Sleep Patterns

Seasonal Sleep Patterns in Migratory Birds: A Model for Bipolar DisorderPDF icon

The migratory songbird, Zonotrichia leucophrys gambelii, shows profound seasonal changes in sleep patterns and behavior. Migratory sparrows show some similarities to patients with bipolar disorder, including a strong seasonal component, periods of dramatically reduced sleeplessness that do not appear to require recovery sleep and analogies between mania and migration; both are characterized by increased goal directed behavior, impulsivity and fragmentation of sleep across the day. In terms of sleep patterns, during the winter birds sleep over twice as much per day than they do during the long days of summer or during migratory periods in the spring or fall. Furthermore, they show striking differences between organization of sleep in the migratory and non-migratory periods, characterized by a loss of clear day-night temporal organization, fragmentation of sleep during the night and increased drowsiness/napping during the day during migration. In fact, during the migratory season, there is no time during the day when sleep propensity is greater than wake propensity, resulting in a sleep pattern similar to insomnia in humans. Given the strong association between insomnia and mood disorders, changes in sleep organization in migrating sparrows may provide clues towards understanding the mechanisms for sleep changes in psychiatric disorders, including possible seasonal influences.

Early Onset of NarcolepsyPDF icon

Narcolepsy is a sleep disorder affecting 0.03 to 0.06% of the Caucasians and Chinese populations. Symptoms commonly start during the second decade of life after the reported onset of puberty. In fact, almost 50% of patients will recall symptoms beginning before age 15 years. Childhood presentations of narcolepsy are not uncommon, but unrecognized. Recognition using the symptoms of sleepiness may be more difficulty in children, as maturational facts affect circadian rhythm and sleep wake behaviors. The purpose of this report is to describe the outcome of an effort intended to diagnose children with narcolepsy by creating a recognition profile, testing for human leukocyte antigen (HLA), multiple sleep latency test (MSLT) and CSF hypocretin level. An estimated incidence in pediatric clinics, and the characteristics of a simplified medical evaluation that we believe establish an unequivocal diagnosis of narcolepsy at an early age. The polymorphism of HCRT in early onset narcolepsy is also reported. In conclusion, the clinical presentation of childhood narcolepsy can resemble that of adult narcolepsy, despite the influence of maturation on changing sleep-wake behavior. Narcolepsy in children is often unrecognized as both symptoms of sleepiness and cataplexy are either not well elicited or understood by doctors. A program of recognition will uncover typical cases. The early onset of cataplexy, the high numbers of SOREMs, and the strong association with HLA marker comprise a diagnostic strategy that can rapidly identify children with narcolepsy and potentially reduce adverse psychosocial outcomes.

Activation of a Subpopulation of Cortical Interneurons During SleepPDF icon

The presence of large amplitude slow waves in the electroencephalogram (EEG) is a primary characteristic that distinguishes cerebral activity during sleep from that which occurs wakefulness.

Although sleep-active neurons have been identified in other brain areas, neurons that are specifically activated during slow wave sleep have not previously been described in the cerebral cortex.

We have identified a population of cells in the cortex that is activated during sleep in three mammalian species. These cortical neurons are a subset of GABAergic interneurons that express neuronal nitric oxide synthase (nNOS). Nitric oxide (NO) has been suggested to be an endogenous sleep regulatory substance. Since Fos expression in these sleep-active nNOS-immunoreactive neurons parallels changes in the intensity of slow wave activity in the electroencephalogram and these neurons are innvervated by neurotransmitter systems previously implicated in sleep/wake control, cortical nNOS-immunoreactive neurons may be part of the long-sought neurobiological substrate that underlies homeostatic sleep regulation.

Dysfunction in the activation of cortical nNOS neurons may cause alterations in sleep homeostasis and sleep disturbances, resulting in sleep that is non-restorative.