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Individuals with schizotypal personality disorder experience interpersonal related ness as problematic and are uncomfortable relating to other people. Although they may express unhappiness about their lack of relationships, their behavior suggests a decreased desire for intimate contacts. As a result, they usually have no or few close friends or con fidants other than a first-degree relative (Criterion A8). They are anxious in social situa tions, particularly those involving unfamiliar people (Criterion A9). They will interact with other individuals when they have to but prefer to keep to themselves because they feel that they are different and just do not "fit in. For example, when attending a dinner party, the individual with schizotypal personality disorder will not become more relaxed as time goes on, but rather may become increasingly tense and suspicious. Schizotypal personality disorder should not be diagnosed if the pattern of behavior oc curs exclusively during the course of schizophrenia, a bipolar or depressive disorder with psychotic features, another psychotic disorder, or autism spectrum disorder (Criterion B). Associated Features Supporting Diagnosis Individuals with schizotypal personality disorder often seek treatment for the associated symptoms of anxiety or depression rather than for the personality disorder features per se. Particularly in response to stress, individuals with this disorder may experience transient psychotic episodes (lasting minutes to hours), although they usually are insufficient in du ration to warrant an additional diagnosis such as brief psychotic disorder or schizophreni form disorder. In some cases, clinically significant psychotic symptoms may develop that meet criteria for brief psychotic disorder, schizophreniform disorder, delusional disorder, or schizophrenia. From 30% to 50% of individuals diagnosed with this disorder have a concurrent diagnosis of major depressive disorder when admitted to a clinical setting. There is considerable co occurrence with schizoid, paranoid, avoidant, and borderline personality disorders. Prevalence In community studies of schizotypal personality disorder, reported rates range from 0. The prevalence of schizotypal personality disorder in clinical populations seems to be infrequent (0%-1. Development and Course Schizotypal personality disorder has a relatively stable course, with only a small propor tion of individuals going on to develop schizophrenia or another psychotic disorder. Schizotypal personality disorder may be first apparent in childhood and adolescence with solitariness, poor peer relationships, social anxiety, underachievement in school, hyper sensitivity, peculiar thoughts and language, and bizarre fantasies. Schizotypal personality disorder appears to aggregate fa milially and is more prevalent among the first-degree biological relatives of individuals with schizophrenia than among the general population. There may also be a modest in crease in schizophrenia and other psychotic disorders in the relatives of probands with schizotypal personality disorder. Pervasive culturally determined characteristics, particularly those regard ing religious beliefs and rituals, can appear to be schizotypal to the uninformed outsider. Gender-Related Diagnostic Issues Schizotypal personality disorder may be slightly more common in males. Schizotypal personality disorder can be distinguished from delusional disorder, schizophrenia, and a bipolar or depressive disorder with psychotic features because these disorders are all characterized by a period of persistent psychotic symptoms. To give an addi tional diagnosis of schizotypal personality disorder, the personality disorder must have been present before the onset of psychotic symptoms and persist when the psychotic symptoms are in remission. There may be great difficulty differentiating children with schizotypal personality disorder from the heterogeneous group of solitary, odd chil dren whose behavior is characterized by marked social isolation, eccentricity, or peculiar ities of language and whose diagnoses would probably include milder forms of autism spectrum disorder or language communication disorders. Communication disorders may be differentiated by the primacy and severity of the disorder in language and by the char acteristic features of impaired language found in a specialized language assessment. Milder forms of autism spectrum disorder are differentiated by the even greater lack of so cial awareness and emotional reciprocity and stereotyped behaviors and interests. Schizotypal personality disor der must be distinguished from personality change due to another medical condition, in which the traits that emerge are attributable to the effects of another medical condition on the central nervous system. Schizotypal personality disorder must also be distinguished from symptoms that may develop in association with persistent substance use. Other personality disorders may be confused with schizotypal personality disorder because they have certain features in common. However, if an individual has personality features that meet criteria for one or more personality disorders in addition to schizotypal person ality disorder, all can be diagnosed. Although paranoid and schizoid personality disor ders may also be characterized by social detachment and restricted affect, schizotypal personality disorder can be distinguished from these two diagnoses by the presence of cognitive or perceptual distortions and marked eccentricity or oddness. Close relation ships are limited in both schizotypal personality disorder and avoidant personality dis order; however, in avoidant personality disorder an active desire for relationships is constrained by a fear of rejection, whereas in schizotypal personality disorder there is a lack of desire for relationships and persistent detachment. Individuals with narcissistic personality disorder may also display suspiciousness, social withdrawal, or alienation, but in narcissistic personality disorder these qualities derive primarily from fears of hav ing imperfections or flaws revealed.

