The Influence of Neuroendocrine and Sleep Disturbances on Recovery from Traumatic Brain Injury

Special Article – Brain Injury Rehabilitation

Phys Med Rehabil Int. 2017; 4(3): 1122.

The Influence of Neuroendocrine and Sleep Disturbances on Recovery from Traumatic Brain Injury

Howell SN¹, Kreber LA¹*, Ashley JG1 and Griesbach GS1,2

¹Centre for Neuro Skills, Bakersfield, CA, USA

²Department of Neurosurgery, David Geffen School of Medicine at UCLA, Los Angeles, California, USA

*Corresponding author: Lisa Kreber, Centre for Neuro Skills, Research Department, 5215 Ashe Road, Bakersfield, CA 93313, USA

Received: August 28, 2017; Accepted: September 26, 2017; Published: October 03, 2017


This article describes the relationship between sleep and neuroendocrine disorders following traumatic brain injury (TBI). There is evidence to support that sleep disorders and neuroendocrine dysfunction can negatively impact recovery and may be the underlying cause of some of the physical, cognitive and emotional symptoms experienced by patients following TBI. We will address the impact of TBI on the neuroendocrine system and sleep-wake cycles within the context of rehabilitation. Specifically, we will focus on the effects of TBI-induced neuroendocrine and sleep alterations and the influences these disorders have on rehabilitation outcomes. Findings from non-injured and injured patient populations are reviewed and support diagnosing and treating sleep disturbances and neuroendocrine dysfunction while the patient is undergoing rehabilitation. A better understanding of the interplay between neuroendocrine functioning and sleep may improve quality of life and rehabilitative outcomes after TBI.

Keywords: Traumatic Brain Injury; Rehabilitation; Outcome; Neuroendocrine Dysfunction; Sleep-Wake Disturbances


The sequelae of chronic traumatic brain injury (TBI) have long term consequences that are addressed within the post-acute rehabilitation setting. Some of these include issues with memory, attention, balance, coordination, and emotional regulation [1]. A better understanding of the underlying mechanisms responsible for these issues is likely to maximize a patient’s recovery. Both sleep and neuroendocrine disorders have been observed following TBI and have been linked to multiple factors that contribute to disability. Disturbances in sleep and neuroendocrine dysfunction have been associated with cognitive impairments including attention, memory and executive function as well as emotional regulation and fatigue [2-6].

This article will describe what is currently known about sleep and neuroendocrine function following TBI. More specifically, the effect of alterations in these systems on chronic outcome will be described. This article will also address the assessment, diagnosis and treatment of sleep and neuroendocrine disorders within the post-acute rehabilitative setting. The ability to detect and treat sleep and neuroendocrine abnormalities can impact the responsiveness to rehabilitation.

Neuroendocrine Function and TBI

Impact of TBI on the neuroendocrine system

Neuroendocrine dysfunction following TBI is not a rare phenomenon and has been investigated in both the acute and chronic phases of rehabilitation [3,7-15].

Structural damage to the neuroendocrine system may be caused by TBI induced white matter damage; thus affecting connectivity in hypothalamic and supra hypothalamic structures. Two-thirds of individuals at autopsy who did not survive their TBI were found to have structural abnormalities of the pituitary, pituitary stalk and/or hypothalamus [16,17]. On a cellular level, the somatotroph cells in the anterior pituitary, which produce growth hormone (GH), and the gondatroph cells, which produce luteinizing hormone (LH) and follicle stimulating hormone (FSH), are vulnerable to damage due to their location in the outer wings of the pituitary lobe and their relatively fragile blood supply [7]. Consistent with this observation, GH and testosterone are the most commonly deficient hormones following TBI [10,18- 21]. Corticotrophic and thyrotrophic cells are less vulnerable to injury given their more central location within the anterior pituitary lobe [7]. These findings are also supported with prevalence studies that indicate that cortisol and thyroid hormones are often less affected following brain trauma [3,10,22]. These findings are not surprising given that low cortisol is associated with increased mortality in patients with moderate to severe TBI (and thus, these individuals may succumb to their injuries prior to being screened for hypoadrenalism) [23]. There is a relative paucity of literature on chronic hypocortisolism, perhaps due to more detectable symptoms and no controversy surrounding cortisol replacement [24].

Prevalence studies of neuroendocrine dysfunction following TBI estimates incidence between 35 to 68% (Table 1). This variability may be due to methodological differences between studies such as patient selection (e.g. age of the patients and injury severity), timing of testing post-TBI, protocols for evaluating hormone levels (i.e. whether a provocative test was used or not), and confounding effects of medications and nutritional status [25].

Citation: Howell SN, Kreber LA, Ashley JG and Griesbach GS. The Influence of Neuroendocrine and Sleep Disturbances on Recovery from Traumatic Brain Injury. Phys Med Rehabil Int. 2017; 4(3): 1122. ISSN:2471-0377