Panic disorder (PD) is typically a distressing, chronic, and recurrent mental disorder associated with a high rate of comorbidity with other mood, anxiety, and substance abuse disorders, increased risk of medical morbidity and mortality, and marked impairment of functioning and reduced quality of life. Most patients with PD first seek treatment in emergency room or general practice settings. In the overwhelming majority of cases, PD patients present with primarily somatic symptoms, many of which are common to medical illnesses. It is, therefore, not surprising that PD is often misdiagnosed and that patients with this disorder often spend years seeking treatment and undergoing costly and unnecessary tests and medical consultations before receiving a correct diagnosis. Better diagnosis and treatment of PD to achieve remission and prevent relapse has the potential to reduce the burden of this illness to the individual and society.

Rasmussen's syndrome (chronic encephalitis with epilepsy) is a rare neurological disorder of unknown cause characterized by severe epilepsy, hemiplegia, dementia, and inflammation of the brain, and progressive functional and structural destruction of a single cerebral hemisphere. While one mechanism underlying the pathogenesis of Rasmussens encephalitis has been hypothesized to be mediated by production of excitotoxic GluR3 autoantibodies to the a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor, other neuropathological etiologies have also been indicated. Proposed therapies have included antiepileptics, steroids, antiviral agents, alpha-interferon, and immunoglobulin. The mainstay of therapy is surgical hemispherectomy. To date, no medical therapies have permanently halted neurologic deterioration.

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.

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.

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.

A growing number of anatomic and physiologic studies have shown that parallel sensory and motor information processing occurs in multiple cortical areas. These findings challenge the traditional model of brain processing, which states that the brain is a collection of physically discrete processing modules that pass information to each other by neuronal impulses in a stepwise manner. New concepts based on neural network models suggest that the brain is a dynamically shifting collection of interpenetrating, distributed, and transient neural networks. Neither of these models is necessarily mutually exclusive, but each gives different perspectives on the brain that might be complementary. Each model has its own research methodology, with functional magnetic resonance imaging supporting notions of modular processing, and electrophysiology (eg, electroencephalography) emphasizing the network model. These two technologies might be combined fruitfully in the near future to provide us with a better understanding of the brain. However, this common enterprise can succeed only when the inherent limitations and advantages of both models and technologies are known. After a general introduction about electrophysiology as a research tool and its relation to the network model, several practical examples are given on the generation of pathophysiologic models and disease classification, intermediate phenotyping for genetic investigations, and pharmacodynamic modeling. Finally, proposals are made about how to integrate electrophysiology and neuroimaging methods.

Integrins are transmembrane heterodimeric (αβ) receptors that transduce mechanical signals between the extracellular milieu and the cell in a bidirectional manner. Extensive research has shown that the integrin beta (β) family is widely expressed in the brain and that they control various aspects of brain development and function. Schizophrenia is a relatively common neurological disorder of unknown etiology and has been found to be closely related to neurodevelopment and neurochemicals in neuropathological studies of schizophrenia. Here, we review literature from recent years that shows that schizophrenia involves multiple signaling pathways related to neuronal migration, axon guidance, cell adhesion, and actin cytoskeleton dynamics, and that dysregulation of these processes affects the normal function of neurons and synapses. In fact, alterations in integrin β structure, expression and signaling for neural circuits, cortex, and synapses are likely to be associated with schizophrenia. We explored several aspects of the possible association between integrin β and schizophrenia in an attempt to demonstrate the role of integrin β in schizophrenia, which may help to provide new insights into the study of the pathogenesis and treatment of schizophrenia.

Converging evidence has suggested that treatment augmentation with a second-generation atypical antipsychotic (SGA) may improve treatment outcomes in major depressive disorder (MDD) patients after an incomplete response to a first-line antidepressant. Cariprazine is a recently approved SGA for MDD augmentation. Herein, we evaluate both continuous (ie, change in depressive symptom severity scores over time) and categorical (ie, remission and response rates) outcomes. Following a full-text review, four randomized controlled trials (RCTs) were included in our meta-analysis, while five studies were included for a qualitative review. Risk ratios (RRs) were calculated for all included randomized controlled studies to determine the relative response and remission rates of cariprazine compared to placebo augmentation. The RR for all-cause dropout was also determined as a proxy for overall acceptability. Two studies found a statistically significant treatment response using cariprazine augmentation. One study observed depressive symptom remission for cariprazine compared to placebo. Our random-effects model revealed moderate antidepressant effects of cariprazine, with a standardized mean difference (SMD) in Montgomery–Åsberg Depression Rating Scale (MADRS) scores of −1.79 (95% CI): −2.89, −0.69). Our pooled response RR and remission RR were calculated as 1.21 (95% CI: 1.05, 1.39, P=0.008) and 0.99 (95% CI: 0.84, 1.17, P=0.91), respectively. The RR for response was statistically significant (P<0.05). However, the RR for remission was not statistically significant. The findings from our meta-analysis include a variable magnitude of effects. Evidence suggests cariprazine may be an effective treatment for MDD; however, further results are needed to clarify this relation.

A medication's pharmacokinetic properties can be as important as its efficacy in determining how successful a treatment is. Formulation plays a critical role in absorption, distribution, and elimination of a drug, which in turn can influence the clinical profile of a medication, including onset and duration of action, consistency of plasma levels, ability to cross the blood-brain barrier, and other factors. Advances in drug delivery technology mean that formulation is now an integral component in the development of a drug. Likewise, formulation is one of the factors that may influence selection of a medication to suit the needs of a particular patient. This article briefly reviews the technologies commonly applied in the development of psychotropic medications, with emphasis on the various oral modified-release formulations, and discusses how formulation can be used to optimize the efficacy and tolerability of psychotropic drugs.

As a general principle, separate treatments are often needed for attention-deficit/hyperactivity disorder (ADHD) and comorbid psychiatric disorders. There are few treatments for mood disorders that also treat ADHD, and vice versa. This discussion will review the literature on agents that are effective for both disorders, or that may potentially be combined. Physicians must bear in mind that none of these agents is approved by the Food and Drug Administration for the treatment of comorbid ADHD and depression.

Patient enrollment in people of color among pivotal trials for multiple sclerosis (MS) and neuromyelitis spectrum disorder (NMOSD) continues to be dismal. It is disappointing that no clinical trial sponsored by a pharmaceutical industry or otherwise, investigating any of the disease-modifying drugs, has tackled this glaring inequity head on. The disease characteristics and phenotype of MS or NMOSD among Blacks and Hispanics are typically aggressive and for this reason alone, if not for any other metric, there needs to a radical shift in allotment of funds devoted to promoting drug research in minority populations.