Development and Course Course is persistent, lasting longer than 3 months, with intermittent exacerbations through out adulthood. Although age at onset is variable, symptoms begin typically in adolescence and early adulthood and persist for several months to years before diagnosis is estab lished. Exacerbation is usually triggered by a change in work or school schedule that requires an early rise time. Individuals who can alter their work schedules to accommo date the delayed circadian sleep and wake timing can experience remission of symptoms. Increased prevalence in adolescence may be a consequence of both physiological and be havioral factors. Hormonal changes may be involved specifically, as delayed sleep phase is as sociated with the onset of puberty. Thus, delayed sleep phase type in adolescents should be differentiated from the common delay in the timing of circadian rhythms in this age group. In the familial form, the course is persistent and may not improve sig^iificantly with age. Predisposing factors may include a longer than average cir cadian period, changes in light sensitivity, and impaired homeostatic sleep drive. Some in dividuals with delayed sleep phase type may be hypersensitive to evening light, which can serve as a delay signal to the circadian clock, or they may be hyposensitive to morning light such that its phase-advancing effects are reduced. Genetic factors may play a role in the pathogenesis of familial and sporadic forms of delayed sleep phase type, including mutations in circadian genes. Diagnostic i/larl(ers Confirmation of the diagnosis includes a complete history and use of a sleep diary or actigraphy. The period covered should include weekends, when social and occupational obligations are less strict, to ensure that the individual exhibits a consistently delayed sleep-wake pattern. Biomarkers such as salivary dim light melatonin onset should be obtained only when the diagnosis is unclear. Functional Consequences of Delayed Sleep Phase Type Excessive early day sleepiness is prominent. The severity of insomnia and excessive sleepiness symptoms varies substantially among individuals and largely de pends on the occupational and social demands on the individual. Delayed sleep phase type must be distinguished from "normal" sleep patterns in which an individual has a late schedule that does not cause personal, social, or occupational distress (most commonly seen in adolescents and young adults). Insomnia disorder and other circadian rhythm sleep-wake dis orders should be included in the differential. Excessive sleepiness may also be caused by other sleep disturbances, such as breathing-related sleep disorders, insomnias, sleeprelated movement disorders, and medical, neurological, and mental disorders. Overnight polysomnography may help in evaluating for other comorbid sleep disorders, such as sleep apnea. The circadian nature of delayed sleep phase type, however, should differen tiate it from other disorders with similar complaints. Comorbidity Delayed sleep phase type is strongly associated with depression, personality disorder, and somatic symptom disorder or illness anxiety disorder. In addition, comorbid sleep disor ders, such as insomnia disorder, restless legs syndrome, and sleep apnea, as well as depres sive and bipolar disorders and anxiety disorders, can exacerbate symptoms of insomnia and excessive sleepiness. Delayed sleep phase type may overlap with another circadian rhythm sleep-wake disorder, non-24-hour sleep-wake type. Sighted individuals with non24-hour sleep-wake type disorder commonly also have a history of delayed circadian sleep phase. Advanced Sleep Phase Type Specifiers Advanced sleep phase type may be documented with the specified "famihal. In this type, specific mutations demonstrate an autosomal dominant mode of inheritance. In the familial form, onset of symptoms may occur earlier (during childhood and early adulthood), the course is persistent, and the severity of symptoms may increase with age. Diagnostic Features Advanced sleep phase type is characterized by sleep-wake times that are several hours earlier than desired or conventional times. Diagnosis is based primarily on a history of an advance in the timing of the major sleep period (usually more than 2 hours) in relation to the desired sleep and wake-up time, with symptoms of early morning insomnia and ex cessive daytime sleepiness. When allowed to set their schedule, individuals with ad vanced sleep phase type will exhibit normal sleep quality and duration for age. Associated Features Supporting Diagnosis Individuals with advanced sleep phase type are "morning types," having earlier sleepwake times, with the timing of circadian biomarkers such as melatonin and core body tem perature rhythms occurring 2-A hours earlier than normal.

