New experimental findings show that schizophrenics, as well as some of their non-schizophrenic relatives, manifest basic cognitive disorders defined in terms of variables from the field of experimental psychology. These basic disorders can be regarded as markers--if not, indeed, as psychological manifestations--of vulnerability to schizophrenia. They can be associated with subjectively experienced forms of non-clinically manifest impairments in psychological functioning. It was therefore hypothesised that schizophrenics, as well as non-schizophrenic subjects vulnerable to schizophrenia, will, in the course of learning processes, develop compensatory efforts which may be more or less effective. It is assumed that effective efforts of this kind will take on special significance in stress situations which would tend to elicit the occurrence of a schizophrenic episode. Effective efforts at compensation for basic disorders should be able to act as a 'buffer' against negative stressor effects (moderator function), thus reducing the danger of a psychotic breakdown. These compensation efforts were studied in 40 inpatients in remission after an acute schizophrenic episode. It was found that significant correlations exist between the extent of subjectively experienced basic disorders and the number and kind of conscious compensation attempts. Although the findings to date are of a preliminary and purely descriptive nature they would seem to justify further research.

Fifty-two adult depressed outpatients fulfilling Research Diagnostic Criteria for Definite Major Depressive Disorder were enrolled in a double-blind study comparing the antidepressant effects of alprazolam versus desipramine. Twenty-nine patients completed the seven week (one week placebo followed by six weeks of active drug) study. The mean daily dose of alprazolam and desipramine at study termination was 3.34 mg and 192 mg respectively. Based on psychometric ratings of depression (Hamilton Scale) and severity of illness (Clinical Global Impressions) there was no significant difference between alprazolam and desipramine at the end of six weeks of active drug treatment. Both medications were well tolerated with drowsiness being the most common side effect of alprazolam, and insomnia, dry mouth, and constipation, the complaints most associated with desipramine.

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Neuroendocrine dysfunction and self-reinforcement deficits were evaluated in 45 individuals exhibiting symptoms of major depression. The dexamethasone suppression test (DST), Beck Depression Inventory (BDI), and Frequency of Self-Reinforcement Questionnaire (FSRQ) were administered to subjects who also were participating in a comparative antidepressant drug study. Subjects with low rates of self-reinforcement tended to exhibit normal DST responses, whereas high self-reinforcers could not be characterized as Seing significantly more or less dysfunctional on the DST. Only one third of this sample of depressives evidenced abnormal DSTs, which suggests that in these cases of depression with normal neuroendocrine functioning, a deficit in self-reinforcement could be related to depression.Recently it has become apparent that numerous possible biological, personality, and environmental factors may function as descriptive and etiological conditions of depression (Craighead, 1980). One of the more extensively researched biological abnormalities is neuroendocrine dysfunction of the hypothalamicpituitary-adrenal (HPA) axis, which is believed to characterize endogenous unipolar depressives. Specifically, limbic and cortical neurotransmitter dysregulation may occasion dysregulation of the HPA axis, which is reflected by abnormal secretion patterns of cortisol (Siever & Davis, 1985). In several studies, Carroll (e.g., Carroll 1982) and his associates have found characteristic patterns of cortisol secretion in depressed patients using the dexamethasone suppression test (DST), an established medical procedure that detects early escape of serum cortisol from suppression by dexamethasone.A positive DST result does not specifically predict depression and may occur in a number of conditions unrelated to affective disorders (Shapiro & Lehman, 1983). In addition, the lack of perfect sensitivity of the DST in predicting depression suggests that all depressives cannot be diagnosed solely with provocative neuroendocrine assessment. In those cases where the DST reveals normal suppression of cortisol, environmental or personality factors, or both, may help to account for the occurrence of depression. There have been studies on the association between depression and general personality disorders (e.g., Soloff,The authors acknowledge the assistance of Peter Hamilton. Nami Kosaka, and Ron Miyaguchi in the collection and analysis of the data.

Fifty-four patients (34 outpatients, 20 inpatients) fulfilling Research Diagnostic Criteria for Definite Major Depressive Disorder were enrolled in a double-blind study comparing the antidepressant effects of alprazolam versus desipramine. The mean daily dose of alprazolam and desipramine at study termination was 3.78 mg and 208 mg respectively. As there were no significant demographic or clinical differences between outpatients and inpatients, both groups were combined in data analysis. Using the Hamilton Depression Rating Scale (HAM-D) both drug groups showed highly significant improvement beginning with the first week of active drug treatment. HAM-D scores continued to decrease through study termination (six weeks of active drug). There were no significant differences when comparing alprazolam and desipramine (outpatients, inpatients, or both groups combined) on any of the subjective or objective psychometrics used in this study. Clinically, only twelve of thirty-four outpatients (35.3%) were felt to be "markedly or moderately" improved, suggesting that neither the outpatient alprazolam nor desipramine patients did particularly well with drug treatment. In terms of drug safety there was no difference between the alprazolam and desipramine in the number of excessive or serious drug side effects. However, five of twenty-nine alprazolam patients had to discontinue therapy because of excessive drowsiness, and two of the alprazolam outpatients had motor vehicle accidents directly related to this adverse event. Alprazolam appeared as effective as desipramine in the pharmacotherapy of this group of depressed outpatient and inpatients. Alprazolam appeared well-tolerated by most subjects although drowsiness was a common--and at times serious--medication side effect.