GH Replacement for GH Deficiency after Traumatic Brain Injury Improves Quality of Life, Depressive Symptoms and Metabolic Status, without Improving Axonal Recovery and Cognition

Presentation Number: SUN 434
Date of Presentation: April 2nd, 2017

Claire Feeney*1, David Sharp2, Peter J Hellyer3, Deborah A Papadopoulou4, David Baxter2, Sagar Jilka2, Timothy Ham2, Mark Midwinter5 and Anthony P. Goldstone2
1Imperial Centre for Endocrinology, London, 2Imperial College, London, 3C3NL, London, 4Imperial College London, London, United Kingdom, 5Royal Centre for Defence Medicine, Birmingham


Growth hormone deficiency (GHD) is a recognised complication following traumatic brain injury (TBI) with reported prevalence rates of 5-10%. GH replacement (GHR) can improve cognition and quality of life following TBI. It is unclear however what is the effect of GHR on white matter recovery following TBI. Diffusion tensor imaging (DTI) is an established magnetic resonance imaging technique used to study axonal injury and repair following TBI.

We conducted a longitudinal study to determine the effects of GHR on neuropsychological recovery, white matter (WM) tract and metabolic status following TBI. 10 patients (9 male, 9 moderate-severe TBI, age median (IQR) 41.7 (22.7, 56.7) years, time since injury 23.5 (20.5, 67.9) months) with GHD following TBI were studied. Patients had DTI scans before and after GHR (duration of treatment 14.2 (10.3, 16.4) months, time between scans 17.1 (13.9, 18.9) months). The neuroimaging outcome measure was fractional anisotropy (FA), a measure of WM tract integrity, in a priori regions of interest (ROI): splenium of corpus callosum (SPCC), anterior thalamic radiculus (ATR) and cingulum hippocampus (CR). Symptom and quality of life (QoL) questionnaires and neurocognitive assessments were completed at both visits, as well as fasting bloods to measure lipids, HOMA-IR and blood pressure (BP) to calculate a metabolic syndrome score (one point for each of raised fasting blood glucose, LDL, BP, and low HDL cholesterol). Patients were compared to a control group of 23 patients without GHD following TBI who were of similar age, gender ratio and time since injury. These patients had identical neuroimaging and cognitive assessments at two time points.

When compared to controls, there was no effect of GHR on FA recovery using a whole brain analysis nor in the ROIs, nor on a variety of neurocognitive domains (group x time interaction P>0.05). However, following GHR in the GHD group there was a significant decrease in the AGHDA-QoL score indicating improvement in symptoms (P=0.004), and in the Beck Depression Inventory II score indicating less depressive symptoms (P=0.001).

At baseline, HOMA-IR was significantly higher in those with GHD compared to those without (median 1.4 vs. 0.9, P=0.002). Total metabolic syndrome score was significantly higher in patients with GHD vs. those without GHD (3.3 vs. 1.5, P=0.001). Following GHR, there was a trend towards a lower metabolic score following treatment (P=0.07), but not in HOMA-IR.

In this small study GHR reduced depressive symptoms and improved QoL in patients with GHD after TBI, with a trend for improved metabolic status, but had no significant effect on WM recovery and cognition. Larger studies will be needed to further examine the effect of GHR on WM integrity and cognition following TBI.


Nothing to Disclose: CF, DS, PJH, DAP, DB, SJ, TH, MM, APG