Assessment of neuroendocrine dysfunction following traumatic brain injury.

Posttraumatic neuroendocrine pathology may be a clinically significant complication following traumatic brain injury (TBI). Metabolic abnormalities are described after TBI in two cases. A 21 year old male injured in a motor vehicle accident admitted in a minimally responsive condition presented with fluctuating high sodium levels, undetectable serum testosterone, and depressed cortisol and thyroid function. Imaging revealed near complete avulsion of the pituitary stalk leading to panhypopituitarism. A 38 year old male admitted for occipital skull fractures and brain contusions presented with hyponatremia and low serum testosterone. Both patients required hormonal replacement and correction of electrolyte abnormalities. A screening protocol adapted for selected patients at risk for endocrine problems is described. While neuroendocrine screening is not advocated in all TBI patients, physicians should be aware of the importance of neuroendocrine dysfunction following TBI.

[1]  T. Sihvonen,et al.  Flexion relaxation of the hamstring muscles during lumbar-pelvic rhythm. , 1997, Archives of physical medicine and rehabilitation.

[2]  M. Miller.  Inappropriate antidiuretic hormone secretion. , 1997, Current therapy in endocrinology and metabolism.

[3]  T. Saito.  SIADH and other hyponatremic disorders: diagnosis and therapeutic problems. , 1996, Nihon Jinzo Gakkai shi.

[4]  S. Knowles,et al.  Hyponatremia and the syndrome of inappropriate secretion of antidiuretic hormone associated with the use of selective serotonin reuptake inhibitors: a review of spontaneous reports. , 1996, CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne.

[5]  E. Elovic.  Pharmacology of attention and arousal in the low level patient. , 1996, NeuroRehabilitation.

[6]  R. Cohen,et al.  Amantadine: A potential adjuvant therapy following traumatic brain injury , 1995 .

[7]  M. Gandelman.  Review of carbamazepine-induced hyponatremia , 1994, Progress in Neuro-Psychopharmacology and Biological Psychiatry.

[8]  W. Butt,et al.  Continuous vasopressin replacement in diabetes insipidus. , 1990, Archives of disease in childhood.

[9]  J. Wilcox,et al.  Psychological effects of amantadine on psychotic subjects. , 1990, Neuropsychobiology.

[10]  A. Viti,et al.  Korsakoff's psychosis due to massive beer intake provoked by diabetes insipidus. , 1988, Southern medical journal.

[11]  Gualtieri Ct.  Pharmacotherapy and the neurobehavioural sequelae of traumatic brain injury , 1988 .

[12]  Z. Barzilay,et al.  Diabetes insipidus in severely brain damaged children. , 1988, Journal of medicine.

[13]  V. Marks,et al.  Post-traumatic diabetes insipidus combined with primary polydipsia. , 1987, Postgraduate medical journal.

[14]  Leramo Ob,et al.  Diplopia and diabetes insipidus secondary to type II fracture of the sella turcica: case report. , 1987 .

[15]  J. D. Clark,et al.  Post‐Traumatic Hypopituitarism: SIX CASES AND A REVIEW OF THE LITERATURE , 1986, Medicine.

[16]  G. Klingbeil,et al.  Anterior hypopituitarism: a consequence of head injury. , 1985, Archives of physical medicine and rehabilitation.

[17]  E. Rolandi,et al.  Evaluation of anterior pituitary function in patients with posttraumatic diabetes insipidus. , 1980, The Journal of clinical endocrinology and metabolism.

[18]  A. Moses,et al.  Permanent diabetes insipidus following head trauma: observations on ten patients and an approach to diagnosis. , 1980, The Journal of trauma.

[19]  Fisher Rs,et al.  Pituitary lesions in craniocerebral injuries. , 1969 .

[20]  N. Winer,et al.  Traumatic hypopituitarism occurring before puberty: survival 35 years untreated. , 1968, The Journal of clinical endocrinology and metabolism.