Ataxic-Hemiparesis, Localization and Clinical Features 363

C. Y. HUANG, M . M E D . , F.R.A.C.P., AND F. S. LUI, M.B., B.S., M.R.C.P.

SUMMARY Five additional cases of ataxic-hemiparesis are reported. In 3 cases, computed tomographyshowed an area of decreased attenuation in the posterior limb of the internal capsule, and in 1 case, 2 areasof attenuation in the corona radiata. A review of previously reported cases suggest that brainstem ataxic-hemiparesis may be separated from supratentorial forms of ataxic-hemiparesis by the presence of nystag-mus, dysarthria, cranial neuropathy, and the absence of sensory abnormality.

Stroke Vol 15, No 2, 1984

ATAXIC HEMIPARESIS IS an unusual clinical syn-drome first described by Fisher and Cole,1 where thereis weakness and ataxia on the same side. Since thenthere has been 10 cases reported, where it has beenpossible to localize the site of the lesion pathologicallyor by means of computed tomography.2"8 We wish toadd 5 more cases studied by computed tomography andsuggest there may be recognizable clinical differencesbetween ataxic hemiparesis caused by a brainstem anda supratentional lesion.

Case ReportCase 1

A 67 year old man, known to be hypertensive and onmedication for 10 years, suddenly developed a sense ofunsteadiness, followed 3 hours later by weakness ofthe left arm in the afternoon. The next morning hefound his left leg to be both numb and weak as well.There was no vertigo, diplopia or headaches. Generalexamination was unremarkable. Blood pressure was145/80, pulse 80 per minute, regular. There were nobruits heard. He was alert, orientated, with normalspeech. There was minimal left facial weakness, with agrade 4/5 left hemiparesis. Stretch reflexes were in-creased on the left, with a positive Babinski sign. Posi-tion and vibration sense was lost on the left and therewas subjective decreased touch and pin prick sensa-tion. There was marked difficulty in performing fin-ger-nose, and heel-shin tests, as well as difficulty withrapid alternate movements on the left. The cranialnerves and fundi were normal. No nystagmus wasseen. On walking he would fall to the left. His fastingblood glucose was found to be elevated on severaloccasions (18.2-20.4 mmol/L). A C.T. scan on thethird day revealed a low density area in the posteriorlimb of the right internal capsule (fig. 1). When seen 1year after discharge, he continued to have an ataxicupper limb, with absent position sense.

Case 2A 71 year old male, known to be hypertensive and

on irregular treatment for some years, suddenly devel-oped a right sided clumsiness and weakness. Therewas no diplopia, vertigo, or headache.

On admission, general examination revealed ablood pressure of 160/100, pulse 80, regular. No bruitwas heard. He was alert, orientated with normal

From the Department of Medicine, University of Hong Kong.Address correspondence to: C. Y. Huang, M.Med., F.R.A.C.P ,

University Department of Medicine, Queen Mary Hospital, PokfulamRoad, Hong Kong.

Received June 22, 1983; revision #1 accepted September 19, 1983.

speech. Cranial nerves and fundi were normal. Therewas a grade 4 right hemiparesis, and on walking hewould fall toward the right. Reflexes were generallybrisk, but more so in the right knee and ankle. Babinskiresponse was present on the right. There was markedataxia in performing the heel-shin and finger-nose testson the right, and rapid alternate movements were alsodefective. Vibration was absent on the right, but othersensation appeared to be normal. C.T. scan on thethird day revealed a low density lesion in the left puta-men/posterior limb internal capsule region (fig. 2). Hisweakness subsided by the fourth day, but there wasstill ataxia at his discharge a week later.

Case 3A 64 year old male, previously well, suddenly de-

veloped weakness of right leg, with unsteadiness ofgait, whilst walking in the street. Some hours later henoted numbness and weakness of the right upper limbas well. There was no diplopia, vertigo or headaches.General examination revealed blood pressure of 170/100, pulse 72, regular. No bruit was heard. He wasalert, orientated, with normal speech. Cranial nervesand fundi were normal. He had a hemiplegia gait, withdragging of his left leg. There was a grade 4 righthemiparesis which included the face. Reflexes wereincreased on the right ankle only, with absent Babinskiresponse. There was decreased pain and touch sensa-tion subjectively on the right with absent right lowerlimb position sense. Finger-nose testing was inaccu-rate, and rapid alternate movement defective in theright upper limb, and heel-shin response defective inthe lower limb. Three days later, the ataxia remained,though the upper limb power had returned to normal.C.T. scan performed on the sixth day revealed twovague areas of low attenuation in the left corona ra-diata, with no enhancement after contrast (fig. 3).

Case 4A previously healthy 72 year old man suddenly de-

veloped right sided weakness and numbness. On ad-mission he had a grade 2 right hemiparesis, withhyper-reflexia and decreased sensation to touch andpin prick on the right. Blood pressure was 190/110,pulse 70 regular. No bruit was heard. Over the nextfew days his power rapidly improved to grade 4, andhis sensation returned to normal. However he was no-ticed then to be ataxic on doing the finger-nose andheel-shin tests, as well as have dysdiadokokinesia, onthe right. C.T. scan showed a low density lesion ex-truding into the posterior limb of the internal capsuleon the left (fig. 4).

