Table 5.
Common Sleep and Circadian Disorders in TBI
| Disorder | General prevalence | Prevalence in TBI4 | Description | Treatments |
|---|---|---|---|---|
| Insomnia | 10–15% | 29% | Difficulty initiating or maintaining sleep, generally characterized as ≥ 30 min sleep latency and/or ≥ 30 min wake after sleep onset, including early morning awakening, with daytime impairment, occurring ≥ 3 nights per week for ≥ 3 months. | Cognitive behavioral treatment for insomnia (CBTI) is considered first-line treatment for primary and comorbid insomnia. Pharmacotherapy and benzodiazepines in particular should be avoided in TBI due to risks of cognitive side effects. |
| Sleep apnea | (Age 30–60) Men: 24% Women: 9% |
25% | Sleep-related breathing disorder characterized by repeated breathing pauses during sleep. Majority is obstructive in nature (i.e., obstructive sleep apnea [OSA]) and caused by partial or total closure of the upper airway. OSA is associated with oxyhemoglobin desaturation and sleep fragmentation due to cortical arousals and increased effort to breathe. Less common is central sleep apnea, characterized by transient reduction in respiratory effort. Sleep apnea can also be mixed. | For moderate or severe OSA, positive airway pressure (PAP) therapies are recommended first-line treatment. PAP uses positive pressure as a pneumatic splint, to gently inflate the airway. Mandibular advancement dental devices can also be effective, particularly in mild-moderate disease. When indicated, weight loss is a cornerstone recommendation. A range of tertiary treatment options exist. |
| Hypersomnias | Narcolepsy: 0.05% Idiopathic hypersomnia: 0.002–0.005% |
Post-traumatic narcolepsy: 4% Post-traumatic hypersomnia: 28% |
Neurologic disorder characterized by excessive daytime somnolence and rapid eye movement (REM) intrusion during wakefulness, as well as cataplexy, sleep paralysis, and hypnogogic hallucinations. Trauma to hypocretin-producing neurons has been shown to induce cataplexy. Hypersomnia that is not due to specific central nervous system abnormality. Trauma can cause non-specific damage to wake producing regions of the brain. |
Treatment is based on symptoms clusters and differential response. Wake promoting agents are classified as either amphetamines or non-amphetamine (e.g., modafinil/ armodafinil). Sodium oxybate is used for narcolepsy with and without cataplexy. Noradrenergic antidepressants such as venlafaxine and duloxetine can also help reduce cataplexy. |
| Periodic limb movement disorder | 3.9% | 19% | Neurologic disorder characterized by involuntary twitching or jerking of limbs during sleep, most often including legs. Frequently overlaps with restless legs syndrome. | Treatment options include benzodiazepines, dopaminergic agents or neuroleptics, or less frequently, anticonvulsants or GABA agonists. When comorbid with OSA, PAP can eliminate PLMs. |
| Circadian rhythm sleep disorders | Unknown | Unknown | Trauma to the circadian pacemaker in the suprachiasmatic nucleus (SCN) of the anterior hypothalamus can disrupt “process C.” Experimental lesions of the SCN have resulted in a complete loss of the circadian rhythm and randomly distributed sleep-wake periods during the 24-hour cycle. | Treatment to modify circadian rhythm includes timed bright light therapy and melatonin. Light therapy is the most potent circadian modulator. A regimented sleep-wake schedule is vital. |
TBI, traumatic brain injury; PLM, periodic limb movements.