1. Age-related Cognitive Decline (780.93)

• DSM-IV-TR criteria
  • Individuals with age-related cognitive decline disorder may report problems remembering names or appointments or may experience difficulty in solving complex problems. This category should be considered only after it has been determined that the cognitive impairment is not attributable to a specific mental disorder or neurological condition.
  • Age-related cognitive decline (ARCD) resembles dementia because memory loss is a major indication of the cognitive dysfunction, but in order for the condition to be considered dementia, the DSM says that memory loss must be present along with a cognitive disturbance such as aphasia, apraxia, agnosia, or a disturbance in executive functioning. It is coded under “Additional Conditions That May Be a Focus of Clinical Attention,” because at this time it is only considered a condition, rather than a disease.
• Associated features
  • Individuals with ARCD are typically around the age of 65 begin to show declining rates of cognitive memory. Individuals with this disorder, experience deterioration in memory, learning, attention, concentration, thinking, use of language, and other mental functions. Even though research has shown that cognition naturally declines with age progression, those with ARCD present with more of a neurological loss than normal age related cognitive loss; however, it is not as severe or as rapidly progressive as those with Alzheimer’s disease or dementia. Individuals with ARCD may also show difficulties in new tasks, complex problem solving and use of language.
• Child vs. adult presentation
  • ARCD is commonly seen in adults around the age of 65. Research has shown that severe brain damage affecting functional cognition can mimic ARCD at any age, but individuals suffering from brain damage would not be considered candidates for ARCD classification. Cognitive skills will peak by age 22 and then show natural regression by around 27, however, the average age for memory decline is around 37 (Salthouse, 2009).
• Gender and cultural differences in presentation
  • Females are much more likely than males to develop age-related cognitive decline, it could have a strong correlation to the general finding that women outlive men. One study has also suggested that it might be due to the decline of estrogenic milieu after menopause (Markowska, 1999).
  • A 2004 Gerontology study performed by Aartsen, Martin, and Zimprich concludes that there is not a gender difference in cognitive function decline, despite more evidence for stronger age-related atrophy of the brain structure in men.
  • Overall culturally, there has not been enough research to show findings of any major cultural differences, although there has been a few studies done in specific areas of the world such as Mexico, Italy, and Israel. Each study showed that educational, cultural, and environmental influences, such as dietary or activity levels, had a significant effect on the development of ARCD.
  • ARCD is the result of a natural process because of an inability to live forever. Just as the skin will lose its firmness, the brain will not perform as it did in its early 20’s. The natural aging process is not culturally valued in the United States, or seen as something to be desired. As the brain ages, memory fades, and as a result, bad decisions and socially unacceptable behavior may occur. Our culture offers retirement/nursing homes as an option to those families who do not have the capabilities to cope with their aging family members. Other cultures, do not offer such remedies, nor do they view aging as undesirable. Many cultures practice family blending as a means of support to family members both young and old.
• Epidemiology
  • Of the older adults who are diagnosed with ARCD, about 30% of them are diagnosed between the ages of 70 to 74, and only about 20% are diagnosed after the age of 75.
  • In a study done about cardiovascular disease and disease related cognitive decline, even healthy older people show a decline in global cognition and memory function with aging. On a conceptual basis and non-sociological status it still remains controversial.
• Etiology
  • Age-related cognitive decline is a condition that is developed over a long period of time, and studies have shown that it is more based on environmental effects than genetic development. Studies have shown that poor dietary and decreased mobility issues can increase risks of developing ARCD. High intake of saturated fatty acids has negative effects on cognition and is linked to contributing to ARCD. Vitamin B6 and B12 deficiencies in older adults have also been thought to lead to ARCD.
  • Other types of individuals have been found to have high risks of developing ARCD. Lower education or lower cognition might also be a cause of ARCD. Individuals with Down syndrome are at an increasingly high risk of developing ARCD, and possibly Alzheimer’s disease, because of their lower than normal cognition and continued decline with age. Studies have also shown that those with a history of depression or mood disorders are at more risk for age-related cognitive decline and later manifest into dementia (Gualtieri & Johnson, 2008).
  • Much research has found that an individual’s socioeconomic status can greatly contribute to functional cognitive decline. In a 2003 Maatrich Brain and Behavior Institute study, it concludes that individuals coming from lower socioeconomic statuses receive substandard education, and therefore, will be more likely to perform jobs that do not require a great amount of cognition. This results in the under-stimulation of cognition, which greatly enhances the risk of getting ARCD earlier in life.
• Empirically supported treatments
  • There is no drugs currently used to treat ARCD, but there are many experimental drugs, herbal remedies, and dietary changes that have been shown to dramatically reduce or reverse the effects of ARCD, or improve cognitive functioning drastically. Experimental drugs such as Hydergine, Gerimal, and Oxiracetam are among the top medical treatments being studied as possible treatments for ARCD, but none have shown more results than the others. Acetyl-L-carnitine has been repeatedly studied in mild cases of ARCD and has shown significantly improved cognitive functioning in a very short time with effects lasting about a month after the studies were stopped. Vitamin B6 and B12 supplements could improve cognition and long-term memory in adults who suffer from those deficiencies.
  • Herbal remedies have been studied with repeated conclusions that ginkgo is the most effective supplement for ARCD. Ginkgo has ingredients in it that enhances memory and concentration, which show moderate improvements in people being treated for ARCD. Mild memory loss has also been shown to be improved by Huperzine A more than some experimental drugs on the market.
  • A healthy diet and exercise has also been shown to be extremely important measure used to prevent and or reduce the effects associated with age-related cognitive decline. Antioxidants that can be found in fruits and vegetables help minimize the risk for ARCD. Also, it has been found that an increase in monounsaturated and polyunsaturated fatty acids will improve cognitive functioning and help prevent against the development of dementia (Solfrizzi, 2008). Staying active and exercising can improve blood flow to the brain and help memory, cognition, and other aspects of the body to prevent, or reduce, the risk of ARCD, or other cognitive disorders.
  • A six year study of more than 3,000 participants suggested that eating fish at least once per week slowed the progression of ARCD by 3-4 years. The Rush University Medical Center study was not able to distinguish what substance from fish caused the actual slow-down in cognitive decline. They did rule-out Omega-3 fatty acids as being associated with their results.
  • There is intense interest in the studies related to the potential of phytochemical-rich foods to prevent age-related neurodegeneration and cognitive decline. Recent evidence has indicated that a group of plant-derived compounds known as flavonoids may exert particularly powerful actions on mammalian cognition and may reverse age-related declines in memory and learning. In particular, evidence suggests that foods rich in three specific flavonoid sub-groups, the flavanols, anthocyanins and/or flavanones, possess the greatest potential to act on the cognitive processes (Spencer, 2010).

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2. Pathological Gambling (312.21)

• DSM-IV-TR criteria:
• A. Persistent and recurrent maladaptive gambling behavior as indicated by five (or more) of the following:
  • (1) is preoccupied with gambling (e.g., preoccupied with reliving past gambling experiences, handicapping or planning the next venture, or thinking of ways to get money with which to gamble)
  • (2) needs to gamble with increasing amounts of money in order to achieve the desired excitement
  • (3) has repeated unsuccessful efforts to control, cut back, or stop gambling
  • (4) is restless or irritable when attempting to cut down or stop gambling
  • (5) gambles as a way of escaping from problems or of relieving a dysphoric mood (e.g., feelings of helplessness, guilt, anxiety, depression)
  • (6) after losing money gambling, often returns another day to get even (“chasing” one’s losses)
  • (7) lies to family members, therapist, or others to conceal the extent of involvement with gambling
  • (8) has committed illegal acts such as forgery, fraud, theft, or embezzlement to finance gambling
  • (9) has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling
  • (10) relies on others to provide money to relieve a desperate financial situation caused by gambling
• B. The gambling behavior is not better accounted for by a Manic Episode.

Associated features

• Pathological gambling (PG) is characterized as a chronic, progressively maladaptive, impulse control disorder that is distinguished by continued acts of PG despite compounding severe negative consequences. Individuals who suffer from PG often have problematic interpersonal relationships. These relationships become increasingly strained during the progression of the disorder. In one extreme, individuals with PG may try to legally finance gambling and living expenses through loans. To a higher extreme, individuals may also commit illegal acts such as forgery, fraud, theft, or embezzlement in order to gain financing.There is evidence to support comorbidity of PG and alcohol and depression. A 1992 study showed that 12.9% of heavy drinkers had a gambling problem as compared to 5% of nondrinkers. Comorbidity rates of PG and major depressive disorder can reach as high as 76%. Other associated features of PG include: unemployment, substance abuse, and suicide attempts. Most pathological gamblers tend to deny their problem and therefore do not get help. The South Oaks Gambling Screen (SOGS) is a very common and validated tool used to assess gamblers. Associated features also include repetitive behaviors which shares features with obsessive compulsive disorder.

Child vs. adult presentation

• Historically, PG has been stereotyped as an adult disorder, but with the vast growth of casino expansion and the creation of internet gambling, adolescent rates of PG have superseded adult prevalence rates by two to four times. According to a 2006 Adolescent Psychiatry article written by Timothy W. Fong, gambling is a media-driven, socially acceptable form of behavior. Fong also states that 86% to 93% of all adolescents have gambled for money at least once, 75% of those did it within the confines of their home, while 85% of parents did not care. He states that adolescent gambling is the most popular risk taking behavior seen in adolescents, trumping cigarettes, alcohol, drugs, and sex. The reasons why adolescents start gambling vs. reasons why adults start gambling are very different. Adolescents start because: it is a form of excitement and relief of boredom, a need to keep playing for spectator success, use gambling as a coping mechanism or relief from daily stress, and lastly, it is a socially acceptable form of competition.

Gender and cultural differences in presentation

• More men are typically diagnosed with pathological gambling than women, and men tend to start sooner. The gender ratio is 2:1 with men being twice more likely than women. Culturally, PG is more prevalent in minority groups. Socioeconomic status also strongly correlates to PG and it is more prevalent in the lower class, who cannot afford to gamble. Pathological gambling affects 2%-5% of Americans, where symptoms and means of gambling vary.

Epidemiology

• As gambling facilities become more prevalent, so do PG prevalence rates. In fact, 2 million Americans are considered to be pathological gamblers, with another 3 million considered being “problematic gamblers,” and 15 million more considered to be at risk. There is a 4% prevalence rate in America, while prevalence rates vary in other countries. Worldwide rates vary from 2% to 6%. Gambling usually begin in early adolescence in men, and from ages 20-40 in women.

Etiology

• The causes do not seem to be biologically related due to the lack of evidence. A psychological cause, however, is more likely. A pathological gambler typically has symptoms of depression or alcoholic tendencies. They usually turn to gambling to get the “high” of winning to escape from everyday problems or more serious life problems.
• PG is consistently associated with blunted mesolimbic-prefrontal cortex activation to nonspecific rewards, whereas these areas show increased activation when exposed to gambling-related stimuli in cue exposure paradigms. Very little is known, and hence more research is needed regarding the neural underpinnings of impulsivity and decision making in PG (van Holst, van den Brink, Veltman, & Gourdriaan, 2010).
• Empirically supported treatments
• Treatment consists of therapy. He/she must first realize that they do indeed have a problem and that they need help. Announcing this to friends and family is usually best. Treatment is based on behavior changes. The counselor will usually start by uncovering the underlying cause of the gambling addiction. If the patient is depressed then the depression is treated accordingly. For the 85% who stay in treatment, it is successful. On average, however, 50% drop out. Aversion therapy is an option. Here the patient is exposed to the stimulus while also being exposed to something that would cause them discomfort. Treatments usually try to help the patient overcome their impulses and learn to control urges. Also, the gambler must learn to overcome the illusion that they will “win the next time.” There are also self-help groups like gamblers anonymous that the patient can join. Groups for the family like Gam-Anon are also available. It is often recommended that he/she never return to gambling. It is also recommended that he/she does not return even to the places that they have gambled. Returning could cause a relapse. Medications such as antidepressants and opioid antagonists (naltrexone) may help also.
• Includes schizophrenia, mood problems, antisocial personality disorder, alcohol, or cocaine addiction.
• Brief intervention, motivational interviewing and cognitive and behaviour therapy are effective treatments. Treatment could be delivered in individual or group-format. Most studies proposed abstinence-based treatments (Khazaal, 2010).
• Dsm5 Proposed Changes
• The work group has proposed that this diagnosis be reclassified from Impulse-Control Disorders Not Elsewhere Classified to Substance Related Disorders which will be renamed to Addiction and Related Disorders
• Disordered Gambling:
• A. Persistent and recurrent maladaptive gambling behavior as indicated by five (or more) of the following:1. is preoccupied with gambling (e.g., preoccupied with reliving past gambling experiences, handicapping or planning the next venture, or thinking of ways to get money with which to gamble
  2. needs to gamble with increasing amounts of money in order to achieve the desired excitement
  3. has repeated unsuccessful efforts to control, cut back, or stop gambling
  4. is restless or irritable when attempting to cut down or stop gambling
  5. gambles as a way of escaping from problems or of relieving a dysphoric mood (e.g., feelings of helplessness, guilt, anxiety, depression)
  6. after losing money gambling, often returns another day to get even (“chasing” one’s losses)
  7. lies to family members, therapist, or others to conceal the extent of involvement with gambling
  8. has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling
  9. relies on other to provide money to relieve a desperate financial situation caused by gambling
  B. The gambling behavior is not better accounted for by a Manic Episode.
  Rationale for Change: Pathological (disordered) gambling has commonalities in clinical expression, etiology, comorbidity, physiology and treatment with Substance Use Disorders
  Lowered Threshold for Pathological (Disordered) Gambling Diagnosis
  Several empirical studies have supported lowering the threshold for a diagnosis of pathological (disordered) gambling. Statistical analyses bearing on this issue are also in progress.
  Eliminate Illegal Act Criterion for Pathological (Disordered) Gambling Diagnosis
  The illegal act criterion of pathological (disordered) gambling has been shown to have a low prevalence with its elimination having little or no effect on prevalence and little effect on the information associated with the diagnosis in the aggregate.
  Severity:
  Recommendations for severity criteria for this disorder are forthcomingDrug Shows Promise in Treating Gambling Addiction

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3. Body Dysmorphic Disorder (300.7)

• DSM-IV-TR criteria
  • A. Preoccupation with an imagined defect in appearance. If slight physical abnormality is present, the person’s concern is markedly excessive.
  • B. The preoccupation causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  • C. The preoccupation is not better accounted for by another mental disorder (e.g., dissatisfaction with body shape and size in Anorexia Nervosa).
• Associated features
  • The preoccupations associated with body dysmorphic disorder (BDD) are commonly described as being repetitive, excessive, obsessive, compulsive, ritualized, distressing, impairing, time-consuming, and somewhat less often, delusional. Symptoms usually appear suddenly, with onset during times of extreme psychosocial stress. The similarities in descriptions of preoccupation frequently cause a misdiagnosis of obsessive-compulsive disorder (OCD), however, the comorbidity of OCD and BDD is relatively common. Other common comorbidities include, but not limited to; mood disorders (major depressive disorder), anxiety disorders (social phobia), substance use, eating disorders (anorexia nervosa), and personality disorders (borderline personality disorder). Examples of preoccupations include behaviors that seek to examine, improve, or hide perceived defects leading to time consuming functional impairments. Activities associated with preoccupations include obsessions in: grooming; mirror checking, hair brushing, hair styling, hair cutting, shaving, washing, and application of makeup. Camouflaging: wearing wigs, hats, make-up, sunglasses, extra clothing and changing body position to hide perceived defect. Medical procedures: numerous dermatological visits, and multiple cosmetic surgeries. Need for reassurance: mirror checking, asking others opinion, and excessive comparison to other people. Diet and exercise: excessive exercise, muscle dysmorphia, steroid usage; excessive diet, anorexia nervosa, and bulimia nervosa (eating disorders). The most common preoccupations of the body focus primarily on the skin, hair, and nose. People diagnosed with BDD typically have poor self-image/esteem, express shame in appearance, feel ugly, unlovable, and have a strong fear of rejection. Suicide ideation, attempts, and completion are significantly high in comparison to other mental disorders; however, the studies are few and only preliminary. Reasons for results suggest that suicidal risk is higher in patients with BDD. High suicidal risks are due to high rates of psychiatric hospitalization, comorbidity prevalence, being single and divorced, low self-esteem, poor social support, and having high levels of anxiety, depression, and hostility.
• Child vs. adult presentation
  • Most research suggests that the onset of BDD begins in early adolescents, although, little research has been done regarding definite onset. The role of body image during pubertal change increases body focus and dissatisfaction. Adolescents typically present more often with body shape and weight concerns related to distress, as opposed to adult presentation of dissatisfaction of specific body parts (i.e., face and hair).
• Gender and cultural differences in presentation
  • Most research suggest BDD in non-discriminative across gender lines. Some research suggests females are more likely to present with associated features resembling weight and shape concerns, eating disorders, and depressive disorders. Sociocultural influences include appearance related pressures. Socially constructed conceptions of perfection and/or beauty portrayed through the media affect both genders without bias. BDD exists in many cultures around the world. The areas having the most research conducted include the United States, Italy, and the United Kingdom. Studies pertaining to prevalence rates cross-cultures have been insignificant in number; the studies done suggest prevalence rates to be very similar.
• Epidemiology
  • Several sources of research agree prevalence rates in the general population vary from 1% – 2%. Prevalence rates tend to increase in clinical settings. Prevalence rates in the medical population of dermatology increase to 11.9%, and in the cosmetic surgery population, an increase of 2% – 7%. People suffering with BDD typically present to cosmetic surgeons for correction of perceived bodily flaw, and inevitably receive no satisfaction or relief from the disorder.
• Etiology
  • The onset of BDD generally begins around the pubertal time of adolescents. The disorder is more commonly chronic and unremitting than it is not. The course of this disorder follows a continuous lifetime course, in that; it is very unlikely for full remission to occur with treatment. Suicidal ideation is higher for this disorder than other mental disorders.
• Empirically supported treatments
  • Serotonin deregulation seems to be common among patients with BDD. Selective serotonin reuptake inhibitor (SSRI) (i.e., fluoxetine hydrochloride) drugs have been empirically proven to decrease the symptoms associated with BDD. Another empirically supported approach is cognitive behavioral therapy (CBT). A combination of SSRI and CBT is the common approach to BDD.
  • Behavioral and/or cognitive-behavioral techniques are typically used to change abnormal activities like avoidance behavior, reassurance seeking, checking, and excessive grooming. For example, exposure in vivo can be used to help people with BDD become more comfortable exposing themselves to social situations.

Links

• Article about Body Dysmorphic Disorder in American population (Need UCO login and password to access article).

Proposed DMS-5 Changes

The work group is recommending that this disorder be reclassified from Somatoform Disorders to Anxiety and Obsessive-Compulsive Spectrum Disorders

A. Preoccupation with a perceived defect(s) or flaw(s) in physical appearance that is not observable or appears slight to others.
B. At some point during the course of the disorder, the person has performed repetitive behaviors (e.g., mirror checking, excessive grooming, skin picking, or reassurance seeking) or mental acts (e.g., comparing their appearance with that of others) in response to the appearance concerns.
C. The preoccupation causes clinically significant distress (for example, depressed mood, anxiety, shame) or impairment in social, occupational, or other important areas of functioning (for example, school, relationships, household).

