Literature DB >> 2063066

[Cerebral crossed diaschisis caused by cerebellar lesion: role of the cerebellum in mental functions].

E Attig1, M I Botez, C Hublet, C Vervonck, J Jacquy, A Capon.   

Abstract

In 3 patients with a stroke limited to the posterior fossa, regional cerebral blood Flows were measured by the 133 Xe inhalation method (the first two cases) or by the SPECT with HMPAO method (the third case). The first patient had a median and paramedian hematoma of the left cerebellar hemisphere and the left dorsolateral portion of the pons. Remote cerebral hypoperfusion, measured 3 months later, was observed in both frontal premotor regions (but more marked in the right hemisphere) and in a circumscribed area of the right temporal region. The second patient had a right-sided ischaemic lesion of the anterior cerebellar lobe and the mesencephalic tectum. Contralateral parietal and rolandic hypoperfusion, measured 7 weeks after the stroke, was observed. The third patient had on old infarct of the right cerebellar hemisphere. The SPECT, measured 17 years later, showed a left fronto-parieto-temporal hypoperfusion and the absence of perfusion in the right cerebellar hemisphere. Preliminary data of neuropsychological assessment in our patients disclosed impairment in visuo-spatial and constructive organization, memory and learning compatible with the published findings in some patients and animals with predominantly cerebellar damage. These interesting findings should be confirmed in a large number of patients with age, sex, and sociocultural matched controls. In the absence of supratentorial insult, and during the hemodynamical stable phase, crossed cerebello-cerebral diaschisis is suggested in our 3 patients. Although it is too early to draw definite conclusions, our findings may: (1) confirm the functional interconnections between the cerebellum and the cerebrum in man and (2) provide functional basis for the behavioral function impairment reported in patients with cerebellar insult. Further rCBF, metabolism, and pathologic studies on this subject are required to elucidate this issue.

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Year:  1991        PMID: 2063066

Source DB:  PubMed          Journal:  Rev Neurol (Paris)        ISSN: 0035-3787            Impact factor:   2.607


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