Twin, family, and adoption studies indicate that genetic factors play a major role in predisposition to schizophrenia. To date, molecular genetic studies have implicated many different chromosomal locations for the disorder. However, no one site replicates across the majority of investigations. This creates an impasse in the study of schizophrenia genetics, because of the large number of chromosomal sites that require further detailed research. It is difficult to plan to move ahead with expensive and labor-intensive research in an attempt to determine the etiologie genetic factor, when any given site proves to be only weakly positive. Therefore, the use of a hypothesis-driven approach may be cost effective, and may ultimately have more power to detect etiologie genes. Several lines of evidence suggest that a neurodevelopmental defect may play an important role in the etiology of this disorder. Neurodevelopment is a complex process in which genetic and nongenetic factors may interact to create the mature differentiated neuron, with its particular network of synaptic connections. A reasonable chance exists that polymorphisms of the genes that control normal development of the central nervous system (CNS) may produce a slightly altered trajectory of brain development, predisposing individuals to schizophrenia. This assumption has led geneticists to begin to study neurodevelopmental genes in schizophrenia subjects. This article reviews and discusses genetic studies of some developmental genes in schizophrenia. Genetic association and linkage studies of neurotrophic factors (brain-derived neurotrophic factor, or BDNF, and neurotrophin-3, or NT-3), neuronal cell adhesion molecule (NCAM), synapsin, and synaptosome-associated protein with a mass of 25 kd (SNAP-25) have proven to be of most interest.

The psychosis, intermittent hyponatremia, and polydipsia (PIP) syndrome is a prevalent, medically serious, and difficult to treat condition in psychiatry, especially common in hospitalized chronic schizophrenic patients. In this paper, the pathophysiology and clinical manifestations of the PIP syndrome are presented as an overview, and a program of medical/pharmacologic, nursing, behavioral, and psychiatric/psychological interventions is presented and discussed. The emphasis throughout this paper is on multidisciplinary treatment approaches for patients with PIP syndrome, including medical, psychiatric, psychosocial, behavioral, and nursing contributions to the evaluation and care of these often difficult patients.

The aim of this study was to evaluate the natural course of mood disorders in 157 patients admitted consecutively to the Dipartimento di Psichiatria, Neurobiologia, Farmacologia e Biotecnologie at Pisa University for an affective or schizoaffective episode and followed for 3 years.

During the follow-up, three patients committed suicide and three died of natural causes. The three suicide patients were diagnosed as suffering from a depressive episode deriving from Bipolar I disorder. Of the remaining 104 patients, 42% had no relapses, 35% had up to three relapses, and 23% had more than three relapses; there were no significant differences between these three groups.

In conclusion, recent treatments seem able to reduce the length and number of relapses in patients with mood disorders. The hyperthymic temperament seems to be a characteristic of compliant patients and a predictor of a good response to treatment. The mortality rate connected with somatic or accidental causes appears to be similar to that of the general population, while the rate of suicide is higher.

Although psychotic symptoms are a recognized manifestation of epilepsy, these are more often associated with seizures of the temporal lobe type. While 10% of children with temporal lobe epilepsy develop a psychotic disorder by adulthood, the literature does not report any cases of psychotic disorders associated with frontal lobe seizures in children. This article presents a unique case of a girl whose frontal lobe seizures were associated with delusional psychotic symptoms. Once her seizure disorder was identified through electroencephalography (EEG) and appropriate anticonvulsant therapy was initiated, her associated psychotic symptoms resolved.

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.

There is a well-established overlap in phenomenology between anorexia nervosa and obsessive-compulsive disorder, and between obsessive-compulsive symptoms and Tourette syndrome (TS). Five cases of eating disorders in patients with obsessive-compulsive symptoms and TS are presented. The identification of four similar cases in the literature putatively marks a subset of eating disorders with a link to TS and to obsessive-compulsive symptomatology. This association may reflect a common underlying neurobiologic imbalance.