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BDD Podcast - an overview and patient experience

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BDD Podcast - an overview and patient experience

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Children don't come with a manual, and parenting can be hard. What is evidence-based parenting training and how can it help? Dr Lucy Maddox interviews Sue Howson and Jane, about their experiences of delivering and receiving this intervention for parents of primary school aged children.
Show Notes and Transcript
Sue...

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Let's Talk About CBT is a podcast about cognitive behavioural therapy: what it is, what it's not and how it can be useful. Dr Lucy Maddox interviews experts in the field including people who have experienced CBT for themselves.

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OCD Podcast - an overview and patient experience

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OCD Podcast - an overview and patient experience

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What are 'intrusiv e thoughts' (we all have them) and what has CBT for OCD got to do with a polar bear? People sometimes talk about being "a little bit OCD", but the reality of obsessive compulsive disorder is much more difficult than a tendency to line your pens up or be super tidy.

Ashley Fulwood talks to Dr Lucy Maddox about his journey towards recovery from OCD with the help of CBT, and Professor Paul Salkovkis explains how CBT works.
Show Notes
Want to know more?
Websites
For more about BABCP check out: babcp.com

To find an accredited therapist: http://cbtregisteruk.com

Ashley's charity, OCD-UK is here, and there is a lot of useful information on their website: https://www.ocduk.org/

And another OCD charity, OCD Action, is here: https://www.ocdaction.org.uk/
Books
Break Free From OCD by Fiona Challacombe, Victoria Bream Oldfield and Paul Salkovskis

Overcoming OCD by David Veale and Rob Wilson

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What are 'intrusive thoughts' (we all have them) and what has CBT for OCD got to do with a polar bear?

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If you run an OCD or BDD support group and would like to list your group on our website, please email office@ocduk.org with the following details and confirmation of the declaration below.

One we have the following information, we will arrange a telephone interview with you to discuss your group, and its suitability for listing for the OCD community. We ask for in order to protect the integrity and independence of support groups and for the welfare of the OCD community. We reserve the right not to list groups at our discretion.

Details about the support group, is it for sufferers, family/friends or open to all

Location of meeting

Image of meeting venue if available

Dates and times of meetings

Is car parking available on-site or nearby

Local travel notes which may help group attendees

Public contact details for group facilitator

Postal address for group facilitator (for internal OCD-UK use only, will not be published)

The group facilitator must confirm the statement below

"I confirm that there is no fee to attend the group, and we promote the use of evidence based therapies (CBT). To avoid conflict of interest I confirm that our support group does not promote any commercial therapy or counselling services affiliated with the group facilitator/s, and that no attempt is made to recruit patients that attend the support group for any private commercial service offered by the group facilitator/s."

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If you run an OCD or BDD support group and would like to list your group on our website, please email office@ocduk.org with the following details and confirmation of the declaration below. One we have the following information, we will arrange a telephone interview with you to discuss your group, and its suitability for listing for the OCD community.

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NHS Panic Disorder Overview and links to recources

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NHS Panic Disorder Overview and links to recources

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Panic disorder is an anxiety disorder where you regularly have sudden attacks of panic or fear.
Everyone experiences feelings of anxiety and panic at certain times. It's a natural response to stressful or dangerous situations.

But someone with panic disorder has feelings of anxiety, stress and panic regularly and at any time, often for no apparent reason.

Symptoms of panic disorder

Anxiety

Anxiety is a feeling of unease. It can range from mild to severe, and can include feelings of worry and fear. Panic is the most severe form of anxiety.

You may start to avoid certain situations because you fear they'll trigger another attack.

This can create a cycle of living "in fear of fear". It can add to your sense of panic and may cause you to have more attacks.

Panic attacks

During a panic attack you get a rush of intense mental and physical symptoms. It can come on very quickly and for no apparent reason.

A panic attack can be very frightening and distressing.

Symptoms include:

a racing heartbeat

feeling faint

sweating

nausea

chest pain

shortness of breath

trembling

hot flushes

chills

shaky limbs

a choking sensation

dizziness

numbness or pins and needles

a need to go to the toilet

ringing in your ears

a feeling of dread or a fear of dying

a churning stomach

a tingling in your fingers

feeling like you're not connected to your body

Most panic attacks last between 5 and 20 minutes. Some have been reported to last up to an hour.

The number of attacks you have will depend on how severe your condition is. Some people have attacks once or twice a month, while others have them several times a week.

Although panic attacks are frightening, they're not dangerous. An attack will not cause you any physical harm, and it's unlikely you'll be admitted to hospital if you have one.

Be aware that most of these symptoms can also be symptoms of other conditions or problems, so you may not always be experiencing a panic attack.

For example, you may have a racing heartbeat if you have very low blood pressure.

When to get help

See a GP if you've been experiencing symptoms of panic disorder.

They'll ask you to describe your symptoms, how often you get them, and how long you have had them.

They may also carry out a physical examination to rule out other conditions that could be causing your symptoms.

It can sometimes be difficult to talk about your feelings, emotions and personal life, but try not to feel anxious or embarrassed.

You may be diagnosed with panic disorder if you have regular and unexpected panic attacks followed by at least a month of continuous worry or concern about having further attacks.

Treatments for panic disorder

Treatment aims to reduce the number of panic attacks you have and ease your symptoms.

Talking therapies and medicine are the main treatments for panic disorder. Your treatment will depend on your symptoms.

Psychological therapies

You can refer yourself directly to a psychological therapies service for treatment based on cognitive behavioural therapy (CBT).

If you prefer, you can see a GP and they can refer you.

Your therapist may discuss with you how you react when you have a panic attack and what you think about.

They can teach you ways of changing your behaviour to help you keep calm during an attack.

You may need to see your GP regularly while you're having CBT so they can assess your progress.

Medicine

If you and your doctor think it might be helpful, you may be prescribed:

Antidepressants can take 2 to 4 weeks before they start to work, and up to 8 weeks to work fully.

Keep taking your medicines, even if you feel they're not working, and only stop taking them if your GP advises you to do so.

Referral to a specialist

If your symptoms do not improve after CBT, medicine and connecting with a support group, your GP may refer you to a mental health specialist such as a psychiatrist or clinical psychologist.

The specialist will carry out an assessment and devise a treatment plan to help you manage your symptoms.

Things you can try yourself

What to do during a panic attack

The next time you feel a panic attack coming on:

do not fight it

stay where you are, if possible

breathe slowly and deeply

remind yourself that the attack will pass

focus on positive, peaceful and relaxing images

remember it's not life threatening

Preventing a further attack

It may help to:

For more help, read how to deal with panic attacks.

You can find mental health apps and tools in the NHS Apps Library.

Support groups

Panic disorder can have a big impact on your life, but support is available. It might help to speak to other people with the same condition, or to connect with a charity.

You may find the following links useful:

Ask your GP about support groups for panic disorder near you.
Find anxiety services in your area

Complications of panic disorder

Panic disorder is treatable and you can make a full recovery. But it's best to get medical help as soon as you can.

If you do not get medical help, panic disorder can escalate and become very difficult to cope with.

You're more at risk of developing other mental health conditions, such as agoraphobia or other phobias, or an alcohol or drug problem.

Having panic disorder may affect your ability to drive. The law requires you to inform the Driver and Vehicle Licensing Agency (DVLA) about a medical condition that could impact your driving ability.

Visit GOV.UK for further information about driving with a disability or health condition.

Causes

As with many mental health conditions, the exact cause of panic disorder is not fully understood.

But it's thought to be linked to a combination of things, including:

a traumatic or very stressful life experience, such as bereavement

having a close family member with panic disorder

an imbalance of neurotransmitters (chemical messengers) in the brain

Panic disorder in children

Panic disorder is more common in teenagers than in younger children.

Panic attacks can be particularly hard for children and young people to deal with. Severe panic disorder may affect their development and learning.

If your child has the signs and symptoms of panic disorder, they should see a GP.

After taking a detailed medical history the GP will carry out a thorough physical examination to rule out any physical causes for the symptoms.

They may refer your child to a specialist for further assessment and treatment. The specialist may recommend a course of CBT for your child.

Screening for other anxiety disorders may also be needed to help find the cause of your child's panic attacks.

Read more about anxiety disorders in children or find out about mental health services for children and young people.

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Panic disorder is an anxiety disorder where you regularly have sudden attacks of panic or fear. Everyone experiences feelings of anxiety and panic at certain times. It's a natural response to stressful or dangerous situations. But someone with panic disorder has feelings of anxiety, stress and panic regularly and at any time, often for no apparent reason.

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A phobia is a fear of a particular thing or situation. Phobias can often have a first triggering event, which then results in the individual feeling very frightened when they then think about, see or are reminded of the feared object / situation.

When a person with a phobia sees or is reminded of the feared object or situation, their mind says they are in danger, which sets off the body's alarm system (adrenaline) resulting in our experiencing many different body sensations. These feelings seem to confirm that we are indeed in terrible danger, and we feel an urge to escape. To stop us experiencing these feelings, we will try to avoid seeing or hearing about the feared object or situation.

Cognitive Behaviour Therapy helps us learn to challenge the unhelpful thoughts and beliefs, combined with gradual exposure to the feared object or situation.

See this page for information about anxiety and the normal body response.

Example of a simple vicious cycle of Phobia

SELF HELP FOR PHOBIAS

Cognitive Behaviour Therapy focuses on learning to challenge the unhelpful thoughts and beliefs, and gradually making changes in our behaviour so that we learn that the feared consequences do not happen, and that it is the anxiety that makes us feel the way we do.

In order to break the vicious cycle of anxiety attacks when exposed to our phobia trigger, we need to change the way we think, and change what we do. Firstly, we can learn about how any anxiety affects our body. This is the body's normal response to danger (or believing we're in danger):

These physical feelings of adrenaline are normal - it is simply the body's alarm system being activated in order to help us escape from a dangerous situation. So it feels dangerous, even if it really isn't.

The feelings will pass. If we could just notice the thoughts and feelings, and not react to them by believing them to be dangerous in themselves, if we could breathe deeply and focus on our breathing and allow the thoughts and feelings to come, and go, then the adrenaline will calm down within a few minutes.

NEEDLE & BLOOD PHOBIAS

With most phobias, the adrenaline response causes our blood pressure to rise, and our heart rate to speed up. This means we are physically unable to faint, even if the adrenaline makes us feel light-headed or dizzy.

However, there are two exceptions to this rule: needle and blood phobias cause a different reaction whereby the increase in blood pressure can be quickly followed by a drop, which causes us to faint. So in cases of needle and blood phobias (and only needle and blood phobias) we can learn to reduce the possibility of fainting, using the applied tension technique.

Sit in a chair and tense the muscles in your arms, legs and body (NOT your head or face) for 10-15 seconds.

Hold the tension until you feel a warmth spread into your face or head.

Release the tension for 20-30 seconds and return your body to its normal sitting state.

Repeat the exercise 5 times over a period of about 5 minutes.

Practise several times a day for at least a week.

After a week, you can start using the technique when you're working through your Avoidance Worksheet doing exposure exercises (for needle and blood phobia).

If this technique triggers headaches, make sure you are tensing ONLY your body, arm and leg muscles, and NOT your face and head muscles.

Thinking Differently - Challenging Thoughts

If we can change the way we think about a situation or about the normal anxiety feelings, then we will not feel so anxious. We can learn to challenge those anxiety-provoking thoughts. We tend to over-estimate the dangerousness of the object or situation and the risk of the worst thing happening, and under-estimate our ability to cope if bad things do happen. Thoughts are not statements of fact. Don't believe everything you think!

Thoughts are just thoughts. We look at life, and situations through distorted lenses. Just because we think this situation or object is dangerous doesn't mean that is how it really is! We are looking at the object or situation, through those very distorted lenses, perhaps as a result of an early experience. There is often an event, earlier in our lives, that happened that could help explain this phobia.

Learn to challenge the unhelpful and distorted thinking:

Thinking Differently: Re-Focus

When we think about being in a situation or when we start to feel anxious, our focus of attention gets totally caught up in the perceived danger and how awful we feel. Our thoughts and the adrenaline makes us feel an overwhelming urge to escape. It can be a horrible experience which leaves us feeling battered and exhausted afterwards - we just want to escape that situation to stop the feelings - and avoid it happening again.

It is very helpful to learn how to change our focus of attention and take more control over how we react to thoughts and feelings. We can learn to just notice the thoughts and physical sensations of anxiety, acknowledge them, then let them pass. Notice the and let it go - turn your focus of attention to something else. First of all, you might learn to focus on your breathing.

Then you might learn and practise Mindfulness skills including Mindful Activity. It's important to practise these skills frequently, every day, so that when you NEED them, you'll be able to use them effectively.

NOW

I am breathing", then notice those sensations in your body
NOW: Mindfulness for Busy People leaflet
MINDFULNESS FOR BUSY PEOPLE

Choose an activity to do mindfully throughout the day, for one, two or five minutes. For example: Drink a cup of tea. Walk. Wash the dishes.

Whatever you are doing, be in that moment, right now. See, hear, smell, touch, feel, breathe.

Simply notice whenever other thoughts and sensations come to mind, then re-focus on your chosen mindful activity.

Be patient and compassionate with yourself.

Describe - rather than judge good or bad, pleasant or unpleasant.

NOW: Mindfulness for Busy People PDF

Doing Differently

Our usual strategy for dealing with phobias, is to avoid our feared object or situation. However, although that helps us avoid becoming anxious, avoiding those objects or situations (where you might be exposed to the fear) just serves to keep the anxiety and panic going because we never find out that things will be ok.

See Overcoming Avoidance to gradually face your fears.

Slowly, we can change what we do. Use the PDF to identify what you don't do or where you don't go, then start by gradually exposing yourself to the least feared situation in the list, using healthy coping strategies in those situations.

Aim to do things gently and gradually, starting with the least feared situation, and gradually work your way up your list to the most feared. For example if you phobia is of enclosed spaces, then your avoidance list may look like this, with the bottom section for your "most feared" completed (after having worked your way up through the list)

It's important that you see the situations through - stick with the anxiety - it will pass.

- there's the again. My body and mind is reacting to the thoughts and anxiety feelings.

- this is just the anxiety talking. Don't believe everything you think! Let's stick with the facts - these thoughts are just opinions ( This situation is safe - the evidence says so. What's the Helicopter view ? The awful danger is imagined and my mind is tricking me. These thoughts and feelings are normal - it's just the body's alarm system doing its job, when it doesn't need to. I can stick with this situation, in order to help me overcome this phobia. It will pass.

- What can I do right now? I can use these strategies:

Where can I put my focus of attention right now? ( Mindfulness & mindful activity). What else can I do that would help me tolerate these thoughts and feelings without reacting to them?

PHOBIAS SELF HELP - this page as PDF

Self Help Resources for Phobias

An Introduction to Coping with Phobias

Introducing Overcoming Phobias: A Practical Guide

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cognitive behavioral therapy for phobias

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A phobia is a fear of a particular thing or situation. Phobias can often have a first triggering event, which then results in the individual feeling very frightened when they then think about, see or are reminded of the feared object / situation.

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Mastering Your Worries: This workbook is designed to provide you with some information about chronic worrying and generalised anxiety disorder and suggested strategies for how you can manage your worrying and anxiety. It is organised into modules that are designed to be worked through in sequence. We recommend that you complete one module before going on to the next. Each module includes information, worksheets, and suggested exercises or activities.

This module provides a general description of anxiety and looks at the symptoms of generalised anxiety disorder.

This module provides an overview of what worrying is, what triggers worrying, and what keeps it going.

This module explores a particular negative belief you might have about worry, that "worrying is uncontrollable". It introduces some helpful techniques to challenge and experiment with this belief.

This module focuses on strengthening your attention so that your mind is not so easily distracted by worries. It will help you stay present-focused, keep your mind on the task at hand and learn to disengage from your worrisome thoughts.

This module explores another negative belief you might have about worry, that "worrying is dangerous". It will guide you through challenging and experimenting with this belief.

This module explores the positive beliefs that you might have about worry and encourages you to challenge and experiment with these beliefs.

Worrying and problem-solving are two very different things. This module describes some valuable strategies for being able to effectively solve problems that you encounter in your day-to-day life.

This module explores more helpful ways of thinking about things that concern you to assist you to feel more capable and less inclined to worry.

This module aims to examine your need for certainty, to look at how this need keeps worrying going, to describe ways of challenging this need, and to discuss how to ultimately accept uncertainty in your life.

This module summarises all the strategies introduced and helps you plan for how to stay on top of your worries in the future, including managing any setbacks that may occur.

Click the link above to download all modules in this workbook at once, as a zip file.

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CCI - Generalised Anxiety Disorder Resources for Clinicians

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Mastering Your Worries: This workbook is designed to provide you with some information about chronic worrying and generalised anxiety disorder and suggested strategies for how you can manage your worrying and anxiety. It is organised into modules that are designed to be worked through in sequence.

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https://www.psychologytools.com/resource/health-anxiety-formulation/

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Many people with a phobia don't need treatment, and avoiding the object of their fear is enough to control the problem.
However, it may not always be possible to avoid certain phobias, such as a fear of flying. In this instance, you may decide to get professional help and advice to find out about treatment options.

Most phobias are curable, but no single treatment is guaranteed to work for all phobias. In some cases, a combination of different treatments may be recommended. The main treatment types are:

Talking treatments

Talking treatments, such as counselling, are often very effective at treating phobias. In particular, cognitive behavioural therapy (CBT) and mindfulness have been found to be very effective for treating phobias.

Cognitive behavioural therapy (CBT)

CBT is a type of counselling that can help you manage your problems by changing the way you think and behave. It can be used to develop practical ways of dealing with your phobia.

One part of the CBT treatment process that's often used to treat simple phobias involves gradual exposure to your fear, so you feel less anxious about it. This is known as desensitisation or exposure therapy.

For example, if you have a fear of snakes (ophidiophobia), your therapist may start by asking you to read about snakes. They may later show you a picture of a snake. They may then arrange for you to visit the reptile house of your local zoo to look at some real snakes. The final step would be for you to hold a snake.

Exposure therapy works by gradually increasing the level of exposure to your fear, which allows you to gain control over your phobia. As the treatment progresses, you should begin to feel less anxious about your phobia.

The National Institute for Health and Care Excellence (NICE) doesn't recommend the use of computerised CBT to treat specific phobias in adults.

Medication

Medication isn't usually recommended for treating phobias, because talking therapies are usually effective and don't have any side effects. However, medication is sometimes prescribed on a short-term basis to treat the effects of phobias, such as anxiety.

There are 3 types of medication recommended for treating anxiety:

Antidepressants

Antidepressants are often prescribed to help reduce anxiety. Selective serotonin reuptake inhibitors (SSRIs) are most often prescribed to treat anxiety, social phobia or panic disorder. These can include:

escitalopram (Cipralex)

sertraline (Lustral)

paroxetine (Seroxat)

Venlafaxine (Efexor), a serotonin and noradrenaline reuptake inhibitor (SNRI) may also be prescribed for anxiety.

Common side effects of these treatments include:

They may also, initially, make your anxiety worse and can cause sexual problems.

Clomipramine (Anafranil) is a type of tricyclic antidepressant (TCA) that's licensed to treat phobias. Side effects include:

Moclobemide (Manerix) is a type of antidepressant from the monoamine oxidase inhibitor (MAOI) group of antidepressants. It's sometimes prescribed to treat social phobia.

Moclobemide interacts with certain types of food, so if you're prescribed this medication, read the information leaflet that comes with it to find out which foods to avoid.

Other possible side effects of moclobemide include:

sleep problems

dizziness

stomach problems

headaches

restlessness

agitation

If you're prescribed antidepressants, it's very important that you don't suddenly stop taking them. Suddenly stopping can cause withdrawal symptoms. See your GP, who can gradually lower your dose.

Tranquillisers

Benzodiazepines are a group of medicines that are categorised as minor tranquillisers. They include medicines such as diazepam (Valium) and are sometimes used on a short-term basis at the lowest possible dose to treat severe anxiety.

Like antidepressants, benzodiazepines should be stopped gradually to avoid withdrawal symptoms.

Beta-blockers

Beta-blockers are often used to treat cardiovascular conditions, such as heart problems and high blood pressure (hypertension). They are also sometimes prescribed to help reduce the symptoms of anxiety, such as palpitations (irregular heartbeat).

Beta-blockers slow down your heart rate and decrease your blood pressure. Propranolol (Inderal) is a beta-blocker that's commonly used to treat anxiety. Possible side effects include:

stomach problems

cold fingers

tiredness

sleep problems

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Many people with a phobia don't need treatment, and avoiding the object of their fear is enough to control the problem. However, it may not always be possible to avoid certain phobias, such as a fear of flying. In this instance, you may decide to get professional help and advice to find out about treatment options.

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Psychology Tools - How Breathing Affects Feelings

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Psychology Tools - How Breathing Affects Feelings

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https://www.getselfhelp.co.uk/docs/models/HealthAnxiety3.pdf

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Psychology Tools - Introspective Exposure

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Psychology Tools - Introspective Exposure

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Obsessive-compulsive disorder and body dysmorphic disorder: treatment | Guidance and guidelines | NICE

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Evidence-based recommendations on treating obsessive-compulsive disorder (OCD) and body dysmorphic disorder (BDD) for adults, young people and children

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Kate d'Ath OCD Psychoeducation Videos on OCD for clients

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Kate d'Ath OCD Psychoeducation Videos on OCD for clients

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1. Katie d'Ath, OCD treatment specialist: Introduction

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CBT Self Help for OCD - Obsessive Compulsive Disorder

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Coping with Panic Attacks: This workbook is designed to provide you with some information about panic attacks and panic disorder and suggested strategies for how you can manage your panic and anxiety. It is organised into modules that are designed to be worked through in sequence. Although it is not necessary that you complete one module before going on to the next, this is recommended. Each module includes information, worksheets, and suggested exercises or activities.

This module describes panic attacks and panic disorder and looks at the symptoms of panic.

The aim of this module is to provide you with some more detailed information on how panic attacks actually develop. This module will also describe how panic attacks develop into panic disorder and what treatment strategies may be useful.

This module describes automatic thoughts and explores how thoughts influence feelings.

This module explores how you can use a thought diary to monitor the unhelpful thoughts that can lead to how you feel about a particular situation.

This module describes a number of common unhelpful thinking styles that can lead to negative emotions.

Module 6 explores how you can examine and challenge unhelpful thoughts by expanding the thought diary described in Module 4.

This module describes how you can summarise how you have challenged unhelpful thoughts by producing a balanced thought.

Core beliefs are often at the root of unhelpful thoughts that are particularly difficult to change. This module looks at core beliefs and how to change them.

The aim of this module is to give you information about how to challenge your beliefs about panic symptoms by actually experiencing them. Research has shown that this is particularly important in being able to successfully overcome panic symptoms and distress about panic symptoms.

