MEDICO LEGAL M A G A Z I N E
ENDOCRINE ASPECTS OF THE TRAUMATIC BRAIN INJURY: MEDICO-LEGAL IMPLICATIONS By Professor Gordana Prelevic, MD, DSc, FRCP, CUEW Consultant Endocrinologist, London Claremont Clinic, London
Introduction Traumatic brain injury (TBI) is a very common injury, particularly among children and young adults. The commonest causes of TBI are: falls (28%), traffic accidents (20%), struck by/against (20%), assaults (12%). It is well known that TBI could be associated with various pituitary hormone deficiencies in more than 25% of patients. Among multiple pituitary deficits, the most common ones are: growth hormone (GH) deficiency present in approximately 25% of patients, adrenocorticotropin hormone (ACTH) deficiency present in approximately 20% of patients and gonadotrophin (LH and FSH) deficiency in approximately 12%. In older age, TBI severity and skull fractures appear to be risk factors for pituitary disorders. The signs and symptoms associated with pituitary hormone deficiencies (hypopituitarism) are nonspecific and often mimic the sequellae of TBI. Because of this, pituitary hormone deficiencies could result in sub-optimal rehabilitation for patients with TBI-induced hypopituitarism. Fatigue is a major symptom and it is also a major symptom of TBI. It is often difficult to differentiate to what extent the symptoms like memory loss, decreased concentration, mood disturbances, increased anxiety and depression, irritability, insomnia and a sense of social isolation are the result of TBI itself and to what extent hypopituitarism might be contributing to these symptoms.
Background The pituitary gland is situated at the base of the brain and connected to the hypothalamus (part of the brain) with numerous nerves and a delicate and
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Sp o n s o re d by:
fragile network of blood vessels. The hypothalamus controls the production and secretion of the pituitary hormones by releasing substances into those fragile blood vessels. The pituitary gland in turn, secretes hormones which control other endocrine glands (adrenal, thyroid, gonads). Because of their anatomical position and delicate network of blood vessels, both the hypothalamus and the pituitary are vulnerable structures and at risk of injury with any severe head trauma. Pituitary dysfunction as a result of TBI may be partial (deficit of one or more pituitary hormones – partial hypopituitarism) or complete (deficit of all pituitary hormones – panhypopituitarism). A systemic review which examined 14 studies including over 1000 patients showed the prevalence of endocrine dysfunction in 15% to 68% of TBI patients (severe 35.3%; moderate 10.9% and mild 16.8%).
Pituitary hormone deficiencies Growth hormone (GH) deficiency is the most common pituitary hormone deficit found at one and three years after TBI and could often be found as an isolated pituitary hormone deficiency. GH deficiency resembles post-traumatic stress disorder including profound fatigue, anxiety, depression, irritability, sleep disturbance, sexual dysfunction, cognitive deficiencies and decreased quality of life. Evaluation for GH deficiency should be considered during the rehabilitation phase after TBI. ACTH deficiency is the second most common hormone deficiency after TBI. This results in low cortisol levels (secondary adrenal insufficiency) or in some cases only in inadequate cortisol responses to stimulatory tests (cortisol level of 500nmol/L or less in response to Synacthen stimulation). In case of the latter cortisol values are in the normal range
