Platelet dysfunction and thrombocytopenia rarely occur during clozapine therapy, but constitute an important source of morbidity and mortality if they are not detected and therapy is discontinued. The manufacturer recommends discontinuing clozapine when the platelet count falls below 100,000/μL and resuming therapy when the count returns to within normal range (150,000–450,000/μL). If thrombocytopenia recurs, clozapine should be permanently discontinued.

The authors report a rare case of long-term thrombocy-topenia persisting 40 months postclozapine treatment. In addition, increased in vitro platelet [14C] serotonin release was observed in the presence of the drug, suggesting an immune-related cause for the thrombocytopenia.

G.W., a 43-year-old African-American man, had been treated in the South Carolina Department of Mental Health since 1974 with a diagnosis of schizophrenia of chronic undifferentiated type, along with severe paranoid, delusional, threatening, and assaulting behavior. There was no history of illicit drug use. He had received intramuscular fluphenazine deconoate and haloperidol, as well as other neuroleptics, with little benefit observed during his years of treatment.

Clozapine was initiated at 25 mg bid on July 2, 1993, and was gradually increased to 650 mg daily over the next 20 months. After 7 weeks on this dose, the patient's platelet count fell from 103,000/μL to 60,000/μL, and clozapine was discontinued. A week later, the count had improved to 109,000/μL; 3 weeks later, with the platelet count at 109,000/μL, clozapine was reintroduced and titration started. However, within 7 days, his platelet count fell to 70,000/μL and clozapine was permanently stopped.

Autistic disorder and catatonia are neuropsychiatric syndromes defined by impairments in social interaction, communication, and restricted, stereotypical motor routines. Assessments of children with these disorders are typically restricted in scope by the patients' limited ability to comprehend directions. The authors performed systematic assessments of dyskinesias on six prepubertal boys with autistic disorder and mental retardation and on one adolescent male with catatonia to determine if this type of information could be routinely obtained. The boys with autistic disorder had more stereotypies and tics, a greater degree of akathisia and hyperactivity, and more compulsions than the adolescent with catatonia. Catatonia was associated with catalepsy and dystonic postures. The authors conclude that the diagnostic accuracy and specificity of neuropsychiatric syndromes may be enhanced by the systematic assessment of the dyskinesias associated with each condition.

Although anxiety and mood disorders are listed as separate disorders in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, they frequently coexist. They may be expressed phenotypically as comorbidities or as the provisional entity mixed anxiety-depressive disorder. Patients with both anxiety and depression are more symptomatic, use more health care resources, and have a worse prognosis than those with a single disorder. Recognizing and treating these patients are challenges for physicians because the symptoms of the two disorders often overlap. Administration of effective treatment, comprising both anxiolytic and antidepressant effects, can reduce patient distress and disability, as well as inappropriate utilization of medical services. Medications such as tricyclic antidepressants, selective serotonin reuptake inhibitors, nefazodone, venlafaxine XR (extended release) and mirtazapine, are highly effective in treating comorbid depression and anxiety. These newer agents now represent the pharmacotherapeutic treatments of choice for the comorbid conditions.

This article focuses on the clinical onset of obsessive-compulsive disorder (OCD), specifically addressing the of onset, gradual and acute onset, and whether there are some types of premorbid conditions or a prodromal phase that predispose individuals to the onset of OCD. Clinical and epidemiological studies have come to different conclusions regarding age at onset as well as regarding differences between the sexes. Data gleaned from research to date have demonstrated a relationship between OCD and obsessive-compulsive personality disorder (OCPD), although OCPD does not appear to be the more prevalent personality disorder among patients with OCD. Preliminary research has suggested that Axis I disorders may predispose individuals to OCD onset; however, the significance of this relationship remains to be clarified. Evidence of the association between OCD and subthreshold obsessive-compulsive syndrome suggests that these disorders lie on a continuum of severity, with some cases developing OCD while others do not.

Although many investigations into the onset of obsessive-compulsive disorder (OCD) suggest the occurrence of potential life events as triggering factors, such an association has not been well studied to date. The purpose of the present paper is to review the literature on OCD onset in order to determine whether OCD is triggered by recent life events, what specific events may serve as triggers, and the clinical and research implications of these factors. Overall, the available studies do not consistently support the theory that OCD is triggered by specific antecedent life events. However, there is a body of evidence to support the theory that the specific life events of pregnancy and birth of a child can trigger OCD. This apparent association has led to the investigation of certain neurohormonal factors, including changes in estrogen or oxytocin levels, that may be of etiopathogenetic significance in OCD. Confirming such associations may allow clinicians to provide more targeted preventive and therapeutic interventions.