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Cauda Equina Syndrome – Symptoms, Causes, Diagnosis and Treatments (aans.org)

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Cauda Equina Syndrome – Symptoms, Causes, Diagnosis and Treatments

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Read a neurosurgeon’s description of cauda equina syndrome (CES), including potential treatments and information on coping with life with CES.

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https://www.youtube.com/watch?v=a23A3nAaO0E

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Ankylosing Spondylitis: Visual Explanation for Students

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https://www.youtube.com/watch?v=dWgZYybq07M

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https://www.youtube.com/watch?v=Z2M9fKGEbxg

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Cauda Equina Syndrome - Everything You Need To Know - Dr. Nabil

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https://my.clevelandclinic.org/health/body/21946-spinal-cord

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Spinal Cord: Function, Anatomy and Structure

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The spinal cord is the tube-like structure that runs from your brain to your lower back. It carries nerve signals that help you move and feel sensations.

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https://www.spine-health.com/conditions/spine-anatomy/lumbar-discs

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The lumbar spine contains a total of 5 intervertebral discs situated between the vertebral bodies. The primary functions of these discs are to:

Distribute compressive loads placed on the spine, providing shock absorption properties

Maintain the distance between the vertebral bodies during movement

Provide flexibility to the spine and prevent excessive movements

Create and maintain the lordotic (backward C-shaped) curve of the lumbar spine

The discs are typically named based on the vertebrae above and below it, for example, the L4-L5 disc.

Characteristics of the Lumbar Discs

The lumbar intervertebral discs have the following distinguishing features:

Size. The lumbar intervertebral discs are the thickest compared to other spinal regions. The discs are also thicker in front than the back.

Height. The lumbar discs become shorter during the day due to the weight of the upper body. It is estimated that sleeping for a minimum of 5 hours helps the discs regain their original shape.

Shape. The form of the lumbar disc changes with movement. When the spine bends forward, the height in the front of the disc decreases while the posterior height increases. The opposite occurs while bending backward.

The discs are secured in place by the anterior (front) and posterior (back) longitudinal ligaments.

Composition of the Lumbar Discs

While the overall composition of the lumbar discs is similar to other discs in the spine, there are a few differences. The lumbar disc typically consists of:

Annulus fibrosus. The outer shell of a lumbar disc is called the annulus fibrosus. This shell is thick and consists of several layers of tough collagen protein fibers, as opposed to a single layer seen in the discs of the neck. The annulus fibrosus provides the main shock-absorbing properties delivered by the disc.

Nucleus pulposus. A softer type of collagen protein fills the central part of the lumbar disc, called the nucleus pulposus. The nucleus pulposus contains 70% to 90% of water and reaches its peak hydration between the ages of 20 to 30 years, following which, dehydration and degeneration begin to occur.

As age advances, the discs may get calcified (deposition of calcium) and hardened, reducing their flexibility.

Read more about Spinal Discs

Vertebral Endplates of the Lumbar Discs

A bi-layered vertebral endplate made of cortical bone and hyaline cartilage is attached to the upper and lower surfaces of the disc and binds the disc to the vertebral body. The bony portion of the endplate is attached to the vertebral body and helps resist compressive loads on the spine. The cartilaginous portion of the endplate helps contain the annulus fibrosus and nucleus pulposus within their normal anatomic borders.

The disc receives a majority of its nutrition through these endplates by absorbing fluids (similar to the action of a sponge) during spinal movements. Excessive forces and high-pressure postures, such as prolonged standing and sitting, can inhibit disc nutrition.

While the lumbar discs provide significant flexibility and protective functions, they are also highly susceptible to injury. In general, the front part of the disc is the strongest and the back and sides are weaker and susceptible to herniation and other disc disorders. Research indicates that 90% of lumbar disc herniations occur at the L4-L5 or the L5-S1 disc space.

Read more about Causes of Lower Back Pain

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The lumbar spine contains a total of 5 intervertebral discs situated between the vertebral bodies. The primary functions of these discs are to: Distribute compressive loads placed on the spine, providing shock absorption properties Maintain the distance between the vertebral bodies during movement Provide flexibility to the spine and prevent excessive movements Create and maintain the lordotic (backward C-shaped) curve of the lumbar spine The discs are typically named based on the vertebrae above and below it, for example, the L4-L5 disc.

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https://www.youtube.com/watch?v=vy1fuqGSjo0

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Common Causes of Low Back Pain - Everything You Need To Know - Dr. Nabil Ebraheim

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https://www.nhs.uk/conditions/back-pain/treatment/

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Back pain will usually improve within a few weeks or months. There are several things you can try to help reduce your pain in the meantime.
There are also some specialist treatments that may be recommended if it's thought simple measures are not likely to be effective on their own.

See a GP or a physiotherapist if your pain is not improving despite trying simple treatments.

Treatments you can try yourself

Stay active

One of the most important things you can do is to keep moving and continue with your normal activities as much as possible.

It used to be thought that bed rest would help you recover from a bad back, but it's now known that people who remain active are likely to recover quicker.

This may be difficult at first, but do not be discouraged - your pain should start to improve eventually. Consider taking painkillers if the pain is stopping you from carrying on as normal.

There's no need to wait until you're completely pain-free before returning to work. Going back to work will help you return to a normal pattern of activity and may distract you from the pain.

Back exercises and stretches

Simple back exercises and stretches can often help reduce back pain. These can be done at home as often as you need to.

For information about exercises and stretches that can help, see:

A GP may be able to provide information about back exercises if you're unsure what to try, or you may want to consider seeing a physiotherapist for advice. Read about how to get access to physiotherapy.

Doing regular exercise alongside these stretches can also help keep your back strong and healthy. Activities such as walking, swimming, yoga and pilates are popular choices.

See exercise video safety information

This exercise video is suitable for most people, but is not tailored to any specific condition, characteristic or person.

Get advice from a GP or health professional before trying it, especially if:

you have any concerns about your health

you are not sure if the exercises are suitable

you have any pre-existing health problems or injuries, or any current symptoms

Stop the exercise immediately and get medical help if you feel any pain or feel unwell.

Painkillers

Non-steroidal anti-inflammatory drug (NSAID) tablets, such as ibuprofen, can help relieve back pain. Many types are available to buy from pharmacies or supermarkets without a prescription.

But NSAIDs are not suitable for everyone, so check the box or leaflet to see whether you can take the medicine first. Speak to a pharmacist if you're not sure.

If you cannot take NSAIDs, alternative medicines such as codeine may help. This is a stronger painkiller that should ideally only be used for a few days, as it can cause addiction if used for longer.

Paracetamol on its own is not recommended for back pain, but it may be used alongside stronger painkillers such as codeine.

Muscle relaxants may be prescribed by a GP if you have painful muscle spasms in your back.

Some muscle relaxants such as diazepam can make you feel drowsy, dizzy or caused blurred vision. Do not drive, cycle or operate machinery if you have these types of side effects.

Hot and cold packs

Some people find that heat (such as a hot bath or a hot water bottle placed on the affected area) helps to ease the pain when back pain first starts.

Cold (such as an ice pack or a bag of frozen vegetables) on the painful area can also help in the short erm. However, do not put ice directly on your skin, as it might cause a cold burn. Wrap an ice pack or bag of frozen vegetables in a cloth or towel first.

Another option is to alternate between hot and cold using ice packs and a hot water bottle. Hot and cold compression packs can be bought at most pharmacies.

Relax and stay positive

Trying to relax is a crucial part of easing the pain as muscle tension caused by worrying about your condition may make things worse.

Read more about:

Although it can be difficult, it helps to stay positive and recognise that your pain should get better. People who manage to stay positive despite their pain tend to recover quicker.

Specialist treatments

Exercise classes

A GP may suggest attending an NHS group exercise programme if they think it might help to reduce your pain.

These programmes involve classes, led by a qualified instructor, where you're taught a mix of exercises to strengthen your muscles and improve your posture, plus aerobic and stretching exercises.

Manual therapy

Manual therapy is the name for a group of treatments where a therapist uses their hands to move, massage and apply careful force to the muscles, bones and joints in and around your spine.

It's usually done by chiropractors, osteopaths or physiotherapists, although chiropractic and osteopathy are not widely available on the NHS.

Manual therapy can help reduce back pain, but it should only be used alongside other measures such as exercise.

There's also some evidence that a therapy called the Alexander technique may help with long-term back pain. However, the National Institute for Health and Care Excellence (NICE) does not currently recommend this treatment.

Psychological support

A GP may suggest psychological therapy, in addition to other treatments such as exercise and manual therapy.

Psychological therapies such as cognitive behavioural therapy (CBT) can help you manage your back pain better by changing how you think about your condition.

While the pain in your back is very real, how you think and feel about your condition can make it worse.

If you've been in pain for a long time, a specialist treatment programme that involves a combination of group therapy, exercises, relaxation, and education about pain and the psychology of pain may be offered.

Surgery and procedures

Surgery for back pain is usually only recommended if there's a specific medical reason for your pain, such as sciatica or a slipped (prolapsed) disc, and other treatments have not helped.

Nerve treatment

A procedure called radiofrequency denervation may sometimes be used if:

you've had back pain for a long time

your pain is moderate or severe

your pain is thought to originate from the joints in your spine

The procedure involves inserting needles into the nerves that supply the affected joints. Radio waves are sent through the needles to heat the nerves, which stops them sending pain signals.

You're awake while the treatment is being done and local anaesthetic is used to numb your back. You will not need to stay in hospital overnight.

As with all procedures, radiofrequency denervation carries a risk of complications, including bleeding, bruising, infection and accidental nerve damage. Discuss the risks with your surgeon before agreeing to treatment.

Spinal fusion surgery

Spinal fusion surgery is another type of surgery for back pain. It may be recommended if there's significant damage to the bones in your back (vertebrae).

Spinal fusion surgery can be used to fuse 2 vertebrae together to strengthen them. This can also help to reduce any related nerve pain as it stops the damaged vertebrae squeezing the nerves that pass through the spine.

It's possible that this type of surgery could cause permanent damage to some of the nerves in your back. This may lead to some partial paralysis in your legs and bowel or urinary incontinence. This complication is estimated to happen in around 1 in every 200 procedures.

Treatments not recommended

A number of other treatments have sometimes been used for non-specific back pain (back pain with no identified cause) but are not recommended by the National Institute for Health and Care Excellence (NICE) because of a lack of evidence.

These include:

belts, corsets, foot orthotics and shoes with "rocker" soles

traction - the use of weights, ropes and pulleys to apply force to tissues around the spine

acupuncture - a treatment where fine needles are inserted at different points in the body

therapeutic ultrasound - where sound waves are directed at your back to accelerate healing and encourage tissue repair

transcutaneous electrical nerve stimulation (TENS) - where a machine is used to deliver small electrical pulses to your back through electrodes (small sticky patches) attached to your skin

percutaneous electrical nerve stimulation (PENS) - where electrical pulses are passed along needles inserted near the nerves in the back

interferential therapy (IFT) - where a device is used to pass an electrical current through your back to try to accelerate healing

painkilling spinal injections (although these can help if you have sciatica)

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Back pain will usually improve within a few weeks or months. There are several things you can try to help reduce your pain in the meantime. There are also some specialist treatments that may be recommended if it's thought simple measures are not likely to be effective on their own.

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Intervertebral disc - Physiopedia (physio-pedia.com)

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The intervertebral disc (IVD) is important in the normal functioning of the spine. It is a cushion of fibrocartilage and the principal joint between two vertebrae in the spinal column. There are 23 discs in the human spine: 6 in the cervical region (neck), 12 in the thoracic region (middle back), and 5 in the lumbar region (lower back).

IVDs allow the spine to be flexible without sacrificing a great deal of strength. They also provide a shock-absorbing effect within the spine and prevent the vertebrae from grinding together. They consist of three major components: the inner, nucleus pulposus (NP), the outer, annulus (AF) and the cartilaginous endplates that anchor the discs to adjacent vertebrae.

The IVD consists of three distinct components (Figure 2):

A central nucleus pulposus (NP);

A peripheral annulus fibrosus (AF);

Two vertebral endplates (VEPs).

Figure 2: Detailed structure of the IVD (adapted from Bogduk 2005)

A gel-like structure that sits at the center of the intervertebral disc and accounts for much of the strength and flexibility of the spine. It is made of 66% to 86% water with the remainder consisting of primarily type II collagen (it may also contain type VI, IX, and XI) and proteoglycans. The proteoglycans include the larger aggrecan and versican that bind to hyaluronic acid, as well as several small leucine-rich proteoglycans. Aggrecan is largely responsible for retaining water within the NP. This structure also contains a low density of cells. While sparse, these cells produce the extracellular matrix (ECM) products (aggrecan, type II collagen, etc.) and maintain the integrity of the NP.

