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US Government Publishing Office. (2021, May 20). National Mental Health Awareness Month Infographic [Infopgraphic]. Gov Info. https://www.govinfo.gov/features/mental-health-awareness-month-2021

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Mental Health Matters Illustration. (2022). [Illustration]. Spreadshirt. https://www.spreadshirt.com/shop/design/mental+health+matters+brain+graphic+bandana-D60fcc86728a196203166bf56?sellable=XyywEgBO2dT4wzZNrpve-610-41

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[Mental Health Illustration]. (2022). Loss Control Learning Center. https://www.mylosscontrolservices.com/learning-center/articles/shining-a-light-on-mental-health-awareness

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Module 1: Introduction & Children's Mental Health Discussion Board Post

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Module 1: Introduction & Children's Mental Health Discussion Board Post

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Hi Class,

My name is Dorothy “Allison” Camp and I am in my final semester of the Mental Health and Wellness Counseling Program here at ASU (wahoo)! I am 27 years old and live in Dallas, TX. I did my undergraduate studies at the University of South Carolina. I am currently in the College Counseling Office as an Associate at a private/independent school with goals to move up into an Associate Director or Director role at my current school. I am also the Varsity Volleyball Assistant Coach at the school and coach club volleyball as well. As an Assistant Director/Director of College Counseling at a high school, learning about dysfunctional behavior will be helpful because there is a fine line of what students share with us in our office as a form of self-reflection necessary to go through the college research/application process successfully, and what we must refer to the school counselor. In addition, understanding potential dysfunctional behaviors in students will help me as a college counselor to advise them on what to share about themselves in their college essays and also would help me share more about them in my counselor letter. Understanding potential dysfunctional behaviors could also help me be a better volleyball coach by seeing warning signs of mental illness in athletes that is on the rise nationally.

After reviewing some data and statistics from the CDC website, I am actually surprised to know that only 9.4% of children are diagnosed with anxiety and 4.4% are diagnosed with depression (Centers for Disease Control and Prevention, 2022). After reviewing data and statistics from the school I work at, this number seems surprisingly low as the percentage of our student body who deals with these struggles are much higher unfortunately. I was also interested in the ratio, specifically in Texas, of the Rates of Mental and Behavioral Health Service Providers by County in 2015. Interestingly, licensed social workers lead the charge in Dallas County with 10.1 per 10,000 children in the county under the age of 17, then psychologists with 8.7 per 10,000, family medicine physicians with 7.8, and falling behind were pediatricians with 5.9 and psychiatrists with 3.6 (Centers for Disease Control and Prevention, 2022a).

Working in a school, I have a few years of experience working with students who have diagnosed (and undiagnosed but self-proclaimed) anxiety, depression, and ADHD. The school I work at is incredibly academically rigorous and holds students to an incredibly high standard - so our office has become a safe place for students to openly share about the challenges they face and their daily struggles while we help them sort it all into useful self-reflection that will lead towards authentic college matches. Helping students articulate their mental health struggles in college essays and applications is a huge part of my job, so I feel confident in the basic understandings of these disorders and my ability to help students reflect and continue moving forward. In terms of stigmas around these behaviors, I have two very different answers. In general and nationally, I certainly think there are negative connotations and stigmas surrounding mental illness and behavioral disorders by people who do not understand them or have never experienced or lived them closely. However, at the school I work at specifically, these behaviors have almost become the “norm” and what is expected. The words “anxious” and “depressed” are tossed around so freely and seemingly as a way for students to prove themselves and how hard they are working. As an adult, this is incredibly interesting but also unnerving to watch play out, as I know how serious true anxiety and depression are.

References:

Centers for Disease Control and Prevention. (2022a, April 19). Behavioral health services in Texas | CDC. Retrieved June 4, 2022, from https://www.cdc.gov/childrensmentalhealth/stateprofiles-providers/texas/index.html

Centers for Disease Control and Prevention. (2022, June 3). Data and Statistics on Children’s Mental Health | CDC. Retrieved June 4, 2022, from https://www.cdc.gov/childrensmentalhealth/data.html

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The Hockaday School Website: How Our School's Counseling Office Works

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The Hockaday School Website: How Our School's Counseling Office Works

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Each Division has a school counselor, a trained mental health professional who understands and responds to the challenges presented by today's diverse student population. A valuable resource for students, parents, faculty, and staff, Hockaday's school counselors do not work in isolation; rather they are integral to the total educational program. They align and work with the school's mission to foster a community of concern and friendship and to instill in every girl a love of learning and an understanding of herself and the ethical principles which guide her life.

The counselors interact with students on a regular basis through a variety of venues, such as making presentations to a class, offering optional workshops, acting as an advisor or club sponsor, or helping an individual student work through a personal problem. Faculty and administrators also look to the counselors for their expertise in social and emotional developmental factors that impact students' learning and functioning in the school community. Parents are also encouraged to contact the school counselor for consultation on parenting strategies, child behavior and developmental concerns, or for help in supporting their student with life events, such as an extended illness, the death of a loved one, or changes in the family.

It should be noted that any one-on-one counseling offered through the school is primarily a short-term, temporary service aimed at facilitating more effective education and socialization of the student within the school community. While the counselors provide immediate crisis intervention and regular consultation during normal school hours, these services do not take the place of long-term, comprehensive psychological counseling.

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Each Division has a school counselor, a trained mental health professional who understands and responds to the challenges presented by today's diverse student population. A valuable resource for students, parents, faculty, and staff, Hockaday's school counselors do not work in isolation; rather they are integral to the total educational program.

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National Library of Medicine Website: Study on Catatonia 

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National Library of Medicine Website: Study on Catatonia 

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Abstract

Catatonia is a psychomotor syndrome that has been reported to occur in more than 10% of patients with acute psychiatric illnesses. Two subtypes of the syndrome have been identified. Catatonia of the retarded type is characterized by immobility, mutism, staring, rigidity, and a host of other clinical signs. Excited catatonia is a less common presentation in which patients develop prolonged periods of psychomotor agitation. Once thought to be a subtype of schizophrenia, catatonia is now recognized to occur with a broad spectrum of medical and psychiatric illnesses, particularly affective disorders. In many cases, the catatonia must be treated before any underlying conditions can be accurately diagnosed. Most patients with the syndrome respond rapidly to low-dose benzodiazepines, but electroconvulsive therapy is occasionally required. Patients with longstanding catatonia or a diagnosis of schizophrenia may be less likely to respond. The pathobiology of catatonia is poorly understood, although abnormalities in gamma-aminobutyric acid and glutamate signaling have been suggested as causative factors. Because catatonia is common, highly treatable, and associated with significant morbidity and mortality if left untreated, physicians should maintain a high level of suspicion for this complex clinical syndrome. Since 1989, we have systematically assessed patients presenting to our psychiatry service with signs of retarded catatonia. In this paper, we present a review of the current literature on catatonia along with findings from the 220 cases we have assessed and treated.

Keywords: Catatonia, Schizophrenia, Benzodiazepines, Electroconvulsive therapy, Extrapyramidal disorders

Core tip: Catatonia is a complex clinical syndrome occurring in more than 10% of patients with acute psychiatric illnesses, and it is associated with multiple life-threatening complications. In the last several decades, renewed interest in this syndrome has led to a great deal of research and debate regarding its diagnosis and treatment. In this paper, we present a review of the current literature on catatonia along with findings from the 220 cases we have assessed and treated since 1989. Catatonia itself is readily treated using low-dose lorazepam, and it also has important implications for how other underlying psychiatric conditions should be treated.

INTRODUCTION

Catatonia is a clinical syndrome characterized by a distinct constellation of psychomotor disturbances. Two subtypes have been described: Retarded and excited. Catatonia of the retarded type is associated with signs reflecting a paucity of movement, including immobility, staring, mutism, rigidity, withdrawal and refusal to eat, along with more bizarre features such as posturing, grimacing, negativism, waxy flexibility, echolalia or echopraxia, stereotypy, verbigeration, and automatic obedience[ 1- 3]. Excited catatonia, on the other hand, is characterized by severe psychomotor agitation[ 4], potentially leading to life-threatening complications such as hyperthermia, altered consciousness, and autonomic dysfunction. This so-called "malignant" or "lethal" catatonia can be rapidly fatal if not appropriately treated[ 5, 6]. The relative prevalence and diagnostic significance of catatonic signs differ among studies and patient populations, but there is general agreement that catatonia occurs in 9%-17% of patients with acute psychiatric illnesses[ 1, 2, 7] and that retarded catatonia is the more frequently observed subtype[ 4, 8- 10].

The catatonic syndrome is associated with other disorders, underscoring the necessity of rapid diagnosis and treatment. In particular, catatonia appears to be a risk factor for the development of neuroleptic malignant syndrome[ 11- 13], which has a mortality rate of approximately 10%[ 14] and may be clinically indistinguishable from malignant catatonia[ 15, 16]. This has important implications for the treatment of catatonia in the context of psychosis, which will be discussed later in this review. Additionally, the immobility and refusal to eat or drink associated with catatonia can give rise to potentially serious medical complications, including dehydration[ 17], malnutrition[ 18, 19], deep vein thrombosis and pulmonary embolism[ 20, 21], pneumonia and other infections[ 17], pressure ulcers[ 19], and muscle contractures[ 18, 19]. The very nature of catatonia can make it challenging, if not impossible, to carry out patient interviews and examinations, thereby interfering with the recognition of underlying diagnoses. These complications of catatonia highlight the importance of recognizing the syndrome and quickly initiating treatment.

Overall, it is clear that catatonia is a common and serious problem that often remains unrecognized. Despite a renewed interest in the disorder over the last several decades[ 22], a number of questions remain regarding its causes and treatment. In this paper, we review the current understanding of the diagnosis, treatment, and pathophysiology of catatonia, and we identify several areas of uncertainty where further research is required.

DIAGNOSIS

Clinical features

While catatonia has long been considered a subtype of schizophrenia or a clinical feature of other medical and psychiatric conditions, the earliest descriptions by Kahlbaum et al[ 23] in fact suggested a unique entity with a distinct clinical course. This proposal was not universally accepted, however, and a great deal of debate has ensued regarding the most appropriate classification of catatonia. Largely due to the influence of Emil Kraepelin, catatonia eventually came to be "officially" seen as a type of schizophrenia[ 24]. Early descriptions of catatonia in both the diagnostic and statistical manual of mental disorders (DSM) and international classification of diseases included it only under the category of schizophrenia, and this view persisted for many years. Things began to change in the 1970's, when multiple reports indicated that catatonia is more closely associated with affective disorders than schizophrenia[ 4, 25]. More recently, it has been proposed that catatonia is also relatively common in patients diagnosed with autism[ 26]. In 1994, catatonia was recognized in the DSM-IV as a disorder that could either complicate general medical conditions or be a specifier in mood disorders. At the same time, there were continued arguments in support of catatonia being its own distinct diagnostic category[ 7, 27].

A number of different criteria have been proposed for the diagnosis of catatonia. In our own ongoing assessment and treatment of consecutively referred patients with catatonia who present to either our acute-care inpatient psychiatric unit or to the consultation-liaison service, we diagnose patients based on the presence of at least four of the catatonic signs originally described by Karl Kahlbaum in 1874[ 1]. These signs, along with their frequency in our patient series, are presented in Table ​Table1. 1 . As we originally reported in 1990[ 1], immobility and mutism are the most common signs, each present in over 90% of patients. In keeping with this finding, the diagnostic criteria proposed by Taylor et al[ 27] include immobility and mutism (along with stupor) as core criteria for catatonia. A systematic effort to identify the catatonic signs with the best diagnostic performance was conducted by Peralta et al[ 2]. Immobility and mutism were again identified as the most common signs, observed in 90.6% and 84.4% respectively of catatonic patients. Rigidity was also common in their sample, observed in 75.0% of catatonic patients. The use of 4 or more catatonic signs as a diagnostic criterion resulted in 100% specificity, but also led to a small number of catatonic patients failing to be identified. As a result, Peralta et al[ 3] suggest the use of three or more catatonic signs as a diagnostic criterion for catatonia, and this recommendation has been supported by more recent work from the same group[ 3]. The DSM-V defines catatonia as the presence of three or more of the following: Catalepsy, waxy flexibility, stupor, agitation, mutism, negativism, posturing, mannerisms, stereotypies, grimacing, echolalia, and echopraxia[ 28]. A number of scales have been developed to quantify catatonic signs[ 29]. While these scales may prove useful for research, we have not found them to be necessary for clinical purposes.

Table 1

Sign % of patients

Immobility

97

Mutism

97

Withdrawal and refusal to eat

91

Staring

87

Negativism

67

Posturing

58

Rigidity

54

Waxy flexibility/catalepsy

27

Stereotypy

25

Echolalia or echopraxia

14

Verbigeration

14

The most important step in the diagnosis of catatonia is recognition of the syndrome's characteristic clinical signs. Immobility and mutism are particularly common, and the appearance of either of these signs in the absence of another explanatory condition should raise the clinical suspicion of catatonia, at which point the presence of other catatonic signs can be determined. In our experience, patients are often incontinent, disheveled, and cachectic depending on the duration of illness. The lack of meaningful responses to external stimuli in these patients should not be interpreted as a lack of awareness of their surroundings. Indeed, many of the patients we have treated reported being completely aware and were able to recall their catatonic state in detail after they recovered.

Differential diagnosis

A number of neurological conditions may appear similar to catatonia, and may even have substantial overlap with respect to pathophysiological mechanisms. The following is a partial list of conditions that, in our experience, have considerable clinical overlap with catatonia and should be carefully considered.

Extrapyramidal side-effects: Extrapyramidal side-effects are commonly associated with both typical and atypical antipsychotic drugs[ 30, 31], so they are of special concern in patients with psychiatric illness. Like patients with catatonia, patients with drug-induced parkinsonism may present with immobility, staring, and rigidity. On numerous occasions we have been asked to see a patient with a tentative diagnosis of catatonia who in fact had antipsychotic-induced parkinsonism. This distinction is an important one to make, since the benzodiazepine medication used to treat catatonia may exacerbate the postural instability that is often associated with parkinsonism. One notable difference between the syndromes is that parkinsonian patients are typically cooperative and interactive, in contrast to catatonic patients who are often withdrawn and negativistic. Also, tremor, which is often present in patients with parkinsonism, is not a feature of catatonia. Unusual features like echophenomena and posturing are typically absent in parkinsonism. We have, however, seen parkinsonian patients whose freezing was mistaken for posturing. Additionally, some patients treated with antipsychotic drugs may develop signs consistent with both catatonia and parkinsonism[ 32]. Other extrapyramidal side-effects may also resemble some aspects of catatonia. For example, the posturing and immobility of catatonic patients can be mistaken for dystonia, while the psychomotor agitation of excited catatonia can appear similar to akathisia. In patients being treated with antipsychotic medication, care must be taken in assessing these clinical features to ensure diagnostic accuracy.

Neuroleptic malignant syndrome: Neuroleptic malignant syndrome is a life-threatening reaction to antipsychotic treatment (including treatment with atypical antipsychotics[ 33]) in which patients develop rigidity, mutism, and delirium accompanied by diaphoresis, hypertension, tachycardia, and fever[ 34, 35]. Autonomic instability helps to distinguish this syndrome from uncomplicated catatonia, but it may sometimes be indistinguishable from malignant catatonia except for the precipitating factor of antipsychotic treatment. Cessation of antipsychotic medication, along with supportive therapy, is often sufficient to treat these patients, but additional pharmacological treatment or electroconvulsive therapy (ECT) may be indicated.

Nonconvulsive status epilepticus: Nonconvulsive status epilepticus can be clinically indistinguishable from catatonia. In both cases, patients can be immobile, mute, rigid, and unable to eat, drink, or cooperate with an examination. Although electroencephalogram (EEG) findings in nonconvulsive status epilepticus can be highly variable, these investigations are nonetheless crucial to making the correct diagnosis[ 36, 37].

Abulia or akinetic mutism: Disorders of diminished motivation exist on a spectrum including abulia (moderate) and akinetic mutism (severe)[ 38]. In the extreme case, neurological dysfunction results in a complete lack of spontaneous speech or movement due to a lack of motivation or drive. Patients are fully aware and visual tracking is preserved. Overt signs of catatonia such as negativism and echophenomena may differentiate the two disorders, but more subtle presentations can make the two conditions difficult to distinguish[ 39]. In such cases, a trial of lorazepam may be helpful in identifying catatonia.

Locked-in syndrome: Locked-in syndrome is usually associated with ventral pontine lesions, and results in near complete paralysis, while blinking and vertical eye movements are spared[ 40]. Patients are aware and, unlike catatonic patients, generally eager to communicate through blinking. However, it should be noted that some patients with locked-in syndrome are unable to blink or move their eyes. As with catatonic patients, EEG investigations are often normal. Abnormalities identified using magnetic resonance imaging (MRI) or brainstem evoked potentials help to identify patients with the locked-in syndrome.

Vegetative state: The vegetative state is characterized by a complete lack of awareness of the self or surroundings, often secondary to a severe cerebral injury[ 41]. The patient makes no voluntary responses to stimuli, and does not visually track objects, but sleep-wake cycles are preserved. Although this definition of the persistent vegetative state is reasonably clear, confidently assessing a lack of awareness can be problematic. EEG and MRI techniques have been used to demonstrate awareness in a disturbing number of patients who otherwise met criteria for a vegetative state[ 42, 43]. Unlike the normal EEG of catatonia, the EEG in vegetative states is almost always abnormal[ 44].

Stiff person syndrome: Stiff person syndrome is an autoimmune disorder frequently presenting with low back and lower extremity stiffness and spasms, as well as exaggerated lumbar lordosis[ 45], which can be mistaken for posturing. Like catatonia, the condition can render patients immobile. Episodes are typically triggered when patients are startled or experience emotional stress. In contrast with what is observed in patients with catatonia, patients with stiff person syndrome are not mute and will often indicate that they are in great pain as a result of the muscle spasms. Since most patients are GAD65 antibody seropositive[ 45], antibody testing may be helpful if there is diagnostic uncertainty. The syndrome generally improves in response to benzodiazepine treatment, perhaps supplemented by adjunctive immunotherapy where appropriate.

