Although the incidence of cancer and cancer-related deaths has declined in recent years, undertreatment of cancer-related pain continues to be a significant problem. By thoroughly assessing chronic malignant pain (CMP) as it relates to cancer and achieving a more complete understanding of the CMP syndromes experienced by cancer patients, psychiatrists and neurologists can formulate accurate diagnoses of patients' clinical pain syndromes and construct well-defined, individual management plans for each patient.

Tic disorders may manifest in a wide variety of clinical presentations, ranging from single tics of relatively short duration to a series of complex tics that may last for years. An understanding of the etiology of various tic disorders is essential to establish a differential diagnosis of Tourette syndrome (TS). Because TS is incurable, improvement in quality of life is the primary goal of pharmacologic therapy. Although neuroleptics have been the most effective medications to date in managing the symptoms of TS, they may have significant adverse effects that limit their use. Several alternative pharmacologic options are either available or under investigation.

There is evidence supporting the presence of abnormalities in certain neurotransmitters, such as dopamine and noradrenaline, and in neuropeptides and other mechanisms, such as the immune system in patients with obsessive-compulsive disorder (OCD). However, the findings implicating serotonin (5-hydroxytryptamine [5-HT]) in the pathophysiology of OCD are increasing at a rate not found in any other psychiatric disorder. These abundant findings foster numerous complex questions that await answers. For example, which 5-HT receptor subtypes or other subcomponents of the 5-HT system are principally involved in OCD pathophysiology, and how do they interact with dysfunctions of other systems? In the search for answers to these critical questions, experimental pharmacology represents a key tool for approaching the complexity of the involvement of 5-HT in OCD, and also suggests new potential therapeutic targets. This article summarizes, in part, the presentations and the discussion of the symposium, “Experimental Pharmacology in OCD,” which was held during the Third International OCD Conference meeting in Madeira, Portugal, in September 1998.

This article reviews recent studies of psychotherapy for treatment of depression. There is evidence that cognitive behavioral and interpersonal therapies are useful treatments for depressed outpatients, roughly comparable to antidepressant pharmacotherapy. Pharmacotherapy and psychotherapy do not, however, necessarily treat the same patients and there is emerging evidence of a neurobiological “boundary” that may delimit therapy response. Psychotherapy plus pharmacotherapy combinations appear particularly useful for outpatients with more severe, recurrent depressions. Depression-focused psychotherapy may also provide an important alternative to an indefinite course of maintenance pharmacotherapy for patients at high risk for recurrence.

Attention-deficit/hyperactivity disorder (ADHD) has an early childhood onset in the majority of cases. This has a considerable impact on the development of the affected individual, both directly (as a result of the symptoms) and indirectly (through the stresses imposed upon school, learning, socialization, and family life). Several lines of evidence point to a genetic component to ADHD. Family studies show a familial aggregation of ADHD, with a five- to sixfold increase in the incidence of ADHD among first-degree relatives. Twin studies reveal a higher concordance rate for ADHD among monozygotic twins compared with dizygotic twins. To date, molecular genetic research has focused on candidate genes in the dopaminergic system. Genes studied include the D2A1 allele of the dopamine D2 receptor gene, the dopamine transporter gene, and the dopamine D4 receptor gene. One of the major limitations to the study of the genetics of behavioral disorders in children has been the overlap among syndromes, including oppositional defiant disorder, conduct disorder, persistent (adult) ADHD, and bipolar disorder. Future research must address weaknesses in existing studies, including small samples sizes, restricted statistical power, and confounding factors such as comorbid illnesses, clinical heterogeneity with variable symptom severity, and unclear phenotypic boundaries.

Tourette syndrome (TS) is a complex neurobehavioral disorder principally characterized by motor and vocal tics. However, features of obsessive-compulsive and attention-deficit/hyperactivity disorders are often present. The basal ganglia and associated brain structures have been implicated in the pathophysiology of TS, as well as in these related conditions. Specifically, it is believed that the neuroanatomically and functionally defined basal ganglia thalamocortical loops are involved in TS. These loops are composed of a sequence of connections originating in the cortex and passing in series through the striatum (caudate and putamen), globus pallidus, and thalamus before returning to the cortical areas of origin. This review concentrates on the neuroimaging findings in Ts, particularly as they relate to alterations in components of the basal ganglia thalamocortical circuits. These neuroimaging data suggest that the major abnormalities in TS involve striatal or cortical dysfunction, as well as dysfunction of dopaminergic systems that regulate basas ganglia neurotransmission.

Alcoholism can result in a number of severe consequences to the central nervous system, including Korsakoff's psychosis, delusions, delirium, Wernicke's encephalopathy, and cerebellar degeneration. Many of these disorders have a substantially higher prevalence than had been previously believed. Neuropathologic and neuroimaging studies have been instrumental in identifying the changes undergone by the alcoholic brain and the factors that may contribute to alcohol-induced brain damage. Biologic differences appear to make women especially susceptible to central nervous system insult from alcohol abuse. The damage caused by alcohol may be associated, in part, with thiamine deficiency, neuronal excitotoxicity, and magnesium wasting.

