Anatomical changes in first-episode schizophrenia broadly coincide with a basal ganglia-thalamocortical circuit. These changes include bilateral reductions in caudate head gray matter, which are absent in chronic schizophrenia. Comparing first-episode schizophrenia and chronic schizophrenia, the authors did not find evidence for the temporolimbic progression of pathology from hippocampus to amygdala, but there was evidence for progression of cortical changes.

The aim of this study was to contribute to the characterization of the entactogen (ecstasy) substance group. The psychopathological, neuroendocrine and autonomic effects of common recreational doses of the entactogen 3,4-methylenedioxyethylamphetamine (MDE), the hallucinogen psilocybin, the stimulant d-methamphetamine and placebo were investigated in a double-blind study with healthy volunteers (n = 32). Psychological effects of the drugs were assessed by means of standardized rating scales, self assessment inventories and free descriptions. The most characteristic effects of MDE were pleasant emotional experiences of relaxation, peacefulness, content and closeness to others. However, significant stimulant and hallucinogen-like effects were also present, although the latter were weaker than the effects of psilocybin. MDE elicited the strongest endocrine and autonomic effects among the three drugs, including robust rises of serum cortisol and prolactin, elevations of blood pressure and heart rate, and a moderate, but significant rise of body temperature. The apparent contrast between psychological and autonomic effects (subjective relaxation versus physical activation) was a unique feature of the MDE state. Our findings are in line with both users' reports and results from previous experimental studies, and support the view that entactogens constitute a distinct psychoactive substance class taking an intermediate position between hallucinogens and stimulants.

Deficits in sensorimotor gating as assessed by prepulse inhibition (PPI) of the startle reflex have been reported in schizophrenia. However, the state or trait nature of these deficits and the relationships with clinical features and psychopathological symptoms are not clear. To explore these issues, we performed a longitudinal study with schizophrenia inpatients. We examined 36 medicated schizophrenia inpatients twice in the course of an acute psychotic episode: recently after admission and after psychopathological improvement 2-3 weeks later. In addition, we examined 18 healthy control subjects twice (two weeks apart). Relative to control subjects, patients with schizophrenia had lower PPI only in the acute, but not in the improved clinical state. Larger PPI deficits were associated with more severe formal thought disorder and bizarre behavior. In the present longitudinal study, PPI deficits in schizophrenic patients appeared to be state dependent. Taking into account recent evidence from the literature we propose that reduced PPI may be a mediating vulnerability marker of schizophrenia: Impairments in sensorimotor mechanisms which subserve PPI of the startle reflex may both predispose individuals to develop psychosis, and, in addition, may covary with the presence of acute positive symptoms.

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