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Patients with signs or symptoms suggesting involvement of other mucosal sites should be referred to an appropriate specialist for an evaluation. For less severe cases with limited oral involvement, topical corticosteroids may be used; but this is uncommon. Pemphigus Ulceration: Example of a large psuedomembrane covered ulcer on the lateral border of the tongue due to pemphigus vulgaris. When bullae rupture, the resultant ulcers are often large and may coalesce (Figure 6). The severity of oral lesions can prevent adequate nutrition due to severe pain during food consumption. In the oral cavity, the gingiva and buccal mucosa are the most commonly affected sites. Lesions can be isolated to the gingiva and sometimes referred to as desquamative or erosive gingivitis (Figure 7B). Microscopically, epithelial separation at the level of the basement membrane without acantholysis is seen. In some refractory instances, corticosteroid treatment is coupled with nonsteroidal immunosuppressants such as azathioprine or mycophenolate. A) Bulla: Example of short-lived bullae on the gingival tissue area buccal to tooth #31. Gingival ulceration: Example of gingival ulceration and sloughing due to an uncontrolled mucous membrane pemphigoid. Ulcerations can be found on any surface including the lips, tongue, and buccal mucosa. Erythema multiforme major, a response to a drug exposure, has both cutaneous and mucous membrane involvement. Intraoral lesions can present as large pseudomembrane-covered ulcers on the buccal mucosa, ventral tongue, and labial vestibule (Figure 8A). Cutaneous lesions (Figure 8B) usually accompany those found in the oral cavity lesions although the oral mucosa can be solely affected. Due to the high risk of bacterial superinfection and sepsis, appropriate cultures should be performed from blood, wounds, and mucosal lesions. This is a self-limited, indolent disorder, generally responding well to conservative management. Affected individuals typically are febrile with widespread superficial ulcers of the oral mucosa both keratinized and non-keratinized (Figure 9). The gingiva is often swollen and ulcerated, which give it the features of acute necrotizing ulcerative gingivitis. Therapy is typically palliative, although systemic acyclovir and other antiviral medication should be considered when the disease is severe or recurrent. Primary herpetic gingivostomatitis: Example of a primary herpetic outbreak in 35 year old male accompanied by headache, fever and overall malaise. Notice the ruptured vesicles on the tongue and the aphthous-like appearing lesion on the soft palate. Bacterial causes of ulceration: Treponema pallidum Syphilis is a well-known disorder with a long history in medicine. The disease is caused by the spirochete Treponema pallidum and has 3 temporally distinct phases. Chancres initially appear as a small papule that elevates, enlarges, erodes, and becomes ulcerated. The lesion is usually punched-out, indurated and approximately 2-3 cm in diameter without a red inflammatory border. Secondary syphilis presents with either oral lesions including red macules, pharyngitis, or isolated/multiple painless, shallow, and highly infectious ulcers surrounded by an erythematous halo. It is primarily characterized by gummas, palatal perforation, and neurological symptoms. Oral ulcers due to systemic conditions Granulomatosis with polyangitis ing vasculitis with granulomatous inflammation.

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A great deal of time is spent in activities necessary to obtain the substance, use the substance, or recover from its effects. Recurrent use of the substance resulting in a failure to fulfill major role obligations at work, school, or home. Continued use of the substance despite having persistent or recurrent social or in terpersonal problems caused or exacerbated by the effects of its use. Important social, occupational, or recreational activities are given up or reduced be cause of use of the substance. Use of the substance is continued despite knowledge of having a persistent or re current physical or psychological problem that is likely to have been caused or ex acerbated by the substance. A need for markedly increased amounts of the substance to achieve intoxication or desired effect. A markedly diminished effect with continued use of the same amount of the sub stance. The characteristic withdrawal syndrome for other (or unknown) substance (refer to Criteria A and B of the criteria sets for other [or unknown] substance withdrawal, p. The substance (or a closely related substance) is taken to relieve or avoid with drawal symptoms. Specify if: In early remission: After full criteria for other (or unknown) substance use disorder were previously met, none of the criteria for other (or unknown) substance use disorder have been met for at least 3 months but for less than 12 months (with the exception that Cri terion A4, "Craving, or a strong desire or urge to use the substance," may be met). In sustained remission: After full criteria for other (or unknown) substance use disor der were previously met, none of the criteria for other (or unknown) substance use dis order have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, "Craving, or a strong desire or urge to use the substance," may be met). Specify if: In a controlled environment: this additional specifier is used if the individual is in an environment where access to the substance is restricted. Instead, the comorbid other (or unknown) substance use dis order is indicated in the 4th character of the other (or unknown) substance-induced disorder code (see the coding note for other (or unknown) substance intoxication, other (or unknown) substance withdrawal, or specific other (or unknown) substance-induced mental disorder). Diagnostic Features the diagnostic dass other (or unknown) substance use and related disorders comprises substance-related disorders unrelated to alcohol; caffeine; cannabis; hallucinogens (phen cyclidine and others); inhalants; opioids; sedative, hypnotics, or anxiolytics; stimulants (including amphetamine and cocaine); or tobacco. Such substances include anabolic ste roids; nonsteroidal anti-inflammatory drugs; cortisol; antiparkinsonian medications; an tihistamines; nitrous oxide; amyl-, butyl-, or isobutyl-nitrites; betel nut, which is chewed in many cultures to produce mild euphoria and a floating sensation; kava (from a South Pacific pepper plant), which