Many endocrine disorders present with symptoms of depression, thus differentiating primary depressive disorders from such endocrine conditions can be challenging. Awareness of the typical clinical picture of endocrine disorders is of primary importance. This article discusses a variety of common and uncommon endocrine disorders and the symptomatology that might suggest a depressive illness, and reviews literature on how endocrinopathies can mimic depression. Emphasis is also placed on the role that stress can play in the pathogenesis of endocrine disorders. Psychiatrists should be familiar with the range of presenting symptoms for endocrine disorders, and they should not rely on the presence or absence of stressors to guide their differential diagnosis between depression and endocrine disorder.

Systematic studies on the genetics of panic disorder as a distinct nosologic entity separate from anxiety disorders date back to the 1980s. It is, therefore, a relatively new topic for psychiatric genetic investigation. For this reason, available data are not numerous, but findings ensuing from “classical” methods, such as family and twin studies, suggest the involvement of genetic mechanisms to a broad extent, confirmed by the most recent studies. The approaches of molecular genetics, particularly linkage analyses and association studies exploring candidate genes, have led to inconclusive results but have also provided interesting findings that need to be tested in future research.

Emphasizing the importance of an interdisciplinary approach in the treatment and management of patients with chronic pain syndromes (CPS), this article reviews, first, non-pharmacologic approaches and modalities for CPS patients, and next, pharmacologic approaches for CPS patients. Flexibility and the use of multiple modalities are emphasized. The article concludes with the controversial subject of the use of long-term analgesic opioid pharmacotherapy in patients with chronic benign pain syndromes.

Social phobia is a common psychiatric disorder that is often associated with significant psychiatric comorbidity and disability. In the past, clinicians have underutilized pharmacotherapy as a treatment option for this disorder. This article provides a review of current pharmacotherapeutic options for social phobia, including a review of the results to date of numerous controlled trials, a description of the recent results of open trials of new and promising agents, and a summary of the information available on the use of pharmacotherapy in the treatment of children and adolescents.

In this article we discuss the procedures that should be followed in order to develop diagnostic tests based on electro-physiologic parameters that would be useful to practicing psychiatrists in their efforts to diagnose mental disorders. To do this, we start by giving an overview of receiver operating characteristic (ROC) analysis, with which a candidate diagnostic test can be characterized mathematically. This methodology allows for an estimate of the overall discriminating power of the diagnostic test and thus can be used to compare the performance of one diagnostic test with that of another. However, ROC analysis cannot be used for optimizing a given diagnostic test (ie, determining the “best” cut-off) and, because it does not incorporate Bayes' theorem, it cannot be used to compare the performances of diagnostic tests when it is given to different risk groups for the target disorder. Both of these problems can be solved by using the concept of information theory. The equation for information gain automatically takes Bayes' theorem into consideration and also provides an intrinsic criterion for finding the cutoff that best discriminates between individuals who do and those who do not have the target disorder. Neither ROC analysis nor information theory are model dependent; however, if the equation for the frequency distribution of the electrophysiologic variable is known for the disease-positive and disease-negative populations, the calculations are greatly simplified. Therefore, the assumption is often made that both of these distributions (or transformations of the distributions) are Gaussian. However, studies have shown that the results of ROC analysis are quite robust to deviations from normality of the underlying distributions.

Savant syndrome, characterized by remarkable islands of mental ability in otherwise mentally handicapped persons, may occur in autistic as well as nonautislic individuals. Overall, approximately 10% of autistic persons exhibit savant abilities; roughly 50% of those with savant syndrome have autism, and the remaining 50% have other forms of developmental disability. Most commonly, savant syndrome takes the form of extraordinary musical abilities, but may also include calendar-calculation, artistic, mathematical, spatial, mechanical, and memory skills. While savant syndrome was first described more than a century ago, only recently have researchers begun to employ a more uniform nomenclature and more standardized testing in an effort to compare the abilities of savants with those of normal persons. Males show signs of savant syndrome approximately four times more often than females. Along with imaging study findings, this fact suggests the presence of a developmental disorder involving left-brain damage with right-brain compensation.

All the research to date implicates serotonin as the major neurotransmitter involved in obsessive-compulsive disorder (OCD). Much of the evidence has come from clinical treatment studies, which have shown the specific antiobsessional effect of drugs that are potent inhibitors of serotonin reuptake. Only the selective serotonin reuptake inhibitors (SSRIs) and the potent inhibitors of serotonin reuptake have been shown to be effective in treating patients with OCD. Serotonin receptor inhibitors and SSRIs have been thoroughly investigated in short- and long-term placebo-controlled studies and all have been found to be effective in OCD.

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.