INVESTIGATIONS

All patients suspected of having catatonia should have EEG testing as a screen for other neurological conditions. This will typically show epileptiform activity in nonconvulsive status epilepticus and slowing in cases of encephalopathy. The EEG in catatonia is typically normal unless there is a concurrent condition that may be causing the abnormality[ 1, 9, 46]. Given that catatonia can develop in the context of a wide array of neurological conditions, brain imaging, preferably by MRI, is recommended[ 1, 47]. In cases of retarded catatonia, immobility generally allows these investigations to be conducted easily. Laboratory investigations should include a complete blood count, blood urea nitrogen, creatinine, muscle and hepatic enzymes, thyroid function tests, electrolytes, blood glucose, and urinalysis to assess for comorbid conditions, causes, or complications of catatonia. Marked dehydration is not uncommon in catatonic patients, and must be attended to. Vital signs should be assessed frequently, as hypertension and fever (often accompanied by elevated creatine phosphokinase, decreased serum iron, and leukocytosis) may herald the onset of malignant catatonia or neuroleptic malignant syndrome if the patient has received antipsychotic agents[ 35, 48- 50]. When possible, a careful review of the patient's recent medications and any changes should be conducted. It is important to determine whether or not a patient has been receiving antipsychotic agents or benzodiazepines, as we have reported, and continue to see, the development of catatonia following abrupt discontinuation of benzodiazepines[ 51, 52].

Unfortunately, the nature of catatonia makes some aspects of a physical and neurological exam impossible. Components of the neurological exam that can usually be assessed include the pupillary reaction, ocular movements, corneal reflex, reaction to pain, the presence of drooling, blink response to threat, reaction to light or sound, frontal release signs, assessment of tone, deep tendon reflexes, and the plantar response.

TREATMENT

A characteristic feature of catatonia is its striking responsiveness to benzodiazepine treatment. We recommend an initial dose of 1-2 mg lorazepam, administered sublingually or intramuscularly. The ability to administer lorazepam intramuscularly is a major advantage, since many catatonic patients refuse to eat or take medication by mouth. A lower lorazepam dose is preferable in patients who are young, elderly, or medically compromised, especially when there is a diagnosis or high likelihood of sleep apnea. If the initial dose is ineffective, it should be repeated in 3 h and again after another 3 h. We have analyzed treatment response in 153 patients treated with lorazepam. In this group, we have observed a response in 132 (85.7%), 90 of whom experienced complete recovery within 3 h. This robust response to low-dose lorazepam has also been reported by others[ 46, 53], but higher doses may be necessary in some cases[ 54, 55]. If a patient responds adequately to benzodiazepine treatment, they should continue on the same dose (provided that this dose is not overly sedating or causing any other problematic side-effects) until treatment of any underlying disorder is underway. Relapse into a catatonic state can occur if benzodiazepines are discontinued before this. In our experience, a subset of patients may develop catatonia whenever attempts are made to discontinue lorazepam, and these patients may require long-term maintenance treatment[ 56]. This phenomenon has also been reported by others[ 57].

It should be noted that patients with long-standing catatonia may not respond as robustly or as rapidly to benzodiazepine treatment as those with acute catatonia[ 54, 58]. We have reported the cases of two brothers, one of whom had been catatonic for 2 wk prior to treatment, while the other had been hospitalized with catatonia for 5 years[ 59]. The first brother recovered completely in 2 wk on a lorazepam dose of 3 mg/d. The second brother, on the other hand, showed only gradual improvement on lorazepam 4 mg/d before being discharged from hospital a year after treatment initiation.

An underlying diagnosis of schizophrenia may be associated with a less robust response to benzodiazepine treatment[ 53]. We have observed a response rate of only 59.1% in patients with schizophrenia, compared with a response rate of over 90% in patients with other psychiatric diagnoses (Table ​(Table2). 2 ). The poorer treatment response in patients with schizophrenia may be related to the chronicity of symptomatology, or it may suggest a distinct underlying pathophysiology, perhaps reflecting the prominence of psychosis affecting their motor behaviour. Nevertheless, benzodiazepines can be effective for treating catatonia in many patients with schizophrenia, and a therapeutic trial is warranted. This is especially the case given the overall safety of benzodiazepine medication.

Table 2

Diagnosis Patients responding (%)

Bipolar disorder ( n = 31)

97

Unipolar depression ( n = 30)

93

Other psychoses ( n = 24)

92

Medical/neurological condition ( n = 11)

82

Schizophrenia ( n = 22)

59

ECT is another highly effective option for the treatment of catatonia[ 9, 60], and even patients who do not respond to benzodiazepines are likely to respond to ECT[ 61, 62]. Despite its effectiveness, ECT has an important drawback: It requires clear consent. Catatonic patients are unable to discuss ECT or consent to its administration, and consent from a substitute decision maker is often difficult to obtain. Because of these problems, and because benzodiazepines are easily administered and have a high margin of safety, we recommend that benzodiazepines be used as the first line of treatment. ECT should be considered in patients who fail to respond to benzodiazepines after several days and surrogate consent should be sought. The exception to this strategy is the patient with malignant catatonia, for whom ECT should be administered early, since the condition has a high rate of mortality if it is not rapidly and effectively treated[ 6, 49].

Of the catatonic patients we have assessed, 77.7% later reported having experienced psychotic symptoms during the catatonic episode. This raises a difficult problem in treatment, since antipsychotic medications may be associated with an increased risk of neuroleptic malignant syndrome in patients with catatonia. White et al[ 12] identified 17 consecutive patients with neuroleptic malignant syndrome, all of whom exhibited catatonic signs prior to antipsychotic exposure. In our own patients, we have observed that 3.6% of catatonic patients treated with antipsychotic medications developed neuroleptic malignant syndrome[ 63]. This is in contrast to an incidence of 0.07%-1.8% in all patients treated with antipsychotic drugs[ 64, 65]. Raja et al[ 11] identified 3 cases of neuroleptic malignant syndrome in a series of consecutive patients presenting to the psychiatric emergency service, all 3 of whom demonstrated catatonic signs and low serum iron prior to the onset of neuroleptic malignant syndrome. The relationship between catatonia and neuroleptic malignant syndrome is not limited to patients treated with typical antipsychotics, as clozapine has also been reported to be a precipitating factor[ 13]. Although more research is required in order to identify which patients are most susceptible to neuroleptic malignant syndrome, we feel that the existing evidence is sufficient to recommend the avoidance of antipsychotic drugs in acutely catatonic patients. In our experience, once catatonic symptoms have been treated by benzodiazepines or ECT and patients are eating, drinking, and walking, antipsychotic treatment can be initiated safely.

Although lorazepam and ECT have long been recognized as effective treatments for patients with catatonia, other options have been suggested. Several case reports have described patients effectively treated with zolpidem[ 66, 67], which, like typical benzodiazepines, may treat catatonia through interactions with GABA-A receptors[ 68]. As well, amantadine and memantine, which act as NMDA antagonists but also interact with a number of other neurotransmitter systems, have shown efficacy in a small number of patients[ 69, 70]. It is not yet clear whether these options are likely to be helpful in the small fraction of patients who do not respond to either lorazepam or ECT.

PATHOPHYSIOLOGY

While the pathophysiology of catatonia is still unclear, several theories have been proposed based on the available data. One possible interpretation of catatonia is that the syndrome is an outward manifestation of intense anxiety[ 22, 71]. The majority of catatonic patients we have treated reported feeling extremely anxious before and during their catatonic episode, to the extent that some believed they were about to die, had already died, or that they needed to remain immobile in order to avoid threats from others. Benzodiazepines reduce anxiety by enhancing chloride conductance through GABA-A receptor ion channels, and may treat catatonia through this mechanism. However, a number of our patients - particularly those with schizophrenia - reported little anxiety during their catatonic episode. This observation does not exclude the possibility that anxiety is an important component of catatonia, but suggests that it is not an essential component for all patients with the syndrome.

A second interpretation of catatonia is that it is essentially a movement disorder similar to parkinsonism. As noted previously, the clinical features of catatonia overlap with those of parkinsonism, which is understood to be caused by dysfunction of the basal ganglia. Since most projection neurons in the basal ganglia are GABAergic, it is plausible that benzodiazepines could treat catatonia by influencing GABA signaling in the basal ganglia. Functional imaging studies have shown that catatonia is associated with altered activity in orbitofrontal, prefrontal, parietal, and motor cortical regions[ 72], suggesting that these cortical structures may also play a role in the pathophysiology of catatonia. This interpretation is reinforced by observations that GABA-A binding is reduced in cortical regions of catatonic patients, motor and affective symptoms are correlated with these abnormalities in GABA-A binding, and cortical abnormalities in catatonic patients are normalized following exposure to lorazepam[ 72].

Whatever the pathophysiology of catatonia may be, it is clear that a wide variety of underlying disorders can be associated with the emergence of catatonic signs. These include mood disorders, nonaffective psychotic disorders, a number of medical and neurological conditions, and genetic disorders[ 73]. How - or if - these diverse etiologies converge upon a final common pathway causing catatonia is unknown, and it is possible that variations in the clinical presentation of catatonia represent distinct underlying mechanisms that would respond preferentially to different treatments. For instance, future research may allow physicians to identify patients who are unlikely to respond to lorazepam treatment and should receive ECT or another pharmacological treatment as a first line option.

CONCLUSION

The syndrome of catatonia encompasses a wide range of psychomotor abnormalities, none of which are present in all patients. Immobility and mutism are especially common, and the presence of these signs should prompt physicians to actively assess other markers of catatonia. The differential diagnosis of catatonia is complex, and catatonia itself can arise from a diverse array of psychiatric and medical etiologies, complicating the investigation of these patients. Affective disorders are the most common underlying psychiatric diagnoses. Fortunately, most catatonic patients rapidly respond to low-dose lorazepam. Some patients, particularly those with long-standing catatonia or schizophrenia, may respond more gradually or not at all to lorazepam, and may require ECT or other pharmacological treatments. We feel that the use of antipsychotics should generally be avoided until the acute catatonic episode has resolved in order to avoid precipitating neuroleptic malignant syndrome. The pathophysiology of catatonia is still poorly understood, and it is unclear whether different constellations of clinical signs might represent distinct underlying mechanisms. Recognizing and treating catatonia usually results in rapid resolution of the syndrome, whereas failing to recognize it may lead to potentially fatal complications including infection, neuroleptic malignant syndrome, and pulmonary embolism. Because of this, physicians should maintain a high level of suspicion for the catatonic syndrome, especially in patients experiencing an acute psychiatric illness.

Footnotes

Conflict-of-interest statement: The authors declare no conflicts of interest regarding this manuscript.

Manuscript source: Invited manuscript

Specialty type: Psychiatry

Country of origin: Canada

Peer-review report classification

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Peer-review started: June 27, 2016

First decision: August 11, 2016

Article in press: October 27, 2016

P- Reviewer: Flyckt L, Müller MJ, Neto MLR S- Editor: Qiu S L- Editor: A E- Editor: Wu HL

References

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23. Kahlbaum KL. Catatonia. Levij Y, Pridan T. Baltimore: Johns Hopkins University Press; 1973. [ Google Scholar]

49. Fricchione G, Mann SC, Caroff SN. Catatonia, lethal catatonia, and neuroleptic malignant syndrome. Psychiatr Ann. 2000;30:347-355. [ Google Scholar]

56. Rosebush PI, Hildebrand A, Mazurek MF. The syndrome of recurring catatonia: treatment and relationship to underlying illness. Proceedings of the 147th Annual Meeting of the American Psychiatric Association. USA: Philadelphia; 1994. p. 129. [ Google Scholar]

63. Rosebush PI, Mazurek MF. Risk of NMS in patients with catatonia (Proceedings of the 149th Annual Meeting of the American Psychiatric Association) USA: New York; 1996. p. 30. [ Google Scholar]

68. Thomas P, Cottencin O, Rascle C, Vaiva G, Goudemand M, Bieder J. Catatonia in French psychiatry: implications of the zolpidem challenge test. Psychiatr Ann. 2007;37:45-54. [ Google Scholar]

Articles from World Journal of Psychiatry are provided here courtesy of Baishideng Publishing Group Inc

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Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology

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Catatonia is a psychomotor syndrome that has been reported to occur in more than 10% of patients with acute psychiatric illnesses. Two subtypes of the syndrome have been identified. Catatonia of the retarded type is characterized by immobility, mutism, ...

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Mental Health America Website: Information on Paranoia and Delusional Disorders

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Mental Health America Website: Information on Paranoia and Delusional Disorders

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Symptoms of paranoia and delusional disorders include intense and irrational mistrust or suspicion, which can bring on feelings of fear, anger, and betrayal. Some beliefs and behaviors of individuals with symptoms of paranoia include mistrust, hypervigilance (constantly looking for threats), difficulty with forgiveness, defensive attitude in response to imagined criticism, preoccupation with hidden motives, fear of being tricked or taken advantage of, trouble relaxing, or being argumentative.

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Symptoms of paranoia and delusional disorders include intense and irrational mistrust or suspicion, which can bring on feelings of fear, anger, and betrayal. Some beliefs and behaviors of individuals with symptoms of paranoia include mistrust, hypervigilance (constantly looking for threats), difficulty with forgiveness, defensive attitude in response to imagined criticism, preoccupation with hidden motives, fear of being tricked or taken advantage of, trouble relaxing, or being argumentative.

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National Alliance on Mental Illness: Information on Schizophrenia

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National Alliance on Mental Illness: Information on Schizophrenia

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Schizophrenia is a serious mental illness that interferes with a person's ability to think clearly, manage emotions, make decisions and relate to others. It is a complex, long-term medical illness. The exact prevalence of schizophrenia is difficult to measure, but estimates range from 0.25% to 0.64% of U.S. adults. Although schizophrenia can occur at any age, the average age of onset tends to be in the late teens to the early 20s for men, and the late 20s to early 30s for women. It is uncommon for schizophrenia to be diagnosed in a person younger than 12 or older than 40. It is possible to live well with schizophrenia.

Symptoms

It can be difficult to diagnose schizophrenia in teens. This is because the first signs can include a change of friends, a drop in grades, sleep problems, and irritability-common and nonspecific adolescent behavior. Other factors include isolating oneself and withdrawing from others, an increase in unusual thoughts and suspicions, and a family history of psychosis. In young people who develop schizophrenia, this stage of the disorder is called the "prodromal" period.

With any condition, it's essential to get a comprehensive medical evaluation in order to obtain the best diagnosis. For a diagnosis of schizophrenia, some of the following symptoms are present in the context of reduced functioning for a least 6 months:

Hallucinations. These include a person hearing voices, seeing things, or smelling things others can't perceive. The hallucination is very real to the person experiencing it, and it may be very confusing for a loved one to witness. The voices in the hallucination can be critical or threatening. Voices may involve people that are known or unknown to the person hearing them.

Delusions. These are false beliefs that don't change even when the person who holds them is presented with new ideas or facts. People who have delusions often also have problems concentrating, confused thinking, or the sense that their thoughts are blocked.

Negative symptoms are ones that diminish a person's abilities. Negative symptoms often include being emotionally flat or speaking in a dull, disconnected way. People with the negative symptoms may be unable to start or follow through with activities, show little interest in life, or sustain relationships. Negative symptoms are sometimes confused with clinical depression.

Cognitive issues/disorganized thinking. People with the cognitive symptoms of schizophrenia often struggle to remember things, organize their thoughts or complete tasks. Commonly, people with schizophrenia have anosognosia or "lack of insight." This means the person is unaware that he has the illness, which can make treating or working with him much more challenging.

Causes

Research suggests that schizophrenia may have several possible causes:

Genetics. Schizophrenia isn't caused by just one genetic variation, but a complex interplay of genetics and environmental influences. Heredity does play a strong role-your likelihood of developing schizophrenia is more than six times higher if you have a close relative, such as a parent or sibling, with the disorder

Environment. Exposure to viruses or malnutrition before birth, particularly in the first and second trimesters has been shown to increase the risk of schizophrenia. Recent research also suggests a relationship between autoimmune disorders and the development of psychosis.

Brain chemistry. Problems with certain brain chemicals, including neurotransmitters called dopamine and glutamate, may contribute to schizophrenia. Neurotransmitters allow brain cells to communicate with each other. Networks of neurons are likely involved as well.

Substance use. Some studies have suggested that taking mind-altering drugs during teen years and young adulthood can increase the risk of schizophrenia. A growing body of evidence indicates that smoking marijuana increases the risk of psychotic incidents and the risk of ongoing psychotic experiences. The younger and more frequent the use, the greater the risk.

Diagnosis

Diagnosing schizophrenia is not easy. Sometimes using drugs, such as methamphetamines or LSD, can cause a person to have schizophrenia-like symptoms. The difficulty of diagnosing this illness is compounded by the fact that many people who are diagnosed do not believe they have it. Lack of awareness is a common symptom of people diagnosed with schizophrenia and greatly complicates treatment.

While there is no single physical or lab test that can diagnosis schizophrenia, a health care provider who evaluates the symptoms and the course of a person's illness over six months can help ensure a correct diagnosis. The health care provider must rule out other factors such as brain tumors, possible medical conditions and other psychiatric diagnoses, such as bipolar disorder.

To be diagnosed with schizophrenia, a person must have two or more of the following symptoms occurring persistently in the context of reduced functioning:

Delusions

Hallucinations

Disorganized speech

Disorganized or catatonic behavior

Negative symptoms

Delusions or hallucinations alone can often be enough to lead to a diagnosis of schizophrenia. Identifying it as early as possible greatly improves a person's chances of managing the illness, reducing psychotic episodes, and recovering. People who receive good care during their first psychotic episode are admitted to the hospital less often, and may require less time to control symptoms than those who don't receive immediate help. The literature on the role of medicines early in treatment is evolving, but we do know that psychotherapy is essential.

People can describe symptoms in a variety of ways. How a person describes symptoms often depends on the cultural lens she is looking through. African Americans and Latinos are more likely to be misdiagnosed, potentially due to differing cultural perspectives or structural barriers. Any person who has been diagnosed with schizophrenia should try to work with a health care professional that understands his or her cultural background and shares the same expectations for treatment.

Treatment

There is no cure for schizophrenia, but it can be treated and managed in several ways.

Related Conditions

People with schizophrenia may have additional illnesses. These may include:

Successfully treating schizohprenia almost always improves these related illnesses. And successful treatment of substance misuse, PTSD or OCD usually improves the symptoms of schizophrenia.

