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PubMed1985

Internight variability of REM latency in major depression: implications for the use of REM latency as a biological correlate.

The internight variability in REM latency in 92 drug-free inpatients with major depressive illness was recorded for 4 consecutive nights and subsequently assessed. Individual coefficients of variation in REM latency [CV = (standard deviation of mean REM latency for 4 recording nights/4-night mean REM latency) X 100] ranged from 5.1 to 121.7, with a mean of 37.0 (SD = 27.3) and a median of 27.4. CV was positively correlated with both age (p less than 0.05) and age at onset of depressive illness (p less than 0.01). Male patients showed more variability in REM latency than female patients (p less than 0.05); likewise, the subgroups of patients who either were incapacitated or had bipolar II illness showed greater variability in REM latency in comparison with the remainder of the sample (p less than 0.05). When the entire patient sample was stratified by CV into three equal subgroups, the subgroup of patients defined by the highest CV presented the longest sleep latency (p less than 0.05) and the shortest REM latency (p less than 0.0001). No other clinical or polysomnographic correlates of REM latency variability were noted nor was REM latency variability related to severity of illness, other subtypes of illness, or clinical response to antidepressant therapy. In selecting REM latency data for assessment of diagnostic sensitivity, the use of the shortest REM latency from at least 3 consecutive nights yielded a higher sensitivity (74%-81%) than did the use of any one individually specified night (50%-56%) or different internight means (49%-52%). The same conclusion applied when patient age was taken into account. These results have implications for standardizing the use of REM latency as a biological correlate in major depression.

Adult↗
PubMed1985

"Paradoxical" shortening of REM latency on first recording night in major depressive disorder: clinical and polysomnographic correlates.

Among 92 inpatients with major depressive disorders, variability in REM latency (RL) during the first two recording nights was assessed by means of an "adaptation coefficient" (AC = night 1 RL--night 2 RL X 100 divided by mean RL for nights 1 and 2). Although mean RL was very similar for both nights (48.1 and 50.7 min), individual ACs showed a gaussian distribution [range: -176.5-171.4; mean: -1.2 (67.3); median: -4.4]. Forty-two patients (45.7%) exhibited shortening of RL on night 2 compared with night 1 (positive AC, corresponding to an "expected" evolution), 48 patients (52.2%) displayed the opposite pattern (negative AC, corresponding to a "paradoxical" evolution), and two patients had identical values on both nights. Extent of increase in RL from first to second night (i.e., extent of "paradoxical" evolution) correlated significantly with increasing duration of current episode, earlier age of onset, and poorer clinical response to tricyclic antidepressants. A cutoff AC of -7 correctly classified 62% of patients according to treatment response. The research diagnostic criteria-based retarded subtype of depression was associated with a more negative AC (i.e., a more "paradoxical" evolution), and the situational subtype was associated with a more positive AC (i.e., a more "expected" evolution) than the remainder of the sample. The subgroup with the most negative ACs (i.e., largest increases in RL from first to second night) also had longer sleep latencies, whereas the subgroup with the most positive ACs (i.e., largest decreases in RL) had higher REM activity and REM density as compared with the remainder of the sample. These results suggest that RL in major depression is not a static parameter and that the study of its within-subject variability can be helpful for diagnostic confirmation and prediction of treatment response.

Adaptation, Physiological↗
PubMed1987

Serial DST, TRH test, and TRH-like immunoreactivity measurements in major affective disorders.

Neuroendocrine functions in depressed patients with major affective disorders were serially investigated by the Dexamethasone Suppression Test (DST), the thyrotropin-releasing hormone (TRH) stimulation test, and the plasma TRH-like immunoreactivity (TRH-LI) measurement. Prior to antidepressant therapy, the sensitivity for nonsuppression to the DST was 36.0%, whereas that for blunted thyroid-stimulating hormone (TSH) response to TRH was 28.0%. Both DST nonsuppression and TSH blunting appeared to be state-related markers for depressed patients. Specifically, a significant increase of maximum TSH response to TRH after 4 weeks of antidepressant therapy was associated with clinical improvement. Plasma TRH-LI in depressed patients was significantly lower than that of healthy controls. It is possible that the lower plasma TRH-LI level is related to the pathophysiology of some depressed patients with major affective disorders.

Adult↗
PubMed1988

Sodium lactate infusions after treatment with tricyclic antidepressants: behavioral and physiological findings.

Fourteen patients with panic disorder were infused with sodium lactate both before and after treatment with tricyclic antidepressants. All patients had panic attacks before treatment, and only five after treatment. There was a significant decrease in measures of anxiety prior to and during infusions after treatment. The patients were able to tolerate more lactate during reinfusions. The comparison of reinfusion panickers and nonpanickers revealed that the reinfusion panickers had higher levels of anxiety, as measured by psychological symptoms on the Panic Description Scale, during both their pretreatment and posttreatment infusions. Tricyclic antidepressants appear to increase the threshold for lactate-induced panic attacks.

Antidepressive Agents, Tricyclic↗
PubMedDate not supplied

State specificity of DST abnormalities in geriatric depression.

Pre-treatment and posttreatment dexamethasone suppression test (DST) results in physically healthy elderly major depressives without dementia demonstrated an association between treatment and DST normalization. Sixty percent of subjects were nonsuppressors at baseline compared to 17% after intensive treatment. DST results normalized in 75% of initial nonsuppressors; none of the initial suppressors converted to nonsuppression. A strong correlation between clinical improvement and decreases in afternoon cortisol levels was identified. Initial suppression status did not influence this association. There was a nonsignificant trend for very high (> 15 micrograms/dl) afternoon cortisol levels to be associated with delusional depression. The advantage of using continuous rather than categorical measures to assess the relationship between reversal of depression and DST results is discussed.

Aged↗