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Subjective excessive daytime sleepiness (SEDS) is a common sequela following traumatic brain injury (TBI) and occupies 14–57% of patients with TBI.1 Post-TBI, SEDS is related to daytime function, reduced cognitive function, and psychiatric disorders such as depression and anxiety; thus, elucidation of its pathogenetic mechanism is clinically important.1 Although the pathogenesis of post-TBI SEDS has not been clearly elucidated, injury of several neural structures, including the hypothalamus, ascending reticular activating system and pontine nuclei, has been suggested as the pathogenetic mechanism of SEDS following TBI.1 Among these neural structures, injury of the hypothalamus, a key regulator of sleep and wakefulness, has been suggested as a convincing pathogenetic mechanism of post-TBI SEDS; however, this has not been clearly demonstrated.
TBI is classified as mild, moderate and severe according to the severity, and mild TBI has been reported in 75–85% of cases of TBI. Patients with mild TBI frequently experience various neurological symptoms derived from neural injury. Diffusion tensor imaging (DTI) has enabled quantitative estimation of neural structures and many studies have demonstrated injury of neural structures following mild TBI. However, no study on injury of the hypothalamus has been reported.
In this study, using DTI, we investigated the relation between SEDS and injury of the hypothalamus in patients with mild TBI.
Fifty-three patients with TBI and 33 age-matched and sex-matched healthy control subjects with no history of neurological, physical or psychiatric illness were recruited for this study. …
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