Consists of "lamellae" or concentric layers of collagen fibres . The fibre orientation of each layer of lamellae alternate and therefore allow effective resistance of multidirectional movements. The AF contains an inner and an outer portion. They differ primarily in their collagen composition. While both are primarily collagen, the outer annulus contains mostly type I collagen, while the inner has predominantly type II. The inner annulus also contains more proteoglycans than the inner. NB collagen Type I: skin, tendon, vasculature, organs, bone (the main component of the organic part of bone) Type II: cartilage (the main collagenous component of cartilage and is more flexible)

An upper and a lower cartilaginous endplate (each about 0.6- 1 mm thick) cover the superior and inferior aspects of the disc. The endplate permits diffusion and provides the main source of nutrition for the disc. The hyaline endplate is also the last part of the disc to wear through during severe disc degeneration.

Plates of cartilage that bind the disc to their respective vertebral bodies.

Each endplate covers almost the entire surface of the adjacent vertebral body; only a narrow rim of bone, called the ring apophysis, around the perimeter of the vertebral body is left uncovered by cartilage.

The portion of the vertebral body to which the cartilaginous endplate is applied is referred to as the vertebral endplate.

The endplate covers the nucleus pulposus in its entirety; peripherally it fails to cover the entire extent of the annulus fibrosus.

The collagen fibrils of the inner lamellae of the annulus enter the endplate and merge with it, resulting in all aspects of the nucleus being enclosed by a fibrous capsule.

The disc is innervated in the outer few millimetres of the annulus fibrosus .

Only the outer third of the AF is vascular and innervated in a non-pathologic state. In ageing and states of inflammation, both nerve growth and granulation tissue growth are stimulated. Additionally, the granulation tissue secretes inflammatory cytokines, which further increases sensitivity to pain sensations.

The IVD is largely avascular, with no major arterial branches to the disc . The outer annular layers are supplied by small branches from metaphysical arteries. Only the outer annulus is vascularized. Blood vessels near the disc-bone junction of the vertebral body as well as those in the outer annulus supply the NP and inner annulus. Glucose, oxygen and other nutrients reach the avascular regions by diffusion. The same process removes metabolites.

Restricted IV joint motion.

Contribution to stability.

Resistance to axial, rotational, bending load.

Preservation of anatomic relationship.

It provides cushioning for the vertebrae and reduce the stress caused by impact.

They act shock absorber for the spine.

They help protect the nerves that run down the spine and between the vertebrae.

Weight bearing: The disc is subjected to various loads, including compressive, tensile and shear stresses . During compressive loading, hydrostatic pressure develops within the NP, which thereby disperses the forces towards the endplates as well as the AF . This mechanism slows the rate applied loads are transmitted to the adjacent vertebra, giving the disc its shock-absorbing abilities .

Movement: The disc is also involved in permitting movements between vertebral bodies, which include:

Axial compression / distraction;

Flexion / extension;

Axial rotation;

Lateral flexion.

Nuclear migration: A symmetric compressive loading disc can cause the NP to migrate in a direction opposite to the compression . For example, during forward bending (or flexion) of the lumbar spine, the NP migrates posteriorly or backwards (Figure 4). Conversely, during backwards bending (or extension), the nucleus is squeezed anteriorly or forwards. This concept is known as the dynamic disc model . Although NP migration has been shown to behave predictably in asymptomatic discs, a variable pattern of migration occurs in people with symptomatic and/or degenerative IVDs .

Figure 4: Direction of nuclear migration within the IVD during spinal movements (adapted from McKenzie 1981)

Disc thickness generally increases from rostral to caudal. The thickness of the discs relative to the size of the vertebral bodies is highest in the cervical and lumbar regions. This reflects the increased range of motion found in those regions.

In the cervical and lumbar regions, the intervertebral discs are thicker anteriorly. This creates the secondary curvature of the spine - the cervical and lumbar lordoses.

There are several terms to describe disc pathologies

1. Disc bulge ie the circumference of disc extends beyond the vertebral bodies.

2. Disc herniation involves the NP. Disc herniation is significant in that it may compress an adjacent spinal nerve. A herniated disc impinges upon the nerve associated with the inferior vertebrae (e.g., L4/L5 herniation affects the L5 nerve root). The most common site of disc herniation is at L5-S1, which may be due to the thinning of the posterior longitudinal ligament towards its caudal end. There are three subtypes of herniations:

Disc protrusion is characterized by the width of the base of the protrusion is wider than the diameter of the disc material that is herniated.

In disc extrusion, the AF is damaged, allowing the NP to herniate beyond the normal bounds of the disc. In this case, the herniated material produces a mushroom-like dome that is wider than the neck connecting it to the body of the NP. The herniation may extend superior or inferiorly relative to the disc level.

In disc sequestration, the herniated material breaks off from the body of the NP.

3. Disc desiccation is common in aging. It is brought about by the death of the cells that produce and maintain the ECM, including proteoglycans, such as aggrecan. The NP shrinks as the gelatinous form is replaced with fibrotic tissue, reducing its functionality, and leaves the AF supporting additional weight. This increased stress leads the AF to compensate by increasing in size. The resulting flattened disc reduces mobility and may impinge on spinal nerves leading to pain and weakness. It is thought to be due to proteoglycan breakdown, which reduces the water-retaining properties of the NP.

NB: Significant research has been put into means of replacing/re-growing the intervertebral discs. The various methods include the replacement of discs with synthetic materials, stem cell therapy, and gene therapy.

There is no intervertebral disc between C1 and C2, which is unique in the spine.

Two major ligaments support the intervertebral discs.

1. The anterior longitudinal ligament is a broadband that covers the anterolateral surface of the spine from the foramen magnum in the skull to the sacrum. This ligament assists the spine in preventing hyperextension and prevents intervertebral disc herniation in the anterolateral direction.

2. The posterior longitudinal ligament covers the posterior aspect of the vertebral bodies, within the vertebral canal, and serves mainly to prevent a posterior herniation of the intervertebral discs, and is therefore responsible for the most herniations being in the postero-lateral direction.

1. Peptan Collagen Available from:https://www.peptan.com/collagen-in-our-bodies/ (last accessed 27.1.2020)

2. Musculoskeletal key Applied anatomy of the lumbar spine Available from:https://musculoskeletalkey.com/applied-anatomy-of-the-lumbar-spine/ (last accessed 27.1.2020)

3. Intervertebral disc. Study.com. Available from https://study.com/academy/lesson/intervertebral-disc-definition-function-disease.html [last accessed 13/10/2020]

4. Reuber, M., et al., Bulging of lumbar intervertebral disks. J Biomech Eng, 1982. 104(3): p. 187-92.

5. Shah, J.S., W.G. Hampson, and M.I. Jayson, The distribution of surface strain in the cadaveric lumbar spine. J Bone Joint Surg Br, 1978. 60-B(2): p. 246-51.

6. Kolber, M.J. and W.J. Hanney, The dynamic disc model: a systematic review of the literature. Phys Ther Rev, 2009. 14(3): p. 181-189.

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The intervertebral disc (IVD) is important in the normal functioning of the spine. It is a cushion of fibrocartilage and the principal joint between two vertebrae in the spinal column. There are 23 discs in the human spine: 6 in the cervical region (neck), 12 in the thoracic region (middle back), and 5 in the lumbar region (lower back).

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Prescription drug abuse - Symptoms and causes - Mayo Clinic
A link explain how to recognize presentations of opioid addiction, causes and preventions

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Overview

Prescription drug abuse is the use of a prescription medication in a way not intended by the prescribing doctor. Prescription drug abuse or problematic use includes everything from taking a friend's prescription painkiller for your backache to snorting or injecting ground-up pills to get high. Drug abuse may become ongoing and compulsive, despite the negative consequences.

An increasing problem, prescription drug abuse can affect all age groups, including teens. The prescription drugs most often abused include opioid painkillers, anti-anxiety medications, sedatives and stimulants.

Early identification of prescription drug abuse and early intervention may prevent the problem from turning into an addiction.

Symptoms

Signs and symptoms of prescription drug abuse depend on the specific drug. Because of their mind-altering properties, the most commonly abused prescription drugs are:

Opioids used to treat pain, for example medications containing oxycodone - such as Oxycontin and Percocet - and those containing hydrocodone - such as Norco

Anti-anxiety medications and sedatives, such as alprazolam (Xanax) and diazepam (Valium), and hypnotics, such as zolpidem (Ambien), used to treat anxiety and sleep disorders

Stimulants, such as methylphenidate (Ritalin, Concerta, others), dextroamphetamine and amphetamine (Adderall XR, Mydayis), and dextroamphetamine (Dexedrine), used to treat attention-deficit/hyperactivity disorder (ADHD) and certain sleep disorders

Opioids

Anti-anxiety medications and sedatives

Stimulants

Constipation

Nausea

Feeling high (euphoria)

Slowed breathing rate

Drowsiness

Confusion

Poor coordination

Increased dose required for pain relief

Worsening or increased sensitivity to pain with higher doses (hyperalgesia)

Drowsiness

Confusion

Unsteady walking

Slurred speech

Poor concentration

Dizziness

Problems with memory

Slowed breathing

Increased alertness

Feeling high

Irregular heartbeat

High blood pressure

High body temperature

Reduced appetite

Insomnia

Agitation

Anxiety

Paranoia

Other signs include:

Stealing, forging or selling prescriptions

Taking higher doses than prescribed

Excessive mood swings or hostility

Increase or decrease in sleep

Poor decision-making

Appearing to be high, unusually energetic or revved up, or sedated

Requesting early refills or continually "losing" prescriptions, so more prescriptions must be written

Seeking prescriptions from more than one doctor

When to see a doctor

Talk with your doctor if you think you may have a problem with prescription drug use. You may feel embarrassed to talk about it - but remember that medical professionals are trained to help you, not judge you. It's easier to tackle the problem early before it becomes an addiction and leads to more-serious problems.

Causes

Teens and adults abuse prescription drugs for many reasons, such as:

To feel good or get high

To relax or relieve tension

To reduce appetite or increase alertness

To experiment with the mental effects of the substance

To maintain an addiction and prevent withdrawal

To be accepted by peers or to be social

To try to improve concentration and academic or work performance

Risk factors

Some people fear that they may become addicted to medications prescribed for medical conditions, such as painkillers prescribed after surgery. But you can reduce your risk by carefully following your doctor's instructions on how to take your medication.

Prescription drug abuse can happen at any age, but commonly begins in teens or young adults.

Risk factors for prescription drug abuse include:

Past or present addictions to other substances, including alcohol and tobacco

Family history of substance abuse problems

Certain pre-existing psychiatric conditions

Exposure to peer pressure or a social environment where there's drug use

Easier access to prescription drugs, such as having prescription medications in the home medicine cabinet

Lack of knowledge about prescription drugs and their potential harm

Older adults and prescription drug abuse

Prescription drug abuse in older adults is a growing problem, especially when they combine drugs with alcohol. Having multiple health problems and taking multiple drugs can put seniors at risk of misusing drugs or becoming addicted.

Complications

Abusing prescription drugs can cause a number of problems. Prescription drugs can be especially dangerous - and even lead to death - when taken in high doses, when combined with other prescription drugs or certain over-the-counter medications, or when taken with alcohol or illegal or recreational drugs.

Medical consequences

Here are examples of serious consequences of prescription drug abuse:

Opioids can cause low blood pressure, a slowed breathing rate and potential for breathing to stop, or a coma. Overdose has a significant risk of death.

Anti-anxiety medications and sedatives can cause memory problems, low blood pressure and slowed breathing. Overdose can cause coma or death. Abruptly stopping the medication may cause withdrawal symptoms that can include nervous system hyperactivity and seizures.

Stimulants can cause dangerously high body temperature, heart problems, high blood pressure, seizures or tremors, hallucinations, aggressiveness, and paranoia.

Physical dependence and addiction

Because commonly abused prescription drugs activate the brain's reward center, it's possible to develop physical dependence and addiction.

Physical dependence. Physical dependence (also called tolerance) is the body's response to long-term use. People who are physically dependent on a drug may need higher doses to get the same effects and may experience withdrawal symptoms when cutting back or abruptly stopping the drug. Physical dependence may also become evident if a drug the body becomes adjusted to over time, even without dosage change, is stopped abruptly.

Addiction. People who are addicted to a drug can have physical dependence, but they also compulsively seek a drug and continue to use it even when that drug causes significant problems in their lives.

Other consequences

Other potential consequences include:

Engaging in risky behaviors because of poor judgment

Using illegal or recreational drugs

Being involved in crime

Motor vehicle accidents

Decreased academic or work performance

Troubled relationships

Prevention

Prescription drug abuse may occur in people who need painkillers, sedatives or stimulants to treat a medical condition. If you're taking a commonly abused drug, here are ways to reduce your risk:

Make sure you're getting the right medication. Make sure your doctor clearly understands your condition and the signs and symptoms. Tell your doctor about all your prescriptions, as well as over-the-counter medications, herbs and supplements, and alcohol and other drug use. Ask your doctor whether there's an alternative medication with ingredients that have less potential for addiction.

