Ataxic hemiparesis

Abstract

Ataxic hemiparesis (AH) is characterized by the simultaneous presence of a pyramidal tract syndrome with homolateral ataxic syndrome. In the first description of AH by Fisher and Cole (1965), they elaborated the core symptoms as weakness and pyramidal signs on one side combined with ipsilateral cerebellar-like Ataxia. However, subsequent reports have expanded the clinical spectrum of AH to include cases with persistent hemisensory deficits and additional symptoms like dysarthria or facial paresis. AH was initially described as a lacunar syndrome correlating with lacunar infarctions. However, recent reports have suggested that AH is not significantly correlated with these infarctions, and in fact a substantial number of studies have demonstrated that lacunar infarction as well as cardioembolic and large-artery atherosclerosis can cause AH. In addition, hemorrhagic strokes, tumors, head trauma, infection, and demyelinating diseases have all been associated with AH. The pons, corona radiata, thalamus, and internal capsule are the most commonly reported lesion sites in AH; however, cortical lesions have also been observed in some AH patients. Regardless of the precipitating insult, specific AH symptoms are thought to result from damage to corticospinal and cerebellar pathways (efferent or afferent), while variations in symptomology reflect the size and precise location of the infarct lesion. Optimal treatment strategies naturally depend on treating the underlying etiology, and to date, have included anticoagulant and antiplatelet drug therapies. The prognosis for AH following ischemic stroke is generally good. This chapter provides an update on the clinical features, lesion topography, treatment, and prognosis of AH.