Abstract
Neuroendocrine dysfunction, long recognized as a consequence of traumatic brain injury (TBI), is a major cause of disability that includes physical and psychological involvement with long-term cognitive, behavioral, and social changes. There is no standard procedure regarding at what time after trauma the diagnosis should be made. Also there is uncertainty on defining the best methods for diagnosis and testing and what types of patients should be selected for screening. Common criteria for evaluating these patients are required on account of the high prevalence of TBI worldwide and the potential new cases of hypopituitarism. The aim of this review is to clarify, based on the evidence, when endocrine assessment should be performed after TBI and which patients should be evaluated. Additional studies are still needed to know the impact of post-traumatic hypopituitarism and to assess the impact of hormone replacement in the prognosis.
Highlights
Neuroendocrine dysfunction has long been recognized as a consequence of traumatic brain injury (TBI) (Cyran, 1914), in moderate and severe cases, the last 10 years have witnessed a better understanding of the frequency of TBImediated hypopituitarism and its clinical implications, with the publication of an increasing number of studies (Benvega et al, 2000; Kelly et al, 2000; Lieberman et al, 2001; Agha et al, 2004; Bondanelli et al, 2004; Popovic et al, 2004; Aimaretti et al, 2005; Leal-Cerro et al, 2005; Herrmann et al, 2006; Schneider et al, 2006; Tanriverdi et al, 2006)
In young adults traumatic brain injury (TBI) is considered one of the main causes of death (Hodgson et al, 2000). It is a major cause of disability that includes physical and psychological involvement with long-term cognitive, behavioral, and social changes (Salazar et al, 2000; Khan et al, 2003)
Neuroendocrine dysfunction has long been recognized as a consequence of TBI (Cyran, 1914), in moderate and severe cases, the last 10 years have witnessed a better understanding of the frequency of TBImediated hypopituitarism and its clinical implications, with the publication of an increasing number of studies (Benvega et al, 2000; Kelly et al, 2000; Lieberman et al, 2001; Agha et al, 2004; Bondanelli et al, 2004; Popovic et al, 2004; Aimaretti et al, 2005; Leal-Cerro et al, 2005; Herrmann et al, 2006; Schneider et al, 2006; Tanriverdi et al, 2006)
Summary
Neuroendocrine dysfunction has long been recognized as a consequence of TBI (Cyran, 1914), in moderate and severe cases, the last 10 years have witnessed a better understanding of the frequency of TBImediated hypopituitarism and its clinical implications, with the publication of an increasing number of studies (Benvega et al, 2000; Kelly et al, 2000; Lieberman et al, 2001; Agha et al, 2004; Bondanelli et al, 2004; Popovic et al, 2004; Aimaretti et al, 2005; Leal-Cerro et al, 2005; Herrmann et al, 2006; Schneider et al, 2006; Tanriverdi et al, 2006).
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