Check in with your doctor. Talk with your doctor on a regular basis to make sure that the medication you're taking is working and you're taking the right dose.

Follow directions carefully. Use your medication the way it was prescribed. Don't stop or change the dose of a drug on your own if it doesn't seem to be working without talking to your doctor. For example, if you're taking a pain medication that isn't adequately controlling your pain, don't take more.

Know what your medication does. Ask your doctor or pharmacist about the effects of your medication, so you know what to expect. Also check if other drugs, over-the-counter products or alcohol should be avoided when taking this medication.

Never use another person's prescription. Everyone is different. Even if you have a similar medical condition, it may not be the right medication or dose for you.

Don't order prescriptions online unless they're from a trustworthy pharmacy. Some websites sell counterfeit prescription and nonprescription drugs that could be dangerous.

Preventing prescription drug abuse in teens

Prescription drugs are commonly misused substances by young people. Follow these steps to help prevent your teen from abusing prescription medications.

Discuss the dangers. Emphasize to your teen that just because drugs are prescribed by a doctor doesn't make them safe - especially if they were prescribed to someone else or if your child is already taking other prescription medications.

Set rules. Let your teen know that it's not OK to share medications with others - or to take drugs prescribed for others. Emphasize the importance of taking the prescribed dose and talking with the doctor before making changes.

Discuss the dangers of alcohol use. Using alcohol with medications can increase the risk of accidental overdose.

Keep your prescription drugs safe. Keep track of drug quantities and keep them in a locked medicine cabinet.

Make sure your child isn't ordering drugs online. Some websites sell counterfeit and dangerous drugs that may not require a prescription.

Properly dispose of medications. Don't leave unused or expired drugs around. Check the label or patient information guide for disposal instructions, or ask your pharmacist for advice on disposal.

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Prescription drug abuse - Symptoms and causes

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Prescription drug abuse is the use of a prescription medication in a way not intended by the prescribing doctor. Prescription drug abuse or problematic use includes everything from taking a friend's prescription painkiller for your backache to snorting or injecting ground-up pills to get high.

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Prescription drug abuse - Diagnosis and treatment - Mayo Clinic
How it's managed

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Prescription drug abuse - Diagnosis and treatment - Mayo Clinic

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Using a prescription medication in a way not intended by the doctor can lead to drug abuse. Learn about risk factors and treatment for drug misuse.

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https://bnf.nice.org.uk/treatment-summary/neuropathic-pain.html
https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Low-Back-Pain
https://www.spine-health.com/conditions/lower-back-pain/early-treatments-lower-back-pain
3 links with general conservative treatment guidance, that I read through, though not essential.

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Low back pain is not unique. An estimated 75-85% of Americans experience some form of back pain during their life. Although low back pain can be quite debilitating and painful, in approximately 90% of cases, it is temporary and pain improves without surgery. However, 50% of patients who suffer from episodes of low back pain will have recurrent episodes within one year. Low back pain is considered to be chronic when it persists for more than 12 weeks.

The Lumbar Spine

The lumbar spine (lower back) consists of five vertebrae (bones) in the lower part of the spine between the ribs and the pelvis. The vertebrae that form the spine in the back are cushioned by small discs, which are located between each of the vertebrae and act as shock absorbers for the spinal bones. These discs are round and flat, with a tough, outer layer (annulus) that surrounds a jelly-like material called the nucleus. Thick ligaments attached to the vertebrae hold the pulpy disc material in place.

Of the 31 pairs of spinal nerves and roots, five lumbar (L1-L5) and five sacral (S1-S5) nerve pairs connect beginning in the lower back area.

Common Causes of Low Back Pain

The symptoms of low back pain show up as pain in the low back that can include pain that goes into the glutes (buttocks), hips or legs. The pain can be sharp, dull, aching, burning or a combination of all of these. It can be constant, intermittent or activity-related.

For more than 30 years, the NREF has funded research and training to improve treatments and care for conditions like low back pain.

Your contribution can make a difference. Learn more about the NREF and make a donation today.

When to Seek Medical Help

Although low back pain is a common occurrence, some features warrant evaluation from a medical professional, such as persistent or worsening back pain; neurologic symptoms, including numbness, weakness, or tingling; or changes in bowel or bladder function.

Diagnosing Low Back Pain

Diagnosis is made by a neurosurgeon based on history, symptoms, physical examination and results of diagnostic studies. Some patients may be treated conservatively; if conservative treatment is ineffective, the physician may order imaging studies of the lower back and other tests, which may include:

Non-surgical Treatment Options

Treatment options include physical therapy, back exercises, weight reduction, steroid injections (epidural steroids), nonsteroidal anti-inflammatory medications, acupuncture, rehabilitation and limited activity. All of these treatment options are aimed at relieving inflammation in the back and irritation of nerve roots. Physicians usually recommend four to six weeks of conservative therapy before considering surgery.

If low back pain occurs after a recent injury - such as a car accident, a fall or sports injury - call your primary care physician immediately. If you have any neurologic symptoms (numbness, weakness, tingling or bowel and bladder dysfunction), seek medical care immediately. If no neurologic problems are present, the patient may benefit by beginning conservative treatment at home for two to three weeks. The physician may recommend anti-inflammatory medications, such as aspirin or ibuprofen, and restrict strenuous activities for a few days.

If low back pain worsens or does not improve after two to three weeks of home treatment, contact the primary care physician. The physician can evaluate and perform an in-office neurologic exam to determine which nerve root is being irritated and to rule out other serious medical conditions. If the physician notes clear signs that the nerve root is being compressed, he/she can prescribe medications to relieve the pain, swelling and irritation. In addition, the doctor may recommend that limiting activities, provide a referral to a pain management specialist or both. If these treatment options do not provide relief within a few weeks, it may be time to consider other diagnostic studies and possibly surgical evaluation.

When Surgery is Necessary

When conservative treatment for low back pain does not provide relief or neurologic symptoms are worsening or severe, surgery may be needed. Candidates for surgery present any of the following:

Reasonably good health

Back and leg pain limits normal activity or impairs quality of life

Progressive neurologic deficits develop, such as leg weakness, numbness or both

Loss of normal bowel and bladder functions

Difficulty standing or walking

Medication and physical therapy are ineffective

If surgery is recommended, neurosurgeons have a variety of options available to help relieve pressure on the nerve roots. If several nerve roots and discs are causing the pain or if degeneration and instability exist in the spinal column, the neurosurgeon may choose: (1) a minimally invasive approach; (2) a more open decompression; or (3) fusing the vertebrae together with bone grafts and stabilizing them with instrumentation, including metal plates, screws, rods and cages, depending on the extent of disease. After such surgery, patients may gain restored mobility in the back, including the ability to bend over. In addition, patients may require postoperative physical therapy.

The benefits of surgery should always be weighed carefully against the risks. Although a large percentage of patients with low back pain report significant pain relief after surgery, it is not guaranteed that surgery will help.

If back pain resolves with non-surgical, conservative treatment, follow-up will likely be on an as-needed basis or if symptoms return. If a patient undergoes surgery, follow-up is different for each type of procedure.

Author Information

Omar Zalatimo, MD, MPH, MHA, FAANS
Director, Functional Neurosurgery LifeBridge Health
Baltimore
The AANS does not endorse any treatments, procedures, products or physicians referenced in these patient fact sheets. This information is provided as an educational service and is not intended to serve as medical advice. Anyone seeking specific neurosurgical advice or assistance should consult his or her neurosurgeon, or locate one in your area through the AANS' Find a Board-certified Neurosurgeon online tool.

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Low back pain is not unique. An estimated 75-85% of Americans experience some form of back pain during their life. Although low back pain can be quite debilitating and painful, in approximately 90% of cases, it is temporary and pain improves without surgery.

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https://www.google.com/url?sa=i&url=https%3A%2F%2Fpsychscenehub.com%2Fpsychinsights%2Fnaltrexone-naltrexone-bupropion-combination-mechanism-of-action-psychopharmacology-and-clinical-application-2%2F&psig=AOvVaw1MEtxgDxGlUoseX7XBqQBO&ust=1646939782373000&source=images&cd=vfe&ved=0CAsQjRxqFwoTCJjF5vjeufYCFQAAAAAdAAAAABAW

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202970/

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Abstract

An epidemic of drug overdose deaths has led to calls for programs and policies to limit misuse and diversion of opioid medications. Any parallel call to consider the risk of iatrogenic addiction when treating pain has been muted in comparison.

We have moved beyond questions of nonmedical use, abuse, and diversion to highlight the role of prescription opioids in causing addiction even when prescribed and used appropriately.

Unfortunately, current evidence is insufficient, and a rapid expansion of longitudinal research is urgently needed to guide clinicians in balancing the need for opioids with the risk of adverse consequences. Meanwhile, medical education should place greater emphasis on the abuse liability of prescription opioids, and providers should endeavor to attenuate risk when possible.

The United States continues to suffer from a startlingly severe epidemic of drug overdose deaths, 1-6 with approximately 46 Americans dying per day in 2010 from an overdose involving prescription opioids. 7 The increase in overdose deaths was directly paralleled by dramatic increases in the sale of opioid pharmaceuticals between 1999 and 2010. 7-13

Attention to this health threat has grown exponentially in recent years, but discussion and interventions have focused almost exclusively on issues such as illegitimate prescribing, nonmedical use, diversion, and overdose. 3-5,7,8,10,11,13-30 These topics are important but pertain primarily to individuals who already engage in nonmedical use of opioids.

A different question is why nonmedical opioid use occurred in the first place. It is universally understood that some small proportion of individuals will intentionally misuse opioid medications for their euphoric effects, and many assume the initial decision to begin doing so is entirely volitional. Largely unaddressed is that some individuals transition to nonmedical use and addiction despite their intention to use medications only as directed and only for pain relief. To date, few articles have alluded to iatrogenic addiction in the context of the current opioid epidemic. 5,22,23,31 None have explicitly called for a disambiguated determination of the role of inadvertent iatrogenic addiction as opposed to the role of intentional misuse and diversion.

We have moved beyond widespread recognition that prescription opioids have contributed to increased fatalities and beyond interventions that bluntly restrict the supply of prescription opioids to prevent misuse and diversion. Instead, we specifically focus on the issue of iatrogenic addiction, the degree to which it is underrecognized, and the need to (1) fully characterize its contribution to the current health crisis, (2) identify patients at risk and intervene early to prevent new cases of opioid use disorders, and (3) consider the issues of acute pain treatment and unscheduled care settings in addition to the more commonly discussed issue of chronic pain management. Most importantly, we seek to remind medical providers that well-intentioned efforts to treat pain may inadvertently lead to opioid use disorders, even if patients follow medical direction precisely. We also suggest urgent steps, including a call to arms for rapid expansion in research activity and better integration of existing evidence into provider education and clinical practice.

OPIOID PRESCRIBING AND OVERDOSE DEATHS

Approximately 15.7 million people in the United States report nonmedical use of prescription drugs, 32 and in 2007, drug overdose surpassed motor vehicle accidents as the leading cause of injury death in the United States. 8 The primary substance contributing to these alarming statistics is prescription opioids. 2 Nonmedical use of prescription opioids is concerning not only because of the risk of fatal overdose but also because it often precedes injection heroin use. 26

This epidemic was predictable. The abuse liability of opioids is well established 10,12,15,33 and a similar phenomenon occurred in the 19th and early 20th centuries, when opioids were prescribed liberally and indiscriminately for all types of pain. 34,35 Physicians undoubtedly, and in most cases unknowingly, contributed significantly to recent increases in opioid-related morbidity and mortality. However, this realization does not by itself illuminate the important question of how often and under what circumstances people have become addicted as a result of appropriate medical use as opposed to nonmedical use.

