Dysarthria is a frequent symptom in cerebral ischaemia. However, speech characteristics of these patients have not previously been investigated in relation to lesion site in a prospective study. We investigated the auditory perceptual features in 62 consecutive patients with dysarthria due to a single, non-space-occupying cerebral infarction confirmed by MRI. Standardized speech samples of all patients were stored within 72 h after stroke onset using a digital tape recorder. Speech samples were assessed independently by two experienced speech therapists, who were unaware of the clinical and neuroradiological findings, using an interval scale ranging from 0 to 6. Separately assessed were features of articulation, phonation, prosody, and the global severity for a total of 31 items. Extracerebellar infarctions (85.5%) were located in the lower motor cortex (14.5%), striatocapsular region (46.8%) and base of the pons (24.2%). Isolated cerebellar infarctions were present in 14.5% of patients. There was a strong correlation between the findings of both examiners, showing identical scores, or only minor differences (<1 on the assessment scale) for 80% of all items. The average severity of dysarthria was 2.9 +/- 1.3. Articulatory abnormalities were the predominant deviation characteristics, affecting in particular the production of consonants. However, phonatory and prosodic abnormalities were also frequently observed speech characteristics. As revealed by factor analysis of speech characteristics the total severity of dysarthria was mainly influenced by the impairment of articulation. Speech parameters describing characteristics of articulation and prosody showed significant side-to-side and area differences, while this effect was lacking for any voice parameter. Left cerebral lesions showed a more severe overall impairment of speech and articulation, independent of lesion topography. Thirty-eight of 62 patients were available for follow-up. Speech evaluation showed normal speech within weeks in 15 out of 38 patients (39.5%). In the other 23 patients overall severity of dysarthria was mild. This is the first prospective study which describes speech characteristics of dysarthria due to acute unilateral cerebral infarctions. We could demonstrate that dysarthria in extracerebellar infarctions was more frequently caused by left-sided lesions and that the severity of dysarthria was more pronounced in left-sided lesions independent from lesion topography. All extracerebellar lesions were located along the course of the cortico-bulbar tract fibres. Compatible with a common pathophysiological basis of dysarthria in these patients, none of the 31 speech items differed significantly between subcortical and brainstem lesions.

Extracerebellar infarcts causing dysarthria were located in all patients along the course of the pyramidal tract. This finding correlates with the frequent occurrence of associated pyramidal tract signs in 90.7% (n = 62) of patients. Isolated cerebellar infarcts leading to dysarthria were in all cases located in the territory of the superior cerebellar artery.

Objectives-The pathophysiology of dysarthria can preferentially be studied in patients with the rare lacunar stroke syndrome of "isolated dysarthria". Methods-A single study was carried out on seven consecutive patients with sudden onset of isolated dysarthria due to single ischaemic lesion. The localisation of the lesion was identified using MRI. The corticolingual, cortico-orofacial, and corticospinal tract functions were investigated using transcranial magnetic stimulation. Corticopontocerebellar tract function was assessed using 99m Tc hexamethylpropylene amine oxime-single photon emission computerised tomography (HMPAO-SPECT) in six patients. Sensory functions were evaluated clinically and by somatosensory evoked potentials. Results-Brain MRI showed the lesions to be located in the corona radiata (n=4) and the internal capsule (n=2). No morphological lesion was identified in one patient.Corticolingual tract function was impaired in all patients. In four patients with additional cortico-orofacial tract dysfunction, dysarthria did not diVer from that in patients with isolated corticolingual tract dysfunction. Corticospinal tract functions were normal in all patients. HMPAO-SPECT showed no cerebellar diaschisis, suggesting unimpaired corticopontocerebellar tract function. Sensory functions were not aVected. Conclusion-Interruption of the corticolingual pathways to the tongue is crucial in the pathogenesis of isolated dysarthria after extracerebellar lacunar stroke. (J Neurol Neurosurg Psychiatry 1999;66:495-501)

The results of this study demonstrate that articulatory movements of the tongue and orofacial muscles are involved in the activation of the rostral paravermal area of the anterior lobe. This location corresponds to the area involved in cerebellar ischemia in patients with dysarthria. Lesions in the upper paravermal area of the right cerebellar hemisphere, the site of coordination of articulatory movements of the tongue and orofacial muscles, may lead to the development of dysarthria that is unrelated to (often concomitant) brainstem infarctions.

Our results indicate the early and in most cases subclinical corticobulbar tract involvement of the central motor pathways to the orofacial muscles and tongue in ALS. TMS of the tongue and orofacial muscles had a higher sensitivity in identifying UMN lesions than that of the upper and lower limbs.