Homolateral ataxia and crural paresis

Perman, Gerald P.; Racy, Anis

doi:10.1212/wnl.30.9.1013

Cited by 52 publications

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“…The majority of patients with hypesthetic ataxic hemiparesis in our series had infarcts localized by CT or MRI to the posterior third of the posterior limb of the internal capsule and contiguous paraventricular region. This distribution is similar to that found by Fisher and Cole, 2 by Huang and Lui, 4 and by Perman and Racy, 36 whose patients with ataxic hemiparesis also had sensory deficits. Verma et al 35 and de Renzi and Nichelli 19 localized infarcts in a similar clinical syndrome to a more anterior and rostral portion of the posterior limb of the internal capsule.…”

supporting

confidence: 90%

Capsular hypesthetic ataxic hemiparesis.

Helgason

Wilbur

1990

Stroke

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Twenty-three patients with hypesthetic ataxic hemiparesis underwent computed tomography or magnetic resonance imaging. Twenty-two patients had infarcts of lacunar or slightly larger size in the contralateral posterior limb of the internal capsule. In 15 patients the infarct extended superiorly into the adjacent paraventricular region, and in seven it extended into the lateral thalmus. In eight patients the infarct was limited to the posterior limb of the internal capsule, and in only two patients was an ipsilateral to capsular pontine lacune found. Despite a location similar to that of pure motor and pure sensory lacunar stroke, hypesthetic ataxic hemiparesis correlates with larger infarcts, most often located in the posterior medial superior territory of the antierior choroidal artery. Some infarcts appeared to be localized immediately posterolateral to this region, in the posterior cerebral artery territory. The presence and extent of infarction is better detected by the addition of magnetic resonance imaging to computed tomography. (Stroke 1990;21:24-33)

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confidence: 90%

Capsular hypesthetic ataxic hemiparesis.

Helgason

Wilbur

1990

Stroke

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“…Ataxic hemiparesis has also been described as a result of lesions in the ventrolateral midbrain 1 ' and superior portion of the posterior limb of the internal capsule. 10 The term ataxic hemiparesis describes a clinical picture and implies neither localization nor pathologic process. Though a cryptic arteriovenous malformation cannot be excluded in this case, a highly localized hypertensive hemorrhage must also be considered since the lesion occurred in the distribution known to be the site of the miliary aneurysm of hypertensive cerebral vascular disease."…”

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confidence: 99%

Pontine hemorrhage presenting as ataxic hemiparesis.

Schnapper¹

1982

Stroke

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“…5 The size of the infarct is usually small, with a diameter of 6 to 10 mm, 2 but larger infarcts have been described in computed tomography (CT) 3 -*• 7 and pathologic stud ies. 2 Although a source of emboli in patients with deep cerebral infarcts is almost never considered, a few experimental 8 and pathologic 1 studies suggest that some may be embolic.…”

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confidence: 99%

Cerebral infarction of the basal ganglia due to embolism from the heart.

Santamaria¹,

Graus²,

Rubio³

et al. 1983

Stroke

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SUMMARY We studied 8 patients with cerebral infarction in the deep territory of the middle cerebral artery (MCA). All patients had a definite cardiac source of emboli and no known factors for thrombosis. Mixed sensory and motor deficit was found in all but one patient and CT scan showed larger lesions than usually reported in lacunar infarcts. Contrast enhancement was seen in all cases in which CT scan was performed in the second or third week. It is concluded that embolic infarcts in deep cerebral territory of MCA from a cardiac source are more frequent than previously reported. This diagnosis has to be consid ered when CT scan demonstrates a deep cerebral infarct.Stroke Patients and MethodsWe reviewed records of all patients with deep cere bral infarcts confirmed by CT seen during the period 1979-1981. Patients with hypertension (blood pres sure equal or more than 160/95 mm Hg in several determinations) diabetes, blood hematocrit greater than 45%, heavy cigarette smoking or vasculitis were excluded. This review yielded 8 patients without known risk factors for a thrombotic disease and with a definite heart disease with high probability of cerebral embolization. Six patients had rheumatic heart disease and mitral valve stenosis, five of them with atrial fi brillation. The disease was diagnosed by clinical histo ry and auscultation. In three cases it was confirmed at surgery. One patient had an aortic prosthetic valve (Starr-Edwards) and anticoagulation had been stopped one year before the stroke because of gastrointestinal bleeding. Another patient had a subacute bacterial en docarditis with blood cultures positive for Streptococ- cus salivarius and infected vegetations were confirmed at surgery. Results Clinical and CT findings are summarized in table 1.The clinical deficit had an abrupt onset, reaching its peak in a few minutes in half of the patients. In two patients, the deficit progressed during the next 3 hours; and in the remaining 2, a fluctuating course over sever al hours was seen before stabilization occurred. Neuro logical examination showed a complete (5 cases) or incomplete (3 cases) hemiplegia, accompanied by hypesthesia in 6 patients. A pure motor hemiplegia was only seen in one case. In three of them, a transitory anosognosia was clearly observed. In a further patient (case 8), the motor hemiplegia was accompanied by an expressive dysphasia. Her language disorder was char acterized by nonfluent conversational speech, naming and reading difficulties, dysgraphia and a normal audi tory comprehension. She was almost normal one year after the stroke. Recovery of the motor and sensory deficit was complete in two patients, moderate in four, and poor in two. EEG was performed on 7 patients. In all but one case, EEG showed a discrete focal slowing. The most common CT abnormality, seen in four cases, was a well-defined low density area placed in caudate, putamen and anterior limb of internal capsule ( fig. 1). In a further 3 cases, CT showed a posterior extension (fig. 2). The patient with aphasia had...

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Homolateral ataxia and crural paresis

Cited by 52 publications

References 0 publications

Capsular hypesthetic ataxic hemiparesis.

Capsular hypesthetic ataxic hemiparesis.

Pontine hemorrhage presenting as ataxic hemiparesis.

Cerebral infarction of the basal ganglia due to embolism from the heart.

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