Sleep Disorders and Sleep Deprivation: An Unmet Public

Sleep Disorders and Sleep Deprivation: An Unmet Public Health Problem
http://www.nap.edu/catalog/11617.html
80 SLEEP DISORDERS AND SLEEP DEPRIVATION
Etiology and Risk Factors
The etiological basis for the comorbidity of sleep disorders and psychiatric
disorders is not well understood. Most potential mechanisms for sleep
changes in psychiatric disorders deal specifically with insomnia and depression.
Possible mechanisms include neurotransmitter imbalance (cholinergicaminergic
imbalance), circadian phase advance, and hypothalamic-pituitaryadrenal
axis dysregulation (Benca, 2005a). Recent evidence implicating
regions of the frontal lobe has emerged from imaging studies using positron
emission tomography. As they progress from waking to non-REM (NREM)
sleep, depressed subjects have smaller decreases in relative metabolism in
regions of the frontal, parietal, and temporal cortex when compared to
individuals who are healthy (Nofzinger et al., 2005). Normally, the transition
from waking to NREM sleep is associated with decreases in these
frontal lobe regions. What appears to occur with depression is that the
decrease is less pronounced. Another finding of the study is that during
both waking and NREM sleep, depressed patients show hypermetabolism
in the brain’s emotional pathways, including the amygdala, anterior cingulate
cortex, and related structures. Because the amygdala also plays a role in
sleep regulation (Jones, 2005), this finding suggests that sleep and mood
disorders may be manifestations of dysregulation in overlapping neurocircuits.
The authors hypothesize that increased metabolism in emotional
pathways with depression may increase emotional arousal and thereby
adversely affect sleep (Nofzinger et al., 2005).
Treatment
Comorbid psychiatric and sleep disorders are treated by a combination
of medication and/or psychotherapy (Krahn, 2005; Benca, 2005a). A major
problem is underdiagnosis and undertreatment of one or both of the
comorbid disorders. One of the disorders may be missed or may be mistakenly
dismissed as a condition that will recede once the other is treated. In
the case of depression, for example, sleep abnormalities may continue once
the depression episode has remitted (Fava, 2004). If untreated, residual
insomnia is a risk factor for depression recurrence (Reynolds et al., 1997;
Ohayon and Roth, 2003). Further, because sleep and psychiatric disorders,
by themselves, are disabling, the treatment of the comorbidity may reduce
needless disability. Insomnia, for example, worsens outcomes in depression,
schizophrenia, and alcohol dependence. Treatment of both conditions
can improve a patient’s functioning and possibly improve adherence with
therapy (Vincent and Hameed, 2003). Another concern is that medication
for one disorder might exacerbate the other (e.g., prescription of sedating
antidepressants for patients with hypersomnolence). The choice of medica-
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