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What is Schizophrenia? | NAMI: National Alliance on Mental Illness

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Discover the symptoms, causes, diagnosis advice, treatment options and related conditions of schizophrenia.

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National Library of Medicine Website: Symptoms, Causes, Treatment of Schizotypal Personality Disorder

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National Library of Medicine Website: Symptoms, Causes, Treatment of Schizotypal Personality Disorder

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Daniel R. Rosell, M.D., Ph.D, 1, ² Shira E. Futterman, Psy.D, 1, ² Antonia McMaster, B.A, 1, ² and Larry J. Siever, M.D 1, ²

Abstract

The study of schizotypal personality disorder (SPD) is important clinically, as it is understudied, challenging to treat, often under-recognized or misdiagnosed, and associated with significant functional impairment. SPD also represents an intermediate schizophrenia-spectrum phenotype, and therefore, can provide a better understanding of the genetics, pathogenesis, and treatment of related psychotic illnesses. In this review we discuss recent findings of SPD related to epidemiology and functional impairment; heritability and genetics; working memory and cognitive impairments; social-affective disturbances; and neurobiology. Additionally, we examine the challenges associated with treating patients with SPD, as well as clinical recommendations. Finally, we address future directions and areas in need of further exploration.

Keywords: Schizotypal, schizophrenia, personality disorder, frontal lobe, temporal lobe, dopamine, working memory, cognition, social cognition, affect processing, magical thinking, perceptual aberration, suspiciousness, paranoia, social anhedonia

Introduction

Introduced in DSM-III, the diagnostic construct of schizotypal personality disorder was derived from two converging lines of investigation: 1) borderline personality conditions, which represented a clinically identified and heterogeneous population of functionally impaired patients that manifested a variety of pervasive disturbances of interpersonal function, cognition, affect, and behavioral control, many of whom exhibited attenuated schizophrenia-spectrum traits; and, 2) studies of non-psychotic family members of patients with schizophrenia who exhibited chronic peculiarities of thought and communication, as well as impoverished social function. Accordingly, early studies of the SPD construct were either related to: 1) confirmation of its utility in identifying non-clinical individuals carrying a genetic vulnerability to schizophrenia; or, 2) clarification of its clinical validity, particularly in comparison with the borderline personality disorder (BPD) construct. Therefore, the significance of defining the diagnosis of SPD was two-fold: It was an important step in the refinement of present-day severe personality disorder syndromes; and, it has yielded an operational definition of an intermediate schizophrenia-spectrum phenotype that can be used to investigate the pathogenesis, genetics, and development of therapeutics of major psychotic disorders. Studies of SPD have increasingly focused on schizophrenia-spectrum issues, and there has been relatively less emphasis on SPD as a clinical syndrome, in and of itself. In this review we will discuss recent findings in SPD and schizotypy related to epidemiology and functional impairment, pathogenesis, cognitive impairment, and neurobiological findings. Additionally, clinical topics will be addressed regarding the phenomenology, differential diagnosis, multidimensionality, and treatment considerations.

Diagnostic Criteria, Psychometric Structure, and Multidimensionality

The SPD diagnostic criteria for DSM-5 are essentially unchanged from DSM-IV-TR, and consist of: ideas of reference; odd beliefs or magical thinking; unusual perceptual experiences and bodily illusions; odd thinking and speech; suspiciousness or paranoid ideation; inappropriate or constricted affect; behavior or appearance that is odd, eccentric, or peculiar; lack of close friends or confidants, other than first-degree relatives; excessive social anxiety that doesn't diminish with familiarity and tends to be associated with paranoid fears. Five of nine criteria are required for a diagnosis of SPD.

SPD (as well as schizotypy in non-clinical populations) has consistently been shown to be a multi-dimensional construct. Although not all studies are in agreement, analyses of SPD have most consistently revealed a 3 factor solution: Cognitive-Perceptual ('odd beliefs,' 'perceptual disturbances,' 'ideas of reference,' and 'paranoia/suspiciousness'), Interpersonal ('no close friends,' 'social anxiety,' +/-'restricted affect'), and Disorganized/Oddness ('odd speech/thought,' 'odd behavior,' -/+ 'restricted affect'). Assignment of 'restricted/inappropriate affect' to either the Interpersonal or Oddness factor appears to depend on whether assessment was performed by 1) self-report in non-clinical populations, as opposed to 2) semi-structured interview of SPD or personality disordered patients, respectively[ 1]. Therefore, as our focus is on clinical populations, and given the greater validity of personality assessment from semi-structured interview compared to self-report, we favor the inclusion of 'restricted affect' in the Oddness domain. More recently, four dimensional factors were resolved among non-psychotic family members of schizophrenia probands, consisting of: Negative Schizotypy, Positive Schizotypy, Interpersonal Sensitivity, and Social Isolation/Introversion [ 2]. This four factor solution is similar to one described using a self-report measure of schizotypy among non-clinical participants [ 3].

Recent findings however have indicated that despite the validity of such a 3-factor solution among the 9 diagnostic criteria of SPD criteria, only the Cognitive-Perceptual and Oddness factors persisted when examining the factor among all DSM-IV personality disorder criteria. Moreover, when all DSM-IV personality disorder criteria were examined, 'paranoia/suspiciousness' was associated with a factor that essentially consisted of Paranoid Personality Disorder (PPD) criteria; 'no close friends' was associated with the same criteria from Schizoid Personality Disorder (SCPD); and, 'social anxiety' was not related to any clinically coherent factor. Moreover, the social anxiety and no close friends criteria of SPD were significantly correlated with a number of personality disorder diagnoses. Thus, the Interpersonal domain (a well as 'paranoia/suspiciousness') did not appear to be useful in discriminating SPD from other personality disorders. Cognitive-Perceptual criteria (namely, ideas of reference, odd beliefs, and perceptual disturbances) have been shown to exhibit high sensitivity and moderate positive predictive value (PPV) in terms of diagnosis of SPD; Oddness criteria (odd behavior, odd speech/thought process, and restricted affect) exhibited the highest PPV for the SPD diagnosis.

Epidemiology and Functional Impairment

The lifetime prevalence of SPD in the United States (US) has recently been estimated to be just under 4%, with slightly higher rates among men (4.2%) than women (3.7%). Likelihood of SPD was greater among black woman, those with a low income, and people who were separated, divorced, or widowed; and, odds of SPD were lower in Asian men. After adjusting for sociodemographic parameters and comorbidities, SPD remained significantly associated with bipolar I and II disorders, PTSD, BPD, and narcissistic personality disorder (NPD). Additionally, even after adjusting for sociodemographic parameters and Axis I and II comorbidities, patients with SPD had significantly greater disability than those without SPD [ 4].

Among a large, Norwegian cohort of treatment-seeking personality disordered patients, 1.37% of patients met criteria for SPD, and 21% reported at least 2 SPD symptoms. One-third of SPD patients were not comorbid with any other personality disorder, one-third had only one additional comorbid personality disorder, and one-third of SPD patients were diagnosed with two or more additional personality disorders. In addition to PPD, antisocial personality disorder (ASPD) also occurred with greater frequency among patients with SPD compared to the total sample of personality disordered patients. Although Cognitive-Perceptual criteria of SPD were strongly associated with a diagnosis of BPD, BPD occurred with no greater frequency among patients with SPD than the total sample of personality disordered patients. SPD exhibited a stronger association with obsessive-compulsive disorder (OCD) than other personality disorders [ 1].

While it is clear that SPD is a clinically and functionally disabling condition, the basis of functional impairment and its relation to other phenomenologically similar personality disorders has not been fully elucidated. In terms of 'real world' functioning, patients with SPD have been shown to be less likely to live independently or have obtained a Bachelor's degree than patients with avoidant personality disorder (AvPD) and healthy control participants. Both patients with SPD and AvPD earned a lower hourly wage compared to healthy control participants, however. Using an interview-based assessment of functional capacity (UCSD Performance-Based Skills Assessment or UPSA), SPD patients demonstrated lower functional capacity than patients with AvPD and healthy control participants. Similar to the role of cognitive dysfunction (working memory, processing speed, executive function) as a major determinant of functional outcomes in schizophrenia, functional capacity in patients with SPD was shown to be significantly correlated to a composite measure of cognitive function. Similar to previous reports, cognitive function among SPD patients was shown to be poorer than among healthy control participants and patients with AvPD [ 5].

Similar results have been found when examining patients with SPD, PPD, SPD and PPD (SPD/PPD), compared to participants without either of these diagnoses. A diagnosis of SPD or PPD was associated with cognitive impairment, and comorbidity of SPD and PPD was not associated with worse cognitive performance over and above either disorder, alone. While a diagnosis of either SPD or PPD was associated with less likelihood of employment than patients without either of these diagnoses, these differences were found to be primarily determined by cognitive impairment. Even after adjusting for cognitive function, however, a diagnosis of SPD was associated with employment at jobs involving less social contact; and a diagnosis of PPD was associated with lower likelihood of having a history of competitive work for more than a year [ 6].

Pathogenesis of SPD

Heritability of SPD

Early studies revealed that SPD was more common among the relatives of schizotypal probands, compared to those of families with non-Cluster A personality disorders [ 7]. Twin studies have provided evidence that SPD is determined by both familial-genetic and unique environmental factors [ 8; 9]. It has also been observed that SPD can manifest in 3 different phenotypic classes, which are associated with differing etio-pathogenic paths [ 10]. A prominent genetic contribution was associated with a phenotypic class of SPD that exhibited exceptionally high levels of odd appearance/behavior, restricted affect/aloofness, as well as lack of close friends. A second SPD class, marked by high levels of magical ideation and perceptual disturbances, was also determined by familial-genetic and unique environmental influences. A third SPD class, however, consisting of moderately high levels of ideas of reference, social anxiety, and suspiciousness, but low levels of odd behavior, odd speech, and constricted affect, did not exhibit heritability, but rather, appeared to be determined entirely by unique environmental influences. In addition to the categorical diagnosis of SPD, the heritability of psychometric schizotypy and associated dimensions has been examined in non-clinical populations. These reports have demonstrated that there are both liability factors that are common and specific to the various schizotypy measures/dimensions, that are determined by genetic and unique environmental influences.

Environmental Factors

Unique environmental factors (i.e., those not shared among all siblings) are strongly suggested to be involved in the development of SPD, schizotypy, and specific schizotypal dimensions. Similar to findings in schizophrenia, prenatal insults, such as influenza exposure during the 6th month of gestation (specifically, week 23) have been associated with higher scores of schizotypal traits in an adult male population [ 11]. A number of forms of psychological trauma [ 12; 13] and chronic stress [ 14] have been associated with SPD. The effect of trauma on the development of schizotypal symptoms, however, appears to be dependent on genetic background. For example, self-reported trauma was associated with schizotypal symptoms in first-degree relatives of schizophrenic, but not bipolar, patients [ 15]. Further, this effect was specific for positive schizotypal symptoms [ 15], consistent with the presence of specific liability factors for particular schizotypy dimensions. Interestingly, among family members of patients with bipolar disorder, self-reported trauma was associated with increased schizotypal symptoms, but only in those carrying a variant of the catechol-O-methyl transferease (COMT) associated with greater dopamine degradation [ 16].

Molecular Genetics

The COMT Val158Met polymorphism is one of the best studied candidate schizotypy genes. The Val allele, which is associated with greater enzymatic activity than the Met allele, has been shown to be correlated with greater levels of self-reported schizotypy [ 17]. There is variability as to whether susceptibility to the pro-schizotypy effects of the Val COMT occurs in non-clinical participants [ 17], only among schizophrenia proband family members [ 18], or among bipolar proband family members with high levels of psychological trauma. Moreover, while it appears the Val allele is associated with specific schizotypal dimensions, findings are mixed, as there is evidence for the Interpersonal/Negative symptoms [ 19; 20], Cognitive-Perceptual/positive symptoms [ 19] Social and Physical Anhedonia [ 18]. Effects of the Val158Met COMT polymorphism on Disorganization symptoms have been particularly mixed, with certain studies showing a positive relationship with the Val allele [ 20], and others with the Met allele [ 21]. Lastly, multiple studies have also implicated the Val158Met COMT polymorphism in cognitive functions that have are impaired in SPD and the schizophrenia spectrum [ 21- 23].

A number of genes, originally identified due to an association with schizophrenia, have been shown to be related to specific schizotypy dimensions and endophenotypes. Variants of the CACNA1C gene, which encodes for a protein involved in the function of L-voltage gated calcium channels, have been associated with schizophrenia and bipolar disorder. We recently performed a study determining the relationship between a CACNA1C polymorphism and schizotypal symptoms and SPD [ 24]. We found that the 'A' allele of the rs10067373 CACNA1C was associated with paranoid ideation among non-clinical, healthy participants; and was more common among patients with SPD relative to healthy control participants. Furthermore, among patients with SPD, this allele was associated with symptoms of paranoia at the level of a statistical trend [ 24]. In a study of a healthy, non-clinical population, common variants of the zinc-finger protein ZNF804A were associated with positive schizotypal symptoms, namely, paranoia and ideas of reference, but not negative schizotypal symptoms nor cognitive performance [ 25]. On the other hand, the Disrupted In Schizophrenia 1 (DISC1) gene, which is involved in neural cell development, is associated with the negative schizotypy dimension, Social Anhedonia, in healthy participants; this effect was specific, as other dimensions, such as Perceptual Aberrations and Physical Anhedonia were not involved [ 26]. In healthy participants, the Interpersonal schizotypy factor has been shown to be related to variants of the p250GAP gene, which is involved in N-methyl-D-aspartate (NMDA) receptor function [ 27].

Neuropsychological and Cognitive Characteristics

Cognitive deficits represent one of the most functionally, clinically, and neurobiologically significant manifestations of SPD and schizotypy. Prefrontal-dependent cognitive processes -- particularly, working memory and context processing -- have received particular focus in studies of the cognitive impairments of SPD. In many ways, the intense focus on cognitive dysfunction in SPD has been largely driven by the critical role of working memory impairments on functional outcomes in schizophrenia and the lack of efficacy of standard treatments on cognitive function. Thus, characterizing working memory and other cognitive domains in SPD can allow for the assessment of novel therapeutic agents and identification of neurobiological correlates of cognitive deficits, without many of the confounds associated with such studies in schizophrenia, e.g., concurrent/past psychotropic medications, stage of illness and psychosis, chronic, severe functional impairment. However, as discussed earlier, attentional and memory difficulties are common complaints of schizotypal patients in the clinical setting, therefore, characterizing the nature of cognitive dysfunction is important for improving treatment outcomes in SPD, as well.

Studies have sought to identify relationships between schizotypal symptoms dimensions and cognitive dysfunction. We have previously demonstrated a correlation between the PASAT (Paced Auditory Serial Addition Test), an auditory, verbal working memory task that is particularly affected in SPD, and the Interpersonal symptom domain [ 28]. Further, it has been described that omission errors in a sustained attention span task were positively correlated with Interpersonal schizotypal traits in a non-clinical population, whereas Disorganization traits were related to false-alarm or commission errors of sustained attention [ 29]. However, findings have been mixed, as working memory deficits have also been shown to be related to higher levels of positive and lower levels of negative schizotypy [ 30].

Current pathophysiologic models of working memory impairment in SPD (and the schizophrenia-spectrum, more broadly), involve a hypodopaminergic state, particularly, in fronto-cortical regions, and subsequent understimulation of dopamine D1 receptors in the dorsolateral prefrontal cortex (DLPFC) [ 31]. A significant body of literature implicates the D1 receptor as a key modulator of DLPFC-dependent working memory function. Studies in neuroleptic-naïve patients with schizophrenia have described increased fronto-cortical D1 receptor availability, which is believed to reflect a compensatory, albeit insufficient, upregulation of D1 receptors owing to understimulation [ 32]. A relationship between greater working memory deficits and higher prefrontal D1 receptor availability in patients with schizophrenia has also been described, which has been interpreted as impaired working memory as a function of D1 receptor understimulation [ 33]. Unpublished studies from our group indicated that while there are no differences in fronto-cortical D1 receptor availability between patients with SPD and healthy controls, similar to what has been observed in schizophrenia, poorer working memory performance, as indexed by the PASAT, was correlated with greater prefrontal D1 receptor availability. We have previously demonstrated that the mixed D1/D2 receptor agonist, pergolide, improves working memory function in patients with SPD [ 34]. Further unpublished findings from our group suggest that direct D1 receptor stimulation in SPD patients, using the high-affinity, full D1 receptor agonist, dihydrexidine, enhance working memory in patients with SPD. Although less well studied than dopaminergic mechanisms, the noradrenergic system may also be involved in the cognitive deficits of SPD. Accordingly, we have described enhancement of context processing in patients with SPD using the alpha-2a adrenergic receptor agonist, guanfacine [ 35].

In terms of anatomical correlates of cognitive dysfunction, we have previously described that the relationship between greater spatial working memory performance and larger ventrolateral prefrontal cortex size, observed in healthy control participants, was absent in patients with SPD [ 36]. The caudate or dorsal striatum, which receives input primarily from dorsolateral prefrontal regions and has been implicated in higher-order cognitive processes, appears to be involved in the cognitive abnormalities of SPD. Specifically, caudate volumes have been shown to be smaller in patients with SPD, and greater volume reduction was related to poorer cognitive performance [ 37]. These findings have been extended to examining more subtle changes in caudate shape abnormalities; greater aberrant morphology of the right caudate in patients with SPD was also related to cognitive impairment [ 38; 39].

Functional imaging studies have also begun to reveal the neural substrates associated with working memory difficulties in SPD. We have previously observed attenuated working memory-associated activation of the left ventral prefrontal cortex, superior frontal gyrus, intraparietal cortex and posterior inferior gyrus in patients with SPD compared to healthy control participants [ 40]. In a more recent study, activation of the left posterior cingulate gyrus, and deactivation of the superior temporal gyrus, insula and middle frontal gyrus were both attenuated during a working memory task in patients with SPD compared to healthy controls [ 41]. Neural network synchronization, as assessed with EEG, during a visual working memory task was decreased in a non-clinical group with high- vs. low-psychometric schizotypy [ 42].

