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Results of the present study provide evidence of: 1) a positive association between bipolar affective disorder and blood type O and a corresponding negative association between the former and blood type A, 2) a positive association between unipolar affective disorder and blood type O, and 3) a positive association between involutional depression and blood type A and a corresponding negative association between the former and blood types B and O. Sex does not appear to modify the ABO blood types' distribution in patients with bipolar, unipolar affective disorder, or involutional depression, and the same holds for early- or late-onset of the illness in patients with bipolar or unipolar affective disorders. Findings in the present study do not support the validity of the bipolar-unipolar distinction of affective disorders, and provide evidence in favour of the view that involutional depression is a genetically distinct nosological entity.

The patterns of prolactin release after bilateral ECT and after 0.4 mg TRH i.v. were studied in 11 female melancholic patients in a 5-min sampling protocol. Mean prolactin peaking times were 10.2 min after ECT and 20.5 min after TRH. The elimination rate coefficients were significantly lower--and the corresponding half-lives longer--for prolactin released by TRH than by ECT. A significant positive correlation of the maximal prolactin responses by the two stimuli was also found.

In order to investigate the effects of 6 weeks' neuroleptic treatment on the pituitary-thyroid axis in 25 male schizophrenic patients, and the diurnal variation in the thyrotropin (TSH) and prolactin (PRL) responses to thyrotropin-releasing hormone (TRH) in these patients, the TRH stimulation test was performed in each of them at 14.00 and 24.00 h of the same day, both before and after 6 weeks' treatment with neuroleptics (chlorpromazine or fluspirilene). Also, serum thyroxine (T4), in vitro radioactive triiodothyronine uptake (RT3 U) and free-thyroxine index (FTI) values were estimated from the pre-TRH blood sample. We found no evidence of diurnal variation in the TSH response to TRH in the schizophrenic patients, before or after 6 weeks' neuroleptic treatment. Only drug-free schizophrenic patients had significantly higher PRL responses to TRH at 14.00 h than those at 24.00 h. After 6 weeks' neuroleptic treatment, schizophrenic patients tended to have lower FTI values; also, they had significantly higher basal TSH and PRL values, as well as significantly augmented TSH and PRL responses to TRH, in comparison to their pretreatment values. These findings render possible the diagnosis of subclinical hypothyroidism in neuroleptic-treated schizophrenic patients.

In this paper the preliminary results from an ongoing investigation on the effect of the MAO-A inhibitor moclobemide on clinicolaboratory variables (antidepressant effect, platelet MAO activity, urinary MHPG and 5-HIAA excretion, plasma prolactin and growth hormone levels and TSH response to TRH) are reported. From the total of 18 patients, 10 (2 males and 8 females) responded favourably (reduction in the HDRS 50% or more) to the treatment. Urine MHPG excretion significantly (p less than 0.001) decreased during treatment, while 5-HIAA secretion showed a less pronounced decrease (p less than 0.05). Plasma PRL and GH remained unchanged, while the TSH-response to TRH increased significantly (p less than 0.025) after 4-week treatment. A significant correlation was found between MHPG pretreatment values and treatment outcome.

1. An experimental antidepressant was studied through sleep laboratory recordings, psychoendocrinological tests and clinical measurements in terms of its efficacy, side effects and effects on sleep. 2. The design included a four-week drug administration period, preceeded and followed by a one week placebo period. 3. In the presence of antidepressant efficacy, the drug did not disturb sleep induction and maintainance. 4. The only effect on sleep stages was an increase of REM sleep during the short-term drug administration period which is contrary to the REM supressant effect of most antidepressants. 5. This finding suggests that REM supression and antidepressant efficacy are not necessarily related. 6. Further, given that the only known action of the drug is its inhibitory effect on GABAergic transmission, one can speculate that GABA mechanisms may be involved in REM sleep modulation.

