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

Abstract

Traumatic brain injury is not a discrete event but an unfolding sequence of damage to the central nervous system. Not only the acute phase but also the subacute and chronic period after injury, i.e., during inpatient rehabilitation, is characterized by multiple neurotransmitter alterations, cellular dysfunction, and medical complications causing additional secondary injury. Neuroendocrine disturbances also influence neurological outcome and are easily overlooked as they often present with diffuse symptoms such as fatigue, depression, poor concentration, or a decline in overall cognitive function; these are also typical sequelae of traumatic brain injury. Furthermore, neurological complications such as hydrocephalus, epilepsy, fatigue, disorders of consciousness, paroxysmal sympathetic hyperactivity, or psychiatric-behavioural symptoms may mask and/or complicate the diagnosis of neuroendocrine disturbances, delay appropriate treatment and impede neurorehabilitation. The present review seeks to examine the interrelation between neuroendocrine disturbances with neurological complications frequently encountered after moderate to severe TBI during rehabilitation. Common neuroendocrine disturbances and medical complications and their clinical implications are discussed.

Identification and Management of Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury

“…Recently, neuroendocrine regulation disturbances observed in the maladaptive response provide new insights for the pathophysiology of PSH (33). In the neurotransmitter system, paroxysm derives from uncontrollable adrenergic outflow resulting in increased circulating catecholamine (34,35).…”

NETs Lead to Sympathetic Hyperactivity After Traumatic Brain Injury Through the LL37-Hippo/MST1 Pathway

“…Sympathetic hyperactivity after TBI is a severe problem in clinical practice. The pathogenesis hypotheses mainly involve diencephalic autonomic epilepsy ( Do et al, 2000 ), cortex-hypothalamus-diencephalon-brainstem disconnection ( Meyfroidt et al, 2017 ), excitatory: inhibitory imbalance ( Baguley, 2008 ), and neuroendocrine ( Renner, 2015 ). These hypotheses are partially reasonable, but they can’t fully explain the phenomenon and lack the exploration of underground pathophysiological mechanisms.…”

Evidence Limitations in Determining Sexually Dimorphic Outcomes in Pediatric Post-Traumatic Hypopituitarism and the Path Forward

“…Past reviews have addressed sex differences in mortality and morbidities after TBI including neurological, endocrine, neuropsychological, psychiatric, and cognitive responses to injury stress [for instance, see (19)(20)(21)(22)]. The incidence of pediatric TBI is bimodal, with one peak occurring between infancy and 4 years of age, and a second around age 15 years (23).…”