Social/Interpersonal and Affective Processing

A significant literature is emerging characterizing the social/interpersonal and affective dimensions of SPD and schizotypy. Pflum et al. have compared performance of two Theory of Mind (ToM) tasks in non-clinical participants selected for either high levels of positive schizotypy (Chapmans Magical Ideation and Perceptual Aberrations scales) or negative schizotypy (Chapmans Social Anhedonia scale). They found that only the positive schizotypy group exhibited ToM impairments, but specifically in a Hinting Task -- a social-cogntive ToM task in which participants have to infer the meaning of a fictitious character's remark [ 43; 44]. No group differences were observed for the Reading the Mind in the Eyes Test (RMET) -- a social- perceptive ToM task in which participants have to infer mental states based on static visual stimuli of facial expressions that only includes peri-orbital features [ 43]. A measure of referential thinking, however, which is related to positive schizotypy, but not specifically Magical Ideation and Perceptual Aberrations, was associated with the RMET, such that greater levels of referential thinking were associated with poorer RMET performance [ 43].

Abbot et al. have performed studies similar to those described above in non-clinical participants with psychometrically determined schizotypy (using the SPQ rather than Chapman's scales) with two different tests of affect recognition [ 45; 46]. In one study using pictures of faces with different emotions, the interpersonal factor of the SPQ (which consists of social anhedonia, constricted affect, and social anxiety) was associated with reduced accuracy of facial affect recognition; moreover, the social anxiety component of the Interpersonal factor was particularly involved in this correlation) [ 46]. No relationship was found, however, for the Cognitive-Perceptual SPQ factor (a measure of positive schizotypy) and facial affect recognition [ 46]. The same group, however, found strikingly differing results when using an affect identification task that involved more complex and dynamic stimuli, i.e., a brief audio/visual vignette of a social interaction [ 45]. Both total schizotypy (total SPQ score) and positive schizotypy (Cognitive-Perceptual SPQ factor) were associated with poorer recognition of positive and negative emotions [ 45]. However, negative schizotypy (Interpersonal SPQ factor) was only associated with impaired recognition of positive emotions [ 45]. The Disorganization SPQ factor was not related to emotion recognition [ 45].

We have recently reported a study using the Empathic Accuracy task (EA) -- a multimodal, dynamic task which assesses how well an individual's assessment of a target's affect is compared to the target's own assessment [ 47] -- in patients with SPD compared to healthy controls [ 48]. Our main finding was that the group of patients with SPD exhibited poorer performance on the EA task when assessing negative affect, compared to controls; but no group differences were observed for assessment of positive affect [ 48]. Moreover, the two groups did not differ on the RMET [ 48]. No clear association was found between severity of SPD symptoms or SPQ total or individual factor scores [ 48]. However, a significant effect was found, indicating greater impairment on negative valence EA performance was associated with poorer social support [ 48]; thus, identifying a correlate between a laboratory social cognitive test and a 'real world' social functional outcome.

In addition to understanding the mental states of others, studies have examined affect processing and regulation in patients with SPD, and characterized the differential contribution of the various schizotypy factors. For example, an early study by Henry et al. examined emotion regulation strategies in non-clinical participants with low and high levels of psychometric schizotypy (as assessed by the SPQ). Generally speaking, participants scoring high on the SPQ exhibited impairments in emotion amplification but not emotion suppression [ 49]. Moreover, it was the Negative or Interpersonal SQP factor --particularly, blunted affect -- that was associated with impaired emotion augmentation [ 49]. Additionally, blunted affect was shown to be associated with an increase use of emotional regulatory process, suppression [ 49]. Using a laboratory task assessing the effect of congruent vs. incongruent emotional primers have identifying the correct emotional valence of a target, Martin et al. demonstrated that a non-clinical group scoring high on Social Anhedonia (a Negative or Interpersonal schizotypy dimension) exhibited greater interference from incongruency of emotional valence between primer and target than did the controls or the schizotypy group scoring high on Cognitive-Perceptual traits (a Positive schizotypy dimension) [ 50].

Brain imaging studies have begun to shed light on the neural substrates of social/interpersonal and affective processes associated with SPD. We've recently demonstrated that patients with SPD exhibit exaggerated habituation of amygdala response to affectively valenced social visual stimuli compared to healthy control participants [ 51]. Premkumar et al. have characterized differences in neural activity patterns in response to social rejection in low- vs. high-schizotypy, non-clinical participants. They found that in response to social rejection activity in the dorsal anterior cingulate cortex (dACC), right superior frontal gyrus, and left ventral prefrontal cortex increased and decreased in the low- vs. high-schizotypy group, respectively [ 52]. Using fMRI, Soliman et al. examined the activity of striatal, cortical, and limbic regions to laboratory induced psychological stress, and demonstrated that non-clinical participants scoring high on Physical Anhedonia (a facet of Negative schizotypy) exhibited greater stress-induced deactivation of striatal and limbic regions compared to control participants and those scoring high on Perceptual Aberration (a facet of Positive schizotypy) [ 53]. Additionally, across all participants, Physical Anhedonia was correlated with stress-associated striatal deactivation [ 53]. Interestingly, as described in the Neurochemistry section, this same group observed in a separate study that participants scoring high for Physical Anhedonia exhibited greater stress-induced release of presynaptic dopamine, compared to controls and participants with high levels of Perceptual Aberrations [ 54].

Neurobiological Studies: Structural and Neurochemical Findings

Structural Neuroanatomy

Numerous studies have examined differences in the size of specific brain regions in SPD and schizotypy in comparison to healthy participants, patients with schizophrenia, and other personality disorders. A number of recent reviews have comprehensively discussed neuroanatomical findings in SPD, therefore, we will highlight overarching patterns and recent studies, here.

Temporal lobe

One of the most consistent findings in SPD has been temporal lobe volume reductions, possibly specific to the left hemisphere. Generally speaking, temporal lobe volume reductions in SPD are similar to those observed in studies of schizophrenia, but occur in a more restricted pattern [ 55- 57]. Although not invariantly observed, reduced size of the left superior temporal gyrus (STG) has received significant attention [ 57; 58]. However, the fusiform and middle temporal gyri have also been found to be reduced, but not the inferior temporal gyrus [ 56]. Recent studies have demonstrated that not only do the temporal lobe volume reductions in SPD occur in a more anatomically restricted manner than they do in in schizophrenia, but temporal lobe volume reductions appear to be progressive over time in schizophrenia, whereas in SPD they are relatively stable [ 56; 57]. Generally speaking, involvement of the left temporal lobe suggests both auditory and language-related processes may be affected. Studies have demonstrated correlations between lower temporal lobe size with poorer logical memory [ 59], the odd speech SPD diagnostic criterion [ 58], and possibly, cognitive-perceptual symptoms [ 55].

Frontal lobe

Frontal lobe findings in SPD are of particular interest given the importance and recent focus on cognitive and working memory impairments in the schizophrenia-spectrum. However, unlike temporal lobe differences in SPD which have been relatively consistent between studies and similar although narrower in scope relative to those of schizophrenia, frontal lobe findings in SPD have been more variable. For example, we have demonstrated prefrontal cortex gray matter volume reduction in schizophrenia compared to both SPD patients and control participants; and no significant differences between the SPD and control groups. Moreover, we found volume differences of Brodmann's area (BA)10 -- a prefrontal region -- in SPD and schizophrenia were contradistinctive. In other words, BA10 was increased in SPD, compared to controls and patients with schizophrenia, and decreased in schizophrenia compared to controls and SPD patients. However, a recent study of neuroleptic-naïve men with SPD demonstrated widespread reductions in cortical gray matter volumes, including the frontal lobe; and no regions were identified with larger cortical volumes [ 60]. To complicate matters further, in studies of healthy, non-clinical participants those with high psychometric schizotypy demonstrated greater prefrontal [ 61] and global cortical gray matter volumes [ 62]. This has led to the hypothesis that general sparing of frontal lobe involvement in SPD, relative to that of schizophrenia, represents a 'protective factor' against the development of frank psychosis.

Striatum

In addition to cortical regions, such as the temporal and frontal lobes, structural and anatomical differences of the striatum have also been examined in patients with SPD. The striatum plays an essential role integrating cortical, thalamic and other subcortical processes in order to promote coherent sensori-motor, cognitive, and emotional/motivational function. While findings have been inconsistent, some general patterns have begun to emerge. Regions composing the associative striatum --most of the caudate and the pre-commissural putamen -- have generally been implicated. Initial reports from our group described smaller putamen volumes of patients with SPD compared to controls, whereas putamen size in patients with schizophrenia was relatively larger than that of control participants [ 63]. No differences of caudate volumes were observed, however. These findings suggested that smaller putamen volumes might reflect a compensatory change against pathogenesis of an overt psychotic syndrome. However, more recently, in a larger study of antipsychotic naïve SPD patients, we observed increased putamen volumes, specifically in the ventral and dorsal aspects [ 64]. Again, no differences in caudate volumes were observed. Interestingly, greater putamen size correlated with less severe paranoid symptoms. Therefore, it was proposed that increased putamen volumes in SPD patients may be a 'protective' factor against development of psychosis. Discrepancy with our earlier study was attributed to differences in sample size, gender ratios, medication history, or heterogeneity of the disorder. Nevertheless, larger putamen size in SPD patients was consistent with larger putamen volumes in schizophrenic patients with better outcomes (possibly reflecting therapeutic sensitivity to antipsychotics) compared to poor-outcome schizophrenia patients [ 65].

A separate group has also examined striatal neuroanatomy in patients with SPD, but have found abnormalities of caudate, rather than putamen, volume and morphology. They have consistently found smaller caudate volumes in SPD patients compared to control participants. Moreover, they have found global and regional morphological abnormalities of the caudate nucleus in patients with SPD, most marked in the right caudate head. Generally speaking, these caudate volume differences correlated with cognitive impairments [ 37- 39; 66].

Other regions and Structural Connectivity

Structural abnormalities of the cingulate gyrus, a limbic cortical region that overlays the internal capsule and is involved in a range of cognitive/attentional and motivational/emotional functions, have also been described in SPD. We have previously observed reduced gray matter volumes in anterior cingulate posterior cingulate [ 55]. Findings in schizophrenia were similar to those of SPD patients, particular with respect to reduced BA31 volumes [ 55]. Furthermore, we have found that comorbidity of SPD in patients with BPD was associated with accentuated or additional gray matter loss of the posterior cingulate, compared to BPD patients without SPD [ 67]. However, not all studies have found volumetric differences in the anterior cingulate in SPD patients [ 68]. One group, however, has described that the right-greater-than-left asymmetry of the anterior cingulate observed in healthy female participants is absent among female patients with SPD [ 69].

Studies have also begun to examine structural connectivity, using diffusion tensor imaging (DTI), which can be used to assess fiber tract integrity [ 70]. In patients with SPD, lower fractional anisotropy (FA) of the uncinate fasciculus (UF), which is involved in fronto-temporal connectivity, was observed in SPD patients compared to healthy control participants [ 71]. However, no differences in the integrity of the cingulum bundle (CB), another important fiber tract bundle involved in connectivity of prefrontal, temporal, and parietal cortices, were observed between SPD patients and healthy control participants. Finally, lower left UF cross-sectional areas predicted poorer cognitive performance, whereas lower right UF areas were correlated with greater SPD Interpersonal symptomatology [ 71]. In accordance with these findings, FA of the right UF has also been shown to correlate with the personality trait, Extraversion, in patients with SPD but not in healthy control participants [ 72]. Our group recently examined the integrity of the anterior limb of the internal capsule (ALIC) which carries fibers between the thalamus and frontal lobe in patients with SPD. We found decreased volumes of the mid-ventral portion of the ALIC in SPD patients compared to controls; and, fewer fiber tracts in the dorsal portion of the ALIC terminating in BA10 but not BA45; and fewer dorsal-ALIC fibers correlated with greater severity of SPD symptomatology [ 73].

Dopamine Neurochemistry

Consistent with the role of the dopaminergic system in schizophrenia, studies have also begun to characterize dopamine neurochemistry in SPD using methods such as positron emission tomography (PET) and single photon emission computed tomography (SPECT) imaging. In an early study from our group [ 74], we used SPECT imaging to characterize striatal presynaptic dopamine release by examining the degree of amphetamine-induced displacement of the D2 receptor radioligand, [123I]IBZM: greater presynaptic dopamine releasing capacity is associated with greater decreases in [123I]IBZM binding after amphetamine challenge. No differences in striatal [123I]IBZM binding were observed between SPD patients and healthy control participants, indicating no significant differences in striatal D2 receptor availability, itself, in SPD patients. However, post-amphetamine decreases in striatal [123I]IBZM binding SPD patients were almost twice that of healthy control participants, suggestive of relatively greater presynaptic dopamine release in SPD patients. Moreover, the degree of presynaptic dopamine release in SPD patients was similar to that observed in patients with remitted schizophrenia, but approximately half that of schizophrenic patients with an acute exacerbation of symptoms [ 74].

Further published studies have examined dopaminergic neurochemistry in healthy, non-clinical participants characterized with well validated self-report scales of schizotypy. Stress-induced striatal dopamine release, as indexed by comparing striatal [11C]raclopride binding during a control and mental arithmetic task, was shown to be elevated only in a group scoring high on a measure of negative schizotypy (Chapmann's Physical Anhedonia scale), but not in a group scoring high on a measure of positive schizotypy group (Chapmann's Perceptual Aberration scale) nor in a control group [ 54].

Examining amephtamine-induced changes in [11C]fallypride binding, the association between presynaptic dopamine release and schizotypal traits was examined in healthy participants assessed with the schizotypal personality questionnaire (SPQ) [ 75]. A positive correlation was found between total schizotypy, as measured by the SPQ, and striatal presynaptic dopamine release. This relationship was found to be primarily related to presynaptic dopamine release in the associative striatum and the Disorganized schizotypal traits [ 75]. Further exploratory analyses indicated a positive correlation between presynaptic dopamine release in a number of other cortical and subcortical regions [ 75]. In a separate study, Disorganized traits, in non-clinical adults assessed with the SPQ, were positively correlated with D2 dopamine receptor availability, as measured by SPECT imaging with [123I]IBZM binding, in the right striatum [ 76]. Lastly, dopamine synthesis capacity in a non-clinical group with subclinical auditory hallucinatory phenomena did not differ from a control group; and schizotypal and other psychosis-spectrum symptoms were not related to dopamine synthesis capacity [ 77].

Unpublished preliminary studies from our group have examined striatal dopamine release using amphetamine-induced [11C]raclopride displacement. These studies suggested greater presynaptic dopamine release, but specifically, in SPD patients under 40 years of age. Further, presynaptic dopamine release in SPD patients under 40 years old, appeared to be positively correlated with cognitive-perceptual (or positive) symptoms and enhanced working memory performance. Presynaptic striatal dopamine, on the other hand, appeared to be inversely correlated with negative symptoms, such as Interpersonal symptoms and social anhedonia in the under-40 SPD patients.

Clinical Perspectives

Identifying SPD and associated traits in the clinical setting can be challenging as manifestations overlap with many other more well-known psychiatric conditions, or may simply be qualified in colloquial terms (e.g., loner) without further diagnostic attribution. Common complaints of patients with SPD or schizotypal traits are related to attentional/cognitive difficulties, social anxiety, difficulty "connecting" to others, and longstanding interpersonal complications related to suspiciousness/paranoia. Superficially healthier SPD patients may present with characteristic anxieties or 'neurotic conflicts' that are, in a more latent manner, determined or exacerbated by underlying magical ideation, odd beliefs, or overvalued ideas.

Therefore, schizotypal patients are not uncommonly diagnosed with attention-deficit disorder (inattentive type); social anxiety disorder; autism-spectrum; dysthymia. Additionally, the role of an underlying odd/magical belief as an aggravating factor of a concurrent symptom disorder (e.g., anorexia, OCD) may be overlooked. what appears anxiety-related complaints or other symptom disorders can be overlooked. Additionally, many of the cognitive/perceptual disturbances that schizotypal patients can bring to a clinician's attention can be quite dramatic or alarming, and even though these phenomena are not associated with patient has a fair degree of intact reality testing, patients may nevertheless receive a diagnosis of a formal psychotic illness. Clinically significant schizotypy can exacerbate the treatment of other clinical syndromes that may be the primary area of focus. For example, schizotypy has been shown to be a potential negative prognostic factor in OCD. We have found that the underlying core beliefs associated with certain disorders can have a more concrete quality or be relatively refractory to insight.

Medications can play either a primary or adjunctive role in treatment of patients with SPD or schizotypal traits. Importantly, however, clinical trials for SPD or specific schizotypal symptoms are rare, and therefore, our recommendations are based on our clinical experience and discussions with colleagues. We have found that attentional and cognitive difficulties are responsive to stimulants, such as those used to treat attention deficit disorder. Although the use of stimulants in those with a vulnerability to psychosis certainly requires close clinical monitoring, we have not found stimulant use in SPD patients to be problematic in this regard. On the contrary, we find that the enhanced cognitive function may limit stress-induced impairment of executive function, and therefore, lessen the propensity more regressive forms of thought processes. Moreover, mood and social anxiety symptoms can also be alleviated during a course of stimulant treatment, however, we do not recommend their use for indications other than attentional or cognitive difficulties. Early evidence from our group also supports a possible role for guanfacine, which also has an indication for attention-deficit disorder [ 35]. We did not observe any benefit of the atypical antipsychotic, risperidone, on cognitive function in patients with SPD. Risperidone (0.25-2 mg), however, has been shown to improve both positive and negative symptomatology in patients with SPD [ 78]. Antipsychotics should be used judiciously in SPD patients, especially since these symptoms are not necessarily the most disturbing to patients, nor are they necessarily the most problematic. Antipsychotics certainly play an important role when SPD patients develop brief psychotic episodes, which they are susceptible to during periods of elevated psychosocial stress. We have also found that benzodiazepines can play in important role in the treatment of anxiety in SPD, however, it is not uncommon that symptoms may only be partially relieved. In contrast to the treatment of generalized anxiety, social anxiety, and panic disorder, we have not been impressed with the effectiveness of serotonin reuptake inhibitors (SRIs) on SPD-associated anxiety. Moreover, we have not found antidepressants to be particularly effective for the dysthymic and anhedonic symptoms of SPD.

