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Biomedical subjects

J Mendlewicz

Publications and source records attributed to J Mendlewicz.

At least 19 recordsLinked to original sources
PubMed1992

Reduced clonidine rapid eye movement sleep suppression in patients with primary major affective illness.

Clonidine hydrochloride, administered intravenously (2 micrograms/kg) during the second non-rapid eye movement period, was significantly less suppressant of rapid eye movement sleep in 10 depressed patients with primary major affective illness, according to Research Diagnostic Criteria, than in three groups of matched subjects (10 normal controls, 10 patients with minor depression, and 10 patients with generalized anxiety). These results suggest that depressed patients with major primary affective illness have down-regulated alpha 2-adrenergic receptors. These findings are consistent with the cholinergic-aminergic balance hypothesis of depression and support the aminergic side of the concept. Finally, the rapid eye movement sleep response to clonidine could provide a new biological marker of affective illness.

Adult↗
PubMed1992

Sleep polygraphic variables in anorexia nervosa and depression: a comparative study in adolescents.

Sleep EEG variables were compared in an adolescent population consisting of 11 anorectic girls, 11 young depressed patients and 11 healthy volunteers matched for age and sex. Anorectic patients differed from depressed patients in a greater number and a higher length of awakenings. In comparison with controls, anorectic patients showed less sleep efficiency, a higher length of awakenings and less REM sleep. When anorectic patients were divided in restricting and bulimic subtypes, the bulimic anorectics showed an increase in stage 3 of sleep. These results do not support a direct association between eating disorders and affective disorders. Sleep EEG variables were not significantly correlated to the Body Mass Index.

Adolescent↗
PubMed1992

Biological and clinical features of recurrent brief depression: a comparison with major depressed and healthy subjects.

Recurrent brief depression (RBD) has recently been proposed as a new subtype of affective disorder characterized by episodes of major depression which last less than two weeks. The aim of this study was to further evaluate the validity of this putative subtype by means of clinical and biological data. DST, TSH response to TRH and sleep EEG variables were compared in 25 RBD patients sex- and age-matched to 25 major depressed (MD) and 25 healthy subjects. Family history, age at onset, and psychiatric comorbidity did not discriminate RBD from MD. Recurrent unipolar depression was found to be more prevalent in MD. Although less severely depressed during the biological tests, patients with RBD did not significantly differ from those with MDD on basis of DST non-suppression, blunted TSH response and shortening of REM latency. Compared to controls, a greater sleep onset latency was observed both in RBD and MD and a lower total sleep time in MD patients only. These results suggest that RBD could be viewed as a subtype of affective disorder sharing many characteristics with MDD.

Adult↗
PubMed1992

5-HT2 receptor antagonism and slow-wave sleep in major depression.

Specific sleep disturbances such as reduced slow-wave sleep (SWS) and decreased serotonergic (5-HT) activity have been observed in depressive disorders. Ritanserin, a specific 5-HT2 receptor antagonist, has been shown to increase SWS in healthy subjects. This study explored the effects of a single dose or ritanserin (5 mg) on sleep electroencephalography in 18 major depressed patients and in 10 control subjects. Ritanserin affected SWS differently in the two groups. Although stage 3 increased significantly in the groups, in contrast to controls, there was no significant effect of ritanserin on stage 4 in depressed patients. In the depressed group, irritability and DSM-III-R melancholic type predicted 40% or the variance of stage 4 increment after ritanserin, as assessed by stepwise multiple regression. These results are in agreement with a potential 5-HT disturbance, particularly at the 5-HT2 receptor level, in some clinical forms of depression.

Adult↗
PubMed1992

Attributional style and depression: a controlled comparison of remitted unipolar and bipolar patients.

Attributional style was investigated in remitted affective disorder patients (23 unipolars and 26 bipolars) and 26 non-psychiatric controls. We found a specific cognitive vulnerability in unipolars. Unipolars attributed negative events to causes that were more stable--but not more internal nor more global--than bipolars and controls, and did not attach more importance to these events. Attributional vulnerability seemed more apparent in patients with longer histories of depression.

Adult↗
PubMed1992

Efficacy of fluvoxamine in severe depression.

The therapeutic efficacy of fluvoxamine has been demonstrated in large numbers of patients participating in comparative double-blind placebo-controlled studies using imipramine as the active reference compound. Overall, patients treated with fluvoxamine for 4 to 6 weeks had significant amelioration of their depression compared with placebo-treated patients. More importantly, the response rate in patients with severe depression was greater than in patients with mild or moderate depression. However, several investigators have observed high placebo response rates, and in some studies there has been a similar response rate to imipramine and placebo treatment. While the high placebo response rate may have resulted from methodological problems, the issue does raise some questions that can only be resolved by further investigation.

Clinical Trials as Topic↗
PubMed1991

Lack of association between HLA-DR antigens and sleep-onset REM periods in major depression.

Narcolepsy is the disease disclosing the strongest association with the HLA system. Almost 100% of cases are associated with HLA-DR2 antigen. Moreover, narcolepsy is often characterized by the occurrence of sleep-onset REM (SOREM) periods. SOREM has also been demonstrated in major depression. To further investigate the relationship between SOREM and HLA-DR2, HLA-DR and HLA-DQ antigens were assessed in 50 research diagnostic criteria (RDC) major depressed patients. Depressed patients were elected for HLA typing on the basis of the presence of at least one SOREM period (n = 29) or three REM latencies above 50 min (n = 21) during three consecutives EEG nights recording. No significant differences were observed in the frequency of HLA-DR or HLA-DQ antigens between patients and controls. These results demonstrate a lack of association between SOREM and HLA-DR2 in major depression, and also do not confirm the presence of an association between antigens encoded by the HLA region of the chromosome 6 and major depressive illness.