The aim of this module is to give you information about exposure to activities and situations in which you are worried that panic attacks might occur.

This module describes how you can reduce your anxiety by gaining control of your breathing.

This final module describes how to maintain gains and continue the progress that has been made throughout the previous modules.

Click the link above to download all modules in this workbook at once, as a zip file.

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Coping with Panic Attacks: This workbook is designed to provide you with some information about panic attacks and panic disorder and suggested strategies for how you can manage your panic and anxiety. It is organised into modules that are designed to be worked through in sequence.

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Professional Reference tools are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines, so you may find the language more technical than the condition leaflets.

This easy-to-use self-administered patient questionnaire is used as a screening tool and severity measure for generalised anxiety disorder (GAD).

The GAD-7 originates from Spitzer RL, Kroenke K, Williams JB, et al; A brief measure for assessing generalized anxiety disorder: the GAD-7. Arch Intern Med. 2006 May 22;166(10):1092-7. GAD-7 © Pfizer Inc. all rights reserved; used with permission.

The GAD-7 score is calculated by assigning scores of 0, 1, 2, and 3, to the response categories of 'not at all', 'several days', 'more than half the days', and 'nearly every day', respectively, and adding together the scores for the seven questions.

Scores of 5, 10, and 15 are taken as the cut-off points for mild, moderate and severe anxiety, respectively. When used as a screening tool, further evaluation is recommended when the score is 10 or greater.

Using the threshold score of 10, the GAD-7 has a sensitivity of 89% and a specificity of 82% for GAD. It is moderately good at screening three other common anxiety disorders - panic disorder (sensitivity 74%, specificity 81%), social anxiety disorder (sensitivity 72%, specificity 80%) and post-traumatic stress disorder (sensitivity 66%, specificity 81%).

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. Egton Medical Information Systems Limited has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

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generalised anxiety disorder assessment (gad7)

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This easy to use self-administered patient questionnaire is used as a screening tool and severity measure for generalised anxiety disorder . [ 13299 :...

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TED Talk: Dr Natascha M Santos 'Debunking the Myths of OCD' 5 min video

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TED Talk: Dr Natascha M Santos 'Debunking the Myths of OCD' 5 min video

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There’s a common misconception that if you like to meticulously organize your things, keep your hands clean, or plan out your weekend to the last detail, you might be OCD. In fact, OCD (Obsessive Compulsive Disorder) is a serious psychiatric condition that is frequently misunderstood by society and mental health professionals alike. Natascha M. Santos debunks the myths surrounding OCD. [Directed by Zedem Media, narrated by Addison Anderson].

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A meta-analysis of treatment outcome and moderators

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A meta-analysis of treatment outcome and moderators

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CBT For Health Anxiety Metanalysis of Treatment outcomes

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Overcoming Health Anxiety: This information package is designed to provide you with some information about health anxiety, including how it develops, how it is maintained, and how to decrease your health worries and concerns. It is organised into modules that are designed to be worked through in sequence. We recommend that you complete one module before going on to the next. Each module includes information, worksheets, and suggested exercises or activities.

This module provides an overview of what health anxiety is, how it can be a problem, and what kind of impact it can have on a person's life.

This module explores, and provides a model of, how health anxiety may develop.

This module explores, and provides a model, of how health anxiety might be triggered and then maintained.

This module explores some attention training exercises aimed at reducing the amount of time you spend focussed on health symptoms and worries.

This module explores how your thoughts can influence your feelings, physiological state, and behaviours. This module then discusses ways to evaluate and overcome unhelpful health related thinking.

This module explores the different ways people check and seek reassurance regarding their health concerns, discusses the difference between helpful and unhelpful checking and reassurance seeking, and introduces strategies to reduce or eliminate these behaviours.

This module explores how avoidance and safety behaviours can keep health anxiety going, and introduces a strategy to gradually reduce and overcome these behaviours.

In this module we will focus on challenging the unhelpful rules and assumptions that can keep you caught in the vicious cycle of health anxiety.

This final module brings all the concepts of this information package together, presents a new model for healthy living, and includes a self-management plan to help you to stay on track in the future.

Click the link above to download all modules in this workbook at once, as a zip file.

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Overcoming Health Anxiety: This information package is designed to provide you with some information about health anxiety, including how it develops, how it is maintained, and how to decrease your health worries and concerns. It is organised into modules that are designed to be worked through in sequence.

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Anxiety  Guided Self Help Guide in Polish Launguage

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MIND: OCD Symptoms, causes, self-help, treatments, useful contacts.

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MIND: OCD Symptoms, causes, self-help, treatments, useful contacts.

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Is a phobia keeping you from doing things you'd like to do? Learn how to recognize, treat, and overcome the problem.

What is a phobia?

Almost everyone has an irrational fear or two-of spiders, for example, or your annual dental checkup. For most people, these fears are minor. But when fears become so severe that they cause tremendous anxiety and interfere with your normal life, they're called phobias.

A phobia is an intense fear of something that, in reality, poses little or no actual danger. Common phobias and fears include closed-in places, heights, highway driving, flying insects, snakes, and needles. However, you can develop phobias of virtually anything. While most phobias develop in childhood, they can also develop in later life.

If you have a phobia, you probably realize that your fear is irrational, yet you still can't control your feelings. Just thinking about the feared object or situation may make you anxious. And when you're actually exposed to the thing you fear, the terror is automatic and overwhelming. The experience is so nerve-wracking that you may go to great lengths to avoid it-inconveniencing yourself or even changing your lifestyle. If you have claustrophobia, for example, you might turn down a lucrative job offer if you have to ride the elevator to get to the office. If you have a fear of heights, you might drive an extra 20 miles in order to avoid a tall bridge.

Understanding your phobia is the first step to overcoming it. It's important to know that phobias are common. (Having a phobia doesn't mean you're crazy!) It also helps to know that phobias are highly treatable. No matter how out of control it feels right now, you can overcome your anxiety and fear and start living the life you want.

Barbara's fear of flying

Barbara is terrified of flying. Unfortunately, she has to travel a lot for work, and this traveling takes a terrible toll. For weeks before every trip, she has a knot in her stomach and a feeling of anxiety that won't go away. On the day of the flight, she wakes up feeling like she's going to throw up. Once she's on the plane, her heart pounds, she feels lightheaded, and she starts to hyperventilate. It gets worse and worse with every flight.

Barbara's fear of flying has gotten so bad that she finally told her boss she can only travel to places within driving distance. Her boss was not happy about this, and Barbara's not sure what will happen at work. She's afraid she'll be demoted or lose her job altogether. But better that, she tells herself, than getting on a plane again.

"Normal" fears vs. phobias or "irrational" fears

It is normal and even helpful to experience fear in dangerous situations. Fear serves a protective purpose, activating the automatic "fight-or-flight" response. With our bodies and minds alert and ready for action, we are able to respond quickly and protect ourselves. But with phobias the threat is nonexistent or greatly exaggerated. For example, it is only natural to be afraid of a snarling Doberman, but it is irrational to be terrified of a friendly poodle on a leash, as you might be if you have a dog phobia.

The difference between normal fear and a phobia

Feeling anxious when flying through turbulence or taking off during a storm

Not going to your best friend's island wedding because you'd have to fly there

Experiencing butterflies when peering down from the top of a skyscraper or climbing a tall ladder

Turning down a great job because it's on the 10th floor of the office building

Getting nervous when you see a pit bull or a Rottweiler

Steering clear of the park because you might see a dog

Feeling a little queasy when getting a shot or when your blood is being drawn

Avoiding necessary medical treatments or doctor's checkups because you're terrified of needles

Normal fears in children

Many childhood fears are natural and tend to develop at specific ages. For example, many young children are afraid of the dark and may need a nightlight to sleep. That doesn't mean they have a phobia. In most cases, they will grow out of this fear as they get older.

For example, the following childhood fears are extremely common and considered normal:

0-2 years - Loud noises, strangers, separation from parents, large objects.

3-6 years - Imaginary things such as ghosts, monsters, the dark, sleeping alone, strange noises.

7-16 years - More realistic fears such as injury, illness, school performance, death, natural disasters.

If your child's fear is not interfering with their daily life or causing them a great deal of distress, then there's little cause for undue concern. However, if the fear is interfering with your child's social activities, school performance, or sleep, you may want to see a qualified child therapist.

Common types of phobias and fears

There are four general types of phobias and fears:

1. Animal phobias such as the fear of snakes, spiders, rodents, and dogs.

2. Natural environment phobias such as a fear of heights, storms, water, and of the dark.

3. Situational phobias (fears triggered by a specific situation) including the fear of enclosed spaces (claustrophobia), flying, driving, tunnels, and bridges.

4. Blood-Injection-Injury phobia, the fear of blood, injury, illness, needles, or other medical procedures.

Some phobias, however, don't fall into one of the four common categories. These include fear of choking, fear of getting a disease such as cancer, and fear of clowns. Other common phobias that don't fit neatly into any of the four categories include:

Social phobia, also called social anxiety disorder, is fear of social situations where you may be embarrassed or judged. If you have social phobia, then you may be excessively self-conscious and afraid of humiliating yourself in front of others. Your anxiety over how you will look and what others will think may lead you to avoid certain social situations you'd otherwise enjoy.

Fear of public speaking-an extremely common phobia-is a type of social phobia. Other fears associated with social phobia include fear of eating or drinking in public, talking to strangers, taking exams, mingling at a party, or being called on in class.

Agoraphobia was traditionally thought to involve a fear of public places and open spaces, but is now believed to develop as a complication of panic attacks.

If you're afraid of having another panic attack, you become anxious about being in situations where escape would be difficult or embarrassing. For example, you're likely to avoid crowded places such as shopping malls and movie theaters. You may also avoid cars, airplanes, subways, and other forms of travel. In more severe cases, you might only feel safe at home.

Signs and symptoms of phobias

The symptoms of a phobia can range from mild feelings of apprehension and anxiety to a full-blown panic attack. Typically, the closer you are to the thing you're afraid of, the greater your fear will be. Your fear will also be higher if getting away is difficult.

Physical symptoms of a phobia include:

Difficulty breathing

Racing or pounding heart

Chest pain or tightness

Trembling or shaking

Feeling dizzy or light-headed

A churning stomach

Hot or cold flashes; tingling sensations

Sweating

Emotional symptoms of a phobia include:

Feeling overwhelming anxiety or panic

Feeling intense need to escape

Feeling "unreal" or detached from yourself

Fear of losing control or going crazy

Feeling like you're going to die or pass out

Knowing that you're overreacting, but feeling powerless to control fear

Symptoms of blood-injection-injury phobia

The symptoms of blood-injection-injury phobia are slightly different from other phobias. When confronted with the sight of blood or a needle, you experience not only fear, but also disgust.

Like other phobias, you initially feel anxious as your heart speeds up. However, unlike other phobias, this acceleration is followed by a quick drop in blood pressure, which leads to nausea, dizziness, and fainting. Although a fear of fainting is common in all specific phobias, blood-injection-injury phobia is the only phobia where fainting can actually occur.

When to seek help for phobias and fears

Although phobias are common, they don't always cause considerable distress or significantly disrupt your life. For example, if you have a snake phobia, it may cause no problems in your everyday activities if you live in a city where you're not likely to run into one. On the other hand, if you have a severe phobia of crowded spaces, living in a big city would pose a problem.

If your phobia doesn't impact your life that much, it's probably nothing to be concerned about. But if avoidance of the object, activity, or situation that triggers your phobia interferes with your normal functioning, or keeps you from doing things you would otherwise enjoy, it's time to seek help.

Consider treatment for your phobia if:

It causes intense and disabling fear, anxiety, and panic

You recognize that your fear is excessive and unreasonable

You avoid certain situations and places because of your phobia

Your avoidance interferes with your normal routine or causes significant distress

You've had the phobia for at least six months

Treating a phobia

Self-help strategies and therapy can both be effective at treating a phobia. What's best for you depends on factors such as the severity of your phobia, your access to professional therapy, and the amount of support you need.

As a general rule, self-help is always worth a try. The more you can do for yourself, the more in control you'll feel-which goes a long way when it comes to phobias and fears. However, if your phobia is so severe that it triggers panic attacks or uncontrollable anxiety, you may want to seek additional support.

Therapy for phobias has a great track record. Not only does it work extremely well, but you tend to see results very quickly-sometimes in as a little as one to four sessions. However, support doesn't have to come in the guise of a professional therapist. Just having someone to hold your hand or stand by your side as you face your fears can be extremely helpful.

Phobia self-help tip 1: Face your fears, one step at a time

It's only natural to want to avoid the thing or situation you fear. But when it comes to conquering phobias, facing your fears is the key. While avoidance may make you feel better in the short-term, it prevents you from learning that your phobia may not be as frightening or overwhelming as you think. You never get the chance to learn how to cope with your fears and experience control over the situation. As a result, the phobia becomes increasingly scarier and more daunting in your mind.

The most effective way to overcome a phobia is by gradually and repeatedly exposing yourself to what you fear in a safe and controlled way. During this exposure process, you'll learn to ride out the anxiety and fear until it inevitably passes. Through repeated experiences facing your fear, you'll begin to realize that the worst isn't going to happen; you're not going to die or "lose it." With each exposure, you'll feel more confident and in control. The phobia begins to lose its power.

It's important to begin with a situation that you can handle, and work your way up from there, building your confidence and coping skills as you move up the "fear ladder."

Make a list. Make a list of the frightening situations related to your phobia. If you're afraid of flying, your list (in addition to the obvious, such as taking a flight or getting through takeoff) might include booking your ticket, packing your suitcase, driving to the airport, watching planes take off and land, going through security, boarding the plane, and listening to the flight attendant present the safety instructions.

Build your fear ladder. Arrange the items on your list from the least scary to the most scary. The first step should make you slightly anxious, but not so frightened that you're too intimidated to try it. When creating the ladder, it can be helpful to think about your end goal (for example, to be able to be near dogs without panicking) and then break down the steps needed to reach that goal.

Work your way up the ladder. Start with the first step and don't move on until you start to feel more comfortable doing it. If possible, stay in the situation long enough for your anxiety to decrease. The longer you expose yourself to the thing you're afraid of, the more you'll get used to it and the less anxious you'll feel when you face it the next time. Once you've done a step on several separate occasions without feeling too much anxiety, you can move on to the next step. If a step is too hard, break it down into smaller steps or go slower.

Practice. The more often you practice, the quicker your progress will be. However, don't rush. Go at a pace that you can manage without feeling overwhelmed. And remember: you will feel uncomfortable and anxious as you face your fears, but the feelings are only temporary. If you stick with it, the anxiety will fade.

Facing a fear of dogs: A sample fear ladder

Step 1: Look at pictures of dogs.

Step 2: Watch a video with dogs in it.

Step 3: Look at a dog through a window.

Step 4: Stand across the street from a dog on a leash.

Step 5: Stand 10 feet away from a dog on a leash.

Step 6: Stand five feet away from a dog on a leash.

Step 7: Stand beside a dog on a leash.

Step 8: Pet a small dog that someone is holding.

Step 9: Pet a larger dog on a leash.

Step 10: Pet a larger dog off leash.

If you start to feel overwhelmed...

While it's natural to feel scared or anxious as you face your phobia, if you start to feel overwhelmed, immediately back off and use the techniques outlined below to quickly calm your nervous system.

Tip 2: Learn to calm down quickly

When you're afraid or anxious, you experience a variety of uncomfortable physical symptoms, such as a racing heart and a suffocating feeling. These physical sensations can be frightening themselves-and a large part of what makes your phobia so distressing. However, by learning how to calm yourself down quickly, you can become more confident in your ability to tolerate uncomfortable sensations and face your fears.

Perform a simple deep breathing exercise. When you're anxious, you tend to take quick, shallow breaths (known as hyperventilating), which actually adds to the physical feelings of anxiety. By breathing deeply from the abdomen, you can reverse these physical sensations and feel less tense, less short of breath, and less anxious. Practice when you're feeling calm until you're familiar and comfortable with the exercise.

Sit or stand comfortably with your back straight. Put one hand on your chest and the other on your stomach.

Take a slow breath in through your nose, counting to four. The hand on your stomach should rise. The hand on your chest should move very little.

Hold your breath for a count of seven.

Exhale through your mouth to a count of eight, pushing out as much air as you can while contracting your abdominal muscles. The hand on your stomach should move in as you exhale, but your other hand should move very little.

Inhale again, repeating the cycle until you feel relaxed and centered.

Practice this deep breathing technique for five minutes twice day. When you're comfortable with the technique, you can use it when you're facing your phobia or in another stressful situation.

Use your senses

One of the quickest and most reliable ways to relieve anxiety is by engaging one or more of your senses-sight, sound, taste, smell, touch-or through movement. But since everyone is different, you'll need to do some experimenting to discover what works best for you.

Movement - Go for a walk, jump up and down, or gently stretch. Dancing, drumming, and running can be especially effective at relieving anxiety.

Sight - Look at anything that relaxes you or makes you smile: a beautiful view, family photos, cat pictures on the Internet.

Sound - Listen to soothing music, sing a favorite tune, or play a musical instrument. Or enjoy the relaxing sounds of nature (either live or recorded): ocean waves, wind through the trees, birds singing.

Smell - Light scented candles. Smell the flowers in a garden. Breathe in the clean, fresh air. Spritz on your favorite perfume.

Taste - Slowly eat a favorite treat, savoring each bite. Sip a cup of coffee or herbal tea. Chew on a stick of gum. Enjoy a mint or your favorite hard candy.

Touch - Give yourself a hand or neck massage. Cuddle a pet. Wrap yourself in a soft blanket. Sit outside in the cool breeze.

Meditation for stress and anxiety relief

When fear or anxiety starts to carry you away, meditating can help stop it in its tracks. And with regular practice, meditation boosts activity in the area of the brain responsible for feelings of serenity, helping to quell fear and panic before they strike.

Tip 3: Challenge negative thoughts about your phobia

When you have a phobia, you tend to overestimate how bad it will be if you're exposed to the situation you fear and underestimate your ability to cope. The anxious thoughts that trigger and fuel phobias are usually negative and unrealistic. By writing down the negative thoughts you have when confronted by your phobia, you can begin to challenge these unhelpful ways of thinking. Many times, these thoughts fall into the following categories:

Fortune telling. For example, "This bridge is going to collapse;" "I'll make a fool of myself for sure;" "I will definitely lose it when the elevator doors close."

Overgeneralization. "I fainted once while getting a shot. I'll never be able to get a shot again without passing out;" "That pit bull lunged at me. All dogs are dangerous."

Catastrophizing. "The captain said we're going through turbulence. The plane is going to crash!" "The person next to me coughed. Maybe it's swine flu. I'm going to get very sick!"

Once you've identified your negative thoughts, evaluate them. Use the following example to get started.

Negative thought: "The elevator will break down and I'll get trapped and suffocate."

Ask yourself the following 4 questions:
1. Is there any evidence that contradicts my negative thought?

Yes, for example: "People are currently using the elevator and it hasn't broken down."

"Even if it did break down, I've never heard of anyone dying from suffocation in an elevator. There are air vents which would stop the air from running out."

"I've never been in an elevator that has broken down."

2. Could you do anything to resolve this situation if it does occur?

"Yes, I could press the alarm or use the telephone to call for assistance."

"I'm fortune telling, as there is no evidence to suggest that the elevator will break down or that I'd suffocate."

"I would tell a friend that the chances of the elevator breaking down are very slim, it's not something you hear about happening very often."

It's also helpful to come up with some positive coping statements that you can tell yourself when facing your phobia. For example:

"I've felt this way before and nothing terrible happened. It may be unpleasant, but it won't harm me."

"If the worst happens and I have a panic attack while I'm driving, I'll simply pull over and wait for it to pass."

"I've flown many times and the plane has never crashed. Statistically, flying is very safe."

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Almost everyone has an irrational fear or two-of spiders, for example, or your annual dental checkup. For most people, these fears are minor. But when fears become so severe that they cause tremendous anxiety and interfere with your normal life, they're called phobias.

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Journal Article: 'What Drives OCD Symptom Change During CBT Treatment?'

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Journal Article: 'What Drives OCD Symptom Change During CBT Treatment?'

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Panic disorder

The main symptoms of panic disorder are attacks of intense fear and discomfort that happen unexpectedly and repeatedly. There may also be physical symptoms such as chest pain, sickness, dizziness, a racing heart beat, breathlessness, sweating or shaking. People with panic disorder may avoid situations that they think might lead to a panic attack. They may also fear or avoid public spaces (this is known as agoraphobia).

A person experiencing a panic attack may go to a hospital accident and emergency department mistakenly thinking they are having a heart attack because their heart rate is so high. If this happens to you, after the healthcare professionals have ruled out any physical cause of your symptoms, they should ask you about any previous treatment, give you information about panic disorder and advise you to see your GP. In most cases, you should not be admitted to hospital if you have had a panic attack.

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Generalised anxiety disorder and panic disorder in adults: management

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The main symptoms of panic disorder are attacks of intense fear and discomfort that happen unexpectedly and repeatedly. There may also be physical symptoms such as chest pain, sickness, dizziness, a racing heart beat, breathlessness, sweating or shaking. People with panic disorder may avoid situations that they think might lead to a panic attack.

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If another person was doing this, you might call it abuse or bullying. Someone who says, over and over: "No. That's not good enough. Do it again." Who torments you and won't let you go to sleep. You might even call it torture.

Except it's happening inside my own head, so I can't get away from it. That's what obsessive compulsive disorder(OCD) feels like: it's a bully I can't escape from.

"Some people think OCD is a joke, or it's just being really neat or tidy. That's not what it's like."

In fact, the World Health Organisation views it as one of the top ten most disabling health conditions there are.

It has even made me feel like I want to burn my house down.

My OCD makes cleaning and tidying difficult. I'll set aside time to sort out a particular room, then just do one thing over and over. It's hard to let anyone else help me, because I feel anxious if someone else touches my belongings. So it can take me months to tidy one room.

I wanted to tidy my spare room. The first thing I did was fold up a duvet. My OCD told me I had to fold that duvet again and again and again. Each time, it wasn't good enough. It kept telling me I had to try again. Just once more. Nope, still not good enough.

After three hours, I phoned the Samaritans and told them I felt like setting my house on fire because my OCD wouldn't let me put anything right.

I realised I had OCD in 2013, while watching the BBC documentary Don't Call Me Crazy. It featured someone with OCD who said: "I was up until 2am straightening some CDs." I'd never heard someone else say something like this before. Suddenly lots of things made sense.

"Talking about it can be really hard because it sounds so ridiculous, like phoning the Samaritans because I couldn't fold a duvet. It might sound absurd, but I felt like I was losing my mind."

I started working for Mind in 2016 and eventually plucked up the courage to start telling people I had OCD. It shouldn't be the case that I'm lucky to work with people who understand, but sadly I know that it's true.