produces sedation, incoordination, weight loss, mild hepati tis, and lung abnormalities; or cathinones (including khвt plant agents and synthetic chem ical derivatives) that produce stimulant effects. Unknown substance-related disorders are associated with unidentified substances, such as intoxications in which the individual can not identify the ingested drug, or substance use disorders involving either new, black mar ket drugs not yet identified or familiar drugs illegally sold under false names. When the substance is known, it should be reflected in the name of the disorder upon coding. Because of increased access to nitrous oxide ("laughing gas"), membership in certain populations is associated with diagnosis of nitrous oxide use disorder. The role of this gas as an anesthetic agent leads to misuse by some medical and dental professionals. With recent widespread availability of the substance in "whippet" cartridges for use in home whipped cream dispensers, nitrous oxide misuse by adolescents and young adults is significant, especially among those who also inhale vola tile hydrocarbons. Some continuously using individuals, inhaling from as many as 240 whippets per day, may present with serious medical complications and mental conditions, including myeloneuropathy, spinal cord subacute combined degeneration, peripheral neuropathy, and psychosis. These conditions are also associated with a diagnosis of ni trous oxide use disorder. Use of amyl-, butyl-, and isobutyl nitrite gases has been observed among homosexual men and some adolescents, especially those with conduct disorder. Membership in these populations may be associated with a diagnosis of amyl-, butyl-, or isobutyl-nitrite use dis order. However, it has not been determined that these substances produce a substance use disorder. Despite tolerance, these gases may not alter behavior through central effects, and they may be used only for their peripheral effects. Substance use disorders generally are associated with elevated risks of suicide, but there is no evidence of unique risk factors for suicide with other (or unknown) substance use disorder. Prevaience Based on extremely limited data, the prevalence of other (or unknown) substance use disorder is likely lower than that of use disorders involving the nine substance classes in this chapter. Development and Course No single pattern of development or course characterizes the pharmacologically varied other (or unknown) substance use disorders. Often unknown substance use disorders will be reclassified when the unknown substance eventually is identified.

Many individuals with gambling disorder believe that money is both the cause of and the solution to their problems. Some individuals with gambling disorder are im pulsive, competitive, energetic, restless, and easily bored; they may be overly concerned with the approval of others and may be generous to the point of extravagance when win ning. Other individuals with gambling disorder are depressed and lonely, and they may gamble when feeling helpless, guilty, or depressed. Up to half of individuals in treatment for gambling disorder have suicidal ideation, and about 17% have attempted suicide. The lifetime prevalence of pathological gambling among African Americans is about 0. Deveiopment and Course the onset of gambling disorder can occur during adolescence or young adulthood, but in other individuals it manifests during middle or even older adulthood. Generally, gam bling disorder develops over the course of years, although the progression appears to be more rapid in females than in males. Most individuals who develop a gambling disorder evidence a pattern of gambling that gradually increases in both frequency and amount of wagering. Most individuals with gambling disorder report that one or two types of gambling are most problematic for them, although some individuals participate in many forms of gambling. Fre quency of gambling can be related more to the type of gambling than to the severity of the overall gambling disorder. For example, purchasing a single scratch ticket each day may not be problematic, while less frequent casino, sports, or card gambling may be part of a gambling disorder. Similarly, amounts of money spent wagering are not in themselves in dicative of gambling disorder. Some individuals can wager thousands of dollars per month and not have a problem with gambling, while others may wager much smaller amounts but experience substantial gambling-related difficulties. Gambling patterns may be regular or episodic, and gambling disorder can be persis tent or in remission. Gambling can increase during periods of stress or depression and during periods of substance use or abstinence. There may be periods of heavy gambling and severe problems, times of total abstinence, and periods of nonproblematic gambling. Nevertheless, some individuals underestimate their vulnerability to develop gambling disorder or to return to gambling disorder following remission. When in a period of re mission, they may incorrectly assume that they will have no problem regulating gambling and that they may gamble on some forms nonproblematically, only to experience a return to gambling disorder. Early expression of gambling disorder is more common among males than among fe males. Individuals who begin gambling in youth often do so with family members or friends. Development of early-life gambling disorder appears to be associated v^ith impulsivity and substance abuse. Many high school and college shidents w ho develop gambling disorder grow out of the disorder over time, although it remains a lifelong problem for some. Mid- and later-life onset of gambling disorder is more common among females than among males. There are age and gender variations in the type of gambling activities and the preva lence rates of gambling disorder. Gambling disorder is more common among younger and middle-age persons than among older adults. Among adolescents and young adults, the disorder is more prevalent in males than in females. Although the proportions of individuals who seek treatment for gambling disorder are low across all age groups, younger individ uals are especially unlikely to present for treatment. Males are more likely to begin gambling earlier in life and to have a younger age at on set of gambling disorder than females, who are more likely to begin gambling later in life and to develop gambling disorder in a shorter time frame.

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