D. The appearance preoccupations are not restricted to concerns with body fat or weight in an eating disorder.
Specify if:
Muscle dysmorphia form of body dysmorphic disorder (the belief that one’s body build is too small or is insufficiently muscular)

Specify whether BDD beliefs are currently characterized by:
Good or fair insight: Recognizes that BDD beliefs are definitely or probably not true, or that they may or may not be true
Poor insight: Thinks BDD beliefs are probably true
Absent insight (i.e., delusional beliefs about appearance): Completely convinced BDD beliefs are true

Rationale:
Criterion A: Changes clarify the criterion’s meaning and aim to make it more acceptable to patients. The changes are not intended to change caseness.

Criterion B: Examples are added to increase awareness of some of the common types of distress or impairment in functioning.
Criterion C: It is recommended that this criterion be limited to eating disorders, as to our knowledge, there are no other disorders that might easily be misdiagnosed as BDD. Before a final recommendation is made, it will be important to examine the DSM-V criteria for eating disorders, and examples of eating disorder NOS, to determine whether criterion C should or should not include eating disorder NOS.
The phrase “not better accounted for” appears to be confusing to some DSM users (for example, it is sometimes misconstrued to mean that BDD cannot be diagnosed if the patient also has an eating disorder, even if the patient also meets criteria for BDD). We recommend alternate wording, such as “is not restricted to,” which may be clearer.
Specifiers: The muscle dysmorphia form of BDD appears to have several important differences from other forms of BDD (e.g., higher rates of suicidality and substance use disorders), and the treatment approach may require some modification. Thus, adding this specifier may have clinical utility.
There appear to be far more similarities than differences between delusional and nondelusional BDD, and thus it is recommended to combine BDD’s delusional and nondelusional variants into a single disorder and to eliminate the delusional variant from the psychosis section. The proposed specifier reflects the broad range of insight (including delusional thinking) that can characterize BDD beliefs. The proposed levels of insight are similar to categories in widely used scales for BDD, and they are the same as those proposed for OCD and olfactory reference syndrome.
Severity:
Yale-Brown Obsessive-Compulsive Scale Modified for BDD (BDD-YBOCS) (Phillips et al., 1997)
Insight dimensions (proposed for OCD, BDD, ORS, Hoarding Disorder): Brown Assessment of Beliefs Scale (BABS) (Eisen et al., 1998)

4. Narcolepsy (347.00)

• DSM-IV-TR criteria
  • A. Irresistible attacks of refreshing sleep that occurs daily over at least 3 months.
  • B. The presence of one or both of the following:
    • Cataplexy (brief episodes of sudden bilateral loss of muscle tone, which is most often associated with intense emotion.)
    • Recurrent intrusions of elements of rapid eye movement (REM) sleep into the transition between sleep and wakefulness, as manifested by either hypnopompic or hypnagogic hallucinations or sleep paralysis at the beginning of end of sleep episodes.
  • C. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or another general medical condition.
• Associated features
  • Narcolepsy is a neurological disorder in which the brain conveys sleep evoking signals at unexpected and inappropriate times. People with narcolepsy experience an inadequate order and length of NREM and REM sleep stages which are disrupted REM sleep episodes during sleep onset instead of after NREM sleep. During a time of excessive sleepiness, an individual with narcolepsy may temporarily experience muscle instability leading to paralysis or cataplexy of the head and body while the person remains awake and entirely conscious. Symptoms also include hypnagogic hallucinations, automatic behavior, insomnia and fragmented sleep associated with excessive day time sleepiness (EDS). Occurrences of narcolepsy may be prompted by sudden emotional reactions such as anger, surprise, fear, or even laughter. The episodes can last anywhere from several seconds to several minutes. Approximately forty percent of individuals with narcolepsy experience comorbidity with depression, anxiety, or substance-related abuse, and some may also experience all symptomatologies associated with narcolepsy.
• Child vs. adult presentation
  • Narcolepsy can occur in children as young as five, but is more prominent during adolescence, though it is also possible for it to develop during young adulthood. Children with narcolepsy also suffer from excessive daytime drowsiness and cataplexy which is most often described as fainting in young children. Children frequently exert confusion and aggressive behaviors when woken up. Frequently, narcolepsy is misdiagnosed in children as a learning disability or attention deficit disorder. However, narcolepsy is usually more difficult to identify in children.
• Gender and cultural differences in presentation
  • Narcolepsy is prevalent in relatively equal rates among males and females; however it has a genetic component that predisposes individuals to develop narcolepsy. Having a close relative that has narcolepsy increases an individual’s risk of developing the disorder by anywhere from twenty to forty times. There are very few variations in the severity and appearance of symptoms between different ethnic groups. Asians usually tend to report less severe incidents of negative emotions and hostility associated with narcolepsy, whereas Caucasian patients tend to report higher rates of cataplexy than many other ethnic groups.
• Epidemiology
  • Studies have shown that Narcolepsy can be found anywhere between 25 and 50 per 100,000 people in European countries, Japan, and the US. Therefore about one in two thousand Americans suffer from narcolepsy. Still the exact prevalence rate continues to remain unclear and the disorder may perhaps affect a bigger section of the population than what is currently estimated.
• Etiology
  • Many advances in determining the cause of narcolepsy have been made in recent years, but a direct causation has not yet been established. Most people who have narcolepsy have low levels of hypocretin, which is a chemical that helps control the level of a person’s wakefulness. The reason for low hypocretin levels, however, is unknown. The main consensus among researchers is genetics. Some scientists think narcolepsy could also be caused by various environmental stressors that occur before the age of onset in the genetically opportunistic individuals. Some factors that could influence development are the individuals BMI, immune response, and other stressful life events. These triggers are still being activated.
• Empirically supported treatments
  • Since there is not a cure for narcolepsy, clinicians strive to improve the patient’s alertness as well as attentiveness during the daytime. Stimulants, antidepressants, and anticataplectics are the types of medications currently used to treat narcolepsy. Stimulants have been around for the longest period of time. Antidepressants are used to suppress the REM sleep and they can help prevent cataplexy, hypnagogic hallucinations, and sleep paralysis. The two types of antidepressants that are commonly used are the selective serotonin reuptake inhibitors (SSRI’s) and tricyclics. GHB, or gammahydroxybutyrate (also known as Sodium oxybate [Xyrem]), gained FDA approval in the year 2002. It is the only drug of its kind (anticataplectic) used to treat patients that experience cataplexy caused by narcolepsy. The Food and Drug and Administration approved a drug called modafinil for excessive daytime sleepiness.
  • Behavioral treatments have also been studied. Adjustments in life-style are necessary for improvement. Some suggestions include following a strict sleep-wake schedule; taking short naps one or two times each day; increasing physical activity and avoiding repetitive tasks as well as potentially dangerous activities such as diving, swimming, and cooking unless under supervision or at a peak alert time.

PROPOSED DSM-5 CHANGES(dsm5.org)
NARCOLEPSY/HYPERCRETIN DEFICIENCY

A. Recurrent daytime naps or lapses into sleep that occurs daily or almost daily over at least the last 3 months (when the patient is untreated).
B. The presence of one or both of the following:
1. Cataplexy defined as brief (a few seconds to 2 minutes) episodes of sudden bilateral loss of muscle tone with maintained consciousness, most often in association with laughter or joking. These episodes must occur at least a few times per month providing the patient is untreated for this symptom.
2. Hypocretin deficiency, as measured using CSF hypocretin-1 immunoreactivity measurements (<1/3 of normal reference values).

C. Do not occur exclusively during the course of another mental or medical disorder but may occur simultaneously with these disorders.
RATIONALE
Rationale: In 2000, it was discovered that most cases with narcolepsy-cataplexy have hypocretin deficiency. Animal models without hypocretin have narcolepsy, establishing causality. Advantage: the name “narcolepsy/hypocretin deficiency” now encompasses a real disease entity with a single etiology and generally consistent set of symptoms. Therapy is more codified for this entity, which was previously “contaminated” by 20-50% (depending of the case series) of patients with other problems. Disadvantage: Some patients with “narcolepsy” but without cataplexy/hypocretin deficiency (generally narcolepsy without cataplexy) could be “undiagnosed”. To mitigate this problem, we insist that the category 307.44 “Primary hypersomnia” be renamed “primary hypersomnia/narcolepsy without cataplexy”

CRITERION B2

Rationale: Recurrent intrusions of elements of REM sleep such as “hypnopompic or hypnagogic hallucinations or sleep paralysis at the beginning or end of sleep episodes” have been shown to occur frequently in normal individuals (especially after sleep deprivation/interruptions), and to be frequently absent in genuine narcoleptic patients. It is neither specific nor sensitive and must be deleted. In contrast, measuring CSF hypocretin-1 immunoreactivity identifies the actual cause of the symptomatology (title change). It also has only very few false positive in patients without a serious associated neurological condition (~0.1%). Advantage: Fewer patients will be diagnosed for life as “narcoleptic” and treated with stimulants unnecessarily if not carelessly. Disadvantage: Some patients diagnosed as “narcolepsy” because they were sleepy and had some sleep paralysis, and hypnagogic hallucinations could feel they are being undiagnosed. To mitigate this problem, we insist that the category 307.44 “Primary hypersomnia” be renamed “primary hypersomnia/narcolepsy without cataplexy”.
A question may be whether or not a positive Multiple Sleep Latency Test (MSLT mean sleep latency ≤8 min, ≥2 Sleep onset REM periods), a nap sleep polysomnography test that has been developed to diagnose narcolepsy, should be added as a third possible criteria. The MSLT is reasonably sensitive (95%) for narcolepsy/cataplexy with hypocretin deficiency. Problematically however, two recent studies have shown it is not very specific, being positive in approximately 2-4% of the general population and probably more in patients with sleep apnea, sleep deprivation or other sleep disorders. Many normal subjects who do not complaint of any symptoms are positive for the test. As the MLT is increasingly used to diagnose narcolepsy independently of the clinical picture, an epidemic of “narcolepsy with cataplexy cases” defined with by a positive MSLT alone is now being diagnosed and aggressively treated, often inappropriately. These subjects often think they have a life long biochemical condition, which is not established. In the revised classification, these subjects will be pulled with “primary Hypersomnia cases”, a mixed bag of cases with sleepiness or excessive sleep of unknown etiologies.
Of note, as it is, the revised classification will remain similar to that of the International Classification of sleep Disorders (ICSD2), except that two instead of 4 categories are included. Narcolepsy/cataplexy would roughly correspond to narcolepsy-cataplexy/hypocretin deficiency. Primary hypersomnia/narcolepsy without cataplexy will be a category merging ICSD2 narcolepsy without cataplexy, hypersomnia with long sleep time, and narcolepsy without long sleep time. As these three entities are not known to be pathophysiologically distinct, and are treated and evaluated similarly, the DSMV will be easier to use than the ICSD2.
RELATIONSHIP TO INTERNATIONAL CLASSIFICATION OF DISEASES-10

Narcolepsy and Cataplexy G47.4
RELATIONSHIP TO INTERNATIONAL CLASSIFICATION OF SLEEP DISORDERS 2nd EDITION

The revised classification will remain similar to that of the ICSD-2, except that two instead of 4 categories are included. Narcolepsy/cataplexy would roughly correspond to narcolepsy-cataplexy/hypocretin deficiency. idiopathic hypersomnia, with/without long sleep time, 327.11, 327.12; narcolepsy with cataplexy 347.01

SEVERITY

1. Stanford Sleep Inventory (1)
2. Epworth sleepiness Scale
3. Multiple Sleep Latency Test

4. Maintenance of Wakefulness test
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5. Conversion Disorder (300.11)

These two videos show a woman experiencing paralysis and uncontrolled muscle movement in and around the facial area caused by Conversion Disorder, which eventually spreads to her entire body. The woman in the video (she goes by the username leleroxit on www.youtube.com) was diagnosed with Conversion Disorder by a specialist in movement disorders.

• DSM-IV-TR criteria
  • A. One or more symptoms or deficits affecting voluntary motor or sensory function that suggest a neurological or other general medical condition.
  • B. Psychological factors are judged to be associated with the symptom or deficit because the initiation or exacerbation of the symptom or deficit is preceded by conflict or other stressors.
  • C. The symptom or deficit is not intentionally produced or feigned (as in Factitious Disorder or Malingering).
  • D. The symptom or deficit cannot, after appropriate investigation, be fully explained by a general medical condition, or by the direct effects of a substance, or as a culturally sanctioned behavior or experience.
  • E. The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of function or warrants medical evaluation.
  • F. The symptom or deficit is not limited to pain or sexual dysfunction, does not occur exclusively during the course of Somatization Disorder, and is not better accounted for by another mental disorder.
• Associated features
  • Some people with Conversion Disorder may display la belle indifference. This is a relative lack of worry about their condition or its implications. Other people may act in a dramatic or histrionic manner though.
  • Individuals being treated for Conversion Disorder may develop dependency issues and embrace an ailing role during the course of their treatment.
  • Symptoms caused by Conversion Disorder usually conflict with established anatomical or physiological knowledge and explanations. Therefore, objective signs that indicate the presence of a traditional abnormality are frequently absent.
  • Laboratory analysis of the condition typically do not yield any findings as well. The absence of any findings is a feature that may indicate that Conversion Disorder is the actual source of the problem(s).
  • Dissociative Disorders, Major Depression, and Histrionic, Antisocial, Borderline, and Dependent Personality Disorders are mental disorders than can be associated with Conversion Disorder.
  • Most conversion symptoms are neurological and usually relate to the loco-motor system. The motor symptoms include convulsions, paralysis, weakness, and dyskinesia. Sensory symptoms include paraesthesia or anesthesia, blindness or speech disorders (Heruti, Levy, Adunski and Ohry, 2002).
• Child vs. adult presentation
  • The symptoms that children with conversion disorder experience are frequently limited to seizure or gait problems. There is a wide range of symptoms that adults with Conversion Disorder may experience. These symptoms may include the loss of sensation, paralysis, blindness, seizures, or a mixed presentation.
  • Conversion Disorder appears in adolescence or early adulthood. Presentation before the age of 10 or after the age of 35 is rare, though some cases have been reported around age 90. Conversion Disorders before the age of 10 are usually limited to walking impairments or convulsions (Heruti, Levy, Adunski and Ohry, 2002).
• Gender and cultural differences in presentation
  • Conversion disorder is diagnosed more frequently in women than in men. An exact ratio has not been established, but most studies indicate that the ratios range between 2:1 and 10:1. It is more common for women with Conversion Disorder to eventually develop Somatization Disorder, but there is a strong relation between Conversion Disorder and Antisocial Personality Disorder among men. It is common for men who experience Conversion Disorder to have suffered an industrial accident or to have been in the Military. It is much more common for women to experience symptoms on the left side of their body than in their right side.
  • There are various links between Conversion Disorder and cultural factors. People in rural settings, lower socioeconomic levels, and with relatively less knowledge of psychology and medicine are diagnosed with Conversion Disorder more frequently than other populations. There is a higher incidence of Conversions Disorder in developing regions than in developed regions, and reports from the developing regions decrease as further development occurs. The conversion symptoms displayed by patients may vary based on their culturally accepted means of demonstrating distress. One must be aware that the religious and healing rituals of certain cultures may include characteristics that could be confused with symptoms of Conversion Disorder.
  • Some symptoms that might be linked to a conversion disorder in the United States may be a “normal expression” of anxiety in other cultures. In London at the National Hospital, the diagnosis of 1% of inpatients. In Iceland, the report is 15 cases per 100,00 persons.
• Epidemiology
  • The prevalence of Conversion Disorder varies according to multiple reports, but the rates generally range from 11/100,000 to 500/100,000 in samples from the general population. About 3% of mental health clinic referrals are due to Conversion Disorder. Conversion Disorder is more likely to develop among older adolescents or young adults, women, and people from lower socioeconomic classes. According to one study, there was 1.2%- 11.5% of psychiatric consultations for hospitalized medical and surgical patients.
• Etiology
  • The exact cause of Conversion Disorder has not been established by empirically supported data, but there are some theories about its development. Many contemporary theories claim that the development of Conversion Disorder is often sudden, and it is triggered by subconscious conflict, unresolved grief, sexual trauma, or other stressful situations. In essence, these theories state that people with Conversion Disorder convert their psychological distress into physical symptoms to avoid any further mental anguish. Disturbances in the central nervous system may increase the likelihood and/or severity of any somatic symptoms.
  • Other factors may influence the development of Conversion Disorder. There is some evidence that Conversion Disorder may be genetically transmitted, but there is not enough data to prove this conclusively. Socioeconomic factors are also known to influence the development of this disorder, but the exact manner in which they impact an individual has not been definitively identified.
  • According to Freud, suppression is the major defense mechanism involved in conversion because of the close relation between conversion conditions and traumatic events in the individual’s life. Freud states that an impulse, or a wish, that cannot be fulfilled due to negative connotations such as fear, shame, quilt, or anger is converted into physical expression (Heruti, Levy, Adunski and Ohry 2002).
• Empirically supported treatments
  • There are no empirically supported treatments for Conversion Disorder, but there are a couple of methods that are believed to help people with this disorder. The most common methods are behavioral or cognitive behavioral treatments. Treatment plans need to be individualized due to the varying symptoms of each person, but there are some general guidelines. It is important to discover any psychological stressors an individual may have that precipitate somatic symptoms to cope with them. It is vital to help individuals recognize these stressors and to help them learn more adaptive methods for dealing with them. Manipulation of the patient’s social environment may be necessary in order to reinforce the patient’s non-symptomatic behavior.
  • Physical rehabilitation, due to motor functional imparities, should be considered an option as soon as possible, after physiological etiologies have been ruled out. Physical rehabilitation addresses the prevention of secondary disabilities due to the disorder.

PROPOSED CHANGES IN DSM-5 (dsm5.org)

The work group is recommending this disorder be renamed from Conversion Disorder to Functional Neurological Symptoms.
Criteria A, B, and C must all be fulfilled to make the diagnosis:
A. One or more symptoms are present that affect motor or sensory function or seizure-like episodes.
B. The symptom, after appropriate medical assessment, is found not to be due to a general medical condition, the direct effects of a substance, or a culturally sanctioned behavior or experience.
C. Physical signs or diagnostic findings that provide evidence of internal inconsistency or incongruity with recognized neurological or medical disorder.