It helped me to realise that, no matter how many times I do something, I'll never feel like it's done and finished. My brain just won't let me. So when my OCD says: "Just fold that duvet one more time," I try to remember that I'll still feel the same whether I do it or not.

Self-care has been really important, too. My OCD wants me to believe I'm a terrible person who can't do anything right. That makes it hard to do nice things for myself. But something simple, like cuddling my cat or listening to music, can make me feel calmer. It has also helped to learn breathing exercises for when I'm really anxious.

Having OCD can feel really isolating. It can really help to talk to other people with similar experiences, or just to read their stories. It's important to remember that you are not alone, and that things can get better.

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If another person was doing this, you might call it abuse or bullying. Someone who says, over and over: "No. That's not good enough. Do it again." Who torments you and won't let you go to sleep. You might even call it torture. Except it's happening inside my own head, so I can't get away from it.

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CBT for Health Anxiety: A Systematic Review and Meta-Analysis

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CBT for Health Anxiety: A Systematic Review and Meta-Analysis

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Obsessive Compulsive Disorder Inventory can be completed online or  downloaded as PDF

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Obsessive Compulsive Disorder Inventory can be completed online or  downloaded as PDF

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Psychiatr Clin North Am. Author manuscript; available in PMC 2013 Jun 17.

Published in final edited form as:

Elizabeth I. Martin, PhD, a,* Kerry J. Ressler, MD, PhD, b, c Elisabeth Binder, MD, PhD, d, e, f and Charles B. Nemeroff, MD, PhD a

INTRODUCTION TO EMOTIONAL PROCESSING

Mood and anxiety disorders are characterized by a variety of neuroendocrine, neurotransmitter, and neuroanatomical disruptions. Identifying the most functionally relevant differences is complicated by the high degree of interconnectivity between neurotransmitter- and neuropeptide-containing circuits in limbic, brain stem, and higher cortical brain areas. Furthermore, a primary alteration in brain structure or function or in neurotransmitter signaling may result from environmental experiences and underlying genetic predisposition; such alterations can increase the risk for psychopathology.

Functional Anatomy

Symptoms of mood and anxiety disorders are thought to result in part from disruption in the balance of activity in the emotional centers of the brain rather than in the higher cognitive centers. The higher cognitive centers of the brain reside in the frontal lobe, the most phylogenetically recent brain region. The prefrontal frontal cortex (PFC) is responsible for executive functions such as planning, decision making, predicting consequences for potential behaviors, and understanding and moderating social behavior. The orbitofrontal cortex (OFC) codes information, controls impulses, and regulates mood. The ventromedial PFC is involved in reward processing1 and in the visceral response to emotions.2 In the healthy brain, these frontal cortical regions regulate impulses, emotions, and behavior via inhibitory top-down control of emotional-processing structures (eg,3).

The emotional-processing brain structures historically are referred to as the "limbic system" ( Fig. 1 ). The limbic cortex is part of the phylogenetically ancient cortex. It includes the insular cortex and cingulate cortex. The limbic cortex integrates the sensory, affective, and cognitive components of pain and processes information regarding the internal bodily state.4,5 The hippocampus is another limbic system structure; it has tonic inhibitory control over the hypothalamic stress-response system and plays a role in negative feedback for the hypothalamic-pituitary-adrenal (HPA) axis. Hippocampal volume and neurogenesis (growth of new cells) in this structure have been implicated in stress sensitivity and resiliency in relationship to mood and anxiety disorders. An evolutionarily ancient limbic system structure, the amygdala, processes emotionally salient external stimuli and initiates the appropriate behavioral response. The amygdala is responsible for the expression of fear and aggression as well as species-specific defensive behavior, and it plays a role in the formation and retrieval of emotional and fear-related memories. ( Fig. 2 depicts the amygdala's involvement in fear circuitry). The central nucleus of the amygdala (CeA) is heavily interconnected with cortical regions including the limbic cortex. It also receives input from the hippocampus, thalamus, and hypothalamus.

Neuroendocrine and Neurotransmitter Pathways

In addition to the activity of each brain region, it also is important to consider the neurotransmitters providing communication between these regions. Increased activity in emotion-processing brain regions in patients who have an anxiety disorder could result from decreased inhibitory signaling by γ-amino-butyric-acid (GABA) or increased excitatory neurotransmission by glutamate.

Well-documented anxiolytic and antidepressant properties of drugs that act primarily on monoaminergic systems have implicated serotonin (5-hydroxytryptamine, 5-HT), norepinephrine (NE), and dopamine (DA) in the pathogenesis of mood and anxiety disorders. Genes whose products regulate monoaminergic signaling have become a prime area of research in the pathophysiology of mood and anxiety disorders, and they are thought to be critical for the mechanism of action of antidepressant drugs. Monoaminergic regulators include transmitter receptors; vesicular monoamine transporter (vMAT), which packages these neurotransmitters into vesicles; the vasopressin (AVP), oxytocin, and vasopressin (AVP), oxytocin, and transmitter-specific reuptake transporters serotonin transporter (SERT), neurotonin transporter, and dopamine transporter; the enzyme monoamine oxidase, which degrades 5-HT, DA, and NE; and the enzyme catecholamine-O-methyltransferase (COMT), which degrades DA and NE.

In the central nervous system, classic neurotransmitters often are packaged and co-released with neuropeptides, many of which are expressed in limbic regions where they can influence stress and emotion circuitry ( Table 1 ). The functional implications of these limbic co-localizations have been addressed in numerous reviews (eg,6-12). Neuropeptides with particularly strong links to psychopathology include cholecystokinin (CCK), galanin, neuropeptide Y (NPY), vasopressin (AVP), oxytocin, and corticotropin-releasing factor (CRF), among others. CCK is found in the gastrointestinal system and vagus nerve and is located centrally in numerous limbic regions (reviewed in13). Galanin is co-localized with monoamines in brainstem nuclei. It influences pain processing and feeding behavior and also regulates neuroendocrine and cardiovascular systems.14-16 NPY is known for its orexigenic effects and is expressed abundantly in the central nervous system, where it is co-localized with NE in the hypothalamus, hippocampus, and amygdala (reviewed in13). Centrally, oxytocin regulates reproductive, maternal, and affiliative behavior.17,18 Central AVP regulates fluid homeostasis but also can co-localize with oxytocin to influence affiliative behavior19 or with CRF to regulate the HPA axis.

Table 1

Neuropeptide

Role in Stress-neurobiology

Role in Psychopathology

Cholecystokinin (CCK)
(Brawman-Mintzer et al., 1997;
Koszycki et al., 2004)

Weak ACTH secretagogue

Anxiogenic
Exogenous CCK evokes anxiety;
patients who have anxiety
disordersare hypersensitive

Galanin (Gal)
(Barrera et al., 2005;
Karlsson and Holmes, 2006)

Increased by physiological
and psychological
stress and pain

Depressogenic
Galanin antagonists are being
developed and possess
antidepressant properties

Neuropeptide Y (NPY)
(Hashimoto et al., 1996;
Heilig, 2004; Martin, 2004; Sajdyk et al., 2004;
Hou et al., 2006;
Yehuda et al., 2006;
Karl and Herzog, 2007)

Increased during stress
Endogenous alarm system
Stress-induced increase
in feeding
Modulate behavior to
cope with
chronic stress.

Oxytocin (OT)
Gimpl and Fahrenholz, 2001)

Weak ACTH
secretagogue

Low OT in CSF is associated
with depression in women

Vasopressin (AVP)
(van Londen et al., 1997; Ma et al., 1999;
Wigger et al., 2004;
Goekoop et al., 2006)

Increased by stress Moderate ACTH
secretagogue
synergize to stimulate
ACTH production
and release

Potentially elevated in
depression

Corticotropin-releasing
factor

Increased by stress Primary ACTH
secretagogue

Elevated in MDD, PD, PTSD;
associated with HPA
axis hyperactivity in MDD and
HPA axis hypoactivity in PTSD

CRF in parvocellular neurons of the hypothalamic paraventricular nucleus is the primary secretagogue for the HPA axis in response to a threatening stimulus. AVP synergizes with CRF in HPA axis activation. In the HPA axis, CRF is released from the paraventricular nucleus and acts on receptors in the anterior pituitary to elicit production and release of adrenocorticotropic hormone (ACTH), which is released systemi-cally and activates production and release of glucocorticoids from the adrenal cortex. In humans, the main stress steroid is cortisol; in rats it is corticosterone. HPA axis activity is regulated by numerous other limbic system structures, including the amygdala, which enhances HPA axis activity, and the hippocampus, which suppresses HPA axis activation ( Fig. 3 ).

Standardized endocrine challenge tests to assess HPA axis activity include the dexamethasone suppression test and the CRF stimulation test. In the dexamethasone suppression test, systemic administration of dexamethasone, a synthetic glucocorticoid, decreases (ie, suppresses) plasma ACTH and cortisol concentrations via negative feedback at the level of the pituitary gland. In the CRF stimulation test, intravenously administered CRF (which does not enter the central nervous system) elevates plasma ACTH and cortisol concentrations by stimulating CRF ₁ receptors in the anterior pituitary. A combination of the dexamethasone suppression test and the CRF stimulation test, the Dex/CRF test, developed by Holsboer and colleagues, generally is considered to be the most sensitive measure of HPA axis activity.

Genetic Contribution to Emotionality

Each anxiety disorder, as well as major depressive disorder (MDD), has both genetic and environmental contributions to vulnerability. In attempts to identify the genetic contribution for psychopathology, the candidate genes have largely been the same across diagnoses. Researchers have tended to concentrate on the genes whose products regulate the HPA axis and monoaminergic signaling. Ongoing research supports the hypothesis that a genetic predisposition may be shared among mood and anxiety disorders, with the individual clinical manifestation being a product of both genetic and environmental influences. In particular, epigenetic factors may permit a remarkably complex range of gene-environment interactions.

Among the limited longitudinal studies available, there is much support for a "developmental dynamic pattern" regarding the influence of genetic factors on individual differences in symptoms of depression and anxiety. In this model, the impact of genes on psychopathology changes so that different developmental stages are associated with a unique pattern of risk factors. This model is in sharp contrast to a "developmental stable model" in which the genetic contribution to psychopathology is mediated by one set of risk factors that do not change with the age of the subject.20

Another approach for assessing the impact of genes on risk for psychopathology focuses not on diagnostic class but on more circumscribed phenotypic characteristics. A recent study assessed anxious behavioral characteristics in children between 7 and 9 years of age. They found shared and specific genetic effects on anxiety-related behavior but no single underlying factor, supporting the hypothesis that genes are involved in the general predisposition for anxiety-related behavior and also for specific symptom subtypes.21

PANIC DISORDER

Anatomical and Neuroimaging Findings in Panic Disorder

Neuroimaging in patients who have panic disorder (PD) under resting conditions and under anxiety- or panic-provoking conditions has identified neuroanatomical alterations associated with symptom severity or treatment response.

Imaging analyses of patients who have PD who are in an anxious (but not panicked) state also have provided important data. Upon presentation of threatening words in fMRI studies, the left posterior cingulate and left medial frontal cortex were activated in these patients.25 Others have shown that presentation of negative emotional words elicits activations in the right amygdala and right hippocampus in patients who have PD.26 When patients who have PD are presented with anxiety-provoking visual stimuli, they exhibit increased activity in the inferior frontal cortex, hippocampus, anterior cingulate cortex (ACC), posterior cingulate cortex (PCC), and OFC.27 Compared with healthy control subjects, patients who had PD exhibited less activation in the ACC and amygdala when shown pictures of angry faces. These latter results were interpreted as a blunted response caused by chronic hyperactivity in these circuits in patients who had PD.28

Neuroendocrine and Neurotransmitter Signaling in Panic Disorder

Amino acid neurotransmitters

Decreased inhibitory signaling has been hypothesized to play an important pathophysiological role in PD. In drug-free patients who had PD, increased benzodiazepine binding in the temporal cortex and right lateral frontal gyrus29 but decreased binding in the left hippocampus30,31 has been observed. In patients who have PD and comorbid MDD treated with antidepressant medications, benzodiazepine binding was decreased in the lateral temporal lobes, left medial inferior temporal lobe, and bilateral OFC. Binding in the insular cortex bilaterally was negatively correlated with panic severity and with comorbid depression.32

Magnetic resonance spectroscopy (MRS) has demonstrated decreased GABA concentrations in the occipital cortex,33 ACC, and basal ganglia34 in patients who have PD compared with control subjects. Although there is no evidence for differences in plasma or cerebrospinal fluid (CSF) GABA concentrations in patients who have PD,33 low baseline CSF GABA concentrations did correlate with a poor therapeutic response to the triazolobenzodiazepine alprazolam or the tricyclic antidepressant imipramine. Interestingly, patients who have PD and who have a family history of mood and anxiety disorders exhibit decreased cortical GABA concentrations (reviewed in35).

Elevated excitatory glutamatergic signaling is associated with panicogenicity, and drugs that reduce glutamate availability are hypothesized to possess anxiolytic properties. For example, LY354740, an agonist on presynaptic metabotropic glutamate receptors (mGluR II), leads to decreased release of glutamate. This drug decreases anxiety-like behavior in the fear-potentiated startle paradigm in experimental animals.36 LY354740 and other presynaptic metabotropic glutamate agonists also exert neuroprotective effects. In human studies, LY354740 and related drugs decrease subjective anxiety in a conditioned-fear paradigm in healthy volunteer subjects. In patients who have PD, mGluR II agonists are protective against panicogenic agents such as carbon dioxide inhalation (reviewed in37).

Monoamines

Monoaminergic drugs, including tricyclic antidepressants and selective serotonin-reuptake inhibitors (SSRIs), are effective in the treatment of PD. Two SSRIs, fluvoxamine and paroxetine, had a more rapid onset of action and a better therapeutic response on PD symptoms than achieved with cognitive behavioral therapy (CBT) (reviewed in38). The dose of paroxetine needed to treat PD optimally is higher than that required for MDD, suggesting that the mechanism by which SSRIs reduce panic symptoms may be distinct from their mechanism of antidepressant action.39 Patients who have PD exhibit an increased anxiogenic response to administration of the 5-HT 2c/5-HT ₃ agonist meta-chlorophenylpiperazine (mCPP).40 In PET studies, 5HT 1A receptor binding is decreased in the cingulate cortex and raphe nucleus of patients who have PD. SPECT studies have revealed decreased SERT binding in the midbrain, bilateral temporal lobe, and thalamus. The magnitude of the decrease correlates with symptom severity and also normalizes in patients who have PD in remission (reviewed in35). Together, these data support a role for serotonergic circuits in the pathogenesis of PD.

Noradrenergic involvement in PD is evidenced by challenge with the α2 antagonist yohimbine. Yohimbine-elicited panic-like anxiety in patients who have PD is associated with elevated cardiovascular activity and increased serum NE concentrations. There is some evidence that the α2 agonist clonidine has an anxiolytic effect. Patients who have anxiety disorders, including PD, often exhibit a blunted growth hormone response to clonidine administration, suggesting that presynaptic NE autoreceptors are supersensitive (reviewed in35). Overall, these data suggest that patients who have PD have alterations in NE circuits, and this system therefore may represent a target for novel treatment development.

Neuropeptides

Although CCK is a well-known panic-inducing agent even in healthy volunteers, few studies have specifically addressed the role of CCK in panic disorder. Chronic imipramine treatment decreases the acute anxiety-inducing effects of CCK, but this finding does not speak to a role for endogenous CCK systems in PD (reviewed in13).

A recent study also identified an association between galanin and symptom severity in female patients who had PD but had no effect on risk for PD. The associated single-nucleotide polymorphisms (SNPs) were within CpG dinucleotides of the galanin promoter, suggesting that epigenetic factors could explain the influence of galanin on PD severity.41

Corticotropin-releasing factor and the hypothalamic-pituitary-adrenal axis

Patients who have PD have been reported to exhibit increased baseline plasma cortisol concentration, which is positively correlated with the risk for a panic attack after lactate administration. These data suggest that elevated baseline plasma cortisol represents a state of anticipatory anxiety, but not panic itself. The underlying biology of elevated basal cortisol concentrations may be related to increases in CRF concentrations in the CSF of patients who have PD (reviewed in35).

The HPA axis in patients who have PD has been assessed at rest over a full circadian cycle, before and after activation by a panicogenic agent that does not independently activate the HPA axis (doxapram) and before and after administration of a panicogenic agent that does activate the HPA axis (the CCK-B agonist pentagastrin). Increased overnight plasma cortisol concentrations corresponding to sleep disruption have been noted in subjects who have PD; this increase is a trait rather than a statedependent marker of PD. In the doxapram challenge study, an exaggerated increase in plasma ACTH was observed in the patients who had PD. Compared with healthy control subjects, plasma ACTH concentrations were elevated following pentagastrin administration in patients who had PD. Taken together, these data support the hypothesis that patients who have PD are hypersensitive to the HPA axis-activating effects of situations that are novel, threatening, and uncontrollable. After the basal state was established reliably, the ACTH response to CRF administration was not altered in patients who had PD, suggesting that the previous studies were confounded by the effects of the novel environment on the HPA axis (reviewed in42).

Genetic Contribution to Panic Disorder

PD is thought to be the most heritable of the anxiety disorders. First-degree relatives of proband patients who have PD have a sevenfold increased likelihood for PD and also have an increased risk for phobic disorders.43-45 Twin studies suggest that 30% to 40% of the variance in vulnerability for PD is derived from genetic factors and the remainder from individual-specific, but not shared, environment/life experiences.43

Linkage studies in families that have PD have been hampered by non-replication and small numbers.45,46 A large analysis including 120 pedigrees with more than 1500 individuals revealed two loci with genome-wide significance on chromosomes 2q and 15q, but these results await further replication.47 A large number of genetic association studies for PD have been published, implicating many genes. A recent review compiled the genes that have been associated with PD in more than one study thus far, although in some cases different polymorphisms within these genes have been associated with PD in different studies, complicating any attempt to draw causal conclusions from these data (reviewed in45). The genes associated with PD in multiple studies are:

In addition to the aforementioned target genes, polymorphisms in SLC6A4, the gene for the serotonin transporter, also have been associated with PD. The association, however, is not with the well-studied promoter-length polymorphism.48 Rather, SNPs within the serotonin transporter gene show association with PD and comorbid PD/social anxiety disorder (SAD). Subjects who have at least one copy of haplotype A-A-G from rs3794808, rs140701, and rs4583306 have 1.7 times the odds of PD than subjects with no copy of this haplotype.49 In combination with associations of other genes within the monoamine system mentioned earlier in this article, these data support the hypothesis that monoaminergic systems are involved in anxiety disorders as a group; their exact role may be disorder specific.

Although most genetic-association studies have investigated only single polymorphism contributions, it is very likely that a combination of polymorphisms in sets of candidate genes act in concert to increase the risk for this disorder. In fact, a recent study investigating the contribution of genetic variants in the CRF and AVP system reported that the strongest results were the combined effects of rs878886 in CRF ₁ and rs28632197 in the gene encoding the vasopressin 1B receptor ( AVP1B).50 A model with two SNPs showed significant associations with PD in both samples separately, and significance improved to P 5 .00057 in the combined sample of 359 cases and 794 controls. Both SNPs are of potential functional relevance, because rs878886 is located in the 3′ untranslated region of the CRF₁ gene, and rs28632197 leads to an arginine-to-histidine amino acid exchange at position 364 of AVP1B, which is located in the intracellular C-terminal domain of the receptor and probably is involved in G-protein coupling. These genetic data support the large body of evidence demonstrating interactions of AVP and CRF systems in anxiety. Another family-based study failed to find an association of four polymorphisms in the CRF₁ locus with PD, but fewer CRF₁ polymorphisms and no AVP1B polymorphisms were tested in this study.51

POSTTRAUMATIC STRESS DISORDER

Anatomical and Neuroimaging Findings in Posttraumatic Stress Disorder

Activation of the amygdala is important for the fear learning associated with PTSD symptoms and with extinction learning associated with PTSD treatment. Amygdala hyperresponsiveness has been identified in numerous studies of patients who have PTSD (reviewed in37). Greater activation of the amygdala in response to viewing fearful faces corresponded with poor prognosis in CBT;52 other studies have shown that severity of PTSD symptoms predicts the magnitude of amygdala activation when encoding memories unrelated to the traumatic event.53

Similarly, sensory gating deficits in patients who have PTSD may result from information processing systems being overpowered by hypervigilance for threat-related stimuli and hyperarousal. A task requiring subjects to inhibit a primed motor response has demonstrated deficits of inhibitory control in patients who have PTSD. In control subjects, inhibitory processing activated the right frontotemporoparietal cortical network. In patients who had PTSD, the left ventrolateral PFC (vlPFC) was activated, and the frontotemporoparietal cortical network was less active. In terms of the behavioral response, increased error correlated with PTSD symptom severity. Increased symptom severity may result in increasingly overwhelmed inhibitory networks. Conversely, decreasing ability to recruit inhibitory control networks may result in more intense symptoms.56

Neurotransmitter and Neuroendocrine Signaling in Posttraumatic Stress Disorder

Amino acid neurotransmitters

Glutamate plays a critical role in hippocampal-dependent associative learning and in amygdala-dependent emotional processing in stressful conditions or following stress exposure. Inappropriate glutamate signaling therefore could contribute to the processing distortion experienced by many patients who have PTSD. In support of the glutamate hypothesis of PTSD, the N-methyl-D-aspartic acid receptor antagonist ketamine is well known for its ability to induce dissociative and perceptual distortions, similar to the processing distortion in patients who have PTSD (reviewed in37).

Recent research has explored the possible therapeutic potential of glutamatergic targets in PTSD. One such drug is the anticonvulsant topiramate. Topiramate inhibits excitatory transmission at kainate and α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors and has demonstrated anxiolytic properties at lower doses than required for anticonvulsant effects, suggesting a unique mechanism of action. Open-label studies using topiramate as either adjunctive or monotherapy have demonstrated some efficacy in diminishing nightmares and flashbacks and in improving overall PTSD symptoms.37

Monoamines

There are numerous reports of hyperactive noradrenergic signaling in PTSD. For example, NE is robustly secreted after exposure to acute physiological stress, and CSF concentrations of NE are tonically elevated in PTSD veterans. There is no evidence of a correlation between NE concentration and symptom severity, however (reviewed in57). As with patients who have PD, yohimbine elicits panic-like anxiety associated with cardiovascular symptoms and increased serum NE in patients who have PTSD relative to healthy control subjects (reviewed in35). Furthermore, patients who have PTSD have been shown to exhibit elevated 24-hour urinary catecholamine excretion.58 Some of the effects of NE on PTSD symptoms may be mediated by interactions between NE and glucocorticoids (eg,59). Drugs targeting the NE system have been assessed in PTSD with varying degrees of success for individual PTSD symptoms (see57 for a thorough review).