ORIGIN OF CURRENT PRACTICE IN PAIN TREATMENT

Factors contributing to increases in opioid prescribing have been detailed elsewhere. 5,12,22,25,29,36 The more permissive attitude toward opioids for pain treatment began in the 1980s, after several reports suggested a low potential for iatrogenic addiction in patients treated with opioids. 33,37,38 Eventually, a 1997 consensus statement concluded there was insufficient evidence to suggest that opioids result in iatrogenic addiction. 39 Belief in the safety of opioids proliferated rapidly throughout the medical education system and has been reaffirmed in several articles, as recently as 2010 by a Cochrane review. 40-42 Other factors included attempts to improve pain management, 39,43 emphasis on patient satisfaction and inclusion of pain relief in patient satisfaction assessments, 44,45 aggressive marketing of opioids by the pharmaceutical industry, 28,46 and welfare and health care reform. 22

The cumulative effect was that medical providers internalized a simple message: pain must be treated adequately, using opioids if needed, without fear of causing iatrogenic addiction. 12,15,33,39,40,47 Of note, there has been and currently remains little opportunity to alter this message in medical education, which provides minimal training on pain management or recognition of substance use disorders. 20,21,48 For example, a survey of formal pain management curriculums in Canadian universities found that, on average, medical students received 16 hours of education in pain management, whereas veterinary students received 87 hours. 49 Other studies have shown that many physicians are aware that their knowledge and confidence in pain management is insufficient, and many do not adhere to clinical guidelines when treating chronic pain. 20,21

ACTUAL RISK OF IATROGENIC ADDICTION

There are no randomized trials and few well-designed longitudinal studies to characterize the rate of iatrogenic addiction or the circumstances by which it occurs. The evidence we do have is limited in quality, ambiguous in terminology, and conflicting in results. 25,33,38-40,47 Overall, more recent evidence tends to indicate a higher rate of iatrogenic addiction than is commonly realized. 50,51 Nonetheless, the most recent systematic review concluded, "The available evidence suggests that opioid analgesics for chronic pain conditions are not associated with a major risk for developing dependence." 40(p688)

The general lack of consistent and reliable information has allowed competing viewpoints, both for and against the assertion that iatrogenic addiction is a frequent consequence of opioid therapy. Knowledge gaps are even more pronounced with respect to acute pain and unscheduled care settings.

Evidence to Date

Studies from the 1980s reported addiction rates after opioid treatment as low as 0.03% to 0.1% in hospitalized patients with no prior addiction history and 5% for patients with chronic noncancer pain. 37,38,52,53 In the early to mid-1990s, studies began to report addiction among patients treated with opioids for acute or subacute pain ranging from 3.8% to 27%, although these studies did not include a definition of addiction and did not specify whether addiction was iatrogenic in etiology. 47 More recent studies have suggested higher rates of opioid misuse, ranging from 3.27% to 56%, depending on specific definitions and outcome measures. 25,54 One large study found that 35% of patients treated long term with opioids met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition 55 criteria for an opioid use disorder. 16

A few studies have addressed the risk of iatrogenic addiction somewhat more directly. Opioid-naïve patients receiving an opioid prescription within seven days of short-stay surgery were 44% more likely to become long-term opioid users within one year than were those not receiving opioids, 17 and prolonged use of opioids has been associated with self-reported patient concern regarding addiction. 18 Another study found that 44% of patients in a methadone maintenance program, who also had chronic pain, reported that opioids prescribed medically for their pain had led to an addiction. 19

Arguments Against Iatrogenic Addiction

Support in favor of prescription opioid safety is intuitively predicated on the belief that opioids carry a low risk of addiction when prescribed and used appropriately. This assertion is not entirely without merit. Pain is a significant health problem, 43,56,57 and there are some reasons to believe that opioids do not, by themselves, lead to addiction, particularly in patients without a history of substance use disorders, mental illness, or chronic pain requiring long-term therapy. 16,25,54,58-63 For example, research suggests that pain may attenuate the euphoric effects of opioids. 64 Furthermore, even if appropriate medical use provides an initial exposure to opioids, that exposure is necessary but not sufficient to cause addiction. Addiction is a complex phenomenon that includes repeated exposure to drugs with abuse liability combined with predisposing environmental and genetic risk factors. 62,63 Many patients can be prescribed high doses of opioid medications for prolonged periods without exhibiting maladaptive patterns of misuse or functional impairments caused by misuse, even after the onset of physiological dependence. 65,66

Arguments for Iatrogenic Addiction

Despite the validity of such arguments, even pain management advocates, who led the initial charge in favor of more aggressive use of opioids, now recognize the imprudence of minimizing the addiction potential of pharmaceutical opioids. 67 First, it is difficult to believe that the parallel rise in prescriptions and associated harms is mere correlation without causation, particularly because of the inherent abuse liability of opioids. 10,12,15,33 If there is a causal relationship, it is difficult to believe that the problem is solely attributable to patients with already existing substance use disorders or that incident cases are solely the result of inappropriate prescribing or intentional misuse. Second, evidence in favor of opioid safety is determined by small and nongeneralizable samples, anecdotal reports, or surveys of provider perception. 15,33,47,50,51 Evidence of this quality certainly does not rule out the possibility of significant risk, and even if risk is very low, it would still cause significant harm because of the frequency with which opioids are prescribed. Finally, there are flaws in the argument that the risk of iatrogenic addiction can be addressed simply by modifying prescribing practices for those with a greater predisposition to addiction. 22 The lifetime prevalence of behavioral health disorders is reported to be as high as 50%, 58,59,68 yet patients without a history of behavioral health disorders may also develop iatrogenic addiction. 22 Thus, history of mental illness or substance use disorder may not provide the sensitivity or specificity required to tailor prescribing practices. 12

Acute Pain and Unscheduled Care Settings

The related topics of acute pain treatment and unscheduled care settings warrant special consideration. Because the probability of addiction is related to the duration of exposure, 69 it is tempting to assume that brief exposures for acute pain (e.g., emergency departments, operative intervention) have a negligible role in iatrogenic addiction, particularly compared to prolonged exposures with chronic pain management. However, there is evidence to challenge this assertion, 17,18 and there are several reasons even unscheduled care settings may contribute to iatrogenic addiction.

Acute care providers prescribe opioids frequently. 14 In the United States, there are more than 129 million emergency department visits annually, 70 and an estimated 39% of emergency department visits are for painful conditions. 71 Even if an initial exposure is insufficient to cause addiction directly, perhaps it is sufficient to trigger initial misuse that could ultimately lead to addiction. In addition, emergency departments and other safety net providers often treat patients repeatedly as patients with acute pain transition to subacute and chronic pain. They also provide care for patients with established chronic pain who experience lost or interrupted access to other care providers.

It is interesting to consider that providers of unscheduled care may be unlikely to recognize iatrogenic addiction as a direct consequence of their own care, because any adverse consequences would occur downstream. If so, it may be that iatrogenic addiction is especially underappreciated in these settings, particularly in the absence of dedicated systems to provide longitudinal outcomes data.

CURRENT MEASURES FOR THE OPIOID EPIDEMIC

Most efforts to address the current opioid epidemic have involved

1. identification of negligent prescribing practices 30;

2. pursuit of abuse-deterrent drug formulations 72,73;

3. measures to prevent misuse and diversion, such as prescription drug monitoring programs and monitoring of chronic pain treatment through urine testing, medication contracts, and mandated electronic prescribing 27,36,74;

4. expanding utilization of medication-assisted therapies 6; and

5. overdose prevention education and naloxone distribution to prevent overdose fatalities. 22,75-78

These interventions, although important, have been discussed elsewhere and do not directly address the problem of how iatrogenic addiction is initiated. However, simply reducing the supply of prescribed opioids available to those affected by substance use disorders, in the absence of diagnosis and treatment, can have unintended consequences, such as switching to heroin as a less expensive or more easily available alternative. 29,79

Various other measures may have some inadvertent effect on the problem of iatrogenic addiction simply by curtailing the degree to which pain is treated (i.e., opioid amount, duration, potency, and frequency of use) and thus the extent of exposure. Recently, emergency physicians have been encouraged to limit the amount and duration of opioid medication provided by any single prescription, avoid replacing lost or stolen prescriptions, and avoid treating chronic pain or refilling opioid prescriptions. 51,80 The Joint Commission on Accreditation of Healthcare Organizations recommendations include the use of multimodal treatment plans, including psychosocial support, coordination of care, promotion of healthful behaviors, and both nonopioid and nonpharmacologic approaches. The commission also acknowledges that not all pain can be eliminated and that in some cases "the best approach may be to start with a non-narcotic." 81(p2) There are also examples of advocacy and policymaker opposition to approval of new high-potency opioid pain medications. 31

Several publications and practice recommendations have recently begun to reintroduce the idea of iatrogenic addiction, but only indirectly and without explicit separation from misuse and diversion. The American College of Emergency Physicians guidelines recommend consideration of the patient's risk for opioid misuse, abuse, or diversion. 82 The Joint Commission on Accreditation of Healthcare Organizations recommends that patients be educated about the potential for addiction when prescribing opioids. 81 The Federation of State Medical Boards similarly recommends providing information to patients regarding the addictive nature of opioids and the potential dangers of misuse. 74 The Food and Drug Administration approved Risk Evaluation and Mitigation Strategy for Extended-Release and Long-Acting Opioid Analgesics requires pharmaceutical companies to make training and educational materials on the safe use of opioid medications available to prescribers and patients. 83-85 Several recent publications have implied that modification of opioid prescribing practices would attenuate the problem of iatrogenic addiction, 5,22,23 and one has explicitly indicated that screening for factors that predispose individuals to substance use disorders could help prevent iatrogenic addiction. 23

RECOMMENDATIONS FOR FUTURE ACTION

Any attempt to develop recommendations to address the issue of iatrogenic addiction in clinical practice is challenged by considerable deficiencies in the available evidence base. Hence, our primary recommendation is to expand the volume of research on iatrogenic addiction with great urgency, and research methods should be sufficiently rigorous to inform clinical practice guidelines. In addition, we need to vastly improve collaborative work across the fields of addiction and medicine to ensure that empirical evidence is transdisciplinary and translated into clinical practice and health policy.

Research

Advances in addiction science have improved our knowledge of opioid abuse liability and risk factors associated with opioid misuse and addiction, but the risk of addiction from appropriate medical use remains poorly defined. Evidence that does exist often does not transfer between siloed disciplines; what may seem obvious in the field of addiction may not be common knowledge to the professionals prescribing opioid medications for pain relief. In our clinical experience, few physicians outside chronic pain management are familiar with the term "iatrogenic addiction," even though both words in that term are in common use separately.

The most fundamental need is for more precise determination of how frequently and under what circumstances iatrogenic addiction occurs. There is knowledge about the individual-, family-, and environment-level factors, including nonmedical use of prescription opioids, which are associated with the development of illicit drug use and addiction. 58-63,86-92 However, there is little understanding of how these and yet other unidentified factors specifically relate to iatrogenic opioid addiction. There is even less understanding of risk factors at the health care system level and how external factors, such as health care setting, prescriber specialty, type of pain, and prescribing patterns are associated with iatrogenic addiction. Characterizing the range of contributory factors would provide a foundation for further research and allow interventions to be targeted proportionally to areas of greatest need. It would also suggest which actions should be avoided to reduce the incidence of iatrogenic addiction.

Perhaps the most important intervention would be the application of tools to appropriately risk-stratify patients before prescribing opioids to manage pain. Presently, there is no available method with adequate sensitivity or specificity to do so, and inaccurate assessments promise unnecessary stigma and inappropriate exclusion from opioid therapy. 12

After it becomes possible to accurately estimate the risk of iatrogenic addiction, there will be a need for research to guide clinicians on how to balance the risk of iatrogenic addiction with the risk of undertreated pain. Currently, there is no clear understanding of how patients or providers should balance these risks, either for individuals with an elevated risk of iatrogenic addiction or for those already suffering from the condition. For example, in cases of elevated risk, we do not know when it is appropriate to forgo opioids, use alternate dosing or abuse-deterrent formulations, or treat as needed but monitor closely. If close monitoring is adopted, we do not know how frequently this should occur, what targets should be selected (e.g., level of euphoria with appropriate use? indications of misuse?), or how best to measure these targets. When iatrogenic addiction has occurred, the best strategies for early recognition and intervention are neither characterized nor empirically tested. In particular, we do not know if, and to what extent, individuals with iatrogenic addiction might require different treatment strategies than are used for other forms of opioid addiction.

Ultimately, newly developed interventions need to be translated into practice. This will be facilitated if evidence is of high quality and developed within the settings and conditions for which the intervention is intended. It will also be vital to incorporate implementation science and effectiveness-implementation hybrid research designs to expedite the translation of empirical findings into clinical practice and public health policies. 93 Such research is inherently multidisciplinary and should include the perspectives of experts in addiction, pain, policy, public health, and ethics as well as health economists, law enforcement officials, advocacy groups, patients, and medical providers.

Education

The full range of available evidence on iatrogenic addiction has not been integrated into medical education to the same degree as has the more selected evidence initially promoted by pain advocates. We suggest several key points of desirable content.

Most fundamentally, providers need to understand the complex etiology and natural progression of opioid addiction and be reminded that appropriate medical use of prescription opioids can, in some unknown proportion of cases, initiate a progression toward misuse and ultimately addiction. The need to learn which patient characteristics are associated with developing addiction directly follows that foundation, as does the need to screen for those factors before prescribing opioid medications. 58-62,86-92 This should be differentiated from the important but different task of screening for opioid use disorders that are already present.

