Psychiatry has a long tradition of believing that too much sex is a bad thing. The classical literature provides detailed accounts of men and women who demonstrated apparently pathological sexual appetites. Since Freud, psychoanalytic authors have held that masturbation is unhealthy, and psychodynamically oriented thinkers have written on Don Juanism and nymphomania.

Peripheral neuropathy associated with human immunodeficiency virus type 1 (HIV-1) infection is a major cause of morbidity in this patient population. Due to the associated chronic pain, its management has come within the purview of neuropsychiatrists. This paper will focus on the primary pathogenic aspects of HIV-1–associated peripheral neuropathies. The specific syndromes of greatest concern are distal sensory polyneuropathy, toxic neuropathy, inflammatory demyelinating polyradiculoneuropathy, and cytomegalovirus-related progressive polyradiculoneuropathy. The treatments available for these conditions and their efficacy are discussed.

Objectives: Possible disease-modifying effects of rivastigmine have been suggested by analyses using a variation of the randomized start design; however, the results were somewhat confounded by differing attrition rates. We report on an alternative method investigating whether increasing doses reduce the rates of cognitive decline in patients who continue treatment.

Methods: The effect of dose on the rate of cognitive decline seen on the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) was explored for patients in a long-term (130-week) extension of a 26-week placebo-controlled trial using two methods: a weighted leas squares regression analysis using each individual's slope, and a weighted analysis of variance (ANOVA) comparing the slopes of patients categorized by dose (≤6 mg/d or >6 mg/d).

Results: The results from 408 patients included in the weighted least squares analysis estimated the rate of decline to attenuate by approximately 1 point/y for every 3 mg/d increase (P<.0001). The average annual rate of decline for patients whose mean dose was >6 mg/d was 4.5 points (95% Cl, 5.1–3.9), while for patients with a mean dose of≥6 mg/d a decline of 8.2 points (95% Cl, 9.1–7.3) was seen.

Conclusion: These data further support earlier results suggesting that rivastigmine reduces the rate of progression of cognitive deterioration in Alzheimer's disease.

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.

Standard pharmacotherapy for the maintenance of treatment of patients with bipolar I disorder consists of lithium, valproate, or carbamazepine. However, many patients fail to respond to monotherapy with any of these agents, and as a result, psychiatrists often resort to polypharmacy. Findings from some open-label trials and retrospective chart reviews suggest this approach may be useful, but in the few controlled trials that have been conducted, the results have been negative. One drug combination that warrants further study as maintenance therapy is lithium plus valproate. Each is approved by the U.S. Food and Drug Administration for treatment of acute mania, and lithium has demonstrated efficacy for maintenance treatment as well. Some preliminary evidence suggests that the combination can be effective for patients who do not respond to monotherapy, and it seems to be no more dangerous than monotherapy. Concomitant administration of lithium plus valproate does not significantly alter lithium pharmacokinetics, and statistically significant changes that arise in valproate pharmacokinetics are not clinically significant. Although it is not known whether the drugs interact to augment response, many of their effects in the central nervous system do differ, and there is no indication of pharmacodynamic interactions that oppose each other. Finally, some evidence suggests that lithium and valproate may differ with regard to clinical variables that predict response to treatment. (J Clin Psychopharmacol 1998;18:38–49)

Bipolar I disorder afflicts approximately 1% of the U.S. adult population, with a median age at onset of 19 years. In many respects, it is a disabling disease. Acute episodes of mania and depression are often protracted with 24% of patients still acutely ill after 1 year has elapsed, 16% after 2 years, and 9% after 5 years. Subsyndromal symptoms, which impose significant morbidity that falls short of meeting full criteria for a mood episode, may occur frequently. Patients with bipolar I disorder are more likely than not to be unemployed or underemployed, less likely to marry and more likely to divorce than matched control subjects, and almost every family perceives the illness as a burden. Even remitted patients manifest poor psychosocial functioning, Ultimately, nearly 19% of patients die from suicide.

Over the past decade, new functional neuroimaging tools have enabled researchers to identify the specific brain regions involved in obsessive-compulsive disorder (OCD). More recently, researchers have perfected several new techniques for stimulating the brain. With some exceptions, these new brain stimulation techniques are regionally specific and less invasive than older methods. As a class, these “somatic interventions” build on prior neuroanatomic information about OCD. This article reviews the past and current status of these brain stimulation methodologies, which promise to revolutionize neuropsychiatric research and therapy over the next 10 to 20 years. As the brain circuits in OCD and the pharmacology within those circuits become better understood, these brain stimulation techniques hold particular promise in helping to understand and perhaps treat OCD.