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Objective: The cognitive and motivational impairments observed in psychotic disorders may reflect early developmental alterations that, when combined with later environmental exposures, may drive the onset of positive psychotic symptoms. The epidemiological predictions of this model were tested. Method: A longitudinal prospective cohort study (the Early Developmental Stages of Psychopathology Study) was conducted with a representative general population sample of adolescents and young adults from Munich (N=3,021), who were 14-24 years of age at baseline. Sociodemographic factors, environmental exposures, and measures of psychopathology and associated clinical relevance were assessed across three waves, covering a period of up to 10 years, by clinical psychologists using the Composite International Diagnostic Interview. Results: Both negative/disorganized and positive psychotic symptoms were frequent (5-year cumulative prevalence rates of around 12%) and occurred in combination more often than predicted by chance. Negative/disorganized symptoms revealed a pattern of sociodemographic associations indicative of developmental impairment, whereas the positive symptoms were associated with environmental exposures such as trauma, cannabis use, and urbanicity. Negative/disorganized symptoms predicted positive symptoms over time, and co-occurrence of positive and negative/disorganized symptoms was predictive of clinical relevance in terms of secondary functional impairment and help-seeking behavior. Conclusions: The results suggest that the negative/disorganized features associated with psychotic disorder are distributed at the population level and drive the ontogenesis of positive psychotic experiences after exposure to environmental risks, increasing the likelihood of impairment and need for care.

Objective: Overwhelming evidence suggests that compromised neuropsychological function is frequently observed in schizophrenia. Neurocognitive dysfunction has often been reported in other psychotic disorders, although there are inconsistencies in the literature. In the context of four distinct diagnostic groups, the authors compared neuropsychological performance among patients experiencing their first psychotic episode. Method: Data were derived from a population-based, case-control study of patients with first-episode psychosis. A neuropsychological test battery was administered to patients with a diagnosis of schizophrenia (N=65), bipolar disorder or mania (N=37), depressive psychosis (N=39), or other psychotic disorders (N=46) following index presentation, as well as to healthy comparison subjects (N=177). The presence of specific and generalized cognitive deficits was examined. Results: The schizophrenia group presented widespread neuropsychological impairments and performed significantly worse than healthy comparison subjects on most neuropsychological measures. Patients with other psychotic disorders and depressive psychosis also demonstrated widespread impairments. Deficits in patients with bipolar disorder or mania were less pervasive but evident in performance scores on verbal memory and fluency tests. Differences between the four patient groups and healthy comparison subjects and among the patient groups were attenuated after controlling for differences in general cognitive ability (IQ). Conclusions: Early in their course, cognitive deficits are present in all psychotic disorders but are most severe and pervasive in schizophrenia and least pervasive in bipolar disorder and mania. (Am J Psychiatry 2010; 167:78-85)

Illlicit methamphetamine abuse represents a major problem in many countries worldwide, including the United States. Prolonged regular smoking or injection of methamphetamine can cause a psychosis, typically characterized by paranoid delusions and auditory hallucinations and often associated with disturbances in mood. These symptoms may persist long after methamphetamine is discontinued and may prove refractory to antipsychotic medications. The authors describe a patient who developed a typical methamphetamine psychosis that persisted despite months of abstinence from methamphetamine and weeks of treatment with antipsychotic medication but that responded promptly to electroconvulsive therapy (ECT) on two separate occasions: on initial presentation and again a year later when the patient relapsed into methamphetamine abuse and developed psychosis again. The authors review the large international literature on methamphetamine psychosis, much of which is from Japan and has not previously been summarized in English. Persistent methamphetamine psychosis has been widely reported in Japan for more than 50 years but is rarely discussed in the American literature, possibly because some such cases are misdiagnosed in the United States as primary psychotic disorders. Given the growing public health problem of methamphetamine abuse in the United States, the distinction between persistent methamphetamine psychosis and a primary psychotic disorder has grown increasingly important. Thus, American clinicians should be alert to the possibility of methamphetamine psychosis and may wish to consider ECT in refractory cases. (Am J Psychiatry 2010; 167:17-23)

Objective: Cognitive models suggest that biased processing of emotional information may play a role in the genesis and maintenance of psychotic symptoms. The role of dopamine and dopamine antagonists in the processing of such information remains unclear. The authors investigated the effect of a dopamine antagonist on perception of, and memory for, emotional information in healthy volunteers. Method: Thirty-three healthy male volunteers were randomly assigned to a single-blind intervention of either a single dose of the dopamine [D.sub.2]/[D.sub.3] antagonist amisulpride or placebo. An attentional blink task and an emotional memory task were then administered to assess the affective modulation of attention and memory, respectively. Results: A significant interaction was observed between stimulus valence and drug on recognition memory accuracy; further contrasts revealed enhanced memory for aversive-arousing compared with neutral stimuli in the placebo but not the amisulpride group. No effect of amisulpride was observed on the perception of emotional stimuli. Conclusions: Amisulpride abolished the enhanced memory for emotionally arousing stimuli seen in the placebo group but had no effect on the perception of such stimuli. These results suggests that dopamine plays a significant role in biasing memory toward emotionally salient information and that dopamine antagonists may act by attenuating this bias.

