Epilepsy is a medical disorder that presents with single or clustered seizures. There are several new drugs that effectively treat epilepsy with few side effects, and treatments of children, women, and the elderly are discussed. In the special population of children, there is a strong emphasis on the cognitive and behavioral benefits of specific therapies.

In the population of epileptic women, seizures most often occur at the start of puberty and menarche, and worsen periodically with each menstrual cycle. Relief of symptoms often occurs at menopause, but a possibility of exacerbation also exists. Women with epilepsy often battle a fear of becoming pregnant. This is a fallacy which must be widely dispelled, as the risk is less than supposed.

Among the elderly, epilepsy often presents after trauma, particularly stroke, and the incidence is three times greater for those over 60 years of age than the general population. Due to various conditions specific to the elderly, misdiagnosis is common. The greatest challenge in treating the elderly is adverse side effects.

Acute agitation is a nonspecific term applied to an array of syndromes and behaviors. It is frequently defined as an increase in psychomotor activity, aggression, disinhibition/impulsivity, and irritable or labile mood. Etiologies of acute agitation include medical disorders, delirium, substance intoxication or withdrawal, psychiatric disorders, and medication side effects. Treatment of acute agitation requires both environmental and pharmacologic intervention. Patients should be calmed with sedating agents early in the course of treatment, allowing for diagnostic tests to take place. Failure to correctly diagnose causes of agitation may lead to delayed treatment for serious conditions, and can even exacerbate agitation.The most common cause of agitation in patients with schizophrenia is psychotic relapse due to medication nonadherence. Pharmacologic treatment options for these patients include lorazepam and antipsychotic agents. Lorazepam causes nonspecific sedation and treats some substance withdrawal, but has little effect on psychosis. First-generation antipsychotics treat psychosis and, at high enough doses, cause sedation, but may induce extrapyramidal side effects (EPS). Some second-generation antipsychoticshave been approved for the treatment of agitation in schizophrenia. These agents treat psychosis with a favorable EPS profile, but are comparatively expensive and cause risks such as hypotension. However, avoiding EPS may reduce patients' resistance to antipsychotic treatment.

In this expert roundtable supplement, Joseph Battaglia, MD, provides an overview of the definition of acute agitation. Next, Delbert, G. Robinson, MD, outlines evaluation methods for actue agitation. Finally, Leslie Citrome, MD, MPH, reviews interventions for acute and ongoing management of agitation.

The World Health Organization estimates that depression is the fourth leading cause of disability worldwide with a lifetime prevalence of ∼15% to 20%. While the antidepressants currently on the market will be effective in most patients, a significant number of patients will experience residual symptoms, treatment-resistance, and relapse. The recent Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study has shed some light on the reality of antidepressant treatment. At first, only one-third of patients on citalopram monotherapy remitted. The other two-thirds who failed to remit saw their likelihood of remission decrease with each successive trial of another antidepressant monotherapy. Thus, after four successive monotherapies were tried over the course of one year, (ie, after four treatments each lasting 12 weeks), only two-thirds of patients achieved remission (Figure 1). Besides this poor prognosis, the patients who required more treatment cycles to get better also had a higher likelihood of relapsing. Once patients reach that point, they are considered treatment-resistant.

In awareness of recent developments and upcoming future changes in the conceptualization of obsessive-compulsive disorders (OCDs), a group of 14 experts with specific experience in this area decided that a consensus statement on the present and future of OCD is timely. The group, with their long-term interest and productivity in the area of OCD, met with the specific aim of providing a global perspective. Ten countries from four continents were represented in this 2-day consensus meeting.

The meeting took place in Cape Town on February 27–28, 2006. The participants were asked to prepare and submit a relevant presentation before the meeting in order to enrich the discussion. Six presentations reviewed the following aspects of OCD: diagnosis, epidemiology, neurobiology, treatment, special populations, and pediatric OCD. A draft consensus was prepared, based on the presentations, recent consensus statements, evidence-based guidelines, and the ensuing discussions.

