Rehabilitation of Moderate-to-Severe Traumatic Brain Injury

Abstract

Traumatic brain injury (TBI) is defined as an alteration in brain function, or other evidence of brain pathology, caused by an external force. Traumatic brain injury is a leading cause of morbidity and disability and is considered a major public health concern. Traumatic brain injury sequelae can lead to long-term impairments in physical, cognitive, behavioral, and social function. Traumatic brain injury rehabilitation requires an interdisciplinary holistic team approach in the management of medical complications, the prevention of further disability, and helping patients return to their highest level of independence. The authors review TBI pathophysiology, grading severity, common medical complications, cognitive rehabilitation, prognosis, and common outcomes used in TBI rehabilitation.

Interrelation between Neuroendocrine Disturbances and Medical Complications Encountered during Rehabilitation after TBI

“…At the same time patients may exhibit obvious clinical signs of functional impairment, while the traditional diagnostic studies may not show any tissue alteration [ 41 ]. Disabilities that may arise as a result of TBI often have physical, cognitive, behavioral, and psychosocial aspects ( Table 1 ) [ 13 , 41 ]. TBI rehabilitation therefore requires comprehensive and individualized rehabilitation programs.…”

“…Thus hormones produced or controlled along the pituitary axis can be dysregulated by TBI. The pituitary gland is particularly susceptible to mechanical and ischemic injuries (secondary to brain swelling or hypoxia) due to the vulnerability of its vascular supply through the infundibulum and firm encasement within the sella turcica [ 13 , 52 ]. Hypopituitarism is defined as a partial or complete loss of one or more of the hormones secreted by the pituitary gland [ 17 ].…”

“…Vasopressin or antidiuretic hormone (ADH) is related to water retention and concentration of urine. An inappropriately high secretion leads to a concentrated urine and hypervolemic hyponatremia, while an insufficient secretion causes diabetes insipidus with a diluted urine, dehydration and/or hypernatremia [ 13 ]. The anterior lobe releases ACTH, GH, prolactin, TSH, follicle stimulating hormone (FSH) and lutenizing hormone (LH).…”

“…These hormones interact with peripheral endocrine glands (e.g., adrenal cortex, liver, thyroid gland, gonads) and endocrine glands within the brain (e.g., hypothalamus and pineal gland). Typical generalized symptoms accompanying a deficiency of most of these hormones ( Table 2 ) as fatigue, depression, anxiety, lack of energy, and cognitive dysfunction cannot be distinguished from the symptomatology frequently encountered after moderate to severe head injury [ 13 , 17 ].…”

“…During the acute event damaged neurons die, but also over the following days and weeks, additional cells die through cellular suicide (apoptosis) and oxidative stress [ 11 ]. The resultant secondary injury is associated with impairments of cerebral blood flow and metabolism, hypoxia, oedema, a cascade of neurochemical changes due to the release of excitotoxic neurotransmitters [ 12 , 13 ] and other dynamic factors (e.g., proinflammatory cytokines, brain-derived neurotrophic factor) influencing neuronal survival and synaptic plasticity [ 14 , 15 ]. Mechanisms of secondary injury influence the extent and type of impairments resulting from TBI, in the subacute and chronic period after injury (during inpatient rehabilitation), as well as during the acute phase.…”