Sleep Disorders in Traumatic Brain Injury

Management of Sleep Disorders

The treatment of TBI-related sleep disorders is the same as for uninjured patients. Continuous positive airway pressure (CPAP) has consistently been shown to be an effective intervention for OSA, and is recommended as first-line therapy. Patients with TBI, particularly those with concomitant insomnia or severe cognitive impairments, present additional challenges.

Castriotta and colleagues^[34] evaluated the impact of therapy for sleep disorders in 57 patients ≥ 3 months post-TBI. They found that 39% had abnormal sleep studies, including 23% with OSA, 3% with PTH, 5% with narcolepsy, and 7% with PLMD. Excessive daytime somnolence was confirmed with MSLT in 21%. The investigators found that, although CPAP effectively ablated obstructive events, it did not improve objective measures of sleepiness. Further investigation for centrally mediated somnolence following head injuries is warranted. Although patients with TBI may have additional causes of persistent sleepiness, treatment of SDB may not resolve objective measures of sleepiness in the patients who have OSA.^[35] Still, because of the additional benefits of CPAP, and the adverse impact that sleep-disordered breathing has on both health and quality of life, CPAP is recommended for most patients with symptomatic OSA.

Because 38% of patients who complain of insomnia may actually have CRSD, an accurate diagnosis may dramatically alter management and outcomes. Melatonin, cognitive behavioral therapy, regimented sleep-wake cycle manipulations, and light-box therapy may be more effective than hypnotics or sedative medications in those with CRSDs.^[19] Shekleton and colleagues^[24] found that patients with TBI had significantly lower evening melatonin production than healthy controls, which may lead to disruption of the circadian regulation of melatonin synthesis and contribute to disruptions in sleep continuity in this population. These investigators concluded that TBI may damage neurologic structures that regulate the sleep-wake cycle, including melatonin synthesis, which may play a role in the development of CRSDs following head injuries. Suppression of melatonin secretion can disrupt sleep continuity and architecture, especially REM sleep.^{[36,37,38,39,40]}

Commonly used sleep medications and sedatives may be contraindicated in patients with TBI and poor sleep. Larson and coworkers^[9] evaluated the effects of commonly used sleep medications on cognition in patients with TBI. They caution that benzodiazepines may lead to residual cognitive impairment after discontinuation, possibly by interfering with neural plasticity and recovery. They recommend trazodone, melatonin, or the melatonin agonist ramelteon for this population.

In TBI patients with centrally mediated hypersomnia, modafinil or armodafinil may improve symptoms and quality of life. In a clinical trial of 53 patients with TBI treated with modafinil or placebo, Jha and colleagues found that modafinil was both safe and well tolerated.^[41] However, no significant improvements in subjective measures of fatigue were appreciated between the 2 groups. In contrast, Kaiser and colleagues found that compared with placebo, 100-200 mg of modafinil improved both subjective and objective measures of sleepiness in patients with TBI.^[42]

Cite this: Jacob F. Collen, Christopher J. Lettieri. Sleep Disorders in Traumatic Brain Injury - Medscape - May 24, 2011.

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