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We read with interest the article by Urbanet al. Using transcranial magnetic stimulation, the authors demonstrated electrophysiological evidence for a central monoparesis of the tongue in patients with isolated dysarthria from stroke.1 As in their patients transcranial magnetic stimulation induced absent or delayed corticolingual responses at the tongue, the authors ascribed isolated dysarthria to interruption of the corticolingual pathways. On the whole, these results seem plausible, but we would like to comment on the underlying mechanism of isolated dysarthria.
As in the case of isolated dysarthria reported by Urbanet al, all of our patients with isolated dysarthria had lacunar infarctions involving the internal capsule and corona radiata.2 Measurement of cerebral blood flow with IMP-SPECT in these patients disclosed frontal cortical hypoperfusion, particularly in the anterior opercular and medial frontal regions. Anterior opercular lesions produce facio-pharyngo-glosso-masticatory paresis (anterior opercular syndrome), and damage to the medial frontal regions, including the supplementary motor area, causes speech expression disorders. White matter lesions can disrupt afferent and efferent fibre connections with cerebral language areas, resulting in dysfunction of these cortices.3 Therefore, we postulated that isolated dysarthria results from interruption of corticosubcortical networks indispensable for speech output, involving the thalamocortical and corticostriatal fibres as well as the corticobulbar fibres. In fact, lacunar infarctions around the internal capsule-corona radiata are likely to undercut these ascending and descending projections.4 5
To assess corticopontocerebellar tract function, Urbanet al investigated cerebellar blood flow in patients with isolated dysarthria using HMPAO-SPECT. The authors concluded that the corticopontocerebellar tract is preserved in isolated dysarthria because of no evidence for cerebellar diaschisis on SPECT. Their SPECT findings on cerebellar blood flow were similar to our results. However, we wonder whether cerebral cortical blood flow was preserved in their patients, because our SPECT study suggested frontal cortical dysfunction as an underlying mechanism of isolated dysarthria. Lingual paresis was clinically evident in three of seven patients reported by Urban et al and in two of 12 by us. This indicates that isolated dysarthria originates in incoordination of multiple organs necessary for articulation as well as a lingual monoparesis. Although interruption of the corticolingual pathways is a likely cause of isolated dysarthria, it should be borne in mind that damage to other descending and ascending projections may contribute to isolated dysarthria.
Urban et al reply:
Okuda et al draw attention to their article on pure dysarthria inStroke 1-1 which we read with much interest. They refer to 12 patients with pure dysarthria, 11 of whom showed multiple bilateral infarctions involving the internal capsule and corona radiata. The main difference to our series of seven patients is the multiple involvement of the brain. We think that single lesions as collected by us1-2 are more appropriate to correlate lesion topography with impaired function. The findings of Okudaet al are in line with our conclusion that interruption of the corticolingual pathway is crucial in the pathogenesis of dysarthria of extracerebellar origin. Obviously, impairment of the corticolingual tract of one hemisphere by a single small lesion is an adequate condition for dysarthria. The patients of Okuda et al had more severe vascular disorder of the brain than our patients as can be concluded from the multiple infarctions. Thus, the bilateral frontal cortical hypoperfusion as disclosed by SPECT in the series of Okudaet al may be due to infarction in other parts of the brain compared with the lesion causing pure dysarthria.