SSRIs have been demonstrated to be of moderate efficacy in PTSD, and sertraline is approved by the Food and Drug Administration to treat this disorder. In patients who had non-combat-related PTSD, paroxetine treatment improved hyperarousal and avoidance symptoms by 8 weeks and improved re-experiencing symptoms by the end of the 12-week study.60 The Institute of Medicine report on treatment of PTSD did not consider the efficacy data on SSRIs to be sufficient when compared with the psychotherapy data.61

Neuropeptides

In healthy soldiers during intense military training, interrogation stress led to an increase in plasma NPY concentrations; plasma NPY concentrations were correlated with cortisol concentrations and with behavioral performance. Combat-exposed men who did not develop PTSD tended to have higher concentrations of plasma NPY than combat-exposed men who had PTSD. These data suggest that NPY could be a neural correlate of resiliency.62

A recent review article identified a potential role for neurokinins in PTSD.35 Neurokinin 2 antagonists did not exhibit anxiolytic properties in preclinical tests in which benzodiazepines were active. The latter are of limited use in PTSD, however. Expression of galanin has been demonstrated to be stress responsive, in that it is decreased by acute stress but returns to normal within several days. If the stress continues and becomes chronic, galanin expression increases. It has been suggested that elevated galanin expression induced by chronic stress leads to increased autoinhibition of NE cell bodies in the locus coeruleus (LC); decreased tonic LC activity could contribute to depressive symptoms in patients who have PTSD (reviewed in35).

Corticotropin-releasing factor and the hypothalamic-pituitary-adrenal axis

Numerous studies have identified HPA axis disruption in patients who have PTSD.63-68 Compared with healthy control subjects, and in contrast to patients who have MDD, cortisol concentration is decreased in plasma, in saliva upon awakening, and in 24-hour urinary measures in combat-exposed patients who have PTSD.69 In a more recent study, a mixed population of civilian patients who had PTSD also exhibited decreased cortisol concentrations; lower plasma cortisol corresponded with greater symptom severity.70 Importantly, there also have been studies showing no difference in circadian salivary or 24-hour urinary cortisol concentrations (eg,71,72).

As in patients who have MDD, CSF concentrations of CRF were found to be higher in patients who had PTSD than in comparison subjects in two studies.73,74 Patients who have MDD typically exhibit a blunted HPA axis response in the CRF-stimulation test, and in veterans of the Vietnam or Korean wars hospitalized for PTSD, the ACTH response to ovine CRF injection also was blunted relative to control subjects and was independent of comorbid MDD diagnosis.75 In contrast, although dexamethasone non-suppression often is observed in patients who have MDD, patients who have PTSD exhibit greater suppression of plasma ACTH and cortisol concentrations.76 Negative findings also have been reported.77 Dexamethasone hypersuppression in patients who have PTSD may result from sensitized central glucocorticoid receptors (GRs) secondary to chronic elevations in CRF. This finding is in sharp contrast to patients who have MDD, in whom chronic CRF overexpression is thought to result eventually in GR desensitization and reduced negative feedback (reviewed in35). Alterations in CRFergic signaling and the HPA axis could result from insufficient glucocorticoid signaling caused by decreased hormone bioavailability or from decreased hormone receptor sensitivity.78

Genetic Contribution to Posttraumatic Stress Disorder

The heritability for PTSD has an estimated range of 30% to 40%, probably resulting from a variety of genes, each with relatively small contributions to the genetic predisposition for this disorder.79-83 Because of the importance of the environmental impact for this disorder, linkage studies in pedigrees cannot be conducted easily. Candidate gene association studies also are confounded by the problem of matching for environmental exposure and largely have been limited by small sample size ( n < 100); therefore these studies would able to detect only large genetic effects.

Because PTSD is the only anxiety diagnosis requiring a prior traumatic event, much research has been devoted to examining gene-by-environment interactions in patients who have PTSD.A complex-repeat polymorphism in the 5′ upstream region of SLC6A4, the gene encoding the serotonin transporter (serotonin transporter-linked polymorphic region, 5-HTTLPR), has been studied in depth by numerous groups. This polymorphism consists of a repetitive region containing 16 imperfect repeat units of 22 bp, located approximately 1000 bp upstream of the transcriptional start site.48,84 The 5-HTTLPR is polymorphic because of the insertion/deletion of units 6 through 8, which produces a short (S) allele that is 44 bp shorter than the long (L) allele. The 5-HTTLPR has been associated with different basal expression and functional activity of the transporter, most likely related to differential transcriptional activity.48,84 The L-allele of this polymorphism has been shown to lead to a higher serotonin reuptake by the transporter and thus less serotonin in the synaptic cleft. The shortSERT allele has been shown to interact with stressful life events (including abuse in childhood)to increase the risk for depression later in life.85-91 This polymorphism recently has been shown to play a role in the genetic underpinnings of PTSD. In hurricane victims, the SERT polymorphism interacts with severity of trauma and level of social support toward the development of PTSD.92

Other genes interacting with early-life stress (ELS) also are strong candidates for influencing susceptibility for PTSD. Preclinical studies indicate that the persistent hyperactivity of the HPA axis associated with ELS is mediated by a hyperactive CRF ₁ system, with chronic overactivity of CRF ₁ in limbic brain regions.93,94 In fact, the authors have shown that a haplotype within the gene encoding CRF ₁ interacts with child abuse to predict depression severity in adults.95 These polymorphisms, however, did not interact with ELS to predict PTSD symptoms.96

Polymorphisms in genes regulating GR activity may alter sensitization of the stress-response pathway during development so that victims of ELS have increased risk for PTSD following traumatic events in adulthood. FKBP5, a co-chaperone of heat shock protein 90, plays a role in regulating the expression of glucocorticoid-responsive genes.97 Increased expression of FKBP5 has been shown to reduce glucocorticoid binding affinity98 and to reduce nuclear translocation of the GR,99 resulting in resistance to glucocorticoid activation. In humans, the rare alleles of the FKBP5, SNPs rs4613916, rs1360780, and rs3800373, were associated with higher FKBP5 expression in blood monocytes as well as with a stronger induction of FKBP5 mRNA by cortisol.100 As an important candidate gene in trauma-related HPA axis disturbances, the putative functional SNPs in FKBP5 are hypothesized to moderate the development of PTSD and/or to alter the impact of early trauma or PTSD on GR.100-102

In support of this hypothesis, there seems to be a positive correlation between the upregulation of FKBP5 mRNA in peripheral blood mononuclear cells induced by acute trauma and the development of the PTSD 4 months later.103 Furthermore, when exposed to medical trauma, pediatric patients who had the rs3800373 and rs1360780 alleles were more likely to exhibit peritraumatic dissociation,104 a strong predictor of PTSD in adulthood.105 In the largest genetics study in PTSD conducted thus far, the authors' group showed that the same alleles increased the risk for adult PTSD symptom severity in adults who had been exposed to child abuse but not to trauma as adults.96 Additional research will be necessary to clarify the gene-environment relationship between early-life trauma versus adult trauma.

SOCIAL ANXIETY DISORDER

Anatomical and Neuroimaging Findings in Social Anxiety Disorder

As with PD and PTSD, amygdala activation has been implicated in symptoms of SAD. Social-cue tasks, such as the viewing of harsh faces, were associated with hyperreactivity in the amygdala and other limbic areas in patients who had SAD. Similarly, in response to viewing negative (but not neutral or positive) affective faces, patients who have SAD exhibited bilateral amygdala activation, which positively correlated with symptom severity and which reversed upon successful treatment. In anticipation of public speaking, subcortical, limbic, and lateral paralimbic activity is increased in patients who have SAD, suggesting elevations in automatic emotional processing. Decreased activity in the ACC and PFC in these subjects suggests a decreased ability for cognitive processing (reviewed in23).

The combined results of imaging analysis in subjects who have SAD suggest dysfunction of a cortico-striato-thalamic network: hyperactivity in the right PFC, striatal dysfunction, and increased hippocampal and amygdala activity with left lateralization. It has been suggested that hyperactivity in the frontolimbic system, including the ACC, which processes negative emotional information and anticipation of aversive stimuli, could result in misinterpretation of social cues (reviewed in23,107).

Neurotransmitter and Neuroendocrine Signaling in Social Anxiety Disorder

Amino acid neurotransmitters

Increased excitatory glutamatergic activity has been reported in patients who have SAD. Compared with matched control subjects, patients who had SAD had a 13.2% higher glutamate/creatine ratio in the ACC as measured by MRS. The glutamate/creatine ratio correlated with symptom severity, suggesting a causal role between excitatory signaling in the ACC and psychopathology (reviewed in37).

Monoamines

The Neurobiology of Anxiety Disorders In addition to benzodiazepines, SSRIs, SNRIs, and monoamine oxidase inhibitors are effective in the treatment of SAD. That SSRI treatment is successful in treating SAD symptoms and reversing some brain abnormalities (eg, elevated amygdala activity) has been cited as evidence for a serotonergic role in the etiology of SAD.107 Data supporting the hypothesis of disrupted monoaminergic signaling in patients who have SAD include decreased 5HT 1A receptor binding in the amygdala, ACC, insula, and dorsal raphe nucleus (DRN). Moreover, trait and state anxiety is elevated in patients who have SAD who have one or two copies of the short SERT allele, and this patient population exhibits amygdala hyperactivity in anxiety-provocation paradigms. Neuroimaging analyses also have revealed decreased density of the dopamine transporter and decreased binding capacity for the D ₂ receptor (reviewed in23). A role for DA in SAD is supported by the finding that patients who have Parkinson's disease have high rates of comorbid SAD (reviewed in107). This co-morbidity, however, could result from insecurity regarding display of the physical symptoms of this movement disorder rather than a common etiology of DA malfunction.

A recent study assessed whether a DA agonist (pramipexole, 0.5 mg) or antagonist (sulpiride, 400 mg) influenced response to anxiogenic challenge such as verbal tasks and autobiographical scripts in patients who had SAD. The anxiogenic effect of the behavioral challenges was significantly increased in patients who had untreated SAD following administration of either drug. After successful treatment with SSRIs, however, administration of pramipexole seemed to dampen the behavioral provocation-induced anxiety, whereas sulpiride administration continued to enhance the anxiogenic effects of these tasks. These authors suggested that instability in the dopaminergic response to social stress contributes to anxiety severity and is normalized only partly by successful treatment, perhaps via SSRI-induced desensitization of postsynaptic D ₃ receptors.108

Neuropeptides

As key effectors of social behavior, the neuropeptides oxytocin and vasopressin are of particular interest in SAD and autistic spectrum disorders. Recently direct oxytocin administration to the amygdala in laboratory animals was shown to decrease activation in this region and to dampen amygdala-brainstem communications, which are known to play a role in the autonomic and behavioral components of fear. Furthermore, preliminary data have shown that genetic variants in the central vasopressin and oxytocin receptors ( AVP1A and OXTR, respectively) influence amygdalar activity. These data support the hypothesis of amygdala hyperactivity in SAD. Future research in this area may elucidate neural underpinning of human social behavior and the genetic risk for disorders including SAD and autism.18

Corticotropin-releasing factor and the hypothalamic-pituitary-adrenal axis

Some evidence indicates sensitization of the HPA axis in patients who have SAD. Psychosocial stress produces a greater increase in plasma cortisol, but not ACTH, in patients who have SAD than in control patients despite similar baseline cortisol concentrations.109 Compared with healthy control subjects or patients who have PTSD, subjects who have SAD tend toward an elevated cortisol response in the Trier Social Stress Test (TSST). The degree of cortisol elevation was correlated with increased avoidance behavior in the approach-avoidance task and the predicted stress-induced increased social avoidance above and beyond effects of blood pressure and subjective anxiety.110 Negative findings also have been reported, however (eg,111,112). For example, an earlier study found that adolescent girls who had social phobia and control subjects exhibited an equal elevation in salivary cortisol following the TSST. To the authors' knowledge, there are no endocrine-challenge studies (Dex-Suppression, CRF-Stimulation, or Dex/CRF) in patients who have SAD.

Genetic Contribution to Social Anxiety Disorder

The Neurobiology of Anxiety Disorders Unfortunately, there are very few studies specifically examining the genetic underpinnings of SAD. Available data suggest that SAD has a high degree of familial aggregation. In a recent meta-analysis in which SAD was grouped with specific phobia and agoraphobia, an association between phobia in probands and their first-degree relatives was identified.43

Twin studies in social phobics suggest that additive genetics is responsible for increased incidence of SAD in monozygotic compared with dizigotic twins and suggest no role for common environmental experiences. Adult twin studies of combined phobia diagnoses (including social phobics) suggest that the additive genetics accounts for 20% to 40% of the variance in diagnosis. This result corresponds with a population-based twin study of adolescents diagnosed with social phobia, MDD, and alcoholism, in which genetics accounted for 28% of the risk variance for SAD. Again, the remaining risk was derived from non-shared environmental experiences. Unlike MDD and PTSD, there is little evidence that early-life trauma influences the risk for developing SAD in adulthood.43

The one genome-wide linkage analysis of SAD implicated a region on chromosome 16 near the gene encoding the norepinephrine transporter. Other genes associated with SAD include (1) a functional variant in ADRB1, the gene encoding the β1-adrenergic receptor, and (2) two SNPs and a 3-SNP haplotype in the gene for COMT in female patients who have SAD (reviewed in107). Because SAD is such a complex phenotype, it has been suggested that it may be more fruitful to search for susceptibility genes by examining intermediate phenotypes, quantitative traits, and comorbidity with other illnesses. In fact, SAD heritability includes disorder-specific but also nonspecific genetic factors. SAD is associated with behavioral inhibition in childhood, low extroversion, and high neuroticism. These personality traits are not SAD specific but are hypothesized to contribute to a spectrum of psychopathology inclusive of mood and anxiety disorders. Furthermore, behavioral inhibition, low extroversion, and high neuroticism are each known to be highly heritable and may largely account for the genetic contribution to SAD.

Genes associated with high behavioral inhibition include CRF and SERT. Internalizing neuroticism is associated with the gene encoding glutamic acid decarboxylase, the rate-limiting enzyme in the synthesis of GABA from glutamate (reviewed in107).

GENERALIZED ANXIETY DISORDER

Anatomical and Neuroimaging Findings in Patients who Have Generalized Anxiety Disorder

In functional imaging studies of adolescent patients who have GAD, resting vlPFC activity is elevated relative to healthy control subjects. Because the vlPFC activity correlates negatively with symptom severity, the elevation in vlPFC metabolism is interpreted as a compensatory response rather than an underlying cause of GAD.114 Because of observed hypermetabolism in the PFC of patients who have GAD, neuronal viability has been assessed in this region as measured by the ratio of N-ace-tylasparate to creatine using proton MRS. For patients who had GAD, neuronal viability was increased in the right dorsolateral PFC in those without early-life stress but was decreased in those who self-reported early-life trauma.115

Functional brain imaging results obtained under resting conditions in patients who have GAD have tended to be inconsistent; provocative anxiety-inducing tasks have produced more robust and interpretable fMRI results. The pattern of brain activity in anxious patients who have GAD correlates well with results from laboratory animal studies in which limbic circuits, particularly the amygdala, play an important role in the fear response (eg,116,117; see118 for a review). In fact, many imaging studies of patients who have GAD show elevated amygdala and insula activation during negative emotional processing (reviewed in23,119,120). In response to viewing angry faces, adolescent patients who had GAD exhibited an elevated right amygdala response; this activation correlated positively with symptom severity. The overactivity in the right amygdala also was correlated negatively with activity in the right vlPFC, suggesting top-down disinhibition as a potential mechanism for elevated amygdala activity.121 Interestingly, strong pretreatment activation of the left amygdala in pediatric patients who had GAD predicted a positive therapeutic response to fluoxetine or CBT.122 These results have been interpreted to suggest that a greater amygdaloid response to negative emotions represents a healthier signal-to-noise ratio. When adult patients who have GAD view fearful faces, lower pretreatment amygdala activity and higher ACC activity predict a positive treatment response to venlafaxine.123 Additional studies will be crucial in determining whether amygdala activation has clinical utility in predicting treatment outcome.

Interconnectivity with brain regions responsible for interpreting social behavior may be one mechanism by which the amygdala plays a substantial role in anxiety disorders. The brain regions responsible for interpreting social behavior include the superior temporal gyrus, thalamus, and PFC. Amygdala hyperactivity may mediate the inaccurate interpretations of social behavior in patients who have GAD.120

Neurotransmitter and Neuroendocrine Signaling in Generalized Anxiety Disorder

Amino acid neurotransmitters

The observed limbic overactivity in patients who have GAD could result from decreased inhibitory neurotransmission, increased excitatory neurotransmission, or a combination of these two processes. Dysregulation of GABA inhibitory neurotransmission has been documented in several anxiety disorders (reviewed in124). GABA A receptor downregulation is observed in patients who have GAD and has been hypothesized to play a role in the etiology of this illness (reviewed in68). In support of this hypothesis is the finding that symptoms of GAD, including excessive worry, hypervigilance, and psychomotor agitation, are treated effectively with GABA A facilitators such as benzodiazepines and barbiturates (reviewed in124). Furthermore, treatment with riluzole, an anti-glutamatergic agent, seems to improve GAD symptoms.125,126

Monoamines

Although all the SSRIs have shown efficacy in GAD, the drug most frequently studied in anxiety is paroxetine, which decreases symptoms of harm avoidance. It is important to note that GAD often is comorbid with other disorders, including MDD, PD, and SAD, each of which also has shown responsiveness to SSRI treatment.39

More concrete evidence supporting a role for 5-HT circuitry in GAD includes challenge with the 5-HT 2c/5-HT ₃ agonist mCPP, which elicits anxiety and anger in patients who have GAD (reviewed in68).

Further evidence for a serotonergic component of GAD is provided by functional brain imaging studies that have found that midbrain SERT density correlates negatively with symptom severity.127,128 Recent studies have replicated the negative correlation between SERT density and anxiety symptoms in GAD, but there is no difference in SERT density in subjects who have GAD as compared with controls.127

Neuropeptides

Patients who have GAD are hypersensitive to exogenously administered CCK agonists,129,130 leading to the study of CCK receptor-selective antagonists as a putative novel class of anxiolytics. One such drug was developed but was not demonstrated to possess anxiolytic efficacy.131 Additional research and development of unique CCK antagonists will be an important step in clarifying the role of CCK in anxiety and its potential as a therapeutic target.

To the authors' knowledge, no studies have specifically examined the role of NPY in GAD. NPY does possess anxiolytic effects in laboratory animals (reviewed in132). These anxiolytic effects may be caused by NPY-CRF interactions; these two neuro-peptides are co-localized in numerous limbic regions and exert opposing effects on the amygdala, LC, and periaqueductal gray matter, the last region is responsible for the motor output for the behavioral stress response.133

Corticotropin-releasing factor and the hypothalamic-pituitary-adrenal axis

Although very few studies have specifically examined HPA axis reactivity in patients who have GAD, there is no evidence of hypercortisolism, dexamethasone non-suppression, or increased CSF CRF concentrations.67,68 That CRF and the HPA axis seem to play a less prominent role in GAD than in other anxiety disorders and MDD is perhaps surprising given that CRF antagonists have been demonstrated to possess anxiolytic effects (134-136; reviewed in137). It is possible that the lack of evidence for a pathophysiological role for CRF circuits in GAD is an artifact of the paucity of endocrine studies in these patients. It is equally likely, however, that the difference in CRF/HPA axis observations in patients who have MDD and patients who have GAD represents a critical biological distinction between these two syndromes.

Genetic Contribution to Generalized Anxiety Disorder

Overall the genetic contribution is thought to be less substantial in GAD than in other anxiety disorders. Studies have shown that first-degree relatives of GAD probands have elevated rates of mood and anxiety disorders in general138 and perhaps have a specifically increased risk for GAD.43 A recent study of more than 3000 twin pairs found modest familial aggregation of GAD with equal heritability in males and females in same-sex or opposite-sex twin pairs; there was no evidence for gender-specific genetic underpinnings of GAD.139 Results from twin studies estimate that approximately 32% of the variance for liability to GAD is caused by additive genetics in male and female twins and that the remaining variance is explained by environment specific to the individual, rather than the shared environment of the twin pair (reviewed in43). Only a handful of genetic-association studies specific for GAD have been reported, and all are thus far unreplicated (eg,140-142).

SUMMARY AND GUIDANCE FOR THE DIAGNOSTIC AND STATISTICAL MANUAL OF MENTAL DISORDERS, EDITION FIVE

Functional Neuroanatomy

The Neurobiology of Anxiety Disorders Commonalities in anxiety disorders include functional hyperactivity in limbic regions, particularly the amygdala, and the inability of higher cortical executive areas to normalize the limbic response to stimuli ( Table 2 ). In contrast to MDD, in which amygdala hyperactivity is observed under resting conditions, provocation paradigms are required to identify amygdalar hyperactivity in patients who have an anxiety disorder.

Table 2

Anatomic Area

Normal and Pathological Sadness

Normal and Pathological Anxiety

Insular cortex

Acute sadness activates dorsal
insula

Acute anxiety activates
ventral insula

Cingulate cortex

Acute anxiety has no effect on ACC
but deactivates the PCC

Amygdala

Not overactive at rest
Overactive during symptom
provocation
Right amygdala most relevant to
anxiety

Additional neuroimaging studies must focus not on individual brain regions but on corticolimbic circuits. Between-laboratory consistency must become a priority throughout the research community to allow interpretation of results across studies. Perhaps most importantly, neuroimaging research must place more emphasis on hypothesis-driven studies. It is hoped that such increased consistency and clear goals will lead to more reliable and robust observations that finally can piece together the diagnosis-specific clinical implications of functional and structural alterations in patients who have mood and anxiety disorders.

Neurotransmitter and Neuroendocrine Signaling

Disruption in neurotransmitter, neuropeptide, and neuroendocrine signaling is not unique to mood and anxiety disorders; a great deal of overlap between diagnostic syndromes should be expected. For example, dysregulation of the generalized stress response is common to numerous medical and psychiatric diagnoses. Repeated, prolonged, or particularly severe stress could increase the magnitude and duration of CRF, glucocorticoid, and catecholaminergic signaling, and these three signaling classes can explain the psychiatric, circulatory, metabolic, and immune manifestations of stress-related illness. In contrast, hypoactivation of the HPA axis as a compensatory mechanism for chronic/severe stress exposure may occur also. HPA axis hyperactivity is seen in MDD, OCD, PD, anorexia, and alcoholism (to name a few), whereas HPA axis hypoactivity is observed in chronic fatigue, fibromyalgia, nicotine withdrawal, PTSD, and the postpartum period. Importantly, the direction of the HPA axis disruption depends on the nature, duration, predictability, and severity of the stressor and also on the age of the subject, individual genetic background, and previous experiences (reviewed in58). The clinical implications of altered monoaminergic signaling probably are influenced by an equally long list of factors. A closer relationship between preclinical and clinical research is essential before it will be possible to begin to piece together the relationship between each of these factors.

