Ph.P. Hubain

Does sleep EEG data distinguish between UP, BPI or BPII major depressions? An age and gender controlled study.

Clinical characteristics and sleep EEG data of 14 unipolar (UPR), 14 bipolar I (BPI) and 14 bipolar II (BPII) patients, matched for age and gender, were investigated during a major depressive episode. We observed a remarkable similarity in the clinical characteristics of the three samples and, concerning sleep EEG data, a trend to a higher percentage of awakening among BPI patients. Pairwise comparisons of the three subgroups showed that only the Newcastle rating scale score reached significant difference between BPI and UPR groups. We observed trends regarding the difference of awakening both between BPI and BPII groups and between BPI and UPR groups, difference of percentage of REM sleep between BPI and BPII groups and difference of Sleep Period Time between BPII and UPR groups. We also observed that the distribution of REM latencies in the BPI subgroup was different from the two others.

Relationship between the Newcastle scale and sleep polysomnographic variables in major depression: a controlled study

In order to investigate the reliability of the endogenous concept of depressive illness with some sleep EEG parameters, we studied 39 male inpatients suffering from a nonbipolar major depressive episode (15 endogenous (MDDE) and 24 nonendogenous (MDDNE)) and 20 age and sex matched normal controls (C). All patients were diagnosed according to the Research Diagnostic Criteria (RDC) and the endogenous character of the episode was assessed with the Newcastle Endogenous Depression Diagnostic Index. We found significant differences for the following variables between the three groups (MDDE, MDDNE and C): sleep period time (SPT), REM latency, stage II, slow wave sleep (SWS), REM latency expressed as a continuous variable and REM latency expressed as a dichotomizing variable with a threshold of 50 min. These variables were used to compare the endogenous and the nonendogenous depressed patients and also the major depressed patients and the normal controls. Significant differences were observed between all depressed patients and control subjects for amount of SWS and REM latency which were both reduced in endogenous and nonendogenous depressed patients. No significant difference was observed between endogenous and nonendogenous depressed patients, except for the REM latency expressed with a threshold of 50 min (more frequently observed in endogenous depressed patients). Our data support the observation that SWS and REM latency are decreased in major depressive patients. However, in this age and sex controlled study, subtyping nonbipolar major depressive disorder for an endogenous character by the Newcastle Endogenous Depression Diagnostic Index (NEDDI) did not reveal further significant differences for sleep EEG variables, except for the shortening of the REM latency expressed as a dichotomizing variable.

TSH response to TRH and EEG sleep in non-bipolar major depression: a multivariate approach.

The TSH response to TRH and selected sleep EEG variables were studied in a homogeneous sample of 280 non-bipolar major depressed inpatients (95 males and 185 females). The TSH response to TRH was blunted in 28% of the sample. delta max TSH was correlated negatively with age, Hamilton rating scale, Newcastle scale, percentage of wake, and positively with basal TSH, percentage of stage II, slow wave sleep, REM sleep and REM latency. delta max TSH was also lower in male patients and in patients suffering from an endogenous or a psychotic subtype of major depression. Basal TSH was only correlated negatively with the Newcastle score. In view of intercorrelations between all these variables, and because of the confounding effect of age, gender and severity on both the TSH response to TRH and sleep EEG variables, a multiple regression analysis was performed and demonstrated that basal TSH and gender were the two variables with the highest contribution to the delta max TSH variance, followed by age and the presence of psychotic symptoms. When controlling strictly for these significant effects, correlation with the severity or with the endogenous character of depression, and with sleep EEG parameters disappeared.