Hypothyroidism can also occur following TBI, though it is reported to be less frequent than other HPA hormone deficiency. At 1-year post-injury the reported prevalence of hypothyroidism is 4.1-6.2% with patients presenting with fatigue, cold intolerance, weight gain, altered menses, hyperlipidemia, hyponatremia, low mood and constipation.2; 4 (See FIGURE 1 for chronic phase screening details.) The neurorehabilitation specialist plays an important role in identifying and treating neuroendocrine deficiencies in the chronic phase following TBI. As the most common medical provider during this phase of recovery, rehabilitation specialists require a clear understanding of signs and symptoms of chronic HPA deficiencies, guidelines for evaluation, and when to refer and principles of treatment. Brain injury rehabilitation often requires a multidisciplinary team collaboratively working together to improve symptoms and function. Identification of HPA deficits may be easiest to determine when patients are engaged with a multidisciplinary neurorehabilitation team, as there is increased interaction with a variety of care providers, and subtle signs and symptoms are more evident. Neuroendocrine deficiency during the chronic phase of TBI can delay rehabilitation, slow recovery and hinder patients’ ability to reach optimum function. Symptoms following TBI can be non-specific (fatigue, sleep disruption, poor attention and memory, decrease mood and increased anxiety) and overlap with those presenting with neuroendocrine deficits. Implementing regular evaluation of screening questions and diagnostic testing during this phase of recovery is important (FIGURE 1). Conclusion Neuroendocrine deficits can occur following all severities of TBI and the absence of intracranial pathology on structural neuroimaging (computer tomography or magnetic resonance brain imaging) does not eliminate the possibility of HPA deficits. Neuroendocrine deficiency after TBI is more common than once thought and can occur in all types of TBI, mild TBI and sport-related concussion included. In the acute phase, screening for AVP deficiency, SIADH and adrenal insufficiency in individuals with signs and symptoms suggestive of these deficiencies is recommended. However, particularly in moderate/severe TBI, a stress response and commonly used medications such as propofol may contribute to transient changes in HPA function and need to be considered. In patients with TBI admitted to the hospital we recommend morning cortisol assessments for day 1-5 and then at again at 2-weeks postinjury; if AI is diagnosed, repeat provocative testing at 2-3 months is recommended. It is not recommended to test for gonadotropin or growth hormone deficiency in the acute phase as there is limited evidence that treatment is beneficial. When and whom to screen is controversial in the chronic phase. For example, Tanriverdi et al. recommended screening at 6 months and 12-months in patients with complicated mild TBI (evidence of intracranial bleed on neuroimaging) and moderate/severe TBI.3 However, Glynn et al recommend similar hormone screening at 3-6 months and 12 months but in moderate/severe TBI only.36 More recently, Mahajan et al. recommended screening at 3-6 months, 12 months, in patients with TBI admitted to hospital for >48 hours or symptomatic patients not admitted or those admitted for < 48 hours.37 We recommend screening for adrenal, gonadal and thyroid deficits at 3-6 months and 12 months post-injury after all severities of TBI, including mild TBI and sport-related concussion with clinical suspicion of hormone deficiency. If any hormone deficits are identified, referral to endocrinology is recommended. At 1-year post-injury, in all severities of TBI, if patients present with signs and symptoms of growth hormone deficiency, we recommend a 30 BRAIN INJURY professional referral to endocrinology for dynamic testing. Opinions differ, but one group suggests if hormone deficits are identified at 12-months post-injury, annual repeat assessment for up to 5 years should be completed (Figure 1).36 All patients with TBI presenting with signs and symptoms of HPA deficits should be screened at the appropriate timepoints after injury to improve symptom burden and enhance recovery. If deficiencies are identified, it is important hormone replacement is not delayed as optimization of a patient’s wellbeing will enhance rehabilitation participation and subsequently improve symptoms and function. Neurorehabilitation teams members such as physiotherapists, occupational therapists, social workers, recreational therapists, nurses, and physical medicine and rehabilitation physicians provide care for patients with TBI at all stages of recovery. Identification and treatment of neuroendocrine deficits during TBI rehabilitation can provide the neurorehabilitation specialist with another important tool to optimize patient’s health. References 1. DEWAN, M. C. et al. Estimating the global incidence of traumatic brain injury. J Neurosurg, v. 130, n. 4, p. 1080-1097, Apr 27 2018. ISSN 1933-0693. Disponível em: < https://www.ncbi.nlm.nih.gov/ pubmed/29701556 >. 2. EMELIFEONWU, J. A. et al. Prevalence of Anterior Pituitary Dysfunction Twelve Months or More following Traumatic Brain Injury in Adults: A Systematic Review and Meta-Analysis. J Neurotrauma, v. 37, n. 2, p. 217226, Jan 15 2020. ISSN 1557-9042. Disponível em: < https://www.ncbi.nlm.nih.gov/pubmed/31111791 >. 3. 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