Adult↗
PubMed1991

Sleep EEG and amitryptiline treatment in depressed inpatients.

We studied the baseline sleep electroencephalogram (EEG) variables and treatment-related sleep changes after 35-46 days of amitryptiline treatment (AMI) in a group of 18 depressed inpatients, mostly suffering from a major depressive disorder endogenous subtype (according to the Research Diagnostic Criteria, RDC), with a short rapid eye movement (REM) latency. The aim of the study was to identify potential sleep "predictors" of clinical response to AMI as well as short-term sleep changes associated with alleviation of depression. Clinical response to the drug was defined as a reduction of more than 50% of the Hamilton Rating Score for Depression (HRSD). Eleven men and 7 women, 25-68 years old, were included in the study. Their sleep was recorded at baseline and after an average of 39 +/- 4 days of AMI treatment, at a mean daily dose of 165 +/- 35 mg. The comparison of responders (n = 9) and nonresponders (n = 9) with Wilcoxon's test showed that responders (1) were more severely depressed at baseline, and (2) had less stage 4 sleep. A discriminant function using baseline HRSD, stage 4 and the number of stage shifts allowed for discrimination between responders and nonresponders with a 100% hit rate. Antidepressant treatment had, however, no differential effect on sleep parameters in the two response groups.

Adult↗
PubMed1991

[Genetics and schizophrenia].

Studies of twins, adoption and familial incidence have demonstrated that heredity plays a role in the genesis of schizophrenia. Owing to recent advances in molecular biology and computerized statistical models, analyses of pedigrees and genetic linkage have made it possible to progress in the identification and mode of transmission of genetic factors in schizophrenia. The methodology and conflicting results of these studies are reviewed, together with modern hypotheses on the mode of transmission of schizophrenia. The contribution of genetic studies to the concept of schizophrenia clinical spectrum and the new strategies of research in genetics are presented.

Genetic Linkage↗
PubMed1991

Circadian and sleep-related endocrine rhythms in schizophrenia.

Plasma levels of prolactin, growth hormone, corticotropin, and cortisol were measured at 15-minute intervals for 24 hours in nine unmedicated male schizophrenic patients and in nine age-matched normal male subjects. Each study was preceded by 3 days of habituation to the laboratory environment. Sleep was polygraphically recorded. The circadian and pulsatile variations present in each hormonal profile were quantitatively characterized with the use of computer algorithms specifically designed for analyses of hormonal fluctuations. The major abnormality of neuroendocrine release that was observed in the schizophrenic patients was an almost threefold enhancement of the sleep-related increase in the prolactin level, associated with an intensified frequency of nocturnal prolactin pulses. This increased stimulatory effect of sleep on prolactin secretion was evident immediately after sleep onset. The normal inhibition of cortisol secretion during early sleep was absent in schizophrenic patients. The major sleep abnormalities were a prolonged sleep latency and a reduction in total rapid eye movement stage sleep. During wakefulness, prolactin and cortisol levels were normal. The 24-hour profile of growth hormone was unaltered in schizophrenic patients, and a sleep-onset growth hormone pulse was observed in all patients. No abnormalities were noted in the levels or temporal organization of corticotropin secretion. Both the amplitude and the timing of the cortisol rhythm were normal. We conclude that, in schizophrenic men, pituitary-adrenal function and circadian time-keeping are normal but prolactin secretion is hyperresponsive to the physiologic stimulus of sleep onset. Schizophrenia thus appears to be characterized by a subset of neuroendocrine disturbances distinct from that observed in major endogenous depression.

Adrenocorticotropic Hormone↗
PubMed1991

Genetic determinants of EEG sleep: a study in twins living apart.

In order to investigate the genetic components of sleep and, in particular, of REM sleep, we performed 3 consecutive all-night EEG recordings in 26 pairs of normal male twins living apart (11 monozygotic and 15 dizygotic). Our results indicate that in man non-genetic rather than genetic influences substantially determine variance in stage REM, in contrast to stages 2, 4 and to delta sleep. In this sample of male twins, waking measures also showed a significant genetic component.

Adult↗
PubMed1991

Sleep-related chronobiological markers of affective illness.

Sleep EEG and neuroendocrine disturbances have been described in the acute phase of affective illness. The question arises as to whether these biological marker disturbances are state- or trait-related. This important issue can be addressed by evaluating changes in sleep EEG and neuroendocrine parameters from a chronobiological approach before and after antidepressant treatment. Among the circadian variables explored in affectively ill patients are REM sleep and slow wave sleep, as well as circadian secretion of plasma GH, cortisol, ACTH and prolactin. Our studies show that depressed patients mainly of the unipolar type secrete more GH and cortisol during the circadian period than control subjects do. GH hypersecretion appears mainly during wakefulness while cortisol hypersecretion is observed during the 24 h space. Temporal disorganization of hormonal secretion is also present since an advance of the quiescent period of the ACTH-cortisol rhythm as well as pre-sleep GH spikes were described in our depressed unipolar patients before treatment. After antidepressive treatment, these chronobiological anomalies tend to normalize, as state biological markers. These observations are giving support to the phase-advance hypothesis of depression.

Adrenocorticotropic Hormone↗