Objective: The 22q11.2 deletion syndrome is the most common known genetic risk factor for the development of schizophrenia. The authors conducted a longitudinal evaluation of adolescents with 22q11.2 deletion syndrome to identify early risk factors for the development of psychotic disorders. Method: Sixty children, 31 with 22q11.2 deletion syndrome and 29 comparison subjects with idiopathic developmental disability matched for age and IQ, underwent a baseline evaluation between 1998 and 2000; of these, 51 children (28 and 23 in the two groups, respectively) underwent follow-up evaluation between 2003 and 2005. A standardized comprehensive psychiatric, psychological, and adaptive functioning evaluation was conducted in both waves. Participants with 22q11.2 deletion syndrome were also genotyped for the catechol O-methyl-transferase (COMT) Met/Val polymorphism and underwent magnetic resonance imaging scans. Results: The two groups had similar baseline neuropsychiatric profiles. At follow-up, 32.1% of subjects with 22q11.2 deletion syndrome had developed psychotic disorders as compared with 4.3% of comparison subjects. In the 22q11.2 deletion syndrome group, baseline subthreshold psychotic symptoms interacted both with the COMT genotype and with baseline symptoms of anxiety or depression to predict 61% of the variance in severity of psychosis at follow-up evaluation. Lower baseline verbal IQ was also associated with more severe psychotic symptoms at follow-up evaluation. Conclusions: Genetic, cognitive, and psychiatric risk factors for the evolution of psychotic disorders in 22q11.2 deletion syndrome during adolescence were identified. Early intervention in the subgroup of children with subthreshold signs of psychosis and internalizing symptoms (especially anxiety symptoms) may reduce the risk of developing psychotic disorders during adolescence.

Objective: The authors reviewed studies published between 1990 and 2003 that reported the prevalence, incidence, and persistence of, as well as the risk factors associated with, psychosis of Alzheimer's disease. Method: PubMed and PsycINFO data-bases were searched by using the terms 'psychosis and Alzheimer disease' and 'psychosis and dementia.' Empirical investigations presenting quantitative data on the epidemiology of and/or risk factors for psychotic symptoms in Alzheimer's disease were included in the review. A total of 55 studies, including a total of 9,749 subjects, met the inclusion criteria. Results: Psychosis was reported in 41% of patients with Alzheimer's disease, including delusions in 36% and hallucinations in 18%. The incidence of psychosis increased progressively over the first 3 years of observation, after which the incidence seemed to plateau. Psychotic symptoms tended to last for several months but became less prominent after 1 year. African American or black ethnicity and more severe cognitive impairment were associated with a higher rate of psychosis. Psychosis was also associated with more rapid cognitive decline. Some studies found a significant association between psychosis and age, age at onset of Alzheimer's disease, and illness duration. Gender, education, and family history of dementia or psychiatric illness showed weak or inconsistent relationships with psychosis. Conclusions: Psychotic symptoms are common and persistent in patients with Alzheimer's disease. Improved methods have advanced the understanding of psychosis in Alzheimer's disease, although continued research, particularly longitudinal studies, may unveil biological and clinical associations that will inform treatments for these problematic psychological disturbances.

Objective: While cognitive deficits are frequently reported in psychotic disorders, it is unclear whether these impairments predate the onset of illness and to what extent they are predictive of later transition to psychosis. Method: The authors studied 37 healthy volunteers and 98 symptomatic, help-seeking patients meeting the inclusion criteria of a treatment program for people at ultra-high risk for psychosis. Of the ultra-high-risk patients, 34 (34.7%) developed psychosis over the course of the investigation. Premorbid and current IQ, attention, memory, and executive functioning were measured with instruments including subtests from the Wechsler Memory Scale--Revised (WMS-R). Analyses compared the ultra-high-risk patients who became psychotic, those who did not become psychotic, and the comparison subjects. Results: Overall, the ultra-high-risk subjects had significantly lower performance IQs than the comparison subjects. Further, impairments were also found in the visual reproduction subtest and the verbal memory index (predominantly owing to lower logical memory scores) of the WMS-R that were specific to the ultra-high-risk-patients who developed psychosis. No other memory, attentional, or executive tasks discriminated between any of the groups. Conclusions: These findings suggest that visuospatial processing impairment and some memory deficits were apparent before the full expression of psychotic illness. Cognitive performance on more complex tasks requiring rapid registration and efficient recall may be compromised before development of first-episode psychosis. Further experimental tasks that challenge these cognitive domains are required to clarify the predictive value of these results.

