Hypothalamic hypothyroidism and hypogonadism in prolonged traumatic coma

Abstract

✓ Prolonged coma after head trauma is associated with depletion of 3′,5′cyclic adenosine monophosphate (cAMP) in the cerebrospinal fluid (CSF). Because cAMP has previously been implicated in neuroendocrine secretion, this study examines the pituitary-hypothalamic function in 15 adult male patients (to exclude the effects of puberty and menses) with traumatic coma lasting longer than 2 weeks. Ventricular CSF cAMP was measured at 2- to 4-day intervals for 10 to 25 days. Simultaneously, plasma hormone concentrations were also determined. In all 15 cases, CSF cAMP and plasma levels of thyroid-stimulating hormone (TSH), thyroxine (T4), free T4, triiodothyronine (T3), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone became subnormal. In 11 patients whose level of consciousness fluctuated, the reduction in plasma T4 and testosterone were proportional to both severity of coma (r > 0.81, p < 0.05) and depletion of CSF cAMP (r > 0.81, p < 0.05). In four patients who remained deeply comatose for 17 to 25 days, the hypothyroidism and hypogonadism persisted. In six patients who regained consciousness, both endocrine defects improved partially or completely. Injection of 1) thyrotrophic-releasing hormone and 2) gonadotrophic-releasing hormone elicited normal or supernormal increases in plasma concentrations of 1) TSH, and 2) LH and FSH, reduced, respectively, suggesting a suprahypophyseal deficiency. These observations demonstrate that suprahypophyseal hypothyroidism and hypogonadism may occur regularly in patients with traumatic coma lasting longer than 2 weeks.