Sleep-wake disturbances following traumatic brain injury (TBI) are increasingly recognized as a serious consequence following injury and as a barrier to recovery. Injury-induced sleep-wake disturbances can persist for years, often impairing quality of life. Recently, there has been a nearly exponential increase in the number of primary research articles published on the pathophysiology and mechanisms underlying sleep-wake disturbances after TBI, both in animal models and in humans, including in the pediatric population. In this review, we summarize over 200 articles on the topic, most of which were identified objectively using reproducible online search terms in PubMed. Although these studies differ in terms of methodology and detailed outcomes; overall, recent research describes a common phenotype of excessive daytime sleepiness, nighttime sleep fragmentation, insomnia, and electroencephalography spectral changes after TBI. Given the heterogeneity of the human disease phenotype, rigorous translation of animal models to the human condition is critical to our understanding of the mechanisms and of the temporal course of sleep-wake disturbances after injury. Arguably, this is most effectively accomplished when animal and human studies are performed by the same or collaborating research programs. Given the number of symptoms associated with TBI that are intimately related to, or directly stem from sleep dysfunction, sleep-wake disorders represent an important area in which mechanistic-based therapies may substantially impact recovery after TBI.

/pdf/sleep-wake-disturbances-after-traumatic-brain-injury-2r6l9tbx1d.pdf

Sleep-Wake Disturbances After Traumatic Brain Injury: Synthesis of Human and Animal Studies.

Sleep in the United States Military.

Key Points Question Is traumatic brain injury associated with long-term risk of cardiometabolic, neurological, or psychiatric comorbidities? Findings In this cohort study including 4351 patients each with mild or moderate to severe TBI and 4351 frequency-matched unexposed patients without TBI, the rates of cardiovascular and endocrine comorbidities after TBI were significantly higher in patients with mild or moderate to severe TBI compared with patients without TBI. The risk of post-TBI comorbidities was higher in all age groups compared with age-matched unexposed patients, particularly in patients younger than 40 years, and post-TBI comorbidities were associated with higher mortality over a 10-year follow-up period. Meaning These findings suggest that patients with TBI in all age groups may benefit from a proactive targeted screening program for chronic multisystem diseases, particularly cardiometabolic diseases, after injury.

https://jamanetwork.com/journals/jamanetworkopen/articlepdf/2791599/izzy_2022_oi_220285_1650462132.01647.pdf

Association of Traumatic Brain Injury With the Risk of Developing Chronic Cardiovascular, Endocrine, Neurological, and Psychiatric Disorders

Traumatic brain injury (TBI) is a major public health concern in the USA and worldwide. Sleep disruption and headaches are two of the most common problems reported by patients after TBI. In this manuscript, we review the current knowledge regarding the relation between post-traumatic sleep disruption and headaches. We also describe the role of the glymphatic system as a potential link between TBI, sleep, and headaches. Recent studies show a reciprocal relation between post-traumatic sleep disruption and headaches: patients with sleep disruption after TBI report more headaches, and post-traumatic headaches are a risk factor for developing disrupted sleep. Despite this clinical association, the exact mechanisms linking post-traumatic sleep disruption and headaches are not well understood. The glymphatic pathway, a newly described brain–wide network of perivascular spaces that supports the clearance of interstitial solutes and wastes from the brain, is active primarily during sleep, and becomes dysfunctional after TBI. We propose a model where changes in glymphatic function caused by TBI and post-traumatic sleep disruption may impair the clearance of neuropeptides involved in the pathogenesis of post-traumatic headaches, such as CGRP. The relation between TBI, post-traumatic sleep disruption, and post-traumatic headaches, although well documented in the literature, remains poorly understood. Dysfunction of the glymphatic system caused by TBI offers a novel and exiting explanation to this clinically observed phenomenon. The proposed model, although theoretical, could provide important mechanistic insights to the TBI-sleep-headache association.

Linking Traumatic Brain Injury, Sleep Disruption and Post-Traumatic Headache: a Potential Role for Glymphatic Pathway Dysfunction.

Davin K. Quinn, M.D., Andrew R. Mayer, Ph.D., Christina L. Master, M.D., and Jesse R. Fann, M.D., M.P.H. From the Department of Psychiatry and Behavioral Sciences, the MIND Research Network, and the Department of Psychology, University of New Mexico, Albuquerque; the Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, and the Division of Orthopedics and Sports Medicine, Children’s Hospital of Philadelphia, Philadelphia; and the Departments of Psychiatry and Behavioral Sciences and of Physical Medicine and Rehabilitation, University of Washington, Seattle.

Prolonged Postconcussive Symptoms.

https://link.springer.com/content/pdf/10.1007%2Fs13311-016-0429-3.pdf

Sleep, Sleep Disorders, and Mild Traumatic Brain Injury. What We Know and What We Need to Know: Findings from a National Working Group

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Sleep, Sleep Disorders, and Mild Traumatic Brain Injury. What We Know and What We Need to Know: Findings from a National Working Group