The Clinical neuropsychologist · 2025
Neuroendocrine dysfunction after TBI: A guide for the clinical neuropsychologist.
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Howell Stefanie N, Masel Brent E
Аннотация
OBJECTIVE: This review aims to provide neuropsychologists with a comprehensive understanding of neuroendocrine dysfunction following traumatic brain injury (TBI), emphasizing post-traumatic hypopituitarism (PTHP) and its implications for cognitive function and rehabilitation.
METHOD: A critical review of current literature on neuroendocrine dysfunction following TBI, including studies on pituitary function, hormone deficiencies, and their effects on cognition, mood, and fatigue. The review integrates findings from endocrinology, neuroscience, and clinical neuropsychology to highlight the importance of interdisciplinary management.
RESULTS: Research indicates that a high proportion of moderate to severe TBI cases may develop PTHP, with growth hormone deficiency (GHD) as the most prevalent dysfunction. While less extensively studied, evidence suggests that individuals with persistent post-mild TBI symptoms may exhibit neuroendocrine dysfunction at similar rates to moderate to severe TBI patients. The impact of hormonal dysregulation on cognition and neuropsychological performance underscores the need for targeted assessment and intervention. Emerging data also suggest that metabolic disturbances, such as altered gut microbiota and amino acid imbalances, may contribute to post-TBI fatigue and cognitive impairment.
CONCLUSIONS: Neuropsychologists play a vital role in identifying and referring patients with suspected neuroendocrine dysfunction for appropriate testing and treatment. Recognizing PTHP as a potential contributor to chronic TBI symptoms may lead to improved patient outcomes through targeted hormonal therapies and interdisciplinary rehabilitation strategies. Increased awareness of the relationship between TBI, pituitary dysfunction, and cognition is essential for optimizing clinical care.
METHOD: A critical review of current literature on neuroendocrine dysfunction following TBI, including studies on pituitary function, hormone deficiencies, and their effects on cognition, mood, and fatigue. The review integrates findings from endocrinology, neuroscience, and clinical neuropsychology to highlight the importance of interdisciplinary management.
RESULTS: Research indicates that a high proportion of moderate to severe TBI cases may develop PTHP, with growth hormone deficiency (GHD) as the most prevalent dysfunction. While less extensively studied, evidence suggests that individuals with persistent post-mild TBI symptoms may exhibit neuroendocrine dysfunction at similar rates to moderate to severe TBI patients. The impact of hormonal dysregulation on cognition and neuropsychological performance underscores the need for targeted assessment and intervention. Emerging data also suggest that metabolic disturbances, such as altered gut microbiota and amino acid imbalances, may contribute to post-TBI fatigue and cognitive impairment.
CONCLUSIONS: Neuropsychologists play a vital role in identifying and referring patients with suspected neuroendocrine dysfunction for appropriate testing and treatment. Recognizing PTHP as a potential contributor to chronic TBI symptoms may lead to improved patient outcomes through targeted hormonal therapies and interdisciplinary rehabilitation strategies. Increased awareness of the relationship between TBI, pituitary dysfunction, and cognition is essential for optimizing clinical care.