In treating schizophrenia there has been a shift in focus, with more attention being paid to early intervention based on the notion that effective treatment at this point can improve outcome. Most of this work has centred on pharmacotherapeutic interventions during the first psychotic break. More recently, attention has turned to the potential value of intervening even earlier, that is during the so-called “prodrome” that has been identified as predating the first psychotic break by as much as 4–5 years. We now have a limited number of published reports addressing this topic and these are reviewed here.

It is just 3 or 4 weeks after my diagnosis of Tourette syndrome (TS). I have been slowly and conscientiously titrating upward the dose of medication prescribed by my neurologist, waiting skeptically, but not without hope, for some amelioration of my tics. A typical scientist/patient, I have downloaded all available information about this drug from the Internet and have been recalculating the increasing dose in mg/kg body weight every few days. Today I have ducked out of my lab and am doing a very hard training run along the Muddy River in Boston, gearing up for my 21st year of spring and summer races, when I am caught unprepared by a flash of insight. I am speeding along the path with a smoothness and crispness of rhythm that I have seldom felt—maybe just one of those rare great days?—when it occurs to me that I am taking a good deep breath every four strides, in-and-out without fail, every four strides. And only at that moment do I realize that I have always suffered from “skipping” breaths, even on the hardest runs, and have always taken it for granted. Indeed, I have always assumed that all other runners' breathing is as ragged as my own. But now—how remarkable!—I am not missing a single precious breath. This, I realize, is because my phonic tic is gone. So my teammates and competitors must have never missed those breaths, not a single one, because they don't have TS!

Many psychiatric disorders are influenced by genetic factors, but the genetic components of complex diseases may not follow clear inheritance patterns. Although the patients may share a common clinical phenotype, the cause of the syndrome may consist of a heterogeneous collection of both genetic and/or environmental components. One method to minimize genetic heterogeneity in studies of complex disorders is to select a very homogenous study population. The average number of families with the same last name, when corrected for population size, is an excellent marker for the degree of homogeneity. We used surname analysis to evaluate the homogeneity of the Portuguese population of Madeira, comparing it with previous data on the homogeneity of populations of mainland Portugal, the Azores, and both rural and urban US populations. The average number of families with the same last name corrected for population size was 33.84 in Madeira, 30.88 in the Azores, and 21.42 in Coimbra (mainland Portugal) compared with 1.13 in rural and 0.38 in urban United States. This surname analysis supports the premise that the Portuguese population is a highly homogenous population, with the highest homogeneity in Madeira and the Azores, making it a good study population for molecular genetic analyses.

Repetitive transcranial magnetic stimulation (rTMS) is a relatively new technique for activating the cerebral cortex through the scalp and skull. By inducing electrical currents in the brain, rTMS is able to produce a variety of effects, including muscle twitching, changes in motor performance, disruption of cognitive and perceptual processes, and changes in mood. Although the technique is noninvasive and easily tolerated by patients and normal subjects, rTMS can produce epileptic seizures and, potentially, other undesirable effects on brain function. Further studies will be required to fully define the safe ranges of the stimulation parameters.

A number of myths exist concerning the psychological impact of breast cancer. Primary among these is the belief that women with breast cancer have greater emotional disability than individuals with other diseases or the population at large. While research has shown that women cope remarkably well with a diagnosis of breast cancer, an understanding of the key periods of anxiety and primary stressors is crucial to the overall psychological and medical management plan. While psychopharmacologic therapy may be indicated for women with breast cancer, it is rarely sufficient and should be combined with effective psychosocial interventions such as group therapy.

Objective: To better understand the efficacy and tolerability of atypical antipsychotics among racial groups, we reviewed data from four short-term (4–6 weeks), fixed-dose, placebo-controlled trials of ziprasidone for black, white, and overall populations of patients with schizophrenia.

Methods: Efficacy of ziprasidone in the black, white, and overall schizophrenic populations was compared to placebo using standard efficacy measures (Positive and Negative Syndrome Scale [PANSS] total, PANSS negative, Brief Psychiatric Rating Scale [BPRS], Clinical Global Impression-Severity [CGI-S], CGI-Improvement [CGI-I]).

Results: Black patients receiving ziprasidone demonstrated statistically significant improvements from baseline in PANSS total, PANSS negative, and BPRS, and improvements in CGI-S and CGI-I (n=99–149) compared with placebo (n=41–66); improvements were comparable to those observed in the overall population (n=451–639) and the white population (n=310–430). Interaction effect (treatment by race) was not significant for any efficacy variables. Ziprasidone was well-tolerated among black patients (n=175). Adjusted mean (least squares mean) overall weight gain in black patients receiving ziprasidone (n=124) was 1.8 kg. There were no increases in total cholesterol, triglycerides, or random glucose in the black population.

Conclusion: Ziprasidone has similar efficacy and safety in black patients with schizophrenia compared with patients in the white and overall populations.