Providers will also need to adopt appropriate strategies for determining when and how opioids should be prescribed. This involves determining not only the risk of iatrogenic addition but also the degree to which opioids are appropriate and necessary. How opioids may be insufficient to treat or may even exacerbate pain 94-97 and may reduce functional status 24 should be understood along with more commonly recognized side effects and benefits. It is interesting that the majority of individuals with chronic pain report not using opioids, and those who do report use of opioids still indicate high levels of chronic pain. 96 Providers should also have more training in alternative approaches to managing pain, particularly in high-risk populations. These include nonopioid pain medications, mixed narcotic agonist-antagonists such as buprenorphine, and physical and occupational therapy. 22,98

Practice

Adding nuance to current practice in pain treatment will be a delicate matter. The push to incorporate addiction risk into medical decision-making should not come at the expense of improvements in pain management. Nonetheless, it may be appropriate to forgo opioids in situations where, on the basis of the best available evidence, the risks of iatrogenic addiction may outweigh the consequences of undertreated pain. When in doubt, shared decision-making approaches may be desirable and, in the setting of chronic pain, could combine the clinical expertise of pain specialists and addiction treatment providers. In addition, alternative pain management strategies should be covered by health insurance so that providers can be reimbursed appropriately for providing these services.

When opioids are prescribed in situations of greater than usual risk, a variety of measures may be necessary. These might include alternate prescribing patterns (e.g., adjusted dosage, potency, duration), patient education on the risks of iatrogenic addiction, and serial evaluation to identify opioid use disorders at the earliest possible stage. Other adjuncts might include more generalized use of pain management contracts, which are currently used only in the context of chronic pain. In the case of patients who have already been diagnosed with a substance use disorder, medication-assisted treatment may be considered in addition to nonopioid pain management. 6

Even when the risk of iatrogenic addiction is not elevated, providers should still be encouraged to advise patients of the risks of iatrogenic addiction and any recommendations to mitigate that risk. Providers commonly warn patients about the danger of sedation when prescribing opioids; warning about the risks of overdose and addiction should be as, if not more, important.

CONCLUSIONS

Pain relief is a core component of routine medical practice, but trends in morbidity and mortality associated with prescription opioids are alarming. Even if iatrogenic addiction occurs in only a small proportion of cases, the health consequences would still be considerable because of the absolute number of patients prescribed opioids annually. Physicians should once again become mindful that prescription opioids may lead to addiction in susceptible patients, even when prescribed and used appropriately. This recognition necessarily requires that the mission to treat pain must be balanced to at least some degree by a mission to prevent opioid abuse and addiction. Unfortunately, methods to achieve this balance are largely unknown. A true call to arms, broadly heralded across many research communities, is urgently needed to guide our response to this health emergency.

References

13. Centers for Disease Control and Prevention. Primary care and public health initiative: balancing pain management and prescription opioid abuse-educational module. 2012. Available at: http://www.cdc.gov/primarycare/materials/opoidabuse. Accessed May 30, 2014.

16. Boscarino JA, Rukstalis MR, Hoffman SN et al. Prevalence of prescription opioid-use disorder among chronic pain patients: comparison of the [ DSM-5 versus DSM-4 diagnostic criteria. J Addict Dis. 2011;30(3):185-194. [ PubMed] Google Scholar]

34. Courtwright DT. Dark Paradise-A History of Opiate Addiction in America. Cambridge, MA: Harvard University Press; 2001. [ Google Scholar]

35. Berridge V, Edwards G. Opium and the People: Opiate Use in Nineteenth Century England. Newhaven, CT: Yale University Press; 1987. [ Google Scholar]

41. Noble M, Treadwell JR, Tregear SJ et al. Long-term opioid management for chronic non cancer pain. Cochrane Database Syst Rev. 2010;(1):CD006605. [[ PMC free article] [ PubMed] Google Scholar]

46. United States General Accounting Office. Prescription drugs: OxyContin abuse and diversion and efforts to address the problem. 2004. Available at: http://www.gao.gov/new.items/d04110.pdf. Accessed December 2, 2013. [ PubMed]

55. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC: American Psychiatric Association; 1994. [ Google Scholar]

56. Dahl JL, Gordon DB.Joint Commission Pain Standards: a progress report APS Bulletin 200212(6)1.11-12 [ Google Scholar]

66. Center for Substance Abuse Treatment. Pain management without psychological dependence: a guide for healthcare providers. Substance Abuse in Brief Fact Sheet Summer. 2006;4(1):1-6. [ Google Scholar]

80. Ohio Prescription Drug Abuse Taskforce. Final Report-Task Force Recommendations. Columbus, OH; October 1, 2010.

84. Willy ME, Graham DJ, Racoosin JA et al. Candidate metrics for evaluating the impact of prescriber education on the safe use of extended-release/long-acting (ER/LA) opioid analgesics. Pain Med. 2014 Epub ahead of print. [[ PubMed] Google Scholar]

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Moving Beyond Misuse and Diversion: The Urgent Need to Consider the Role of Iatrogenic Addiction in the Current Opioid Epidemic

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An epidemic of drug overdose deaths has led to calls for programs and policies to limit misuse and diversion of opioid medications. Any parallel call to consider the risk of iatrogenic addiction when treating pain has been muted in comparison.We have ...

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https://www.youtube.com/watch?v=Z2M9fKGEbxg

this guy sounds like he knows what he's talking about, says he's a Dr? idk

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Cauda Equina Syndrome - Everything You Need To Know - Dr. Nabil

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https://geekymedics.com/the-vertebral-column/

nice layout and easy to go through

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The collection of bones stacked vertically upon one another to form the spine is what we know as the vertebral column. Each of these bones is called a vertebra (plural: vertebrae).

The vertebral column comprises 33 vertebrae, each separated by fibrocartilaginous intervertebral discs.

There are five distinct regions of the vertebral column where vertebrae share distinct characteristics that allow for specific joints to form and movements to be produced. Each of these regions is assigned a letter and a number, as described below.

This article focuses on the osteology of the vertebral column.

The vertebral column is a rigid, bony structure that serves several important functions:

Support: carrying the weight of the body above the vertebra and transmitting this through the pelvis to the legs

Movement: forms the central axis of the body by which the trunk and legs can move

Protection: contains the spinal canal, forming an osseous cylinder around the spinal cord

Axis: forms an axis that structures can attach to, such as the ribs and head

There are five distinct regions of the vertebral column.

From superior to inferior, these are:

1. Cervical - 7 vertebrae (C1 = highest; C7 = lowest)

2. Thoracic - 12 vertebrae (T1 = highest; T12 = lowest)

3. Lumbar - 5 vertebrae (L1 = highest; L5 = lowest)

4. Sacral - 5 fused vertebrae (S1 = highest; S5 = lowest)

5. Coccygeal - 3-4 fused vertebrae (Co1 = highest; Co3 = lowest)

Before we describe each of these regions and some examples of atypical vertebrae, we will consider the similarities in their basic structure.

Body

Almost all vertebrae in the human vertebral column contain a vertebral body.

The vertebral body becomes larger and provides more stability as the vertebral column moves inferiorly from the cervical region.

This is, in part, due to the increased mass placed on each vertebral body.

The vertebral body is surrounded by cortical (compact) bone.

Within the cortical bone is a dense network of trabecular bone.

This trabecular bone is of vital importance to haematopoiesis, or blood cell production, as it contains red bone marrow.

The vertebral bodies of two adjacent vertebrae are connected to intervertebral discs. These discs help to cushion shock as forces are transmitted through the vertebral column and also contributes to improving the range of motion between vertebrae.

Two projections exit either side of a vertebra posteriorly: the pedicles.

Pedicles

With a name derived from the Latin pediculus, meaning " little foot," the pedicles are two small posterior projections of the vertebral body.

They help to form the lateral margin of the spinal canal, and give rise to four important structures:

Lamina (posteriorly)

Articular processes (superiorly and inferiorly)

Transverse processes (laterally)

The vertebral arch refers to the semicircular ring of bone that connects the two vertebral pedicles.

The vertebral arch forms the posterior margin of the spinal canal. When the lamina and pedicles are referred to collectively, they are known as the vertebral arch.

The laminae have a postero-inferior extension known as the spinous process.

Articular processes

The articular processes are small protrusions of bone extending from the junction between the pedicles and laminae.

This process can extend superiorly to form the superior articular process, or inferiorly to form the inferior articular process.

At the tips of these articular processes are articular facets, which form a (zygapophyseal) joint with adjacent vertebrae to improve stability within the vertebral column.

Transverse processes

The transverse processes of the vertebral column are projections of bone that arise from the same place as the articular processes and travel laterally.

They serve different purposes in different regions of the spine, such as carrying blood vessels or forming attachment sites for the ribs.

Spinous processes

The spinous processes are postero-inferior projections of bone that exit the vertebral arch posteriorly from the midline.

They assist in limiting movements in certain regions of the spine and are a site for many ligaments to attach to.

Before introducing each vertebral region, we will explore the different joints in the vertebral column. Here, we focus on the joints common to each region.

There are three major joints in each vertebra:

Intervertebral joint (1 per vertebra)

Superior articular joints (2 per vertebra: left and right)

Inferior articular joints (2 per vertebra: left and right)

The inferior surface of a vertebral body is attached to an intervertebral disc, which then attaches to the superior surface of a vertebral body beneath it.

Intervertebral discs have two components:

Peripheral annulus fibrosis:

Dense types I and II collagen providing structural integrity and osseous attachments

Central nuclear pulposus:

High proteoglycan content to absorb water

Major shock absorber and pressure distributor

Becomes flatter proportional to time spent erect or standing

On each vertebra, there are two superior articular processes with facets and two inferior articular processes with facets. These form the zygapophyseal, or facet, joints of the vertebral column.

The orientation of the articular facets dictates the movements allowed in each vertebral region.

For example, the thoracic spine has an anterior-posterior orientation of the facets, allowing lateral movement but limiting flexion and extension.

Anterior and posterior longitudinal ligaments

They form a long line, running from the cervical region to the sacrum

Attach to the anterior and posterior surfaces of the vertebral bodies, respectively

Limits excessive extension and flexion of the vertebral column, respectively

Ligamentum flavum (yellow or golden ligament)

Attaches between the laminae of each vertebra

Very thick and strong

Limits excessive flexion of the vertebral column

Interspinal ligament

Between spinous processes of adjacent vertebrae

Limits excessive flexion of the vertebral column

Supraspinous ligament

Runs from spinous process to spinous process, in a line down the vertebral column

Limits excessive flexion of the vertebral column

Vertebral regions

Now that we have covered the common features of most typical vertebrae, we will discuss each vertebral region and highlight some characteristics that make bones in that region specifically identifiable. As we go, refer to these three images of the cervical, thoracic and lumbar spines to see the differences we discuss.

Cervical vertebrae

There are seven cervical vertebrae in the human vertebral column. They are the superior-most vertebral column group, and have several identifying features that are explained in more detail in the atypical vertebrae article:

Small vertebral body

Large, triangular-shaped vertebral foramen

Transverse foramina

Bifid spinous process

Cervical vertebrae having small vertebral bodies is the result of two important considerations:

1. The mass being transmitted through the cervical vertebrae is relatively small, and does not need a large base of support; and

2. The spinal cord is at its widest diameter in the cervical region, and a small vertebral body allows for a larger vertebral foramen

Transverse foramen in the cervical region have a distinct transverse foramina (hole). These transverse foramina allow the vertebral arteries to travel up the side of the vertebral column before entering the skull through the foramen magnum.

The vertebral arteries usually enter the transverse foramen of C6-C1, but can sometimes pass through the C7 transverse foramina as well.

Thoracic vertebrae

There are twelve thoracic vertebrae in the human vertebral column. They serve as the dorsal attachment site for the ribs, which form the majority of the lateral margin of the thoracic cavity (thorax), and line the thoracic inlet and outlet.

There are several identifying features of the typical thoracic vertebrae:

Heart-shaped vertebral body

Circular vertebral foramen

Anteriorly-posteriorly facing articular facets

Transverse processes with costal facets

Inferiorly pointing spinous process

Demi-facets

Each typical thoracic vertebrae has two demi-facets (half-facets) that are located on the superior and inferior lateral aspects of the thoracic vertebral body. These are positioned such that adjacent thoracic vertebrae each attach to a common rib.

Each typical rib will then attach to a single transverse process to improve the stability of the ribs and thoracic cage.

Lumbar vertebrae

The lumbar vertebrae are the last of the individual vertebrae in the vertebral column. There are five lumbar vertebrae, and each provides significant support to the body mass above the vertebral level. As a result of this, they have the largest vertebral bodies.

There are only a handful of spinal nerves left to branch from the spinal cord in the lumbar region, and the lumbar vertebrae have a small triangular vertebral foramen.