Genetic Contribution

The Neurobiology of Anxiety Disorders When attempting to identify the genetic contribution toward susceptibility for psychopathology, the candidate genes are largely the same across diagnoses and tend to be genes whose products regulate the HPA axis and monoaminergic signaling. These similarities, however, do not preclude important clinical distinctions between diagnostic classes within anxiety disorders or between anxiety disorders and MDD. Some genetic factors are nonspecific but influence the risk for psychopathology in general. Others are diagnosis specific. Moreover, the impact of individual diagnosis-specific genetic risk factors may vary over time, depending on the developmental stage and previous experience of each subject.

Overall, the decision to classify MDD, PD, PTSD, SAD, and GAD as distinct disorders must be based not only on clinical phenomenology but also on pathophysiology, genetics, course of illness, and treatment response data. Neuroendocrine, neurotransmitter, and neuroanatomical differences between patients who have mood or anxiety disorders and healthy control subjects must be interpreted with care ( Table 3 ). Brain regions and neurotransmitter systems implicated in mood and anxiety disorders have wide-ranging functions, many of which may be unrelated to the etiology of psychiatric disorders. Finally each of these disorders clearly represents the result of complex gene-environment interactions. The clinical phenotype may well be determined largely by individual differences in multiple genes that exhibit functional polymorphisms. It is hoped that continued research will begin to uncover more consistent findings across laboratories, methodologies, and subjects. At that point, a new discussion of diagnostic criteria may be relevant.

Table 3

Neurotransmitter

Normal and Pathological Sadness

Normal and Pathological Anxiety

GABA

Inconsistent
GABA-A agonists not approved for
MDD by the Food and Drug
Administration

Decreased
GABA-A receptor density in GAD;
GABA-A agonists are anxiolytic
Affinity for GABA-A predicts
efficacy of benzodiazepines

Serotonin

Decreased 5HIAA CSF
concentrations in suicide victims
Normal in non-suicidal MDD
patients
Blunted prolactin response to 5-HT
agonists

Decreased 5HIAA CSF
concentrations in some studies

SERT

Decreased density in midbrain
Density correlates negatively with
anxiety symptoms in MDD

Density correlates negatively with
anxiety symptoms in GAD

5HT1A

-

Anxiolytic as DRN autoreceptors
Anxiogenic as hippocampus
postsynaptic receptors

5HT2

Desensitized by antidepressants

Anxiogenic
Antagonists are anxiolytic

Norepinephrine

Unchanged in GAD

Acknowledgments

This work was supported by National Institute of Health (NIH) grants MH-541380, MH-77083, MH-69056, MH-58922, MH-42088, MH071537, and DA-019624; the Doris Duke Clinical Scientist Award, and the Burroughs Wellcome Fund. K.J.R. has received awards and/or funding support from Lundbeck, Burroughs Wellcome Foundation, Pfizer, the National Alliance for Research in Schizophrenia and Depression (NARSAD), the National Institute of Mental Health (NIMH), and the National Institute on Drug Abuse and has a consulting agreement with Tikvah Therapeutics for N-methyl-D-as-partic acid-based therapeutics. C.B.N currently serves on the scientific advisory boards of American Foundation for Suicide Prevention (AFSP), AstraZeneca, NARSAD, Quintiles, Janssen/Ortho-McNeil, and PharmaNeuroboost. He holds stock/equity in Corcept; Revaax, NovaDel Pharma, CeNeRx, and PharmaNeuroboost. He is on the board of directors of the AFSP, George West Mental Health Foundation, NovaDel Pharma, and Mt. Cook Pharma, Inc. He holds a patent on the method and devices for transdermal delivery of lithium (US 6,375,990 B1) and the method for estimating serotonin and norepinephrine transporter occupancy after drug treatment using patient or animal serum (provisional filing April, 2001). In the past year, he also served on the Scientific Advisory Board for Forest Laboratories, received grant support from the NIMH, NARSAD, and AFSP, and served on the Board of Directors of the American Psychiatric Institute for Research and Education. E.B. is co-inventor on the following patent applications: FKBP5: a novel target for antidepressant therapy, international publication number: WO 2005/054500; and Polymorphisms in ABCB1 associated with a lack of clinical response to medicaments, international application number: PCT/EP2005/005194. She receives grant support from NARSAD and the Doris Duke Charitable Foundation. In the past 2 years, she has received grant support from Pfizer Pharmaceuticals (Young Investigator award) and GlaxoSmithKline.

REFERENCES

13. Schatzberg AF, Nemeroff CB, editors. Textbook of psychopharmacology. ed. 3. Washington (DC): The American Psychiatric Publishing; 2004. pp. 717-765. 847-68, 913-35. [ Google Scholar]

49. Strug LJ, Suresh R, Fyer AJ, et al. Panic disorder is associated with the serotonin transporter gene (SLC6A4) but not the promoter region (5-HTTLPR) Mol Psychiatry. 2008 [[ PMC free article] [ PubMed] Google Scholar]

61. Committee on Treatment of Posttraumatic Stress Disorder, Institute of Medicine. Treatment of posttraumatic stress disorder: an assessment of the evidence. Washington (DC): National Academies Press; 2008. [ Google Scholar]

108. Hood S, Potokar J, Davies S, et al. Dopaminergic challenges in social anxiety disorder: evidence for dopamine D3 desensitisation following successful treatment with serotonergic antidepressants. J Psychopharmacol. 2008 Oct 6; [Epub ahead of print] [[ PubMed] Google Scholar]

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The Neurobiology of Anxiety Disorders: Brain Imaging, Genetics, and Psychoneuroendocrinology

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Psychiatr Clin North Am. Author manuscript; available in PMC 2013 Jun 17. Published in final edited form as: Elizabeth I. Martin, PhD, a, * Kerry J. Ressler, MD, PhD, b, c Elisabeth Binder, MD, PhD, d, e, f and Charles B.

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What are 'intrusiv e thoughts' (we all have them) and what has CBT for OCD got to do with a polar bear? People sometimes talk about being "a little bit OCD", but the reality of obsessive compulsive disorder is much more difficult than a tendency to line your pens up or be super tidy.

Ashley Fulwood talks to Dr Lucy Maddox about his journey towards recovery from OCD with the help of CBT, and Professor Paul Salkovkis explains how CBT works.
Show Notes
Want to know more?
Websites
For more about BABCP check out: babcp.com

To find an accredited therapist: http://cbtregisteruk.com

Ashley's charity, OCD-UK is here, and there is a lot of useful information on their website: https://www.ocduk.org/

And another OCD charity, OCD Action, is here: https://www.ocdaction.org.uk/
Books
Break Free From OCD by Fiona Challacombe, Victoria Bream Oldfield and Paul Salkovskis

Overcoming OCD by David Veale and Rob Wilson

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What are 'intrusive thoughts' (we all have them) and what has CBT for OCD got to do with a polar bear?

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CBT for Panic disorder- Journal Article by Freedman & Addesky (2009)

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Coping with Depression: This workbook is designed to provide you with some information about depression and suggested strategies for how you can manage your mood. It is organised into modules that are designed to be worked through in sequence. Although it is not necessary that you complete one module before going on to the next, this is recommended.

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Change Factors in the process of CBT for OCD

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Change Factors in the process of CBT for OCD

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International OCD Foundation: Contamination Fact Sheet

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International OCD Foundation: Contamination Fact Sheet

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In recognition of our psychological treatment expertise, CEDAR is now the sole commissioned provider of IAPT training in the South West. We have worked in collaboration with key professionals in the field to create the PWP workbooks and manuals used for IAPT training across the UK. Additionally, we have developed workbooks for Psychological Wellbeing Practitioners to utilise whilst working with patients.

You can download a copy of our workbooks here:Managing Your Worries - Paul Farrand, Joanne Woodford and Faye Small

Managing Your Worries - Paul Farrand, Joanne Woodford and Faye Small

Managing Your Worries

Unhelpful Thoughts: Challenging and Testing Them Out - Paul Farrand, Joanne Woodford and Katie Jackson
Unhelpful Thoughts

From Problems to Solutions: Finding your Way Forward - Paul Farrand, Joanne Woodford and Faye Small
Problems to Solutions

Enhancing resilience - Finding inner strength to manage the demands of clinical practice - Professor Paul Farrand and Heather Stonebank

Other useful IAPT publications

Reach Out 3rd Edition (.pdf)
National programme student materials to support the delivery of training for Psychological Wellbeing Practitioners delivering Low Intensity interventions, 3 rd edition
David Richards & Mark Whyte*Copyright Rethink Mental Illness www.rethink.org, Registered Charity Number 271028.

A recovery programme for depression.
Karina Lovell & David Richards*Copyright Rethink Mental Illness 2012 www.rethink.org, Registered Charity Number 271028.

Oxford Guide to Low Intensity CBT Interventions
James Bennett-Levy (Editor), David Richards (Editor), Paul Farrand (Editor), Helen Christensen (Editor), Kathy Griffiths (Editor), David Kavanagh (Editor), Britt Klein (Editor), Mark A. Lau (Editor), Judy Proudfoot (Editor), Lee Ritterband (Editor), Jim White (Editor), Chris Williams (Editor)*Oxford University Press (2010). Available from most book shops

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In recognition of our psychological treatment expertise, CEDAR is now the sole commissioned provider of IAPT training in the South West. We have worked in collaboration with key professionals in the field to create the PWP workbooks and manuals used for IAPT training across the UK.

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Patient experience of CBT treatment for OCD - Sarah

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Patient experience of CBT treatment for OCD - Sarah

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1. How would you describe CBT? How was your experience of it? What was it like?

I had 20 sessions of CBT for OCD. Before this, I had struggled with anxiety and depression for many years and had tried a number of other therapies. CBT was different, it was a lot more structured - we set an agenda at the beginning of every session. This took a bit of getting used to, but meant we used our time much more productively. CBT also felt more collaborative, which was very empowering. My therapist was the expert on CBT principles, I was the expert on how my mind worked. Sometimes she suggested I do things that were difficult, but I always understood her reasoning, the process was very transparent.

I have heard CBT described as more of a doing therapy than a talking therapy and this feels true to my experience - the approach is quite scientific. The talking bit was important though.

2. What did you find most useful?

We did a lot of what CBT refers to as behavioural experiments: activities designed to test beliefs and predictions in the real world. Before the experiment the therapist would ask what I thought would happen and how strongly I believed this would occur. Afterwards we would compare this with the outcome.

The therapist also taught me some useful cognitive techniques such as the downward arrow technique, which identifies the beliefs underlying particular thoughts (or what I call the fear beneath the fear) and also generating alternative explanations for events.

3. Was there anything you would have changed about it?

The main things was that I wish I had had CBT a lot sooner! Although the time limited nature of the treatment was helpful in many ways I wish it could have been a bit more flexible - I think I would have benefited from more sessions in "blocks" e.g. 16 sessions, then a break of a few months and then a further 8-10 sessions. It would also have been great if the therapist had the time available to come out "on location" for behavioural experiments and exposure therapy.

4. Did it make any difference to your life? If so, what was different?

CBT has made a huge difference to my life. I can do things that I could not do before, such as cook for other people. The time and energy I used to expend on checking is now free for other things. I still experience intense anxiety in certain situations, but this is less frequent and my overall anxiety levels are much better. I still feel some way from recovered or able to live a fulfilling life, but I have a much clearer sense of how to get to this point.

5. What would you say to someone considering having it?

Mainly, go for it!

I think that he transparency of CBT means that you will know relatively quickly whether it is helpful for you, which is not the case with all therapies.

The caveat would be to be prepared for it to be challenging and to be aware that you will have to do some work between sessions. Do make the the time to do this as the benefit will be much greater if you do. Tell the therapist if he or she asks you to do something which feels to difficult or which you don't understand the reasons for. Finally, make sure you are getting "proper" CBT. OCD Action has a good checklist of what CBT for OCD should look like [LINK https://www.ocdaction.org.uk/resource/what-cognitive-behavioural-therapy-cbt]

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british association for behavioural & cognitive psychotherapy

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I had 20 sessions of CBT for OCD. Before this, I had struggled with anxiety and depression for many years and had tried a number of other therapies. CBT was different, it was a lot more structured - we set an agenda at the beginning of every session.

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Coping with Physical Alarms (CCI) Exposure Part 1

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Coping with Physical Alarms (CCI) Exposure Part 1

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Psychology Tools: OCD Formulation Worksheet

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Psychology Tools: OCD Formulation Worksheet

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Skip to main content

Worksheet

An important treatment implication of the cognitive behavioral model of OCD is that clinicians can work at the level of the meaning of the intrusion. This can be contrasted with traditional exposure and response prevention, which can be framed as an intervention at the level of the compulsion or neutralizing behavior. The Obsessive Compulsive Disorder (OCD) Formulation worksheet is a case conceptualization tool for cognitive behavioral therapists.

Downloads

Description

The essential insight of the cognitive behavioral model of obsessive compulsive disorder (OCD) is that it is the client's interpretation of the intrusion which drive the distress and maladaptive responses (Salkovskis, Forrester & Richards, 1998). Intrusive thoughts, images, urges, and doubts are very common and entirely normal (Purdon and Clark, 1993, 1994): what gives intrusions their emotional power in OCD is the meaning that clients assign to them. Individuals with OCD commonly interpret the occurrence or content of their intrusions as:

Meaning something bad about them and/or that something bad will happen, and

Believing that they are personally responsible for preventing harm to themselves and/or others

Interpreting intrusions through the lens of responsibility has a number of effects including: increased discomfort, increased focus of attention on the intrusions, increased accessibility of the intrusions, active attempts to reduce the intrusions, and attempts to decrease or discharge the responsibility that the individual perceives is associated with them. Although these efforts can lead to short-term reductions in anxiety, in the long-term they increase preoccupation with the intrusive thoughts and maintain the pattern of responses to them.

An important treatment implication of the cognitive behavioral model of OCD is that clinicians can work at the level of the meaning of the intrusion. This can be contrasted with traditional exposure and response prevention, which can be framed as an intervention at the level of the compulsion or neutralizing behavior. Clients can be helped to develop an alternative, less-threatening, interpretation of what the intrusions mean (theory b), and then to test this alternative through a process of information-gathering which might include symptom monitoring, behavioral experiments, and exposure exercises. The Obsessive Compulsive Disorder (OCD) Formulation worksheet is a case conceptualization tool for cognitive behavioral therapists.

Instructions

This worksheet is designed as a case conceptualization tool for therapists. If it is used with clients it can help to structure a discussion about how the client's experiences and reactions interact. Case conceptualization is considered to be most effective when it is collaborative exploration of a client's difficulties rather than presented as a 'completed solution' (Kuyken, Padesky, Dudley, 2011). If the worksheet is used in session with a clients it is best introduced as a tentative tool for exploration. The therapist might introduce it by saying "some people's OCD responses fit the pattern on this diagram. I wonder if we could we explore some of your thoughts, feelings, and reactions and see what kind of pattern they follow?".

1. Ask the client to think of a recent time when they experienced an intrusion

2. Help the client to focus on the meaning of the intrusion:
"What does it say about you that you had this intrusion / thought / image / doubt / urge?"
"What would other people think of you if they knew you had this thought?"
"How responsible do you feel for preventing this event from happening?"
"If other people knew you had this thought how responsible would they think you are for preventing [negative outcome] from happening?"

3. Help the client to describe their responses to interpreting the intrusion in this way:
"What do you do to cope?"
"What do you do to prevent the worst from happening?" "What do you pay extra attention to or look out for?"
"What do you feel when you think about things in this way?"

4. Explore the consequences of the client's reactions and consider whether any of these reactions might act to reinforce the cycle. A common pattern to look for is that reactions lead to short-term improvements (e.g. feeling safer) but either no change to, or a worsening of, the sequence in the long-term.

References

Kuyken, W., Padesky, C. A., & Dudley, R. (2011). Collaborative case conceptualization: Working effectively with clients in cognitive-behavioral therapy. Guilford Press.

Purdon, C., & Clark, D. A. (1993). Obsessive intrusive thoughts in nonclinical subjects. Part I. Content and relation with depressive, anxious and obsessional symptoms. Behaviour Research and Therapy, 31(8), 713-720.

Purdon, C., & Clark, D. A. (1994). Obsessive intrusive thoughts in nonclinical subjects. Part II. Cognitive appraisal, emotional response and thought control strategies. Behaviour Research and Therapy, 32(4), 403-410.

Salkovskis, P. M., Forrester, E., & Richards, C. (1998). Cognitive-behavioural approach to understanding obsessional thinking. The British Journal of Psychiatry, 173(S35), 53-63.

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Obsessive Compulsive Disorder (OCD) Formulation - Psychology Tools

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Skip to main content An important treatment implication of the cognitive behavioral model of OCD is that clinicians can work at the level of the meaning of the intrusion. This can be contrasted with traditional exposure and response prevention, which can be framed as an intervention at the level of the compulsion or neutralizing behavior.

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RCT comparing outcomes for OCD patients: EMDR and CBT

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RCT comparing outcomes for OCD patients: EMDR and CBT

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Patient experience of CBT treatment for OCD - Frank

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Patient experience of CBT treatment for OCD - Frank

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My name is Frank and a year ago I came to the end of a course of treatment for OCD at the Centre for Anxiety Disorders and Trauma, where I had 20 weekly sessions of cognitive behavioural therapy - CBT. I've been asked to write something about it, for people with OCD who may be considering a course of CBT. If that's you, you may be wondering about the treatment - about what you've heard and read. You may have spent years living in fear, shifting from one object of anxiety to another, scrabbling around, making small adjustments that mean you can just about carry on functioning. And now someone talks to you about challenging those fears, rather than buying them off with rituals and avoidance. You may be thinking, that sounds hard. Too hard, maybe.

People who've been through medical conditions often say that the treatment was tough - they worked at it, they 'beat' the condition and so on. It's the language of struggle, of fighting. I'd like to tell you that CBT isn't so difficult - not when you're guided and helped, as you will be.

Perhaps right now, you're thinking about your worst OCD fear - the thing that makes your life most gruelling, that stops you in the street and makes you feel nauseous. Even if, like me, you've had OCD for a long time and your fears have turned into a rag-bag of nagging ideas, you probably have a number-one terror that seems beyond reach, beyond challenge. Maybe you're thinking, how could I ever approach that? How can I think about it in a different way, how can I make it less massive?

If you've never had CBT, it's bound to seem mysterious. Mental health conditions feel mysterious too, especially in their early stages - where on earth did that come from? So it may make the whole thing easier to imagine if I compare it to another condition - one that's more up front and evident. Since 1980, I've been a type-1 diabetic, which means I need to inject myself with insulin several times a day. As a child, I used to read about diabetes or listen to diabetics being interviewed on TV and think, how on earth do you go about pushing a needle into your own body? The idea seemed impossible, and I was glad I'd never have to do it. Or so I thought.

Then after a long spell of ill-health, I was diagnosed with diabetes. I had to think again about the injections. The medical team took it slowly. They gave me a few days to get less sick, they showed me how injections are done, they gave me an orange to practise on - it takes a similar amount of pressure, apparently - in general, they encouraged me. And before long, the task didn't seem quite so enormous. You know that to regain some control over your life, you need to do your jabs yourself. And you set yourself down to try it.

You put the needle to your skin and push... and it doesn't hurt. Not usually, and never very much. It isn't your skin that's the barrier, it's your fear - and you can get past both of them. Afterwards, I felt excited - elated, even. I felt healthier, stronger and in control - as much as you can be in this unpredictable life (which is another thing it's important to think about when you have OCD!).

When I started my CBT treatment at CADAT, I felt the same fears. I'd had OCD for years, bent my life out of shape to appease it, been in thrall to it, in fact. Appeasing the fear had been the only relief I got, so all the rituals and avoiding seemed like magic spells of protection - they brought me scraps of comfort, at a huge, huge price. I didn't want to think about the day when I'd abandon the most 'powerful' of them. I pushed it to the back of my mind, and thought if it gets too much, I can twist the treatment, do just enough to get by, make life easier for a year or so, maybe. Because anyone who's had various therapies for OCD knows that we will stop short of a breakthrough if we can - we tweak the condition, do what we can to improve it without addressing it at its most basic, crucial level.

I'd done that before, but CBT has improved vastly since I first did it in the late 90s, when therapists were still telling us to take our minds off OCD by snapping rubber bands against our arms. At CADAT, the therapy and the therapists are brilliant. It's very focused, totally shaped for and aimed at your condition. The therapists have enough time to take you to the crucial turning point and beyond - the point at which you start to act against your fears, with what they call anti-OCD behaviour. That is, you don't find a route around the OCD, you confront it and do things that challenge it. I find myself wanting to say 'transgress against it', even though I accept it isn't entirely helpful - it makes the fear seem masterful, like the boss of the situation, although as you'll discover, it isn't really like that.

The therapy starts slowly. No one will throw your worst nightmare into your lap and say 'Deal with it.' You'll talk, you'll learn new ways to think about OCD (and about life, which as it turns out is more important than OCD). First you'll challenge some target behaviours that feel within reach. But sooner or later, yes - you will stand at that turning point, the worst of your fears, and you'll have to take a step forward. You'll confront something that feels out of reach and you will act against it, because if you don't, you'll slip backwards. It will be a troublesome moment, but it will not be impossible. Far from it.

Because you will be helped. You'll have new ways of thinking, and it will feel like having tools for the job - you can reach into your toolbox and pick strategies that make the work easier. Your therapist will be there for you, and it won't be as bad as you imagine right now. For me, it did feel like my first insulin injection - I was helped through the barriers and I was surprised how little it hurt. I even felt the same sense of elation afterwards. (Elation makes me suspicious, but I suppose it's better than fear.)

The CBT wasn't all about anti-OCD behaviour. I needed to think about the idea that, yes, life is fragile. There is no magic bullet for that, however much we wish there were. In fact, there is no magic, full stop. Bad things will happen to us, but those things will be unpredictable - they will happen whatever we do, whether we walk under ladders or not. No one enjoys thinking about the precarious nature of life, but surprisingly, taking on that notion makes living feel easier, not more grim - it won't stop the bad stuff happening, but at least you won't be to blame for it. If you've spent your life thinking about magical defences, it's hard to ditch OCD talismans completely. But the treatment will help.

I still get the OCD fears. I'd be lying if I said I had no slip-ups. But during the last year, there have been several points where I've known I could go badly wrong, if I let myself, and fall into a behaviour that will end up seriously corrupting my life. Each time, I've been able to think it through and make a better choice. That's thanks to the treatment I had at CADAT, and to my therapist and her assistant.