The clinical manifestation of epileptic seizures may vary widely from patient to patient, depending on the region of the brain involved. Over the centuries, many seizure classific systems have been used, and the current most widely used classification system is that of the International League Against Epilepsy (ILAE). The ILAE system divides seizures into those of partial onset and those of generalized onset, depending on whether the initial clinical manifestations indicate that one cortical region or both hemispheres are involved at the onset of the seizure. Partial seizures are then divided into simple partial seizures, in which a fully conscious state is retained, or complex partial seizures, in which consciousness is impaired. A more recent classification system based purely on symptom features and signs has been proposed, and this system may provide advantages for localization, and especially for surgical evaluation. Epilepsy is a condition characterized by recurrent unprovoked seizures. Epilepsy may be idiopathic, cryptogenic, or symptomatic. Idiopathic epilepsies are generally genetic, and while man such syndromes have been described, advances in molecular genetics will undoubtedly reveal many more syndromes in near future. Cryptogenic epilepsies are those in which an underlying cause is suspected, but the etiology remains undetected. Epilepsies for which there is an underlying structural cause or major metabolic derangement are considered symptomatic. Common causes and diagnostic evaluation are described in this article.

Stemming from the finding that nicotine potentiates haloperidol-induced catalepsy in rats, nicotine in the form of nicotine gum and as transdermal nicotine patch (TNP) has been used in open-label studies to obtund motor and vocal tics of children (age≥8 years, weighi≥25 kg), adolescents, and adults. Reduction of tics was seen during chewing of nicotine gum; the improvement lasted no longer than 1 hour after chewing. With a TNP in subjects who were not responding well to a variety of dopamine blockers, with some also receiving clonidine or a variety of selective serotonin reuptake inhibitors, motor and vocal tics were obtunded 45% over baseline in 85% of 35 subjects within 30 minutes to 3 hours after TNP application. Moreover, the relief of symptoms with a single 7-mg TNP, remaining on the skin for 24 hours, persisted for a variable period of time ranging from 1 to 120 days with an average of 10±2 days. Application of a second TNP for 24 hours when symptoms began to return resulted in a similar reduction in tic severity and frequency, which persisted an average of l3±3 days. Nicotine alone, without D2 blockers, was successful in reducing premonitory urges to tic. After follow-up of 3 to 5 years, 19 of 35 patients continued to use the TNP in gradually decreasing frequency and with gradual reduction in dose of D2 blockers. However, 16 patients (45%), as they grew into middle adolescence, discontinued use of the TNP, stating that they objected to the nausea induced by the patch. There was no evidence of habituation to nicotine. Side effects were not life threatenting; the most disturbing side effect was nausea, appearing 1 to 4 hours after the application of the patch and lasting 1 to 3 hours. There was no change in blood pressure; pulse rate increased from 5 to 10% within 3 hours but returned to baseline after 24 hours. Unsolved problems using TNP are mentioned and a putative mechanism for nicotine effectiveness in Tourette syndrome is briefly discussed.

Depression is one of the most prevalent disorders in the general population, causing personal and social disability and impairment. Major studies assessing the diagnosis and management of depression have shown that it is often underdiagnosed and undertreated. A pan-European study aimed at assessing the extent and consequences of depression in six different countries is reported in this article. Different types of depressive profiles are analyzed and their respective management has been compared. The importance of improving diagnosis and treatment of depression is underlined. Appropriate management of depression depends on the recognition of depressive symptoms by patients, their possibility of seeking care, and the ability of the primary care physician to recognize the disorder and prescribe the appropriate medicines. Improvement in all of these fields is necessary.

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.

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.

This short-term, open-label study investigates short- and long-term effects of the selective serotonin reuptake inhibitor (SSRI) fluvoxamine for the treatment of trichotillomania (TTM). Additionally, this study aimed to test the hypothesis that the presence of hair pulling compulsiveness is predictive of SSRI response. Nineteen subjects meeting the Diagnostic and Statistical Manual of Mental Disorders, Third Edition Revised, (DSM-III-R) criteria for TTM were treated with fluvoxamine at doses up to 300 mg/day. Random regression analysis of change across time for patients who completed the study (n=14) and those who dropped out (n=5) revealed statistically significant improvements in Physician Rating Scale, hair-pulling episodes, Trichotillomania Impairment Scale, and Trichotillomania Symptom Severity Scale, but not in estimated amount of hair pulled. In addition, the percentage of patients' focused or compulsive hair-pulling symptoms was predictive of treatment response. Unfortunately, all three subjects who entered long-term treatment displayed substantial movement back toward baseline by the end of 6 months. We concluded that fluvoxamine produces moderate reductions in symptoms during the short-term treatment of TTM and that the presence of focused or compulsive hair pulling may be predictive of treatment response. However, responses may be short lived when treatment is extended.

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.