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.

Cervical dystonia (CD), also known as spasmodic torticollis, is the most common of the focal dystonias. Muscle hypertrophy is present in nearly all patients, and neck pain is associated with CD in about 80% of patients. Remissions can occur in about 20% of patients, though most last under a year.

Medical therapies have not generally worked well for patients with CD, and are typically associated with many side effects. Botulinum toxin (BT), which causes fewer side effects, has been considered the treatment of choice. Beyond medical therapy, various surgeries for CD have been performed for many decades. Of surgical treatments now in use, selective peripheral denervation is the most common.

In CD, botulinum toxin type A (BT-A) targets pain, dystonic posturing, limited range of motion, and tremor. BT type B (BT-B) is a serotype of BT that is ontogenetically distinct from the type A toxin. There have been three randomized, multicenter, double-blind, placebo-controlled trials of BT-B. It appears that BT-B is a safe and effective treatment for patients with CD who are responsive or resistant to BT-A.

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.

Major depressive disorder (MDD) is a highly prevalent, debilitating disorder that is often chronic, recurrent, and costly, with the economic burden in the United States for the year 2000 exceeding $83 billion. Recent data from the National Comorbidity Survey Replication (NCS-R) indicate that MDD has a lifetime prevalence of 16.2% and a 12-month prevalence of 6.6% in the US. Among those reporting at least one episode of MDD in the previous 12 months, mean episode duration was 16 weeks. Roughly 60% of patients experienced role impairment that was “severe” or “very severe,” and nearly 80% reported comorbid disorders as defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, with MDD only rarely being primary. Although 51.6% of patients with MDD received health care treatment for the illness, treatment was “adequate,” as defined by the Agency for Health Care Policy and Research and the American Psychiatric Association guidelines (ie, ≥4 outpatient visits with any type of physician for pharmacotherapy that included use of either an antidepressant or a mood stabilizer for ≥30 days or ≥8 outpatient visits with any professional in the specialty mental health sector for psychotherapy lasting a mean of ≥30 visits) in 41.9% of treated cases. Only 21.6% of all MDD patients in the NCS-R, therefore, received minimal guideline-level treatment.

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.

In discussion of the best practices for patients with fibromyalgia (FM), it is key to Introduce commentary about what FM is as a clinical condition, how clinicians should assess for FM, and the pharmacologic approaches to management.

The first widely accepted criteria for the classification for FM were published in 1990 as the American College of Rheumatology criteria for FM. However, the condition has long been described in medical history. In the 1800s, a condition similar to FM was labeled “neurasthenia” and was further defined by researchers in the medical literature. During the early 1900s, symptoms associated with FM were labeled “fibrositis,” which was based on the mistaken idea that there were inflammatory changes in peripheral connective tissue. It was not until the mid-1970s when pioneering work by Smythe and Moldofsky defined central nervous system abnormalities, including significant sleep pathology, in patients with this condition that led to the increased recognition by researchers and clinicians that FM was a central pain phenomenon.

Following this critical development, use of the term “fibromyalgia” began and was codified in the 1990 criteria, intended for use in research settings to standardize classification of FM. The 1990 criteria classify the condition as involving chronic widespread pain for at least 3 months. Patients must also exhibit tenderness of at least 11 of 18 tender points.

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.

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.

Fever (pyretotherapy) was used for psychosis during the turn of the 19th century, but pyretotherapy (ie, the treatment of a disorder by inducing fever) fell out of use after the introduction of convulsive methods. Here, we report on a case of schizoaffective disorder and review classical and recent literature on fever and psychosis. The patient developed auditory hallucinations, persecutory delusional ideas, and was terrified soon upon his arrival in a foreign country. After being treated for 12 days with olanzapine and haloperidol, he developed a fever due to urinary infection; his creatine phosphokinase levels were high, prompting the suspension of antipsychotics. Psychotic symptom resolution followed immediately fever abatement. Antipsychotics were reintroduced at lower dosages. He was discharged asymptomatic with a prescription of olanzapine 15 mg/day and haloperidol 3 mg/day. The time course of symptom resolution in this patient suggests that fever had a beneficial role in this case. The associations between body temperature changes and psychotic symptoms need to be further studied.

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.

This is the second published case report of Lleuprolide acetate for depot suspension (LD)-induced mania. Both reports detail a patient with a prior psychiatric history of both depressive and hypomanic episodes. While depression is a predictable and documented side effect of LD and menopause (especially in those with a previoushistory of symptoms), manic reactions are rare and unexplained. Possible causative mechanismsbehind the LD-induced manic episodes are discussed, and we suggest that patients with a single previous hypomanic episode are at risk for LD-induced mania.

Patients with cancer may report neuropsychiatric abnormalities including cognitive impairment, behavioral disturbances, and psychiatric disorders that potentially worsen their quality of life, reduce their treatment response, and aggravate their overall prognosis. Neuropsychiatric disturbances have a different pathophysiology, including immuno-inflammatory and neuroendocrine mechanisms, as a consequence of oncologic treatments (chemo- and radio-therapy). Among clinicians involved in the management of such patients, psychiatrists need to pay particular attention in recognizing behavioral disturbances that arise in oncologic patients, and determining those that may be effectively treated with psychotropic medications, psychotherapeutic interventions, and an integration of them. Through the contribution of different clinicians actively involved in the management of oncological patients, the present review is ultimately aimed at updating psychiatrists in relation to the pathophysiological mechanisms responsible for the onset of cognitive, affective, and behavioral syndromes in these patients, along with epidemiologic and clinical considerations and therapeutic perspectives.