Abstract
Ataxic hemiparesis (AH) is characterized by the occurrence of unilateral weakness and pyramidal signs combined with ipsilateral cerebellar-like ataxia. AH was initially considered a lacunar syndrome because it correlated with lacunar infarctions, but subsequent reports have suggested that it is not, in fact, significantly correlated with these infarctions. Indeed, studies have shown that not only lacunar infarction but also cardioembolic and large-artery atherosclerosis can cause AH, with others showing that hemorrhagic strokes, tumors, head trauma, infection, and demyelinating diseases are 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 patients with AH. Regardless of the precipitating insult, specific AH symptoms probably result from damage to afferent or efferent cerebellar pathways, while variability in those symptoms probably reflects the size and location of the infarction. Optimal treatment strategies naturally depend on treating the underlying etiology and, to date, have primarily included antithrombotic therapies. The prognosis for AH following ischemic stroke is generally good. In this chapter, the clinical features, lesion topography, treatment, and prognosis of AH are detailed.
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Hiraga, A. (2020). Ataxic Hemiparesis. In: Manto, M., Gruol, D., Schmahmann, J., Koibuchi, N., Sillitoe, R. (eds) Handbook of the Cerebellum and Cerebellar Disorders. Springer, Cham. https://doi.org/10.1007/978-3-319-97911-3_74-2
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