Presentation

HOMOLATERAL ATAXIA AND CRURAL PARESIS: coined by Fisher later renamed the syndrome "ataxic
hemiparesis," meaning

any combination of weakness and incoordination, out of proportion to weakness, on the same
side of the body.

The usual clinical features as described by Fisher and Cole include

- "weakness of the lower limb, especially the ankle and toes, and a Babinski sign,
-
-
associated with striking dysmetria of the arm and leg on the same side."[7]
-

- Some of the patients also had transient paresthesias

- Dysarthria (less common)
- Nystagmus (less common)
- Gait deviation toward the affected side (less common)

ABSENT cortical signs:

aphasia, agnosia, neglect, apraxia, or hemianopsia

Causes
Lesions that simultaneously interrupt

- pyramidal systems (weakness) and

- adjoining frontopontocerebellar systems (ataxia) produce ataxic hemiparesis.

Locations

The corona radiata and the anterior limb of the internal capsule are common sites of injury.

Fisher reported 3 autopsied cases (coined ataxia-hemiparesis in this paper) that showed contralateral lacunar
infarcts in the upper basis pontis.[59, 60]

A computed tomography (CT)-based series of patients with ataxic hemiparesis has also shown lesions in the

- internal capsule (posterior limb),

- Capsular ataxic-hemiparesis will cause the syndrome by involving the corticospinal tract as well as the frontopontine
fibres in the posterior limb of the internal capsule. Although capsule ataxia hemiparesis seems frequently to be
associated with sensory loss, sensory loss is not essential for ataxia to be present, as in Iragui and McCutchen's case,
and our case 4 (FS LUI)
- corona radiata,
- lentiform nucleus, and
- thalamus.[43, 70, 71]

Overall, no distinct clinical features differentiate lacunar infarctions originating in the capsule from
those in the pons.[72]

In addition to small, deep infarcts, larger anterior cerebral artery infarcts have been recognized as a cause of
ataxic hemiparesis with leg-predominant weakness.

Ataxic hemiparesis also has been described in several nonischemic lesions, particularly hemorrhages[73, 74] and
tumors[75, 76] .

Disease course
Overall, improvement occurs within days or weeks. Occasionally, the hemiparesis improves, and the ataxia
remains.[77]