Catechol-O-methyltransferase (COMT) inhibitors are a new class of medication being developed for the treatment of Parkinson's disease (PD). The enzyme COMT metabolizes levodopa and dopamine, both peripherally and centrally. Coadministration of a COMT inhibitor with levodopa creates an increase in peripheral and central levodopa bioavailability, as well as higher central dopamine concentrations. Because these actions improve the duration of response to levodopa, the COMT inhibitors should prove to be useful adjunctive therapies in PD patients.

Panic disorder occurs frequently with different forms of cardiovascular disease and hypertension. The 13 panic symptoms described in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) often overlap with manifestations of cardiovascular disorders, raising problems in the differential diagnosis. In order to explore in greater detail the phenomenology of panic symptoms in cardiovascular patients, the Structured Clinical Interview for Panic-Agoraphobic Spectrum (SCI-PAS) was administered to 111 patients with hypertension and 29 patients with a recent myocardial infarction.

With regard to the frequency of endorsement of many of the symptoms assessed on the SCI-PAS, more than 40% of the cardiovascular patients who failed to meet the DSM-IV criteria for panic disorder did not significantly differ from the 10% of cardiovascular patients who did fulfill the criteria for panic disorder. A third distinct subgroup comprising 48.6% of the cardiovascular patients reported a significantly smaller number of SCI-PAS symptoms than the other two groups.

These preliminary findings suggest the existence of a relatively large proportion of cardiovascular patients who present with physical and psychological symptoms that are potentially related to panic disorder and that may provoke considerable subjective distress. Further studies are needed to clarify the nature of these symptoms and their potential interference with treatment and symptomatology of cardiovascular disease.

The growth of gambling across the United States over the past decade has created significant difficulties for pathological gamblers. The rise in problem gambling, coupled with an increasing strain on social and health care services for treatment of gamblers and their families, has resulted in an urgent need for innovative interventions that target patients, health care providers, educational institutions, government, media, and the gambling industry. This article describes the impact of gambling from a consumer-protection perspective, and offers approaches to promoting public awareness of compulsive gambling as a pervasive problem that affects multiple areas of society.

Brain lesions cause different level change in cerebral function. They may conflict with the existing antagonistic mechanisms between the dorsal and ventral brain. At a clinical level, a dorsal brain lesion may constitute praxis disorders, while a ventral lesion may represent preventive inhibition. Further instinctive symptoms originate in the cingulate gyrus and its connections with the thalamic peduncle. This area may be an importan obsessive-compulsive disorder (OCD) pathway, that is utilized therapeutically during neurosurgical interventions in OCD.

Evidence continues to mount that anticonvulsants represent broad-spectrum central nervous system agents which are highly efficacious in the treatment of core psychiatric symptoms. The US Food and Drug Administration has extended the use of anticonvulsants beyond the treatment of epilepsy, to include wide-reaching neuropsychiatric illnesses such as mania, migraine, panic disorder, and trigeminal neurologia. From the perspective of psychiatric disorders, the most exciting development about these newer agents is the emergence of persuasive evidence that they are effective in treating mood disorders. Depakote and Tegretol have been joined by Neurontin and Lamictal as agents shown to be useful in the treatment of bipolar, and possibly unipolar, depression.

Recently, both clinical and research attention has focused specifically on the use of Neurontin and Lamictal as alternatives to standard, agents for the treatment of mood and anxiety disorders. Because many patients with bipolar disorder experience continued symptomology despite standard treatment, further study of these novel agents for the treatment of affective disorders is warranted.

During the past decade, an increasing interest has been shifted from the study of neuroreceptors to their links with second-messenger pathways. In the present article, we shall briefly review the methodological tools for evaluating adenylyl cyclase activity in several human brain and peripheral models, as well as the studies suggesting its involvement in the pathophysiology of mood disorders. We shall present also some preliminary data obtained in our laboratory providing evidence for the measurement of serotonin-sensitive adenylyl cyclase activity in human brain postmortem.

Obsessive-compulsive disorder (OCD) is a psychiatric disorder in which the patient suffers from recurrent intrusive ideas, impulses, thoughts (obsessions), and/or patterns of behavior (compulsions) that are ego-alien and produce anxiety if resisted. The ego-dystonic nature of OCD is one of the hallmarks of this disorder. OCD can be a disabling condition because the obsessions and compulsions are time-consuming and interfere with patients' everyday activities and their relationships with friends and family. In severe cases, OCD conflicts even with the simplest tasks of daily living.

