The proportion of pregnancies exposed to either second-generation antipsychotics (SGAs) or first-generation antipsychotics (FGAs) varies between 0.3%–2% of all pregnancies, but, until now, little is known about the potential neurobehavioral teratogenicity of antipsychotics. Assessing this safety facet is the aim of this article. PubMed, Scopus, and Google Scholar were searched for eligible articles. PubMed (1954 to May 2016) was searched using several medical subject headings, variously combined. PubMed search results were also limited using the search filter for human studies published in English. Scopus and Google Scholar searches were filtered for article title (antipsychotics/neuroleptics, pregnancy). After excluding duplicates, 9,250 articles were identified and 29 met the following inclusion criteria: only articles that provided original/primary data on neurodevelopmental outcome in human offspring older than 4 months of age, independently of the study design, were selected for review. Indeed, some relevant neurodevelopmental milestones are achieved at this time. Length of study and neurodevelopmental assessment methodology did not influence the study selection. Unfortunately, published data on neurodevelopmental teratogenicity of SGAs mainly derive from case reports and small case-series studies. Even findings emerging from case-control and prospective/retrospective studies are of limited clinical relevance because of their small sample sizes. Limited data are also available on FGAs. Hence, we have to conclude that the long-term neurodevelopmental outcomes for children exposed in utero remain unclear. Low to very low quality evidence of retrieved data makes impossible to confirm or exclude potential long-lasting untoward effects on infant neurocognitive development associate with antenatal exposure to either SGAs or FGAs.

It is becoming clear that post-traumatic stress disorder (PTSD) is not simply a psychiatric disorder, but one that involves pervasive physiological impairments as well. These physiological disturbances deserve attention in any attempt at integrative treatment of PTSD that requires a focus beyond the PTSD symptoms themselves. The physiological disturbances in PTSD range over many systems, but a common thread thought to underlie them is that the chronic effects of PTSD involve problems with allostatic control mechanisms that result in an excess in what has been termed “allostatic load” (AL). A pharmacological approach to reducing AL would be valuable, but, because of the large range of physiological issues involved – including metabolic, inflammatory, and cardiovascular systems – it is unclear whether there exists a simple comprehensive way to address the AL landscape. In this paper, we propose that the cannabinoid system may offer just such an approach, and we outline evidence for the potential utility of cannabinoids in reducing many of the chronic physiological abnormalities seen in PTSD which are thought to be related to excess AL.

Sexual health is important to overall health and quality of life. Sexual problems have been associated with relationship problems and may interfere with overall health and they may also be a marker for other undiagnosed comorbid medical conditions. In order for healthcare professionals to manage the sexual health concerns of their patients, it is important for them to understand what constitutes good sexual health. To that end, it is necessary to have a working knowledge of the evolving theoretical models offered to describe a healthy sexual response as well as an understanding of the neurobiology of sexual function. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Revised lists six primary female sexual disorders: hypoactive sexual desire disorder, sexual aversion disorder, female sexual arousal disorder, female orgasmic disorder,dyspareunia, and vaginismus. Despite a growing awareness of the high prevalence of sexual disorders they are not typically identified nor treated. There are a number of reasons why clinicians fail to identify and treat sexual problems including insufficient training in sexual medicine and communication skills, time-constraints, and embarrassment. Treatment for female sexual problems is usually individualized and may include a combination of office-based education and basic counseling, cognitive-behavioral psychotherapy, pharmacotherapy, and treatment of concomitant medical conditions.

Successful treatment of pediatric disorders has necessitated the development of alternative medication formulations, as children may prefer alternative dosage forms to tablets or capsules. This is especially true for attention-deficit/hyperactivity disorder (ADHD), which is one of the most common chronic pediatric conditions and often involves children with a variety of overlapping physical, psychological, or neurodevelopmental disorders. A special challenge for developing alternative dosage forms for ADHD treatment is the incorporation of a once-daily long-acting formulation. Traditional ADHD medication formulations have been limited, and issues surrounding prescribed dosing regimens—including poor medication adherence, difficulty swallowing, and the lack of dosing titration options—persist in ADHD treatment. In other disease areas, the development of alternative formulations has provided options for patients who have issues with consuming solid dosage forms, particularly children and individuals with developmental disorders. In the light of these new developments, several alternative formulations for ADHD medications are under development or have recently become available. This article reviews the various strategies for developing alternative dosage forms in other disease areas and discusses the application of these strategies in ADHD treatment. Alternative dosage forms may increase medication adherence, compliance, and patient preference and, therefore, improve the overall treatment for ADHD.