The literature on psychotherapy for patients with SPD is close to non-existent. Stone's manuscript of his clinical experience treating schizotypal patients psychotherapeutically, although close to 30 years old, remains highly relevant [ 79]. Psychotherapy with SPD patients can be limited by a variety of possible interpersonal complications. On the one hand, paranoia and limited capacity/desire to form close personal relationships can be a barrier for developing a therapeutic alliance. On the other hand, in SPD patients with the capacity and desire to form relationships, complications can arise during periods of treatment intensification and separation. Patients with SPD may experience a blurring of the boundaries between themselves and the therapist as treatment advances. For example, a high functioning SPD patient in psychotherapy began expressing a feeling that she and the therapist 'knew each other from someplace else' after the therapist had linked the patients symptomatic, excessive conscientiousness with her description of her siblings as being unreliable during childhood. This was taken as an indication to the therapist that this standard psychotherapeutic intervention may not have suitable at that time. Additionally, SPD patients may either be unable to tolerate regular or extended periods of separation; alternatively, they may have difficulty experiencing continuity between sessions -- as if the work of each session wasn't cumulative, but rather, was just another "new" session.

Peculiarities of thought and semantic processing make it very difficult for SPD patients to be understood and/or communicate complex emotional and psychological states and concepts that are typically required in psychotherapy. Furthermore, SPD patients can have a limited capacity to think about their mental states abstractly; or, they may find the process to be disconcerting or destabilizing. We have also noted that SPD patients exhibit a striking capacity for disavowal of certain realities, which further complicates the process of psychotherapy as the anxiety associated with certain external consequences plays less of a motivating role for psychological change.

Vivid perceptual/dissociative disturbances that are associated with elaborate magical beliefs require a delicate psychotherapeutic approach, as SPD patients can simultaneously (albeit in an unintegrated manner) recognize these thoughts and experiences as symptoms, yet at the same time, ascribe them to reality. Therefore, a challenge for the psychotherapist is to be able to tolerate and help the patient tolerate these complicated and troubling experiences.

Lastly, there is significant individual variability in terms of what types of psychotherapeutic interventions SPD patients could benefit from; and, ultimately, this can only be assessed empirically during the initial and extended evaluation process. Therefore, once clinically significant schizotypy has been identified, this should prompt the clinician to pay particularly close attention to various factors, such as: the ability of the patient to form a therapeutic alliance; the patient's expectation of what are reasonable psychotherapeutic goals, and psychotherapy is supposed to work.

Conclusions

SPD is significant both as a clinical syndrome and, from a research perspective, as an intermediate schizophrenia-spectrum phenotype. From a clinical standpoint, SPD is relatively understudied, compared to other personality disorders, and a great deal needs to be understood with respect to both pharmacological and psychotherapeutic interventions. SPD can be challenging to identify, as diagnostic phenomena may be a) difficult to elicit, b) attributed to more familiar diagnoses, or c) go unrecognized. Other important phenomena, namely, cognitive deficits (attentional, executive function, and working memory impairments), may not lead one to consider a diagnosis of SPD as they are not formally represented in the DSM diagnostic criteria. Nevertheless, such cognitive impairments are strongly associated with SPD and play an important role in determining functional outcomes. Recognition of SPD may be aided by appreciation of its multidimensional nature, typically represented in terms of Cognitive-Perceptual, Oddness/Disorganized, and Interpersonal/Negative domains. SPD is a heritable condition, consisting of both genetic and environmental factors (e.g., psychological trauma). There are factors that contribute to the development of SPD itself, as well as its component domains (e.g., Cognitive-Perceptual). In terms of the neurobiology of SPD, there are shared and divergent elements with respect to schizophrenia. For example, both SPD and schizophrenia exhibit decreased left temporal lobe volumes; however, in SPD, temporal lobe volume abnormalities are anatomically more circumscribed, and less progressive over time than in schizophrenia. Frontal lobe and striatal anatomical abnormalities have also been identified in SPD; however, these findings have been less consistent, and may also consist of compensatory or 'protective' factors that limit progression to full psychosis. Dopaminergic neurochemistry in striatal and cortical regions appears to play an important role in SPD and schizotypal traits in non-clinical participants. Areas in need of future focus include characterization of schizotypy in child and adolescent populations, including further understanding of relationship with autism-spectrum conditions; studies on psychopharmacological and psychotherapeutic treatments; characterizing neural correlates and therapeutics of cognitive impairment.

Footnotes

Compliance with Ethics Guidelines: Conflict of Interest: Daniel R. Rosell has received support for travel and payment from writing or reviewing manuscript from the Department of Veterans Affairs.

Shira E. Futterman has received a grant from the National Institute of Mental Health.

Antonia McMaster has received a grant from the National Institute of Mental Health.

Larry J. Siever has received grants and travel support from the National Institute of Mental Health and the Department of Veterans Affairs. He also received travel support from the Mental Illness Research, Education and Clinical Centers. Dr. Siever also has receive payment for writing or reviewing manuscripts from the Department of Veterans Affairs, the Mental Illness Research, Education and Clinical Centers, and Mount Sinai.

Human and Animal Rights and Informed Consent: This article does not contain any studies with human or animal subjects performed by any of the authors.

References

Papers of particular interest, published recently, have been highlighted as:

* Of importance

** Of major importance

41*. Vu MA, Thermenos HW, Terry DP, et al. Working memory in schizotypal personality disorder: fMRI activation and deactivation differences. Schizophr Res. 2013 This is a recent, and one of the few studies to examine functional neural correlates of working memory in SPD. [[ PubMed] Google Scholar]

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Schizotypal Personality Disorder: A Current Review

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Daniel R. Rosell, M.D., Ph.D, 1, 2 Shira E. Futterman, Psy.D, 1, 2 Antonia McMaster, B.A, 1, 2 and Larry J. Siever, M.D 1, 2 The study of schizotypal personality disorder (SPD) is important clinically, as it is understudied, challenging to treat, often under-recognized or misdiagnosed, and associated with significant functional impairment.

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Cleveland Clinic Website: Information on Trichotillomania

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Cleveland Clinic Website: Information on Trichotillomania

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Overview

Missing patches of hair are a possible sign of trichotillomania.

What is trichotillomania?

Trichotillomania (often abbreviated as TTM) is a mental health disorder where a person compulsively pulls out or breaks their own hair. This condition falls under the classification of obsessive-compulsive disorder (OCD). When it's severe, it often has extremely negative effects on a person's happiness, well-being and overall quality of life.

Trichotillomania (pronounced trick-oh-till-oh-main-ee-uh) comes from three Greek words:

Tricho: hair.

Tillo: pull.

Mania: excessive behavior or activity.

What is the difference between trichotillomania and obsessive-compulsive disorder?

TTM falls under the overall category of obsessive-compulsive disorder, but it has some key differences from OCD itself.

Obsessions. OCD involves obsessions, which are thoughts or urges that a person can't control and doesn't want. TTM doesn't involve obsessions.

Feeling of reward. When people with TTM pull out their hair, they often feel relief or other positive emotions. OCD doesn't involve positive feelings in that way.

Who does it affect?

TTM is especially common in children and adolescents. In young children and infants, it's usually a short-lived concern and goes away on its own. The more serious form most commonly starts between ages 10 and 13.

In children, it happens equally between men and women. In adults, women outnumber men with this condition by as much as 9 to 1.

How common is this condition?

TTM is relatively uncommon. Research studies estimate it affects 0.5% to 3.4% of adults at some point in their lifetime.

How does this condition affect my body?

People with TTM compulsively pull out their hair, usually one strand at a time. Many people will pull hair from the same spot. The most common places people pull hair from are their scalp, eyelashes and eyebrows, and pubic hair.

The effects of trichotillomania also depend on the age at which it happens. Children commonly pull their hair in this way, but that behavior is often a self-soothing act. Children often grow out of this behavior and don't have any long-term negative effects. Adolescents, teenagers and adults with this condition tend to have much more severe problems.

Mental health effects

People with TTM commonly feel anxiety, embarrassment or shame about this condition. This can affect their work and social lives. Many people with this condition don't seek treatment because they feel embarrassed or ashamed.

Trichophagia

About 20% of people with this condition eat their hair after pulling it, a condition known as trichophagia (from Greek words "tricho" for hair and "phagia" for eating). This can lead to hairball-like blockages in their digestive tract. Those blockages are sometimes dangerous and often cause damage that needs surgery to repair.

People with TTM commonly hold back from telling their healthcare provider about this even after revealing details about TTM. This is often because they're waiting until they feel they can trust their provider more before sharing that amount of detail.

Hair, skin and tissue damage

People who pull out their hair often cause damage to their skin and tissue just underneath the skin's surface, especially if they use any kind of personal care tool like tweezers. Skin and tissue damage sometimes need repair or skin grafting to fix. Damage to skin caused by hair pulling can also cause permanent hair loss in affected areas.

Symptoms and Causes

What are the symptoms of trichotillomania?

According to the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders Fifth Edition (better known as the DSM-5), the diagnosis of TTM requires a person to meet five criteria:

1. Repeated pulling out of hair that causes hair loss.

2. Trying multiple times to stop this behavior or do it less often.

3. Feeling that hair pulling negatively affects your life, especially your work and social life.

4. The hair pulling or hair loss isn't happening because of another condition (such as a skin-related disorder or problem).

5. The hair pulling isn't happening because of another mental health condition. An example of this is body dysmorphia, where hair pulling happens because a person believes there's a problem with their appearance and is trying to fix it).

Some people with TTM pull their hair deliberately, such as when they feel a hair is out of place or looks different from others around it. Other people pull their hair automatically without thinking about it.

What causes trichotillomania?

While experts suspect several possible factors could lead to TTM, there aren't any confirmed causes of this condition. Some of the suspected factors include:

Genetics. TTM may happen because of certain DNA mutations. More research is needed to confirm this.

Changes in brain structure or chemistry. People with TTM often have changes to certain areas in their brains or differences in their brain chemistry.

Coping mechanism. Many people with TTM describe it as starting after a stressful time in their life. Others describe it starting because of boredom and that pulling their hair became a habit over time.

Other conditions that happen with TTM

There are several mental health conditions that a person is much more likely to have along with TTM. These can happen either as separate conditions or because of TTM (especially anxiety and depression). These include:

OCD (this condition is a common misdiagnosis for people who, in reality, have TTM).

Major depressive disorder.

Anxiety disorders.

Substance use disorders (alcohol and drugs).

Is it contagious?

No, TTM isn't contagious, and it can't spread to others. While some experts suspect it might be something you can inherit from your parents, more research is necessary to confirm that.

Diagnosis and Tests

How is trichotillomania diagnosed?

Diagnosing TTM involves a combination of a physical exam, where your healthcare provider looks for visible signs of the condition. They'll also ask questions about your health history, current circumstances and anything else that might have a connection to a medical problem.

TTM is a relatively straightforward condition to diagnose, but people with this condition often hide it out of shame or embarrassment. That can make it harder for your healthcare provider to diagnose this condition based solely on asking questions. That's why a specific type of skin test may also help.

What tests will be done to diagnose it?

In some cases, a " punch biopsy " (where your healthcare provider takes a skin sample for lab analysis) is necessary to confirm a diagnosis of TTM. This test can also rule out other skin conditions that might be the true cause of hair loss or hair pulling.

In cases where your healthcare provider suspects a blockage from swallowed hair, you might also undergo other diagnostic tests. These include imaging tests like a computerized tomography (CT) scan, blood testing for anemia and more.

Management and Treatment

How is it treated, and is there a cure?

Treating TTM often involves therapy, medication or a combination of both. Ongoing research shows some medications for other mental health conditions might help TTM, but more research is necessary before any specific medication becomes a part of the standard care.

What medications and treatments are used?

Medication alone often isn't enough to treat TTM. Healthcare providers may use combinations of medications, therapy techniques or both.

Medications

Medications that may treat, either on their own or in combinations, TTM include:

Antidepressants. Selective serotonin reuptake inhibitors (commonly referred to as SSRIs) and tricyclic antidepressants can sometimes help with reducing the impulse to pull hair.

Antipsychotics. These medications help balance your brain chemistry. While the name sounds like they have only one use, they actually treat many conditions, including dementia, bipolar disorder and schizophrenia.

Anticonvulsants. These medications typically help treat seizures and other disorders that affect muscle movements, but they also can help with TTM.

Nutraceuticals. These are nutrition products, such as amino acid supplements, that can help treat medical conditions.

Therapies

Therapy methods that may help treat TTM include:

Habit reversal therapy. This method involves helping you become more aware of your behaviors and activity patterns. By helping you become more aware, this therapy teaches you to break habits like hair pulling. This method has the best odds of success out of any treatment option for TTM.

Group therapy and peer support. People with TTM may benefit from specific types of group therapy or support.

People with TTM with hair loss or scarring may need to see other healthcare providers and specialists. In some cases, a dermatologist can help treat related skin problems or damage. Plastic and reconstructive surgeons may also help with skin grafting for affected areas of your body. Other healthcare providers can also offer solutions related to hair regrowth; though, regrowth isn't always an option.

Complications/side effects of the treatment

The possible side effects that can happen with medications depend on the medications themselves, as well as your medical history and circumstances. Your healthcare provider can tell you more about possible side effects, including potential trouble signs and how you should react if you see those signs. They're the best source of information about this because they can tailor the information they give you to your specific health needs, situation and circumstances.

How to take care of myself/manage symptoms?

TTM isn't a condition you should diagnose on your own. That's because a trained and experienced mental healthcare provider is better prepared to determine if you have TTM or another health condition. It's also not something you should treat on your own, partly because both medication and therapy methods often need a prescription or other input from a healthcare provider.

How soon after treatment will I feel better?

The time it takes for you to feel better from medication, therapy or a combination of the two can be very different from person to person. Your healthcare provider can tell you more about what you can expect as you undergo treatment and what you can do to help yourself through the process.

Prevention

How can I reduce my risk or prevent this condition?

TTM is a mental health condition, which means it isn't preventable. There's also no known way of reducing your risk of developing it.

Outlook / Prognosis

What can I expect if I have this condition?

TTM isn't usually a danger to your physical health (except in rare cases, especially when a person develops a digestive tract blockage from hair they've swallowed). However, it can be very disruptive and damaging to your mental health and quality of life.

Because people with TTM often feel ashamed or embarrassed of this condition, most avoid treatment. Those who avoid or delay treatment are much more likely to have issues like permanent hair loss, scarring and more severe mental health problems.

How long does TTM last?

The available research, while limited, shows that people with TTM have this condition for an average of about 22 years. In some cases, the condition is a lifelong problem. People also often describe that the condition has phases, becoming more or less severe for periods of time. Overall, early diagnosis and treatment are the best chance for limiting how long this condition lasts and how severely it impacts your life.

What's the outlook for this condition?

The overall outlook for this condition depends partly on the age of the person who has it. Infants and children with TTM often have the best outlook, with the condition commonly going away on its own.

However, the older a person gets - especially from adolescence onward - the greater the odds that treating the condition becomes difficult. TTM on its own is rarely a life-threatening problem. But its impacts on a person's life, especially their mental health, are often severe. Because of this, early diagnosis and treatment are very important.

Living With

How do I take care of myself?

If you have TTM, it's important to see a healthcare provider (or multiple providers) with specialized training and experience in treating this condition. They can best guide you on what you can do to minimize the impact of this condition on your life.

In general, healthcare providers recommend the following:

Be honest about what you're experiencing. TTM is a medical condition that affects your mind and behaviors. Much like you would see a healthcare provider for a broken bone or an ear infection, you should also see a healthcare provider for mental health conditions like TTM. They can help treat your condition and help you deal with any negative emotions you're facing in connection with it.

See your healthcare provider(s) as recommended. This is especially important for therapy sessions and other mental health visits.

Take medications as prescribed, if prescribed. Medications can often help decrease how strongly or often you feel the urge to pull your hair.

When should I go to ER?

People with TTM who swallow their hair have a higher risk of blockages in their digestive tract. These blockages often cause severe or even life-threatening complications. The following symptoms are likely with a blockage and mean you should call your healthcare provider or go to the hospital:
A note from Cleveland Clinic
Trichotillomania, or hair pulling, can have a severe effect on your mental health. People with this condition often feel ashamed, embarrassed or guilty because of it. If you have TTM or know someone who does, it's important to remember this is a medical condition and that hair pulling is very difficult to control or stop on your own. But with treatment, it's possible to limit how often you pull your hair or stop pulling it. That can help you live a life where your hair and appearance don't make you feel anxious or ashamed, so you can focus on things that matter most to you.

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Trichotillomania (often abbreviated as TTM) is a mental health disorder where a person compulsively pulls out or breaks their own hair. This condition falls under the classification of obsessive-compulsive disorder (OCD). When it's severe, it often has extremely negative effects on a person's happiness, well-being and overall quality of life.

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Anxiety and Depression Association of America Website: Information on Body Dysmorphic Disorder

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Anxiety and Depression Association of America Website: Information on Body Dysmorphic Disorder

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Body Dysmorphic Disorder (BDD) | Anxiety and Depression Association of America, ADAA

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Understanding Body Dysmorphic Disorder (BDD). People who have body dysmorphic disorder (BDD) think about their real or perceived flaws for hours each day. They can't control their negative thoughts and don't believe people who tell them that they look fine.

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International OCD Foundation Website: Information on Obsessive Compulsive Disorder

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International OCD Foundation Website: Information on Obsessive Compulsive Disorder

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What is OCD? | International OCD Foundation

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Obsessive compulsive disorder (OCD) is a mental health disorder that affects people of all ages and walks of life, and occurs when a person gets caught in a cycle of obsessions and compulsions. Obsessions are unwanted, intrusive thoughts, images, or urges that trigger intensely distressing feelings.…

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The Hockaday School's Website: How our School's Learning Support Team Works

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The Hockaday School's Website: How our School's Learning Support Team Works

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The Dr. William B. Dean Academic Learning Support Program seeks to help all Hockaday students PK-12 reach their maximum potential. All students at Hockaday are welcome to receive help from The Dr. William B. Dean Academic Learning Support Program - whether or not they have a diagnosed learning difference. Ultimately, the department's goals are to empower all students in self-advocacy in order to meet success and to assist teachers in the practice of differentiating instruction through best practices.

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The Dr. William B. Dean Academic Learning Support Program seeks to help all Hockaday students PK-12 reach their maximum potential. All students at Hockaday are welcome to receive help from The Dr. William B. Dean Academic Learning Support Program - whether or not they have a diagnosed learning difference.

