Emerging pharmacotherapy for treatment of traumatic brain injury: targeting hypopituitarism and inflammation
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Updated: Apr 9, 2026
Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Irene Paterniti1, Marika Cordaro2, Michele Navarra3
1a 1 University of Messina, Department of Biological and Environmental Sciences , Viale Ferdinando Stagno D'Alcontres, 31 - 98166 Messina, Italy +390906765208 ; salvator@unime.it.
Introduction:
Traumatic brain injury (TBI) is a common cause of morbidity and mortality in the developed world. In particular, TBI is an important cause of death and disability in young adults with consequences ranging from physical disabilities to long-term cognitive, behavioural, psychological and social defects.
Areas Covered:
There is a large body of evidence that suggest that TBI conditions may adversely affect pituitary function in both the acute and chronic phases of recovery. 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. Diagnosis of hypopituitarism and accurate treatment of pituitary disorders offers the opportunity to improve mortality and outcome in TBI conditions.
Expert Opinion:
The aim of this paper is to review the history and pathophysiology of TBI and to summarize the best evidence of TBI as a cause of pituitary deficiency. Moreover, in this article we will describe the multiple changes which occur within the hypothalamic-pituitary-thyroid axis in critical illness, giving rise to 'sick euthyroid syndrome', focus our attention on thyroid hormones circulating levels from the initial insult to critical illness.