D. The symptom causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.

Both the Somatic Symptom Disorders Work Group and the Anxiety, Obsessive-Compulsive Spectrum, Posttraumatic, and Dissociative Disorders Work Group are discussing how conversion disorder relates to the Dissociative Disorders

Rationale:
Major Change #1: Rename Somatoform disorders to Somatic Symptom Disorders and combine with PFAMC and Factitious Disorders
The workgroup suggests combining Somatoform Disorders, Psychological Factors Affecting Medical Condition (PFAMC), and Factitious Disorders into one group entitled “Somatic Symptom Disorders” because the common feature of these disorders is the central place in the clinical presentation of physical symptoms and/or concern about medical illness. The grouping of these disorders in a single section is based on clinical utility (these patients are mainly encountered in general medical settings), rather than assumptions regarding shared etiology or mechanism.
Major Change #2: De-emphasize medically unexplained symptoms
Remove the language concerning medically unexplained symptoms for reasons specified above. The reliability of such judgments is low (Rief, 2007). In addition, it is clear that many of these patients do in fact have considerable medical co-morbidity (Creed, Ng). Medically unexplained symptoms are 3 times as common in patients with general medical illnesses, including cancer, cardiovascular and respiratory disease compared to the general population (OR=3.0 [95%CI: 2.1 to 4.2] (Harter et al 2007). This de-emphasis of medically unexplained symptoms would pertain to somatization disorder, hypochondriasis, undifferentiated somatoform disorder, and pain disorder. We now focus on the extent to which such symptoms result in subjective distress, disturbance, diminished quality of life, and impaired role functioning.
Major Change 3: Modify Criteria for Conversion Disorder

Changes are made in an effort to simplify the criteria for conversion disorder. First, we suggest removing the requirement that the clinician actively establish that the patient is not feigning. This is because (a) it is probably clinically impossible to prove that a patient is not feigning (Sharpe, 2003) and (b) there is no evidence that feigning of conversion symptoms is more common than feigning of other mental disorders. However as with other disorders positive evidence of feigning remains an exclusion, thereby differentiating conversion from factitious disorder and malingering.
Second, we suggest removing the requirement that the clinician has to establish that there are associated psychological factors . This is because (a) as with feigning, it is very difficult to reliably establish that relevant psychological factors are present in all cases and (b) the research evidence suggests that psychological factors can often be found but are not specific and have only a weak association with the diagnosis (Roelofs, 2005). The association with psychological factors has therefore been relegated to accompanying text rather than remaining a clinical requirement for diagnosis.
Third, we emphasize the importance of obtaining positive evidence of the diagnosis from appropriate neurological assessment and testing. Current diagnostic criteria require that the symptom, after appropriate medical assessment, is found not to be due to a general medical condition. In contrast to most other somatic symptoms, it can be usually be reliably determined whether neurological symptoms are due to an organic disease (Stone et al 2009). Additionally there are also findings on neurological assessment and investigation that positively suggest the symptoms are those of conversion (such as Hoovers sign for motor weakness or absence of seizure activity on an EEG during apparent seizures for seizures) (Hallett 2005; Reuber 2004; Stone 2005).

We suggest retaining Conversion Disorder in the Somatic Symptom Disorders section of the DSM. Conversion remains a condition defined by a somatic symptom that causes disability or distress and therefore sits comfortably in the new Somatic Symptom Disorders category that replaces somatoform disorders on grounds of utility. The alternative placement of this diagnosis is with dissociative disorders. The argument for moving conversion there is that the mental mechanisms involved are similar. However dissociation is a hypothetical process and moving conversion would (a) risk making an unjustified assumption about cause (b) lose the utility of grouping with other conditions that present with a somatic symptom.

SEVERITY

There are few widely employed measures of severity in factitious disorder or conversion disorder.

For conversion disorder, the severity scoring might best be based on the severity of the associated disability (using a simple rating of mild, moderate and severe)
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6. Pyromania (312.33)

• DSM-IV-TR criteria
  • A. Deliberate and purposeful fire setting on more than one occasion.
  • B. Tension or affection arousal before the act.
  • C. Fascination with, interest in, curiosity about, or attraction to fire and its situational contexts (e.g., paraphernalia, uses, consequences).
  • D. The fire setting is not done for monetary gain, as an expression of sociopolitical ideology, to conceal criminal activity, to express anger or vengeance, to improve one’s living circumstances, in response to a delusion or a hallucination, or as a result of impaired judgment (e.g., in dementia, Mental Retardation, Substance Intoxication).
  • E. The fire setting is not motivated by monetary gain, sociopolitical ideology, anger or revenge, psychotic thinking (delusions or hallucinations), or to conceal criminal activity.
  • The fire setting is not better accounted for by Conduct Disorder, a Manic Episode, or Antisocial Personality Disorder.
• Associated features
  • Individuals with pyromania often have a difficult time controlling themselves, specifically in situations that are harmful to themselves and others. Those with head injuries or epilepsy are at an increased risk of developing and impulse control disorder. Researchers have noticed an increase in impulse control disorders in older patients with Parkinson’s disease due to the effect of the dopaminergic drugs. There has also been a correlation with pyromania to learning disabilities, as well as cruelty to animals; these problems could suggest a higher risk of violence in the future. There is also high comorbidity with disorders, such as: substance abuse disorders, obsessive compulsive disorder, anxiety disorders, and mood disorders.
  • In one study, arsonists have more often received psychiatric treatment, prior to committing their index offence, and had a history of severe alcohol abuse more often in comparison to the controls. The arsonists turned out to be less likely to suffer from a major psychotic disorder.
  • Child vs. adult presentation( Labree, Nijman, van Marie, & Rassin, 2010).
• The age of onset for pyromania is approximately 18 years. It is extremely rare for a child younger than adolescence to develop Pyromania. It is also rare for older adults to develop pyromania.
  • Fire setting in children may be a way of relieving tension or stress. This outward expression of tension/stress may be associated with depression, suicidal thoughts, poor coping abilities, and repeated interpersonal conflicts.
  • It is rare for children to have it, but it can occur in children as young as three. Most of the time, parents recognize the behaviors and get it treated before it becomes a problem.
  • Features such as temperament, parental psychopathology, social and environmental factors and possible neurochemical predispositions have been hypothesized to cause childhood pyromania.
• Gender and cultural differences in presentation
  • Males have a much higher risk for developing pyromania. Approximately 90% of those diagnosed with Pyromania are male. There are no cultural differences in presentation of this disorder. People from many different cultures will show the same symptoms.
  • Pyromania in childhood appears to be rare. Juvenile fire setting is usually associated with Conduct Disorder, Attention-Deficit/Hyperactivity Disorder, or Adjustment Disorder.
  • Pyromania occurs much more often in males, especially those with poorer social skills and learning difficulties.
• Epidemiology
  • It is a very rare disorder, about less than 1% of the populations has it.
  • Most of the research done on Pyromania has not focused on the epidemiology. It is only known that there is a higher prevalence of Pyromania in men than women.
  • It is known that about 9% of the population has impulse control problems which include pyromania.
  • Only 14% of fires are started by people with pyromania and other mental disorders.
  • The majority of epidemiological studies have focused on pyromania in childhood and adolescence, and have reported prevalence rates to be between 2.4% and 3.5% (Dell’Osso, Altamaura, Allen, Marazziti and Hollander 2006).
• Etiology
  • Although little research has been done on the etiology of Pyromania, it is believed that the cause can be targeted during childhood. Many researchers say that possible causes can be an abusive family environment or mild brain trauma. Other factors of pyromania are: antisocial behaviors and attitudes, people seeking sensation and adventure, people seeking attention, a lack of social skills with others, and a lack of fire-safety knowledge and/or ignorance of the dangers involved. Environmental factors include things such as: poor supervision from parents, peer pressure, and stressful life events.
• Empirically supported treatments
  • Counseling and medication are both preferred for treating pyromania. Behavior modification is the best treatment found so far for treating this disorder in hopes of getting a response to social limits.
    • Treatment of adults and children with pyromania is often individualized based on the patient’s presenting problems and history. Treatment of children with this disorder often begins with an assessment of the child’s life and includes the evaluation of such factors as stressors on the child, home discipline, and supervision of the child. This assessment is generally followed by a case-management approach, rather than a medicinal approach, where the treatment is tailored to the child and involves a variety of approaches, such as anger management and communication skills.
    • Treatment of adults with pyromania is often approached differently. Because adult patients with this disorder tend to be uncooperative, they are generally treated with a combination of medication and psychotherapy. Usually the patient is treated with a selective serotonin reuptake inhibitor, but there have also been multiple case reports of tricyclic antidepressants and mon-amine oxidase inhibitors being useful in impulse control disorders. There haven’t been very many carefully controlled studies that use strict diagnostic criteria on adult patients diagnosed with pyromania or other impulse-control disorders.
  • Treatments work in 95% of children that exhibit signs and symptoms of pyromania.

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7. Intermittent Explosive Disorder (312.34)

This is a short video by Dr. Gary Solomon explaining what Intermittent Expolsive Disorder is and the symptoms that go along with the disorder.

• DSM-IV-TR criteria
  • A. Several discrete episodes of failure to resist aggressive impulses that result in serious assaultive acts or destruction of property.
  • B. The degree of aggressiveness expressed during the episodes is grossly out of proportion to any precipitating psychosocial stressors.
  • C. The aggressive episodes are not accounted for by another mental disorder (e.g., Antisocial Personality Disorder, Borderline Personality Disorder, a Psychotic Disorder, a Manic Episode, Conduct Disorder, or Attention-Deficit/Hyperactivity Disorder) and are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., head trauma, Alzheimer’s disease)
• Associated features
  • Some individuals see their impulses as stressful and destructive before, during and after they react to these impulses. These reactions can cause problems socially in their relationships, school, and/or jobs. Individuals with Intermittent Explosive Disorder can sometimes suppress their anger, to an extent, and react in a less destructive manner. Individuals with narcissistic, obsessive, paranoid, or schizoid traits may be especially prone to having explosive outbursts of anger when under increased stress. Some individuals may also report that their aggressive episodes are often preceded or accompanied by symptoms such as tingling, tremor, palpitations, chest tightness, head pressure, or hearing an echo. Individuals may describe their aggressive impulses as extremely distressing. The disorder may result in job loss, school suspension, divorce, difficulties with interpersonal relationships or other impairment in social or occupational spheres, accidents, hospitalization, financial problems, incarcerations, or other legal problems.
  • Signs of generalized impulsivity or aggressiveness may be present between explosive episodes. Individuals with Intermittent Explosive Disorder may report problems with chronic anger and frequent “sub threshold” episodes, in which they experience aggressive impulses but either manage to resist acting on them or engage in less destructive aggressive behaviors.
• Child vs. adult presentation
  • In children, they may react with a temper, hyperactivity, or destructive actions such as tearing up objects, setting objects on fire, or taking from others. There is no exact age of when Intermittent Explosive Disorder begins, however it is believed to occur from childhood to late teens or twenties.
  • Intermittent explosive behavior or episodic aggressive outbursts often begin in childhood, adolescence or early adulthood and follow a chronic course. In a study of 27 patients who were diagnosed with IED, 75% of those reported that their explosive behavior began in adolescence, with a mean age of onset of 14 years old, and a mean duration of 20 years old (Olvera 2002).
• Gender and cultural differences in presentation
  • The episodic violent behavior is more frequent in men than women. Amok is uncontrolled, severe violent behavior where a person would declare it was amnesia. This is known to be seen more in the southeastern area of Asia. But, has also been seen in Canada and the United States. However, Amok does not occur frequently, but in a single episode.
• Epidemiology
  • Very little is known about Intermittent Explosive Disorder; it is seen as a very rare disorder. Most studies, however, indicate that it occurs more frequently in males. The most common age of onset is the period from late childhood through the early 20s. The onset of the disorder is frequently abrupt, with no warning period. Patients with IED are often diagnosed with at least one other disorder—particularly personality disorders, substance abuse (especially alcohol abuse) disorders, and neurological disorders.
• Etiology
  • Some studies suggest that abnormalities of the brain that are responsible for regulating behavioral arousal and inhibition could be the cause. Developmental problems or Neurological symptoms maybe a cause. There may be an imbalance of serotonin or testosterone levels. However, if a physician believes it is due to physiological problems, it may be diagnosed as a General Medical Condition instead. It may also be a cause of exposure in family situations at a young age, or a genetic factor. Also, lower levels of brain glucose (sugar) metabolism in patients who act in “impulsively aggressive” ways.
  • Impulsive aggression is thought to be mainly defensive in nature, driven by fear, anger and a cognitive distortion of environmental conditions, with extremely high autonomic arousal (Olvera 2002).
  • Neurobiological studies of aggression suggest that numerous neurotransmitters are disrupted. A disruption in the serotonergic system, in particular, low cerebral spinal fluid levels of 5-hydroxyindoleacetic acid, a serotonin metabolite, have been found in IED individuals (Olvera 2002).
• Empirically supported treatments
  • Some treatments are seen in certain medications such as anti-convulsion, anti-anxiety, mood regulators, or anti-depressants. Also, some forms of group therapy such as anger management have been seen as helpful. Some medications include: carbamazepine (an antiseizure medicine), propranolol (a heart medication), and lithium (used to treat Bipolar type two manic-depression disorder).

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8. Kleptomania (312.32)

This is a short clip of Dr. Gary Solomon explaining what activities a person diagnosed with kleptomania might do.

• DSM-IV-TR criteria
  • A. Recurrent failure to resist impulses to steal objects that are not needed for personal use or for their monetary value.
  • B. Increasing sense tension immediately before committing the theft.
  • C. Pleasure, gratification, or relief at the time of committing the theft.
  • D. The stealing is not committed to express anger or vengeance and is not in response to a delusion or a hallucination.
  • E. The stealing is not better accounted for by a Conduct Disorder, a Manic Episode, or Antisocial Personality Disorder.
• Associated features
  • Kleptomania is an irresistible impulse to steal, stemming from emotional disturbance rather than economic need. It is also said that it is a recurrent failure to resist stealing. It is most observed in patients who are “chemically dependent” or also have mood, anxiety, or eating disorders. It is possible that people with kleptomania could also be dealing with major depression, panic attacks, social phobia, anorexia nervosa, bulimia nervosa, substance abuse, and obsessive compulsive disorder. People with this disorder get a thrill from stealing and randomly have an overwhelming urge to do so. Strangely enough, they often feel guilty after committing theft and surreptitiously return the stolen items. If the items, usually of lesser importance, aren’t returned they are hoarded, discarded, or given away. In less severe instances of kleptomania, things are borrowed and not returned.
    Kleptomania is not to be confused with the regular act of stealing. Whether planned or impulsive, a normal thief steals for the objects value or usefulness. Many times they are teenagers or gang members that view theft as a rite of passage, form of rebellion, or commit them just for a dare.
• Child vs. adult presentation
  • It is difficult to assess the differences in presentation of Kleptomania among children and adults. This is because Kleptomania typically presents itself during late adolescence or early adulthood. It is rare for Kleptomania to manifest itself during a person’s early childhood or late in their life. This is because it is hard to distinguish if children are stealing because of a disorder or if it is because they do not know any better.
• Gender and cultural differences in presentation
  • In preliminary evidence, clinical samples suggest that approximately two-thirds of individuals with Kleptomania are female. Kleptomania in cultural differences are not stated.
• Epidemiology
  • Kleptomania is a rare condition that appears to occur in fewer than 5% of identified shoplifters. Studies suggest that the prevalence in the general population may be around 0.6%. Studies also suggest that it is more prominent in females. Other studies, interestingly, have found an exceptionally high correlation of kleptomania in patients with bulimia of 65%. Also, approximately 7% of patients have a correlation with histories of OCD.
• Etiology
  • One theory suggests that receiving the thrill of stealing can aid in alleviating symptoms in people who are clinically depressed. They never seek aid in the act of theft and never plan to steal with others. There can be favored objects or environments where theft occurs, but detection of kleptomania, even by family, is difficult and the problem mostly goes undetected.
  • There is no known cause for kleptomania. It is possible that it is genetically related especially from first-degree relatives. There also tends to be a sharp inclination for kleptomania to coexist with OCD, bulimia nervosa, and clinical depression.
• Empirically supported treatments
  • Actually finding a diagnosis is typically difficult given that patients do not seek medical help for this complaint. It is also difficult to detect in the initial psychological assessments. It is most commonly addressed when one comes in for other reasons like depression, bulimia, or are simply emotionally unstable. They may prefer certain objects and settings, but these may not be described by the patient. Initial psychological evaluations may reveal a past of inadequate parenting, conflicting relationships, or a point of severe stressors such as having to make a move from one home to another.
  • There tends to be little or no system on the course of Kleptomania. There are, however, three typical courses that can be described as: “sporadic with brief episodes and long periods of remission; episodic with protracted periods of stealing and periods of remission; and chronic with some degree of fluctuation.” Though they are convicted numerous times for shoplifting, the disorder could go on for years.
    Treatments will vary concerning this disorder. It starts with an extensive psychological assessment. The patient will undergo therapy that targets impulse control and any and all coexisting mental disorders. They gain a comprehensible understanding of their specific triggers in order to prevent relapse. Psychotherapies, such as cognitive-behavioral therapy and rational emotive therapy, will be included in the treatment. Other psychotherapies include covert sensitization, aversion therapy, and systematic desensitization.
  • Several medications have been shown to work, but the possibility of the patient having another mental disability should also be taken into account. Antidepressants are the most widely used medicine to treat kleptomania, which includes Prozac. These are serotonin reuptake inhibitors. Side effects often occur, so patients should consult doctor if any occur. Mood stabilizers can also be used to even out the patient’s mood. This will help the patient not have rapid or uneven mood changes that may trigger them to steal something. An example of this includes lithium which is shown to possibly be helpful. Benzodiazepines can also be used but the effectiveness often varies patient to patient and they may cause the patient to become dependent on the drug. These medications are central nervous system depressants, also known as tranquilizers. Examples of these include Xanax and Klonopin. Lastly, there are addiction medications. Revia falls into this category. Revia is known as an opioid antagonist and is most commonly prescribed for kleptomania. This particular drug blocks the part of the brain that feels pleasure with certain addictive behaviors, which in turn should reduce the patients urge to steal.

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9. Depersonalization Disorder (300.6)

This is a video of a woman who was diagnosed with depersonalization disorder. In the video she gives a good description of what it feels like when a person is experiencing an episode caused by depersonalization disorder.