Maybe it's best not to think too much about the most challenging moments in CBT - not before you start, anyhow. Coming face to face with fear and then living with it - perhaps that seems like an unreal ambition to you now. It did to me, back in 2016. But it isn't unreal at all. The thought of confronting OCD is much, much worse than actually doing it. You will be smashing some of your personal idols, but that will turn out to be a good thing - not just in terms of managing your OCD, but also of living a bolder, more productive, less cowed life.

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british association for behavioural & cognitive psychotherapy

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My name is Frank and a year ago I came to the end of a course of treatment for OCD at the Centre for Anxiety Disorders and Trauma, where I had 20 weekly sessions of cognitive behavioural therapy - CBT. I've been asked to write something about it, for people with OCD who may be considering a course of CBT.

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Information Sheet - What is Health Anxiety

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Information Sheet -What are Safety Behaviours

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Dr Blenkiron has previously developed digestible summaries of NICE guidance for mental health services, including summaries on generalised anxiety, panic, depression, obsessive-compulsive disorder and post-traumatic stress. Each uses the principles of the Stepped Care Model so that it is applicable across primary and secondary care. The focus is upon the clinical content of the guideline, which includes the triad of a) screening, identification and education about the disorder b) evidence based psychological treatments (in particular cognitive behaviour therapy- CBT) and c) drug treatments. These summaries have been used as educational aides within workshops and lectures for NHS community mental health teams, trainee psychiatrists in North Yorkshire, Leeds University MSc Course and in national CBT workshops for the Royal College of Psychiatrists via their Centre for Learning and Conferences in 2012 and 2013. These summaries have proved very popular with healthcare professionals and so their development will continue. This submission concentrates on the summary produced for the social anxiety disorder guideline.

The initial response to the summaries has been very positive, and further research is planned to ascertain their usefulness. As part of an educational evaluation project, all professionals who attend Dr Blenkiron's CBT training workshops locally and nationally are asked to rate their knowledge, skills and confidence before and after attending each workshop. A specially devised feedback form is used which includes four 10-point rating scales. Preliminary results have shown a significant increase in participants' self rated knowledge (up by 13%), skills (20%) and confidence (16%) after attending the workshop series. The median score for post workshop factual knowledge (assessed independently via multiple choice questions) is 77%, and participants' median rating for educational value of workshop content (including the NICE summaries) is 9/10 (very good to excellent).

Although it is difficult to assess the impact on practice directly, adherence to NICE guidelines is evaluated through a systematic trust-wide NHS audit programme. In the meantime other opportunities are being pursued to promote the summaries locally within secondary care and also more widely, for example through the IAPT (Improving Access to Psychological Therapies) Programme.

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Summary of NICE guideline on social anxiety disorder for use by healthcare professionals

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Dr Blenkiron has previously developed digestible summaries of NICE guidance for mental health services, including summaries on generalised anxiety, panic, depression, obsessive-compulsive disorder and post-traumatic stress. Each uses the principles of the Stepped Care Model so that it is applicable across primary and secondary care.

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OxCADAT ResourcesResources for cognitive therapy for PTSD, social anxiety disorder and panic disorder.Social Anxiety Disorder

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Social anxiety training videos Social anxiety training manual Social anxiety questionnaires and therapy materials

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Cognitive behavioral therapy for postpartum panic disorder: a case series

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Cognitive behavioral therapy for postpartum panic disorder: a case series

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Abstract

Background

Clinical anxiety is common during the perinatal period, and anxiety symptoms often persist after childbirth. Ten to 30 % of perinatal women are diagnosed with panic disorder (PD)-far more than the 1.5-3% rate among the general population. Although cognitive behavioral therapy (CBT) has been determined to be an effective treatment for PD, few studies have been conducted on CBT effectiveness in treating postpartum PD and, to the best of the knowledge of the present authors, no research has been conducted on postpartum PD among Japanese women. In this manuscript, we report on our administration of CBT to three postpartum patients with PD, detailing the improvement in their symptoms.

Case presentation

All patients in this study were married, in their thirties, and diagnosed using the Mini-International Neuropsychiatric Interview as having PD with agoraphobia. The Panic Disorder Severity Scale (PDSS) was used to evaluate patients' panic symptoms and their severity. All patients received a total of 16 weekly 50-min sessions of CBT, and all completed the treatment. All patients were exceedingly preoccupied with the perception that a "mother must protect her child," which reinforced the fear that "the continuation of their perinatal symptoms would prevent them from rearing their children". After treatment, all participants' panic symptoms were found to have decreased according to the PDSS, and two no longer met clinical criteria: Chihiro's score changed from 13 to 3, Beth's PDSS score at baseline from 22 to 6, and Tammy's score changed from 7 to 1.

Conclusions

CBT provides a therapeutic effect and is a feasible method for treating postpartum PD. It is important that therapists prescribe tasks that patients can perform collaboratively with their children.

Peer Review reports

Background

Postpartum women's mental heath

In the field of women's health, anxiety and depression symptoms are common in the postpartum period [ 1]. A recent literature review reported that generalized anxiety disorder, PD, obsessive compulsive disorder (OCD), and post-traumatic stress disorder are frequently diagnosed in postpartum women [ 2]. Specifically, the prevalence of clinically significant anxiety and depression, which is the most common mental condition during the postpartum period, has been observed at a rate of 10-20% in developed countries and approximately 30% in developing countries [ 3]. Also, the prevalence rates of PD in the general population range from 1.5 to 3.5% [ 4]; meanwhile, although using a small sample, a previous study showed that 11% of postpartum women have PD [ 5]. Thus, PD is more common in postpartum women than in the general population. PD is characterized by both recurrent and unexpected panic attacks, with at least one of the attacks having been followed by 1 month (or more) of one (or more) of the following: (a) persistent concern about having additional attacks; (b) worry about the implications of the attack or its consequences (e.g., losing control, having a heart attack, "going crazy"); (c) a significant change in behavior related to the attacks. PD is often (but not always) diagnosed alongside agoraphobia [ 4]. Untreated anxiety can have negative long-term consequences for both mother and child [ 6, 7]. Hence, it is importance to improve of symptoms by evidenced-based interventions. In the National Institute for Health and Care Excellence (NICE) guidelines, selective serotonin reuptake inhibitors (SSRIs) and Cognitive Behavioral Therapy (CBT), which have established effectiveness, are recommended as primary options for the treatment of PD [ 8]. However, SSRIs can cause adverse effects for fetus and infants and, thus, postpartum women are reluctant to take them [ 9]; regular exposure to SSRIs in the uterus is related to postnatal mental-health problems and an increased risk of fatal heart failure (hazard ratio: 1.17-1.38) [ 10, 11].

CBT for PD

The CBT model for treating PD indicates that patients with PD can misinterpret normal physical sensations such as increased breathing, palpitations, and dizziness, and this can lead to panic attacks [ 12]. The CBT model seeks to help patients with PD understand that their internal physical sensations are normal, pursuing this outcome through behavioral experiments; for example, causing excessive breathing by asking the patient to run, or spinning the patient on a chair to make them dizzy. In Japan, we already reported feasibility of CBT for adult patients with PD by 2 single arm trials [ 13, 14]; We also confirmed a significant reduction of PD symptoms reporting a 60-80% improvement rate.

The use of CBT to address PD has been consistently found to be effective by meta-analysis including randomized controlled trials (RSTs) [ 15]. However, the effects of CBT are understudied. CBT's previous research on perinatal depression and on effectiveness of psychotherapy for non-perinatal adult PD by the rigid systematic review has important implications for perinatal PD [ 2, 16]. The recent review by meta-analysis including 20 RCTs, including 3623 women, show that CBT as psychotherapy significant improved depression symptoms [ 16]. In addition, the review suggested that the intervention group had a lot of cured women than the control group that treatment as usual at almost of RCTs: Short term Odds Ratio: 6.57; Long term Odds Ratio: 2.00). In other words, CBT improve perinatal depression twice to sextuple as much as usual care. Although CBT models for depression and PD have different the hypotheses for maintenance of mood or anxiety, Intervention by CBT have targets of cognitions and behaviors in common. Therefore, CBT may be able to reduce panic symptoms as well as depression for perinatal PD. In addition, since literary prior research was in the Western culture area [ 2], it is important to consider CBT for perinatal PD in Eastern Asia as Japan.

Responsibility in the postpartum patient with PD

A previous case series reported a mother who had become concerned that her child was isolated from the community and felt disappointed in herself [ 17]. The women experienced distressing symptoms, such as chest pain, palpitations, shortness of breath, dizziness, tightening of throat, blurry vision, amplified sounds, and tingling in extremities. They could not leave their homes, worrying about bad influence on their children. This mother's suffering can be interpreted as a response to her love for her child reported that participants expressed feelings of guilt, avoidance, distancing and were completely distressed and overwhelmed by the responsibilities of motherhood.

A sense of responsibility for child care can promote excessive control of perinatal physiological and healthy responses. Obsessive compulsive disorder is a disease that strives excessively to fulfill one's own sense of responsibility for things that can't be originally controlled. The leading cognitive models of OCD posited that "inflated responsibility" beliefs play as a vulnerability and maintenance cognitive factor for obsessional thinking [ 18, 19]. Previous study by random-effect meta analyses included twenty-two studies ( n = 8541, 48 effect sizes overall) suggested that "inflated responsibility beliefs may be associated also with symptoms of different forms of psychopathology other than OCD, specifically anxiety disorders. A possible explanation could be that responsibility beliefs play as a transdiagnostic cognitive factor for both OCD and anxiety disorders [ 20]". Hence, it would probably be necessary to implement CBT to help such mothers recognize their responsibilities as mothers and the relationships they should have with their children. Additionally, postpartum PD can be caused by catastrophically misunderstanding physiological responses, because women can feel fear as a result of sensing abnormal respiration, dizziness, and changes in body temperature. Therefore, psychological education on the physiology of pregnancy may also be therapeutically important.

Objective of this study

The objective of this study was to investigate the adaptability of CBT for postpartum PD of Japanese patients. Here, we present the results from clinical practice about postpartum PD of three patients. All patients had inflated responsibility for anxiety symptoms and physical sensation. In the current study, we focus on the CBT model of postpartum PD. We performed a retrospective study by three case series to assess the efficacy and feasibility of our CBT model for adult PD [ 21].

Case presentation

Participants

Participants were three women aged 36 to 38 years who met DSM-IV-TR criteria for PD [ 4]. Two patients had been referred by the obstetrics-gynecology to our psychiatry unit in Teikyo University Chiba Medical Center to treat their anxiety. Another patient had been referred by the psychiatry to our CBT center in Chiba University to improve her PD more. To distinguish among the three women in this manuscript, they have been assigned the fictitious names of "Chihiro," "Beth," and "Tammy." Table 1 shows the patients' characteristics: all participants have two infants. Range of children' age was 0 to 4. Each patient had a supportive family and husband to whom each had been married for at least 7 years. Only Beth had lived in northern Europe, returned hometown to give birth her second child. Once her PD had improved, Beth planned to return to the country where her husband worked. These patients showed an increase in panic-related symptoms during the postpartum period and received CBT within 6 months of childbirth.

Table 1 Characteristics of the three patients

In the assessment session before CBT, first author conducted interviews using the Mini-International Neuropsychiatric Interview (M. I. N. I.) [ 22, 23, 24], all patients exhibited sufficient criteria for PD diagnosis. Further, according to standard practice, the severity of their PD was measured using the Panic Disorder Severity Scale (PDSS) [ 25, 26]; Panic symptom severity levels ranged from mild to severe. The PDSS scores are shown in Table 2. None of the participants had previously received any cognitive behavioral intervention. Chihiro and Beth are reluctant to take regular medications, instead preferring to receive exclusively CBT introduced by their doctor (Second author: Sato K). Tammy already received pharmacotherapy and showed an improvement in symptoms. However, she hoped to receive CBT to further reduce the remaining panic symptoms. Tammy was also introduced to this psychotherapy by her doctor.

Table 2 Outcomes at pre-, middle-, and post-CBT

Measures

To provide data on the effectiveness of the therapy, participants completed assessment surveys reporting panic, general anxiety, and mood during daily life in the first, middle, and final CBT sessions. The primary outcome was measured using the PDSS [ 25, 26]. The PDSS is a 5-point Likert-type scale ranging from 0 (not severe) to 4 (severe). The PDSS is a seven-item clinical interview rating scale that assesses the core features of PD. The seven items include (1.) the frequency of panic attacks and episodes with limited episodes, (2.) panic attacks and LSE distress, (3.) anticipatory anxieties, (4.) avoidance, (5.) fear and avoidance of panic-related sensations, (6.)occupational dysfunction, and (7.) social dysfunction. Evaluation using this scale takes 10-15 min. As a preliminary analysis, the PDSS survey shows useful psychopathological characteristics [ 27]. To measure general anxiety and mood, generalized anxiety symptoms and depressive symptoms were measured by the patients' therapists using the Generalized Anxiety Disorder-7 (GAD-7) scale and the Patient Health Questionnaire-9 (PHQ-9), respectively [ 28, 29, 30]. The GAD-7 was designed to identify probable cases of generalized anxiety disorder and to assess symptom severity. The items featured on the GAD-7 describe the most prominent diagnostic features of the DSM-IV diagnostic criteria A, B, and C for generalized anxiety disorder [ 4]. In accordance with the GAD-7, subjects are asked how often, during the last 2 weeks, they have been bothered by each of the seven core symptoms of generalized anxiety disorder: (a) feeling nervous, anxious, or on edge; (b) uncontrollable worrying; (c) worrying too much; (d) trouble relaxing; (e) restlessness; (f) feeling annoyed or irritable; (g) feeling afraid as if something awful might happen. The PHQ-9 consists of nine items to assess the presence of the nine diagnostic criteria for major depression according to DSM-IV [ 4]. The PHQ-9 evaluates the presence of the following symptoms over the previous two-week period: (a) depressed mood, (b) anhedonia, (c) sleep problems, (d) feelings of tiredness, (e) changes in appetite or weight, (f) feelings of guilt or worthlessness, (g) difficulty concentrating, (h) feelings of sluggishness or worry, and (i) suicidal ideation. Items on both the GAD-7 and PHQ-9 are answered on a four-point Likert scale from 0 to 3 as follows: 0 (never), 1 (several days), 2 (more than half of the days), and 3 (most days).

Therapist and supervisor

As the aim of this case series was to learn how to adapt CBT for postpartum PD, it was essential that the therapy and supervision be conducted by individuals fully trained in adult PD. All sessions were delivered by Matsumoto K., an experienced clinical psychologist who had been trained in CBT for anxiety disorder during a clinical placement at the Center for Cognitive Behavioral Therapy, Chiba University Graduate School of Medicine, Japan. Matsumoto K had been provided weekly individual face-to-face supervision by Shimizu E who developed the CBT model for PD.

Treatment

Therapy was delivered in accordance with the standard adult protocol (i.e., 16 individual 50-min sessions). The CBT model is administered once per session, with the exception of the "behavior experiments," which were repeated five times in a row. After each session, Matsumoto K carefully reviewed the session and discussed with Shimizu E the effect panic seemed to have on the patient's cognition and behaviors, along with plans for the next session. All patients completed 16 sessions of the CBT model [ 21].

The following treatment components were conducted with the aid of worksheets delivered during the session and also as homework:

1. 1)
Assessment and goal setting: The therapist performed hearing of mental health history, evaluated severity of panic symptoms by PDSS, and provided feedback to patients. Through this, the patients could gain an understanding of themselves (including their symptomology), establish therapeutic goals, and increase their focus on addressing PD by CBT. In Session 1, the patients were asked, as homework, to think of the thoughts and behaviors related to a feeling of panic that they experience or perform in their daily lives.

2. 2)
Psycho-education regarding the CBT model: The application of Seki and Shimizu's CBT model was determined collaboratively with the postpartum women, based on their own thoughts, images, and safety-behaviors [ 21]. The model used paper- or digital-based visual aids created by the therapist to help the patients easily understand their panic. In the course of relaxation, the therapist relieved the patients' physical tension by instructing them in normal, rhythmic breathing; sometimes, the therapist demonstrated this by performing the behaviors him/herself.

3. 3)
Case formulation: Fig. 1 depicts Chihiro's model. The relationship among the three elements of 1) attention to internal information from body sensations, 2) critical misinterpretation, and 3) safety behavior combined to invariably cause the patients to maintain their panic levels [ 31]. The therapist illustrated this vicious cycle of panic to the patients using a visual aid.

4. 4)
Safety behaviors: Therapist helped the patients identified safety behaviors. To examine the functions of the patients' safety behaviors, in Session 4, two ways of role-playing (both with and without safety behaviors) were demonstrated. In the first trial, the patients were asked to focus their attention on themselves and think of a panic attack, while also performing their habitual safety behaviors (including maintaining an internal attention condition). In the second trial, they were encouraged to focus externally, not to perform safety behaviors, and instead to involve themselves in their situation (external attention condition). Typically, patients with PD discover that the habitual safety behaviors by which they perceive internal physical sensations (being self-focused and evaluative) makes them feel more anxious. It is important that patients empirically recognize their unconscious safety behaviors and maintain an awareness of their internal and external attention conditions. As homework, patients were recommended to repeat the two approaches on a daily basis.

5. 5)
Re-constructing the catastrophic self-image associated with internal physical sensations: During panic-related episodes, visual images that caused pain may also occur, along with symptoms of post-traumatic stress disorder [ 32], and these can last longer than the instigating thought. If the patient converts the visual image into a linguistic format (i.e., through speaking or writing it), it disappears more quickly [ 33]. Based on the negative emotions arising from critically exaggerated interpretations of physical sensations, patients with PD overestimate the true threat and create catastrophic images [ 34]. In Session 5, in order to establish an identification of images, the patients first, with their eyes closed), were asked to express the most catastrophic image that, for them, can cause a panic attack involving symptoms such as palpitations and hyperventilation (e.g., dying on the street because an ambulance does not arrive). Next, the meaning of the image was discussed, such as through considering evidence and falsifications, intelligently reconstructing the meaning of the image in order to increase the patients' confidence. Finally, the therapist encouraged the patients to create positive images, and discussed with the patients the relationship between the safety behaviors and the image.

6. 6)
Attention-shift training: Patients with PD tend to excessively focus their attention on internal physical sensations (palpitations, hyperventilation, dizziness, etc.) [ 35], and become hypersensitive to unusual sensations [ 36], thus making, anxiety symptoms more likely to occur. Therefore, it is necessary to direct attention to external, non-physical sensations (sounds, colors, figures). In addition, for patients who try to remain focused on external attention to avoid the fear of internal feelings (a safety behavior), the goal is to be able to freely and flexibly shift between internal and external attention.

7. 7)
Behavioral experiments regarding catastrophic beliefs: It was necessary to conduct behavioral experiments across multiple sessions, including interceptive exposure and in vivo exposure. Hence, we collaboratively devised experiments to examine the patients' catastrophic beliefs regarding their physical sensations. During the experiments, in order to collect new information about their panic, patients were encouraged to stop performing their safety behaviors and to focus their attention externally. This was designed to help patients realize that the feared catastrophic outcome is less likely to occur than they originally believed (see Additional file 1 for examples with the postpartum patients). Behavioral experiment was administered in session 7 to session 11, which was repeated five times in a row. Patients were recommended for exposure to select methods based on their diagnosed level agoraphobia, based on the anxiety hierarchy chart.

8. 8)
Re-scripting early panic memories associated with negative images: Patients with anxiety disorder are more likely to recall content relating to threats [ 37], which makes them hypersensitive to stimuli related to threats and more likely to retain such stimuli in their memory [ 38]. Therefore, after the first intense panic attack, some patients experience the event as a trauma. As part of this CBT intervention, after identifying the traumatic memories, the patients addressed these memories using techniques and empathic words learned through CBT. This process overwrites the implications of the event and attributes a more positive meaning to a panic attack. The patients had reduced mental defeat and increased cognitive flexibility, through "imagery re-scripting," so that they came to be able to manage the meaning of images and memories associated with the first panic attack situation [ 39].

9. 9)
Modifying pre- and post-event processing: By reflecting on behaviors during and results after a panic attack, a patient tries to confirm the correctness of their safety behaviors as ritual actions. As a result, they develop increased confidence in false beliefs. Consequently, patients with PD must cease engaging in such pre- and post-event processing. By writing down their ruminations and recording the specific nature of their worry surrounding an event and analyzing the relative merits and demerits of such thoughts, patients can usually choose not to engage in such habits in future.

10. 10)
Opinion survey regarding others' evaluations of a catastrophic situation: Even if the worst situation (such as hyperventilation and fainting) occurs, patients need to be aware that others will not evaluate them as negatively as they believe. To assess the criteria and viewpoints of others, public opinion surveys were conducted.

11. 11)
Schema work: Negative nonfunctional beliefs/assumptions (schema) were identified in this session. For example, an extreme cautionary warning is: "I must always be careful about chest palpitations." For this, the conditional belief is: "I could die unless I carefully monitor myself for chest palpitations." Meanwhile, the unconditional belief is: "No matter what I do, I will suddenly die." To address this, patients were asked to create positive functional beliefs/assumptions instead of relying on schema, and to write them on cards so that they could be referred to at any time. For example, "If I feel heart palpitations, it is not an actual heart attack; for example, I can still walk." As homework, patients were asked to recite the contents of the cards they created every day and record evidence of positive emotions supporting the new belief.

12. 12)
Preventing relapse: The therapist listened to the skills and knowledge the patients had acquired through their treatment and gave them feedback regarding their demonstrated level of awareness. In addition, to generalize what the patients had learned from previous PD-related episodes, the therapist held collaborative discussions with the patients.

Patient 1's case-formulation

Patient 1 - Chihiro

Chihiro was 36 years old at the first session. She graduated from college and worked full-time as a retailer for a decade. She then married in her early thirties and retired from full-time work, taking a part-time position as a clerk. After 2 years, Chihiro became pregnant; she consequently retired from her career and began living a happy life at home. Chihiro's decision to retire was an easy one; caring for her children was her priority. Four years later, she had a second child, for whom she had hoped and planned. For this second pregnancy, Chihiro needed to be hospitalized and underwent a cesarean section. Immediately after hospitalization, Chihiro began to experience symptoms of anxiety, such as feelings of compression, stuffiness, cold sweats, and a strong fear that she was "about to scream and lose control." However, as the birth of her child was imminent, the nurse asked Chihiro to "please stay in your room," so she remained in her hospital room, experiencing repeated panic attacks. Chihiro gave birth without complications, and she felt relief upon meeting the new member of her family. Unfortunately, Chihiro's panic attacks did not cease after discharge, so she visited a psychiatrist for help. Chihiro thought, "if I keep having panic-attack symptoms, I will not be able to be a good mother because I won't be able to do things such as take the children to the park." The second author, who became Chihiro's attending psychiatrist, diagnosed her with PD and agoraphobia using DSM-IV-TR criteria [ 4]. At the time, because Chihiro was lactating (as it was 2 months after childbirth), CBT was initially administered without medicinal intervention, but Chihiro suffered a strong panic attack after the fifth session. After this, her doctor prescribed her an SSRI (25 mg of sertraline). From the seventh session, the level of sertraline was increased to 50 mg, and this continued until the final CBT session.