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National Institute of Mental Health Website: Information on Attention-Deficit/Hyperactivity Disorder (ADHD)

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National Institute of Mental Health Website: Information on Attention-Deficit/Hyperactivity Disorder (ADHD)

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National Institute of Mental Health (NIMH)

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What is ADHD?

Attention-deficit/hyperactivity disorder (ADHD) is marked by an ongoing pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development. People with ADHD experience an ongoing pattern of the following types of symptoms:

Inattention means a person may have difficulty staying on task, sustaining focus, and staying organized, and these problems are not due to defiance or lack of comprehension.

Hyperactivity means a person may seem to move about constantly, including in situations when it is not appropriate, or excessively fidgets, taps, or talks. In adults, hyperactivity may mean extreme restlessness or talking too much.

Impulsivity means a person may act without thinking or have difficulty with self-control. Impulsivity could also include a desire for immediate rewards or the inability to delay gratification. An impulsive person may interrupt others or make important decisions without considering long-term consequences.

What are the signs and symptoms of ADHD?

What are the risk factors of ADHD?

How is ADHD treated?

How can I find a clinical trial for ADHD?

Where can I learn more about ADHD?

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Learn about attention-deficit/hyperactivity disorder, including signs and symptoms, risk factors, treatments, and tips for staying organized with ADHD.

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Autism Speaks Website: Information on Autism Symptoms, Diagnosis, Causes, etc.

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Autism Speaks Website: Information on Autism Symptoms, Diagnosis, Causes, etc.

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Autism, or autism spectrum disorder (ASD), refers to a broad range of conditions characterized by challenges with social skills, repetitive behaviors, speech and nonverbal communication. According to the Centers for Disease Control, autism affects an estimated 1 in 36 children in the United States today.

We know that there is not one autism but many subtypes, most influenced by a combination of genetic and environmental factors. Because autism is a spectrum disorder, each person with autism has a distinct set of strengths and challenges. The ways in which people with autism learn, think and problem-solve can range from highly skilled to severely challenged. Some people with ASD may require significant support in their daily lives, while others may need less support and, in some cases, live entirely independently.

Several factors may influence the development of autism, and it is often accompanied by sensory sensitivities and medical issues such as gastrointestinal (GI) disorders, seizures or sleep disorders, as well as mental health challenges such as anxiety, depression and attention issues.

Signs of autism usually appear by age 2 or 3. Some associated development delays can appear even earlier, and often, it can be diagnosed as early as 18 months. Research shows that early intervention leads to positive outcomes later in life for people with autism.

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What is autism spectrum disorder (asd)? Click here to read the definition, learn about different types of autism and how to help autistic kids.

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American Association on Intellectual and Developmental Disabilities Website: Intellectual Disabilities Criteria and Information

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American Association on Intellectual and Developmental Disabilities Website: Intellectual Disabilities Criteria and Information

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Intellectual Functioning

Intellectual functioning-also called intelligence-refers to general mental capacity, such as learning, reasoning, problem solving, and so on.

One way to measure intellectual functioning is an IQ test. Generally, an IQ test score of around 70 or as high as 75 indicates a significant limitation in intellectual functioning.

Adaptive Behavior

Adaptive behavior is the collection of conceptual, social, and practical skills that are learned and performed by people in their everyday lives.

Conceptual skills-language and literacy; money, time, and number concepts; and self-direction.
Social skills-interpersonal skills, social responsibility, self-esteem, gullibility, naïveté (i.e., wariness), social problem solving, and the ability to follow rules/obey laws and to avoid being victimized.

Practical skills-activities of daily living (personal care), occupational skills, healthcare, travel/transportation, schedules/routines, safety, use of money, use of the telephone.

Standardized tests can also determine limitations in adaptive behavior.

Age of Onset

The condition originates during the developmental period, which is defined as before the age of 22. Intellectual disability is one of several conditions known collectively as developmental disabilities.

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Intellectual functioning-also called intelligence-refers to general mental capacity, such as learning, reasoning, problem solving, and so on. One way to measure intellectual functioning is an IQ test. Generally, an IQ test score of around 70 or as high as 75 indicates a significant limitation in intellectual functioning.

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Nationwide Childrens Hospital Website: Information on Conduct Disorders in Children

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Nationwide Childrens Hospital Website: Information on Conduct Disorders in Children

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What Symptoms Should Parents Look for?

There are four basic types of behavior that characterize conduct disorder:

Physical aggression (such as cruelty toward animals, assault or rape).

Violating others' rights (such as theft or vandalism).

Lying or manipulation.

Delinquent behaviors (such as truancy or running away from home).

Conduct disorder is characterized by aggression toward others and a callous disregard for their rights and needs. Adolescents and teens with conduct disorder can find acts of aggression, deceit and coercion to be gratifying. Your child may meet the criteria for conduct disorder if you find them engaging in several of the below behaviors:

Many young people with conduct disorder will have trouble:

Feeling and expressing empathy or remorse.

Showing emotion toward others.

Performing well in the school or community and blaming others for poor performance.

They often misinterpret the actions of others as being hostile or aggressive. They respond by escalating the situation into verbal or physical conflict.

In adolescents and teens, conduct disorder may be associated with other difficulties, including:

In younger children, it can be more of a challenge to distinguish signs of conduct disorder from more typical "acting out".

At times, these same symptoms can be seen in children without the disorder. The difference is frequency, intensity, and duration, as well as to what extent it impacts their functioning. In children with conduct disorder, these behaviors happen much more frequently.

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There are four basic types of behavior that characterize conduct disorder: Physical aggression (such as cruelty toward animals, assault or rape). Violating others' rights (such as theft or vandalism). Lying or manipulation. Delinquent behaviors (such as truancy or running away from home).

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National Library of Medicine: Study on Antisocial Personality Disorder

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National Library of Medicine: Study on Antisocial Personality Disorder

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Continuing Education Activity

This activity reviews the evaluation and treatment of antisocial personality disorder (ASPD). ASPD is a deeply ingrained and dysfunctional thought process that focuses on social exploitive, delinquent, and criminal behavior most commonly known due to the affected individual's lack of remorse for these behaviors. ASPD falls into 1 of 4 cluster-B personality disorders within the DSM V, which also includes narcissistic, borderline, and histrionic personality disorders. This activity reviews the role of the an interprofessional team in evaluating, treating, and improving the care for patients with this condition.

Objectives:

Identify the psychopathology of antisocial personality disorder

Summarize the diagnostic criteria of Antisocial personality disorder.

Outline the treatment and management options available for Antisocial personality disorder.

Summarize interprofessional team strategies for improving care coordination and communication to advance the treatment of antisocial personality disorder and improve outcomes.

Access free multiple choice questions on this topic.
Introduction

Antisocial personality disorder (ASPD) is a deeply ingrained and rigid dysfunctional thought process that focuses on social irresponsibility with exploitive, delinquent, and criminal behavior with no remorse. Disregard for and the violation of others' rights are common manifestations of this personality disorder, which displays symptoms that include failure to conform to the law, inability to sustain consistent employment, deception, manipulation for personal gain, and incapacity to form stable relationships.[1]

The Diagnostic and Statistical Manual of Mental Disorders (DSM 5) classifies all ten personality disorders into three clusters (A, B, and C). Antisocial personality disorder falls into 1 of 4 cluster-B disorders, which also includes borderline, narcissistic, and histrionic. All of these disorders characteristically present with dramatic, emotional, and unpredictable interactions with others.[2] Antisocial personality disorder is the only personality disorder that is not diagnosable in childhood. Before the age of 18, the patient must have been previously diagnosed with conduct disorder (CD) by the age of 15 years old to justify diagnostic criteria for ASPD.[1]

Many researchers and clinicians argue this diagnosis, with concerns of significant overlap with other disorders, including psychopathy. However, others counter that psychopathy is simply a subtype of antisocial personality disorder, with a more severe presentation. Recent literature states that although a heterogeneous construct that can subdivide into multiple subtypes that share many similarities and are often comorbid but not synonymous, individuals with ASPD must be characterized biologically and cognitively to ensure more accurate categorization and appropriate treatment.[3]

Etiology

Although the precise etiology is unknown, both genetic and environmental factors have been found to play a role in the development of ASPD. Various studies in the past have shown differing estimations of heritability, ranging from 38% to 69%. Environmental factors that correlate to the development of antisocial personality disorder include adverse childhood experiences (both physical and sexual abuse, as well as neglect) along with childhood psychopathology (CD and ADHD).[4]

Other studies stress the importance of both shared and non-shared environmental factors, including both family dynamics and peer relations on the development of ASPD. Research has focused on establishing the exact gene contributing to ASPD, and much evidence is pointing toward the 2p12 region of chromosome 2 and variation within AVPR1A. Interactions of specific genes with the environment have been an area of study as well, with evidence of variation in the oxytocin receptor gene (OXTR) contributing to the broad ranges of behavior elicited in antisocial personality disorder due to its effect on the influence of deviant peer affiliation.[5]

Epidemiology

The estimated lifetime prevalence of ASPD amongst the general population falls within 1 to 4%.[6][7] Due to the predicting factor of the initial diagnosis of conduct disorder before the age of 15, this assumption can be quite broad as CD does not always get adequately evaluated.[8] Gender distribution tends to be skewed towards males, with 3 to 5 times more likelihood of being diagnosed with ASPD than females, with 6% men and 2% women within the general population.[9] Substance abuse has been found to show a significant correlation to the diagnosis of antisocial personality disorder,[10] while education and intelligence displays a negative correlation,[9][11] with a higher prevalence of ASPD amongst those with lower IQs and reading levels.[12] Research has shown reductions in the prevalence rate with increasing age in criminal populations,[13] as well as epidemiological samples.[9] Changes in personality traits with age and increased mortality with the behavior of antisocial personality disorder have been hypothesized to justify this age-dependent alteration.[14]

History and Physical

Before performing a comprehensive psychiatric assessment of the patient, a careful history and physical examination is necessary. "The DSM-5 diagnostic criteria for Antisocial Personality Disorder

1. A pervasive pattern of disregard for and violation of the rights of others, since age 15 years, as indicated by three (or more) of the following:

1. Failure to conform to social norms concerning lawful behaviors, such as performing acts that are grounds for arrest.

2. Deceitfulness, repeated lying, use of aliases, or conning others for pleasure or personal profit.

3. Impulsivity or failure to plan.

4. Irritability and aggressiveness, often with physical fights or assaults.

5. Reckless disregard for the safety of self or others.

6. Consistent irresponsibility, failure to sustain consistent work behavior, or honor monetary obligations.

7. Lack of remorse, being indifferent to or rationalizing having hurt, mistreated, or stolen from another person.

2. The individual is at least age 18 years.

3. Evidence of conduct disorder typically with onset before age 15 years.

4. The occurrence of antisocial behavior is not exclusively during schizophrenia or bipolar disorder."

Evaluation

No current diagnostic modalities, such as tests including serology, are currently accepted standards in diagnosing antisocial personality disorder. However, genetic testing and neuroimaging have been used to evaluate potential causes and patterns, respectively, with ASPD (see Etiology section above). Patients with antisocial personality disorder are at a higher risk of contracting certain viral infections and sexually transmitted diseases associated with high-risk behavior, including hepatitis C and human immunodeficiency virus, as well as increased mortality rates due to accidents, traumatic injuries, suicides, and homicides.[15][16][17]

Treatment / Management

Although there has been a multitude of interventions tested in the past, an appropriate algorithm fails to exist today. Literature suggests early treatment intervention with conduct disorder in children as the least costly and most effective with treating ASPD.[18] However, researchers have employed certain psychopharmacology and psychotherapy throughout literature, but due to the severity of potential harms in adulthood, intricate consideration are necessary when delineating a treatment course.[19]

Most of the needs of antisocial personality disorder are addressable in the outpatient setting. Hospitalization is not cost-effective as it provides little to no benefit to those with ASPD, and it is very costly. Also, the presence of those with ASPD in a psychiatric hospital disrupts the environment, thus affecting the treatment of other patients in need of therapeutic care. Hospitalization is reserved for treating co-occurring conditions or possible complications, such as substance intoxication/withdrawal or recent suicidal behavior.

Insufficient evidence exists to support any psychological intervention in adults with ASPD.[20] No pharmacological intervention has been shown to treat ASPD, but medications are highly recommended to treat co-occurring conditions. Aggressive behavior is treatable with second-generation antipsychotics as first-line therapy, including risperidone (2 to 4mg/day), quetiapine (100 to 300mg/day). Second and third-line therapies for aggression include selective serotonin reuptake inhibitors (SSRI), sertraline (100 to 200mg/day) or fluoxetine (20mg/day), and mood stabilizers; lithium and carbamazepine (dosed at recommended levels for bipolar disorder), respectively. Anticonvulsants, such as oxcarbazepine and carbamazepine, can be used to aid with impulsivity. Bupropion and atomoxetine are often used to treat associated ADHD due to their non-addictive nature.

Differential Diagnosis

Narcissistic personality disorder (cluster B personality disorder with overlap; exploitive and uncompassionate, but not aggressive or deceitful)

Borderline personality disorder (cluster B personality disorder with overlap; manipulative, but for reassurance and nurture)

Substance use disorder (Impulsivity and irresponsibility due to substance influence must be ruled out before diagnosing ASPD. ASPD can be diagnosed if substance use is co-occurring)

Prognosis

Of those children with conduct disorder, 25% of girls and 40% of boys will meet the diagnostic criteria for antisocial personality disorder. Boys exhibit symptoms earlier than girls, who often only elicit these symptoms in puberty. Children who do not develop conduct disorder and progress to the age of 15 without antisocial behaviors will not develop ASPD. Childhood conduct disorder is a reliable prognosticator of adulthood ASPD.[1] The small percentage of adults with antisocial personality disorder who never met the criteria or never received an assessment for conduct disorder, tend to have milder symptoms.[21]

Antisocial personality disorder, although a chronic condition with a lifelong presentation, has had moderations shown with advancing ages, with the mean remitted age of 35 years old. Those with less baseline symptomatology showed better-remitted rates. Studies in the past revealed remission rates of 12 to 27% and 27 to 31% rates of improvement, but not remitted. Crime rates and severity reflect this relation as well, with peak crime statistics in late teens and higher severity of crimes at younger ages. Those with later presentations of antisocial behavior showed less severe behavioral problems. Those who were either never imprisoned or imprisoned for longer periods displayed greater remission rates than those imprisoned for shorter periods. This finding indicated that short-term incarceration could be somewhat preventive for future antisocial behavior.[1]

Complications

Many individuals diagnosed with antisocial personality disorder remain a burden to their families, coworkers, and closely associated peers, such as neighbors, despite becoming less troublesome with age. Mental health comorbidities and associated addictive disorders, as well as higher mortality rates due to suicides and homicides, only add to this burden. Most of those who improve with age remain unable to re-claim their lost prospects, including education, domestication, and employment. Those patients who did show remission were more likely to have spousal or family ties, with better social support.[1]

Deterrence and Patient Education

Antisocial personality disorder is one of the best-documented disorders in all of literature pertaining to psychiatry, including etiology, epidemiology, pathophysiology, neuroanatomy, heritability, and interventional treatment. However, an established treatment algorithm and specialized psychopharmacology currently fail to exist.

Better preventative measures are necessary as many of those with ASPD may only have an evaluation upon incarceration after inflicting harm. One is not apt to seek help for ASPD symptomatology. Many only seek assistance for co-occurring mental disorders or only present for court-mandated assessments.

Even with the remission rates in advanced ages, antisocial personality disorder causes much turmoil to the patient and the patient's surrounding community. The lives of those with ASPD remain negatively impacted even after remission.

Enhancing Healthcare Team Outcomes

The diagnosis, categorization, and management of ASPD is quite complex and multifaceted, often only presenting after harm has already taken place. Management of the disorder is best with an interprofessional team dedicated to the treatment of mental health disorders. People with antisocial personality disorder are at risk of incarceration due to the violent and deceitful nature of the behaviors elicited in ASPD. Hospitalization provides no benefit to a patient with ASPD and can actually create a disruptive hospital environment to others who truly need hospitalization for therapeutic purposes. The majority of these individuals are noncompliant with therapy and often fail to show up at clinics. Thus, management can be difficult.

The physician overseeing the case almost inevitably needs to be a psychological specialist; they can work collaboratively with the patient's family physician, but the complexity of this diagnosis requires specist-level care. Nursing staff should also have specialized psychological training, so they have received adequate training on ways to approach and cope with these individuals, as well as to be able to recognize therapeutically significant signs and behaviors that need to be brought to the treating physician's attention. They can also assess patient compliance as well as give their impressions of treatment effectiveness. A pharmacist should also provide consultation on the medications used, verifying dosing and checking carefully for drug interactions, and reporting to the nurse or physician if there are any concerns. Only with a collaborative interprofessional team approach patients with antisocial personality disorder receive optimal care leading to better outcomes. [Level 5]

References

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Antisocial personality disorder (ASPD) is a deeply ingrained and rigid dysfunctional thought process that focuses on social irresponsibility with exploitive, delinquent, and criminal behavior with no remorse.

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Johns Hopkins Medicine Website: Information on Oppositional Defiant Disorder

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Johns Hopkins Medicine Website: Information on Oppositional Defiant Disorder

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What is oppositional defiant disorder (ODD) in children?

Oppositional defiant disorder (ODD) is a type of behavior disorder. It is mostly diagnosed in childhood. Children with ODD are uncooperative, defiant, and hostile toward peers, parents, teachers, and other authority figures. They are more troubling to others than they are to themselves.

What causes ODD in a child?

Researchers don’t know what causes ODD. But there are 2 main theories for why it occurs:

Developmental theory. This theory suggests that the problems start when children are toddlers. Children and teens with ODD may have had trouble learning to become independent from a parent or other main person to whom they were emotionally attached. Their behavior may be normal developmental issues that are lasting beyond the toddler years.

Learning theory. This theory suggests that the negative symptoms of ODD are learned attitudes. They mirror the effects of negative reinforcement methods used by parents and others in power. The use of negative reinforcement increases the child’s ODD behaviors. That’s because these behaviors allow the child to get what he or she wants: attention and reaction from parents or others.

Which children are at risk for ODD?

