Pathological gambling is an understudied disorder that causes significant distress to sufferers, their families, and society. Despite its prevalence among the general population, the impact of pathological gambling remains largely unrecognized by many health care providers. Although a discrete entity, pathological gambling shares salient characteristics with addiction and obsessive-compulsive disoders, and is comorbid with these and other conditions such as attention-deficit hyperactivity disorder in a large number of cases. Recognizing these similarities has significant implications for treatment, as pharmacologic therapies used for these disorders, including serotonergic and mood-stabilizing agents, have shown some degree of efficacy in pathological gambling.

Trichotillomania (TTM, repetitive hair pulling) is a complex underdiagnosed syndrome that often causes considerable psychological distress and physical disfigurement. Although many aspects of hair pulling bear similarity to compulsions of obsessive-compulsive disorder (OCD), TTM lacks obsessions associated with OCD. The phenomenology of TTM also is similar to tics in Tourette Syndrome (TS) and overlaps with TS in both limited structural neuroimaging data and in terms of treatment response to pharmacotherapy with dopamine antagonists.

In order to study potential comorbid relationships between TTM, TS, and OCD, a total of 61 patients with either TS, OCD, or OCD comorbid with TS were assessed using structured interviews as part of a phenomenological study of these groups. Post hoc analyses indicated significantly higher proportions of hair pulling in those subjects with OCD comorbid with TS compared to subjects with either OCD or TS alone.

These data, in conjunction with clinical phenomenology, neuroimaging results, and response to pharmacotherapy suggest the possibility that some forms of TTM may be more closely related to tic disorders than OCD. Futher research is needed to clarify and confirm these observations of putative relationships between TTM and TS and potential treatment implications.

Twin, family, and adoption studies indicate that genetic factors play a major role in predisposition to schizophrenia. To date, molecular genetic studies have implicated many different chromosomal locations for the disorder. However, no one site replicates across the majority of investigations. This creates an impasse in the study of schizophrenia genetics, because of the large number of chromosomal sites that require further detailed research. It is difficult to plan to move ahead with expensive and labor-intensive research in an attempt to determine the etiologie genetic factor, when any given site proves to be only weakly positive. Therefore, the use of a hypothesis-driven approach may be cost effective, and may ultimately have more power to detect etiologie genes. Several lines of evidence suggest that a neurodevelopmental defect may play an important role in the etiology of this disorder. Neurodevelopment is a complex process in which genetic and nongenetic factors may interact to create the mature differentiated neuron, with its particular network of synaptic connections. A reasonable chance exists that polymorphisms of the genes that control normal development of the central nervous system (CNS) may produce a slightly altered trajectory of brain development, predisposing individuals to schizophrenia. This assumption has led geneticists to begin to study neurodevelopmental genes in schizophrenia subjects. This article reviews and discusses genetic studies of some developmental genes in schizophrenia. Genetic association and linkage studies of neurotrophic factors (brain-derived neurotrophic factor, or BDNF, and neurotrophin-3, or NT-3), neuronal cell adhesion molecule (NCAM), synapsin, and synaptosome-associated protein with a mass of 25 kd (SNAP-25) have proven to be of most interest.

Nonepileptic seizures (NES) are clinical events that can resemble almost any seizure phenotype, but are behavioral and emotional manifestations of psychological distress, conflict, or trauma. Intractable NES is a disabling disorder that drastically affects patients' emotional well-being. Differential diagnosis, assessment, and treatment of NES is complex, with differentials scattered across an array of neurological and psychiatric disorders. This paper provides an overview of issues related to the diagnosis and treatment of NES. It highlights characteristics and risk factors of the disorder, issues in differential diagnosis, and treatment considerations.

Bullying is an omnipresent problem with high prevalence in children and adolescents. There are many antibullying state laws and practices in place however its real level impact is ambiguous at best. We studied the prevalence of bullying in the United States, examine the practices, laws, and interventions in place to prevent bullying and its real-life impact. Various studies have reported that the ground-level change brought about by these policies and programs varies and is not quite significant. The effectiveness of existing policies and legislations remains unclear and measurable objective change or impact is not yet observed. Therefore, a rethink of the strategies is needed. The focus must be on community-level programs and interventions with inclusive approaches involving all the stakeholders are critical for addressing this menace.