Objective: The urban environment and familial liability are risk factors for psychotic illness, but it is not known whether a biological synergism exists between these two proxy causes. Method: The amount of biological synergism between familial liability (defined as a family history of delusions and/or hallucinations necessitating psychiatric treatment) and a five-level rating of population density of place of residence was estimated from the additive statistical interaction in a general population risk set of 5,550 individuals. Results: Both the level of urbanicity (adjusted summary odds ratio=1.57, 95% Cl= 1.30-1.89) and familial liability (adjusted odds ratio=4.59, 95% C1=2.41-8.74) increased the risk for psychotic disorder, independently of each other. However, the effect of urbanicity on the additive scale was much larger for individuals with evidence of familial liability (risk difference= 2.58%) than in those without familial liability (risk difference=0.40%). An estimated 60%-70% of the individuals exposed to both urbanicity and familial liability had developed psychotic disorder because of the synergistic action of the two proxy causes. Conclusions: Given that familial clustering of psychosis is thought to reflect the effect of shared genes, the findings support a mechanism of gene-environment interaction in the causation of psychosis.

Objective: The authors' goal was to investigate the suggestion of previous investigations that prenatal viral exposures might increase the later risk of psychotic disorders. Method: They conducted a follow-up study in young adulthood of a birth cohort that was previously documented, by clinical examination and serological testing, to have in utero rubella exposure during the 1964 rubella epidemic. Data were also obtained from an unexposed birth cohort and from the Epidemiological Catchment Area survey. Young adult subjects were administered a standard psychiatric diagnostic interview. The authors compared the proportions of subjects with nonaffective psychosis in the exposed and unexposed cohorts. Results: The rubella-exposed subjects, most of whom were exposed in the first trimester, demonstrated a substantially greater risk for nonaffective psychosis than the subjects who were not exposed to rubella (relative risk=5.2). Conclusions: There is an association between clinically and serologically diagnosed prenatal viral infection and nonaffective psychosis in adulthood.

Drugs of abuse can produce temporary and even more long-lasting psychotic symptoms, but whether affected individuals are more prone to psychosis in the absence of drugs is not known. To evaluate the hypothesis that those experiencing transient cocaine-induced paranoia are more vulnerable to psychosis, 20 cocaine-dependent men with at least three years of continuous use were studied. Subjects had used at least five grams of cocaine per week and were currently involved in a substance abuse treatment program. Half of these men reported episodes of paranoia that occurred only when they binged with cocaine. Subjects were evaluated with two scales: the Perceptual Aberration Scale and the Magical Ideation Scale, which measure perceptual distortions and abnormal beliefs in causation, respectively. The scores were strongly correlated with a history of cocaine-induced paranoia; the 10 men who had experienced paranoia had more abnormal scores than men who never had such experiences. Eighty percent of those identified as prone to psychosis were in the group that reported paranoia, and 90 percent of those who were not prone to paranoia were in the group that did not report having had these experiences. The probability scores derived from these data were well above 80 percent. This suggests that heavy cocaine users who experience paranoia may be more prone to psychosis than cocaine users who do not. (Consumer Summary produced by Reliance Medical Information, Inc.)

Although clinical and laboratory evidence indicates that people who use alcohol and other psychoactive drugs are at risk for psychotic experiences (delusions, hallucinations), epidemiological studies of real populations have not been carried out. To address this issue, a prospective study of 4,994 adults (aged 18 to 49) was performed to identify subjects who reported at least one psychotic experience during the first year of the study. A positive response to one or more of the 12 questions on the Diagnostic Interview Schedule constituted a self-reported psychotic experience. Slightly more than 11 percent of the group (507 'cases') met this criterion, and they were matched to 'noncases' in the same census tract of the general population. Cases and noncases were then compared with respect to drug use habits. Results showed that habitual drug use was associated with psychotic experience, with different drugs having different risk factors. Thus, daily use of marijuana was associated with a 2.4-fold elevated risk (cases versus controls), while daily cocaine use (involving 11 people in the entire study) was associated with a 7-fold higher risk. Alcohol disorder (but not heavy use of alcohol) carried a risk for cases that was 2.6 times that for controls, with a much higher risk for men than women. Overall, the findings suggested that regular use of alcohol, marijuana, and cocaine is associated with a considerably elevated risk of psychotic experience, while occasional use of these substances is not. (Consumer Summary produced by Reliance Medical Information, Inc.)

Psychosis link to child sex abuse Children who are sexually abused before they are 16 are 10 times more likely to develop schizophrenia in later life, according to research published [...]

Objective: The authors address Whether a possible age-at-on-set cohort effect may have introduced a bias into anticipation studies of schizophrenia. Method: A retrospective review of the medical records of all admissions for psychotic disorders (N=877) was conducted. All subjects with a confirmed DSM-IV diagnosis of schizophrenia and age-at-onset data were included (N=419). For analyses, subjects were placed into one of three successive birth cohorts: 1905-1944 (N=96), 1945-1964 (N=200), and 1965-1984 (N= 123). Results: The mean age at first appearance of psychotic symptoms and, similarly, the mean age at first hospitalization significantly decreased over time in successive birth cohorts (25.3, 23.3, and 20.4 years, respectively, for age at first appearance of psychotic symptoms). Conclusions: This potential birth cohort effect for age at onset of schizophrenia needs to be incorporated into genetic models. (Am J Psychiatry 2001; 158:489-492)

FROM THE ANNUAL MEETING OF THE AMERICAN PSYCHIATRIC ASSOCIATION HONOLULU - Synthetic marijuana, known as 'spice,' appears to have induced psychosis in 10 young service members in the US. Naval [...]