Male patients suffering from borderline personality disorder (n = 13), major depression (n = 13) or schizophrenia (n = 13) were investigated on several psychopathological (HDRS, BPRS) and neuroendocrinological (DST and TSH, PRL, GH responses to TRH) parameters. Comparisons were made between the borderline group and the other groups of patients. Borderline patients differed from schizophrenics psychopathologically (BPRS) and neuroendocrinologically (DST). Also, borderline patients differed from major depressives in the HDRS, but behaved like them concerning DST. Our findings support the hypothesis that there are neuroendocrinological similarities between borderline personality disorder and major depressive patients, especially on the hypothalamo-pituitary-adrenal axis.

The clinical, electrophysiological and muscle biopsy findings of 7 cases with a peculiar form of X-linked hereditary degenerative motor neuron disease are presented. It is suggested that the disease might be a separate clinical entity with the following characteristics: (1) sex-linked recessive inheritance, (2) unusual but not invariable late onset, (3) slow progression, (4) facial-bulbar and proximal spinal muscle involvement, (5) consistent fasciculations, sometimes massive and more pronounced about the lips, chin and tongue, (6) fine tremor of the hands, (7) muscle cramps usually preceding the other symptoms, and (8) gynaecomastia as a frequent but not a constant feature.

Fifteen male paranoid schizophrenics underwent an initial 4-week therapy with haloperidol 7.5 mg/day, and a subsequent 4-week treatment with haloperidol 15 mg/day, p.o. (group I). Another 15 male paranoid schizophrenics received an initial 4-week treatment with haloperidol 30 mg/day, and a subsequent 4-week therapy with haloperidol 60 mg/day, p.o. (group II). In each group of patients, serum prolactin (PRL), luteinizing hormone (LH) and testosterone (T) levels were measured before treatment and at the end of the two consecutive periods of treatment. A dose-related increase in serum PRL levels was found in both groups of medicated patients. Serum LH levels were not significantly affected by haloperidol treatment. A significant decrease in serum T levels was detected only in group II medicated patients, i.e., in the patients who were treated with relatively high daily doses (30 or 60 mg/day) of haloperidol.

The red cell 2,3 DPG, the most important factor for oxygen delivery in the tissues, was found to be increased in Parkinsonism patients compared with controls. The aging process seems not to be a factor in the increased 2,3 DPG concentration. Other factors relevant to raised 2,3 DPG level such as physical activity, increased oxygen requirements, and metabolic changes are discussed.

The authors assayed plasma dopamine beta-hydroxylase activity, platelet monoamine oxidase (MAO) activity, plasma prolactin, the urinary monoamine metabolites 3-methoxy-4-hydroxyphenylglycol (MHPG), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA), and urinary cAMP from 18 delusional and 22 nondelusional depressed inpatients. No significant differences between the two groups were found.

The mean values of serum thyroxine (T4), in vitro radioactive triiodothyronine uptake and free-thyroxine index (FTI) in 41 drug-free schizophrenic patients did not differ significantly from those of euthyroid controls. Following 6 weeks' treatment of 24 schizophrenics with chlorpromazine, trifluoperazine or clozapine, a significant decrease in serum T4 and FTI was noted after chlorpromazine and clozapine, whereas after trifluoperazine only serum T4 decreased, but not FTI. The questions arising from these findings are discussed and the need for a future investigation of serum triiodothyronine and serum TSH in schizophrenic patients before and after neuroleptic treatment is stressed.

Serum prolactin (PRL), luteinizing hormone (LH) and testosterone (T) levels were estimated in a group of 30 male paranoid schizophrenics before and after 4 weeks treatment with chlorpromazine and/or trihexyphenidyl, and in a group of 14 healthy male individuals. After treatment with chlorpromazine (100 mg t.i.d., p.o.), 10 patients presented a significant increase in serum PRL values and a significant decrease in serum T values. A significant increase in serum PRL values was also found in 10 patients who were treated with chlorpromazine (100 mg t.i.d., p.o.) plus trihexyphenidyl (5 mg t.i.d., p.o.). No significant difference in any of the investigated endocrine parameters was detected in 10 patients after 4 weeks administration of trihexyphenidyl (5 mg t.i.d., p.o.). Following chlorpromazine treatment with or without concomitant administration of trihexyphenidyl, 20 patients showed a significant increase in serum PRL levels and a significant decrease in serum LH and T levels.