| 정지성 뇌병변후 발생한 지연성 운동장애 |
| 천화영, 최일생 |
| 연세대학교 의대 신경과 |
| Delayed-onset movement disorders after static brain lesions |
| Hwa Young Cheon, M.D. , Il Saing Choi, M.D. |
| Dept of neurology , Yonsei Univ. College of Medicine |
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| Abstract |
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We studied 55 patients with static brain lesions who developed delayed-onset movement disorders. Of these, 29(52.7%) had pakinsonism, 17(30.9%) dystonia, 6(10.9%) chorea, 2(3.6%) tremor, and I(I.8%) myoclonus. The precipitating insults included carbon mono-oxide, poisoning in 32(58.2%), 6(10.9%), encephalitis in 5(9.1%)head injury, stoke and hypoxia, in 6(10.9%) patients each. Among the four Patients with initial insult occurring at age 2years or younger(infant group), all had dystonia. Distribution of dystonia was focal in one(25%), segmental in two(50%), and unilateral in one patient(25%). The mean latency between the original injury and the onset of movement disorder was 378.03+277.13 weeks. Among the 11 patient initial insults occurring between ages 5 and 17(childhood group), 7 had dystonia, 3 parkinsonism, 1chorea. The distribution of dystonia was focal in one, segmental in five, and unilateral in one patient; the mean latency between the original injury and the onset of movement disorder was 91.3+,230.1 weeks. Among the 40patients with initial insults occurring at ages 23 or older (adult group), 26(65.0%) had parkinsonism, 6(15.0%) dystonia, 5(12.5%) chorea, 2(5.0%) tremor, 1(2.5%) myoclonus. The distribution of dystonia in patient was focal in two(33.0%), and segmental in four(67.7%) patients. The mean latency of movement disorder onset in the 40 patients, of the adult group was 17.25+43.67weeks. Brain injury at a young age was associated with a longer latency to onset of subsequent movement disorder. Among the 45 initial brain computed tomography, 28 (62.2%) had abnormal findings; 14(31.1%) low density lesion in the basal ganglia, 7(15.6%) low density lesions in the cerebral white matter, 2(4.4%) low density lesion in the cerebral white matter and basal ganglia, and 5(l1.1%) cortical atrophy. Seventeen (37.8%) had normal neuroimaging finding. Many, but not all, patients had lesionon on brain imaging, but there was no clear correlation between the sites of damage on imaging and the clinical manifestation. |
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