Isolated dysarthria due to extracerebellar lacunar stroke: a central monoparesis of the tongue

Abstract

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)

Transient Hemiglossal Denervation during Acute Internal Capsule Infarct in the Setting of Dysarthria−Clumsy Hand Syndrome

“…3 Of additional note, despite the close anatomic proximity of the corticolingual and corticofacial motor tracts, corticofacial tracts are primarily contralateral, without bilateral uncrossed fibers, so that corticofacial infarction most often results in facial paresis. 7 Unilateral findings in this case support the existence of predominant contralateral innervation from the motor cortex to the hypoglossal nucleus. Lack of tongue deviation on physical examination in this case could be explained by transient or incomplete denervation of the tongue that was in the process of recovering, preserved contralesional corticolingual innervation of the hypoglossal nucleus maintaining normal bilateral tongue function, or tongue apraxia preventing full tongue protraction, thus masking deviation.…”

“…3 Tongue movement dysfunction is inconsistently seen in patients with dysarthria, even with abnormal corticolingual conduction measured by TMS, and is attributable to bilateral innervation. 7 Even with motor impairment, physical findings may be masked by apraxia, because tongue deviation may only be detected at full protraction. 3 Of additional note, despite the close anatomic proximity of the corticolingual and corticofacial motor tracts, corticofacial tracts are primarily contralateral, without bilateral uncrossed fibers, so that corticofacial infarction most often results in facial paresis.…”

“…2 Commonly, supranuclear hypoglossal palsy is associated with ipsilesional arm weakness and supranuclear facial palsy, dysarthria, and dysphagia, presumably due to the close anatomic relationship of the respective motor pathways. 6,7 While the hypoglossal nerve is a lower motor neuron, crossed and uncrossed upper motor neuron corticolingual fibers extend from both hemispheres to the hypoglossal nuclei. 5 Following unilateral infarction, TMS of the affected hemisphere fails to produce an ipsilateral or contralateral lingual response, whereas TMS of the unaffected hemisphere produces a bilateral lingual response, even in the setting of unilateral lingual paralysis.…”

“…[2][3][4][5][6][7] We report a case of transient reversible hemiglossal denervation edema on MR imaging, contralateral to acute internal capsule infarction in the clinical setting of DCHS. A neuroanatomic basis is discussed.…”

Pure Dysarthria Resulting from a Small Cortical Infarction Located at the Left Middle Frontal Gyrus

“…In the majority of cases, pure dysarthrias are caused by subcortical lesions, but in some cases cortical lesions cause pure dysarthria (2,3,(5)(6)(7). All extracerebellar infarctions were more frequent and more severe, when caused by left-sided lesions and were located along the course of cortico-bulbar tract fibers (8).…”