The identifying features of the lumbar vertebrae include:

Bean-shaped, large vertebral body

Small, triangular vertebral foramen

Laterally-facing superior and inferior articular facets

Short and posteriorly projecting spinous process

Sacral vertebrae

The sacrum is formed by 5 fused vertebrae that form an inverted triangle, with the base lying atop the apex.

Superiorly the sacrum connects to the intervertebral disc of L5/S1

Inferiorly, the sacrum connects to the coccygeal vertebrae

Laterally, the sacrum connects to the ilium of the pelvis via several dense, strong ligaments that help form the sacroiliac joint (SIJ)

The sacral nerves travel through the sacral canal to exit via the dorsal and ventral sacral foramina.

Lumbarisation and sacralisation are two recognised anatomical variants:

Lumbarisation refers to the separation of S1 from the rest of the sacrum

Sacralisation refers to the fusion of L5 to the sacrum

They are of little significance but may increase or decrease (respectively) range of motion in the lumbosacral region

Coccygeal vertebrae

The coccyx is formed by 3 (and occasionally 4) fused coccygeal vertebrae, also known as the tailbone.

Co1 and Co2 are invariably present, but Co3 can be absent or detached from the other two coccygeal vertebrae.

There are no vertebral arches in the coccygeal vertebrae, and thus, no vertebral canal can form in this region.

Clinical relevance

Clinical relevance - lateral curvature: scoliosis

Scoliosis refers to lateral curvature of the spine that may occur in any vertebral region, but more commonly the thoracolumbar spine.

It can be brought about by improper posture from muscular or skeletal abnormalities and may present at any age. It affects women more than men.

The signs and symptoms are location dependent, but pain is common. If thoracic scoliosis, dyspnoea and restrictive lung function patterns may be seen. In lumbar scoliosis, abdominal pain and 'tightening' of abdominal viscera are common.

Conservative therapy with physiotherapy, braces and exercise management can be corrective in mild disease. More advanced disease may need surgical intervention.

Clinical relevance - anterior/posterior curvature: kyphosis and lordosis

Kyphosis usually refers to pathological and excessive flexion of the primary spinal curves: the thoracic or the sacral curvatures.

Thoracic kyphosis is almost exclusively discussed in the medical world and presents with a heavily stooped posture and back pain.

It is commonly the product of lower bone mineral density causing osteopaenic or osteoporotic crush fractures of the thoracic vertebrae.

Lordosis refers to a pathological and excessive extension of the secondary spinal curves: the cervical or lumbar curvatures.

Lumbar lordosis is almost exclusively discussed in the medical world and presents with anteriorly rotated hips and excess extension of the lumbar spine (a "hollow back", or "Saddleback").

Common causes of lumbar lordosis may be tight hip flexors and erector spinae muscle groups, pregnancy, and pubertal growth spurts.

Clinical relevance - disc herniation

The intervertebral disc is the major shock absorber of the vertebral column.

The superior half of intervertebral discs send organised sheets of type I collagen fibres superiorly to attach the base of a superior vertebral body; and the inferior half of the intervertebral discs send these organised sheets inferiorly to the top of an inferior vertebral body.

Thus, a point of weakness in the intervertebral disc is this (vertically) middle portion of the disc, where there are disarrayed type I collagen fibres. The weakest portion of the intervertebral disc is the middle of the posterolateral portion, where the contents of a disc may slip through and protrude into the vertebral canal to cause spinal cord or nerve compression.

The most common locations for disc herniation are the lower cervical regions and lower lumbar regions. In both regions, the primary complaint is a shooting or radiating pain on movement of the spine or limb. Later in the disease course, motor dysfunction can occur.

Physical examination example

To assess for disc herniation in the lumbar region, the supine leg raise test is completed. Reproducing symptoms in the first 30 degrees of hip flexion is a positive sign, and suggests the need for further workup for lumbar disc herniation.

There are several stages of disc herniation, in order:

1. Disc degeneration: The nucleus pulposus bulges mildly into the annulus fibrosis

2. Disc prolapse: The nucleus pulposus bulges through the annulus fibrosis, which remains intact

3. Disc extrusion: The nucleus pulposus ruptures through the annulus fibrosis

4. Disc sequestration: The nucleus fibrosis and annulus fibrosis both rupture

References

Reference images

1. Dr Johannes Sobotta [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)]

2. BodyParts3D/Anatomography [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)]

3. Jmarchn [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)]

4. Beatricebalciunaite [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]

5. Anatomography [CC BY-SA 2.1 jp (https://creativecommons.org/licenses/by-sa/2.1/jp/deed.en)]

6. Anatomography [CC BY-SA 2.1 jp (https://creativecommons.org/licenses/by-sa/2.1/jp/deed.en)]

7. Anatomography [CC BY-SA 2.1 jp (https://creativecommons.org/licenses/by-sa/2.1/jp/deed.en)]

8. BruceBlaus [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]

9. Weiss HR [CC BY 2.0 (https://creativecommons.org/licenses/by/2.0)]

10. BruceBlaus [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]

11. Gunel Malikova [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]

12. Dawson, E. G., An, H. S. Herniated Discs: Definition, Progression, and Diagnosis by Edgar G.

13. Dawson, SpineUniverse, Accessed April 27, 2019

14. https://www.spineuniverse.com/conditions/herniated-disc/herniated-discs-definition-progression-diagnosis

Reference texts

Moore, K. L., Dalley, A. F., & Agur, A. M. (2013). Clinically oriented anatomy. Lippincott Williams & Wilkins.

Sinnatamby, C. S. (2011). Last's Anatomy, International Edition: Regional and Applied. Elsevier Health Sciences.

Editor

William Maish

# data[].attributes.attachment_link.title
The Vertebral Column | Bones of the Spine | Geeky Medics

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The collection of bones stacked vertically upon one another to form the spine is what we know as the vertebral column. Each of these bones is called a vertebra (plural: vertebrae). The vertebral column comprises 33 vertebrae, each separated by fibrocartilaginous intervertebral discs.

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https://www.nhs.uk/conditions/lumbar-decompression-surgery/what-happens/

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If you and your consultant decide you could benefit from lumbar decompression surgery, you'll be put on a waiting list.
Your doctor or surgeon should be able to tell you how long you're likely to have to wait. Read more about NHS waiting times.

Before the operation

To help you recover from your operation and reduce your risk of complications, it helps if you're as fit as possible before surgery.

As soon as you know you're going to have lumbar decompression surgery, it's advisable to stop smoking (if you smoke), eat a healthy, balanced diet and take regular exercise.

Pre-operative assessment

You'll be asked to attend a pre-operative assessment appointment a few days or weeks before your operation.

During this appointment, you may have some blood tests and a general health check to make sure you're fit for surgery, as well as an X-ray or magnetic resonance imaging (MRI) scan of your spine.

This assessment is a good opportunity to discuss any concerns you may have or ask questions about your operation.

You should be told who will be doing your operation and you may be introduced to them. Lumbar decompression surgery is carried out either by a neurosurgeon or an orthopaedic surgeon with experience in spinal surgery.

Read more about having an operation and general advice about going into hospital.

The operation

You'll be admitted to hospital either on the day of your operation or the day before. Your surgeon and anaesthetist will explain what will happen during the operation. This will give you the opportunity to ask any questions you may have.

Before the operation, you'll be asked to sign a consent form to confirm that you know what's involved and the potential risks.

You'll usually be asked not to eat or drink for about 6 hours before the operation.

During lumbar decompression surgery, you'll usually lie face down on a special curved mattress to allow the surgeon better access to the affected part of your spine and reduce the pressure on your chest, abdomen and pelvis.

The operation is carried out under general anaesthetic, which means you'll be asleep during the procedure and won't feel any pain. The whole operation takes at least an hour, but it may take much longer, depending on its complexity.

The exact level of decompression required will be determined using an X-ray. An incision will be made in the middle of your back, running vertically along your spine. The length of the incision will depend on:

how many vertebrae and/or discs need to be treated

the complexity of the surgery

whether fusion has been considered

The muscles in your back will be lifted from the back bone, to expose the back of the spine. The affected tissues or nerves will be removed little by little, taking the pressure off the spinal cord or nerves. Once adequate decompression has been achieved, the muscles will be stitched back together and the incision will be closed and stitched up.

Surgical procedures

The aim of lumbar decompression surgery is to relieve the pressure on your spinal cord or nerves, while maintaining as much of the strength and flexibility of your spine as possible.

Depending on the specific reason you're having surgery, a number of different procedures may need to be carried out during your operation to achieve this.

Three of the main procedures used are:

laminectomy - where a section of bone is removed from one of your vertebrae (spinal bones) to relieve pressure on the affected nerve

discectomy - where a section of a damaged disc is removed

spinal fusion - where 2 or more vertebrae are joined together with a bone graft

Laminectomy

A laminectomy removes areas of bone or tissue that are putting pressure on your spinal cord.

The surgeon makes an incision (cut) over the affected section of spine down to the lamina (bony arch of your vertebra), to access the compressed nerve. The nerve will be pulled back towards the centre of the spinal column and part of the bone or ligament pressing on the nerve will be removed.

To complete the operation, the surgeon will close the incision using stitches or surgical staples.

Discectomy

A discectomy is carried out to release the pressure on your spinal nerves caused by a bulging or slipped disc.

As with a laminectomy, the surgeon will make an incision over the affected area of your spine down to the lamina.

The surgeon will gently pull the nerve away to expose the prolapsed or bulging disc, which they'll remove just enough of to prevent pressure on the nerves. Most of the disc will be left behind to keep working as a shock absorber.

To complete the operation, the surgeon will close the incision with stitches or surgical staples.

Spinal fusion

Spinal fusion is used to join 2 or more vertebrae together by placing an additional section of bone in the space between them.

This helps to prevent excessive movements between 2 adjacent vertebrae, lowering the risk of further irritation or compression of the nearby nerves and reducing pain and related symptoms.

The additional section of bone can be taken from somewhere else in your body (usually the hip) or from a donated bone. More recently, synthetic (man-made) bone substitutes have been used.

To improve the chance of fusion being successful, some surgeons may use screws and connecting rods to secure the bones.

Afterwards, the surgeon will close the incision with stitches or surgical staples.

Your surgeon can give you more information about which procedures are going to be performed during your surgery.

Keyhole surgery

Spinal decompression surgery is usually performed through a large incision in the back. This is known as "open" surgery.

In some cases, it may be possible for spinal fusion to be carried out using a "keyhole" technique known as microendoscopic surgery. This is performed using a tiny camera and surgical instruments inserted through a small incision in your back. The surgeon is guided by viewing the operation on a video monitor.

Microendoscopic surgery is complicated and isn't suitable for everyone. Whether it's suitable for you depends on the exact problem in your lower back. There's also a slightly higher risk of accidental injury during this operation than with an open operation.

Some of the techniques used during microendoscopic surgery, such as using a laser or a heated probe to burn away a section of damaged disc, are relatively new. Therefore, it's still uncertain how effective or safe they may be in the long term.

An advantage of microendoscopic surgery is that it usually has a much shorter recovery time. In many cases, people can leave hospital the day after surgery has been completed.

Interspinous distraction

Interspinous distraction is a new type of lumbar surgery for spinal stenosis. This technique involves making a small incision above your spine and placing a metal device, known as a spacer, between 2 vertebrae, so that they can't move onto the underlying nerve.

Interspinous distraction appears to be safe in the short term, but as it's a new technique, it's uncertain how it will fare in the long term. One possible risk is that the spacer could move out of position and require further surgery to correct.

The National Institute for Health and Care Excellence (NICE) has more information about interspinous distraction procedures for lumbar spinal stenosis (PDF, 92kb).

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Lumbar decompression surgery - How it's performed

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If you and your consultant decide you could benefit from lumbar decompression surgery, you'll be put on a waiting list. Your doctor or surgeon should be able to tell you how long you're likely to have to wait. Read more about NHS waiting times.

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https://www.spineuniverse.com/conditions/herniated-disc/herniated-discs-definition-progression-diagnosis
Useful on herniated discs

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Herniated Discs: Definition, Progression, and Diagnosis

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This informative article explains herniated discs in easy-to-understand language. Learn what a herniated disc really is, how we develop them, where we can feel pain from them, and how doctors diagnosis them.