Epidemiological trends in global suicides have been of serious concern in the last decade. The burden of higher expectations in the assessment of suicidal behaviors on mental health professionals is mounting. However, the suicidal risk assessment has many evolving and moving parts, and is one of the most heavily researched fields in psychiatry. Although it is clear from current empirical research that suicide cannot accurately be predicted, the standard of care from regulatory bodies and professional organizations dictates the use of established measures and following consensus guidelines. However, the legal system has different parameters to assess for the deviation from these standards and views it from a different vantage point. Therefore, it is imperative to know these critical multifaceted panoramas of suicide assessment. Considering the gaps within suicide risk assessment tools, we propose that appropriate documentation and thorough treatment planning are key to navigating the complex medicolegal risks. These approaches are useful for risk management and improve clinical outcomes, quality of care, and overall patient safety.

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.

Historically, drugs that increase central cholinergic transmission have primarily been investigated for relieving cognitive symptoms in mild-to-moderate Alzheimer's disease. These efforts have led to the somewhat unexpected findings that cholinergic therapy has a beneficial effect on selected neuropsychiatric symptoms in AD across disease stages. In Parkinson's disease with dementia and dementia with Lewy bodies, cholinergic deficits are more severe than in AD, and there is emerging evidence that cholinesterase inhibitors are efficacious in treating core symptoms of attentional disturbance and psychosis. Recent data also suggest a rational basis for cholinergic therapy in vascular dementia. The cognitive and neuropsychiatric effects of cholinergic therapy observed in AD and other dementias form the crux of an integrative model of cholinergic therapeutic efficacy that encompasses the diverse central nervous system actions of acetylcholine and its complementary interactions with central monoamine transmitters. This heuristic framework highlights the broader therapeutic potential of cholinergic therapy for symptom-based indications in other neuropsychiatric disorders.

Pharmacological challenge tests provide a method of assessing the functional responsiveness of serotonin (5-HT) receptor subtypes in the human brain. A number of selective agonist ligands for the 5-HT1B/1D receptor are available for human use; however, these compounds do not distinguish between 5-HT1B and 5-HT1D receptors, which is somewhat of a disadvantage. Acute administration of sumatriptan, rizatriptan, and zolmitriptan all increase plasma growth hormone in healthy subjects, possibly via activation of postsynaptic 5-HT1D receptors. This response is blunted in major depression. Sumatriptan lowers plasma prolactin, perhaps via activation of presynaptic 5-HT1B receptors. This response is not altered during repeated treatment with selective serotonin reuptake inhibitors (SSRIs), suggesting that 5-HT1B receptors retain the ability to restrain 5-HT outflow during short-term SSRI treatment.

Systematic investigations indicate that some of the recognized psychiatric disorders can be identified among those with mental retardation due to chromosomal abnormalities. We report a psychotic patient with mild mental retardation (intelligence quotient: 68) and minor anomalies that had a chromosomal aberration not previously described in a psychotic patient. Our patient highlights the importance of the cytogenetic study in psychiatric patients with comorbid mental retardation or minor anomalies. In addition, her psychosis symptoms may be helpful to propose a new candidate gene for psychosis.

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.

We appear to be on the brink of a new epoch of treatment for Alzheimer's disease. Compelling evidence suggests that Aβ42 secretion is the triggering event in the pathogenesis of Alzheimer's disease, and that tau aggregation may be an important secondary event linked to neurodegeneration. Prophylactic administration of anti-amyloid agents designed to prevent Aβ accumulation in persons with subclinical disease is likely to be more effective than therapeutic interventions in established Alzheimer's disease. Drug development programs in Alzheimer's disease focus primarily on agents with anti-amyloid disease-modifying properties, and many different pharmacologic approaches to reducing amyloid pathology and tauopathy are being studied. Classes of therapeutic modalities currently in advanced-stage clinical trial testing include forms of immunotherapy (activeβ-amyloid immunoconjugate and human intravenous immunoglobulin), a γ-secretase inhibitor, the selective Aβ42-lowering agent R-flurbiprofen, and the anti-aggregation agent tramiprosate. Non-traditional dementia therapies such as the HMG-CoA reductase inhibitors (statins), valproate, and lithium are now being assessed for clinical benefit as anti-amyloid disease-modifying treatments. Positive findings of efficacy and safety from clinical studies are necessary but not sufficient to demonstrate that a drug has disease-modifying properties. Definitive proof of disease-modification requires evidence from validated animal models of Alzheimer's disease; rigorously controlled clinical trials showing a significantly improved, stabilized, or slowed rate of decline in cognitive and global function compared to placebo; and prospectively obtained evidence from surrogate biomarkers that the treatment resulted in measurable biological changes associated with the underlying disease process.