![]() ![]() ![]() Arch Gen Psychiatry 42(11):1098–1104Ĭonus P, Ward J, Lucas N, Cotton S, Yung AR, Berk M, McGorry PD (2010) Characterisation of the prodrome to a first episode of psychotic mania: results of a retrospective study. Biol Psychiatry 39(6):411–418Ĭasper RC, Redmond DE Jr, Katz MM, Schaffer CB, Davis JM, Koslow SH (1985) Somatic symptoms in primary affective disorder: presence and relationship to the classification of depression. Bipolar Disord 9(7):671–678īreslau N, Roth T, Rosenthal L, Andreski P (1996) Sleep disturbance and psychiatric disorders: a longitudinal epidemiological study of young adults. Neurosci Lett 368(2):123–126īerk M, Conus P, Lucas N, Hallam K, Malhi GS, Dodd S, Yatham LN, Yung A, McGorry P (2007) Setting the stage: from prodrome to treatment resistance in bipolar disorder. Neurosci Lett 355(1–2):37–40īenedetti F, Serretti A, Colombo C, Lorenzi C, Tubazio V, Smeraldi B (2004b) A glycogen synthase kinase 3-beta promoter gene single nucleotide polymorphism is associated with age at onset and response to total sleep deprivation in bipolar depression. J Affect Disord 116(3):170–175īenedetti F, Bernasconi A, Lorenzi C, Pontiggia A, Serretti A, Colombo C, Smeraldi E (2004a) A single nucleotide polymorphism in glycogen synthase kinase 3-beta promoter gene influences onset of illness in patients affected by bipolar disorder. ![]() Bipolar Disord 5(3):169–179īauer M, Glenn T, Grof P, Rasgon N, Alda M, Marsh W, Sagduyu K, Schmid R, Adli M, Whybrow PC (2009) Comparison of sleep/wake parameters for self-monitoring bipolar disorder. Sleep 26(7):902–906īaldessarini RJ, Tondo L, Hennen J (2003) Treatment-latency and previous episodes: relationships to pretreatment morbidity and response to maintenance treatment in bipolar I and II disorders. It may also tentatively suggest that sleep may be altered prior to the first manic episode in subjects at high risk.Īnnie V, Charles MM (2003) Actigraphy in the assessment of insomnia. This study provides further evidence that sleep and circadian timing are profoundly altered in patients with bipolar disorder. In particular, both groups described recurring insomnia and hypersomnia, sensitivity to shifts in circadian rhythm, difficulties awakening and prolonged sleep latency. The results of participants with an elevated risk of developing the disorder had subjective and lifetime characteristics that were largely analogous to those of patients with manifest bipolar disorder. The subjective and lifetime sleep characteristics of bipolar patients differed significantly from healthy controls. Patients with bipolar disorder had longer sleep latency and duration compared with healthy controls as determined by actigraphy. In addition, participants wore an actimeter for six nights. Twenty-two patients with bipolar I and II disorder, nine persons with an elevated risk of developing the disorder and 28 healthy controls were evaluated with a structured interview to characterize subjective and lifetime sleeping habits. This study aims to explore the objective, subjective and lifetime sleep characteristics of patients with manifest bipolar disorder and persons with an elevated risk of developing the disease. A deficit in sleep regulation may be a vulnerability factor with aetiological relevance in the development of the disease. There is accumulating evidence that sleep is also altered in euthymic states. Sleep is highly altered during affective episodes in patients with bipolar disorder.
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