Cited by 70Pituitary Gland Disorders and TreatmentsTraumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury Research

Traumatic brain injury: Endocrine consequences in children and adults

Richmond, Erick, Rogol, Alan D.·2014·Endocrine

Abstract

Traumatic brain injury (TBI) is a common cause of death and disability in young adults with consequences ranging from physical disabilities to long-term cognitive, behavioral, psychological and social defects. Recent data suggest that pituitary hormone deficiency is not infrequent among TBI survivors; the prevalence of reported hypopituitarism following TBI varies widely among published studies. The most common cause of TBI is motor vehicle accidents, including pedestrian-car and bicycle car encounters, falls, child abuse, violence and sports injuries. Prevalence of hypopituitarism, from total to isolated pituitary deficiency, ranges from 5 to 90 %. The time interval between TBI and pituitary function evaluation is one of the major factors responsible for variations in the prevalence of hypopituitarism reported. Endocrine dysfunction after TBI in children and adolescents is common. Adolescence is a time of growth, freedom and adjustment, consequently TBI is also common in this group. Sports-related TBI is an important public health concern, but many cases are unrecognized and unreported. Sports that are associated with an increased risk of TBI include those involving contact and/or collisions such as boxing, football, soccer, ice hockey, rugby, and the martial arts, as well as high velocity sports such as cycling, motor racing, equestrian sports, skiing and roller skating. The aim of this paper is to summarize the best evidence of TBI as a cause of pituitary deficiency in children and adults.

Integrity signals

Registry

Crossref · 10.1007/s12020-013-0049-1

Cites

42 of 42 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • TBI can trigger substantial neuroendocrine alterations, often manifesting days to months after the initial insult.

    “Beyond the immediate structural and functional cerebral damage, TBI can trigger substantial neuroendocrine alterations, often manifesting days to months after the initial insult [5,6,7].”
  • During the acute phase after TBI, serum cortisol levels typically rise in response to stress and neuroinflammation, later declining towards baseline as the injury stabilizes.

    “During the acute phase, serum cortisol levels typically rise in response to stress and neuroinflammation, later declining towards baseline as the injury stabilizes [7,48,49].”
  • As the injury evolves, children may shift from a compensated adrenal response to partial or complete hypothalamic-pituitary-adrenal axis failure.

    “As the injury evolves, children may shift from a compensated adrenal response to partial or complete hypothalamic–pituitary–adrenal axis failure [7].”
  • Post-traumatic endocrine dysfunction is an underrecognized but clinically significant sequela of pediatric TBI with potential long-term consequences for growth, puberty, metabolism, and quality of life.

    “Beyond acute neurological injury, post-traumatic endocrine dysfunction has emerged as an underrecognized but clinically significant sequela, with potential long-term consequences for growth, puberty, metabolism, and overall quality of life.”
  • Many endocrine sequelae after pediatric TBI manifest months to years after the initial trauma, complicating timely diagnosis.

    “Importantly, many endocrine sequelae manifest months to years after the initial trauma, complicating a timely diagnosis.”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Richmond, E., & Rogol, A. D.
Affiliations
  • Hospital Nacional de Niños (CR)
  • University of Virginia (US)
Corresponding author
Rogol, Alan D.
Venue
Endocrine
Published
2013-09-13
Volume
45
Issue
1
Pages
3-8
ISSN
  • 0969-711X (ISSN-L)
  • 1355-008X
  • 1559-0100
OpenAlex
W2076601163
Cited by
70
References
42
Citations by year
2026: 4 · 2025: 2 · 2024: 3 · 2023: 5 · 2022: 6 · 2021: 4 · 2020: 6 · 2019: 7 · 2018: 4 · 2017: 8 · 2016: 7 · 2015: 12 · 2014: 2
FWCI
1.03
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
Keywords
traumatic brain injury, hypopituitarism, pituitary hormone deficiency, endocrine dysfunction, children and adolescents, sports-related head injury, motor vehicle accidents, falls
MeSH terms
Adolescent, Adult, Brain Injuries, Child, Hormones, Humans, Hypopituitarism, Pituitary Gland, Human Growth Hormone, Hormone Replacement Therapy

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review