Our findings indicate that the hand area in the cerebral motor cortex is located in the middle to lower portion of the anterior wall of the central sulcus, that is, in Brodmann area 4. We present our 8 patients showing isolated hand palsy due to a discrete cortical infarction on MRI to expand the knowledge about cortical localization of the hand area.

Background and Purpose: Dysarthria characterized by slurring with imprecise articulation without evidence of aphasia is a frequent symptom in the acute phase of cerebral ischemia, although there is little knowledge on its anatomic specificity and spectrum of associated clinical characteristics regarding diffusion-weighted imaging (DWI). Methods: An investigation of 101 consecutive patients with sudden-onset dysarthria due to a single or multiple lesions on DWI, corresponding to 8.7% of 1,160 patients with ischemic stroke, was made. The presence of lesions of the cranial arteries was sought by magnetic resonance angiography and reviewed with a three-dimensional rotating cineangiographic method. Results: Dysarthria was mostly associated with a supratentorial lesion (63%) and with a classic lacunar stroke syndrome in 45% of patients. Lacunar lesions on DWI were found in 69 (68%) patients, while only 45 of the patients (65%) with a lacunar infarct presented a classic lacunar syndrome with dysarthria. Pure dysarthria occurred in 15% of patients, dysarthria + pure motor hemiparesis in 14%, dysarthria + ataxic hemiparesis in 11%, dysarthria + clumsy hand syndrome in 7%, dysarthria + pure sensory stroke in 3%, dysarthria + central facial paresis in 8% and lingual paresis occurred in 2%. The lesions were due to small-artery disease in 41%, large-artery disease in 15%, cardioembolism in 10% and a mixed etiology in 3%. The cause of stroke was not identified in 17 patients. Lesions on DWI were found mainly in the corona radiata (n = 18), middle cerebral artery territory, including the motor cortex and/or insular cortex (n = 13), striatocaudate nuclei (n = 11), primary motor cortex (n = 10), internal capsule (n = 7), pons (n = 25), pontobulbar junction (n = 5) and the thalamomesencephalic junction (n = 4). Isolated cerebellar infarctions (n = 6) or associated brainstem lesions (n = 6) affected mostly the superior cerebellar artery or the posterior inferior cerebellar artery territory. Conclusion: Cortical involvement was more frequent in patients with pure dysarthria than those with dysarthria and additional neurological signs, while the frequency of pontine involvement was higher in patients with additional neurological signs than those with pure dysarthria. One third of the patients with dysarthria had multiple lesions on DWI, and the most common cause of stroke was small-artery disease. Pure dysarthria, dysarthria with lingual paresis, dysarthria with clumsy hand and dysarthria with facial paresis had predictive value for lacunar lesions.

Homonymous visual-field defects in our patients improved within 6 months. Restoration of the lower quadrants and especially the peripheral zones was noted. Incomplete damage to the striate cortex, which has a varying pattern of vascular supply, could explain this finding. Magnification factor theory, which is the increment of the receptive-field size of striate cortex cells with visual-field eccentricity, may explain the more significant improvement in the peripheral zones.

Epilepsy needs multi-dimensional analysis because of its chronic nature, frequently accompanying psychiatric disorders, its negative effects on QOL and the important role social support plays. The clinicians' handling of patients at an early stage can play an important role in preventing the negative results of epilepsy.

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