Neuroendocrine Disturbances after Brain Damage: An Important and Often Undiagnosed Disorder

Abstract

Traumatic brain injury (TBI) is a common and significant public health problem all over the world. Until recently, TBI has been recognized as an uncommon cause of hypopituitarism. The studies conducted during the last 15 years revealed that TBI is a serious cause of hypopituitarism. Although the underlying pathophysiology has not yet been fully clarified, new data indicate that genetic predisposition, autoimmunity and neuroinflammatory changes may play a role in the development of hypopituitarism. Combative sports, including boxing and kickboxing, both of which are characterized by chronic repetitive head trauma, have been shown as new causes of neuroendocrine abnormalities, mainly hypopituitarism, for the first time during the last 10 years. Most patients with TBI-induced pituitary dysfunction remain undiagnosed and untreated because of the non-specific and subtle clinical manifestations of hypopituitarism. Replacement of the deficient hormones, of which GH is the commonest hormone lost, may not only reverse the clinical manifestations and neurocognitive dysfunction, but may also help posttraumatic disabled patients resistant to classical treatment who have undiagnosed hypopituitarism and GH deficiency in particular. Therefore, early diagnosis, which depends on the awareness of TBI as a cause of neuroendocrine abnormalities among the medical community, is crucially important.

Kickboxing review: anthropometric, psychophysiological and activity profiles and injury epidemiology

“…TBI is a well-known public health problem around the world, and it is associated with increased morbidity, mortality and long-term disability [65]. For instance, kickboxing is well established to be associated with a risk of TBI [31].…”

Social dysfunction after pediatric traumatic brain injury: A translational perspective

“…The narrow pituitary stalk is vulnerable to direct damage by mechanical compression, shearing or vascular injury, or indirectly compromised by brain swelling (Dusick et al, 2012; Reifschneider et al, 2015). Haemorrhage, necrosis and fibrosis of the pituitary stalk, anterior and posterior pituitary have been reported upon autopsy after fatal TBI (Klose and Feldt-Rasmussen, 2015; Kornblum and Fisher, 1969; Tanriverdi and Kelestimur, 2015), and amongst survivors of adult TBI, pituitary atrophy is evident by MRI up to at least 11 months post-injury (Maiya et al, 2008). Further, rodent studies have identified an inflammatory response in the hypothalamus, associated with impaired growth hormone levels, even in the absence of overt pituitary damage (Osterstock et al, 2014).…”

Traumatic brain injuries

“…The most common abnormalities are growth hormone (GH) deficiency and hypogonadism, whilst adrenocorticotrophic hormone (ACTH) and thyroidstimulating hormone (TSH) deficiencies are diagnosed less often104,105 . Almost 50% of TBI patients have anti-diuretic hormone deficiency severe enough to cause central diabetes insipidus in the acute phase following the injury, but this deficiency often resolves within 3 months105,106 .PTHP can result in a multitude of acute and chronic symptoms107 . For example, GH deficiency may result in changes in body composition and a reduction in quality of life including depression, whilst hypothyroidism may cause weight gain, low mood and blunted cognition107 .…”

“…Almost 50% of TBI patients have anti-diuretic hormone deficiency severe enough to cause central diabetes insipidus in the acute phase following the injury, but this deficiency often resolves within 3 months105,106 .PTHP can result in a multitude of acute and chronic symptoms107 . For example, GH deficiency may result in changes in body composition and a reduction in quality of life including depression, whilst hypothyroidism may cause weight gain, low mood and blunted cognition107 . Most crucially, acute adrenal insufficiency may occur within days of TBI in some patients, with the ensuing adverse consequences of hypotension, hyponatraemia and hypoglycaemia, which require emergent treatment.…”

“…Most crucially, acute adrenal insufficiency may occur within days of TBI in some patients, with the ensuing adverse consequences of hypotension, hyponatraemia and hypoglycaemia, which require emergent treatment. PTHP is also relevant in the context of mild TBI; a recent study demonstrated a prevalence of GH deficiency of 1% in a cohort of patients with a history of concussion108 and even higher prevalence has been reported in athletes with a history of repetitive head trauma107 . For example, high prevalence (25-30%) of hypopituitarism with GH and ACTH deficiency has been reported in amateur kick boxers and retired American football players that may result in poor quality of life, erectile dysfunction and metabolic syndrome109,110 .…”