Nocturnal sweating and temperature in depression

Avery, David; Shah, Saloni; Eder, Derek N.; Wildschiødtz, Gordon

doi:10.1111/j.1600-0447.1999.tb10864.x

Cited by 61 publications

(28 citation statements)

References 32 publications

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“…Depressed patients often have ‘flattened’ diurnal rhythms as nocturnal temperatures remain high. 28,29 Remission is usually associated with a decrease in nocturnal temperature and a restoration of normal rhythms. 28,30 …”

Section: Abnormal Circadian Rhythms In Major Depressive Disorder (Mdd)mentioning

confidence: 99%

Circadian dysregulation of clock genes: clues to rapid treatments in major depressive disorder

et al. 2014

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Conventional antidepressants require 2–8 weeks for a full clinical response. In contrast, two rapidly acting antidepressant interventions, low-dose ketamine and sleep deprivation (SD) therapy, act within hours to robustly decrease depressive symptoms in a subgroup of major depressive disorder (MDD) patients. Evidence that MDD may be a circadian-related illness is based, in part, on a large set of clinical data showing that diurnal rhythmicity (sleep, temperature, mood and hormone secretion) is altered during depressive episodes. In a microarray study, we observed widespread changes in cyclic gene expression in six regions of postmortem brain tissue of depressed patients matched with controls for time-of-death (TOD). We screened 12 000 transcripts and observed that the core clock genes, essential for controlling virtually all rhythms in the body, showed robust 24-h sinusoidal expression patterns in six brain regions in control subjects. In MDD patients matched for TOD with controls, the expression patterns of the clock genes in brain were significantly dysregulated. Some of the most robust changes were seen in anterior cingulate (ACC). These findings suggest that in addition to structural abnormalities, lesion studies, and the large body of functional brain imaging studies reporting increased activation in the ACC of depressed patients who respond to a wide range of therapies, there may be a circadian dysregulation in clock gene expression in a subgroup of MDDs. Here, we review human, animal and neuronal cell culture data suggesting that both low-dose ketamine and SD can modulate circadian rhythms. We hypothesize that the rapid antidepressant actions of ketamine and SD may act, in part, to reset abnormal clock genes in MDD to restore and stabilize circadian rhythmicity. Conversely, clinical relapse may reflect a desynchronization of the clock, indicative of a reactivation of abnormal clock gene function. Future work could involve identifying specific small molecules capable of resetting and stabilizing clock genes to evaluate if they can rapidly relieve symptoms and sustain improvement.

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Section: Abnormal Circadian Rhythms In Major Depressive Disorder (Mdd)mentioning

confidence: 99%

Circadian dysregulation of clock genes: clues to rapid treatments in major depressive disorder

et al. 2014

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“…In contrast, in H mice, the core temperature was lower than in NH mice during the light period, but it rose to NH levels during the dark period. Interestingly, depressed patients also exhibit disruptions of the body temperature rhythm (Avery et al, 1999;Bunney and Bunney, 2000).…”

Section: Locomotor Activity and Sleep-wakefulness Cycles Under Baselimentioning

confidence: 99%

“…It is associated with characteristic sleep impairments, notably difficulties in falling asleep, reduction of the rapid eye movement (REM) sleep latency, sleep fragmentation, and early morning awakenings (Adrien, 2002;Benca, 2000). In addition, abnormalities of circadian rhythms, affecting notably nycthemeral variations in rest-activity, and body temperature, have been described in depressed patients (Avery et al, 1999;Bunney and Bunney, 2000;Souetre et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Popa

