Libido is the drive to have a sexual activity. Gonadal hormones play a major role in activating and maintaining libido in both men and women. Other hormones, though, interact with them in influencing sexuality, such as prolactin and also brain neurotransmitters. The role of hormones declines with age and sexuality becomes more mind-induced. Nevertheless, some aspects of sexuality remain linked to hormones. For example, a reduction of central arousability is typical of hypogonadal state. However, it is not clear at what level of androgen deficiency the loss of libido begins and if adequate external stimuli can overcome a partial deficiency.

The majority of studies that have examined the usefulness of pharmacotherapies selective for serotonin (5-hydroxytryptamine; 5-HT) as a treatment for alcohol dependence have been standard, double-blind clinical trials that include patients with a variety of clinical presentations. Almost all of the early studies evaluated heavy social drinkers and found only a modest advantage for 5-HT pharmacotherapies in reducing the number of drinks per day. Also, the advantage of these pharmacotherapies was observed primarily when these agents were given at higher daily dosages than suggested prescribing practices for use as an antidepressant. The few studies that evaluated treatment-seeking patients found that 5-HT pharmacotherapies were not instrumental in reducing drinking rates compared with placebo. These results led to a dampening of enthusiasm for use of these agents in treating alcohol dependence. However, more recent investigations have begun to target subgroups with potential abnormalities in 5-HT neurotransmission. The thinking is that these medications should be most useful in alcohol-dependent individuals who have more clearly delineated suggestive signs of 5-HT dysfunction, such as concomitant depression or anxiety. Although few results are available to date, there is growing evidence to suggest that alcohol-dependent subgroups are differentially responsive to 5-HT pharmacotherapies with respect to drinking-related outcomes. This may explain the modest and variable 5-HT pharmacotherapeutic effects that were reported in the earlier studies, which included large heterogeneous patient groups. Further investigations are needed to confirm these initial optimistic results.

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.

Karl Ludwig Kahlbaum originally described catatonia as a psychomotor disease that encompassed motor, affective, and behavioral symptoms. In the beginning of the 20th century, catatonia was considered to be the motoric manifestation of schizophrenia; therefore, neuropathologic research mostly focused on neuroanatomic substrates (ie, the basal ganglia underlying the generation of movements). Even though some alterations were found in basal ganglia, the findings in these subcortical structures are not consistent. Recently, there has been a reemergence of interest into researching catatonia. Brain imaging studies have shown major and specific alterations in a right hemispheric neural network that includes the medial and lateral orbitofrontal and posterior parietal cortex. This neural network may be abnormally modulated by altered functional interactions between γ-aminobutyric acid (GABA)-ergic and glutamatergic transmission. This may account for the interrelationship among motor, emotional, and behavioral alterations observed in both clinical phenomenology and the subjective experiences of patients with catatonia. Such functional interrelationships should be explored in further detail in catatonia, which may also serve as a paradigmatic model for the investigation of psychomotor and brain function in general.

This paper discusses the National Bioethics Advisory Commissions (NBAC's) report on research involving persons with mental disorders that may affect decisionmaking capacity. After placing the NBAC recommendations into their historic context, the authors propose a strategy to enroll decisionally incapacitated subjects into neuropsychiatric research. The authors maintained that their proposed consensus model for research authorization, utilizing subject advocates, fosters valuable clinical research while protecting potentially vulnerable subjects.

Depression and apathy are the two most frequent behavioral complications of stroke. This article reviews the prevalence of these conditions in poststroke patients, as well as their clinical correlates, longitudinal course, and possible mediators. A number of controlled clinical trials of the efficacy of various drugs in the treatment of poststroke depression are also reviewed.

Infection with human immunodeficiency virus type 1 (HIV-1 ) leads rapidly to infection of the brain and subsequent neuropsychological impairment, including subclinical impairment, minor cognitive-motor disorder, and HIV-1–associated dementia (HAD). This article reviews HAD and the factors involved in its pathogenesis; the effectiveness of antiretroviral therapy; the prevalence of HIV-1 and subtypes; and the role of chemokines and cytokines as the capstones associated with neuropathology due to inflammation.

Although the concept of pharmacotherapyfor attention-deficit/hyperactivity disorder (ADHD) was first introduced more than 60 years ago, treatment of this disorder remains more controversial than ever. It is hoped, however, that the recent Consensus Development Conference (CDC) Statement on the diagnosis and treatment of ADHD will not only help answer some of the questions surrounding management of this disorder, but also lend needed scientific weight to debate in this area. While more research in ADHD is needed, the CDC partic ipants pointed to a solid body of evidence showing that careful medication management can result in noticeable improvement in several measures, with little risk of adverse events.

Brain ischemia is a process of delayed neuronal cell death, not an instantaneous event. The concept of neuroprotection is based on this principle. Diminished cerebral blood flow initiates a series of events (the “ischemic cascade”) that lead to cell destruction. This ischemic cascade is akin to a spreading epidemic starting from a hypothesized core of ischemia and radiating outward. If intervention occurs early, the process may be halted.

