| Project/Area Number |
62570358
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Chiba University |
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Principal Investigator |
KOJIMA Shigeyuki Department of Neurology, Chiba University, School of Medicine, 医学部・神経内科, 助手 (40170245)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1988: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1987: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Ataxic hemiparesis / Crossed cerebellar atrophy / Corticopontocerebellar pathways / Cerebrocerebellar correlation / 大脳小脳連関 / 多発性硬化症 / 皮質・橋・小脳路 / 大脳・小脳連関 / 皮質橋路 |
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| Research Abstract |
The pathomechanism of the crossed cerebellar atrophy and ataxic hemiparesis, which seem to correlate with frontal ataxia, was investigated clinicoradiologically.
1. Crossed cerebellar atrophy. Crossed cerebellar atrophy was demonstrated by CT in 8 of the 130 patients who suffered from unilateral supratentorial cerebrovascular diseases. Of these 8 patients, 6 had cerebral infarction in the fronto-temporal lobe and 2 had cerebral hemorrhage (putaminal and thalamic hemorrhages respectively). It was observed that in 5 of the 8 patients with crossed cerebellar atrophy, atrophy was present in both crus cerebri and basis pontis and no dilatation or deformity of the fourth ventricle was seen in the 8 patients. The CT findings suggest that crossed cerebellar atrophy is not caused by the retrograde transsynapyic degeneration of the dentatorubrothalamic pathways but the anterograde trans-synaptic degeneration of the corticopontocerebellar pathways, especially from the fronto-temporal lobe.
2. Ataxic hemiparesis from demyelinating lesion in the crus cerebri. Two patients with multiple sclerosis are described who had ataxic hemiparesis and in whom MRI revealed localized lesion in the crus cerebri of midbrain on the side opposite the affected limbs. They had no deep sensory disturbance, and in one patient somatosensory evoked potentials were normal. The lesion demonstrated by MRI had not reached the midbrain tegmentum including the decussation of superior cerebellar peduncles or red nucleus. In these two patients, the MRI findings suggest that ataxic hemiparesis is caused by the interruption of cortico-pontine pathways and corticospinal tract in the crus cerebri.
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