Endocrine changes after pediatric traumatic brain injury

Rose, Susan R.; Auble, Bethany

doi:10.1007/s11102-011-0360-x

Cited by 46 publications

(32 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…An alternative possibility is that sexual anhedonia may reflect injury-induced disturbances in the endocrine system and reduced levels of key neuropeptides and androgens [67], [77], [78]. Recent clinical studies have highlighted the prevalence of endocrine disturbances after TBI in both children and adults [79], [80], [81], whereby pituitary function may appear normal acutely but become impaired over months post-injury [82], [83].…”

Section: Discussionmentioning

confidence: 99%

Sociosexual and Communication Deficits after Traumatic Injury to the Developing Murine Brain

et al. 2014

View full text Add to dashboard Cite

Despite the life-long implications of social and communication dysfunction after pediatric traumatic brain injury, there is a poor understanding of these deficits in terms of their developmental trajectory and underlying mechanisms. In a well-characterized murine model of pediatric brain injury, we recently demonstrated that pronounced deficits in social interactions emerge across maturation to adulthood after injury at postnatal day (p) 21, approximating a toddler-aged child. Extending these findings, we here hypothesized that these social deficits are dependent upon brain maturation at the time of injury, and coincide with abnormal sociosexual behaviors and communication. Age-dependent vulnerability of the developing brain to social deficits was addressed by comparing behavioral and neuroanatomical outcomes in mice injured at either a pediatric age (p21) or during adolescence (p35). Sociosexual behaviors including social investigation and mounting were evaluated in a resident-intruder paradigm at adulthood. These outcomes were complemented by assays of urine scent marking and ultrasonic vocalizations as indices of social communication. We provide evidence of sociosexual deficits after brain injury at p21, which manifest as reduced mounting behavior and scent marking towards an unfamiliar female at adulthood. In contrast, with the exception of the loss of social recognition in a three-chamber social approach task, mice that received TBI at adolescence were remarkably resilient to social deficits at adulthood. Increased emission of ultrasonic vocalizations (USVs) as well as preferential emission of high frequency USVs after injury was dependent upon both the stimulus and prior social experience. Contrary to the hypothesis that changes in white matter volume may underlie social dysfunction, injury at both p21 and p35 resulted in a similar degree of atrophy of the corpus callosum by adulthood. However, loss of hippocampal tissue was greater after p21 compared to p35 injury, suggesting that a longer period of lesion progression or differences in the kinetics of secondary pathogenesis after p21 injury may contribute to observed behavioral differences. Together, these findings indicate vulnerability of the developing brain to social dysfunction, and suggest that a younger age-at-insult results in poorer social and sociosexual outcomes.

show abstract

Section: Discussionmentioning

confidence: 99%

Sociosexual and Communication Deficits after Traumatic Injury to the Developing Murine Brain

et al. 2014

View full text Add to dashboard Cite

show abstract

“…In the prospective and retrospective studies available, the pediatric population shows an incidence rate of pituitary dysfunction in 16-61% of patients, 1-5 years after injury, compared with the 23-69% seen in adults. 26,58 Variation in reported rates may be the result of differences in inclusion criteria and diagnostic methods (e.g., baseline testing vs. provocative testing). Nonetheless, pituitary dysfunction following TBI is an important syndrome to identify and treat.…”

Section: Incidence and Time Course Of Hormonal Changesmentioning

confidence: 99%

“…26,58 Damage to the pituitary from both primary and secondary injuries is likely to be responsible for the acute impairment and the development of persistent dysfunction seen in many patients. Acute MRI scans and numerous pathological reports have shown evidence of hemorrhage, swelling, infundibular stalk transection, and necrotic lesions in the acute time frames after injury ( <1week).…”

Section: Potential Mechanisms Of Damage and Recovery Of The Pituitarymentioning

confidence: 99%

“…A growing body of evidence also points toward TBI being a cause of hypopituitarism in the adolescent population. 26 This is of particular importance, as the highest risk of TBI occurs within the early adolescent and adolescent age groups. 27 Disruption of pituitary function could have important clinical consequences, as the neuroendocrine system is an integral part of development.…”

mentioning

confidence: 99%

See 1 more Smart Citation

The Effects of Repeat Traumatic Brain Injury on the Pituitary in Adolescent Rats

Greco¹,

Hovda²,

Prins³

2013

Journal of Neurotrauma

View full text Add to dashboard Cite

Adolescents are one of the highest groups at risk for sustaining both traumatic brain injury (TBI) and repeat TBI (RTBI). Consequences of endocrine dysfunction following TBI have been routinely explored in adults, but studies in adolescents are limited, and show an incidence rate of endocrine dysfunction in 16-61% in patients, 1-5 years after injury. Similar to in adults, the most commonly affected axis is growth hormone (GH) and insulin-like growth hormone 1 (IGF-1). Despite TBI being the primary cause of morbidity and mortality among the pediatric population, there are currently no experimental studies specifically addressing the occurrence of pituitary dysfunction in adolescents. The present study investigated whether a sham, single injury or four repeat injuries (24 h interval) delivered to adolescent rats resulted in disruption of the GH/IGF-1 axis. Circulating levels of basal GH and IGF-1 were measured at baseline, 24 h, 72 h, 1 week, and 1 month after injury, and vascular permeability of the pituitary gland was quantified via Evans Blue dye extravasation. Changes in weight and length of animals were measured as a potential consequence of GH and IGF-1 disruption. The results from the current study demonstrate that RTBI results in significant acute and chronic decreases in circulation of GH and IGF-1, reduction in weight gain and growth, and an increase in Evans Blue dye extravasation in the pituitary compared with sham and single injury animals. RTBI causes significant disruption of the GH/IGF-1 axis that may ultimately affect normal cognitive and physical development during adolescence.

show abstract

“…First and foremost, TBI is a common cause of pituitary dysfunction, which is recognized as a sequela [8,9]. Thirty-to-fifty per cent of TBI patients suffer from hypopituitarism [10][11][12]. Broadly, hypothalamic-pituitary dysfunction was identified in nearly 70% of patients following TBI [13].…”

Section: Introductionmentioning

confidence: 99%