ODD is more common in boys than in girls. Children with the following mental health problems are also more likely to have ODD:

Mood or anxiety disorders

Conduct disorder

Attention-deficit/hyperactivity disorder (ADHD)

What are the symptoms of ODD in a child?

Most symptoms seen in children and teens with ODD also happen at times in other children without it. This is especially true for children around ages 2 or 3, or during the teen years. Many children tend to disobey, argue with parents, or defy authority. They may often behave this way when they are tired, hungry, or upset. But in children and teens with ODD, these symptoms happen more often. They also interfere with learning and school adjustment. And in some cases, they disrupt the child’s relationships with others.

Symptoms of ODD may include:

Having frequent temper tantrums

Arguing a lot with adults

Refusing to do what an adult asks

Always questioning rules and refusing to follow rules

Doing things to annoy or upset others, including adults

Blaming others for the child’s own misbehaviors or mistakes

Being easily annoyed by others

Often having an angry attitude

Speaking harshly or unkindly

Seeking revenge or being vindictive

These symptoms may look like other mental health problems. Make sure your child sees his or her healthcare provider for a diagnosis.

How is ODD diagnosed in a child?

If you notice symptoms of ODD in your child or teen, you can help by seeking a diagnosis right away. Early treatment can often prevent future problems.

A child psychiatrist or qualified mental health expert can diagnose ODD. He or she will talk with the parents and teachers about the child’s behavior and may observe the child. In some cases, your child may need mental health testing.

How is ODD treated in a child?

Early treatment can often prevent future problems. Treatment will depend on your child’s symptoms, age, and health. It will also depend on how bad the ODD is.

Children with ODD may need to try different therapists and types of therapies before they find what works for them. Treatment may include:

Cognitive-behavioral therapy. A child learns to better solve problems and communicate. He or she also learns how to control impulses and anger.

Family therapy. This therapy helps make changes in the family. It improves communication skills and family interactions. Having a child with ODD can be very hard for parents. It can also cause problems for siblings. Parents and siblings need support and understanding.

Peer group therapy. A child develops better social and interpersonal skills.

Medicines. These are not often used to treat ODD. But a child may need them for other symptoms or disorders, such as ADHD.

How can I help prevent ODD in my child?

Researchers don’t know what causes ODD. But certain approaches can help prevent the disorder. Young children be helped by early intervention programs that teach them social skills and how to deal with anger. For teens, talk therapy (psychotherapy), learning social skills, and getting help with schoolwork can all help reduce problem behaviors. School-based programs can also help to stop bullying and improve relationships among teens.

Parent-management training programs are also important. These programs teach parents how to manage their child’s behavior. Parents learn positive reinforcement methods, and also how to discipline their child.

How can I help my child live with ODD?

Early treatment for your child can often prevent future problems. Here are things you can do to help:

Keep all appointments with your child’s healthcare provider.

Take part in family therapy as needed.

Talk with your child’s healthcare provider about other providers who will be involved in your child’s care. Your child may get care from a team that may include counselors, therapists, social workers, psychologists, and psychiatrists. Your child’s care team will depend on his or her needs and how serious the disorder is.

Tell others about your child’s conduct disorder. Work with your child’s healthcare provider and school to develop a treatment plan.

Reach out for support. Being in touch with other parents who have a child with ODD may be helpful. If you feel overwhelmed or stressed out, talk with your child’s healthcare provider. He or she may direct you to a support group for caregivers of children with ODD.

When should I call my child’s healthcare provider?

Call your child’s healthcare provider right away if your child:

Feels extreme depression, fear, anxiety, or anger toward him or herself or others

Feels out of control

Hears voices that others don’t hear

Sees things that others don’t see

Can’t sleep or eat for 3 days in a row

Shows behavior that concerns friends, family, or teachers, and others express concern about this behavior and ask you to seek help

Call 911 if your child has suicidal thoughts, a suicide plan, and the means to carry out the plan.

Key points about ODD in children

Oppositional defiant disorder (ODD) is a type of behavior disorder. Children with ODD are uncooperative, defiant, and hostile toward peers, parents, teachers, and other authority figures.

Developmental problems may cause ODD. Or the behaviors may be learned.

A child with ODD may argue a lot with adults or refuse to do what they ask. He or she may also be unkind to others.

A mental health expert often diagnoses ODD.

Therapy that helps the child interact better with others is the main treatment. Medicines may be needed for other problems, such as ADHD.

Next steps

Tips to help you get the most from a visit to your child’s healthcare provider:

Know the reason for the visit and what you want to happen.

Before your visit, write down questions you want answered.

At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you for your child.

Know why a new medicine or treatment is prescribed and how it will help your child. Also know what the side effects are.

Ask if your child’s condition can be treated in other ways.

Know why a test or procedure is recommended and what the results could mean.

Know what to expect if your child does not take the medicine or have the test or procedure.

If your child has a follow-up appointment, write down the date, time, and purpose for that visit.

Know how you can contact your child’s provider after office hours. This is important if your child becomes ill and you have questions or need advice.

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Oppositional Defiant Disorder (ODD) in Children

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Oppositional defiant disorder (ODD) is a type of behavior disorder. It is mostly diagnosed in childhood. Children with ODD are uncooperative, defiant, and hostile toward peers, parents, teachers, and other authority figures.

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American Counseling Association: Code of Ethics

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American Counseling Association: Code of Ethics

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Texas Education Agency: Educators' Code of Ethics

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Texas Education Agency: Educators' Code of Ethics

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The Educators' Code of Ethics is set forth in Texas Administrative Code to provide rules for standard practices and ethical conduct toward students, professional colleagues, school officials, parents, and members of the community.

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The Educators' Code of Ethics is set forth in Texas Administrative Code to provide rules for standard practices and ethical conduct toward students, professional colleagues, school officials, parents, and members of the community.

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US Department of Human Health Services Office on Women's Health: Information on Premenstrual Dysphoric Disorder

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US Department of Human Health Services Office on Women's Health: Information on Premenstrual Dysphoric Disorder

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National Eating Disorders Association Website: Avoidant Restrictive Food Intake Disorder

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National Eating Disorders Association Website: Avoidant Restrictive Food Intake Disorder

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Avoidant Restrictive Food Intake Disorder (ARFID)

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Avoidant Restrictive Food Intake Disorder (ARFID) is a new diagnosis in the DSM-5, and was previously referred to as “Selective Eating Disorder.” ARFID is similar to anorexia in that both disorders involve limitations in the amount and/or types of food consumed, but unlike anorexia, ARFID does not i…

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Mayo Clinic Website: Information on Binge-Eating Disorder

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Mayo Clinic Website: Information on Binge-Eating Disorder

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Overview

Binge-eating disorder is a serious eating disorder in which you frequently consume unusually large amounts of food and feel unable to stop eating.

Almost everyone overeats on occasion, such as having seconds or thirds of a holiday meal. But for some people, excessive overeating that feels out of control and becomes a regular occurrence crosses the line to binge-eating disorder.

When you have binge-eating disorder, you may be embarrassed about overeating and vow to stop. But you feel such a compulsion that you can't resist the urges and continue binge eating. If you have binge-eating disorder, treatment can help.

Symptoms

Most people with binge-eating disorder are overweight or obese, but you may be at a normal weight. Behavioral and emotional signs and symptoms of binge-eating disorder include:

Eating unusually large amounts of food in a specific amount of time, such as over a two-hour period

Feeling that your eating behavior is out of control

Eating even when you're full or not hungry

Eating rapidly during binge episodes

Eating until you're uncomfortably full

Frequently eating alone or in secret

Feeling depressed, disgusted, ashamed, guilty or upset about your eating

Frequently dieting, possibly without weight loss

Unlike a person with bulimia, after a binge, you don't regularly compensate for extra calories eaten by vomiting, using laxatives or exercising excessively. You may try to diet or eat normal meals. But restricting your diet may simply lead to more binge eating.

The severity of binge-eating disorder is determined by how often episodes of bingeing occur during a week.

When to see a doctor

If you have any symptoms of binge-eating disorder, seek medical help as soon as possible. Binge-eating problems can vary in their course from short-lived to recurrent or they may persist for years if left untreated.

Talk to your medical care provider or a mental health professional about your binge-eating symptoms and feelings. If you're reluctant to seek treatment, talk to someone you trust about what you're going through. A friend, loved one, teacher or faith leader can help you take the first steps to successful treatment of binge-eating disorder.

Helping a loved one who has symptoms

A person with binge-eating disorder may become an expert at hiding behavior, making it hard for others to detect the problem. If you have a loved one you think may have symptoms of binge-eating disorder, have an open and honest discussion about your concerns.

Provide encouragement and support. Offer to help your loved one find a qualified medical care provider or mental health professional and make an appointment. You might even offer to go along.

Causes

The causes of binge-eating disorder are unknown. But genetics, biological factors, long-term dieting and psychological issues increase your risk.

Risk factors

Binge-eating disorder is more common in women than in men. Although people of any age can have binge-eating disorder, it often begins in the late teens or early 20s.

Factors that can increase your risk of developing binge-eating disorder include:

Family history. You're much more likely to have an eating disorder if your parents or siblings have (or had) an eating disorder. This may indicate that inherited genes increase the risk of developing an eating disorder.

Dieting. Many people with binge-eating disorder have a history of dieting. Dieting or restricting calories during the day may trigger an urge to binge eat, especially if you have symptoms of depression.

Psychological issues. Many people who have binge-eating disorder feel negatively about themselves and their skills and accomplishments. Triggers for bingeing can include stress, poor body self-image and the availability of preferred binge foods.

Complications

You may develop psychological and physical problems related to binge eating.

Complications that may be caused by binge-eating disorder include:

Poor quality of life

Problems functioning at work, with your personal life or in social situations

Social isolation

Obesity

Medical conditions related to obesity, such as joint problems, heart disease, type 2 diabetes, gastroesophageal reflux disease (GERD) and some sleep-related breathing disorders

Psychiatric disorders that are often linked with binge-eating disorder include:

Depression

Bipolar disorder

Anxiety

Substance use disorders

Prevention

Although there's no sure way to prevent binge-eating disorder, if you have symptoms of binge eating, seek professional help. Your medical care provider can advise you on where to get help.

If you think a friend or loved one has a binge-eating problem, steer her or him toward healthier behavior and professional treatment before the situation worsens. If you have a child:

Foster and reinforce a healthy body image, regardless of body shape or size

Discuss any concerns with your child's primary care provider, who may be in a good position to identify early indicators of an eating disorder and help prevent its development

The Mayo Clinic experience and patient stories

Our patients tell us that the quality of their interactions, our attention to detail and the efficiency of their visits mean health care like they've never experienced. See the stories of satisfied Mayo Clinic patients.

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Binge-eating disorder - Symptoms and causes

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Binge-eating disorder is a serious eating disorder in which you frequently consume unusually large amounts of food and feel unable to stop eating. Almost everyone overeats on occasion, such as having seconds or thirds of a holiday meal. But for some people, excessive overeating that feels out of control and becomes a regular occurrence crosses the line to binge-eating disorder.

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Johns Hopkins Medicine Website: Information on Bulimia Nervosa

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Johns Hopkins Medicine Website: Information on Bulimia Nervosa

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Bulimia is an eating disorder. It is characterized by uncontrolled episodes of overeating, called bingeing. This is followed by purging with methods such as vomiting or misuse of laxatives. Bingeing is eating much larger amounts of food than you would normally eat in a short period of time, usually less than 2 hours.

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American Addiction Center Website: Information on Anorexia

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American Addiction Center Website: Information on Anorexia

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Anorexia is a mental health disorder that is recognized in the official American Psychiatry Association guide, the Diagnostic and Statistical Manual of Mental Disorders - 5 (DSM-5).

Anorexia is often discussed in the media or society at large without any reference to its different phases. A person begins to develop anorexia-involved thoughts and actions often long before anyone notices that the disorder is present.

Phases of Anorexia

Anorexia is often associated with its later stages, as the effects are typically highly visible on the affected individual. As a result, the public's conception of anorexia is skewed toward the latter end of its timeline. A more expansive understanding of anorexia could be helpful to individuals who develop this eating disorder. The earlier risks or symptoms can be detected, the more likely it is that appropriate and effective intervention can occur.

Individuals who experience anorexia do not follow the same trajectory of development, nor will they experience the same symptoms. Although there are no established stages, for illustrative purposes, consider the disorder as being spread out over six stages. The following discussion describes some of the hallmarks of each of these phases.

During the first stage, individuals move from mere contemplation of restricting their diets and/or engaging in an intensive exercise program to beginning these activities. At this point, an onlooker may think the person is only being health-conscious or trying to "get in shape." The individual who is dieting and exercising may not yet have a specific intention to go to extremes to meet weight loss goals. At this point, the main health risk will be the side effects associated with sudden weight loss and the risk of developing a more severe case of anorexia or adding in bulimic practices.

When a person loses weight too fast, the following side effects may emerge:

Liver problems: Rapid loss of weight is a risk factor for developing liver damage that may owe to the sudden change in the person's fatty acid levels.

Gallstones: These are hard cholesterol deposits that can cause nausea and abdominal pain. They may progress to the point that the gallbladder needs to be removed.

Lean muscle loss: Losing weight quickly can significantly reduce fat-free mass in the body (i.e., lean muscle tissue and bone), which in turn causes the metabolism to slow down.

Lost skin elasticity: Loose skin may develop on arms, legs, and the abdomen as fat shrinks away faster than the skin can contract.

In the second phase, individuals typically begin to obsess about their level of food intake and/or exercise. As they progress to the third phase, they may keep a detailed journal of daily caloric intake, exercises performed, and subsequent calories burned. As time progresses, a review of these journal entries may reveal less caloric intake and more calories burned. As the food and/or exercise obsession takes hold, individuals will likely be heard complaining about their bodies.

Individuals in this phase often suffer from malnutrition. The following are some of the health risks associated with malnutrition:

Osteoporosis due to low calcium levels in the blood that results in brittle bones

A deterioration of organs, typically with the most damage to the liver and intestines followed by the heart and kidneys

Dehydration

Deficiency in essential vitamins and minerals

Muscle and cartilage deterioration

During the fourth stage, individuals with anorexia may celebrate their body appearance in various ways, such as counting their exposed ribs or checking to see if their collarbone or spine protrudes. These activities may be kept hidden. Individuals may feel good about their thinness but have a sense that others would be concerned. To protect their eating disorder, they may hide its symptoms from others. This stage can be thought of as the beginning of a dangerous downward spiral. Individuals with anorexia may experience any number of serious side effects at this point (discussed below).

The fifth stage may involve a malnourished person "upping the ante," so to speak. The individual may want to accelerate weight loss through extreme behaviors, such as starving to the point of fainting. During this stage, fainting may occur often.

In the sixth stage, the disorder continues to spiral out of control. In addition to fainting spells, the individual may experience any of the following serious health effects:

Suicidal thoughts

In females, loss of menstruation

Substance abuse

In males, lowered testosterone

Anemia

Mitral valve prolapse (abnormal heart rhythms)

Depress, anxiety, or mood disorders

Heart failure

Obsessive-compulsive disorder (OCD)

Gastrointestinal problems, such as irritable bowel syndrome

Low potassium, chloride, and sodium levels (electrolyte balance problems)

Anorexia can be a fatal disorder. Of all mental health disorders, anorexia has the highest rate of fatalities. On average, 5-20 percent of individuals with anorexia will have a fatal outcome. The longer an individual experiences anorexia, the greater the likelihood of fatality. Thankfully, this disorder is treatable, and many, if not all, of the negative health effects can be reversed with proper care.

A Personal Story of Anorexia and Recovery

The Alliance for Eating Disorders Awareness has published, on its official website, the personal story of a young woman named Brenda. Starting in 6th grade, and continuing for nearly 11 years, Brenda considered anorexia to be her friend and thought that a life without her anorexic practices was not worth living. Brenda could never imagine herself in recovery; to her, that would have been like abandoning a much loved and trusted partner. Brenda starved herself, ate then purged, and excessively exercised for years.
Brenda's anorexic behaviors began after a dance teacher advised her that a dance career would be a challenge for her because of her body weight, shape, and size.
Brenda's father was overweight, and she believed that would predispose her to being overweight too. Brenda also trusted her dance teacher, a person she greatly admired and wanted to please. Brenda escalated her efforts to excel in dance, but in severely unhealthy ways. From 7th to 12th grade, Brenda would purge after eating and push her body to be what she perceived to be "perfect" for a dancer, though a doctor would have considered her significantly underweight and malnourished. Being a dancer helped Brenda to deny the reality of her anorexia.

When Brenda entered college, she decided to stop dancing and thought her anorexia would disappear. It did not. Brenda found herself on the college rowing team, rowing up to four hours a day, and obsessing about each calorie she consumed. Although college is a social environment, Brenda withdrew from other students to hide her anorexic practices. She felt she had a problem that made her unlovable. Eventually, during crew training practice, Brenda collapsed.

The Road to Health

Anorexia is a treatable condition that can be effectively addressed with proper rehabilitative care. It's imperative that those suffering from anorexia seek comprehensive care that includes medical supervision and therapeutic counseling. While AAC facilities do not treat anorexia, various reputable centers across the country treat this disorder. With inclusive care, true recovery is possible.

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What Are the Consequences & Health Risks of Anorexia

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Anorexia is a mental health disorder that is recognized in the official American Psychiatry Association guide, the Diagnostic and Statistical Manual of Mental Disorders - 5 (DSM-5). Anorexia is often discussed in the media or society at large without any reference to its different phases.

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National Eating Disorders Association's Parent Toolkit:
https://www.nationaleatingdisorders.org/sites/default/files/Toolkits/ParentToolkit.pdf

Kelty Eating Disorders Parents Survive to Thrive Guide:
https://keltyeatingdisorders.ca/wp-content/uploads/2016/09/BCMH026_EatingDisorder_FullGuide_v6-Web.pdf

Dallas Eating Recovery Center Website:
https://www.eatingrecoverycenter.com/recovery-centers/dallas

Dallas Center for Change Inpatient Eating Disorder Facility:
https://centerforchange.com/treatment/levels-of-care/acute-inpatient-treatment/

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Texas Education Agency Website: 504 Plans in Education

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Texas Education Agency Website: 504 Plans in Education

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What is Section 504

The U.S. Department of Education enforces Section 504 of the Rehabilitation Act of 1973, as amended, (Section 504) a civil rights statute which prohibits discrimination against individuals with disabilities. The Office for Civil Rights (OCR) also enforces Title II of the Americans with Disabilities Act of 1990 (Title II), which extends this prohibition against discrimination to the full range of state and local government services, programs, and activities (including public schools) regardless of whether they receive any Federal financial assistance. The Americans with Disabilities Act Amendments Act of 2008 (Amendments Act), effective January 1, 2009, amended the Americans with Disabilities Act of 1990 (ADA) and included a conforming amendment to the Rehabilitation Act of 1973 (Rehabilitation Act) that affects the meaning of disability in Section 504. The standards adopted by the ADA were designed not to restrict the rights or remedies available under Section 504. The Title II regulations applicable to free appropriate public education issues do not provide greater protection than applicable Section 504 regulations. This guidance focuses primarily on Section 504.