• DSM-IV-TR criteria
  • A. Persistent or recurrent experiences of feeling detached from, and as if one is an outside observer of, one’s mental processes or body (e.g., feeling like one is in a dream).
  • B. During the depersonalization experience, reality testing remains intact.
  • C. The depersonalization causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  • D. The depersonalization experience does not occur exclusively during the course of another mental disorder, such as Schizophrenia, Panic Disorder, Acute Stress Disorder, or another Dissociative Disorder, and is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., temporal lobe epilepsy)
• Associated features
  • Associated features may include anxiety or depression. Sometimes, individuals have a hard time with sense of time and may have somatic manifestations. Comorbidity can include Panic Disorder, Borderline Personality Disorder, Post-Traumatic Stress Disorder, Obsessive-compulsive Disorder, Dysthymic Disorder, Acute Disorder, or Major Depressive disorders. Individuals with Depersonalization disorder may have personality disorders as well.
  • Individuals with Depersonalization have difficulty describing their symptoms and may fear that these experiences signify that they are “crazy.” Derealization may also be present and is experienced as the sense that the external world is strange or unreal. The individual may perceive an uncanny alteration in the size or shape of objects, and people may seem unfamiliar or mechanical.
• Child vs. adult presentation
  • The disorder is more likely to occur in late adolescence to adulthood.
• Gender and cultural differences in presentation
  • From various studies, equal numbers of men and women are diagnosed. Individuals from individualistic societies are more likely to suffer from the disorder (see Etiology).
  • In clinical samples, this disorder is diagnosed at least twice as often in women than in men.
• Epidemiology
  • Although much of the general population experiences a depersonalization experience (whether caused by a traumatic experience or danger, or a drug induced experience), only about 2.4% of the population has been diagnosed with depersonalization disorder.
  • A transient experience of depersonalization develops in nearly one-third of individuals exposed to life-threatening danger and in close to 40% of patients hospitalized for mental disorders.
• Etiology
  • Similar to the other dissociative disorders, scientists link severe childhood abuse to depersonalization disorders. Brain imaging including pet scans show sensory cortex abnormalities. Positron emission tomography scans used to assess brain glucose metabolism show abnormalities in the sensory cortex including the temporal, occipital, and parietal lobes. The sensory cortex controls the senses and perception of an individual’s body in space. Lower levels of nerve cell responses in the area of the brain that controls emotion may correlate to the emotional detachment that individual’s feel during an episode of depersonalization. Western cultures where individuals live in a more individualistic society may be more likely to suffer from a depersonalization disorder. Individualism is stressed in most Western cultures and may have an effect on an individual’s sense of self. Also, it is thought that trauma and childhood abuse (physical, emotional, and/or sexual) could be a factor to depersonalization disorder.
• Empirically supported treatments
  • There are currently no empirically supported treatments for this condition. For the most part, DPD remains resistant to traditional treatment measures. Psychotherapeutic techniques like cognitive behavioral therapy have been used to treat this disorder, but none of them have an established effectiveness. Pharmacological options continue to be researched. Some possible options that could be used to treat this condition include selective serotonin reuptake inhibitors, anticonvulsants, and opioid antagonists.
  • Also some medications like benzodiazepine tranquilizers (lorazepam and clorazepate) and tricyclic antidepressants (amitriptyline and doxepin) can be helpful in treatment for Desensitization Disorder.
  • Despite anecdotal reports that serotonin reuptake inhibitors may improve depersonalisation, there is no proven efficacious treatment for depersonalisation disorder (Simeon, Guralnik, Schmeidler, & Knutelska, 2004).

PROPOSED CHANGES IN DSM-5 (dsm5.org)

Either (1), (2), or both:

A1. Depersonalization: Persistent or recurrent experiences of feeling detached from, and as if one is an outside observer of, one’s mental processes or body (e.g., feeling as though one is in a dream; sense of unreality of self or body; or time moving slowly)

A2. Derealization: Persistent or recurrent experiences of unreality of surroundings (e.g., world around the person is experienced as unreal, dreamlike, distant, or distorted)

B. During the depersonalization or derealization experience, reality testing remains intact
C. The depersonalization or derealization symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
D. The depersonalization or derealization symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., complex partial seizures).
E. The depersonalization or derealization symptoms are not restricted to the symptoms of another mental disorder (e.g.,schizophrenia, panic disorder, acute stress disorder, posttraumatic stress disorder, major depressive disorder, or another dissociative disorder).
Specify if:
a) Depersonalization only

b) Derealization only

RATIONALE FOR CHANGE

D and E: Changes allow comorbid diagnoses to be made when warranted.
SEVERITY
Brief Dissociation Scale (Carlson E & Dahlenberg C, 2009)

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10. Dissociative Identity Disorder (300.14)

This is a video of a man named Tony who has Dissociative Identity Disorder. It is believed that Tony has 53 or more distinct identities or personality states.

The video above is an interview with former NFL running back Herschel Walker. In the interview he briefly discusses his experience with Dissociative Identity Disorder.

• DSM-IV-TR criteria
  • A. The presence of two or more distinct identities or personality states (each with its own relatively enduring pattern of perceiving, relating to, and thinking about the environment and self).
  • B. At least two of these identities or personality states recurrently take control of the person’s behavior.
  • C. Inability to recall important personal information that is too extensive to be explained by ordinary forgetfulness.
  • D. The disturbance is not due to the direct physiological effects of a substance (e.g., blackouts or chaotic behavior during Alcohol Intoxication) or a general medical condition (e.g., complex partial seizures). Note: In children, the symptoms are not attributable to imaginary playmates or other fantasy play.
• Associated features
  • Several symptoms are characteristic:
    • Fluctuating symptom pictures
    • Fluctuating levels of function from highly effective to disabled
    • Severe headaches or other pains
    • Time distortions, time lapses, and amnesia
    • Depersonalization and Derealization – Depersonalization occurs when a person feels unattached to him or herself. During this phenomenon, it is almost as if you can see yourself from another view point. Derealization is when you experience surroundings or people as if they are new, eccentric, or dreamlike when they are clearly not.
    • Patients can lose time; they can end up in places and not know how they arrived there or why. They also may find objects that they do not identify or handwriting that they do not think they wrote.
    • Individuals with Dissociative Identity Disorder frequently report having experienced severe physical and sexual abuse, especially during childhood. However, children’s minds can produce distorted images or memories, so it is hard to tell how accurate they are. Some past experiences can be cleared up through objective evidence. Some individuals may have post traumatic symptoms such as nightmares, flashbacks, and startle responses.
    • Certain identities can control their pain levels or other physical symptoms, which some individuals will self-mutilate and have suicidal thoughts. They may also experience relationships that contain both sexual and physical abuse. The identities or personality states persistently take control over the person’s behavior. These alternate identities are frequently diverse from the individual’s personality. Also, it could be of a different name, age, gender, or even race.
    • Comorbidity occurs with Post- Traumatic Stress Disorder.
• Child vs. adult presentation
  • There are no reliable figures on the diagnosis of children. However, it has increased during the 1990s. A child acting like someone else is perfectly normal. They are trying to get a sense of self. Of course, if some trauma happens in a child’s life, the result may go beyond simply mimicking another person. It may go as far as to creating alter personality states so they can create a fantasy world in order to escape real life. The average age is in early childhood, generally by the age of four. The average time period for the first symptom to occur to diagnosis is 6-7 years. The disorder may go dormant after 40 years of age but may reappear during episodes of stress or trauma or with substance abuse.
• Gender and cultural differences in presentation
  • Dissociative Identity Disorder has been found in individuals from a several different cultures all around the world. It is diagnosed 3 to 9 times more often in adult females than in adult males; in childhood, the female-to-male ratio may be even more, but the data is limited. Males tend to have fewer identities than females. Males have approximately 8 identities. Females tend to have around 15 or more.
• Epidemiology
  • The studies do not give an exact estimate, however the numbers have increased drastically. A reason for this is because it could have been misdiagnosed as schizophrenia or bipolar disorders. Also, people have become more aware of child sexual abuse, which is a leading cause of DID. DID may be present in about 1% of the general population. India, Switzerland, China, and Germany’s prevalence rates range from 0.015% to 0.9%. The Netherlands is 2%. The U.S. ranges from 6 to 10% and Turkey at the highest with 14%.
  • However, scientists claim that a person having multiple personalities is bizarre, and the support for it is not credible. Some therapists maintain that using hypnosis and frequent prompting of alters bring about the indwelling identities. Even though, some patients do not show symptoms before the treatment has occurred. There is substantial support for the claim that therapists and the media are creating alters rather than discovering them.
• Etiology
  • The causes are not yet confirmed, but there are some theoretical predictions of what causes DID. They are overwhelming stress, physical and sexual abuse especially in childhood, inadequate childhood nurturing, and the disability to separate recollections with what actually happens. The most common reason is childhood abuse; most of the cases reported deal with abuse. Some children tend to make up “happy places” that they can disappear to, to get away from the violence. If it happens often enough, the children may not be able to tell the difference between that and reality. It is also more common when an individual has biological relatives that also have the disorder.
• Empirically supported treatments
  • Treatment is done to try to reconnect the different personalities to one functional identity. Sometime if that does not work, a clinician may try to do something to help with the symptoms. Some of the things are long-term psychotherapy, cognitive and creative therapies, and medications for comorbid disorders or doing some kind of behavioral therapy. Some may face a longer, slower process which may only help with symptom relief. However, the ones that are still attached to the abusers may have the most difficult time. Some medications for Dissociative Identity Disorder are antidepressants, anti-anxiety drugs, or tranquilizers to help reduce the symptoms.

PROPOSED DSM-5 CHANGES (dsm5.org)
Dissociative Identity Disorder

A. Disruption of identity characterized by two or more distinct personality states or an experience of possession, as evidenced by discontinuities in sense of self, cognition, behavior, affect, perceptions, and/or memories. This disruption may be observed by others or reported by the patient.
B. Inability to recall important personal information, for everyday events or traumatic events, that is inconsistent with ordinary forgetfulness.

C. Causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

D. The disturbance is not a normal part of a broadly accepted cultural or religious practice and is not due to the direct physiological effects of a substance (e.g., blackouts or chaotic behavior during Alcohol intoxication) or a general medical condition (e.g., complex partial seizures). NOTE: In children, the symptoms are not attributable to imaginary playmates or other fantasy play.
specify if

a) With non-epileptic seizures or other conversion symptoms

b) With somatic symptoms that vary across identities (excluding those in specifier a)
The workgroup is still considering whether Criterion C is necessary. The specifiers are still under consideration.

RATIONALE FOR CHANGE

A. Clarification of language, including indicating that different states can be reported or observed, reducing use of Dissociative Identity Disorder Not Otherwise Specified. Including Trance and Possession Disorder by mentioning “experience of possession” increases global utility.

B. Noting that amnesia for everyday events is a common feature.
C. This criterion is included in DSM-IV Dissociative Identity Disorder. Including it may help differentiate normative cultural experiences from psychopathology.

D. Addition from DSM-IV Dissociative Trance Disorder to increase cross-cultural applicability

Specifiers:

a) A substantial proportion of patients with Dissociative Identity Disorder have conversion symptoms, which are related to their dissociative disorder and require special clinical attention and treatment.

b) Some Dissociative Identity Disorder patients have dissociative variations in somatic symptoms that require clarification for differential medical diagnosis and treatment.

DSM-5 CHANGES FOR DISSOCIATIVE DISORDER NOT OTHERWISE SPECIFIED(300.15)

This category is for disorders in which the predominant feature is a dissociative symptom (i.e. a subjective loss of integration of information or control over mental processes that, under normal circumstances, are available to conscious awareness or control, including memory, identity, emotion, perception, body representation, motor control, and behavior) that does not meet the criteria for any specific Dissociative Disorder. Examples include:

1. Clinical presentations similar to Dissociative Identity Disorder that fail to meet full criteria for this disorder. Examples include presentations in which a) there are not two or more distinct personality states, or b) amnesia for important personal information does not occur.
2. States of dissociation that occur in individuals who have been subjected to periods of prolonged and intense coercive persuasion (e.g., brainwashing, thought reform, or indoctrination while captive).
3. Dissociative trance, characterized by narrowing of awareness of immediate surroundings or stereotyped behaviors or movements that are experienced as being beyond one’s control. The dissociative trance is not a normal part of a broadly accepted collective cultural or religious practice.
4. Loss of consciousness, stupor, or coma not attributable to a general medical condition.
5. Ganser syndrome: the giving of approximate answers to questions (e.g., 2 plus 2 equals 5) when not associated with Dissociative Amnesia.
6. Acute reactions to stressful events, lasting less than one month, that are characterized by mixed dissociative symptoms, such as depersonalization, derealization, amnesia, disruptions of consciousness, and/or stupor that cause marked distress or impairment and are not restricted to the symptoms of another mental disorder, e.g., Acute Stress Disorder, Delirium, or another dissociative disorder.
7. Acute states, lasting less than one month, characterized by mixed dissociative symptoms (e.g., amnesia, dissociative flashbacks, disruptions of consciousness) and psychotic symptoms (e.g., catatonia, auditory or visual hallucinations, delusions, grossly disturbed behavior) that cause marked distress or impairment and do not meet criteria for Acute Stress Disorder, a Psychotic Disorder, Delirium, or another dissociative disorder.

An additional example of acute presentations with mixed dissociative symptoms that do not fulfill criteria for the specified dissociative disorders is being considered for inclusion in Dissociative Disorder Not Otherwise Specified.
Rationale
Changes to be consistent with alterations in Dissociative Identity Disorder and the definition of dissociation.

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11. Dissociative Fugue (300.13)

• DSM-IV-TR criteria
  • A. The predominant disturbance is sudden, unexpected travel away from home or one’s customary place of work, with inability to recall one’s past.
  • B. Confusion about personal identity or assumption of a new identity (partial or complete).
  • C. The disturbance does not occur exclusively during the course of Dissociative Identity Disorder and is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g.., temporal lobe epilepsy).
  • D. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
• Associated features
  • Dissociative Fugue was formerly known as Psychogenic Fugue, it is comorbid with Bipolar Disorder, Major Depressive Disorder, and Schizophrenia, as well as PTSD, Substance Related disorders, Panic and Anxiety Disorders, Eating Disorders, and Somatoform Disorders. Note: Dissociative Fugue is often mistaken for malingering. This happens because the disorder enables people to escape their responsibilities or undesirable or dangerous situations; therefore it is seen as if a person is taking the ‘easy-way-out’. A person in the midst of a Dissociative Fugue episode may appear only slightly confused or they may appear to have no symptoms at all and attract no attention. Eventually, however, the person will begin to show significant signs of confusion or distress as they become aware of memory loss or confusion about their identity. This amnesia is characteristic of the disorder. When the fugue ends, the person may experience depression, grief, shame, and suicidal impulses.
• Child vs. adult presentation
  • Dissociative Fugue usually begins in adulthood. There is little information about the presentation of this disorder in children. When it does affect children, it is most commonly due to severe trauma such as sexual abuse, but even then it does not usually present until adulthood.
• Gender and cultural differences in presentation
  • Some research revealed that this condition most often occurs in females, but the reason is unknown. One source stated that females are at a rate six to nine times higher than males, and it increases as age increases. This pattern is most likely associated with the stresses on a woman to be both mother and a family provider and caretaker, in conjunction with the societal pressures and gender prejudices. Most studies however, believed that Dissociative Fugue is equally prevalent across genders.
    There is little information on the cultural differences in presentation of Dissociative Fugue. It is important to remember that what may be considered dissociative in one culture may be seen as normal in another. Cultures prone to warfare are more likely to experience the distressing pressures of war, which is a common causal traumatic event of this disorder. Various cultures with defined “running” syndrome may have symptoms that meet diagnostic criteria for Dissociative Fugue, such as the amok in Western Pacific cultures.
• Epidemiology
  • This is a relatively rare disorder, actually the rarest of the dissociative disorders, affecting about only 2 in 1000 people in the United States. The prevalence rate is estimated at 0.2%. It is much more common however among people who have been in wars, accidents, natural disasters, or other highly traumatic or stressful events.
• Etiology
  • Episodes of Dissociative Fugue are usually triggered by very stressful events. Traumatic experiences such as war, natural disasters, accidents, and sexual abuse during childhood, often increase the incidence of the disorder. More personal types of stress, like the shocking death of a loved one or unbearable pressures at work or home, might also lead to the unplanned travel and amnesia that is characteristic of Dissociative Fugue.
• Empirically supported treatments
  • Most fugues last for only hours or days, and then often disappear on their own. The goal of treatment is to assist the person to come to terms with the trauma or stress that triggered the fugue in the first place. Another goal of treatment is to help develop new coping methods to prevent further fugue episodes. As with most disorders, the particular treatment approach depends on the individual and the severity of his or her symptoms. The most likely treatment however will include a combination of psychotherapy, cognitive therapy, medication, family therapy, creative therapy, and clinical hypnosis. Psychotherapy is the main treatment for dissociative disorders such as Dissociative Fugue. Such treatments aim to increase insight into problems. Cognitive therapy focuses on changing dysfunctional thinking patterns. Medication is useful when the person also suffers from depression or anxiety. Family therapy aims to teach the family more about the disorder and learn about the symptoms of recurrence. Creative therapies, such as music therapy and art therapy, let the person express themselves in safe manners. Clinical hypnosis uses intense relaxation, concentration, and focuses attention to achieve an altered state of awareness. This is risky however because of the risk of creating false memories. The prognosis for Dissociative Fugue is often very good because the episodes do not usually last longer than a few months and people generally recover quickly. Efforts to restore the memories of what happened during the fugue are usually unsuccessful or take a long time to be recovered.
• Illustrative case
  • A case study was reported in Psychology Today (Drawing a Blank, October 2007) and was also reported in Maclean’s Magazine (The Man Who Lost Himself, May 2007) about a man named Jeff Ingram. A short summary of this case goes as follows: Ingram, 40, is a former mill worker in Olympia, Washington. He left his home one morning headed for Alberta to visit a terminally ill friend. A few days later he woke up on a street in Denver with no idea of who he was. Ingram became confused, angry, and worried when he was being questioned by the hospital’s receptionist because he had no knowledge of his identity. Even months after being reunited with his family, Ingram still had no pre-fugue memories, including that of his three year relationship with then-fiancée. In order to prevent such confusion in the future, Ingram ordered GPS shoes and had his identity information tattooed on him. He also wears a zip disk with medical information around his neck. It is believed that the possible trigger of Ingram’s fugue episode was the stress of his friend’s battle of cancer. A more detailed article can be found in Maclean’s magazine (May 2007).

PROPOSED DSM-5 CHANGES: (dsm5.org)
The DSM-5 workgroup is proposing that this disorder be subsumed into an existing disorder. Dissociative Amnesia(to become a subtype of Dissociative Amnesia).
Rationale:The literature, reviewed in the Dissociative Disorders literature review, makes it clear that dissociative amnesia, usually for identity, is the primary feature, and travel is an inconsistent one. Also, the disorder is extremely rare, so inclusion as a subtype of Dissociative Amnesia seems reasonable.

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12. Trichotillomania (312.39)

The video above contains a woman explaining her struggles with trichotillomania.

• DSM-IV-TR criteria
  • A. Recurrent pulling out of one’s hair resulting in noticeable hair loss.
  • B. An increasing sense of tension immediately before pulling out the hair or when attempting to resist the behavior.
  • C. Pleasure, gratification, or relief when pulling out the hair.
  • D. The disturbance is not better accounted for by another mental disorder and is not due to a general medical condition (e.g., a dermatological condition.)
  • E. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
• Associated Features
  • Individuals with Trichotillomania are often seen by the public as having a habit of playing with their hair. The individual will examine the hair root, twirl it off, pull the strand of hair between their teeth, or may eat their hair. They usually do not pull their hair out in the presence of anyone except family members. The individual suffering from this disorder will deny that they pull out their hair, and will attempt to hide the resulting baldness. If the case is extreme, the individual may have urges to pull others hair, but often can refrain. Dolls, pets, carpet, and sweaters are often pulled on like hair, and nail biting, scratching, gnawing, and excoriation are often associated with this disorder.
• Child vs. Adult presentation
  • The mean age of onset is 9 to 14 years old. It is more common during the first 20 years of someone’s life. There is not a difference in presentation between child and adults, however.
• Gender and cultural differences in presentation
  • When presented in children, the rates between genders tend to be relatively equal. However, when Trichotillomania is present in an adult, it is more common in females. It has been found that 70-90% of pre-adolescents and adults that have this are female. This finding of an off-balance male-to-female ratio may be a result of the true gender ratio of the condition, or it could be due to treatment seeking curve formed due to cultural or gender based attitudes regarding acceptance of the associated features of this disease.
• Epidemiology
  • Trichotillomania is now believed to be more common than it once was. Studies show that today the lifetime prevalence rate of this disorder is 0.6%.
• Etiology
  • There is evidence of a genetic predisposition, in which mutations found in a gene known as SLITRK1 have been linked to trichotillomania as well as to Tourette syndrome, a neurological disorder that causes a person to make unusual movements and sounds
  • Neurochemical problems can also play a role in Trichotillomania. Some studies suggest that abnormalities in the natural brain chemicals serotonin and dopamine may play a role in trichotillomania.
• Empirically supported treatments

Proposed Dsm5 Changes (Dsm5.org)

The work group is recommending that this disorder be reclassified from Impulse Control Disorders Not Elsewhere Classified to Anxiety and Obsessive-Compulsive Spectrum Disorders
A. Recurrent pulling out of one’s hair resulting in hair loss.
B. The hair pulling causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
C . The hair pulling is not due to a general medical condition (e.g., a dermatological condition).
D. The hair pulling is not restricted to the symptoms of another mental disorder (e.g., hair pulling due to preoccupation with appearance in Body Dysmorphic Disorder).