As with members of other cultural and religious groups, patients within the Orthodox Jewish community present with their own distinct clinical psychiatric issues related to their unique beliefs and practices. This article reviews the existing literature and anecdotal experience on the psychopharmacologic assessment and treatment of Orthodox Jewish patients. Specific aspects examined include this group's perceived intense stigma in receiving treatment, the priority this community places on cognitive functioning, and how the influence of Jewish laws on marriage and sexual practices impacts one's treatment decisions. The relevance of Jewish dietary laws, the Sabbath, and the community's interest in alternative treatments are also discussed. The limited ethno-psychopharmacology research related to Orthodox Jewish psychiatric patients is reviewed. We conclude that understanding issues such as these is critical if one is going to work within this cultural system in order to successfully address their mental health issues. However, the dearth of controlled research in this community needs to be addressed to provide more effective treatment.

The origins of the word “shame” recall the concept of the infraction of integrity both as scandal and as individualization. The human experience of shame stretches along a continuum from modesty to disabling interpersonal terror. Unlike other basic affects, its emergence is a fundamental moment in the process of self-awareness and self-object differentiation. Neglected by psychiatry because it was regarded as a moral concept, today it is possible to hypothesize that it has a biologic basis that one can attempt to describe in terms of corticothalamic pathways. In this respect, like other affects, it could be considered as a cognitive shortcut to activate specific and evolutionally useful behavioral patterns, such as concealment or a request for affiliation. It is fairly ubiquitous in psychopathology, but is clinically much more structured in its abnormal expressions in anxiety disorders, particularly social phobia, obsessive-compulsive disorder, eating disorders, body dysmorphic disorder, and even in bipolar mood disorder. In schizophrenia it has been described as being one stage in the construction of delusion. Its presence is connected to interpersonal relationship (altruism) though it seems absent in autism. The assessment of shame experiences in psychiatric patients could be useful for both pharmacological and psychotherapeutic strategies, and could provide a categorization of a new psychopathology based on abnormal affects.

The issues surrounding generic drug substitution in patients with epilepsy are complex.The substitution of one formulation of an antiepileptic drug (AED) for another is controversial. Well-reasoned and defensible cases can be made both for and against such substitution. Although regulatory agencies require that generic and proprietary drugs have similar pharmacokinetic bioequivalence data, their therapeutic efficacy may not necessarily be identical. The paroxysmal nature of epilepsy, the narrow therapeutic index of some AEDs, the need to. individualize therapy to achieve seizure control, and the negative consequences of uncontrolled epilepsy distinguishes epilepsy from other clinical conditions. Epilepsy management with AEDs requires careful dose titration and consistent drug exposure at the optimal level for each patient, which can be altered if a different formulation of the AED is substituted. Unexpected variability in plasma concentrations could occur when a patient who has been receiving one formulation of an AED (generic or brand) receives an alternate formulation.Thus, no substitutions should be made for people with epilepsy without the knowledge and approval of the prescribing physician. Patients should be consulted about the substitution, with all risks and benefits carefully explained.

Modern formulations of psychiatric disorders hypothesize that mother nature goes awry, causing both genetic and epigenetic disease actions. Genetic disease actions are the consequences of naturally inherited risk genes that have an altered sequence of DNA. This altered DNA sequence theoretically leads to the production of altered gene products in neurons, causing inefficient information processing in various brain circuits, and biasing those circuits towards developing symptoms of a mental illness. Epigenetic disease actions are theorized either to activate risk genes to make an altered gene product or to activate normal genes to make normal gene products but at the wrong time. Epigenetic disease mechanisms theoretically turn normal genes into risk genes by causing normal genes to be expressed in neurons when these genes should be silenced or by causing normal genes to be silenced when they should be expressed.

