Most episodes of bipolar patients are cross-sectionally associated with sleep rhythm abnormalities. Insomnia and hypersomnia are both found in bipolar depression and mania. Mania is strongly associated with decreased need for sleep. Changes in sleep–wake cycle, and in sleep structure can be occurred in course of bipolar disorder (BD). The short sleep duration is associated with more severe symptomatology, while both short and long sleep duration are associated with poorer function and quality of life in BD. Episodes of BD have been associated with sleep polysomnographic changes. The most common finding is abnormalities of rapid eye movement (REM) sleep typically shorter latency and increased density in both manic and depressive episodes. Previous studies showed prospective evidence of a complex association between sleep length and mood change in BD. Reduced sleep is recognized as a part of diagnostic criteria as well as a trigger of manic episodes. Episodes of BD can be precipitated by zeitgeber challenges, such as seasonal change and time-zone travel. Sleep disturbance is regarded as the most common prodromal symptoms of mania and bipolar depression, and often precedes deterioration in clinical state and worsens further during an episode. Manipulation of sleep (sleep deprivation) is also one of the most effective antidepressant. Indeed abnormalities of sleep rhythms proposed to endophenotypes or marker of bipolar disorders. The sleep may have a particular importance for emotional processing and emotion regulation. The sleep disturbance considerably increases negative mood, irritability, and affective volatility. The investigations show evidence for circadian and the same brain regions subserve sleep dysfunction as a causal pathway to BD. Sleep functions and neurotransmitters are implicated in mood disorder. Symptoms of BD have been associated with polymorphisms in circadian genes in animal and human studies. Effective treatments for acute episodes moderate circadian parameters, while relapse can be precipitated by zeitgeber challenges, such as light manipula¬tion. Related data suggest that ‘circadian instability’ may act as a trait-like vulnerability to BD. At least two neurotransmitter systems (dopaminergic and serotonergic systems) are crucial in the link between sleep rhythms and emotion. Dopaminergic system regulates sleep-wake and mood disorders while serotonergic pathways are involved in sleep function. It is particularly notable that an independent literature argues for dopaminergic and serotonergic systems as critical pathways in BD. Apart from the immediate clinical implications of poor sleep, evidence also suggests that biological rhythm disturbance is etiologically involved in BD. Besides prospective data linking sleep to mood in BD, sleep changes precede episodes (especially mania) and correlate with symptom severity. Most particularly, manipulation of sleep improves bipolar depression and can induce mania in patients. This conclusion is consistent with present clinical practice, in which sleep is a fundamental relapse prevention strategy. Stabilization of daily rhythms is accepted as therapeutic in consensus treatment guidelines. There is consensus that biological rhythms have a crucial role in the emotion dysregulation in BD. Clinical studies also suggest that disturbed sleep reduces quality of life in BD. Therefore evidence suggests that outcomes in BD can be improved by dealing with sleep difficulties across phases of the disorder. Studies on circadian rhythms and sleep have led searching nonpharmacological therapies of mood disorders that can be used in daily practice. These therapies (chronotherapeutics) demonstrate good efficacy in the treatment, and are based on controlled exposures to environmental stimuli that act on biological rhythms. Chronotherapeutics include manipulations of the sleep–wake rhythm such as partial and total sleep deprivation, and sleep phase advance as well as manipulations of the exposure to the light–dark cycle such as light therapy and dark therapy. Sleep deprivation is a same-day powerful treatment for bipolar and unipolar depression. Using combinations of zeitgeber manipulation and pharmacotherapy is the most common and the most resistant manifestation in treatments of BD. Maintenance of the therapeutic effect beyond the next sleep phase is a target of current research. Combined sleep deprivation, sleep phase advance, and timed light are suggested as an effective adjunctive intervention for bipolar depression in a recent study. Stabilization of sleep rhythm is a core component in most adjunctive psychosocial treatments for BD, including cognitive behavioral therapy. Improvement of sleep quality is an important compo¬nent of rhythm stabilization, and has functional benefits in its own right. Management of the sleep-wake cycle is a frequently reported well-being strategy amongst people with BD. Therefore; chronotherapeutic interventions are an important topic for further research. Future studies into these interventions should seek to determine moderators (e.g., light sensitivity, severity and diagnosis, temperament, gender) and media¬tors (e.g., light-dark cycle exposure, sleep quality, sleep structure, circadian rhythm, and daytime arousal) of treatment outcome in BD. In conclusion; sleep disturbances are central to the pathophysiology of BD. They are not only a key symptom of bipolar patients, but also the earliest indicator of new mood episode. Continuing research in this area is the priority for future research between sleep and BD.