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Chronobiological Therapy for Mood Disorders

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Chronobiological Therapy for Mood Disorders THEMED ARTICLE y Mood disorders Perspective For reprint orders, please contact [email protected] Chronobiological therapy for mood disorders Expert Rev. Neurother. 11(7), 961–970 (2011) Sara Dallaspezia†1 and Alteration of the sleep–wake cycle and of the sleep structure are core symptoms of a major Francesco Benedetti1 depressive episode, and occur both in course of bipolar disorder and of major depressive disorder. Many other circadian rhythms, such as the daily profiles of body temperature, cortisol, thyrotropin, 1Department of Clinical Neurosciences, Scientific Institute and University prolactin, growth hormone, melatonin and excretion of various metabolites in the urine, are Vita-Salute San Raffaele, Milano, Italy disrupted in depressed patients, both unipolar and bipolar individuals. These disrupted rhythms †Author for correspondence: seem to return to normality with patient recovery. Research on circadian rhythms and sleep Istituto Scientifico Universitario have led to the definition of nonpharmacological therapies of mood disorder that can be used Ospedale San Raffaele, Dipartimento di Neuroscienze Cliniche, San Raffaele in everyday practice. These strategies, named chronotherapeutics, are based on controlled Turro, Via Stamira d’Ancona 20, exposures to environmental stimuli that act on biological rhythms, and demonstrate good 20127 Milano, Italy efficacy in the treatment of illness episodes. They include manipulations of the sleep–wake Tel: +39 226 433 156 Fax: +39 226 433 265 rhythm (such as partial and total sleep deprivation, and sleep phase advance) and of the exposure [email protected] to the light–dark cycle (light therapy and dark therapy). In recent years, an increasing literature about the safety and efficacy of chronobiological treatments in everyday psychiatric settings has supported the inclusion of these techniques among the first-line antidepressant strategies for patients affected by mood disorders. KEYWOrdS: bipolar disorder • chronotherapeutics • depression • light therapy • mood disorder • sleep deprivation Alteration of the sleep–wake cycle and of the body temperature, cortisol, thyrotropin, prolac- sleep structure are core symptoms of a major tin, growth hormone, melatonin and excretion depressive episode, and occur in both of the of various metabolites in urine [5,6], and most of courses of bipolar disorder and of major depres- them seem to normalize with patient recovery. sive disorder. Approximately 90% of depressed Polymorphisms in molecular clock genes, patients complain of poor quality of sleep, with which play a pivotal role in maintaining circa- sleep disturbances appearing weeks before the dian rhythms, show not only an association with recurrence of mood episodes [1] and worsening affective disorder, but also seem to influence in the days preceding the recurrence [2]. Sleep in symptomatology characteristics and response major depression is characterized by disturbances to treatment [7]. Moreover, some drugs used to of sleep continuity, a reduction of slow-wave treat mood disorders interact with clock genes. sleep and a disinhibition of rapid eye movement Chronic treatment with fluoxetine increases (REM) sleep, involving a shortening of REM expression of CLOCK and Bmal1 in the hippo- latency and an increase of REM density [3]. campus [8], valproate alters the expression of In bipolar disorder, the relationship between several circadian genes in the amigdala [9], and sleep disturbances has been documented for both lithium salts inhibit glycogen synthase kinase-3b depressive and manic episodes, with features that expression [10] and lengthen the circadian period are peculiar to the episode polarity. Most fac- in several animals, including humans [11]. tors known to precipitate a manic recurrence of Circadian rhythm and sleep research have led illness could be related to the genesis of mania to the definition of nonpharmacological therapies through a marked reduction in sleep. Moreover, a of mood disorder that can be used in everyday decreased need for sleep is a fundamental marker practice [12]. These clinical interventions, named of the manic state [4]. chronotherapeutics, are based on controlled expo- Many other circadian rhythms have been sures to environmental stimuli that act on bio- found to be disrupted in depressed patients, logical rhythms. The use of psychiatric chrono- both unipolar and bipolar individuals. These therapeutic techniques in everyday psychiatric disrupted rhythms include the daily profiles of work is a rather new achievement and is almost www.expert-reviews.com 10.1586/ERN.11.61 © 2011 Expert Reviews Ltd ISSN 1473-7175 961 Perspective Dallaspezia & Benedetti exclusive to the