Obsessive-compulsive symptoms (OCS) are relatively common and clinically significant phenomena in schizophrenia patients, suggesting the existence of a separate schizo-obsessive subgroup of the disorder. Although a majority of schizo-obsessive patients have typical ego-dystonic OCS, a meaningful proportion exhibits diagnostically challenging psychopathological phenomena, psychotic in content and obsessive in form. We report the clinical and functional magnetic resonance imaging characteristics of a schizophrenia patient who developed auditory hallucinations with musical content and obsessive in form. We suggest that “obsessive musical hallucinations”, that integrate both psychotic and obsessive-compulsive disorder (OCD)-related features, may be mediated by the brain networks believed to be involved in OCD and in auditory musical hallucinations.

Platelet dysfunction and thrombocytopenia rarely occur during clozapine therapy, but constitute an important source of morbidity and mortality if they are not detected and therapy is discontinued. The manufacturer recommends discontinuing clozapine when the platelet count falls below 100,000/μL and resuming therapy when the count returns to within normal range (150,000–450,000/μL). If thrombocytopenia recurs, clozapine should be permanently discontinued.

The authors report a rare case of long-term thrombocy-topenia persisting 40 months postclozapine treatment. In addition, increased in vitro platelet [14C] serotonin release was observed in the presence of the drug, suggesting an immune-related cause for the thrombocytopenia.

G.W., a 43-year-old African-American man, had been treated in the South Carolina Department of Mental Health since 1974 with a diagnosis of schizophrenia of chronic undifferentiated type, along with severe paranoid, delusional, threatening, and assaulting behavior. There was no history of illicit drug use. He had received intramuscular fluphenazine deconoate and haloperidol, as well as other neuroleptics, with little benefit observed during his years of treatment.

Clozapine was initiated at 25 mg bid on July 2, 1993, and was gradually increased to 650 mg daily over the next 20 months. After 7 weeks on this dose, the patient's platelet count fell from 103,000/μL to 60,000/μL, and clozapine was discontinued. A week later, the count had improved to 109,000/μL; 3 weeks later, with the platelet count at 109,000/μL, clozapine was reintroduced and titration started. However, within 7 days, his platelet count fell to 70,000/μL and clozapine was permanently stopped.

Over the past century researchers have attributed the symptoms that today are labeled as Tourette syndrome to various etiologies. Although most investigators have accepted Gilles de la Tourette's initial description of a symptom complex of tics and involuntary vocalizations, most have rejected his claim that “tic disease” resulted from hereditary degeneration. Subsequent investigators have offered an array of contradictory etiological explanations including viewing these symptoms as a subset of choreas, a result of insufficient inhibition, a failure to control infantile habits, a sequel to encephalitis and other infections, or the result of unconscious psychosexual childhood conflict. With the advent of effective pharmacologic treatments in the 1960s, psychiatrists, often urged on by the parents of afflicted children, began to insist that the disorder resulted from organic factors, most likely connected to transmission of the neurotransmitter dopamine and signaling in the basal ganglia. Since the 1970s, research has focused on a variety of possible organic substrates, but disputes over which symptoms to include in the syndrome's phenotype continue to constrain efforts to locate its etiology.

Irreversible monoamine oxidase inhibitor (MAOI) antidepressants have significant efficacy in treatment-resistant unipolar depression, but in some instances patients may not achieve remission. Among the adjunctive and augmentation strategies, certain second-generation antipsychotics (SGAs) have approval for inadequate responders to antidepressant therapy, including aripiprazole, brexpiprazole, and quetiapine, with lurasidone and the olanzapine/fluoxetine combination indicated for bipolar depression. Clinicians may eschew SGA options in part due to the limited literature on SGA–MAOI combinations, with only one published case involving aripiprazole, and none for olanzapine, lurasidone, or brexpiprazole. In addition to the limited publication history on SGA–MAOI treatment, clinicians may also be deterred by uncertainty regarding SGA mechanisms and the risk of serotonin syndrome or other adverse outcomes. This paper describes the case of a 54-year-old male with a history of psychotic unipolar depression treated with a combination of phenelzine, aripiprazole, and quetiapine, and reviews the 12 published cases of SGA–MAOI combination therapy with a focus on the pharmacological basis for serotonin syndrome, and the SGA mechanisms that should not be associated with a risk for this syndrome.