Sleep Laboratory Studies with Trazodone inInsomnia Related to Depression and Dysthymia

Overview

Summary:
Utilizing polysomnography (PSG) and psychometry, objective and subjective sleep andawakening quality was investigated in 11 patients with nonorganic insomnia (F51.0) related toa depressive episode (F32) or recurrent depressive disorder (F33) and 11 patients with nonorganicinsomnia related to dysthymia (F34.1), as compared with 2 age- and sex-matched normal controlgroups. Both affective disorders demonstrated decreased sleep efficiency as well as prolongedsleep latency and an increased number of nocturnal awakenings. Moreover, in depression totalsleep time was reduced and early morning awakening increased; in dysthymia there was anincrease in wakefulness during the total sleep period (TSP). Concerning sleep architecture bothpatient groups showed an increase in S1, a decrease in S2 and a nonsignificant decrease in S3+S4,while SREM was significantly increased only in dysthymics. Also snoring was only increased inthe latter, while the PLM index showed an increase in both groups. Subjective sleep and awakeningquality as well as subjective well-being and mood were deteriorated in both groups. Drivewas reduced only in depressed patients, affectivity and morning wakefulness only in dysthymics.Morning psychomotor activity was deteriorated in both groups, memory and reaction time variabilityonly in dysthymic patients. Concerning psychophysiological variables, only depressed patientsshowed a significant increase in morning and evening systolic and diastolic blood pressure.In an acute, placebo-controlled cross-over design study, the acute effects of 100 mg trazodone,a serotonin reuptake inhibitor with sedative action due to 5-HT2 and
1 receptor blockade, wereinvestigated in both patient groups. As compared with placebo, trazodone induced an increase in sleep efficiency, total sleep time (TST) and TSP as well as a decrease in wakefulness during theTSP and early morning awakening in depressed patients. Similar findings occurred in dysthymics,though the level of statistical significance was not reached. Concerning sleep architecture,a significant increase in slow-wave sleep (S3+S4) was seen in both groups. In depression S2 wassignificantly increased, in dysthymia SREM significantly decreased and REM latency significantlyprolonged. The snoring index showed no significant changes, the apnea-hypopnea index wasreduced in depression, the PLM index in dysthymia. Subjective sleep quality improved significantlyin depression. There were no significant changes in the morning thymopsyche or noopsyche,except for an improvement of numerical memory in depression. Dysthymics exhibited a significantdecrease in systolic blood pressure, while in depressives diastolic values were significantlydecreased. In conclusion, both affective disorder groups showed significant changes in objectiveand subjective sleep and awakening quality as compared with normal controls, which were counteractedby trazodone 100 mg. This suggests a key-lock principle in regard to diagnosis andtreatment of nonorganic insomnia due to affective disorder with this drug.

Key words:
nonorganic insomnia, depression, dysthymia, controls, polysomnography, subjectivesleep quality, awakening quality, psychometry, trazodone.