Research interest in OCD has been growing steadily in the past decade. A search on MEDLINE reveals an over 300% increase in citations on OCD from 1986 to 1998. These range across the spectrum of research fields, from genetic studies, brain imaging, and neurobiological research examining the underlying pathogenesis of OCD to epidemiological studies evaluating the course of clinical symptoms, comorbidities, and outcomes. Each area represents an important piece in the complex jigsaw puzzle of OCD.

The etiology and treatment of obsessive-compulsive disorder has been explained from a social learning and neurobiological model. In this article a third model is proposed: the biobehavioral model, which encompasses a learning and neurochemical viewpoint. The authors suggest that behavior therapy and medications may operate in the same manner and that behavior therapy may need to be reconceptualized. Animal and human research supporting the interaction of behavioral change and neurochemical processes is presented. The authors also posit that urges precede anxiety and that compulsions are performed in response to the anxiety. Also, obsessions are viewed as secondary to compulsions. The mechanism of how behavior and cognitive-behavioral therapy may produce neurochemical changes is discussed.

The lumping together of the seven deadly sins—pride, covetousness, jealousy, sloth, lust, gluttony, and anger—is, of course, a theological categorization rather than a medical nosology. Nevertheless, these seven sins are oddly reminiscent of various symptoms of a common medical disorder—one that has received increasing neuroscientific investigation in recent years—obsessive-compulsive disorder (OCD). Is such a parallel between sin and symptom purely coincidental, or is modern neurobiology able to provide a more coherent explanation?

Interestingly, the term “obsession” derives from the Roman Catholic concept of obsession—a state of being possessed by the devil. Indeed, obsessions—defined as recurrent intrusive and senseless thoughts and images—are some of the most overwhelming and distressing of psychiatric symptoms. While it is true that hallucinations and delusions lead to a loss of contact with reality, people with obsessions suffer from the very fact that they cannot resist ideas that they know full well to be irrational. Thus, OCD sufferers find themselves having to perform compulsions—recurrent rituals that relieve anxiety—but which are not realistically connected to the preceding obsessions or are clearly excessive.

In this article, we present rationales for using complex combination therapy in treatment-refractory bipolar patients and discuss the agents available for use in this therapeutic approach. We review a case example of successful remission that was achievable only with complex combination therapy, and examine its theoretical implications. Practical approaches to devising the optimal complex combination treatment for individual patients are explained, and we look to the development of new methodologies and a more systematic database for decision making in the future.

The endogenous peptide 5-HT–moduline has been characterized as a novel neuropeptide that binds to 5-HT1B receptors in the brain areas in which it is released. By inducing structural changes in these receptors, this peptide prevents 5-HT binding, thereby desensitizing the receptors and inhibiting serotonergic function. This novel mechanism may help to explain differential effects of the serotonergic system in varying areas of the brain that are innervated by the same or few neurons. In addition, dysfunction or disruption of the 5-HT–moduline system may contribute to psychiatric disorders such as depression and anxiety, and may have important implications for the development of new therapeutic agents for these disorders.

This article describes a new approach to the understanding and treatment of pathological gambling (PG). In order to foster an understanding of the pathological variations of gambling, gambling as a “normal,” widespread behavior that spans cultures and centuries is briefly reviewed, as is the current socioeconomic impact of gambling on society. PG is interpreted as an excessive exaggeration of a normal behavior (a behavioral excess disorder, or BED), similar to exaggerations of cleaning, grooming, loving, working, or shopping.

Particular developmental deficits in certain individuals and their resulting vulnerabilities make these persons prone to “getting lost” in excessive gambling activities. PG fulfills three important functions that serve to maintain these behaviors. Most frequently, it serves the intraindividual function of distraction from a cognitive, emotional, or physiologic negative state (NEST). A second, much less frequent intraindividual function is that of fast socioeconomic self-destruction in persons who develop presuicidal depression before they start gambling. In the worst disease course of this subtype, patients enter a dramatic “last game”; when they lose, “fate has decided” that they should kill themselves immediately thereafter. A third function fulfilled by PG is interactional, ie, in the “I can't be with or without you” type of relationship.

