Some of the profound effects alcohol has on the brain were discovered years ago through pathological studies at autopsy. However, the recent development of new tools for structural and functional brain imaging has enabled researchers to expand upon this earlier knowledge. For example, some imaging studies have revealed that chronic alcohol consumption causes cortical loss, some of which is reversible with abstinence. Other studies have found that alcohol acts as a global central nervous system depressant, with chronic use resulting in reduced activity that can take a month or more to recover. Finally, imaging tools are also beginning to shed light on which brain regions are active when an alcoholic has the urge to drink.

The science of infertility has advanced rapidly over the past decade, in many respects without regard to the enormous demands that are placed on all participants undergoing an infertility work-up and treatment. Among these demands are a variety of potential psychological effects that must be addressed in the initial patient visit with continued counseling throughout the infertility work-up process. This article reviews the psychological factors that may affect individual patients and couples experiencing infertility, with special attention given to the common manifestations of stress. The need for physicians to provide early and ongoing attention to emotions is emphasized, and a biopsychosocial approach to infertility evaluations is outlined.

Substance use disorder (SUD) pedigrees identified through an attention deficit/hyperactivity disorder (ADHD) proband may be helpful in teasing apart the genetic risks for both ADHD and SUD (ie, alcohol or drug use). Pedigrees segregating for both SUD and ADHD may represent a subset of both of these common disorders that share a related genetic basis. We determined the number of SUD and ADHD pedigrees in a sample of 175 ADHD probands. We found 52 ADHD pedigrees, indicating that at least 29.7% were familial cases. We also found 50 SUD pedigrees; 13 families contained both an alcohol and a drug pedigree, 35 families were alcohol-only pedigrees, and two families were drug-only pedigrees. The incidence of drug-only pedigrees is significantly higher (P<0.01) in families with familial ADHD. This was also true for families with both drug and alcohol pedigrees (P<0.01). The total number of SUD pedigrees and the families with alcohol-alone pedigrees were not significantly different in ADHD pedigrees compared with nonfamilial ADHD families.

The unique clinical presentation of Tourette syndrome (TS) and its symptomatic response to dopamine antagonists are widely cited as evidence for the central role of the limbic-motor interface in the pathophysiology of TS. Nonetheless, the true neuropathology of TS remains elusive, even though significant advances have been made in understanding complex interconnected circuitries within the limbic system and basal ganglia. Neuropathologic and neuroimaging studies—plagued by small samples, clinical heterogeneity, and a number of interpretative problems—are generally supportive of pathology within the orbitofrontal cortex, striatum, and their efferent projections in TS. The specific patterns of abnormalities vary widely across these studies, clouding attempts to define a unifying neuropathology for this disorder. Converging yet circumstantial evidence for frontal cortical, and basal ganglia pathology in TS comes also from studies infields ranging from neuroimmunology to neuropsychology, and from the clinical overlap between TS and disorders such as obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, and Sydenhams chorea. As a “model” neuropsychiatric disorder, TS has stimulated advances in several areas of neurobiology research, yet we still await a real understanding of its pathophysiology in order to move from empirically driven therapeutics to the development of targeted effective treatments.

This article presents a rationale for the hypothesis that an autoimmune mechanism might be involved in the pathogenesis of some forms of obsessive-compulsive aborder (OCO). Existing clinical studies suggesting that some individuals with OCD may have an autoimmune-mediated disorder are briefly summarized. A case example where intravenous immunoglobulin G has been successfully used to treat an adult with OCD spectrum disorder is presented. Preclinical data demonstrating that fragments from the group Αβ hemolytic streptococcus cell wall M proteins can generate antibodies that bind to rat and human tissue are also presented.

To gain a better understanding and a more complete assessment of chronic pain syndrome, the psychosocial, psychological, psychodynamic, and psychiatric aspects of this condition should be included in patient evaluation. As illustrated in the two case studies presented, this approach leads to clearer recognition of the biological and psychosocial needs of patients, and allows for more effective treatment measures to be taken.

Tourette syndrome (TS) has been conceptualized as a psychological problem, a neurological problem, and more recently a neurobehavioral problem. Each conceptual model has had an impact on how persons with TS view themselves and how practitioners view individuals with TS, as well as an impact on what both clinicians and patients expect from diagnosis and treatment. This article reviews the common comorbid psychiatric disorders and their relationship to TS, and discusses how the evolving conceptions of TS have impacted psychologically on persons with tics and TS, as well as on the providers who treat them.

This case study describes the psychoanalytic treatment of a young woman presenting with symptoms of overwhelming anxiety, panic, and conversion. The emphasis is on technique with detailed reporting on the psychoanalytic process. Attention is paid to transference-countertransference paradigms at critical junctures in the treatment. The role of clinical supervision in the unfolding of the process is described also. This patient developed an identifiable transference neurosis during the course of the treatment, which became the focus of the analysis. Follow-up observations on this patient are also presented, as she returned for a brief course of treatment 4 years following initial termination.

Until recently, several weeks of treatment were required in order to obtain a clinically significant antidepressant response using pharmacotherapy. The present study, using the mouse forced swimming test, investigated possible antidepressant augmentation strategies, together with the probable mechanisms involved in such potentiations. It is clear from this and other similar studies that it is possible to enhance the activity of antidepressant drugs with the addition of other compounds (ie, clonidine, quinine, glyburide, pindolol, or buspirone). These data indicate that direct/indirect manipulation of serotonergic receptor systems potentiates the effect antidepressant drugs (ie, selective serotonergic reuptake inhibitors) in the mouse forced swimming test, and thus establish this model as a reliable preclinical tool for the investigation of possible antidepressant augmentation strategies. It also appears that this model can be used as a method for identifying the mechanisms involved in such treatment strategies.

As the Human Genome Project completes the first human genome sequence, attention has turned to how this information can be used to understand disease. The availability of sequences for all genes will allow a comprehensive evaluation of each gene's contribution to disease. Approaches involving collecting specific gene variants and monitoring expression levels using DNA microarrays facilitate collecting information about DNA and RNA in a rapid and highly parallel manner. Developing an extensive catalogue of polymorphisms will become increasingly important in the context of studies of complex genetic diseases such as schizophrenia and bipolar disorder.

Sydenham's chorea is currently recognized as the only neurologic sequela of rheumatic fever. Recent evidence suggests that there may be a spectrum of neurobehavioral disturbances, particularly including tics and obsessive-compulsive disorder, that develops following streptococcal infection by the process of molecular mimicry, whereby antibodies directed against bacterial antigens cross-react with brain targets. This proposed postinfectious, immune-mediated condition has been termed “pediatric autoimmune neuropsychiatric disorders after streptococcal infection” (PANDAS). This article reviews research evidence in favor and also against the PANDAS concept and discusses the implications of the hypothesis.

This paper outlines potential research applications of the unquantified (paper or digital) electroencephalography (EEG) in psychiatry. Three main areas are highlighted: first, the need for thorough familiarity with the unquantified EEG is emphasized, including the ability to confidently recognize all normal and abnormal activities that could influence further analysis of the record as well as artifacts that can contaminate the tracings; second, the fact that definitive studies relating EEG abnormalities to psychiatric symptomatology and clinical response are lacking; and third, the potential for EEG to be utilized as a tool to decrease the risk of invasive research studies is discussed.