Abstract
Crossed cerebellar atrophy (CCA) was investigated by using X-ray CT scan to establih its incidence, mechanism, its relation with cerebral lesions in 130 caes suffering from unilateral supratentorial cerebrovascular diseases. These 130 cases consisted of 83 males and 47 females with cerebral infarction (65 cases) and cerebral hemorrhage (65 cases). The patients' average age was 57.6 years.
Crossed cerebellar atrophy wa demontrated in 8 of the 130 cases (6.2%). Of these 8 cases, six had massive cerebral infarction in the middle cerebral artery area. These six cases accouted for 9.2% of the 65 cases with cerebral infarction. The six cases of CCA caused by cerebral infarction had lesions in the frontal and temporal lobes as a common lesion. Two had a cerebral hemorrhage in the putamen and in the thalamus, respectively, and these 2 cases accounted for 3.1% of hte 65 cases of cerebral hemorrhage. Of these 2 cases, the one with putaminal hemorrhage, hemorrhagic lesion was extended to the temporal and parietal lobes. And the another one with thalamic hemorrhage, the lesion was extended to the internal capsule and corona radiata. The attack of the cerebrovascular disease had occured in these patients with CCA more than 2 months previously.
It was observed that in 5 of the 8 cases with CCA, atrophy was present in the basis pedunculi and the basis pontis on the side of the cerebral lesion. However, no dilation nor deformity of the fourth ventricle was present in any of the patients, suggesting that none of the CCA patients had atrophy of the dentate nucleus.
Pathologically, it is thought that CCA is caused by the transsynaptic degeneration of the cortico-ponto-cerebellar pathway or the dentate-rubro-thalamic pathway. The cortico-ponto-cerebellar pathway begins chiefly in the frontal and temporal lobes, and it passes through the basis pedunculi and the basis pontis. So, the cases of CCA who had massive cerebral lesion in the frontal and temporal lobes or atrophy of the basis pedunculi and basis pontis suggest the presence of the transsynaptic degeneration of the cortico-ponto-cerebellar pathway. But in the case of the thalamic hemorrhage, who had not the hemorrhagic lesion in the frontal and temporal lobes, atrophy of the basis peduncli and basis pontis was not observed. Though dilation or deformity of the fourth ventricle is not observed in this case, presence of the degeneration of the dentate-rubro-thalamic pathway cannot be denied.
Thus, our clinical investigation suggests that CCA is caused by both the transsynaptic degeneration of the cortico-ponto-cerebellar pathway and the dentate-rubro-thalamic pathway.