Interventions have been directed toward salvaging the ischemic penumbra. Hypothermia decreases the size of the ischemic insult in both anecdotal clinical and laboratory reports. In addition, a wide variety of agents have been shown to reduce infant volume in animal models. Pharmacologic interventions that involve thrombolysis, calcium channel blockade, and cell membrane receptor antagonism have been studied and have been found to be beneficial in animal cortical stroke models. Human trials of neuroprotective therapies have been disappointing. Other than thrombolytics, no agents, have shown an unequivocal benefit. The future of neuroprotection will require a logical extension of what has been learned in the laboratory and previous human trials. A sensible approach to the use of multiple-agent cocktails used in combination with thrombolytics is likely to offer the highest chance for benefit.

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.

The modern therapeutic approach to most psychiatric diseases involves a combination of well-supervised psychotherapy, pharmacotherapy, and electroconvulsive therapy. Patients who fail to adequately respond to these modern treatment methods and remain severely disabled may be considered for surgical intervention. Cingulotomy, capsulotomy, subcaudate tractotomy, and limbic leucotomy are the most common psychosurgical procedures performed today, with response rates in the 35% to 65% range. Modern stereotactic techniques have reduced complication rates, but controversy remains regarding the optimal surgical procedure. The major psychiatric diagnostic categories that might respond to surgery include treatment-refractory major affective disorders, obsessive-compulsive disorder, and chronic anxiety states. Surgery should be considered as one part of an entire treatment plan and must be followed by an appropriate psychiatric rehabilitation program. It should only be carried out by an expert multidisciplinary team consisting of a neurologist a neurosurgeon, and a psychiatrist with experience in these disorders. Surgical intervention remains a reasonable therapeutic option for select patients with a disabling psychiatric disease and may be underutilized.

The study of the psychobiological bases of boredom has been limited by the vagueness of its clinical constructs and the difficulties in applying adequate experimental models. The theoretical background of previous research mainly has been based upon cognitive and behavioral psychology by using neuropsychological constructs, such as arousal, attention, motivation, sensation-seeking, and the reward system. Recently acquired data depict a complex and fragmentary picture. In this article, the author presents a review of the literature as well as some personal considerations on this intriguing topic.

The increasing evidence for a neurobiologic basis for alcoholism has spurred the search for pharmacologic agents to treat alcohol abuse. The complex set of symptoms and behaviors that characterizes alcoholism has been linked to dopaminergic and opioid neurotransmitter systems, suggesting that opioid antagonists, such as naltrexone, may alter the positive reinforcement effects and craving involved in alcoholism. Laboratory and clinical investigations of naltrexone have demonstrated the potential for this agent to reduce craving, increase the aversive effects of alcohol, decrease drinking days, and increase abstinence. While naltrexone and other opioid antagonists, such as nalmefene, may be effective components of an alcohol-treatment program, they should only be used in combination with psychosocial interventions, such as support groups and psychotherapy.

Psychotic anxiety has not been systematically included in standard psychopathologic and diagnostic literature, presumably because anxiety is implicitly perceived to be an emphatically comprehensible consequence of the cognitive symptoms of psychosis. This review gives an overview of neurophysiologic studies that indicate different pathogenic mechanisms for different types of psychosis. Convergent and complementary structural and functional imaging findings, biochemical and neuropsychological data allow conjecture as to neurophysiologic-psychopathologic links in cycloid psychosis. Intriguing results suggest that in cycloid psychosis, a generalized hyperasousal related to the tonus of the noradrenergic system may be the basic disturbance causing the delusionary and perceptual psychotic distortions. The findings are specific for cycloid psychoses, which are diagnosed as polymorphous psychosis in the International Classification of Diseases and Related Health Problems, 10th Edition. Furthermore, these findings are consistent with the author's hypothesis that the emotional derailment is the primary disturbance in cycloid psychosis (anxiety-elation). In contrast, cognitive disturbances are secondary and remit after the exceptional emotional state is rebalanced.

The historical development of the concept of catatonia in affective disorders and contemporary papers on this topic are reviewed. In addition, data from a current study on the frequency of catatonia in mixed mania are reported. Differences between catatonic and noncatatonic patients with mixed mania are presented and their relevance to clinical practice is discussed.

This article reviews the use of pharmacologic agents to treat nonparaphilic compulsive sexual behaviors (paraphilia-related disorders). Recent data suggest that serotonergic antidepressants, especially serotonin reuptake inhibitors (SRIs), may be effective in treating nonparaphilic sexual behaviors characterized by hypersexuality. The rationale, prescriptive use, and limitations of SRIs are reviewed, as are the proposed mechanisms of action, prescriptive use, and side effects of medications that lower serum testosterone (including triptorelin and the antiandrogens medroxyprogesterone acetate and cyproterone acetate). The potential use of psychostimulants, mood stabilizers, and atypical antipsychotics for paraphilia-related disorders in specific clinical situations is discussed. Practical guidelines, augmentation strategies with adjunctive psychopharmacologic agents, and indications regarding pharmacologic combinations of the above medications are suggested.