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this diagram shows the pathology of AS (showing the genetic and environmental factors)

1) the bacteria penetrate the mucosal barrier
2) activating the macrophages and dendritic cells
3) these cells produce increased IL-23 acting on T-cells, Neutrophils and Mast cells to make IL-17
4a) IL-17 drives inflammation causing the SACROILIITIS and ENTHESITIS.
4b) the dendrites present the antigens that activate the T-cells and TNF which then produces the IL-22
4c) production of IL-22 is thought to cause the new bone formation typical of AXIAL spondyloarthropathies

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https://teachmesurgery.com/orthopaedic/spine/radiculopathy/#:~:text=A%20radiculopathy%20is%20a%20conduction,causing%20paraesthesia%20and%2For%20anaesthesia.

this was quite a nice website that helped me to understand the basics of radiculopathies

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Radiculopathy - Red Flag Symptoms - Symptomatic Management - TeachMeSurgery

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A radiculopathy is a conduction block in the axons of a spinal nerve or its roots, with impact on motor axons causing weakness and on sensory axons causing paraesthesia and / or anaesthesia

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I used the same extra resource as Maisie

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file:///C:/Users/sarai/Downloads/Referred%20pain%202022%20lecture%20notes.pdf

the lecture notes that were uploaded on blackboard I found to be very useful in summarising this LO and also explained the different mechanisms of referred pain very well

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https://www.youtube.com/watch?v=sHdAGSa1Opc

sums up everything for spondys

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crash course

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NICE guidelines

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https://www.ncbi.nlm.nih.gov/books/NBK470173/

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Continuing Education Activity

Ankylosing spondylitis (AS) is a chronic, inflammatory disease of the axial spine. Chronic back pain and progressive spinal stiffness are the most common features of this disease. Involvement of the spine, sacroiliac joints, peripheral joints, digits, and entheses are characteristic. Impaired spinal mobility, postural abnormalities, buttock pain, hip pain, peripheral arthritis, enthesitis, and dactylitis are all commonly associated with ankylosing spondylitis. This activity reviews the evaluation and management of ankylosing spondylitis and highlights the role of the interprofessional team in evaluating and improving care for patients with this condition.

Objectives:

Identify the etiology of ankylosing spondylitis.

Describe the workup of a patient with ankylosing spondylitis.

Review the management options available for ankylosing spondylitis.

Summarize interprofessional team strategies for improving care and outcomes in patients with ankylosing spondylitis.

Access free multiple choice questions on this topic.
Introduction

Ankylosing spondylitis (AS) is a chronic, inflammatory disease of the axial spine that can manifest with various clinical signs and symptoms. Chronic back pain and progressive spinal stiffness are the most common features of the disease. Involvement of the spine and sacroiliac (SI) joints, peripheral joints, digits, entheses are characteristic of the disease. Impaired spinal mobility, postural abnormalities, buttock pain, hip pain, peripheral arthritis, enthesitis, and dactylitis ("sausage digits") are all associated with AS.

Extraskeletal organs may also be affected by this disease. The most common extraarticular manifestations of AS include inflammatory bowel disease (up to 50%), acute anterior uveitis (25% to 35%), and psoriasis (approximately 10%). AS is also associated with an increased risk of cardiovascular disease. The cause of this increased risk has been postulated to be due to the systemic inflammation evident in AS. Pulmonary complications are also associated with AS, as diminished chest wall expansion and decreased spinal mobility predispose patients to a restrictive pulmonary pattern.

Finally, AS predisposes people to at least a two-fold increased incidence of vertebral fragility fractures. These patients are also at increased risk of atlantoaxial subluxation, spinal cord injury, and, rarely, cauda equina syndrome.[1][2][3]

Etiology

The cause of ankylosing spondylitis (AS) remains largely idiopathic, but there seems to be a correlation between the prevalence of AS in a given population and the prevalence of human leukocyte antigen (HLA)-B27 in that same population. Among people who are HLA-B27 positive, the prevalence of AS is approximately 5% to 6%. In the United States, the prevalence of HLA-B27 varies among ethnic groups. According to a 2009 survey, prevalence rates of HLA-B27 were 7.5% among non-Hispanic Whites, 4.6% among Mexican-Americans, and 1.1% among non-Hispanic Blacks.[4][5]

Epidemiology

Ankylosing spondylitis (AS) is typically diagnosed in people younger than 40 years, and about 80% of patients develop first symptoms when they are younger than 30 years. Less than 5% of patients present when they are older than 45 years. AS is more common among men than women. There is an increased risk in relatives of affected patients.[6]

Pathophysiology

Ankylosing spondylitis (AS) is a chronic inflammatory disease with an insidious onset. Progressive musculoskeletal, and often extraskeletal, signs and symptoms are characteristic of the disease. The rate of progression can vary from one patient to the next. The primary pathology of spondyloarthropathies is enthesitis with chronic inflammation, including CD4 and CD8 T lymphocytes and macrophages. Cytokines, particularly tumor necrosis factor-α (TNF-α) and transforming growth factor-β (TGF-β), are also important in the inflammatory process by leading to inflammation, fibrosis, and ossification at sites of enthesitis.

History and Physical

A comprehensive, full-body evaluation should be performed in patients suspected of having ankylosing spondylitis (AS) due to the pervasive nature of the disease and susceptibility to multi-organ system involvement. Almost all patients will complain of back pain to some degree. The characteristic type of back pain in AS is "inflammatory" in nature. Inflammatory back pain typically exhibits at least four of the five following characteristics: age of onset less than 40 years, insidious onset, improvement with exercise, no improvement with rest, and pain at night with an improvement upon arising. Spinal stiffness, immobility, and postural changes, especially hyperkyphosis, are also commonly seen. History and physical exam should address all systems, as AS can have several axial and peripheral musculoskeletal manifestations, as well as extra-articular features. A detailed medical history should be obtained to rule in/out any correlated conditions (e.g., psoriasis, inflammatory bowel disease, uveitis, among others).

Evaluation

Laboratory findings in ankylosing spondylitis (AS) are generally nonspecific but may help assist with diagnosis. About 50% to 70% of patients with active AS have elevated acute phase reactants, such as erythrocyte sedimentation rate (ESR) and elevated C-reactive protein (CRP). A normal ESR and CRP, however, should not exclude the disease.[7][8][9]

A number of imaging abnormalities, especially those affecting the spine and sacroiliac joints, are characteristic of AS. In fact, according to the assessment of spondyloarthritis international society (ASAS) 2009 axial SpA criteria, evidence of sacroiliitis on imaging (radiographic or MRI) is a major inclusion criterion for AS. A standardized plain radiographic grading scale exists for sacroiliitis, which ranges from normal (0) to most severe (IV), as detailed below.

0: Normal SI joint width, sharp joint margins

II: Sclerosis, some erosions

III: Severe erosions, pseudo dilation of the joint space, partial ankylosis

In the first few years of AS, plain radiographic changes in the SI joints can be very subtle, but within the first decade will usually become more obvious. Subchondral erosions, sclerosis, and joint fusion are the most obvious abnormalities, and these radiographic changes are typically symmetric.

A series of plain radiographic changes characteristic of AS can progressively develop over the course of the disease. An early sign is "squaring" of the vertebral bodies, best seen on lateral x-ray. This is seen as a loss of normal concavity of the anterior and posterior borders of the vertebral body due to inflammation and bone deposition. Romanus lesions, or the "shiny corner sign," can also be seen on this radiographic view in the early stages. These lesions are characterized by small erosions and reactive sclerosis at the corners of the vertebral bodies. Late-stage findings include ankylosis (fusion) of the facet joints of the spine, syndesmophytes, and calcification of the anterior longitudinal ligament, supraspinous ligaments, and interspinous ligaments. This calcification may be seen on imaging as the "dagger sign," which is represented as a single radiodense line running vertically down the spine on frontal radiographs. The classic radiographic finding in late-stage AS is the "bamboo spine sign," which refers to the vertebral body fusion by syndesmophytes. A bamboo spine typically involves the thoracolumbar or lumbosacral junctions. It is this fusion of the spine that predisposes the patient to progressive back stiffness.

While plain radiography is the first-line imaging modality in AS, MRI may be needed to reveal more subtle abnormalities such as fatty changes or inflammatory changes. Active SI joint inflammatory lesions appear as bone marrow edema (BME) on short tau inversion recovery (STIR) and T2-weighted images with fat suppression. It should be noted that the presence of BME on MRI can also be seen in up to 23% of patients with mechanical back pain and 7% of healthy people.[10]

Treatment / Management

Treatment goals should focus on relieving pain and stiffness, maintaining axial spine motion and functional ability, and preventing spinal complications. Non-pharmacologic interventions should include regular exercise, postural training, and physical therapy. First-line medication therapy is with long-term, daily non-steroidal anti-inflammatory drugs (NSAIDs). Should NSAIDs not provide adequate relief, they can be combined with or substituted for tumor necrosis factor inhibitors (TNF-Is) such as adalimumab, infliximab, or etanercept. Response to NSAIDs should be assessed four to six weeks after initiation and twelve weeks following initiation of TNF-Is. Systemic glucocorticoids are not recommended, but local steroid injections may be considered. Specialist referrals may be warranted based on the patient's clinical picture, potential complications, and extra-articular manifestations of the disease. Rheumatologists may assist in a formal diagnosis, management, and monitoring, while dermatologists, ophthalmologists, and gastroenterologists may assist with associated non-musculoskeletal features of AS.[11][1][12]

Differential Diagnosis

Certain diseases and conditions can mimic ankylosing spondylitis (AS) and must be ruled out. These include, but are not limited to:

Diffuse idiopathic skeletal hyperostosis (DISH)

Each of these diagnoses has similarities with AS, but their differences should be ruled in or out for accurate diagnosis.

Mechanical back pain can be differentiated from AS by the onset of symptoms, as mechanical back pain can present at any age, while AS typically presents before age 40. Unlike AS, pain improves with rest, and morning stiffness is mild and short-lived. Mechanical back pain is also not associated with peripheral arthritis or extraskeletal manifestations, as AS is.

Lumbar spinal stenosis (LSS) is a narrowing of the spinal canal that exerts pressure on the spinal cord. Like AS, it may present with chronic back pain and morning stiffness. Unlike AS, however, LSS usually presents in patients older than 60 years, is not associated with peripheral arthritis or extraskeletal features, and response to NSAIDs is variable.

Rheumatoid arthritis (RA) is another chronic inflammatory disorder of the joints that often presents with progressive back pain and morning stiffness in patients 40 or younger, similar to AS. However, peripheral arthritis is extremely common in RA, unlike in AS. In addition, rheumatoid nodules are pathognomonic for RA but are not usually present with AS.

Diffuse idiopathic skeletal hyperostosis (DISH) is a degenerative disorder characterized by ossification in the spine occurring primarily in the anterior longitudinal ligament, paravertebral tissues, and peripheral aspect of the annulus fibrosus. Similar to AS, the DISH may present with a history of postural changes and back pain. Unlike AS, which is an inflammatory disorder, the DISH does not have inflammatory characteristics such as morning stiffness or improvement with exercise but not with rest. DISH also shows no evidence of sacroiliitis on radiographs.

Prognosis

While the younger age of onset in ankylosing spondylitis (AS) patients is associated with poorer function outcomes, severe physical disability is uncommon. Most patients remain fully functional and able to work. Patients with the severe, long-standing disease have greater mortality compared with the general population, predominantly due to cardiovascular complications.

Complications

Ankylosing spondylitis (AS) has articular and extra-articular complications. These include:

Deterrence and Patient Education

Patient education is very important in the management of ankylosing spondylitis (AS). Patients should be educated about the long-term nature of the illness and the use and toxicities of medications. Inform patients that proper exercise programs are useful in reducing symptoms, to remain functional, physical therapy is highly recommended. Both water therapy and swimming are known to help maintain fitness and lower morbidity. Because of pulmonary involvement in AS, smoking cessation is recommended.

Pearls and Other Issues

Pitfalls: The possibility of vertebral fracture should always be considered in patients with ankylosing spondylitis (AS), even after minor trauma. Patients with AS are at increased risk of vertebral fracture and subluxation, especially of the cervical spine. Therefore, these patients are more susceptible to neurologic compromise.

Prevention of disease morbidity can be achieved with exercise, physical therapy, tailored pharmacologic intervention, and regimented follow-up appointments with providers.

Enhancing Healthcare Team Outcomes

Ankylosing spondylitis (AS) is a systemic disorder that can affect many organ systems and hence an interprofessional team approach is recommended to avoid the morbidity.

Rheumatologist to evaluate and manage the acute symptoms and address any coexisting spondyloarthropathies.

Gastroenterologist to assess for inflammatory bowel disease

Ophthalmologist to assess for anterior uveitis

Cardiologist to assess for heart block or valvular involvement

Physical therapy to help with function

Neurologist to assess for nerve compression syndromes

Pharmacist to monitor for drug interactions and dependence on analgesics

Nurse to educate the patient on the management of daily living activities

There are many reports indicating that an interprofessional approach to ankylosing spondylitis can improve function, lower pain and increase the quality of life.[13][14] (Level II)

Evidence-based Medicine

Meta-analysis of many studies has revealed that those who participate in an exercise program have a much better outcome than those who lead a sedentary lifestyle. (Level II) Unfortunately, those patients with large symptom burden at the time of diagnosis usually have poor response rates and are often lost to follow up. One way to retain these patients is by starting an education program early in the disease.[15][16][17] (Level V)

References

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Ankylosing spondylitis (AS) is a chronic, inflammatory disease of the axial spine that can manifest with various clinical signs and symptoms. Chronic back pain and progressive spinal stiffness are the most common features of the disease. Involvement of the spine and sacroiliac (SI) joints, peripheral joints, digits, entheses are characteristic of the disease.