• The work group is considering an additional criterion that addresses urges to pull one’s hair or attempts to resist hair pulling.

Rationale for Change

Name: The term “mania” seems inappropriate for trichotillomania. However, changing too rapidly to a more descriptive term (eg hair-pulling disorder) may be confusing for clinicians, hence we propose to retain trichotillomania in parentheses

A: Hair loss may not always be noticeable in those suffering from this disorder.

B and C: Patients with chronic hair-pulling may or may not meet criteria B or C. Those who do and do not meet these criteria do not appear distinguishable on a range of clinical validators.

D: The exclusion criterion may be more clinically useful if it lists disorders that may be misdiagnosed as trichotillomania. For purposes of clarity and consistency, we have used the phrase “not restricted to” in the hierarchy criterion of other disorders in our section.

Severity: Massachusetts General Hospital Hairpulling Scale (MGH-HPS) (Keuthen et al., 1995)

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13. Somatization Disorder (300.81)

In the video above Dr. Soheil Ahaddian explains what Somatization Disorder is and the symptoms that appear with it.

• DSM-IV-TR criteria
  • A history of many physical complaints beginning before age 30 years that occur over a period of several years and result in treatment being sought or significant impairment in social, occupational, or other important areas of functioning.
  • Each of the following criteria must have been met, with individual symptoms occurring at any time during the course of the disturbance:
    • (1) four pain symptoms: a history of pain related to at least four different sites or functions (e.g., head, abdomen, back, joints, extremities, chest, rectum, during menstruation, during sexual intercourse, or during urination)
    • (2) two gastrointestinal symptoms: a history of at least two gastrointestinal symptoms other than pain (e.g., nausea, bloating, vomiting other than during pregnancy diarrhea, or intolerance of several different foods)
    • (3) one sexual symptom: a history of at least one sexual or reproductive symptom other than pain (e.g., sexual indifference, erectile or ejaculatory dysfunction, irregular menses, excessive menstrual bleeding, vomiting throughout pregnancy)
    • (4) one pseudo-neurological symptom: a history of at least one symptom or deficit suggesting a neurological condition not limited to pain (conversion symptoms such as impaired coordination or balance, paralysis or localized weakness, difficulty swallowing or a lump in throat, aphonia, urinary retention, hallucinations, loss of touch or pain sensation, double vision, blindness, deafness, seizures; dissociative symptoms such as amnesia; or loss of consciousness other than fainting.
  • C. Either (1) or (2):
    • (1) after appropriate investigation, each of the symptoms in Criterion B cannot be fully explained by a known general medical condition or the direct effects of a substance (e.g., a drug of abuse, a medication)
    • (2) when there is a related general medical condition, the physical complaints or resulting social or occupational impairment are in excess of what would be expected from the history, physical examination or laboratory findings
  • D. The symptoms are not intentionally produced or feigned (as in Factitious Disorder or Malingering)
• Associated features
  • Associated features of Somatization Disorder (SD) include: vomiting, chest pain, dizziness, headaches, stomachaches, pain during sex, diminished sex drive, pain while passing urine, erectile dysfunction, irregular menstruation, joint pain, and back pain. Other types of symptoms are possible, but these are the most common. These symptoms are usually severe enough to interfere with patients’ daily lives and relationships. They are not to be taken lightly.
  • Individuals diagnosed with Somatization Disorder make colorful, often exaggerated complaints. The complaints are often lacking in specific factual information. A checklist approach to diagnostic interviewing may be less effective than a thorough review of medical treatments and hospitalizations in documenting the pattern of frequent somatic complaints.
• Child vs. Adult presentation
  • Children experience many of the same symptoms adults suffer from. The age of onset is typically during adolescence and the diagnosis criteria needs to be met by the 20s. If chronic, individuals rarely remit completely. Boys and girls experience symptoms equally until adolescence is reached. Once adolescence is reached, more girls report having somatization disorder than boys. Children tend to experience somatization disorder after a traumatic event in their life has taken place, such as divorce or death of a loved one.
• Gender and cultural differences in presentation
  • Somatization disorder is more prevalent in women than it is in men. Some studies provide that as much as two percent of women suffer from somatization disorder. The ratio of men to women that suffer from somatization disorder is about ten to one.
  • Somatization disorder is found all over the world. Many cultures present with the same symptoms that are mentioned above, but others are different. Cross-cultural studies indicate that the symptoms people with somatization disorder experience may vary greatly from culture to culture. Some symptoms specific to South Asia and Africa include burning sensations in the hands and feet and the feeling of worms crawling or ants crawling under the skin, respectively. Prevalence is about 0.2% to 2% in women and less than 2% in men.
• Epidemiology
  • Somatization Disorder is not commonly found in the population. About 2% of women have it and 0.2% of men have it. Many people that suffer from somatization disorder also have anxiety disorders or depression or both.
• Etiology
  • Somatization disorder is caused by stress. The patient does not want to feel stress or anxiety so the patient transmits these feelings into physical symptoms. Some people also associate a stigma onto psychological therapy and if they feel pain or other symptoms they can go to a medical doctor and not a psychologist.
• Empirically supported treatments
  • There is not a known treatment for somatization disorder, but there are ways to manage symptoms. Cognitive behavioral therapy is used to help the patient change and manage their thoughts. Patients are also encouraged to become more active. Anti-depressants can also be used to manage symptom, these treat by alleviating the depression or dysthymia. It is extremely difficult to treat but a combination of medical management and cognitive-behavioral therapy may be helpful.
  • While empirical support may be lacking, there is a growing consensus that suggests that somatization disorder should be managed instead of treated. This simply means that primary care physicians, therapists, or any other caregivers should help patients control the behavior caused by SD instead of trying to cure it. An important goal of this method is preventing any unnecessary medical or surgical investigations. This could be accomplished by following five recommendations:
    • 1. One long-term and supportive relationship with a primary care physician that understands the situation should be established. This can prevent doctor shopping and lead to more coordinated support.
    • 2. Establish an appointment schedule for check-ups rather than seeing the patient on demand. This is done to avoid the reinforcement of abnormal behaviors caused by the disorder.
    • 3. A caregiver may regard certain physical complaints as a form of communication as well as possible evidence of a disease.
    • 4. The use of psychotropic drugs and analgesic medication should be minimized.
    • 5. Adaptive and positive behavior should be encouraged and promoted while sick role behavior is ignored whenever possible.

Propoesd DSM5 Changes (DSM5.org)
Reclassifiaction to Complex Somatic Symptom Disorder
Complex Somatic Symptom Disorder includes: previous diagnoses of Somatization Disorder, Undifferentiated Somatoform Disorder, Hypochonddiasis, Pain Disorder Associated With Both Psychological Factors and a General Medical Condition, and Pain Disorder Associated with Psychological Factors
To meet criteria for CSSD, criteria A,B, and C are necessary.
A. Somatic Symptoms

One or more somatic symptoms that are distressing and/or result in significant disruption in daily life.
B. Excessive Thoughts, Feelings, and Behaviors related to these somatic symptoms or associated health concerns:

At least two of the following are required to meet this criterion:
(1) High level of health-related anxiety.
(2) Disproportionate and persistent concerns about the medical seriousness of one’s symptoms.
(3) Excessive time and energy devoted to these symptoms or health concerns

C. Chronicity: Although any one symptom may not be continuously present, the state of being symptomatic is chronic (at least 6 months).
For patients who fulfill the CSSD criteria, the following optional specifiers may be applied to a diagnosis of CSSD where one of the following dominates the clinical presentation:
XXX.1 Predominant somatic complaints (previously, somatization disorder)
XXX.2 Predominant health anxiety (previously, hypochondriasis). If patients present solely with health-related anxiety with minimal somatic symptoms, they may be more appropriately diagnosed as having an anxiety disorder.
XXX.3 Predominant Pain (previously pain disorder). This classification is reserved for individuals presenting predominantly with pain complaints who also have many of the features described under criterion B. Patients with other presentations of pain may better fit other psychiatric diagnoses such as adjustment disorder or psychological factors affecting a medical condition.
For assessing severity of CSSD, metrics are available for rating the presence and severity of somatic symptoms (see for instance PHQ, Kroenke et al, 2002). Scales are also available for assessing severity of the patient’s misattributions, excessive concerns and preoccupations (see for instance Whiteley inventory, Pilowsky , 1967).

Rationale:

Major Change #1: Rename Somatoform Disorders to Somatic Symptom Disorders and combine with PFAMC and Factitious Disorders

The workgroup suggests combining Somatoform Disorders, Psychological Factors Affecting Medical Condition (PFAMC), and Factitious Disorders into one group entitled “Somatic Symptom Disorders” because the common feature of these disorders is the central place in the clinical presentation of physical symptoms and/or concern about medical illness. The grouping of these disorders in a single section is based on clinical utility (these patients are mainly encountered in general medical settings), rather than assumptions regarding shared etiology or mechanism.

Major Change #2: Combine Somatization disorder, hypochondiasis, undiffereniated somatoform disorder, and pain disorder into a new category entitled “Complex Somatic Symptom Disorder” (CSSD)

Combine somatization disorder, hypochondriasis, undifferentiated somatoform disorder, and pain disorder into a new category entitled “Complex Somatic Symptom Disorder” (CSSD) which emphasizes the symptoms plus the patients’ abnormal cognitions (Barsky, Lowe, Rief). The term “complex” is intended to denote that in order for this diagnosis to be made, the symptoms must be persistent and must include both somatic symptoms (criterion A) as well as cognitive distortions (criterion B).
This is a major change in the diagnostic nomenclature, and it will likely have a major impact on diagnosis. It clarifies that a diagnosis of CSSD is inappropriate in the presence of only unexplained medical symptoms. Similarly, in conditions such as irritable bowel syndrome, CSSD should not be coded unless the other criterion (criterion B—attributions, etc) is present.
It is unclear how these changes would affect the base rate of disorders now recognized as somatoform disorders. One might conclude that the rate of diagnosis of CSSD would fall, particularly if some disorders previously diagnosed as somatoform were now diagnosed elsewhere (such as adjustment disorder). On the other hand, there are also considerable data to suggest that physicians actively avoid using the older diagnoses because they find them confusing or pejorative. So, with the CSSD classification, there may be an increase in diagnosis.
The proposal is to group together these heretofore separately recognized disorders because in fact, there are 3 diverse sources suggesting considerable overlap among them.
1. A 2009 study found that 52% of physicians surveyed indicated that there was “a lot of overlap” and an additional 38% thought that there was “some overlap” across these disorders. In contrast, less than 2% of physician respondents felt that these were “distinctly different disorders (Dimsdale, Sharma, & Sharpe, unpublished).
2. There are limited data regarding overlap in clinical settings. One primary care study, for instance, found that 20% of somatization disorder patients also had hypochondriasis (Escobar, 1998). In primary care patients, somatization disorder was 5 times ( Fink et al 2004) to 20 times (Barsky et al 1992) more common in hypochondriasis patients as compared to primary care patients without hypochondriasis.
3. Treatment interventions are similar in this group of disorders. Cognitive behavior therapy (CBT) and antidepressant medications appear to be the most promising therapeutic approaches for hypochondriasis, somatization disorder, and pain disorder (Kroenke 2007; Sumathipala 2007). Although several variations of CBT have been employed, they share many elements in common. These include the identification and modification of dysfunctional and maladaptive beliefs about symptoms and disease, and behavioral techniques to alter illness and sick role behaviors and promote more effective coping. The literature on the use of antidepressants is more limited, but it too does not suggest any major distinctions in therapeutic response across these different disorders. In addition to these patient centered commonalities of treatment, all of these disorders benefit from specific interventions with the patient’s non-psychiatric physician (e.g. scheduling regular appointments as opposed to prn appointments, limiting testing and procedures unless clearly indicated) (Allen 2002).
A key issue is whether the guidelines for CSSD describe a valid construct and can be used reliably. A recent systematic review (Lowe, submitted for publication) shows that of all diagnostic proposals, only Somatic Symptom Disorder reflects all dimensions of current biopsychosocial models of somatization (construct validity) and goes beyond somatic symptom counts by including psychological and behavioral symptoms that are specific to somatization (descriptive validity). Predictive validity of most of the diagnostic proposals has not yet been investigated.

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14. Undifferentiated Somatoform Disorder (300.82)

• DSM criteria
  • A one or more physical complaints (e.g. fatigue, loss of appetite, gastrointestinal or urinary complaints).
  • B Either 1 or 2:
    1. after appropriate investigation, the symptoms cannot be fully explained by a known general medical condition or the direct effects of a substance (e.g. a drug of abuse, a medication)
    2. when there is a related general medical condition, the physical complaints or resulting social or occupational impairment is in excess of what would be expected from the history, physical examination, or laboratory findings
  • C The symptoms cause clinically significant distress or impairment in social, occupational, or other important area of functioning.
  • D the duration of the disturbance is at least 6 months.
  • E The disturbance is not better accounted for another mental disorder (e.g. another Somatoform Disorder, Sexual Dysfunction, Mood Disorder, Anxiety Disorder, Sleep Disorder, or Psychotic Disorder).
  • F The symptom is not intentionally produced or feigned (as in Fictitious Disorder or Malingering).
• Associated Features
  • The symptoms of this disorder vary from person to person. The most common symptoms associated with this disorder are mostly physical complaints. These include:
    • pain
    • fatigue
    • appetite loss
    • various gastrointestinal problems
  • The characteristic that defines this disorder is that although the person complains, no evidence can be found that these physical symptoms actually exist. Even with lab test and exams by doctors, no physical signs can be supported to prove that the person actually has these symptoms.
• Child vs. adult presentation
  • Undifferentiated somatoform disorder is more common in adults than children.
• Gender and cultural differences
  • The highest frequency of unexplained physical complaints occurs in young women of low socioeconomic status, but such symptoms are not limited to any gender, age, or sociocultural group.
• Epidemiology
  • Undifferentiated Somatoform Disorder is relatively common. About four to eleven percent of the population will experience this disorder at some point in their life. This disorder is also comorbid with anxiety and depression. About fifty percent of people also suffer with these comorbid disorders.
• Etiology
  • Some people believe that in the development of Undifferentiated Somatoform Disorder, causes could include problems in the family when the person was a child. Other explanations are that the person experiences stress or depression. A final possible cause is the patient worrying about every little change or sensation their body has.
• Empirically Supported Treatments
  • Most treatments are done via psychotherapy. These treatments focus on the stressors that cause the patient to think something is happening to their body. If the patient already suffers from depression or stress, treating this problem can help lead to making the symptoms of the disorder go away or at least subside for a while. Most treatments will try to help the person manage stress, as well as differentiate between psychological stressors and physiological pain.

• Dsm5 Proposed Changes (Dsm5.org)

The work group is recommending that this disorder be subsumed into a new disorder: Complex Somatic Symptom Disorder

Major Change #1: Rename Somatoform Disorders to Somatic Symptom Disorders and combine with PFAMC and Factitious Disorders

The workgroup suggests combining Somatoform Disorders, Psychological Factors Affecting Medical Condition (PFAMC), and Factitious Disorders into one group entitled “Somatic Symptom Disorders” because the common feature of these disorders is the central place in the clinical presentation of physical symptoms and/or concern about medical illness. The grouping of these disorders in a single section is based on clinical utility (these patients are mainly encountered in general medical settings), rather than assumptions regarding shared etiology or mechanism.

Major Change #2: Combine Somatization disorder, hypochondiasis, undiffereniated somatoform disorder, and pain disorder into a new category entitled “Complex Somatic Symptom Disorder” (CSSD)

Combine somatization disorder, hypochondriasis, undifferentiated somatoform disorder, and pain disorder into a new category entitled “Complex Somatic Symptom Disorder” (CSSD) which emphasizes the symptoms plus the patients’ abnormal cognitions (Barsky, Lowe, Rief). The term “complex” is intended to denote that in order for this diagnosis to be made, the symptoms must be persistent and must include both somatic symptoms (criterion A) as well as cognitive distortions (criterion B).
This is a major change in the diagnostic nomenclature, and it will likely have a major impact on diagnosis. It clarifies that a diagnosis of CSSD is inappropriate in the presence of only unexplained medical symptoms. Similarly, in conditions such as irritable bowel syndrome, CSSD should not be coded unless the other criterion (criterion B—attributions, etc) is present.
It is unclear how these changes would affect the base rate of disorders now recognized as somatoform disorders. One might conclude that the rate of diagnosis of CSSD would fall, particularly if some disorders previously diagnosed as somatoform were now diagnosed elsewhere (such as adjustment disorder). On the other hand, there are also considerable data to suggest that physicians actively avoid using the older diagnoses because they find them confusing or pejorative. So, with the CSSD classification, there may be an increase in diagnosis.
The proposal is to group together these heretofore separately recognized disorders because in fact, there are 3 diverse sources suggesting considerable overlap among them.
1. A 2009 study found that 52% of physicians surveyed indicated that there was “a lot of overlap” and an additional 38% thought that there was “some overlap” across these disorders. In contrast, less than 2% of physician respondents felt that these were “distinctly different disorders (Dimsdale, Sharma, & Sharpe, unpublished).
2. There are limited data regarding overlap in clinical settings. One primary care study, for instance, found that 20% of somatization disorder patients also had hypochondriasis (Escobar, 1998). In primary care patients, somatization disorder was 5 times ( Fink et al 2004) to 20 times (Barsky et al 1992) more common in hypochondriasis patients as compared to primary care patients without hypochondriasis.
3. Treatment interventions are similar in this group of disorders. Cognitive behavior therapy (CBT) and antidepressant medications appear to be the most promising therapeutic approaches for hypochondriasis, somatization disorder, and pain disorder (Kroenke 2007; Sumathipala 2007). Although several variations of CBT have been employed, they share many elements in common. These include the identification and modification of dysfunctional and maladaptive beliefs about symptoms and disease, and behavioral techniques to alter illness and sick role behaviors and promote more effective coping. The literature on the use of antidepressants is more limited, but it too does not suggest any major distinctions in therapeutic response across these different disorders. In addition to these patient centered commonalities of treatment, all of these disorders benefit from specific interventions with the patient’s non-psychiatric physician (e.g. scheduling regular appointments as opposed to prn appointments, limiting testing and procedures unless clearly indicated) (Allen 2002).
A key issue is whether the guidelines for CSSD describe a valid construct and can be used reliably. A recent systematic review (Lowe, submitted for publication) shows that of all diagnostic proposals, only Somatic Symptom Disorder reflects all dimensions of current biopsychosocial models of somatization (construct validity) and goes beyond somatic symptom counts by including psychological and behavioral symptoms that are specific to somatization (descriptive validity). Predictive validity of most of the diagnostic proposals has not yet been investigated.