Tardive dyskinesia (TD) is a heterogeneous, hyperkinetic movement disorder induced by dopamine-receptor blocking agents that presents a unique challenge in the treatment of psychosis. Although acceptance of TD as a serious consequence of antipsychotic treatment was resisted initially, subsequent research by many investigators in psychopharmacology contributed to a rich store of knowledge on many aspects of the disorder. While basic neuroscience investigations continue to deepen our understanding of underlying motor circuitry, past trials of potential treatments of TD focusing on a range of theoretical targets were often inconclusive. Development of newer antipsychotics promised to reduce the risk of TD compared to older drugs, but their improved tolerability unexpectedly enabled an expanding market that paradoxically both increased the absolute number of patients at risk and diminished attention to TD which was relegated to legacy status. Fortunately, development and approval of novel vesicular monoamine transporter inhibitors offered evidence-based symptomatic treatment of TD for the first time and rekindled interest in the disorder. Despite recent progress, many questions remain for future research including the mechanisms underlying TD, genetic predisposition, phenomenological diversity, whether new cases are reversible, how to implement best practices to prevent and treat TD, and whether the development of novel antipsychotics free of the risk of TD is attainable. We owe our patients the aspirational goal of striving for zero prevalence of persistent symptoms of TD in anyone treated for psychosis.

Impulsive violence may be the behavioral consequence of inefficient information processing within specific neuronal networks. Analogous to the hypothetical pathophysiology of addiction, maladaptations within reward pathways may shift goal-directed behaviors to impulsive reactions and then to compulsive habits, in order to create impulsive violence.

Marshall is a 6-year-old child who displayed significant symptoms of hyperactivity, impulsivity, defiance, and temper tantrums since 2 years of age. Marshall lives with his mother, a single parent, and two siblings, ages 4 and 1. His problematic behavior, defiance, and argumentativeness were significant problems at home for his mother, which often made her late to work in the morning. These behaviors were also problematic in the evenings at dinnertime and at bedtime not only for his mother but also for the whole family. Marshall was also having social problems at school including being increasingly shunned by other children because of his aggressiveness and impulsivity as well as being defiant and argumentative with his teachers.

His mother initially sought out her pediatrician, who indicated that Marshall was too young for medication and that better discipline techniques were necessary. Medical workup at that point was unrevealing of any significant condition responsible for Marshall's behavior. Marshall's mother continued to pursue a psychiatric evaluation for Marshall, and a formal psychiatric evaluation revealed diagnoses of attention-deficit/hyperactivity disorder (ADHD), combined type, and oppositional defiant disorder (ODD). Paper and pencil instruments were used including the Swanson, Nolan, and Pelham (SNAP) form for assessing ADHD and ODD symptoms. On the form, both Marshall's mother and teacher indicated that he was significantly elevated in both ADHD and ODD symptom domains, and target symptoms were identified: hyperactivity, impulsivity, short attention span, difficulty with follow through, defiance, argumentativeness, tantrums, and the beginnings of aggressiveness.

Attention-deficit/hyperactivity disorder (ADHD) is a genetic disorder that affects both children and adults. Genetic studies have shown the heritability of ADHD to be higher than other psychiatric disorders. In addition, imaging studies have revealed various structural anomalies in the brain.

Often ADHD persists into adulthood. The presentation of ADHD into adulthood most often results from childhood onset of ADHD. Symptoms of inattention and functional behavior tend to persist. These symptoms may often be less obvious, with less overt hyperactivity and impulsiveness.

Stimulant medications remain the predominant choice for the treatment of ADHD. They are safe and offer good response. Common adverse reactions can usually be removed by changing the dose and the timing of medication administration. Of the second-line agents for treating ADHD, the tricyclic antidepressants have generated the most studies and have proved fairly efficacious.