Endocrine abnormalities in severe traumatic brain injury —a cue to prognosis in severe craniocerebral trauma?

Abstract

Patients with severe craniocerebral trauma (sCCT) display metabolic and endocrine changes. The question is raised whether hormonal patterns give cues to the prognosis of outcome or not. In 21 patients the function of the adrenocortical, gonadal, thyroid and human growth hormone (hGH)-insulin system was assessed. LH, FSH, TSH, prolactin and hGH were stimulated. 3 groups of patients were formed. Group I: patients in acute phase with a Glasgow Coma Score (GCS) more than 6 (group Ia) and less than 6 (group Ib). Group II: patients in transition to traumatic apallic syndrome (TAS). Group III: patients with full-blown or resolving TAS. The values of group Ia comprised low T3, T4 and testosterone, elevated insulin, normal hGH. Group Ib had hypothyroid T3 and T4 and an attenuated response of LH, TSH, prolactin and hGH to stimulation. Group III: there was seen an endocrine normalisation with elevated T4 and TBG and an altered response of hGH and prolactin to stimulation. Endocrine abnormalities were not helpful in predicting which course, either to better or to worse, a given patient would follow.

Hypopituitarism after traumatic brain injury

“…In this regard, only a few authors have evaluated the relationship between outcome from TBI and the presence of pituitary dysfunction. As mentioned above, either positive or negative relationships between pituitary dysfunction and outcome from TBI have been observed in the early, acute phase post-TBI (41,46,47,61). We did not find any statistical correlation between outcome measures and presence of pituitary dysfunction, both in patients examined over a 5-year period after TBI (5) and in patients evaluated during the early rehabilitation period (48).…”

“…A decrease in GH bursts frequency has been detected 24 -48 h after severe trauma, indicating a relative hyposomatotropinism (45). A blunted GH response to arginine (ARG) stimulation has been found in patients with severe TBI and very poor outcome (41). Gottardis et al (46) reported that a GH-releasing hormone (GHRH) test elicited a significant (43).…”

“…In a study on post-traumatic central hypothyroidism, domestic and vehicle accidents represented the main causes of TBI (81). Severity of TBI and secondary cerebral damage have been suggested as risk factors for the development of PTHP (30,41,79). In the past, the risk of developing pituitary dysfunction was considered as strictly dependent on the severity of TBI, particularly when associated with skull and facial fractures, cranial nerve injury and a prolonged period of unconsciousness (64,76,78).…”

Neuroendocrine Disturbances Following Head Injuries

“…As mentioned above, either positive or negative relationships between pituitary dysfunction and outcome from TBI have been observed in the early, acute phase post-TBI. (39,40,41,42) We did not find any statistical correlation between outcome measures and presence of pituitary dysfunction, both in patients examined over a 5-years period after TBI (5) and in patients evaluated during the early rehabilitation period. (43) Autopsy studies demonstrated a high incidence (14-74%) of anatomical lesions in the hypothalamic-pituitary region; this suggests, therefore, that hypopituitarism might contribute to the poor prognosis of the TBI patients.…”

The Case of Hypopituitarism in Traumatic Brain Injury

“…A number of studies have assessed the acute neuroendocrine changes following TBI, in order to investigate their correlation to trauma severity, metabolic derangement and variables that may predict outcome (Cernak et al, 1999;Cohan et al, 2005;Della et al, 1998;Feibel et al, 1983;Hackl et al, 1991). The clinical implications of these findings remain unclear.…”