Yacoubi²,

Vaugeois³

et al. 2005

Neuropsychopharmacol

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In depressed patients, sleep undergoes marked alterations, especially sleep onset insomnia, sleep fragmentation, and disturbances of the Rapid Eye Movement (REM) sleep. Abnormalities of rest-activity rhythms and of hypothalamic-pituitary-adrenocortical function have also been described in these patients. In the present study, we examined the presence of such abnormalities in a recently developed line of mice (Helpless mice-H) that exhibit depression-like behaviors in validated tests, compared to the nonhelpless (NH) line derived from the same colony. Experiments were essentially carried out in females for which previous studies showed marked differences between H and NH lines. Compared to NH mice, the H line exhibited (i) lower basal locomotor activity, (ii) sleep fragmentation, shift towards lighter sleep stages, and facilitation of REM sleep reflected by increased amounts and decreased latency, (iii) larger response to the REM sleep promoting effect of muscarinic receptor stimulation (by arecoline). In contrast, H and NH mice were equally responsive to the REM sleep inhibitory effect of 5-HT 1A receptor stimulation (by 8-OH-DPAT). In addition, a deficiency in delta power enhancement after sleep deprivation was observed in the H group, and acute immobilization stress in this group failed to elicit a REM sleep rebound and was associated with a long-lasting raise in serum corticosterone levels. These results further validate H mice as a depression model and suggest they might be of particular interest for investigating the neurobiological mechanisms and possibly genetic substrates underlying sleep alterations associated with depression.

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“…24 -30 One study found that depressed patients sweat more at night than control subjects but only during the 20 minutes just before the onset of rapid eye movement sleep. 31 Sweating increases with increasing depths of nonrapid eye movement sleep. It is reduced during rapid eye movement sleep in the absence of emotionally charged dreams despite increases in brain glucose metabolism, increased temperature in many parts of the brain, increase skin sympathetic activity, and increased heart rate.…”

Section: How Have Night Sweats Been Defined?mentioning

confidence: 99%

“…It is reduced during rapid eye movement sleep in the absence of emotionally charged dreams despite increases in brain glucose metabolism, increased temperature in many parts of the brain, increase skin sympathetic activity, and increased heart rate. [31][32][33][34][35][36] Nonthermoregulatory regulation of sweating could also be involved in some people who report night sweats. Sweating can result from a wide variety of medications that affect the sympathetic nervous system, the thermoregulatory center, or the sweat glands; and from sleep stage disturbances, autonomic nervous system disorders, medullary and spinal cord abnormalities, reductions in serum osmolality or abnormalities of osmoreceptor function, hypercapnia, and direct sweat gland stimulation by pressure, heat, trauma, or toxins.…”

Section: How Have Night Sweats Been Defined?mentioning

confidence: 99%

Night Sweats: A Systematic Review of the Literature

Mold

Holtzclaw

McCarthy

2012

The Journal of the American Board of Family Medicine

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Background: Much of primary care involves helping patients manage symptoms. Nighttime sweating is a symptom linked to menopause, malignancies, autoimmune diseases, and infections. However, in primary care settings, night sweats are commonly reported by persons without these conditions.Methods: We conducted a literature review, focusing on questions about definition, mechanisms, incidence/prevalence, measurement, clinical causes, evaluation, treatment, and prognosis. We limited our search to English language studies of adult humans published since 1966. Because studies of estrogen and androgen deficiency states had been reviewed by others, we excluded them. Search criteria were developed for each question. Publications meeting criteria were reviewed by the first 2 authors and consensus was reached through discussion.Results: Prevalence estimates ranged from 10% among older primary care patients to 60% among women on an obstetrics inpatient unit. Life expectancy of primary care patients reporting night sweats did not appear to be reduced. Although many clinical causes have been suggested, most are not well supported. Algorithmic approaches to evaluation are not evidence-based. Alpha adrenergic blockers may reduce night sweats in patients taking serotonin reuptake inhibitors. Thalidomide and thioridazine may benefit some terminal cancer patients with night sweats.

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Nocturnal sweating and temperature in depression

Abstract: The nocturnal sweating rates in the depressed patients suggest that impaired sweating is not the cause of the high nocturnal temperature commonly found in depressed patients.

Cited by 61 publications

References 32 publications

Circadian dysregulation of clock genes: clues to rapid treatments in major depressive disorder

Circadian dysregulation of clock genes: clues to rapid treatments in major depressive disorder

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Night Sweats: A Systematic Review of the Literature

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