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15. Pain Disorder (307)

• DSM-IV-TR criteria
  • A. Pain in one or more anatomical sites is the predominant focus of the clinical presentation and is of sufficient severity to warrant clinical attention.
  • B. The pain causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  • C. Psychological factors are judged to have an important role in the onset, severity, exacerbation, or maintenance of the pain.
  • D. The symptom or deficit is not intentionally produced or feigned (as in Factitious Disorder or malingering).
  • E. The pain is not better accounted for by a Mood, Anxiety, or Psychotic Disorder and does not meet criteria for Dyspareunia.
    • Code as follows:
    • 307.80 Pain Disorder Associate With Psychological Factors: psychological factors are judged to have the major role in the onset,severity, exacerbation, or maintenance of the pain. (If a general medical condition is present, it does not have a major role on the onset,severity, exacerbation, or maintenance of the pain.) This type of Pain Disorder in not diagnosed if criteria are also met for Somatization Disorder.
    • Specify if:
    • Acute: duration of less than 6 months
    • Chronic: duration of 6 months or longer
    • 307.89 Pain Disorder Associated with both psychological factors and general medical condition: both psychological factors and a general medical condition are judged to have important roles in the onset, severity, exacerbation, or maintenance of the pain. The associated general medical condition or anatomical site of the pain(see below) is coded on Axis III
    • Specify if:
    • Acute:duration of less than 6 months
    • Chronic: duration of 6 months or longer
    • Note: The following is not considered to be a mental disorder and is included here to facilitate differential diagnosis.
    • Pain Disorder Associated with a General Medical Condition: a general medical condition has a major role in the onset, severity, exacerbation, or maintenance of the pain. (If psychological factors are present, they are not judged to have a major role in the onset, severity, exacerbation, or maintenance of the pain.) The diagnostic code for the pain is selected based on the associated general medical condition if one has been established(see Appendix G) or on the anatomical location of the pain if the underlying general medical condition is not yet clearly established-for example, low back(724.2) sciatic (724.3), pelvic (625.9), headache (784.0), facial (784.0), chest (786.5), joint (719.4), bone (733.9), abdominal (789.0), breast (611.71), renal(788.0), ear (388.70), eye (379.91), throat(784.1), tooth (525.9), and urinary (788.0).
  • Associated features
    • Pain may severely disrupt different aspects of a person’s daily life. It may lead to unemployment, disability, and family problems. It may also have an effect on Iatrogenic Opiod Dependence or Abuse and Benzodiazepine Dependence or Abuse as well as Substance Dependence or Abuse. It is also associated with severe depression with terminal illness as well as a risk to suicide. It may lead to inactivity and social isolation, reduction in physical endurance, and fatigue. Also, other associated features include: musculoskeletal conditions, neuropathies, malignancies. There is comorbidity with Osteoporosis, Osteoarthritis, and Fibromyalgia.
  • Child vs. Adult presentation
    • It may occur at any age but there are not any known differences.
  • Gender and cultural differences
    • Females will appear to experience certain chronic pain conditions, most migraine and tension-type headaches and musculoskeletal pain more often than males.
    • It is different in each individual therefore it is hard to determine cultural differences.
  • Epidemiology
    • 10-15 % of adults in the United States
    • Depressive Disorders, Alcohol Dependence, and chronic pain may be more common in the first degree biological relatives with Pain Disorder.
  • Etiology
    • Pain disorder may develop due to a conversion mechanism and some patients may have what is called a “pain-prone personality:” where they have old feelings of guilt and worthlessness about themselves, and they constantly feel that they are in need of punishment, pain gives them this.
      *Physical pain may play such a role, and the onset of the pain may be seen in these patients when things seem to be going otherwise unexpectedly well in their lives. There is some connection between this personality style and a history of childhood abuse. Others, often women, experience pain for which no cause can be found. It appears unexpectedly, usually after a stress, and may fade away in days or it can last years.
  • Empirically supported treatments
    • It’s associated with a General Medical Condition may be treated with a course of general pain killers. This term is used for any patient who has pain that is mainly caused, worsened or maintained by a general medical condition, so long as any psychological factors play at most a minor role. This is not considered to be a mental disorder.
  • DSM-5 Changes (taken from DSM5.org)

The work group is recommending that this disorder be subsumed into a new disorder: Complex Somatic Symptom Disorder.
The following optional specifiers may be applied to a diagnosis of CSSD where one of the following dominates the clinical presentation:
XXX.3 Pain disorder. This classification is reserved for individuals presenting predominantly with pain complaints who also have many of the features described under criterion
B. Patients with other presentations of pain may better fit other psychiatric diagnoses such as major depression or adjustment disorder.

Rationale:
Major Change #1: Rename Somatiform disorders to Somatic Symptom Disorders and combine with PFAMC factitious disorders

The workgroup suggests combining Somatoform Disorders, Psychological Factors Affecting Medical Condition (PFAMC), and Factitious Disorders into one
group entitled “Somatic Symptom Disorders” because the common feature of these disorders is the central place in the clinical presentation of physical symptoms and/or concern about medical illness. The grouping of these disorders in a single section is based on clinical utility (these patients are mainly encountered in general medical settings), rather than assumptions regarding shared etiology or mechanism.

Major Change #2: Combine Somatization disorder hypochodriasis, undifferentiated somatiform disorder, and pain disorder into a new category entitled “Complex Somatic System Disorder” (CSSD).

Combine somatization disorder, hypochondriasis, undifferentiated somatoform disorder, and pain disorder into a new category entitled “Complex Somatic Symptom Disorder” (CSSD) which emphasizes the symptoms plus the patients’ abnormal cognitions (Barsky, Lowe, Rief). The term “complex” is intended to denote that in order for this diagnosis to be made, the symptoms must be persistent and must include both somatic symptoms (criterion A) as well as cognitive distortions (criterion B).

This is a major change in the diagnostic nomenclature, and it will likely have a major impact on diagnosis. It clarifies that a diagnosis of CSSD is inappropriate in the presence of only unexplained medical symptoms. Similarly, in conditions such as irritable bowel syndrome, CSSD should not be coded unless the other criterion (criterion B—attributions, etc) is present.
It is unclear how these changes would affect the base rate of disorders now recognized as somatoform disorders. One might conclude that the rate of diagnosis of CSSD would fall, particularly if some disorders previously diagnosed as somatoform were now diagnosed elsewhere (such as adjustment disorder). On the other hand, there are also considerable data to suggest that physicians actively avoid using the older diagnoses because they find them confusing or pejorative. So, with the CSSD classification, there may be an increase in diagnosis.
The proposal is to group together these heretofore separately recognized disorders because in fact, there are 3 diverse sources suggesting considerable overlap among them.
1. A 2009 study found that 52% of physicians surveyed indicated that there was “a lot of overlap” and an additional 38% thought that there was “some overlap” across these disorders. In contrast, less than 2% of physician respondents felt that these were “distinctly different disorders (Dimsdale, Sharma, & Sharpe, unpublished).
2. There are limited data regarding overlap in clinical settings. One primary care study, for instance, found that 20% of somatization disorder patients also had hypochondriasis (Escobar, 1998). In primary care patients, somatization disorder was 5 times ( Fink et al 2004) to 20 times (Barsky et al 1992) more common in hypochondriasis patients as compared to primary care patients without hypochondriasis.
3. Treatment interventions are similar in this group of disorders. Cognitive behavior therapy (CBT) and antidepressant medications appear to be the most promising therapeutic approaches for hypochondriasis, somatization disorder, and pain disorder (Kroenke 2007; Sumathipala 2007). Although several variations of CBT have been employed, they share many elements in common. These include the identification and modification of dysfunctional and maladaptive beliefs about symptoms and disease, and behavioral techniques to alter illness and sick role behaviors and promote more effective coping. The literature on the use of antidepressants is more limited, but it too does not suggest any major distinctions in therapeutic response across these different disorders. In addition to these patient centered commonalities of treatment, all of these disorders benefit from specific interventions with the patient’s non-psychiatric physician (e.g. scheduling regular appointments as opposed to prn appointments, limiting testing and procedures unless clearly indicated) (Allen 2002).
A key issue is whether the guidelines for CSSD describe a valid construct and can be used reliably. A recent systematic review (Lowe, submitted for publication) shows that of all diagnostic proposals, only Somatic Symptom Disorder reflects all dimensions of current biopsychosocial models of somatization (construct validity) and goes beyond somatic symptom counts by including psychological and behavioral symptoms that are specific to somatization (descriptive validity). Predictive validity of most of the diagnostic proposals has not yet been investigated.
Severity:

Severity metrics are readily available for somatic symptoms (viz PHQ, Kroenke 2002) and for the cognitive distortions and misattributions associated with CSSD (viz Whiteley Index, Pilowsky. 1967).

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16. Dissociative Amnesia (formerly Psychogenic Amnesia) (300.12)

• DSM-IV-TR criteria
  • The predominant disturbance is one or more episodes of inability to recall important personal information, usually of a traumatic or stressful nature, that is too extensive to be explained by ordinary forgetfulness.
  • The disturbance does not occur exclusively during the course of Dissociative Identity Disorder, Dissociative Fugue, Post traumatic Disorder, Acute stress Disorder, or Somatization Disorder and is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a neurological or other general medical condition (e.g., Amnestic Disorder Due to Head Trauma).
  • The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
• Diagnostic Features
  • The essential feature of Dissociative Amnesia is an inability to recall important personal information. Dissociative Amnesia most commonly presents as a retrospectively reported gap or series of gaps in recall for aspects of the individual’s life history. This acute form is more likely to occur during wartime or in response to a natural disaster or other form of severe trauma.
    • Localized amnesia
      • The individual fails to recall events that occurred during a circumscribed period of time, usually the first few hours after the event (e.g., the uninjured survivor of a car accident in which a person has been killed may not be able to recall anything that happen from the time of the accident until two days later).
    • Selective Amnesia
      • The person can recall some, but not all, of the events during a circumscribed period of time (e.g., a combat veteran can recall only parts of a series of violent combat experiences).
    • Generalized Amnesia
      • The person has a failure of recall encompasses the person’s entire life.
    • Continuous Amnesia
      • It is defined as the inability to recall events subsequent to a specific time up to and including the present.
    • Systematized Amnesia
      • The person’s loss of memory for certain categories of information, such as all memories relating to one’s family or to a particle person.
  • Individuals who exhibit these latter three types of Dissociative Amnesia may ultimately be diagnosed as having a more complex form of Dissociative Disorder (e.g., Dissociative Identity Disorder).
• Associated Features
  • Some individuals may report depressive symptoms, anxiety, depersonalization, trance states, analgesia, and spontaneous age regression. Other problems that have been reported include sexual dysfunction, impairment in work and interpersonal relationships, self-mutilation, aggressive impulses, and suicidal impulses and acts. Individuals with Dissociative Amnesia may also meet the criteria for Conversion Disorder, a Mood Disorder, a Substance-Related Disorder, or Personality Disorder. Associated laboratory findings.Individuals with Dissociative Amnesia often display high hypnotizability as measured by standardized testing.
• Child vs. Adult Presentation
  • This disorder is especially difficult to assess in preadolescent children, because it may be confused with inattention, other childhood disorders, or learning disorder. Outside observation or evaluations by several different examiners may be used to make an accurate diagnosis.
• Epidemiology
  • In the last twenty years there has been an increase in reported case that involves previously forgotten early-childhood traumas. It has been debated if this is due to the growing awareness of this disorder, or the over diagnosed in Individuals who are highly suggestible.
• Etiology
  • Has been linked to overwhelming stress, which could be due to a traumatic event (war, abuse, or disasters). There may also be a genetic link to Dissociative Amnesia. *Note: Many people with this disorder tend to have close relatives with similar conditions.
• Empirically supported treatments
  • Psychotherapy, for mental and emotional disorders uses psychological techniques designed to encourage communication of conflicts and increase insight into problems.
  • Cognitive therapy, focusing on changing dysfunctional thinking patterns and the resulting feelings and behaviors.
  • Pharmacotherapy, there is no medication to treat the dissociative disorders themselves; however, a person with a dissociative disorder who also suffers from depression or anxiety might benefit from treatment with a medication such as an antidepressant or anti-anxiety medicine.

PROPOSED DSM-5 CHANGES (DSM5.org)

Dissociative Amnesia

A. Inability to recall important personal information, usually of a traumatic or stressful nature, that is inconsistent with ordinary forgetting. Note: There are two primary forms of Dissociative Amnesia: (1) localized amnesia for a specific event or events, and (2) Dissociative Fugue: generalized amnesia for identity and life history. Fugue may be accompanied by either purposeful travel or bewildered wandering.
B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
C. The memory loss is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a neurological or other general medical condition (e.g., Amnestic Disorder Due to Head Trauma).
D. The memory loss is not restricted to the symptoms of another mental disorder (e.g., inability to remember an important aspect of the traumatic event in Posttraumatic Stress Disorder or Acute Stress Disorder, or amnesia occurring as a symptom of Dissociative Identity Disorder or Somatization Disorder).
Specify if:
Dissociative Fugue subtype:
1. Amnesia includes inability to recall one’s past, confusion about personal identity, or assumption of a new identity (partial or complete)

2. Sudden, unexpected travel away from home or work.

Rationale:
Minor wording changes for clarity.

B and C switched.

Changes to new C allow comorbid diagnoses to be made when warranted.

Severity:
Brief Dissociation Scale (Carlson E & Dahlenberg C, 2009)

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17. Dementia of the Alzheimer’s Type (294.1x)

• Diagnostic criteria
  • A. The development of multiple cognitive deficits manifested by both
    • (1) memory impairment (impaired ability to learn new information or to recall previously learned information)
    • (2) one (or more) of the following cognitive disturbances:
      • (a) aphasia (language disturbance)
      • (b) apraxia (impaired ability to carry out motor activities despite intact motor function)
      • (c) agnosia (failure to recognize or identify objects despite intact sensory function)
      • (d) disturbance in executive functioning (i.e. planning, organizing, sequencing, abstracting)
  • B. The cognitive deficits in Criteria A1 and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning.
  • C. The course is characterized by gradual onset and continuing cognitive decline.
  • D. The cognitive deficits in Criteria A1 and A2 are not due to any of the following:
    • (1) other central nervous system conditions that cause progressive deficits in memory and cognition (e.g. cerebrovascular disease, Parkinson’s disease, Huntington’s disease, subdural hematoma, normal-pressure hydrocephalus, brain tumor)
    • (2) systemic conditions that are known to cause dementia (e.g. hypothyroidism, vitamin B12 or folic acid deficiency, niacin deficeincy, hypercalcemia, ceurosyphilis, HIV infection)
    • (3) substance-induced conditions
  • E. The deficits do not occur exclusively during the course of a delirium.
  • F. The disturbance is not better accounted for by another Axis I disorder (e.g. Major Depressive Disorder, Schizophrenia).

Code based on presence or absence of a clinically significant behavioral disturbance:

• 294.10 Without Behavioral Disturbance: if the cognitive disturbance is not accompanied by any clinically significant behavioral disturbance.
• 294.11 With Behavioral Disturbance: if the cognitive disturbance is accompanied by a clinically significant behavioral disturbance (e.g., wandering, agitation).

Specify subtype:

• With Early Onset: if onset is at age 65 years or below
• With Late Onset: if onset is after age 65 years

Coding note: Also code 331.0 Alzheimer’s disease on Axis III. Indicate other prominent clinical features related to the Alzheimer’s disease on Axis I (e.g., 293.83 Mood Disorder Due to Alzheimer’s Disease, With Depressive Features, and 310.1 Personality Change Due to Alzheimer’s Disease, Aggressive Type).

Associated Features

• Dementia of Alzheimer’s Type is increasingly diagnosed in individuals with Down Syndrome and those with a history of head trauma. Brain atrophy is present in the majority of individuals diagnosed with Dementia of Alzheimer’s Type, and they generally have wider cortical sulci and larger cerebral ventricles than would be expected given the normal aging process.
• Few motor and sensory signs are seen in the first years of illness. Also, myoclonus and gait disorder may appear as the illness progresses. 10% of individuals with Dementia of the Alzheimer’s Type begin having seizures.

Child vs. Adult presentation

• This disorder is not seen in children, it is present in adults only. Very few cases are seen before age 50. Late onset of Dementia of Alzheimer’s Type is more typical than early onset, meaning that the age of onset is typically after age 65 years.

Epidemiology

• The prevalence rates of Dementia of Alzheimer’s Type increases dramatically with increasing age, rising from .6% in males and .8% in females at age 65 to 11% in males and 14% in females by age 85. As age increases so do the prevalence rates; at age 90 the rates rise to 21% in males and 25% in females, and by age 95 the prevalence rates are as high as 36% in males and 41% in females. Unfortunately, 40%-60% are moderate to severe cases.

• DSM-5 proposed changes (DSM5.org)

1. Removing the term “Dementia” and adding “Major Neurocognitive Disorders”
2. Adding a category of “Minor Cognitive Disorders”
3. Categorizing behavioral disturbances, particularly the syndromes of psychosis and depression, associated Neurocognitive Disorders
4. Selecting specific domains as well as measures of severity of cognitive functional impairment

• Major Neurocognitive Disorder (DSM-5)

Disorders subsumed under this overarching category would include, but not limited to, the following: Dementia Due to a General Medical Condition, Dementia Not Otherwise Specified, Dementia of the Alzheimer’s Type, Vascular Dementia, Dementia Due to Multiple Etiologies, Amnestic Disorder Due to a General Medical Condition, and Amnestic Disorder Not Otherwise Specified. Some individuals meeting criteria for Cognitive Disorder Not Otherwise Specified may also meet criteria for this disorder. Certain specific etiologies would be coded as subtypes, such as the Alzheimer’s Disease Subtype of Major and Minor Neurocognitive Disorders.

Major Neurocognitive Disorder
A. Evidence of significant cognitive decline from a previous level of performance in one or more of the domains outlined above based on:
1. Reports by the patient or a knowledgeable informant, or observation by the clinician, of clear decline in specific abilities as outlined for the specific table above.
AND
2. Clear deficits in objective assessment of the relevant domain (typically > 2.0 SD below the mean [or below the 2.5th percentile] of an appropriate reference population [i.e., age, gender, education, premorbid intellect, and culturally adjusted])

B. The cognitive deficits are sufficient to interfere with independence (e.g., at a minimum requiring assistance with instrumental activities of daily living, i.e., more complex tasks such as finances or managing medications)
C. The cognitive deficits do not occur exclusively in the context of a delirium.