These gambling-related vulnerabilities are discussed against the background of recent studies from: (1) cognitive psychological and animal experiments regarding the prediction of future events; (2) functional brain imaging studies in obsessive-compulsive disorder; and (3) gambling experiments (prediction of future events) in patients with specific lesions in the orbitofrontal cortex. This article outlines the basics of strategic-systemic behavior therapy for these conditions, and summarizes results of the first outcome and follow-up studies.

We present the case of a 27-year-old man treated unsuccessfully for 1 year for chronic cough, who was thought to suffer from psychogenic cough. Vocal tic was suspected by a liaison psychiatry service, and treatment with low-dose haloperidol was successful. This case suggests that more attention to tic syndromes is needed before qualifying persistent idiopathic cough as psychogenic.

The application of computers in psychiatry affords clinicians endless possibilities in terms of information gathering, processing, and sharing. Some systems have been designed and are currently in use, expanding the knowledge of psychiatric pathology and its treatment. This review highlights the uses of computers in psychiatry and the progress being made in this area.

Separation anxiety has long been of interest in psychiatry. The term refers to both a phenomenon of normal psychological development and to the symptoms of a common childhood psychiatric disorder, classified in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), and the International Statistical Classification of Diseases and Related Health Problems, Tenth Edition (ICD 10), as separation anxiety disorder. Available epidemiological studies suggest a prevalence rate of this disorder of about 4%. Treatment studies using cognitive behavioral therapy and/or medication are reported in the literature. There is also evidence that symptoms of separation anxiety may occur in adulthood, though this is far less widely known. We consider childhood and adult separation anxiety to be a component of panic spectrum, described in other papers of this issue.

A small and somewhat confusing literature addresses the question of outcome of childhood separation anxiety disorder, with support for a weak association between childhood separation anxiety and adult panic disorder. We believe there is a suggestion of a stronger association of the childhood condition with persistence of a similar syndrome of adult separation anxiety. Symptoms of adult separation anxiety may be a manifestation of panic spectrum, as we suggest. Such symptoms may represent a separate, specific clinical entity, or symptomatic separation anxiety may occur as a manifestation of a range of Axis I disorders, and may respond to treatment of these disorders. In any case, we urge researchers and clinicians to begin to attend to the possibility that adult psychiatric patients may suffer from clinically significant symptoms of adult separation anxiety.

The neurobiology of trichotillomania (TTM) has only recently received attention from the neuropsychiatrie community, and the number of studies in this area is limited. Nevertheless, there is tentative support for the hypothesis that serotonergic, dopaminergic, and opioid systems mediate hair-pulling symptoms, and that corticostriatal circuits also play a role. An understanding of the neurobiology of TTM may be of value not only for the treatment of this disorder, but also for other stereotypic behaviors.

Although the precise etiological nature of autism—the most common development disorder—remains elusive, two main biological factors have been suggested. One is related to a possible neurochemical dysfunction at the level of the serotonergic system; the other underlines the presence of neuroanatomical abnormalities in different areas, in particular, in the cerebellum.

The authors propose a unifying hypothesis linking serotonin (5-hydroxytryptamine, or 5-HT) to the cerebellum on the basis of the observation of a specific 5-HT receptor subtype, 5-HT5A, in this area. The 5-HT5A receptors may be involved in the pathophysiology of autism, and perhaps, in autism-related disorders, since they are mainly expressed in Purkinje's cells. Future studies with specific drugs that interact with 5-HT5A receptors should permit the testing of this hypothesis through the evaluation of the receptors themselves in autopsied brain samples or in vivo by positron emission tomography. Theoretically, such compounds might prove effective in the treatment of autism.

In an effort to aid the clinician in the differential diagnosis of catatonic states, we assessed the nature of electroencephalography (EEG) findings in both medical and psychiatric forms of catatonia. An exhaustive review of the literature on catatonia due to a general medical condition (CDGMC) was performed in addition to a prospective review of catatonic patients at The Ohio State University Neuwpsychiatric Facility.

A total of 105 patients had documented, specific clinical and EEG information, with neurologic conditions accounting for 82.8% of case reports. Results from the case series of 31 episodes of catatonia indicate that there is an increased likelihood of diffuse slowing in patients with CDGMC versus psychiatric catatonia. Given the observed rate of abnormalities, EEG is an important but underutilized tool in the differential diagnosis of catatonic disorders.