The Prevalence of Neuroendocrine Deficits after TBI of Any Severity
In prior posts we have discussed the importance of evaluating possible neuroendocrine deficits, principally hypopituitarism, after a traumatic brain injury (TBI).
The pituitary gland is a pea-sized gland that sits in a rigid bony enclosure called the sella turcica, while the fragile pituitary stalk attaches it to the hypothalamus. Rapid brain movement from impacts can cause the brain to shift, stretching, twisting, or tearing the delicate stalk – resulting in abnormal hormone production.
As we have previously discussed, with reference to the literature, the most common chronic pituitary hormone deficit after TBI is growth hormone deficiency (GHD). Patients with GHD may present with significant fatigue, poor sleep, cognitive dysfunction, decreased exercise tolerance, reduced muscle mass and strength, dyslipidemia, anxiety, depression, and osteoporosis. It was initially thought that these deficits only appeared following moderate to severe TBI and were not common. This has proven to be inaccurate, a misunderstanding caused in part by inadequate screening – the most common screening test for GHD, the IGF-1 blood test, has been shown to lack specificity and sensitivity for the diagnosis of GHD in the TBI population. As discussed in prior posts, the only reliable means of assessing GHD in this population is “dynamic” testing such as the glucagon stimulation test (also sometimes referred to as “provocative” testing or “stimulation” testing.)
The current state of the science on this issue is described in a literature review published in May, 2026: Debert and Lithgow, Evaluation of neuroendocrine deficits following traumatic brain injury: The role of the neurorehabilitation specialist. Growth Hormone and IGF Research 84 (2026) 101702.
One of the key findings in the review is that hypopituitarism is a prevalent contributor to disability after any severity of TBI:
“Hypopituitarism is a prominent contributor to disability after TBI, occurring in approximately 28-32% of patients and can arise after any severity of TBI, including mild TBI and sport-related concussions even in the absence of intracranial pathology on structural imaging (e.g. computer tomography (CT) or magnetic resonance imaging (MRI).) If left untreated neuroendocrine deficits can increase morbidity and mortality, impede participation in rehabilitation, and have long-term consequences for recovery.“
The authors note that growth hormone deficiency after TBI is the most common chronic (persisting more than one year) pituitary deficit, producing the symptoms described above.
The authors also note that the IFG-1 blood test “has been shown to lack specificity and sensitivity for diagnosis of GHD in the TBI population” and that “patients at risk of GHD post-TBI” should “be referred to an appropriate center for dynamic testing using glucagon stimulation test, insulin tolerance test, or other dynamic testing….”
One of issues addressed by authors is the cost of treating GHD, which can sometimes be lifelong. It is not surprising that the medical/insurance industry sometimes resists recognizing medical conditions like GHD deficiency that require expensive treatment, even where there is strong scientific consensus and where the treatment can materially improve the quality of a patient’s life.