The experiential core of the obsessive mind rests on subtle, primary mental phenomena (such as obsessions and so called “sensory phenomena”) which precede and trigger behavioral compulsions. Converging evidence supports a possible pathophysiological role for altered corollary discharge (phenotypically expressed in sensorimotor symptoms and contributing to a reduced Sense of Agency [SoA]), in the neurodevelopment of obsessions and “sensory phenomena.” In phenomenological terms, “sensory phenomena” may represent the subjective experiential resonance of an individual history of persistent inaccurate sensory predictions, whereas accompanying manifestations, such as the obsessive need for order and symmetry, may represent a compensatory attempt to mitigate “sensory phenomena” (eg, by increasing the sensory predictability of the surrounding world). Since disturbances of both SoA and Sense of Ownership have been thematized as potential pathogenetic factors in the neurodevelopment of the psychotic mind, a dimensional account of altered sensorimotor prediction may partly explain the affinities (and high comorbidity) between obsessive–compulsive disorder and schizophrenia spectrum disorders.

Genetic study holds potential for understanding the etiology of a number of serious psychiatric disorders. In the case of obsessive-compulsive disorder (OCD), many investigators agree that there is a strong genetic component to its development. In this article, we review the scientific evidence gleaned from different types of studies that has led to a better understanding of the nature of the inherited factors in OCD.

Anticonvulsants are being used clinically as monotherapy and adjuncts in mental illnesses other than affective disorders. This review focuses on the literature for anticonvulsants and lithium in substance use disorders, anxiety disorders, and schizophrenia. Given the abuse potential and other difficulties with prescribing benzodiazepines for alcohol and benzodiazepine withdrawal, anticonvulsants have been considered as an alternative. Promising therapeutic effects have been demonstrated in many of the anxiety disorders, with the greatest number of trials and positive results in posttraumatic stress disorder. Although anticonvulsant and lithium augmentation for schizophrenia is common in practice and has been studied in double-blind, randomized, controlled trials, the sum of the evidence has been inconclusive.

What is the current knowledge concerning the pharmacologic treatment of human sexual dysfunction? A number of interventions, including oral phophodiesterase inhibitors and intracorporeal agents with vasodilatory effects, are available to treat male erectile disorder. Serotonergic drugs have been shown to be effective in the treatment of rapid ejaculation. Various lines of research suggest that high dosages of androgenic agents may eventually have a role in the treatment of decreased libido in females. There may be a role for phophodiesterase inhibitors in the treatment of a subgroup of women with arousal disorders. Normal sexual function involves successful integration of biological, psychological, and interpersonal influences. Clinical psychiatry with its biopsychosocial model should incorporate the treatment of human sexual dysfunction within its purview.

Various terms have been used to describe mania when it is accompanied by depressive symptoms. In this article, we attempt to define and discuss 3 of these terms: dysphoric mania, mixed state, and mania with mixed features specifier. We conclude that whatever term is used, it is important to be aware that mania is more often unpleasant than pleasant, and that the unpleasantness is not limited to depression.

Pharmacogenetics brought the promise of matching individuals with treatments that would be efficacious while minimizing adverse events. This has been long needed in psychiatry, where treatment options have been empirical and treatment choices have been made largely based on clinical judgment. The efficacy and tolerability of antidepressants, the most common drugs used in mood disorders, have been widely studied in pharmacogenetics. Genetic association studies have been reported for pharmacokinetic genes such as the CYP450 isoenzymes or MDR1, and pharmacodynamic genes such as the serotonin transporter (SLC6A4) or the serotonin 2A receptor (HTR2A). However, despite the large number of reports, clinically useful predictors are still scarce for antidepressant monotherapy. Pharmacogenetic predictors of efficacy for mood stabilizers such as lithium and anticonvulsants have not had a dissimilar fate, and clinically meaningful markers are yet to emerge. The lack of consistent results may be in part due to small samples of heterogeneous populations and lack of consensus on phenotype definitions. Current pharmacogenetic recommendations include testing for HLA-B*1502 when using carbamazepine in Asian ancestry populations to prevent Stevens–Johnson syndrome, CYP2D6 genotypes when using pimozide, and CYP2D6 in polypharmacy to minimize drug interactions. This review, which is aimed at clinicians, lays the basis for understanding strengths and weaknesses of pharmacogenetic studies and outlines current clinical uses of these biomarkers.

Antidepressants have been available since the 1950s, when the monoamine oxidase inhibitors were first discovered. Since then, our armamentarium of antidepressants has progressively expanded with the discovery of the tricyclic antidepressants (TCAs) in the 1960s, the selective serotonin reuptake inhibitors (SSRIs) in the 1980s, and, subsequently, the serotonin norepinephrine reuptake inhibitors (SNRIs), and other agents possessing a diverse mechanism of action including buproprion, and mirtazapine.

Panic disorder seems to be mediated by the neuronal circuitry and neurochemical systems that have evolved to respond to external threatening stimuli. Distant threats activate prefrontal cortex (involved in complex planning of avoidance strategies), while immediate threats activate midbrain structures (involved in fast reflexive behaviors). Panic disorder may, however, also involve more specific interoceptive mechanisms. For example, the association between respiratory dysfunction and panic disorder has bolstered a false suffocation alarm hypothesis. Genetic and environmental contributors to panic disorder are beginning to be delineated. Effective pharmacotherapy and psychotherapy are able to normalize the relevant psychobiology.

