JNNP

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER


[Advanced]
Journal of Neurology, Neurosurgery, and Psychiatry 2008;79:753-759; doi:10.1136/jnnp.2007.132837
Copyright © 2008 by the BMJ Publishing Group Ltd.
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Read responses to this article
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this link to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Add article to my folders
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Behan, L A
Right arrow Articles by Agha, A
PubMed
Right arrow PubMed Citation
Right arrow Articles by Behan, L A
Right arrow Articles by Agha, A

REVIEW

Neuroendocrine disorders after traumatic brain injury

L A Behan1, J Phillips2, C J Thompson1, A Agha1

1 Academic Department of Endocrinology, Beaumont Hospital and RCSI Medical School, Dublin, Ireland
2 Academic Department of Neurosurgery, Beaumont Hospital and RCSI Medical School, Dublin, Ireland

Correspondence to:
Dr Amar Agha MD, Academic Department of Endocrinology, Beaumont Hospital and RCSI Medical School, Dublin, Ireland; amaragha{at}beaumont.ie


ABSTRACT
Traumatic brain injury (TBI) is the most common cause of death and disability in young adults living in industrialised countries, in which 180–250 persons per 100 000 per year die or are hospitalised as a result. Neuroendocrine derangements after TBI have received increasing recognition in recent years because of their potential contribution to morbidity, and possibly mortality, after trauma. Marked changes of the hypothalamo-pituitary axis have been documented in the acute phase of TBI, with as many as 80% of patients showing evidence of gonadotropin deficiency, 18% of growth hormone deficiency, 16% of corticotrophin deficiency and 40% of patients demonstrating vasopressin abnormalities leading to diabetes insipidus or the syndrome of inappropriate anti-diuresis. Longitudinal prospective studies have shown that some of the early abnormalities are transient, whereas new endocrine dysfunctions become apparent in the post-acute phase. There remains a high frequency of hypothalamic-pituitary hormone deficiencies among long-term survivors of TBI, with approximately 25% patients showing one or more pituitary hormone deficiencies. This is a higher frequency than previously thought and suggests that most cases of post-traumatic hypopituitarism (PTHP) remain undiagnosed and untreated. PTHP has been associated with adverse outcome both in the acute and chronic phases after injury. These data underscore the need for the identification and appropriate timely management of hormone deficiencies, in order to optimise patient recovery from head trauma, improve quality of life and avoid the long-term adverse consequences of untreated hypopituitarism.




eLetters:

Read all eLetters

Omental transplantation for post-traumatic hypopituitarism
Hernando Rafael
JNNP Online, 3 Jul 2008 [Full text]

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
Terms and conditions relating to subscriptions purchased online  ¦  Website terms and conditions  ¦  Privacy policy
Copyright © 2008 by the BMJ Publishing Group Ltd.