The natural history of post-traumatic neurohypophysial dysfunction

Abstract

Background and objectives: Posterior pituitary function remains poorly investigated after traumatic brain injury (TBI). We report the results of a study designed to prospectively define the natural history of post-traumatic diabetes insipidus (DI) and syndrome of inappropriate antidiuretic hormone secretion (SIADH) using standard reliable methodology. Design and methods: 50 consecutive patients with severe or moderate TBI (initial Glasgow Coma Scale (GCS) score 3/15 -13/15) were prospectively studied on three occasions: at the acute phase and at 6 months and at 12 months following TBI. In the acute phase, DI was diagnosed either by the presence of hypernatraemia in association with hypotonic polyuria or by the water-deprivation test (WDT) and, at 6 and 12 months by the WDT in all patients. Normative data on response to the WDT were obtained from healthy matched volunteers. Functional outcome was assessed using the Glasgow Outcome Scale (GOS). Results: 13 patients (26%) had DI in the acute post-TBI phase, of whom nine patients recovered by 6 months and one additional patient recovered by 12 months. Of the remaining three patients with permanent DI, two had partial vasopressin deficiency. Acute-phase peak plasma osmolality correlated negatively with the initial GCS scores (r ¼ 2 0.39, P ¼ 0.005) and with the GOS scores (r ¼ 20.45, P ¼ 0.001). Seven patients had SIADH in the acute phase of TBI but none did at 6 or 12 months. No new cases of DI or SIADH were noted after the acute phase.Conclusion: This prospective study shows that posterior pituitary dysfunction is common following TBI. Most cases recover completely but there is an appreciable frequency of long-term DI which can be subtle and should be recognized and managed appropriately.

Prevalence of Pituitary Hormone Dysfunction, Metabolic Syndrome, and Impaired Quality of Life in Retired Professional Football Players: A Prospective Study

“…[7][8][9][10][11][12][13][14][15]45,46 In contrast, corticotroph, thyrotroph, and posterior pituitary deficiencies are less common, with rates averaging 8%, 5%, and 2% respectively. [7][8][9][10][11][12][13][14][15]45,46 In the present study of mTBI subjects who sustained repetitive head impact with a median of 5 concussions in their football career, a similar pattern of hormonal deficiency was observed involving the somatotroph and gonadotroph axes with sparing of corticotroph, thyrotroph, and posterior pituitary function. GHD remained the most common HD in our cohort, despite adjustment for BMI for the diagnostic cut point for GHD.…”

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

“…Other signaling mechanisms could include trans-synaptic (Koliatsos et al, 2004) as well as anterograde and retrograde neuronal degeneration from the site of injury to the more distal sites (Sorensen et al, 1996;Bechmann and Nitsch, 1997), also eventually affecting some of the endocrine functions. While we know something about the effects of TBI on endocrine function based on human studies (Ceballos, 1966;Agha et al, 2004aAgha et al, , 2004bAgha et al, , 2005aAgha et al, , 2005bAimaretti et al, 2004Aimaretti et al, , 2005bBondanelli et al, 2004;Herrmann et al, 2006;Powner et al, 2006;Schneider et al, 2006;Tanriverdi et al, 2006), there is still some uncertainty about the mechanisms by which long-term alterations in the endocrine system (like suppression of serum GH in TBI subjects) evolve over time, and whether such changes could be prevented by therapeutic interventions.…”

Post‐traumatic hypopituitarism: report of a child case

“…Post‐traumatic central diabetes insipidus is frequently transient,6, 10 although spontaneous recovery from anterior pituitary hormone deficiency is rare 10. In one series, only 3 of 19 children (aged 4 months–15 years) with acute central diabetes insipidus secondary to severe brain injury survived the acute attack of central diabetes insipidus 8. Therefore, the occurrence of acute onset central diabetes insipidus may be a poor prognostic factor for survival in patients with TBI.…”