D. The cognitive deficits are not wholly or primarily attributable to another Axis I disorder (e.g., Major Depressive Disorder, Schizophrenia)
Rationale for Change

Major Neurocognitive Disorder (including what was formerly known as Dementia) is a disorder with greater cognitive deficits in at least one (typically two or more) of the following domains:
Complex attention (planning, decision-making, working memory, responding to feedback/error correction, over-riding habits, mental flexibility),
Executive ability (planning, decision-making, working memory, responding to feedback/error correction, overriding habits, mental flexibility),
Learning and memory(immediate memory, recent memory [including free recall, cued recall, and recognition memory])
Language(expressive language [including naming, fluency, grammar and syntax] and receptive language),
Visuoconstructional-perceptual ability (construction and visual perception),and
Social cognition (recognition of emotions, theory of mind, behavioral regulation).
The cognitive deficits must be sufficient to interfere with functional independence. Important changes from the DSM-IV criteria include: change in nomenclature (MNCD or Dementia), not necessarily requiring memory to be one of the impaired domains, allowing cognitive deficit limited to one domain. In the introductory text, we offer a table that offers more details about the assessment of each domain in the form of specific symptoms of decline that can be elicited or observed, and assessment procedures that can be used to document the cognitive impairment and quantify its severity.

• The term “dementia” is replaced by Major Neurocognitive Disorder, which is conceptualized as including what was formerly known as dementia as well as entities like amnestic disorder. “Dementia” is an accepted term for older adults (e.g., with Alzheimer’s disease)—although even in this setting it has acquired a pejorative or stigmatizing connotation, it is less well accepted among younger adults with deficits related to e.g., HIV or head injury.
• This rewording focuses on decline (rather than deficit—consistent with the requirement in the basic definition of an acquired disorder) from a previous level of performance.
• The previous criteria for dementia used Alzheimer’s disease as their prototype and thus required memory impairment as a criterion for all dementias. There is growing recognition that, in other neurocognitive disorders (e.g., HIV-related cognitive decline, cerebrovascular disease, frontotemporal degeneration, traumatic brain injury, etc.), other domains such as language or executive functions may be impaired first, or exclusively, depending on the part of the brain affected and the natural history of the disease.
• The terminology for the cognitive domains has been updated to reflect current usage in neuropsychology and neurology.
• The new definition, consistent with DSM-wide changes, focuses first on performance rather than disability. In the introductory table, we provide for each domain examples of specific symptoms or observations consistent with the Major level of decline and objective assessments. This encourages the use of objective measures, including formal neuropsychological testing where feasible with lesser exclusive reliance on individual judgment.
• The presence of both symptoms/observations and objective assessment is included to ensure specificity. This is a larger issue for Minor Neurocognitive Disorder but included here for parallel structure of the criteria.
• NOTE: The committee is in the process of refining criteria A1 and A2 to achieve a balance between preferred formal neuropsychological assessment and what may feasible in some clinical settings. They welcome input on this issue.
• The new language preserves the traditional function-based threshold for dementia but tries to operationalize it more clearly as a loss of independence.
• NOTE: The committee is still refining criterion D and discussing to what extent Major Neurocognitive Disorder should be diagnosed in the setting of disorders like schizophrenia and depression (although this concern applies primarily to Minor Neurocognitive Disorder). They also realize that issues of this nature are being addressed at the DSM-wide level, and are awaiting input of these larger discussions, as well as public input on this issue.

• Minor Neurocognitive Disorder(DSM-5)

A. Evidence of minor cognitive decline from a previous level of performance in one or more of the domains outlined above based on:
1. Reports by the patient or a knowledgeable informant, or observation by the clinician, of minor levels of decline in specific abilities as outlined for the specific domains above. Typically these will involve greater difficulty performing these tasks, or the use of compensatory strategies.
AND
2. Mild deficits on objective cognitive assessment (typically 1 to 2.0 SD below the mean [or in the 2.5th to 16th percentile] of an appropriate reference population (i.e., age, gender, education, premorbid intellect, and culturally adjusted). When serial measurements are available, a significant (e.g., 0.5 SD) decline from the patient’s own baseline would serve as more definitive evidence of decline.
B. The cognitive deficits are not sufficient to interfere with independence (Instrumental Activities of Daily Living are preserved), but greater effort and compensatory strategies may be required to maintain independence.
C. The cognitive deficits do not occur exclusively in the context of a delirium.

D. The cognitive deficits are not wholly or primarily attributable to another Axis I disorder (e.g., Major Depressive Disorder, Schizophrenia).
Rationale for Change

Minor Neurocognitive Disorder has been added to recognize the substantial clinical needs of individuals who have mild cognitive deficits in one or more of the same domains but can function independently (i.e., have intact instrumental activities of daily living), often through increased effort or compensatory strategies. This syndrome, known in many settings as Mild Cognitive Impairment may be particularly critical, as it may be a focus of early intervention. Early intervention efforts may enable the use of treatments that are not effective at more severe levels of impairment and/or neuronal damage, and, in the case of neurodegenerative disease, may enable a clinical trial to prevent or slow progression.

• Minor Neurocognitive Disorder is added to account for individuals with minor levels of cognitive impairment who may require assessment and treatment, but are not sufficiently impaired the Major diagnosis. To some extent, this entity will take care of individuals currently coded as Cognitive Disorder NOS without specific criteria. This change is driven by the need of such individuals for care, and by clinical; epidemiological; and radiological, pathological and biomarker research data suggesting that such a syndrome is a valid clinical entity with prognostic and potentially therapeutic implications. Prime examples are the prevalent neurocognitive disorders associated with various neuromedical conditions such as traumatic brain injury, HIV, substance-use-related brain disorders, diabetes, and early/mild stages of neurodegenerative disorders like Alzheimer’s disease and of cerebrovascular disease. As these conditions are increasingly seen in clinical practice, clinicians have a pressing need for reliable and valid diagnostic criteria in order to assess them and provide services including treatment of associated mood symptoms, further investigation of brain function, identification of treatable causes, and, for progressive disorders, appropriate early interventions.
• The Neurocognitive Disorders Work Group is aware that the specific term “minor” can be challenged on the grounds that it implies lack of need for services and are open to alternative suggestions. They chose “minor” rather than “mild” to be parallel with “major” and to be able to maintain the mild, moderate, and severe distinction within Major NCD.
• The combination of symptoms/observations and objective assessment is critical in Minor Neurocognitive Disorder to maintain specificity: a report of a change in abilities protects against overcalling the disorder in those with lifelong poor performance (sincedecline can only be inferred from a single observation), and objective assessment protects against overcalling the disorder in “the worried well.”
• The Neurocognitive Disorders Work Group is in the process of refining these criteria to achieve a balance between preferred formal neuropsychological assessment and what may be feasible in some clinical settings. The issue is particularly difficult for Minor Neurocognitive Disorder because at lesser levels of cognitive impairment symptom reports may be unavailable or unreliable, observation may be less informative, the interpretation of objective assessments is complicated by variable premorbid abilities, and simpler assessments are likely to be insensitive. They welcome input on this issue.
• The Neurocognitive Disorders Work Group is still refining criterion D and discussing to what extent Minor Neurocognitive Disorder should be diagnosed in the setting of disorders like schizophrenia and depression. They also realize that issues of this nature are being addressed at the DSM-wide level and are awaiting input of these larger discussions, as well as public input on this issue.
• Alzheimer’s Disease Subtype of Major or Minor Neurocognitive Disorders (DSM-5)

A. Major: Meets criteria for Major Neurocognitive Disorder, with memory being one of the impaired domains.
Minor: Meets criteria for Minor Neurognitive Disorder with memory impairment AND there is clear supporting evidence for the Alzheimer etiology (e.g. a positive test for a known mutation in an Alzheimer’s disease associated gene), or with evolving research, documentation based on biomarkers or imaging.
B. Early and prominent impairment in the Memory domain (rarely, other domains such as visuoconstructive perceptual domain may be prominently affected, but Alzheimer’s disease would not be diagnosed without clear supporting imaging, biomarker or genetic evidence).
Major:Deficits are observed in at least one other domain, often Executive Ability, and as the disease progresses, in additional domains.
Minor:Only Memory may be affected, but deficits in Executive Abilities are common.
C. The course is characterized by gradual onset and continuing cognitive decline
D. Evidence from history, examination, and investigations that deficits are not wholly or primarily attributable to other disorders. However, other such disorders may coexist.
RATIONALE FOR CHANGE

Alzheimer’s disease is a neurodegenerative disorder, typically seen in late life, but can occur earlier. It is marked by insidious onset, gradual decline, and typically an early prominent memory loss. For Major Neurocognitive Disorder this typical clinical picture has excellent predictive value for the Alzheimer subtype and is all that is required for a diagnosis of the Alzheimer subtype, although additional evidence adds to the certainty of diagnosis. For less typical clinical profiles such as posterior coritical atrophy or visual variant of AD, additional supportive evidence such as typical neuroimaging patterns of atrophy is required. For Minor Neurocognitive Disorder, because of the modest predictive value of the clinical picture alone and the significant social consequences of an Alzheimer diagnosis, the Alzheimer’s disease subtype is not commonly diagnosed. However, such a diagnosis is possible if there is sufficient information available (e.g., a positive genetic test for dominantly inherited AD, or as the field develops, evidence that certain imaging markers, atrophy of medial temporal lobe structures on MRI, temporoparietal hypometabolism on FDG PET, amyloid deposition on PET scanning or markers for tau and abeta in the CSF are sufficiently predictive of an underlying AD pathology).
While patients in memory disorders clinics who meet current research criteria for Mild Cognitive Impairment (similar to Minor Neurocognitive Disorder with impaired memory) progress to dementia of the Alzheimer type at the rate of 12-15% per year and have neuropathological evidence of both neurodegeneration and cerebrovascular disease, population-based studies show a much lower rate of progression with some individuals improving. Research is ongoing into what specific features of MCI might reliably indicate the presence of prodromal Alzheimer’s disease. Until those features can be identified, the Neurocognitive Disorders Work Group does not feel that the predictive value of Minor Neurocognitive Disorder (minor NCD) with memory impairment is sufficient for a diagnosis of Alzheimer’s disease. However, such a diagnosis might be made in an individual with an autosomal dominant family history or positive test for a mutation in an autosomal dominant “AD gene”, or, after further research, with clearly predictive biomarkers or imaging studies.

• This is an area in which knowledge is evolving rapidly; the procedures described above are increasingly used in clinical practice at tertiary care centers and outside the US. It is possible some of them will enter standard use in the near future.
• Previous terminology was revised to recognize the clinical and pathological evidence that comorbidity is the norm in the population at large, that having cerebrovascular disease does not preclude also having Alzheimer’s disease and vice versa, and in the presence of both, it is not useful to arbitrarily assign causality to one or the other.
• There is little scientific rationale for retaining the distinction between early and late onset, as the underlying pathology is the same, and the threshold of age 65 is arbitrary at best.
  • Criteria for Psychosis of AD:
  • A. Characteristics symptoms: Delusions or auditory or visual hallucinations
  • B. Primary diagnosis: AD: Chronology of onset of symptoms of dementia prior to onset of psychotic symptoms
  • C. Duration: >1 month, although the delusions and hallucinations may be intermittent; symptoms cause clinically significant distress or functional disruption
  • D. Symptoms not exclusively during delirium
  • E. Symptoms not due to direct physiological effects of a substance and cannot be better accounted for schizophrenia or other psychotic disorder
  • Rationale
  • (1) Public health importance: High prevalence & incidence
  • (2) Associated with: More agitation, aggression, More rapid cognitive decline, Greater caregiver distress, earlier institutionalization, and higher cost of care
  • (3) Persistence or recurrence common
  • (4) Aggregates in families
  • (5) Clinical differences between AD + Psychosis and both AD without psychosis and Psychosis without AD
  • (6) Specific treatment considerations
  • Criteria for Depression of AD:
  • A. 3 (or more) of 10 listed symptoms under Major Depressive Disorder
  • B. Primary diagnosis: AD
  • C. Duration: > 2 weeks; Symptoms cause clinically significant distress or functional disruption
  • D. Symptoms not exclusively during delirium
  • E. Symptoms not due to direct physiological effects of a substance and cannot be better accounted for by another disorder

  Rationale

  • (1) Public health importance: High prevalence and incidence
  • (2) Associated with: Higher mortality and Higher cost of care
  • (3) Persistence or recurrence common
  • (4) Clinical differences between AD + depression and both AD without depression and Depression without AD
  • (5) Specific treatment considerations

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• 18. Vascular Dementia (290.4x)

• A video documentary of a man caring for his father who has Vascular Dementia can be found at http://current.com/groups/culture/85771461_julius-and-dementia.htm.
• • DSM-IV-TR criteria
    • A. The development of multiple cognitive deficits manifested by both
      • (1) memory impairment (impaired ability to learn new information or to recall previously learned information)
      • (2) one (or more) of the following cognitive disturbances:
        • (a) aphasia (language disturbances)
        • (b) apraxia (impaired ability to carry out motor activities despite intact motor function)
        • (c) agnosia (failure to recognize or identify object despite intact sensory function)
        • (d) disturbances in executive functioning (i.e. planning, organizing, sequencing, abstracting)
    • B. The cognitive deficits in Criteria A1 and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning.
    • C. Focal neurological signs and symptoms (e.g., exaggeration of deep tendon reflexes, extensor plantar response, pseudobulbar palsy, gait abnormalities, weakness of an extremity) or laboratory evidence indicative of cerebrovascular disease (e.g., multiple infarctions involving cortex and underlying white matter) that are judged to be etiologically related to the disturbance.
    • D. The deficits do not occur exclusively during the course of a delirium.
      • Code based on predominant features:
        • 290.41 With Delirium: if delirium is superimposed on the dementia
        • 290.42 With Delusions: if delusions are the predominant feature
        • 290.43 With Depressed Mood: if depressed mood (including presentations that meet full symptom criteria for a Major Depressive Episode) is the predominant feature. A separate diagnosis of Mood Disorder Due to a General Medical Condition is not given.
        • 290.40 Uncomplicated: if none of the above predominates in the current clinical presentation
      • Specify if:
        • With Behavioral Disturbance
    • Coding note: Also code cerebrovascular condition on Axis III.
  • Associated features
    • Individuals with Dementia may become spatially disoriented and have difficulty with spatial tasks. Poor judgment and poor insight is also fairly common in Dementia. Sometimes individuals with this disorder may display no awareness of the loss of their cognitive abilities. Suicidal tendencies have also been seen in individuals with Dementia. Disinhibited behavior, slurred speech, motor disturbances, and delusions have also been associated with Dementia.
  • Child vs. adult presentation
    • The age of onset of Vascular Dementia is typically earlier than that of Dementia of Alzheimer’s Type.
  • Gender and cultural presentation
    • This disorder seems to be more common in males than in females.
  • Epidemiology
    • Vascular Dementia is much less common than Dementia of Alzheimer’s Type
  • Empirically Supported Treatment

DSM 5 Changes: (DSM5.org)

Proposed Revision:The work group is recommending that this disorder be subsumed into a new disorder:Major Neurocognitive Disorder. Work on a subtype for vascular etiology is currently in progress.

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• 19. Primary Insomnia (307.42)

