Sleep Disorders in Patients with Traumatic Brain Injury: A Review

• Published in: CNS drugs 2011-03, Vol.25 (3), p.175-185
• Main Authors: Castriotta, Richard J., Murthy, Jayasimha N.
• Format: Article
• Language: English
• Subjects: Adult and adolescent clinical studies; Biological and medical sciences; Brain; Brain Injuries - complications; Care and treatment; Complications and side effects; Diagnosis; Disorders of higher nervous function. Focal brain diseases. Central vestibular syndrome and deafness. Brain stem syndromes; Dosage and administration; Epidemiology; Head injuries; Humans; Injuries; Injuries of the nervous system and the skull. Diseases due to physical agents; Medical sciences; Medicine & Public Health; Memory; Nervous system (semeiology, syndromes); Neurology; Neuropharmacology; Neurosciences; Organic mental disorders. Neuropsychology; Pharmacology. Drug treatments; Pharmacotherapy; Polysomnography; Psychiatry; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Psychopharmacology; Questionnaires; Review Article; Risk factors; Sleep apnea; Sleep disorders; Sleep Wake Disorders - diagnosis; Sleep Wake Disorders - etiology; Sleep Wake Disorders - physiopathology; Stimulants; Trauma; Traumas. Diseases due to physical agents; Traumatic brain injury
• ISSN: 1172-7047; 1179-1934
• DOI: 10.2165/11584870-000000000-00000

Traumatic brain injury (TBI) is a global problem and causes long-term disability in millions of individuals. This is a major problem for both military and civilian-related populations. The prevalence of sleep disorders in individuals with TBI is very high, yet mostly unrecognized. Approximately 46% of all chronic TBI patients have sleep disorders, which require nocturnal polysomnography and the Multiple Sleep Latency Test for diagnosis. These disorders include sleep apnoea (23% of all TBI patients), post-traumatic hypersomnia (11%), narcolepsy (6%) and periodic limb movements (7%). Over half of all TBI patients will have insomnia complaints, most often with less severe injury and after personal assault, and half of these may be related to a circadian rhythm disorder. Hypothalamic injury with decreased levels of wake-promoting neurotransmitters such as hypocretin (orexin) and histamine may be involved in the pathophysiology of excessive sleepiness associated with TBI. These sleep disorders result in additional neurocognitive deficits and functional impairment, which might be attributed to the original brain injury itself and thus be left without specific treatment. Most standard treatment regimens of sleep disorders appear to be effective in these patients, including continuous positive airway pressure for sleep apnoea, pramipexole for periodic limb movements and cognitive behavioural therapy for insomnia. The role of wake-promoting agents and CNS stimulants for TBI-associated narcolepsy, post-traumatic hypersomnia and excessive daytime sleepiness requires further study with larger numbers of patients to determine effectiveness and benefit in this population. Future research with multiple collaborating centres should attempt to delineate the pathophysiology of TBI-associated sleep disorders, including CNS-derived hypersomnia and circadian rhythm disturbances, and determine definitive, effective treatment for associated sleep disorders.