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Common differential diagnoses for back pain

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https://www.medicalnewstoday.com/articles/318465#Radiculopathy-symptoms

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Radiculopathy: Causes, symptoms, and treatment

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Radiculopathy describes a nerve being pinched by the spine. This can cause discomfort, weakness, and numbness, and can be treated with medication and physical therapy. This article explains the causes of this painful condition, how it is diagnosed, and how a person might go about preventing the onse…

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https://www.ncbi.nlm.nih.gov/books/NBK537200/

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Continuing Education Activity

Cauda equina and conus medullaris syndromes have overlap in anatomy and clinical presentation. The cauda equina is a group of nerves and nerve roots stemming from the distal end of the spinal cord, typically levels L1-L5 and contains axons of nerves that give both motor and sensory innervation to the legs, bladder, anus, and perineum. Cauda equina syndrome (CES) results from compression and disruption of the function of these nerves and can be inclusive of the conus medullaris or distal to it, and most often occurs when damage occurs to the L3-L5 nerve roots. This activity reviews the cause and presentation of cauda equina and conus medullaris syndromes and highlights the role of the interprofessional team in their management.

Objectives:

Review the causes of cauda equina and conus medullaris syndromes .

Describe the presentation of cauda equina and conus medullaris syndromes.

Summarize the treatment of cauda equina and conus medullaris syndromes.

Explain the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by cauda equina and conus medullaris syndromes.

Access free multiple choice questions on this topic.
Introduction

Cauda equina and conus medullaris syndromes have overlap in anatomy and clinical presentation. Therefore, for the purpose of this discussion, they will be grouped, and notable differences highlighted. The conus medullaris is the terminal end of the spinal cord, which typically occurs at the L1 vertebral level in the average adult.[1] Conus medullaris syndrome (CMS) results when there is compressive damage to the spinal cord from T12-L2.[1] The cauda equina is a group of nerves and nerve roots stemming from the distal end of the spinal cord, typically levels L1-L5 and contains axons of nerves that give both motor and sensory innervation to the legs, bladder, anus, and perineum.[2] Cauda equina syndrome (CES) results from compression and disruption of the function of these nerves and can be inclusive of the conus medullaris or distal to it, and most often occurs when damage occurs to the L3-L5 nerve roots.[1] Both syndromes are neurosurgical emergencies as they can present with back pain radiating to the legs, motor and sensory dysfunction of the lower extremities, bladder and/or bowel dysfunction, sexual dysfunction and saddle anesthesia.[3] CMS and CES also carry a high risk of litigation as delays in diagnosis and management can lead to devastating life-long impairment.

Etiology

Cauda equina syndrome and conus medullaris syndrome result from compression of the spinal cord and nerves/nerve roots arising from L1-L5 levels. The most common cause of compression in 45% of CES is a herniated lumbar intervertebral disc.[3] Other causes include epidural abscess, spinal epidural hematoma, diskitis, tumor (either metastatic or a primary CNS cancer), trauma (particularly when there is retropulsion of bone fracture fragments), spinal stenosis and aortic obstruction.[4] Rare reported cases exist in which CES was associated with chiropractic manipulation, placement of interspinous devices, and thrombosis of the inferior vena cava.[4]

Epidemiology

Cauda equina syndrome and conus medullaris syndrome are rare, with an estimated prevalence of 1 in 30,000 to 100,000 people per year.[5] Estimates of annual incidence are between 1.5 to 3.4 per million people.[5] It occurs in 3% of all disc herniations.[5] Cauda equina syndrome and conus medullaris syndrome are most common in young men, possibly due to this population group being more likely to experience compressive thoracolumbar trauma.[5] One study estimated that in the U.S. we would expect to see 1016 new causes of cauda equina syndrome and 449 new cases of conus medullaris per year.[5]

History and Physical

A thorough history is necessary, with detailed questions regarding recent falls, trauma or injuries, use of anticoagulation, presented spinal instrumentation, intravenous drug use, history of malignancy, chiropractic manipulation, and constitutional symptoms like fevers/chills.[3]

Patients can present with:

Back pain and sciatica (seen in as many as 97% of patients)

Weakness and changes in sensation in the lower extremities

Bladder dysfunction (disruption of autonomic fibers results in either retention or incontinence in up to 92% of patients)

Bowel dysfunction (retention or incontinence in up to 72% of patients)

Saddle anesthesia or decreased sensation in the perineum (in up to 93% of patients)

Sexual dysfunction (impotence in men)[3]

The symptoms above when presenting in isolation, are neither specific nor sensitive for CMS/CES. However, several of the signs and symptoms mentioned above taken as a constellation should raise clinical suspicion.[2] These symptoms also lack significant positive predictive value for the syndromes, especially early on.[6] However, the onset of perineal anesthesia associated with bladder dysfunction is typical of the start of CES and the time at which the clock starts on diagnosis and management.[2] It is important also to note that painless urinary retention often has the greatest predictive value as a stand-alone symptom, but it is unfortunately indicative of late, often irreversible CMS/CES.[7]

Once clinical suspicion is established based on history, a thorough neurological examination is paramount. Findings to watch for include:

Motor or sensory deficits in the legs - usually bilateral but can also be unilateral and asymmetrical (particularly in cases with an incomplete injury)

Lower motor neuron signs in the legs - areflexia, hypotonia, atrophy (in cases of chronic cord compression resulting in CES)

Absent or decreased rectal tone

Absent or decreased bulbocavernosus reflex

Palpable bladder indicating urinary retention[3]

It is important to note that in the case of isolated conus medullaris syndrome, deficits of the lower extremities are more often bilateral and symmetric. Also, upper motor neuron signs can be present, such as spasticity and hyperreflexia.[1]

Evaluation

The gold standard method of evaluation for CMS/CES is obtaining urgent MRI imaging with sagittal and axial T1 and T2 sequences.[2] There has not been a specific timeframe established for "door to MRI time" in the ED, but early MRI and neurosurgical or orthopedic consultation is imperative. An ideal goal for MRI is one hour from the patient presentation.[2] For patients with contraindications to MRI, such as those with metal implants, a CT myelogram is a viable option.[2] This imaging modality has limited utility as it requires injecting contrast through a spinal tap to visualize the spinal cord and its associated structures. A bladder scan checking for a post-void residual volume should also be obtained to evaluate for urinary retention.[2]

Treatment / Management

Prompt neurosurgical or orthopedic consultation is necessary in cases of cauda equina and conus medullaris syndromes, as the treatment is surgical decompression via laminectomy with or without subsequent discectomy, or via sequestrectomy.[2]

Differential Diagnosis

The differential diagnosis centers on non-compressible causes of spinal cord dysfunction such as:

Prognosis

Several studies have looked at prognosis and outcomes based on the timing of surgical decompression. Early intervention by surgical decompression in patients with conus medullaris and cauda equina syndromes is associated with a better prognosis, particularly when surgery occurs within 48 hours of initial presentation.[6] The longer the compression continues, the worse the permanent structural and functional impairment, and the poorer the prognosis.[2] It is important to note that the presence of bladder dysfunction prior to surgery has been linked to poorer outcomes regardless of the timing of decompression, although early decompression is still the recommendation for a better prognosis irrespective of clinical status at initial presentation.[2]

Complications

Complications in cauda equina syndrome and conus medullaris syndrome occur in a large percentage of those diagnosed. One study looked at 63-day outcomes on micturition, defecation, saddle anesthesia, sexual function, and sciatica in cauda equina syndrome. The data indicate that a large percentage of patients still experience residual symptoms irrespective of their time to surgical decompression.[3] Micturition deficits such as retention requiring self-catheterization or presence of suprapubic or indwelling catheters and incontinence still presented in 47.7% of patients.[3] Dysfunction with defecation decreased post-operatively significantly, but 41.8% of patients still had problems at 63 days post-operatively.[3] Sexual dysfunction persisted in 53.3% of patients, and saddle anesthesia in 56.6%.[3] Sciatica was present in 47.5% of patients.[3] The best predictors of outcome are neurological status at presentation and degree of injury. Incomplete injuries tend to have better outcomes.[3]

Deterrence and Patient Education

Patients presenting with sciatica and no other evidence of CES/CMS in the history or exam should receive counsel on the possible development of other related symptoms such as bladder or bowel dysfunction, impotence, and saddle anesthesia. These patients must be given strict return precautions in the event they develop other symptoms pointing to CES/CMS. Patients who are suspected to have CES/CMS and are undergoing evaluation for these syndromes need to remain informed and updated on their investigations (MRI, bladder scan, etc.) and pending surgical consultations. Patients who receive a definitive diagnosis need counseling on complication rates and must receive a realistic prognosis based on their degree of injury. Due to the nature of sensitive lifelong sequelae resulting from these syndromes, cases with CES/CMS have a high involvement in medicolegal litigation.[8] For physicians, it is vital to document the history and physical exam thoroughly and accurately and reach the diagnosis as promptly as possible. In court cases involving CES, a positive association exists between time to surgical decompression greater than 48 hours and an adverse decision for the physician involved.[8] The degree of functional loss did not affect court rulings in the cases studies.[8]

Enhancing Healthcare Team Outcomes

The involvement and effective collaboration of the entire healthcare team is essential in any patient encounter, but even more so in cases where the presentation requires urgency in proper diagnosis and management. Due to the high degree of functional impairment arising from CES/CMS, speedy diagnosis and subsequent treatment via surgical decompression are important. The efficiency of the medical system must begin with the person responsible for triaging appropriately in the emergency department, where a significant proportion of patients with CES/CMS initially present for evaluation. After the initial triage, nurses and physicians must work together to keep the patient updated on the suspected diagnosis, workup, and test results. The radiologist must know the reason for ordering the MRI these patients and given the clinical history and suspected diagnosis early.

MRI imaging is considered the gold standard imaging modality to asses of CES/CMS, Class I evidence. Many studies recommend obtaining MRI within an hour from presentation. Furthermore, it is paramount that prompt neurosurgical consultation take palce promptly, as surgical decompression is required. Many studies have been done that show decompression within 48 hours is best, although some studies recommend the timing be closer to under 24 hours, Class II evidence. It is challenging to design large RCTs to obtain Class I evidence for the timing of surgical decompression for obvious ethical reasons.[9] Despite prompt surgical intervention, patients will experience residual symptoms. It is vital to counsel patients on this possibility. The primary care provider also has a vital role in further outpatient management postoperatively.

References

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Cauda Equina And Conus Medullaris Syndromes

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Cauda equina and conus medullaris syndromes have overlap in anatomy and clinical presentation. Therefore, for the purpose of this discussion, they will be grouped, and notable differences highlighted.

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https://www.practicalpainmanagement.com/pain/neuropathic/referred-pain-vsorigin-pain-pathology

Also used the lecture

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https://learn.capsule.ac.uk/case/4505
This capsule case is very relevant to this week. apologies if you have completed this one already.

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Questions

1. What are Dermatomes and myotomes?

2.Which nerve fibres carry pain and what are the differences between them?

3. Which nerve supplies the gluteal muscles, posterior thigh and posterior lower leg and where does it originate?

4. What condition does pain in the area indicate?

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Answers

1. - area of skin where the sensory nerves derive from a single nerve root.
- groups of muscles where the motor fibres are served by a single spinal root.

2. - A-delta fibres, myelinated, fast sensory conduction, mediate sharp, pricking, stinging pain.
- C-fibres non-myelinated, slow sensory conduction, mediate burning, dull, aching pain.

3. - sciatic nerve
- L4,L5, S1, S2, S3,

4. - Sciatica
- pain indicates compression of the sciatic nerve due to impingement of L5 or S1 nerve roots.

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After the onset of cauda equina symptoms, what is the ideal max time frame to surgically treat patients to provide significant advantage in improving sensory & motor deficits and continence?

-24 hours

-36 hours

-48 hours

-72 hours

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What isn’t a red flag for cauda equina syndrome?

-Saddle anaesthesia

-Bowel incontinence

-Muscle spasms in lower leg

-Urinary retention

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Where is the cauda equina located?

-Lumbar region only

-Sacral region only

-Lumbar to sacral region

-Lumbar to coccygeal region

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- arrange urgent spinal surgical admission that day
-arreflexia and reduced tone
-left box in complete and right box is incomplete
- 48 hours
-muscle spams in lower leg