Section 504 prohibits discrimination on the basis of disability in programs or activities that receive Federal financial assistance from the U.S. Department of Education. For more details, please refer to the United States Department of Education Section 504 Frequently Asked Questions document.

Students protected under Section 504

Section 504 covers qualified students with disabilities who attend schools receiving Federal financial assistance. To be protected under Section 504, a student must be determined to: (1) have a physical or mental impairment that substantially limits one or more major life activities; or (2) have a record of such an impairment; or (3) be regarded as having such an impairment. Section 504 requires that school districts provide a free appropriate public education (FAPE) to qualified students in their jurisdictions who have a physical or mental impairment that substantially limits one or more major life activities. For more details, please refer to the United States Department of Education Section 504 Frequently Asked Questions document.

Evaluation

At the elementary and secondary school level, determining whether a child is a qualified disabled student under Section 504 begins with the evaluation process. Section 504 requires the use of evaluation procedures that ensure that children are not misclassified, unnecessarily labeled as having a disability, or incorrectly placed, based on inappropriate selection, administration, or interpretation of evaluation materials. For more details, please refer to the United States Department of Education Section 504 Frequently Asked Questions document.

Placement

Once a student is identified as being eligible for regular or special education and related aids or services, a decision must be made regarding the type of services the student needs. For more details, please refer to the United States Department of Education Section 504 Frequently Asked Questions document.

Procedural Safeguards

Public elementary and secondary schools must employ procedural safeguards regarding the identification, evaluation, or educational placement of persons who, because of disability, need or are believed to need special instruction or related services. For more details, please refer to the United States Department of Education Section 504 Frequently Asked Questions document.

How to file a complaint

Online: You may file a complaint with OCR using OCR's electronic complaint form at the following website: http://www.ed.gov/about/offices/list/ocr/complaintintro.html.

Mail or Facsimile: You may mail or send by facsimile information to the address or phone number available at this link. You may use OCR's Discrimination Complaint Form or write your own letter. If you write your own letter, please include:

The complainant's name, address and, if possible (although not required), a telephone number where the complainant may be reached during business hours;

Information about the person(s) or class of persons injured by the alleged discriminatory act(s) (names of the injured person(s) are not required);

The name and location (city and state) of the institution that committed the alleged discriminatory act(s); and

A description of the alleged discriminatory act(s) in sufficient detail to enable OCR to understand what occurred, when it occurred, and the basis for the alleged discrimination.

Email: You may email OCR's Discrimination Complaint Form or your own signed letter to . If you write your own letter, please include the information identified above

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The U.S. Department of Education enforces Section 504 of the Rehabilitation Act of 1973, as amended, (Section 504) a civil rights statute which prohibits discrimination against individuals with disabilities. The Office for Civil Rights (OCR) also enforces Title II of the Americans with Disabilities…

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US Department of Education Website: Info on the Individuals with Disabilities Education Act

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US Department of Education Website: Info on the Individuals with Disabilities Education Act

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Individuals with Disabilities Education Act

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The Individuals with Disabilities Education Act (IDEA) is a law that makes available a free appropriate public education to eligible children with disabilities throughout the nation and ensures special education and related services to those children.

The IDEA governs how states and public agencies provide early intervention, special education, and related services to more than 8 million (as of school year 2022-23) eligible infants, toddlers, children, and youth with disabilities.

Infants and toddlers, birth through age 2, with disabilities and their families receive early intervention services under IDEA Part C. Children and youth ages 3 through 21 receive special education and related services under IDEA Part B.

Additionally, the IDEA authorizes:

Formula grants to states to support special education and related services and early intervention services.

Discretionary grants to state educational agencies, institutions of higher education, and other nonprofit organizations to support research, demonstrations, technical assistance and dissemination, technology development, personnel preparation and development, and parent-training and -information centers.

Congress reauthorized the IDEA in 2004 and most recently amended the IDEA through Public Law 114-95, the Every Student Succeeds Act, in December 2015.

In the law, Congress states:

Disability is a natural part of the human experience and in no way diminishes the right of individuals to participate in or contribute to society. Improving educational results for children with disabilities is an essential element of our national policy of ensuring equality of opportunity, full participation, independent living, and economic self-sufficiency for individuals with disabilities.

Other Laws for Children with Disabilities

The U.S. Department of Education's Office for Civil Rights (OCR) provides additional resources of interest for individuals with disabilities and their families.

OCR does not enforce the IDEA; however, OCR does enforce the Rehabilitation Act of 1973, Section 504 and Americans with Disabilities Act of 1990, Title II rights of IDEA-eligible students with disabilities.

To learn more, visit the OCR's Frequently Asked Questions About Section 504 and the Education of Children with Disabilities.

Visit OCR's website for additional resources.

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About IDEA - Individuals with Disabilities Education Act

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The IDEA is a law that makes available a free appropriate public education to eligible children with disabilities throughout the nation and ensures special education and related services to those children.

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National Institute of Mental Health Website: Bipolar Disorder Symptoms, Causes, Prevention, Treatment

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National Institute of Mental Health Website: Bipolar Disorder Symptoms, Causes, Prevention, Treatment

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National Institute of Mental Health (NIMH)

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Overview

Bipolar disorder (formerly called manic-depressive illness or manic depression) is a mental illness that causes unusual shifts in a person's mood, energy, activity levels, and concentration. These shifts can make it difficult to carry out day-to-day tasks.

There are three types of bipolar disorder. All three types involve clear changes in mood, energy, and activity levels. These moods range from periods of extremely "up," elated, irritable, or energized behavior (known as manic episodes) to very "down," sad, indifferent, or hopeless periods (known as depressive episodes). Less severe manic periods are known as hypomanic episodes.

Bipolar I disorder is defined by manic episodes that last for at least 7 days (nearly every day for most of the day) or by manic symptoms that are so severe that the person needs immediate medical care. Usually, depressive episodes occur as well, typically lasting at least 2 weeks. Episodes of depression with mixed features (having depressive symptoms and manic symptoms at the same time) are also possible. Experiencing four or more episodes of mania or depression within 1 year is called "rapid cycling."

Bipolar II disorder is defined by a pattern of depressive episodes and hypomanic episodes. The hypomanic episodes are less severe than the manic episodes in bipolar I disorder.

Cyclothymic disorder (also called cyclothymia) is defined by recurring hypomanic and depressive symptoms that are not intense enough or do not last long enough to qualify as hypomanic or depressive episodes.

Sometimes a person might experience symptoms of bipolar disorder that do not match the three categories listed above, and this is referred to as "other specified and unspecified bipolar and related disorders."

Bipolar disorder is often diagnosed during late adolescence (teen years) or early adulthood. Sometimes, bipolar symptoms can appear in children. Although the symptoms may vary over time, bipolar disorder usually requires lifelong treatment. Following a prescribed treatment plan can help people manage their symptoms and improve their quality of life.

Signs and symptoms

Risk factors

Treatments and therapies

Join a study

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Learn about bipolar disorder, including signs and symptoms, types, risk factors, how it is diagnosed, and potential treatments and therapies.

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Mayo Clinic Website: Major Depressive Disorder Symptoms, Causes, Prevention, Treatment

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Mayo Clinic Website: Major Depressive Disorder Symptoms, Causes, Prevention, Treatment

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Overview

What is depression? A Mayo Clinic expert explains.

Learn more about depression from Craig Sawchuk, Ph.D., L.P., clinical psychologist at Mayo Clinic.

Hi, I'm Dr. Craig Sawchuk, a clinical psychologist at Mayo Clinic. And I'm here to talk with you about depression. Whether you're looking for answers for yourself, a friend, or loved one, understanding the basics of depression can help you take the next step.

What is depression?

Depression is a mood disorder that causes feelings of sadness that won't go away. Unfortunately, there's a lot of stigma around depression. Depression isn't a weakness or a character flaw. It's not about being in a bad mood, and people who experience depression can't just snap out of it. Depression is a common, serious, and treatable condition. If you're experiencing depression, you're not alone. It honestly affects people of all ages and races and biological sexes, income levels and educational backgrounds. Approximately one in six people will experience a major depressive episode at some point in their lifetime, while up to 16 million adults each year suffer from clinical depression. There are many types of symptoms that make up depression. Emotionally, you may feel sad or down or irritable or even apathetic. Physically, the body really slows down. You feel tired. Your sleep is often disrupted. It's really hard to get yourself motivated. Your thinking also changes. It can just be hard to concentrate. Your thoughts tend to be much more negative. You can be really hard on yourself, feel hopeless and helpless about things. And even in some cases, have thoughts of not wanting to live. Behaviorally, you just want to pull back and withdraw from others, activities, and day-to-day responsibilities. These symptoms all work together to keep you trapped in a cycle of depression. Symptoms of depression are different for everyone. Some symptoms may be a sign of another disorder or medical condition. That's why it's important to get an accurate diagnosis.

What causes depression?

While there's no single cause of depression, most experts believe there's a combination of biological, social, and psychological factors that contribute to depression risk. Biologically, we think about genetics or a family history of depression, health conditions such as diabetes, heart disease or thyroid disorders, and even hormonal changes that happen over the lifespan, such as pregnancy and menopause. Changes in brain chemistry, especially disruptions in neurotransmitters like serotonin, that play an important role in regulating many bodily functions, including mood, sleep, and appetite, are thought to play a particularly important role in depression. Socially stressful and traumatic life events, limited access to resources such as food, housing, and health care, and a lack of social support all contribute to depression risk. Psychologically, we think of how negative thoughts and problematic coping behaviors, such as avoidance and substance use, increase our vulnerability to depression.

The good news is that treatment helps. Effective treatments for depression exist and you do have options to see what works best for you. Lifestyle changes that improve sleep habits, exercise, and address underlying health conditions can be an important first step. Medications such as antidepressants can be helpful in alleviating depressive symptoms. Therapy, especially cognitive behavioral therapy, teaches skills to better manage negative thoughts and improve coping behaviors to help break you out of cycles of depression. Whatever the cause, remember that depression is not your fault and it can be treated.

To help diagnose depression, your health care provider may use a physical exam, lab tests, or a mental health evaluation. These results will help identify various treatment options that best fit your situation.

Help is available. You don't have to deal with depression by yourself. Take the next step and reach out. If you're hesitant to talk to a health care provider, talk to a friend or loved one about how to get help. Living with depression isn't easy and you're not alone in your struggles. Always remember that effective treatments and supports are available to help you start feeling better. Want to learn more about depression? Visit mayoclinic.org. Do take care.

Depression is a mood disorder that causes a persistent feeling of sadness and loss of interest. Also called major depressive disorder or clinical depression, it affects how you feel, think and behave and can lead to a variety of emotional and physical problems. You may have trouble doing normal day-to-day activities, and sometimes you may feel as if life isn't worth living.

More than just a bout of the blues, depression isn't a weakness and you can't simply "snap out" of it. Depression may require long-term treatment. But don't get discouraged. Most people with depression feel better with medication, psychotherapy or both.
Depression care at Mayo Clinic
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Symptoms

Although depression may occur only once during your life, people typically have multiple episodes. During these episodes, symptoms occur most of the day, nearly every day and may include:

Feelings of sadness, tearfulness, emptiness or hopelessness

Angry outbursts, irritability or frustration, even over small matters

Loss of interest or pleasure in most or all normal activities, such as sex, hobbies or sports

Sleep disturbances, including insomnia or sleeping too much

Tiredness and lack of energy, so even small tasks take extra effort

Reduced appetite and weight loss or increased cravings for food and weight gain

Anxiety, agitation or restlessness

Slowed thinking, speaking or body movements

Feelings of worthlessness or guilt, fixating on past failures or self-blame

Trouble thinking, concentrating, making decisions and remembering things

Frequent or recurrent thoughts of death, suicidal thoughts, suicide attempts or suicide

Unexplained physical problems, such as back pain or headaches

For many people with depression, symptoms usually are severe enough to cause noticeable problems in day-to-day activities, such as work, school, social activities or relationships with others. Some people may feel generally miserable or unhappy without really knowing why.

Depression symptoms in children and teens

Common signs and symptoms of depression in children and teenagers are similar to those of adults, but there can be some differences.

In younger children, symptoms of depression may include sadness, irritability, clinginess, worry, aches and pains, refusing to go to school, or being underweight.

In teens, symptoms may include sadness, irritability, feeling negative and worthless, anger, poor performance or poor attendance at school, feeling misunderstood and extremely sensitive, using recreational drugs or alcohol, eating or sleeping too much, self-harm, loss of interest in normal activities, and avoidance of social interaction.

Depression symptoms in older adults

Depression is not a normal part of growing older, and it should never be taken lightly. Unfortunately, depression often goes undiagnosed and untreated in older adults, and they may feel reluctant to seek help. Symptoms of depression may be different or less obvious in older adults, such as:

Memory difficulties or personality changes

Physical aches or pain

Fatigue, loss of appetite, sleep problems or loss of interest in sex - not caused by a medical condition or medication

Often wanting to stay at home, rather than going out to socialize or doing new things

Suicidal thinking or feelings, especially in older men

When to see a doctor

If you feel depressed, make an appointment to see your doctor or mental health professional as soon as you can. If you're reluctant to seek treatment, talk to a friend or loved one, any health care professional, a faith leader, or someone else you trust.

When to get emergency help

If you think you may hurt yourself or attempt suicide, call 911 in the U.S. or your local emergency number immediately.

Also consider these options if you're having suicidal thoughts:

Call your doctor or mental health professional.

Contact a suicide hotline.

In the U.S., call or text 988 to reach the 988 Suicide & Crisis Lifeline, available 24 hours a day, seven days a week. Or use the Lifeline Chat. Services are free and confidential.

U.S. veterans or service members who are in crisis can call 988 and then press "1" for the Veterans Crisis Line. Or text 838255. Or chat online.

The Suicide & Crisis Lifeline in the U.S. has a Spanish language phone line at 1-888-628-9454 (toll-free).

Reach out to a close friend or loved one.

Contact a minister, spiritual leader or someone else in your faith community.

If you have a loved one who is in danger of suicide or has made a suicide attempt, make sure someone stays with that person. Call 911 or your local emergency number immediately. Or, if you think you can do so safely, take the person to the nearest hospital emergency room.

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Causes

It's not known exactly what causes depression. As with many mental disorders, a variety of factors may be involved, such as:

Biological differences. People with depression appear to have physical changes in their brains. The significance of these changes is still uncertain, but may eventually help pinpoint causes.

Brain chemistry. Neurotransmitters are naturally occurring brain chemicals that likely play a role in depression. Recent research indicates that changes in the function and effect of these neurotransmitters and how they interact with neurocircuits involved in maintaining mood stability may play a significant role in depression and its treatment.

Hormones. Changes in the body's balance of hormones may be involved in causing or triggering depression. Hormone changes can result with pregnancy and during the weeks or months after delivery (postpartum) and from thyroid problems, menopause or a number of other conditions.

Inherited traits. Depression is more common in people whose blood relatives also have this condition. Researchers are trying to find genes that may be involved in causing depression.

Risk factors

Depression often begins in the teens, 20s or 30s, but it can happen at any age. More women than men are diagnosed with depression, but this may be due in part because women are more likely to seek treatment.

Factors that seem to increase the risk of developing or triggering depression include:

Certain personality traits, such as low self-esteem and being too dependent, self-critical or pessimistic

Traumatic or stressful events, such as physical or sexual abuse, the death or loss of a loved one, a difficult relationship, or financial problems

Blood relatives with a history of depression, bipolar disorder, alcoholism or suicide

Being lesbian, gay, bisexual or transgender, or having variations in the development of genital organs that aren't clearly male or female (intersex) in an unsupportive situation

History of other mental health disorders, such as anxiety disorder, eating disorders or post-traumatic stress disorder

Abuse of alcohol or recreational drugs

Serious or chronic illness, including cancer, stroke, chronic pain or heart disease

Certain medications, such as some high blood pressure medications or sleeping pills (talk to your doctor before stopping any medication)

Complications

Depression is a serious disorder that can take a terrible toll on you and your family. Depression often gets worse if it isn't treated, resulting in emotional, behavioral and health problems that affect every area of your life.

Examples of complications associated with depression include:

Excess weight or obesity, which can lead to heart disease and diabetes

Pain or physical illness

Alcohol or drug misuse

Anxiety, panic disorder or social phobia

Family conflicts, relationship difficulties, and work or school problems

Social isolation

Suicidal feelings, suicide attempts or suicide

Self-mutilation, such as cutting

Premature death from medical conditions

Prevention

There's no sure way to prevent depression. However, these strategies may help.

Take steps to control stress, to increase your resilience and boost your self-esteem.

Reach out to family and friends, especially in times of crisis, to help you weather rough spells.

Get treatment at the earliest sign of a problem to help prevent depression from worsening.

Consider getting long-term maintenance treatment to help prevent a relapse of symptoms.

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Depression (major depressive disorder) - Symptoms and causes

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Depression is a mood disorder that causes a persistent feeling of sadness and loss of interest and can interfere with your daily functioning.

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ASCA School Counselor Professional Standards & Competencies Website

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ASCA School Counselor Professional Standards & Competencies Website

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Module 4: Bipolar & Depressive Disorders Infographic

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Module 4: Bipolar & Depressive Disorders Infographic

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Module 3: Educating Others on Feeding and Eating Disorders Presentation

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Educating Others on Feeding and Eating Disorders_ How Parents & College Counseling Can Work Together

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Module 2: Anxiety Education and Intervention Infographic

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Module 2: Anxiety Education and Intervention Infographic

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