  • Diagnostic Criteria
    • A. The predominant complaint is difficulty initiating or maintaining sleep, or nonrestorative sleep, for at least one month.
    • B. The sleep disturbance (or associated daytime fatigue) causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
    • C. The sleep disturbance does not occur exclusively during the course of Narcolepsy, Breathing-Related Sleep Disorder, Circadian Rhythm Sleep Disorder, or a Parasomnia.
    • D. The disturbance does not occur exclusively during the course of another mental disorder (e.g., Major Depressive Disorder, Generalized Anxiety Disorder, a delirium).
    • E. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition.
  • Associated features
    • Many individuals with Primary Insomnia have a history of light sleep prior to the development of this disorder. Anxious over concern with general health and increased sensitivity to the daytime effects of mild sleep loss have been noticed within Primary Insomnia. Also, interpersonal, social, and occupational problems may develop as a result of over concern with sleep, increased daytime irritability, and poor concentration.
    • Individuals with severe Primary Insomnia may have concentration problems and greater functional impairment, lower productivity, and increased health care utilization.
    • Individuals with this disorder may have a history of mental disorder, particularly Mood and Anxiety Disorders.
  • Child vs. adult presentation
    • Complaints of Insomnia are more prevalent with increasing age. Young adults more often complain of difficulty falling asleep, whereas midlife and elderly adults are more likely to have difficulty with maintaining sleep and early morning awakening.
  • Gender and cultural differences
    • Primary Insomnia is more prevalent in females than in males.
  • Epidemiology
    • One-year prevalence rates are as high as 30%-45% in adults. The prevalence rates for the general adult population is approximately 1%-10% and up to 25% in the elderly.
    • Primary Insomnia typically begins in young adulthood or middle age and is very rare in children or adolescents.
  • Etiology
    • Most cases of Primary Insomnia develop after a sudden onset of psychological, social, or medical stress, and typically persist long after the original causal factors resolve, due to the development of heightened arousal and negative conditioning.
• Treatment
• Orexin-A and -B (also known as hypocretin-1 and -2) are neuropeptides produced in the lateral hypothalamus that promote many aspects of arousal through the OX1 and OX2 receptors. In fact, they are necessary for normal wakefulness, as loss of the orexin-producing neurons causes narcolepsy in humans and rodents. This has generated considerable interest in developing small-molecule orexin receptor antagonists as a novel therapy for the treatment of insomnia. Orexin antagonists, especially those that block OX2 or both OX1 and OX2 receptors, clearly promote sleep in animals, and clinical results are encouraging: Several compounds are in Phase III trials. As the orexin system mainly promotes arousal, these new compounds will likely improve insomnia without incurring many of the side effects encountered with current medications (Scammel & Winrow, 2010). Acupuncture and cupping have shown significant effects in treating insomnia in college students (Zhang, Ren, & Zhang, 2010).
• PROPOSED CHANGES IN DSM-5 (DSM5.org)
• Insomnia Disorder
• A. The predominant complaint is dissatisfaction with sleep quantity or quality made by the patient (or by a caregiver or family in the case of children or elderly).
• B. Report of one or more of the following symptoms:
• -Difficulty initiating sleep; in children this may be manifested as difficulty initiating sleep without caregiver intervention
• -Difficulty maintaining sleep characterized by frequent awakenings or problems returning to sleep after awakenings (in children this may be manifested as difficulty returning to sleep without caregiver intervention)
• -Early morning awakening with inability to return to sleep
• -Non restorative sleep
• -Prolonged resistance to going to bed and/or bedtime struggles (children)
• C. The sleep complaint is accompanied by significant distress or impairment in daytime functioning as indicated by the report of at least one of the following:
• -Fatigue or low energy
• -Daytime sleepiness
• -Cognitive impairments (e.g., attention, concentration, memory)
• -Mood disturbance (e.g., irritability, dysphoria)
• -Behavioral problems (e.g., hyperactivity, impulsivity, aggression)
• -Impaired occupational or academic function
• -Impaired interpersonal/social function
• -Negative impact on caregiver or family functioning (e.g., fatigue, sleepiness
• D. The sleep difficulty occurs at least three nights per week.
• E. The sleep difficulty is present for at least three months.
• F. The sleep difficulty occurs despite adequate age-appropriate circumstances and opportunity for sleep.
• Duration:
• 1. Acute insomnia (<1 month)
• 2. Sub acute insomnia (1-3 months)
• 3. Persistent insomnia (> 3 months)
• Clinically Comorbid Conditions:
• -Psychiatric disorder (specify)
• -Medical disorder (specify)
• -Another disorder (specify)
• Rationale For Changes
• This new terminology reflects a change in paradigm, recommended by NIH (2005), and widely adopted in the sleep community. Making a reliable differential diagnosis between “Primary Insomnia” and “Insomnia related to another disorder” implies that a clinician can identify the cause and the consequence of the main condition, a determination that is often difficult, if not impossible to make. We recommend using “Insomnia Disorder” whenever diagnostic criteria are met, whether or not there is a co-existing psychiatric, medical, or another sleep disorders. The presence of any of these disorders can still be coded separately. Adopting this new paradigm/terminology would preclude using criteria C, D, E from DSM-IV.
• CRITERION A
• The addition of dissatisfaction to the insomnia definition may improve detection of clinically significant insomnia relative to a single focus on insomnia symptoms. Also, dissatisfaction is more strongly related to daytime impairments compare to insomnia symptoms alone.
• References:
• Ohayon, M. M. (2002). “Epidemiology of insomnia: What we know and what we still need to learn.” Sleep Medicine Reviews 6(2): 97-111.
• Ohayon, 2009. Secondary analyses.
• Early morning awakening can be the only presenting insomnia symptom and this does not necessarily have the same presentation or significance as nocturnal awakenings with difficulty returning to sleep. This addition may enhance specificity of symptoms/diagnosis and, potentially, treatment.
• References:
• Hohagen, F., C. Kappler, et al. (1994). “Sleep onset insomnia, sleep maintaining insomnia and insomnia with early morning awakening–temporal stability of subtypes in a longitudinal study on general practice attenders.” Sleep17(6): 551-554.
• Morin, C. M., M. LeBlanc, et al. (2006). “Epidemiology of insomnia: prevalence, self-help treatments, consultations, and determinants of help-seeking behaviors.” Sleep Medicine 7(2):
• CRITERION B
• The examples of impairments may facilitate assessment of the impact of insomnia on daytime functioning.
• References:
• Buysse, D. J., W. Thompson, et al. (2007). “Daytime symptoms in primary insomnia: a prospective analysis using ecological momentary assessment.” Sleep Medicine 8(3): 198-208.
• Edinger, J. D., M. H. Bonnet, et al. (2004). “Derivation of research diagnostic criteria for insomnia: report of an American Academy of Sleep Medicine Work Group.” Sleep 27(8): 1567-96.
• CRITERION C
• The frequency of occurrence of insomnia symptoms is an important determinant of morbidity/impairment. Although arbitrary, the proposed cut-point is consistent with ICD-10 and with those typically used in clinical research. This change would contribute to harmonizing criteria across diagnostic nosologies.
• References:
• Ohayon (2009). Secondary analysis
• CRITERION D
• The 1-month threshold is a very short period of time to define insomnia as chronic and persistent. Insomnia lasting only 1 month might be better conceptualized as an episode of insomnia rather than an insomnia disorder. Morbidity may also increase with insomnia duration longer than one month.
• References:
• Ohayon (2009). Secondary analyses.
• Morin, C. M., Belanger, L. et al. (2009). “The natural history of insomnia: a population-based 3-year longitudinal study.”Arch Intern Med 169(5): 447-53.
• CRITERION E
• Consistent with the Research Diagnostic Criteria, this specification can be helpful to distinguish clinical insomnia from volitional sleep deprivation.
• References
• Edinger, J. D., M. H. Bonnet, et al. (2004). “Derivation of research diagnostic criteria for insomnia: report of an American Academy of Sleep Medicine Work Group.” Sleep 27(8): 1567-96.
• COMORBID CONDITIONS
• Although we wish to move away from the previous conceptualization of insomnia as primary or secondary, it would be helpful to still code the presence of any comorbid psychiatric, medical, or other sleep disorders.
• Relationship to International Classification of Diseases 10
• Nonorganic Insomnia F 51.0, Disorders of initiating and maintaining sleep (insomnias) G 47.0
• Relationship to International Classification of Sleep Disorders 2nd Edition
• Psychophysiological, paradoxical and idiopathic insomnia 307.42
• SEVERITY
• 1. Insomnia Severity Index
• 2. PROMIS Sleep-Wake Disurbance Self-Report (preliminary in development now)
• 3. Women’s Health Initiative Insomnia Rating Scale
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• 20. Factitious Disorder (300.19)

  • DSM-IV-TR criteria
    • A. The patient is intentionally producing or pretending to have physical or psychological symptoms or signs of illness.
    • B. The patient’s motivation is to assume the role of a sick person.
    • C. There are no external motives that explain the behavior.
  • Associated Features
    • Includes intentionally fabricating physical or psychological symptoms without having any actual illnesses. Motivation must lie in assuming the sick role and not for personal gain as in malingering.
    • It can have predominantly psychological signs and symptoms, or predominantly physical signs and symptoms or a combination of psychological and physical signs and symptoms.
    • Patients may do things to make it look like they are ill and need medical attention such as; contaminating urine sample, ingesting harmful substances like bacteria to invoke some sort of physical proof that they need care, taking hallucinogens, purposefully infecting minor cuts or scrapes to increase the severity and increase the medical attention administered. Can be seen in patient who seeks attention, sympathy, or leniency in some situations.
    • Patients may have long medical histories with many hospital admissions. Their records are usually vague and inconsistent.
    • The patient may have an unusual knowledge of the supposed disease as if they just had definitions to go off of without any true experience.
    • They could be employed in a medical setting.
    • Their hospital visits are usually around hospitals and weekends when the experienced staff is not working so they will have a less likely chance of being caught but still get the same treatment.
    • The person will probably receive few hospital visits even if they claim to be an important figure.
    • The patient may be unusually comfortable with invasive procedures, uncomfortable surgeries, or a drastic diagnosis.
    • Their hospital behavior could be classified as controlling, hostile, attention-seeking, or disruptive.
    • They may only present symptoms when they think they are being watched or when thought to be under surveillance and may disprove of surveillance.
    • They are abusing medications, most commonly pain-killers.
    • The illness that is being played out fluctuates, often with rapid progression.
    • Self-inflicted wounds are most abundant.
  • Munshausen
    • Munchausen Disorder is another term for Factitious Disorder.
    • This is also known as Hospital Addiction Syndrome or Hospital Hopper Syndrome.
    • This has the same diagnostic criteria as Factitious Disorder, seeking attention for being sick. Most often seeking sympathy and care. Sometimes multiple surgeries are performed before diagnosing this disorder.
  • Munchausen Syndrome by proxy
    • Referred to in the DSM-IV-TR as Factitious Disorder by proxy, is a disorder in which someone delivers harm to someone else, most often a child, in order to gain attention. Its been described as an extended form of child abuse; it’s only difference is that it’s done for some sort of gain.
    • Münchausen syndrome by proxy (MSBP), is a psychiatric disorder, a particular form of child abuse. An impaired emotional relationship exists mainly between the mother and her child. According to the variety of victims’ symptoms, all medicine doctors may deal with this syndrome in every day clinical practice. Still insufficient knowledge about the syndrome and its’ rare consideration in the differential diagnosis result in only severe, potentially lethal cases recognition. For many years the rest remains a source of a long-term physical and mental injuries in victims (Berent, Florkowski, & Galecki, 2010).
    • Brief overview of Munchausen by Proxy
  • Ganser Syndrome
    • Gasner Syndrome is a separate type of Factitious Disorder. This disorder involves a patient giving absurd or exaggerated responses to simple questions. It can also be when a patient gives approximate answers to simple questions. The symptoms include clouded consciousness, altered reality, confusion, stress, loss of identity, etc.
  • Epidemiology
    • FD often goes undetected therefore making it difficult to accurately determine how many people are afflicted.
    • It has been shown that there is a much higher prevalence of physical factitious symptoms than psychological factitious symptoms.
    • Only a few select studies have been done to show its prevalence. A large teaching hospital in Toronto reported that 10 of 1,288 patients referred to a consultation service had FD (0.8%). The National Institute for Allergy and Infectious Disease reported that 9.3% of patients referred for fevers of unknown origin had factitious disorder. A clinic in Australia found that 1.5% of infants brought in for serious illnesses by parents were cases of Munchausen syndrome by proxy.
  • Etiology
    • Little is known about the true causes of FD because of poor follow up after hospital visits. There are a few theories; brain imaging has shown some biological associations with FD especially with Gasner Syndrome.
    • FD might be attempted to re-enact some unresolved parental issues, or to re-enact a particularly enjoyable hospital visit.
    • It also might be a form of masochism.
    • It could just be attention seeking behavior or a need for care and nurturance
    • It’s been speculated that FD may be an attempt to gain control over an authority figure such as a doctor.
    • FD is often common amongst people who received extensive medical treatment as children for real physical disorders, experienced extreme family problems or abuse during childhood,
  • Treatment
    • Medication has yet to prove successful in treating FD, some mood disorder medications have proven effective if they have other personality disorders.
    • Most long term treatment is dropped by someone with FD.
    • Psychotherapy and Family Therapy are some of the only treatments that have shown benefit, these often require what the patient doesn’t have that caused this disorder, such as a caring family or someone willing to go through long term therapy with them.

DSM5 changes (dsm5.org)

The work group proposed that Factitious Disorder be reclassified to Somatic Symptom Disorders.

Factitious Disorder

To make this diagnosis, all 4 criteria must be met.
1. A pattern of falsification of physical or psychological signs or symptoms, associated with identified deception.

2. A pattern of presenting oneself to others as ill or impaired.
3. The behavior is evident even in the absence of obvious external rewards.
4. The behavior is not better accounted for by another mental disorder such as delusional belief system or acute psychosis.

Major Change #1: Rename somatiform disorders to Somatic Symptom Disorders and combine with PFAMC and Factitious Disorders

The workgroup suggests combining Somatoform Disorders, Psychological Factors Affecting Medical Condition (PFAMC), and Factitious Disorders into one group entitled “Somatic Symptom Disorders” because the common feature of these disorders is the central place in the clinical presentation of physical symptoms and/or concern about medical illness. The grouping of these disorders in a single section is based on clinical utility (these patients are mainly encountered in general medical settings), rather than assumptions regarding shared etiology or mechanism.
Major Change #2: De-emphasize unexplained symptoms

Remove the language concerning medically unexplained symptoms for reasons specified above. The reliability of such judgments is low (Rief, 2007). In addition, it is clear that many of these patients do in fact have considerable medical co-morbidity (Creed, Ng). Medically unexplained symptoms are 3 times as common in patients with general medical illnesses, including cancer, cardiovascular and respiratory disease compared to the general population (OR=3.0 [95%CI: 2.1 to 4.2] (Harter et al 2007). This de-emphasis of medically unexplained symptoms would pertain to somatization disorder, hypochondriasis, undifferentiated somatoform disorder, and pain disorder. We now focus on the extent to which such symptoms result in subjective distress, disturbance, diminished quality of life, and impaired role functioning.

Minor Change: Factitious Disorders
The work group proposes minor modifications to factitious disorders. Most importantly, it eliminates the distinction between factitious disorders involving physical vs psychological symptoms. It clarifies who is the patient in circumstances previously diagnosed as “factitious disorder by proxy.” This is now termed “factitious disorder on other.”
Additional minor changes in the factitious disorder descriptions were made to emphasize objective identification rather than inference about intentionality or possible underlying motivation. “Intentional production or feigning” was thus removed and replaced with “a pattern of falsification”. The wording “pattern of falsification” attempts to emphasize that the diagnosis should follow an objective characterization of a set of behaviors, without perceived inference about the intentionality or possible underlying motivation for these behaviors. “…associated with identified deception” was inserted to state that the behaviors showed evidence of deception as identified by the observer. Again, this wording emphasizes behaviors being observed, rather than inference about intent. Finally, item A4 was added to clarify that factitious disorder is not diagnosed when it is accounted for by another mental disorder such as an acute psychosis.
Severity:
There are few widely employed measures of severity in factitious disorder or conversion disorder.
For factitious disorder, one might grade severity levels as “1” when symptoms alone are reported (“bright red blood in stool”), as “2” when a lab test was modified (e.g. introducing blood into a urine sample), as “3” when patients make themselves sick or as “4” when patients’ actions lead to life threatening illness.

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• 21. Primary Hypersomnia (307.44)

  • DSM-IV-TR criteria
    • The patient experiences excessive sleepiness for at least one month. This can include prolonged sleep at night or additional sleep in the daytime.
    • The patient experiences significant distress or functional impairment due to excessive sleepiness.
    • The excessive sleepiness is not better accounted for by insomniaand does not occur exclusively during the course of another Sleep Disorder (e.g. Narcolepsy, Breathing-Related Sleep Disorder, Circadian Rhythm Sleep Disorder, or a Parasomnia) and cannot be accounted for by an inadequate amount of sleep.
    • The disturbance does not occur exclusively during the courseof another mental disorder.
    • The condition cannot occur exclusively with any other mental disorder, physical medical condition, or substance use.

Proposed DSM 5 changes (DSM5.org)

• A. The predominant complaint is unexplained hypersomnia (excessive sleep) or/and hypersomnolence (sleepiness in spite of sufficient nocturnal sleep), for at least 3 months, occurring 3 or more times per week.1. Hypersomnia (excessive sleep) is defined by a prolonged nocturnal sleep episode or daily sleep amounts (>9 hours/day).2. Hypersomnolence is defined by excessive daytime sleepiness with recurrent daytime naps or lapses into sleep that occurs daily or almost daily over at least the last 3 months (when the patient is untreated) and daily sleep amounts > 6 hours. To document hypersomnolence, the Multiple Sleep Latency Test must show a mean sleep latency below 8 minutes, with or without Sleep Onset REM Periods (SOREMPs). If the patient has more than 2 SOREMPs, the condition may be called “narcolepsy without cataplexy”. B. The sleep periods are non-restorative (unrefreshing) or so prolonged in length that this causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.C. The hypersomnia is not better accounted for by insomnia and does not occur exclusively during the course of another Sleep Disorder (e.g., Narcolepsy with Cataplexy, Sleep-Related Breathing Disorder, Circadian Rhythm Sleep Disorder, or a Parasomnia) and cannot be accounted for by an inadequate amount of sleep. D. The disturbance does not occur exclusively during the course of another mental or medical disorder but may occur simultaneously with these disorders.E. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication).Clinically Comorbid Conditions:
  1. Mental/Psychiatric Disorder (specify)
  2. Medical Disorder (specify)

• Rationale:

• Narcolepsy without cataplexy is defined based on a positive Multiple Sleep Latency Test but no cataplexy. Its symptoms are identical to hypersomnia without long sleep time. Most of these cases are not caused by hypocretin deficiency. The treatment of narcolepsy without cataplexy is similar to that of primary hypersomnia. There is no proof that narcolepsy without cataplexy and primary hypersomnia are distinct disease entities. Advantage: Simplifies the classification. Disadvantage: Some patients with “narcolepsy” but without cataplexy/hypocretin deficiency (generally narcolepsy without cataplexy) would now go into the category 307.44 “primary hypersomnia/narcolepsy without cataplexy”. As the cause of 307.44 is unknown, this is a “softer” diagnosis.

Criterion A:

Rationale, advantage and disadvantage: It is not a major change, but rather a clarification. The term “Hypersomnia” originally meant “increased sleep amounts”; it is distinct from “hypersomnolence (daytime sleepiness). The The two interacts, and both may be present. There are no disadvantages. The three month criteria is more standard.

Criterion B:

• Rationale, advantage and disadvantage: It is not a major change, but rather a clarification. By definition, sleep must be non-restorative or unrefreshing and cause distress. If the subjects sleeps a lot but feels fine, he/she would be characterized as a long sleeper. It would really become pathological only if extremely long and unmanageable socially.

Criterion C, D, & E: are primarily in the wording.

Relationship to International Classification of Diseases -10:
Nonorganic hypersomnia F51.1, Disorders of Excessive Somnolence (hypersomnias) G47.1

Relationship to International Classification of Sleep Disorders 2nd edition: The revised classification will remain similar to that of the ICSD-2, except that two instead of 4 categories are included. Primary hypersomnia/narcolepsy without cataplexy will be a category merging ICSD-2 narcolepsy without cataplexy, hypersomnia with long time sleep, and narcolepsy without long time sleep. As these three entities are not known to be pathophysiologically distinct, and are treated and evaluated similarly. Narcolespy withou cataplexy 347.00

Severity:

1. Epworth sleepiness Scale

2. Multiple Sleep Latency Test
3. Maintenance of Wakefulness test

• 22. Kleine Levin Syndrome (Sleeping Beauty Syndrome)

  • Proposed addition to DSM-V.
  • Criteria
    • A. The patient experiences recurrent episodes of excessive sleep (>11 hours/day).
    • B. Episodes occur at least once a year, and are generally 2 days to 4 weeks in duration.
    • C. During episodes, when awake, cognition is abnormal with feeling of unreality or confusion. Behavioral abnormalities such as megaphagia or hypersexuality may occur in some episodes.
    • D. The patient has normal alertness, cognitive functioning, and behavior between the episodes.
  • E. The condition is not better accounted for by another mental disorder (e.g, mood disturbance), and is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or another general medical condition (e.g. a metabolic disorder).

TREATMENT-
Treatment for KLS has not been established, although lithium has been used in limited cases with insignificant efficacy. Gabapentin has shown some promise in being effective for the prevention of hypersomnia attacks. There is considerable speculation that the recurrent hypersomnia and behavior disturbance are related to epilepsy-like neuronal discharge from the thalamus due to dysfunction in GABAnergic receptors (Itokawa et al., 2009).

For more information, check out the KLS Foundation: http://www.kleinelevin.com/

• Segment about Kleine Levin Syndrome http://klsfoundation.org/kleine/levin/video_article/strange_brain/

• Dsm5 proposed changes (dsm5.org)

• A. The patient experiences recurrent episodes of excessive sleep (>11 hours/day).
• B. Episodes occur at least once a year, and are generally 2 days to 4 weeks in duration.
• C. During episodes, when awake, cognition is abnormal with feeling of unreality or confusion. Behavioral abnormalities such as megaphagia or hypersexuality may occur in some episodes.
• D. The patient has normal alertness, cognitive functioning, and behavior between the episodes.
• E. The condition is not better accounted for by another mental disorder (e.g, mood disturbance), and is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or another general medical condition (e.g. a metabolic disorder).
• Rationale for change
• There is increasing evidence that the disorder is a genuine disease entity based on its consistent description in term of clinical presentation, demographics (70% male, adolescent), evolution (eventually disappears), and therapeutic response (almost nothing is effective). It may be misdiagnosed as depression or other psychiatric consequences, with devastating consequences.
• Relationship to International Classification of Diseases- 10
• Other Sleep Disorders: Kleine-Levin Syndrome G47.8
• Relationship to International Classification of Sleep Disorders 2nd Edition
• Recurrent Hypersomnia 327.13
• Severity
• Recommendations for severity criteria for this disorder are forthcoming.

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