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The UAB-TBIMS provides this website as an auxiliary resource for primary care of patients with TBI.The contents of this website were developed under a grant from the National Institute on Disability, Independent Living, and Rehabilitation Research (NIDILRR grant number 90DPTB0029). NIDILRR is a Center within the Administration for Community Living (ACL), Department of Health and Human Services (HHS). The contents of this website do not necessarily represent the policy of NIDILRR, ACL, HHS, and you should not assume endorsement by the Federal Government.
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Reasons for Sleep Disturbances after Traumatic Brain Injury

Sleep disturbance may disrupt recovery via obstructing neuroplasticity, compromising vascular functioning, and/or compromising metabolic functioning. Sleep disruption increases oxidative stress and neuroinflammation, resulting in neurodegeneration. Disrupted sleep decreases synaptogenesis and memory consolidation. Sleep deprivation also dramatically reduces ATP production, prolonging inflammation and resulting in cell death. It may also result in an increased volume of neurofibrillary tangles and tauopathies. 3

There are numerous pathways which have been proposed to explain the relationship between sleep disturbance and TBI. Sleep disturbance may result from damage to sleep-wake regulating centers.4 Direct cortical damage resulting from TBI may be responsible for numerous forms of sleep disturbance. For example, hypersomnia may result from lesions in the reticular activating system, posterior hypothalamus, basal forebrain, and/or thalamus. Sleep disordered breathing may result from damage to the medullary respiratory center. Sleep movement disorders may arise from damage to the lenticulostriate region. Excessive sleepiness may also result from extensive loss of orexin secreting neurons in the hypothalamus following TBI. This neurotransmitter is a key sleep regulator and reduced levels can lead to excessive sleepiness.1

There are also potential secondary contributors to sleep dysfunction following TBI. These include physical and psychosocial factors such as pain, depression, anxiety, medicolegal issues, neuroendocrine disturbance, post-traumatic epilepsy, trauma-induced brain damage, genetic predisposition, analgesic pharmacotherapy, anticonvulsive drugs, and neuropsychological deficits.4,5 Fatigue may also result from impaired attention and processing speed, requiring greater cognitive effort to complete tasks.4

Mazwi, N., Fusco, H., & R. Zafonte (2015). Sleep in traumatic brain injury. In Handbook of Clinical Neurology, Vol. 128. J. Grafman and A.M. Salazar, Eds. Elsevier.

Singh, K., Morse, A., Tkachenko, N., & S. Kothare (2016). Sleep disorders associated with traumatic brain injury – A review. Pediatric Neurology, 60, 30-36.

Lucke-Wold, B., Smith, K., Nguyen, L., Turner, R., et al. (2015). Sleep disruption and the sequelae associated with traumatic brain injury. Neuroscience and Biobehavioral Reviews, 55, 68-77.

Ponsford, J., & K. Sinclair (2014). Sleep and fatigue following traumatic brain injury. Psychiatric Clinics of North America, 37, 77-89.

Baumann, C. (2016). Sleep and traumatic brain injury.   Sleep Medicine Clinics, 11, 19-23.

Larson, E., & F. Zollman (2010). The effect of sleep medications on cognitive recovery from traumatic brain injury. Journal of Head Trauma Rehabilitation, 25, 1, 61-67.

800-UAB-MIST - 24-hour hotline for physicians to consult with a UAB specialist.


MD Learning Channel
Ask a Question
Feedback & Comments
PCPs & ADA Compliance


The UAB-TBIMS provides this website as an auxiliary resource for primary care of patients with TBI.The contents of this website were developed under a grant from the National Institute on Disability, Independent Living, and Rehabilitation Research (NIDILRR grant number 90DPTB0029). NIDILRR is a Center within the Administration for Community Living (ACL), Department of Health and Human Services (HHS). The contents of this website do not necessarily represent the policy of NIDILRR, ACL, HHS, and you should not assume endorsement by the Federal Government.
NIDILRR