treatment of mood disorders, with antidepressant Chronotherapeutic interventions, such as manipulations of the effects of different chronotherapeutic approaches described in all sleep–wake rhythms and of the light–dark cycle, can certainly depressive conditions. Mainly developed in European countries trigger mania when patients are in euthymic conditions. When over the last five decades [13], these techniques evolved from both repeated total SD (three cycles in a week) was administered to the empirical observation of impressive clinical changes following 206 patients affected by bipolar disorder type I as an antidepres- random exposure to environmental stimuli (e.g., immediate mood sant intervention during a major depressive episode, a 4.85% improvement in sleep-deprived depressed patients), and from (4.54% if patients were receiving lithium salts) switch rate into neuro biological models of behavior [14]. They include manipula- mania was observed. This switch rate is similar to those observed tions of the sleep–wake rhythm (e.g., partial and total sleep depri- with SSRIs and placebo, lower than those reported with tryci- vation [SD] and sleep phase advance [SPA]) and of the exposure clic antidepressants [26], and much lower than those reported to the light–dark cycle (light therapy [LT] and dark therapy) [15]. (10–29%) in bipolar patients receiving antidepressant drugs as maintenance treatment [27,28]. Moreover, the severity of mania Sleep deprivation was rather mild or moderate in the majority of patients, and Clinical aspects less than half needed to combine antipsychotic medication with The clinical effects of SD in thousands of depressed patients world- mood stabilizers to return to euthymia [29]. These low rates were wide have been reported in more than 60 studies. The common confirmed when LT was combined with repeated total SD, thus effect is a rapid (within 24–48-h) reversal of depressive symptoms. confirming the favorable side-effect profile of chonotheraputic Positive antidepressant effects of SD have been reported in dif- treatment in this respect [24]. Hence, the obvious benefit of over- ferent depressive conditions, but better effects have been shown in coming the need for unwieldy treatment of bipolar depression endogenous major depression compared with secondary depres- with antidepressant drugs, which leads to the quandary of choos- sion [16], and in the treatment of bipolar disorder compared ing between a high risk of relapse in the absence of maintenance with unipolar disorder [17]. The reported response rates to SD treatment with antidepressants, and a risk of development of are similar to those observed with antidepressant drugs, ranging treatment-emergent mania in roughly a quarter of bipolar patients from 50 to 80% of treated patients. The response to SD has been administered antidepressant drugs [28,30]. shown to be influenced by the same functional polymorphisms It is still unclear how many hours of SD are needed to achieve that influence the efficacy of antidepressant drugs, thus suggest- its full antidepressant effect. The typical antidepressant SD is ing common mechanisms of action [18]. In particular, significant called ‘total’ SD because wake is prolonged throughout the night associations have been observed with gene variants affecting the of treatment. It begins with the extension of daytime wake into promoter of the serotonin transporter [19], the serotonin recep- the night and lasts about 36 h until the evening of the day after. tor 2A [20], the catechol-O-methyltransferase [21] and the glycogen Researchers still argue whether a short nap can stop the powerful synthase kinase-3b promoter [22]. effect of SD. Considering the available data, it could be supposed Clinical predictors of response to SD also include the presence that the interaction between naps and lack of response may be of diurnal mood fluctuation and melancholic features. Moreover, linked with yet undefined individual characteristics, and that a brain imaging studies demonstrated that depressed patients who full antidepressant response to SD can well occur independent had a favorable clinical response to SD had higher relative meta- of possible napping. Even if most of the studies showed a mood bolic rates in the ventral anterior cingulate, medial prefrontal cor- worsening, not only after napping [31], but also after subjectively tex and posterior subcallosal cortex at baseline than either normal unrecognized microsleeps [32], others did not, or even reported volunteers or depressed patients who did not respond to SD [23]. an improvement in mood after short naps [33]. Moreover, some While antidepressant drugs show long response latencies, researchers have suggested a circadian variation of propensity to response to SD becomes clinically relevant in a matter of hours relapse into
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