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외상성 뇌손상 후 수면-각성 리듬 교란을 동반한 환자의 증례
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  • 외상성 뇌손상 후 수면-각성 리듬 교란을 동반한 환자의 증례
  • A Patient with the Disrupted Sleep-Wake Rhythm after Traumatic Brain Injury
저자명
김은지, 김성헌, 이정희
간행물명
신경정신의학KCI
권/호정보
2019년|58권 3호|pp.252-258 (7 pages)
발행정보
대한신경정신의학회|한국
파일정보
정기간행물|KOR|
PDF텍스트(0.89MB)
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서지반출

국문초록

Many patients with a traumatic brain injury (TBI) experience a range of sleep problems. Although some studies investigated the pathophysiology of sleep-wake cycle disturbances in TBI patients, it has not been clarified. This paper presents a middle aged female patient who showed sleep deprivation and sleep-wake cycle disturbances for approximately three months after TBI. The improvement in the subjective and objective sleep quality was shown by the sleep diary and actigraphy during this period. Moreover, the dim light melatonin onset (DLMO) had been delayed before returning to the normal range in 3 months. In addition, the patient showed an improvement in the neurocognitive function, including attention, memory and language function, along with a consolidation of the sleep-wake cycle. This case showed that the sleep disturbance following a TBI was probably caused by the disrupted melatonin rhythm based on the abnormality of the DLMO. In addition, the cognitive dysfunction after TBI could be associated with sleep-wake cycle disturbances because its gradual improvement occurred as the sleep disturbance diminished. Further studies on the change in circadian rhythm after a brain injury related to neurocognitive impairment are required.

영문초록

Many patients with a traumatic brain injury (TBI) experience a range of sleep problems. Although some studies investigated the pathophysiology of sleep-wake cycle disturbances in TBI patients, it has not been clarified. This paper presents a middle aged female patient who showed sleep deprivation and sleep-wake cycle disturbances for approximately three months after TBI. The improvement in the subjective and objective sleep quality was shown by the sleep diary and actigraphy during this period. Moreover, the dim light melatonin onset (DLMO) had been delayed before returning to the normal range in 3 months. In addition, the patient showed an improvement in the neurocognitive function, including attention, memory and language function, along with a consolidation of the sleep-wake cycle. This case showed that the sleep disturbance following a TBI was probably caused by the disrupted melatonin rhythm based on the abnormality of the DLMO. In addition, the cognitive dysfunction after TBI could be associated with sleep-wake cycle disturbances because its gradual improvement occurred as the sleep disturbance diminished. Further studies on the change in circadian rhythm after a brain injury related to neurocognitive impairment are required.

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