In the first CBT session, we noticed that Chihiro constantly focused her attention on her throat. Such a habit made her hypersensitive to throat discomfort. Conversely, Chihiro also held the belief that "if I pay too much attention to my throat, I will suffer a panic attack." To verify Chihiro's catastrophic beliefs regarding physical sensations, the therapist and Chihiro undertook behavioral experiments by performing activities that caused her to feel fearful (e.g, taking the elevator, going to the cinema and sitting in the middle of the venue, exercising, going out with her children), without performing safety behaviors; in one task, in order to simulate a breathless experience Chihiro was asked to climb stairs quickly, which she performed with the therapist in the hospital, as follow:

KM: If your speculation is correct (if you don't cope with it right away you will asphyxiate), you must always get a panic attack when you feel of dyspnea, right?

Chihiro: I agree. Even with this care, I always feel like my throat is full.

KM: Another way of thinking is explained in the CBT model of PD. It is a hypothesis that you are catastrophically interpreting the physical sensations and focusing attention on internal information has made it easier to notice the unpleasant physical sensations.

Chihiro: That might be true. It is too difficult for me to protect my children if panic attach occurs to me, so that I always be concerning about the condition of my throat after a panic attack has occurred.

KM: It is a natural thing to happen to a healthy person to feel tightness when exercising or doing activities. Chihiro's breathlessness may also be healthy and harmless. Dare, Could you do activities that feel of dyspnea and reassess the danger? First task is climbing the stairs of this hospital with me, from the first floor to the ninth floor.

Chihiro: Well.... OK, I will try.

KM: Brave decision. Let's challenge now!

To expose Chihiro to compression and breathlessness from physical internal sensations, the following homework tasks based on behavioral experiments were established: to expose internal sensations such as breathless or compression, she would exercise by climbing up and down a low platform for 10 min, wrap threads for cooking around her wrists, and use a hug string when hugging her baby. Through the series of behavioral experiments, Chihiro learned that her fear of physical sensations was unfounded. After performing the experiments, Chihiro found it easier to go out with her children. Finally, she was able to bring her children to a show for children, which required her to get on a limited express train whose doors remain sealed for over 10 min after the train has departed. She was glad that her children, especially the eldest son, seemed very happy to be able to go out with their mother. Chihiro's PDSS scores for panic symptoms fell from 13 pre-treatment to 3 post-treatment: GAD-7 scores from 10 to 5; PHQ-9 scores from 7 to 7 (see details in Table 3).

Table 3 Patients' performance in each session

In Chihiro's case, the change in the her living environment seemed to cause the absence of a change in the PHQ-9 value from before and after treatment, despite marked improvement in panic symptoms. In Japan, there is customary for a postpartum daughter live for a while at her mother's house. After a daughter has recovered from the fatigue of childbirth, she will return to her husband's home. At the end of the treatment program, Chihiro was returning home with her children, and so she no longer had the support of her parents' constant presence. Therefore, the relative increase in Chihiro's nurturing role may explain the post-treatment PHQ-9 score (the same value recorded during pre-treatment).

Patient 2 - Beth

Beth was 38 years old at the first session. After graduating from university, Beth worked full-time as a general clerk for 15 years. Marrying in her mid-thirties, she soon gave birth to her first child at the age of thirty-six. On an otherwise normal day when Beth had been driving, she suffered a panic attack. She felt a sharp panic manifest in the form of a rapid heartbeat, breathlessness, and serious fear. Since then, Beth often experienced palpitations, difficulty breath, trembling, and high levels of fear, both in her car and at home. In the past, Beth had been treated with psychosomatic medicine, and further anti-anxiety medicine was prescribed (specifically ethyl loflazepate, as well as other medications whose details are unknown to the authors) to her to take regularly for 1 year, but it was ineffective. Further, due to circumstances regarding her husband, she relocated to a European country, and her treatment was temporarily suspended. Although Beth wanted to take walks with her child in the beautiful European townscape, she never did because she feared "if I feel dizzy and my breathing gets difficult, I may faint; and this will reflect badly on my husband and could have a negative effect on his career."

Beth's strongest supporter was her husband, who listened to her problems and anxieties every day. Beth was able to go out with her husband and baby every weekend, and this made her happy. Then, Beth was pleased to find that not long after moving to Europe, she had become pregnant with her second child. However, her anxieties about her panic attacks also increased. Approximately 10 months after moving abroad, Beth returned to Japan to give birth. After giving birth she felt unable to fulfill her responsibilities as a mother with respect to her baby's care and education, saying "I can't bring my child anywhere as it is, and I feel depressed all day if I do not go out." As a result, she visited a psychiatric department for the purpose of curing her panic and anxiety. Using DSM-IV-TR criteria, Beth was diagnosed with PD with agoraphobia [ 4]. As Beth wanted to breastfeed her baby, she consulted with the attending psychiatrist carefully and decided to undergo individual CBT rather than pharmacologic therapy.

As part of the CBT, Beth performed role play that involved boarding a train. She was asked to notice her strong anxiety when she became worried and to pay attention to her respiration. Although she appropriately engaged in external attention during the session, she later reported that she was unable to do so during homework because her child's "playing was very noisy, and I could not concentrate." Consequently, we adjusted the task to flexibly accommodate and bring attention to the sounds of children playing as well as her physical sensations. Beth answered, "I will do it while breastfeeding," and later reported that she had succeeded, stating that: "I became confident in my ability to flexibly manage my attention, and I was able to go to a hairdresser for the first time in a few months." In a behavioral experiment, Beth sat on a rotating chair, and was spun around five times, making her dizzy. She then rushed up some stairs (with the therapist behind her as a safety precaution). Through this activity, Beth experienced heavy breathing and dizziness. Additionally, focusing on her internal physical sensation allowed her to develop the reasonable interpretation that "if I feel difficulty breathing, I will not succumb to a little dizziness."

Beth also believed that "when a person feels dizziness or shortness of breath, because my husband's boss or colleague and their wife will not respect a person whose family member has a PD, it reflects badly on my husband." To help her understand that others would not make this evaluation, the therapist first confirmed that Beth herself did not negatively evaluate others based on their spouse's physical symptoms as follows:

KM: "If your friend raise panic attack in front of you, would you evaluate her or him as a bad mother/wife?"

Beth: "No at all."

KM: "Why do you evaluate yourself negatively?" "Is that reasonable?"

Beth: "Well, now that you say that, I may be too harsh for myself."

Next, we performed an opinion survey with 10 people, affirming that, if a person collapses from a panic attack, none believed that "that person's family can't be trusted," or "that person's family can't function." The people recruited for the survey were Beth's three family members (father, mother, and husband) and seven colleagues of the authors. These efforts allowed Beth to become aware that "people do not think critically about others in a negative way," and somewhat relieved the anxiety that caused Beth's panic attacks as follows:

KM: "According to the questionnaire, no one answered that they could not trust anyone who had panic attacks. How would you interpret this result?"

Beth: "Unsurprisingly everyone was kind, they don't evaluate negatively. I found that I was the most critical of my own symptoms."

In the final session, Beth told the therapist that "I would like to take my children to a beautiful national park near my residence in Europe," to which she later returned. Her panic symptoms pre- and post-treatment changed from 22 to 6 on the PDSS scale, respectively. Her GAD-7 scores changed from 10 to 4, and PHQ-9 scores changed from 6 to 4 (see details at Table 3).

Patient 3 - Tammy

Tammy was 36 years old while first session. Tammy is the mother raising two children. After graduating from high school, Tammy began working full-time. Then, at the age of 29, Tammy got married. After her marriage, she took a part-time job in sales, which she retained until she gave birth to her first child. Later, she gave birth to a second child, a daughter. Tammy wanted to raise more children so, at the age of 36, she planned to become pregnant again. Soon after becoming pregnant, Tammy was sitting in her car on a sunny summer day waiting for a traffic signal when she suddenly suffered a panic attack: "my head felt hot, I could not breathe; the panic made me so scared that I returned home." While delighting in her pregnancy, a sufficiently stressful situation to cause another panic attack did not arise for some time. However, Tammy suffered a miscarriage and her emotional state changed. She suffered a panic attack when visiting to a familiar beauty salon by herself. The feeling of heat when hot water was poured onto her hair made Tammy afraid: "my head was hot, I became afraid! I could not run away from there, as I was fixed into a chair." Leaving the beauty salon allowed her to calm herself; however, anticipating further panic attacks, she returned home without having her hair cut.

A month later, Tammy continued to experience troubles in daily life, such as sudden panic attacks and fear when going out. As a result, Tammy went to a psychiatrist who was recommended to her by her family physician. Using DSM-IV-TR criteria, the psychiatrist diagnosed her with PD and agoraphobia [ 4], prescribed 1.0 mg of ethyl loflazepate. The effect of this pharmacotherapy was remarkable, as Tammy stated that "my daily life has become much easier," but anticipatory anxiety remained. Therefore, Tammy decided to undergo CBT, a decision she made by consulting with her psychiatrist 4 months after beginning pharmacotherapy. Considering Tammy had responsibilities in raising her children, we agreed to conduct CBT via video-conferencing in order to ensure that treatment could be provided at a regular frequency through 50-min weekly sessions.

After explaining the CBT model for PD and formulating a protocol based on Tammy's panic symptoms, activities to simulate these symptoms were affected. Tammy found that efforts to focus on the dryness in her throat and breathing kept her constantly aware of those sensations, and that her safety behaviors in this regard were taking deep breaths or having a drink of water. Through role playing, we verified that her safety behaviors were maintaining her anxiety. As a result, Tammy agreed to engage in daily life without performing safety behaviors. For example, Tammy often noticed her breathing when lying down and observing her child sleeping (in Japanese culture, mothers lying beside pre-school children is considered to be a good child-rearing method). In recognition of this behavior, tasks in behavioral experiments involving exposure to internal senses were established, including breathing through a straw, excessive breathing, putting warm water on her face, and submerging her face in hot water while in the bath. Every task served to reinforce a new belief that breathlessness is not related to panic attacks. Tammy later reported that: "I can start house keep, but I cannot carry on doing them." Therapist found that she had traumatic memory about panic attack. She changed the meaning of trauma memory to a safer thing: from "I suffer from panic symptoms that never recover to helpless" to "I know how to cope with panic and the panic attack will vanish over time." In intervention for her traumatic memory, She advised past-herself that "I know you were afraid. Don't worry, paying attention to bodily sensations and uneasy thoughts makes you uncomfortable, so you should read some magazines or engage in some other behaviors that distract you."

Tammy used empathic words to give advice to her past self. Additionally, Tammy was fearful of getting on a train, but, by regularly performing an activity involving boarding a bus or train, she was finally able to board a bullet train and remain on board for over an hour. The severity levels of her pre- and post-treatment panic symptoms decreased from 7 to 1, respectively, as measured by the PDSS. GAD-7 scores changed from 3 to 2 and PHQ-9 scores changed from 2 to 2 (see details in Table 2).

Discussion & Conclusion

The present case series concerned the efficacious application of CBT to treat three women with PD related to reproductive events. Specifically, it involved the use of the Seki and Shimizu CBT model [ 21], which has been demonstrated to be effective for adult patients with PD; the model comprises 16 weekly 50-min sessions. In this case series, all patients performed all aspects of CBT and consequently showed improvements in their panic symptoms. They all experienced panic attacks during the postpartum period and had safety behaviors that reinforced their excessive anxiety regarding their physical conditions and physical sensations. These feelings seemed to evolve from their viewpoints regarding the duty of a mother to raise her children. It is possible that women after childbirth judge normal autonomic nervous system responses, such as anxiety, shortness of breath, palpitations, etc., to be a great threat to her own and her children's lives, and consequently pay excessive attention to their physical sensations and safety behaviors [ 42]. All patients were socially required to play a role as a mother, and they were hoping to fill the role one their-self. Such physiological and social contexts during pregnancy and after birth may affect all elements of the CBT model vicious cycle, such as occurrence of physical symptoms, schema, automatic thinking, self-image, safety behavior, and anxiety symptoms. We suggest that it is important for postpartum PD to intake that context in each session, since CBT tasks that are directly related to protecting and caring for children were more performed than others.

In a previous study, it was indicated that beliefs concerning inflated responsibility for causing or preventing harm to oneself or others plays a critical role in the maintenance of compulsive checking behaviors and other form of obsessive behavior characteristic of OCD [ 43]. The findings of the present case series accord with those of previous studies that have shown that attitudes toward child rearing and responsibility as a mother influence the manifestation of symptoms of PD. Therefore, in order to prevent PD and unnecessary anxiety in this population, it is suggested that during the postpartum period women be provided with psycho-education on perinatal physiology and mental health. Also, a belief that closely resembles OCD was observed in the three patients in the present study: "inflated responsibility" [ 44], this involves the belief that a threat can be avoided depending on one's own efforts, resulting in the threat being excessively estimated. The definition of "responsibility" in obsessive-compulsive disorder is that there is an important force that can cause or prevent the consequences one fears [ 45]. With regard to the beliefs that affect the onset of mental illness, PD is characterized by interpreting the physical sensation catastrophically [ 12]. We found that perinatal PD patients often have responsibility which prompts fear or anxiety concerning their ability to take care of the baby. As a result of this observation, we suggest that catastrophic interpretation of responsibility be used to predict the onset of perinatal PD. The finding among Japanese PD patients in the perinatal period support the previous findings that perception of responsibility is a risk factor which can be used in cross-diagnosis of anxiety disorder and obsessive-compulsive disorder [ 19].

In CBT, it is important to set tasks that can improve patients' standard of living, and to have the patients continue to perform these tasks in their own living environments [ 46, 47]. In these case studies, all patients were instructed to bring their children to the city park or the shopping mall, and, upon doing so, they consequently reported a strong sense of accomplishment. It is thought that setting tasks that mothers can perform with their children is important for motivation, and such tasks also have high levels of utility in everyday life. Considering that mothers seem to fall into a vicious cycle of panic as a result of their obligations to protect their children and their sense of responsibility regarding child rearing, it is natural that tasks involving the role of a mother being used as motivation. The findings of our report further support that it is critical to establish behavior al experiments and homework tasks that involve children, particularly for mothers with postpartum PD.

When raising multiple children, it may be difficult to visit a hospital frequently. In the series of these cases, Chihiro and Beth received support from their parents, who took care of the children during their daughters' CBT sessions. However, Tammy did not receive support from her parents, so it was difficult for her to visit our facility at least once a month; consequently, she underwent CBT via video-conferencing. Two recent systematic reviews, through meta-analyses, suggested that Internet-based CBT (ICBT) were significantly effective in reducing anxiety from which a patient with anxiety disorder suffered [ 48, 49]. The effectiveness of ICBT for OCD during pregnancy has been reported in a trial involving RCT design [ 50], several studies reported the effectiveness on ICBT for PD [ 51, 52, 53, 54, 55]. To examine the feasibility of ICBT for adult patients with PD, we conducted a clinical trial using a videoconference system, as a result of which the symptoms of panic and agoraphobia were significantly reduced [ 13]. Hence, ICBT, which is composed of web-based treatment programs, involves minimal guidance, allows for correspondence via e-mail, telephone, or video-conferencing, and allows therapists to deliver effective treatment to patients at home on a flexible schedule. Such ICBT approach promises to be useful for pregnant women with PD.

This study is limited in several ways. First, this study is observed retrospectively, it cannot be explained with a causal relationship. To prove the causation of postpartum PD in pregnant women by their strength of their sense of responsibility, future research has to investigate the risk of perinatal PD in a cohort study. The second limitation relates to cultural differences. This study is the first in the world to report the efficacy of the application of the CBT model to Japanese women suffering from postpartum PD, and, as such, should not be extrapolated to the other populations without further research on those specific populations. Since similar studies have not yet been conducted in other countries, this paper cannot predict the efficacy of the CBT model to non-Japanese patients. The final limitation is the failure to ascertain conclusively the effectiveness of the CBT model for perinatal PD. This study cannot claim certain effectiveness, because the series included only three case studies. In order to examine the efficacy of the CBT model for postpartum PD in the future, it is necessary to conduct clinical trials designed to include random controls.

In the present case studies, the patients showed improvements regarding their panic symptoms pre- and post-intervention and did not report any adverse events. Our results show the viability of CBT for patients with PD after childbirth.

Availability of data and materials

Abbreviations

CBT:

Cognitive behavioral therapy

GAD-7:

Generalized Anxiety Disorder-7

ICBT:

Internet-based cognitive behavioral therapy

MINI:

Mini-International Neuropsychiatric Interview

NICE:

National Institute for Health and Care Excellence

OCD:

Obsessive compulsive disorder

PD:

Panic disorder

PDSS:

Panic Disorder Severity Scale

PHQ-9:

Patient Health Questionnaire-9

RCTs:

Randomized controlled trials

SSRI:

Selective serotonin reuptake inhibitors

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Acknowledgements

Mr. Yoichi Seki PhD. and Kohei Yoshino MD. We would like to express our appreciation to Mr. Yoichi Seki PhD. as clinical psychologist and to Mr. Kohei Yoshino (MD) as psychiatrist. They gave keen clinical insights and suggestions regarding this manuscript. The authors would like to express their gratitude to the all of the participants and collaborators. This work was supported by JSPS KAKENHI 18 K03130.

Funding

This study was supported by Japan Society for the Promotion of Science (JSPS) KAKENHI Grant-in-Aid for Scientific Research C, Grant Numbers 18 K03130). The funding sources had no role in the design and conduct of the study.

Author information

Affiliations

1. Research Center for Child mental Development, Chiba University, Chiba, Japan

Kazuki Matsumoto, Sayo Hamatani & Eiji Shimizu

2. Department of Psychiatry, Teikyo University Chiba Medical Center, 3426-3, Anegasaki, Ichihara-shi, Chiba, Japan

Kazuki Matsumoto, Koichi Sato, Sayo Hamatani & Yukihiko Shirayama

3. Research Fellow of japan Society for the Promotion of Science, Chiba, Japan

Sayo Hamatani

4. Department of Cogntiive Behavioral Physiology, Guraduate School of Medicine, Chiba University, Chiba, Japan

Eiji Shimizu

Contributions

All authors declare here that the manuscript has been completed by fully fulfilling their respective roles: KM conducted investigations and interventions on all patients for symptoms. Also, in preparing this paper, KM made effort in the entire process; KS established a comprehensive treatment plan including CBT for cases as a doctor of two patients, managed and supervised it, and made planning and guidance on this case scries; SH conducted a peer supervision of all patients and advised and examined the technology on intervention. In addition, she taught the essential points on the case by paper; YS instructed all authors except the last author for treatment through conferences held within their affiliated institution for 2 cases. Also consideration was given to the procurement and management of materials for intervention by therapists; ES was the primary physician of one patient and supervised as a senior therapist for the intervention of all cases. In addition, overall guidance and supervision on case reports were carried out. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Kazuki Matsumoto.

Ethics declarations

Ethics approval and consent to participate

The authors assert that all procedures contributing to this work comply with the ethical standards of the relevant national and institutional committees on human experimentation and with the Helsinki Declaration of 1975, as revised in 2008. All patients were treated as part of a routine clinical service and the project was considered clinical audit. This research was approved the ethics committee of Chiba University (R000032149), registered under the following research name: "Observational epidemiology database study on cognitive behavioral therapy of the anxiety disorder" (UMIN000028099) on the University hospital Medical Information Network Center.

Consent for publication

All patients provided informed written consent for publication.

Competing interests

The authors declare that they have no competing interests.

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# data[].attributes.attachment_link.title
Cognitive behavioral therapy for postpartum panic disorder: a case series

# data[].attributes.attachment_link.description
Background Clinical anxiety is common during the perinatal period, and anxiety symptoms often persist after childbirth. Ten to 30 % of perinatal women are diagnosed with panic disorder (PD)-far more than the 1.5-3% rate among the general population.

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Recommendations

The following guidance is based on the best available evidence. The full guideline gives details of the methods and the evidence used to develop the guidance.

Box 1 Depression definitions (taken from DSM-IV)

Subthreshold depressive symptoms: Fewer than 5 symptoms of depression.

Mild depression: Few, if any, symptoms in excess of the 5 required to make the diagnosis, and symptoms result in only minor functional impairment.

Moderate depression: Symptoms of functional impairment are between 'mild' and 'severe'.

Severe depression: Most symptoms, and the symptoms markedly interfere with functioning. Can occur with or without psychotic symptoms.

Not that a comprehensive assessment of depression should not rely simply on a symptom count, but should take into account the degree of functional impairment and/or disability (see section 1.1.4).

This guideline is published alongside NICE's guideline on depression in adults with a chronic physical health problem, which makes recommendations on the identification, treatment and management of depression in adults aged 18 years and older who also have a chronic physical health problem.

People have the right to be involved in discussions and make informed decisions about their care, as described in making decisions about your care.

Making decisions using NICE guidelines explains how we use words to show the strength (or certainty) of our recommendations, and has information about prescribing medicines (including off label use), professional guidelines, standards and laws (including on consent and mental capacity), and safeguarding.

1.1 Care of all people with depression

1.1.1 Providing information and support, and obtaining informed consent

1.1.1.3 Inform people with depression about self-help groups, support groups and other local and national resources.

1.1.1.4 Make all efforts necessary to ensure that a person with depression can give meaningful and informed consent before treatment starts. This is especially important when a person has severe depression or is subject to the Mental Health Act.

1.1.2 Advance decisions and statements

1.1.2.1 For people with recurrent severe depression or depression with psychotic symptoms and for those who have been treated under the Mental Health Act, consider developing advance decisions and advance statements collaboratively with the person. Record the decisions and statements and include copies in the person's care plan in primary and secondary care. Give copies to the person and to their family or carer, if the person agrees.

1.1.3 Supporting families and carers

1.1.3.1 For families or carers who are involved in supporting a person with severe or chronic (symptoms more or less continuously for 2 years or more) depression, see recommendations in the NICE guideline on supporting adult carers on identifying, assessing and meeting the caring, physical and mental health needs of families and carers.

1.1.4 Principles for assessment, coordination of care and choosing treatments

1.1.4.1 When assessing a person who may have depression, conduct a comprehensive assessment that does not rely simply on a symptom count. Take into account both the degree of functional impairment and/or disability associated with the possible depression and the duration of the episode.

