Background and Purpose-Isolated dysarthria, termed pure dysarthria, develop
s rarely after stroke, and its pathophysiology remains unclear. To clarify
the underlying mechanism of pure dysarthria, we investigated lesion sites a
nd cerebral blood flow in patients with pure dysarthria.
Methods-We examined 12 patients with pure dysarthria who underwent MRI and
cerebral blood flow study. To visualize cortical blood flow, a three-dimens
ional display was generated from single-photon emission computed tomography
(SPECT). Regional cerebral blood now of the patients was semiquantitativel
y measured with SPECT and N-isopropyl-p[I-123]iodoamphetamine as a tracer a
nd compared with that of 11 control subjects.
Results-On MRT, multiple lacunar infarctions were noted bilaterally in 11 p
atients, all of whom had lesions involving the internal capsule or corona r
adiata. The other patient had a unilateral internal capsule-corona radiata
infarction. Three-dimensional display showed frontal cortical hypoperfusion
in 8 patients. Since interhemispheric differences of blood flow were not s
ignificant in any region of the 12 patients, the mean of left and right cor
tical blood flow was analyzed. Compared with the control subjects, cortical
perfusion was significantly reduced in the patients' frontal regions, spar
ing the sensorimotor, temporal, and parietal cortices and the cerebellum. R
eductions of perfusion were rather pronounced in the anterior opercular, me
dial prefrontal and premotor, and anterior cingulate regions.
Conclusions-Pure dysarthria results mainly from multiple lacunar infarction
s, which induce frontal cortical hypoperfusion, probably due to interruptio
n of corticosubcortical networks. We conclude that frontal cortical hypoper
fusion, particularly in the anterior opercular and medial frontal regions,
plays an important role in the development of pure dysarthria.