Although many investigations into the onset of obsessive-compulsive disorder (OCD) suggest the occurrence of potential life events as triggering factors, such an association has not been well studied to date. The purpose of the present paper is to review the literature on OCD onset in order to determine whether OCD is triggered by recent life events, what specific events may serve as triggers, and the clinical and research implications of these factors. Overall, the available studies do not consistently support the theory that OCD is triggered by specific antecedent life events. However, there is a body of evidence to support the theory that the specific life events of pregnancy and birth of a child can trigger OCD. This apparent association has led to the investigation of certain neurohormonal factors, including changes in estrogen or oxytocin levels, that may be of etiopathogenetic significance in OCD. Confirming such associations may allow clinicians to provide more targeted preventive and therapeutic interventions.

What exactly is known today about the impact of the adult form of attention-deficit/hyperactivity disorder (ADHD) in society?:

In a recent study to examine the societal impact of attention-deficit/hyperactivity disorder (ADHD), 500 patients diagnosed with ADHD and 501 participants with no substantial signs or symptoms of ADHD were studied. Subjects were asked several questions about their quality of life, employment, job satisfaction, and other aspects of their well-being and functionality. Income, which is an important marker for the degree of productivity for an individual in society, was also assessed. ADHD can profoundly affect the performance of individuals in the workplace (Slide 1), and this study found that having ADHD reduced an individual's income by an average of ∼$10,000 per year. If that loss of income is extrapolated to all adults in the United States who have ADHD, it suggests that the economy is losing around $70 billion a year to $115 billion a year in productivity, as measured by loss of income. The range was broad because different models with varying assumptions were applied to project income loss over time. Nevertheless, based on these numbers, it is reasonable to estimate that the population is losing ∼$100 billion annually in productivity due to ADHD.

Income loss was found at all levels of education, but it was greatest among patients who had advanced degrees of education; so it seems that the disease may have a more pronounced impact on income among those in the higher income brackets.

Atherosclerotic disease accounts for ~25% of ischemic strokes. Atherosclerotic stroke is caused mainly by embolic events from the carotid artery bifurcation or the aortic arch, although intracranial thrombosis can occur, more often in African Americans, Asians, and diabetes patients. Primary prevention of stroke is critical for patients with risk factors for atherosclerosis, including hypertension, diabetes, smoking and hypercholesterolemia. Stroke can be prevented in patients with established atherosclerotic disease by identification and management of patients with carotid artery stenosis by non-invasive testing. Particular attention must be paid to patients with transient symptoms of brain ischemia.

Emerging therapies for Alzheimer's disease offer hope to patients and their caregivers. Future treatments will probably include combination approaches with agents that modify amyloid processing, deposition, and clearance. One example, the AD vaccine, reduced amyloid burden and changed behavior in animal models of AD, but the human trial was halted when several subjects developed brain inflammation. Anti-inflammatory agents have epidemiologic support, but clinical trials have been disappointing, possibly related to inadequate study with anti-inflammatory agents that modify amyloid processing. Agents that target known cardiovascular risk factors, such as hypercholesterolemia, hypertension, and insulin resistance, have epidemiologic, preclinical, and clinical evidence to warrant further investigation. Heavymetal chelators, antioxidants, neurotrophic factors, glutaminergic modulators, and agents that modify hyper-phosphorylation of Tau are other approaches in research and development.

In the treatment of sexual addiction and compulsivity, the family unit is often neglected. Yet this disorder has a major impact not only on the identified patient, but also on the spouse or partner (the coaddict) and on the family as a whole. Moreover, the family unit is the context in which the sexual addict continues to live, and the mental health of the partner has a significant impact on the sexual addicts recovery. Increasing evidence points to a family history of addiction or dysfunction as a primary contributor to both sexual addiction and coaddiction in adulthood. When compulsive sexual behaviors are present within a family, treatment of both members of the couple improves the couple's relationship as well as the mental health of each partner. In addition, treatment of children in such a family can help break the cycle of sexual addiction and prevent its perpetuation into the next generation.

Attention-deficit/hyperactivity disorder (ADHD) is a lifelong condition that begins in childhood and continues with adult manifestations related to the core symptoms. Approximately 50% to 75% of children with ADHD continue to meet criteria for the disorder as adolescents and adults. Adults with the disorder increasingly present to primary care physicians, psychiatrists, and other practitioners for diagnosis and treatment. Understanding the diagnosis of ADHD in adults requires knowledge of age-dependent decline of symptoms over time. Retrospective recall of symptoms and impairment are valid methods of diagnosing the disorder. ADHD is also a brain disorder with a strong neurobiologic basis, complex etiology, and genetic component. Genetic and environmental vulnerabilities give rise to abnormalities in the brain and subsequent behavioral and cognitive deficits, which may produce the symptoms associated with ADHD. Magnetic resonance imaging studies of ADHD have provided evidence that abnormalities in the brain are caused by the disorder itself rather than treatment of the disorder. Psychiatric comorbidity is common among patients with ADHD and tends to complicate treatment. Acute and long-term use of long-acting stimulant formulations (methylphenidate and amphetamine compounds) have shown robust efficacy and tolerability consistent with the treatment response established in children with ADHD. Non-stimulant medications have demonstrated efficacy as well, and may be preferred in patients with tic and substance use disorders.