1.1.4.2 In addition to assessing symptoms and associated functional impairment, consider how the following factors may have affected the development, course and severity of a person's depression:

any history of depression and comorbid mental health or physical disorders

any past history of mood elevation (to determine if the depression may be part of bipolar disorder)

any past experience of, and response to, treatments

the quality of interpersonal relationships

living conditions and social isolation.

1.1.4.4 When assessing a person with suspected depression, be aware of any learning disabilities or acquired cognitive impairments, and if necessary consider consulting with a relevant specialist when developing treatment plans and strategies.

1.1.4.6 Always ask people with depression directly about suicidal ideation and intent. If there is a risk of self-harm or suicide:

assess whether the person has adequate social support and is aware of sources of help

arrange help appropriate to the level of risk (see section 1.3.2)

advise the person to seek further help if the situation deteriorates.

1.1.5 Effective delivery of interventions for depression

1.1.5.2 Consider providing all interventions in the preferred language of the person with depression where possible.

1.2 Stepped care

The stepped-care model provides a framework in which to organise the provision of services, and supports patients, carers and practitioners in identifying and accessing the most effective interventions (see figure 1). In stepped care the least intrusive, most effective intervention is provided first; if a person does not benefit from the intervention initially offered, or declines an intervention, they should be offered an appropriate intervention from the next step.

Complex depression includes depression that shows an inadequate response to multiple treatments, is complicated by psychotic symptoms, and/or is associated with significant psychiatric comorbidity or psychosocial factors.

Collaborative care for step 3 is only for depression where the person has a chronic physical health problem and associated functional impairment.

1.3 Step 1: recognition, assessment and initial management

1.3.1 Case identification and recognition

1.3.1.2 If a person answers 'yes' to either of the depression identification questions (see recommendation 1.3.1.1) but the practitioner is not competent to perform a mental health assessment, they should refer the person to an appropriate professional. If this professional is not the person's GP, inform the GP of the referral.

1.3.1.3 If a person answers 'yes' to either of the depression identification questions (see recommendation 1.3.1.1), a practitioner who is competent to perform a mental health assessment should review the person's mental state and associated functional, interpersonal and social difficulties.

1.3.1.4 When assessing a person with suspected depression, consider using a validated measure (for example, for symptoms, functions and/or disability) to inform and evaluate treatment.

1.3.1.5 For people with significant language or communication difficulties, for example people with sensory impairments or a learning disability, consider using the Distress Thermometer and/or asking a family member or carer about the person's symptoms to identify possible depression. If a significant level of distress is identified, investigate further.

1.3.2 Risk assessment and monitoring

1.3.2.1 If a person with depression presents considerable immediate risk to themselves or others, refer them urgently to specialist mental health services.

1.3.2.3 Advise a person with depression and their family or carer to be vigilant for mood changes, negativity and hopelessness, and suicidal ideation, and to contact their practitioner if concerned. This is particularly important during high-risk periods, such as starting or changing treatment and at times of increased personal stress.

1.4 Step 2: recognised depression - persistent subthreshold depressive symptoms or mild to moderate depression

1.4.1 General measures

Depression with anxiety

1.4.1.1 When depression is accompanied by symptoms of anxiety, the first priority should usually be to treat the depression. When the person has an anxiety disorder and comorbid depression or depressive symptoms, consult the NICE guideline for the relevant anxiety disorder (see find guidance) and consider treating the anxiety disorder first (since effective treatment of the anxiety disorder will often improve the depression or the depressive symptoms).

Sleep hygiene

1.4.1.2 Offer people with depression advice on sleep hygiene if needed, including:

establishing regular sleep and wake times

avoiding excess eating, smoking or drinking alcohol before sleep

creating a proper environment for sleep

taking regular physical exercise.

Active monitoring

1.4.1.3 For people who, in the judgement of the practitioner, may recover with no formal intervention, or people with mild depression who do not want an intervention, or people with subthreshold depressive symptoms who request an intervention:

discuss the presenting problem(s) and any concerns that the person may have about them

provide information about the nature and course of depression

arrange a further assessment, normally within 2 weeks

make contact if the person does not attend follow-up appointments.

1.4.2 Low-intensity psychosocial interventions

Delivery of low-intensity psychosocial interventions

1.4.2.2 Individual guided self-help programmes based on the principles of CBT (and including behavioural activation and problem-solving techniques) for people with persistent subthreshold depressive symptoms or mild to moderate depression should:

include the provision of written materials of an appropriate reading age (or alternative media to support access)

be supported by a trained practitioner, who typically facilitates the self‑help programme and reviews progress and outcome

consist of up to six to eight sessions (face-to-face and via telephone) normally taking place over 9 to 12 weeks, including follow-up.

1.4.2.3 CCBT for people with persistent subthreshold depressive symptoms or mild to moderate depression should:

be provided via a stand-alone computer-based or web-based programme

include an explanation of the CBT model, encourage tasks between sessions, and use thought-challenging and active monitoring of behaviour, thought patterns and outcomes

be supported by a trained practitioner, who typically provides limited facilitation of the programme and reviews progress and outcome

typically take place over 9 to 12 weeks, including follow-up.

1.4.3 Group cognitive behavioural therapy

1.4.3.1 Consider group-based CBT for people with persistent subthreshold depressive symptoms or mild to moderate depression who decline low‑intensity psychosocial interventions (see recommendation 1.4.2.1).

1.4.4 Drug treatment

1.4.4.1 Do not use antidepressants routinely to treat persistent subthreshold depressive symptoms or mild depression because the risk-benefit ratio is poor, but consider them for people with:

a past history of moderate or severe depression or

initial presentation of subthreshold depressive symptoms that have been present for a long period (typically at least 2 years) or

subthreshold depressive symptoms or mild depression that persist(s) after other interventions.

1.5 Step 3: persistent subthreshold depressive symptoms or mild to moderate depression with inadequate response to initial interventions, and moderate and severe depression

1.5.1 Treatment options

1.5.1.1 For people with persistent subthreshold depressive symptoms or mild to moderate depression who have not benefited from a low-intensity psychosocial intervention, discuss the relative merits of different interventions with the person and provide:

1.5.1.2 For people with moderate or severe depression, provide a combination of antidepressant medication and a high-intensity psychological intervention (CBT or IPT).

1.5.1.4 For people with depression who decline an antidepressant, CBT, IPT, behavioural activation and behavioural couples therapy, consider:

counselling for people with persistent subthreshold depressive symptoms or mild to moderate depression

short-term psychodynamic psychotherapy for people with mild to moderate depression.

Discuss with the person the uncertainty of the effectiveness of counselling and psychodynamic psychotherapy in treating depression.

1.5.2 Antidepressant drugs

Choice of antidepressant

For additional considerations on using antidepressants and other medications (including the assessment of the relative risks and benefits) for women who may become pregnant, please refer to the BNF and individual drug summary of product characteristics. For women in the antenatal and postnatal periods, also see also the NICE guideline on antenatal and postnatal mental health.

1.5.2.1 Discuss antidepressant treatment options with the person with depression, covering:

the choice of antidepressant, including any anticipated adverse events, for example side effects and discontinuation symptoms (see recommendation 1.9.2.1), and potential interactions with concomitant medication or physical health problems

their perception of the efficacy and tolerability of any antidepressants they have previously taken.

1.5.2.2 When an antidepressant is to be prescribed, it should normally be an SSRI in a generic form because SSRIs are equally effective as other antidepressants and have a favourable risk-benefit ratio. Also take the following into account:

SSRIs are associated with an increased risk of bleeding, especially in older people or in people taking other drugs that have the potential to damage the gastrointestinal mucosa or interfere with clotting. In particular, consider prescribing a gastroprotective drug in older people who are taking non-steroidal anti-inflammatory drugs (NSAIDs) or aspirin.

Fluoxetine, fluvoxamine and paroxetine are associated with a higher propensity for drug interactions than other SSRIs.

Paroxetine is associated with a higher incidence of discontinuation symptoms than other SSRIs.

1.5.2.4 When prescribing drugs other than SSRIs, take the following into account:

The increased likelihood of the person stopping treatment because of side effects (and the consequent need to increase the dose gradually) with venlafaxine, duloxetine and TCAs.

The specific cautions, contraindications and monitoring requirements for some drugs. For example:

the potential for higher doses of venlafaxine to exacerbate cardiac arrhythmias and the need to monitor the person's blood pressure

the possible exacerbation of hypertension with venlafaxine and duloxetine

the potential for postural hypotension and arrhythmias with TCAs

the need for haematological monitoring with mianserin in elderly people.

Non-reversible monoamine oxidase inhibitors (MAOIs), such as phenelzine, should normally be prescribed only by specialist mental health professionals.

Dosulepin should not be prescribed.

Starting and initial phase of treatment

1.5.2.5 When prescribing antidepressants, explore any concerns the person with depression has about taking medication, explain fully the reasons for prescribing, and provide information about taking antidepressants, including:

the gradual development of the full antidepressant effect

the importance of taking medication as prescribed and the need to continue treatment after remission

potential side effects

the potential for interactions with other medications

the risk and nature of discontinuation symptoms with all antidepressants, particularly with drugs with a shorter half-life (such as paroxetine and venlafaxine), and how these symptoms can be minimised

the fact that addiction does not occur with antidepressants.

Offer written information appropriate to the person's needs.

1.5.2.6 For people started on antidepressants who are not considered to be at increased risk of suicide, normally see them after 2 weeks. See them regularly thereafter, for example at intervals of 2 to 4 weeks in the first 3 months, and then at longer intervals if response is good.

1.5.2.7 A person with depression started on antidepressants who is considered to present an increased suicide risk or is younger than 30 years (because of the potential increased prevalence of suicidal thoughts in the early stages of antidepressant treatment for this group) should normally be seen after 1 week and frequently thereafter as appropriate until the risk is no longer considered clinically important.

1.5.2.8 If a person with depression develops side effects early in antidepressant treatment, provide appropriate information and consider one of the following strategies:

monitor symptoms closely where side effects are mild and acceptable to the person or

stop the antidepressant or change to a different antidepressant if the person prefers or

in discussion with the person, consider short-term concomitant treatment with a benzodiazepine if anxiety, agitation and/or insomnia are problematic (except in people with chronic symptoms of anxiety); this should usually be for no longer than 2 weeks in order to prevent the development of dependence.

1.5.2.9 People who start on low-dose TCAs and who have a clear clinical response can be maintained on that dose with careful monitoring.

1.5.2.10 If the person's depression shows no improvement after 2 to 4 weeks with the first antidepressant, check that the drug has been taken regularly and in the prescribed dose.

1.5.2.11 If response is absent or minimal after 3 to 4 weeks of treatment with a therapeutic dose of an antidepressant, increase the level of support (for example, by weekly face-to-face or telephone contact) and consider:

1.5.2.12 If the person's depression shows some improvement by 4 weeks, continue treatment for another 2 to 4 weeks. Consider switching to another antidepressant as described in section 1.8 if:

1.5.3 Psychological interventions

Delivering high-intensity psychological interventions

1.5.3.3 For all people with depression having IPT, the duration of treatment should typically be in the range of 16 to 20 sessions over 3 to 4 months. For people with severe depression, consider providing two sessions per week for the first 2 to 3 weeks of treatment.

1.5.3.5 Behavioural couples therapy for depression should normally be based on behavioural principles, and an adequate course of therapy should be 15 to 20 sessions over 5 to 6 months.

1.6 Treatment choice based on depression subtypes and personal characteristics

There is little evidence to guide prescribing in relation to depression subtypes or personal characteristics. The main issue concerns the impact of other physical disorders on the treatment of depression. Refer to the NICE guideline on depression in adults with a chronic physical health problem for further information.

1.6.1.1 Do not routinely vary the treatment strategies for depression described in this guideline either by depression subtype (for example, atypical depression or seasonal depression) or by personal characteristics (for example, sex or ethnicity) as there is no convincing evidence to support such action.

1.6.1.2 Advise people with winter depression that follows a seasonal pattern and who wish to try light therapy in preference to antidepressant or psychological treatment that the evidence for the efficacy of light therapy is uncertain.

1.7 Enhanced care for depression

1.7.1.1 Medication management as a separate intervention for people with depression should not be provided routinely by services. It is likely to be effective only when provided as part of a more complex intervention.

1.7.1.2 For people with severe depression and those with moderate depression and complex problems, consider:

1.8 Sequencing treatments after initial inadequate response

Some people have depression that does not respond well to initial treatment. This section describes strategies to adopt if this occurs.

1.8.1 Drug treatments

1.8.1.1 When reviewing drug treatment for a person with depression whose symptoms have not adequately responded to initial pharmacological interventions:

check adherence to, and side effects from, initial treatment

increase the frequency of appointments using outcome monitoring with a validated outcome measure

be aware that using a single antidepressant rather than combination medication or augmentation (see recommendations 1.8.1.5 to 1.8.1.9) is usually associated with a lower side-effect burden

consider reintroducing previous treatments that have been inadequately delivered or adhered to, including increasing the dose

consider switching to an alternative antidepressant.

Switching antidepressants

1.8.1.3 Do not switch to, or start, dosulepin because evidence supporting its tolerability relative to other antidepressants is outweighed by the increased cardiac risk and toxicity in overdose.

1.8.1.4 When switching to another antidepressant, which can normally be achieved within 1 week when switching from drugs with a short half‑life, consider the potential for interactions in determining the choice of new drug and the nature and duration of the transition. Exercise particular caution when switching:

from fluoxetine to other antidepressants, because fluoxetine has a long half-life (approximately 1 week)

from fluoxetine or paroxetine to a TCA, because both of these drugs inhibit the metabolism of TCAs; a lower starting dose of the TCA will be required, particularly if switching from fluoxetine because of its long half-life

to a new serotonergic antidepressant or MAOI, because of the risk of serotonin syndrome (features include confusion, delirium, shivering, sweating, changes in blood pressure and myoclonus)

from a non-reversible MAOI: a 2-week washout period is required (other antidepressants should not be prescribed routinely during this period).

Combining and augmenting medications

'Augmentation' is when an antidepressant is used with a non-antidepressant drug and 'combination' is when two antidepressants are used together.

1.8.1.5 When using combinations of medications (which should only normally be started in primary care in consultation with a consultant psychiatrist):

select medications that are known to be safe when used together

be aware of the increased side-effect burden this usually causes

discuss the rationale for any combination with the person with depression, follow GMC guidance if off-label medication is prescribed, and monitor carefully for adverse effects

be familiar with primary evidence and consider obtaining a second opinion when using unusual combinations, the evidence for the efficacy of a chosen strategy is limited or the risk-benefit ratio is unclear

document the rationale for the chosen combination.

1.8.1.6 If a person with depression is informed about, and prepared to tolerate, the increased side-effect burden, consider combining or augmenting an antidepressant with:

an antipsychotic such as aripiprazole, olanzapine, quetiapine or risperidone or

another antidepressant such as mirtazapine or mianserin.

In October 2009, this was an off-label use of aripiprazole, olanzapine, quetiapine and risperidone. See NICE's information on prescribing medicines.

1.8.1.7 When prescribing lithium:

monitor renal and thyroid function before treatment and every 6 months during treatment (more often if there is evidence of renal impairment)

consider ECG monitoring in people with depression who are at high risk of cardiovascular disease

monitor serum lithium levels 1 week after initiation and each dose change until stable, and every 3 months thereafter.

1.8.1.8 When prescribing an antipsychotic, monitor weight, lipid and glucose levels, and side effects (for example, extrapyramidal side effects and prolactin-related side effects with risperidone).

1.8.1.9 The following strategies should not be used routinely:

Augmentation of an antidepressant with a benzodiazepine for more than 2 weeks as there is a risk of dependence.

Augmentation of an antidepressant with buspirone, carbamazepine, lamotrigine or valproate as there is insufficient evidence for their use. (Valproate must not be used in women or girls of childbearing potential, including young girls who are likely to need treatment into their childbearing years; see the MHRA safety advice on risks of using valproate during pregnancy.)

Augmentation of an antidepressant with pindolol or thyroid hormones as there is inconsistent evidence of effectiveness. In October 2009, this was an off-label use of buspirone, carbamazepine, lamotrigine, valproate, pindolol, and thyroid hormones. See NICE's information on prescribing medicines.

1.9 Continuation and relapse prevention

1.9.1.2 Review with the person with depression the need for continued antidepressant treatment beyond 6 months after remission, taking into account:

the number of previous episodes of depression

the presence of residual symptoms

concurrent physical health problems and psychosocial difficulties.

Using medication for relapse prevention

1.9.1.5 When deciding whether to continue maintenance treatment beyond 2 years, re-evaluate with the person with depression, taking into account age, comorbid conditions and other risk factors.

1.9.1.7 People who have had multiple episodes of depression, and who have had a good response to treatment with an antidepressant and an augmenting agent, should remain on this combination after remission if they find the side effects tolerable and acceptable. If one medication is stopped, it should usually be the augmenting agent. Lithium should not be used as a sole agent to prevent recurrence.

Psychological interventions for relapse prevention

Delivering psychological interventions for relapse prevention

1.9.1.10 Mindfulness-based cognitive therapy should normally be delivered in groups of 8 to 15 participants and consist of weekly 2-hour meetings over 8 weeks and four follow-up sessions in the 12 months after the end of treatment.

1.9.2 Stopping or reducing antidepressants

1.9.2.1 Advise people taking antidepressant medication that, before stopping it, they should discuss this with their practitioner. [2019]

1.9.2.2 Advise people that if they stop taking antidepressant medication abruptly, miss doses or do not take a full dose, they may have discontinuation symptoms such as:

restlessness

problems sleeping

unsteadiness

abdominal symptoms

altered sensations (for example electric shock sensations in the head)

altered feelings (for example irritability, anxiety or confusion).

Explain that whilst the withdrawal symptoms which arise when stopping or reducing antidepressants can be mild and self-limiting, there is substantial variation in people's experience, with symptoms lasting much longer (sometimes months or more) and being more severe for some patients. [2019]

1.9.2.3 When stopping an antidepressant, gradually reduce the dose, normally over a 4-week period, although some people may require longer periods, particularly with drugs with a shorter half-life (such as paroxetine and venlafaxine). This is not required with fluoxetine because of its long half-life.

1.10 Step 4: complex and severe depression

Referral to specialist mental health services should normally be for people with depression who are at significant risk of self-harm, have psychotic symptoms, require complex multiprofessional care, or where an expert opinion on treatment and management is needed.

1.10.1.1 The assessment of a person with depression referred to specialist mental health services should include:

their symptom profile, suicide risk and, where appropriate, previous treatment history

associated psychosocial stressors, personality factors and significant relationship difficulties, particularly where the depression is chronic or recurrent

associated comorbidities including alcohol and substance misuse, and personality disorders.

1.10.1.2 In specialist mental health services, after thoroughly reviewing previous treatments for depression, consider reintroducing previous treatments that have been inadequately delivered or adhered to.

1.10.1.3 Use crisis resolution and home treatment teams to manage crises for people with severe depression who present significant risk, and to deliver high-quality acute care. The teams should monitor risk as a high-priority routine activity in a way that allows people to continue their lives without disruption.

1.10.1.4 Medication in secondary care mental health services should be started under the supervision of a consultant psychiatrist.

1.10.1.5 Teams working with people with complex and severe depression should develop comprehensive multidisciplinary care plans in collaboration with the person with depression (and their family or carer, if agreed with the person). The care plan should:

identify clearly the roles and responsibilities of all health and social care professionals involved

develop a crisis plan that identifies potential triggers that could lead to a crisis and strategies to manage such triggers

be shared with the GP and the person with depression and other relevant people involved in the person's care.

1.10.2 Inpatient care, and crisis resolution and home treatment teams

1.10.2.1 Consider inpatient treatment for people with depression who are at significant risk of suicide, self-harm or self-neglect.

1.10.2.2 The full range of high-intensity psychological interventions should normally be offered in inpatient settings. However, consider increasing the intensity and duration of the interventions and ensure that they can be provided effectively and efficiently on discharge.

1.10.2.3 Consider crisis resolution and home treatment teams for people with depression who might benefit from early discharge from hospital after a period of inpatient care.

1.10.3 Pharmacological management of depression with psychotic symptoms

1.10.3.1 For people who have depression with psychotic symptoms, consider augmenting the current treatment plan with antipsychotic medication (although the optimum dose and duration of treatment are unknown).

1.10.4 Electroconvulsive therapy (ECT)

The recommendations in this section update the depression aspects only of NICE's technology appraisal guidance on the use of electroconvulsive therapy.

1.10.4.1 Consider ECT for acute treatment of severe depression that is life‑threatening and when a rapid response is required, or when other treatments have failed.

1.10.4.2 Do not use ECT routinely for people with moderate depression but consider it if their depression has not responded to multiple drug treatments and psychological treatment.

1.10.4.3 For people whose depression has not responded well to a previous course of ECT, consider a repeat trial of ECT only after:

reviewing the adequacy of the previous treatment course and

considering all other options and

discussing the risks and benefits with the person and/or, where appropriate, their advocate or carer.

1.10.4.4 When considering ECT as a treatment choice, ensure that the person with depression is fully informed of the risks associated with ECT, and with the risks and benefits specific to them. Document the assessment and consider:

the risks associated with a general anaesthetic

current medical comorbidities

potential adverse events, notably cognitive impairment

the risks associated with not receiving ECT.

The risks associated with ECT may be greater in older people; exercise particular caution when considering ECT treatment in this group.

1.10.4.7 Assess clinical status after each ECT treatment using a formal valid outcome measure, and stop treatment when remission has been achieved, or sooner if side effects outweigh the potential benefits.

1.10.4.8 Assess cognitive function before the first ECT treatment and monitor at least every three to four treatments, and at the end of a course of treatment.

1.10.4.9 Assessment of cognitive function should include:

orientation and time to reorientation after each treatment

measures of new learning, retrograde amnesia and subjective memory impairment carried out at least 24 hours after a treatment.

If there is evidence of significant cognitive impairment at any stage consider, in discussion with the person with depression, changing from bilateral to unilateral electrode placement, reducing the stimulus dose or stopping treatment depending on the balance of risks and benefits.

1.10.4.10 If a person's depression has responded to a course of ECT, antidepressant medication should be started or continued to prevent relapse. Consider lithium augmentation of antidepressants.

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Depression in adults: recognition and management

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The following guidance is based on the best available evidence. The full guideline gives details of the methods and the evidence used to develop the guidance. Subthreshold depressive symptoms: Fewer than 5 symptoms of depression. Mild depression: Few, if any, symptoms in excess of the 5 required to make the diagnosis, and symptoms result in only minor functional impairment.

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Internet-based CBT for social phobia and panic disorder

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Treatment satisfaction with cognitive-behavioural therapy among children and adolescents with anxiety and depression: A systematic review and meta-synthesis

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Treatment satisfaction with cognitive-behavioural therapy among children and adolescents with anxiety and depression: A systematic review and meta-synthesis