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364 STROKE VOL 15, No 2, MARCH-APRIL 1984

FIGURE 1. Showing low density area in the posterior limb of FIGURE 3.the right internal capsule. (Case I) (Case 3)

Low density area seen in the left corona radiata.

Case 5A previously healthy 57 year old woman, developed

mild unsteadiness in her gait suddenly. Four days later,she woke up from her sleep, with a hoarse voice, andleft sided weakness and clumsiness. On admission, shehad a normal blood pressure 140/80, pulse 70 per min-ute, regular.

There was no definite abnormality found in the cra-nial nerves. Nystagmus was not present. There was aleft facial weakness with grade 4 left hemiparesis, andhyper-reflexia on the left. No sensory loss could bedetected. She fell to the left on walking. Ataxia onperforming finger-nose and abnormality in rapid alter-nate movement was present in the left upper limb.

Heel-shin test was normal in the legs. C.T. scan on theseventh day revealed no abnormality.

DiscussionFisher and Cole1 originally described the syndrome

of ataxic-hemiparesis under the name of homolateralataxia and crural paresis. They described 14 patients,who all had a picture of leg weakness, and homolateralataxia, without face or arm weakness, and normal sen-sation in all but one. Two of the patients had nystag-mus. In one of the cases an infarct was found in theposterior limb of the internal capsule. But as he alsohad other infarcts, clinicopathological correlation waslimited. Since then, Fisher2 has reported 3 cases where

FIGURE 2. Showing low density area in the posterior limb ofthe left internal capsule and the putamen. (Case 2)

FIGURE 4. Low density area on the left posterior limb of inter-nal capsule. (Case 4)

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ATAXIC HEMIPARESIS/tfHang and Lui 365

infarct was found in the basis pontis opposite the sideof the neurological deficit. All 3 patients had face andarm weakness as well, though in one of them, the toesand ankles were very much weaker, and in anothershoulder and grip weakness was more noticed. Threeother cases of ataxic-hemiparesis have also been de-scribed in the brainstem. Schnapper3 described a casedue to pontine haemorrhage documented by C.T. scan,causing nystagmus, face, arm, and leg paresis, andataxia. Sakai, Murakami and Ito4 described a case withweakness of right arm, and leg, and slight facial asym-metry, with dysarthria, and left trigeminal weakness.C.T. scan revealed a pontine infarction. Bendheim andBerg5 described a case of a 10 year old boy with acutelymphocytic leukemia, who developed a right ataxic-hemiparesis which involved the face as well as limbequally. C.T. scan showed a mass lesion presumablydue to leukemia infiltration, in the left rostral midbrainand caudal thalamus. Three cases of ataxic hemipare-sis6"8 have previously been documented by C.T. scansto have infarct in the posterior limb of the internalcapsule. The face have been spared in all 3 cases, andIchikawa, Tsutsumishita and Fujioka reported that thefoot was selectively weak, in their case. In our 3 casesof supratentional infarcts causing ataxic-hemiparesishowever, the face, have all been involved as well.

In discussing the possible site of lesions causing thesyndrome, Fisher had suggested internal capsule, co-rona radiata, midbrain as well as basis pontis as possi-ble sites. Lesions have now been demonstrated in allthese sites in ataxic-hemiparesis. Of 8 cases of infarctsdemonstrated on computed tomography, only 1 casewas seen in the brainstem. This however is likely to bedue to difficulties with demonstrating a brainstem in-farct with computed tomography. A review of theclinical features (table 1) suggest that the brainstemlesions causing ataxic-hemiparesis may cause a differ-

ent clinical picture from that seen in supratentionallesions. Nystagmus was noted in 4/6 of brainstemcases, dysarthria in 2 and trigeminal weakness wasnoted in 1 case. Sensory testing were all reported asbeing normal. On the other hand, nystagmus, dysarth-ria, and cranial neuropathy were absent in supraten-tional cases, and 6 out of 7 cases had abnormality onsensory testing. These features may serve to separatethe two groups of ataxic-hemiparesis. If this is true,then our case 5, who had hoarseness of voice at onset,and a normal sensory finding, may have had a negativeC.T. scan because the pontine lesion was not easilyseen.

Although the original clinical cases of Fisher andCole stressed the selective weakness, subsequent casesof ataxic-hemiparesis have shown more widespreadand symmetrical involvement. Fisher has documentedvariable distribution and severity in hemiparesis due toa pontine lesion.2 However Ichikawa, Tsutsumishitaand Fujioka's case of capsular infarct also showedselective foot weakness. Thus, selective weakness, es-pecially of the lower limb may not necessarily indicatea brainstem lesion.

As in other cases of lacunar syndromes, ataxic-hemiparesis is not necessarily just due to lacuna.Haemorrhage, as well as tumour may be responsive.Apart from the single cases of leukaemic infilterate, 22of the 26 cases reported had hypertension. Transientischaemic attacks was also documented in 9 patientsand progression in deficits described in eight. Thus,large vessel disease may be present in some of thecases of ataxic-hemiparesis. However, angiogramstudies have only been reported by Perman and Racy,6

who showed bilateral carotid and vertebral stenosis intheir case. More long term studies of the natural histo-ry are necessary to document whether ataxic-hemipa-resis patients behave as typical lacunar syndromes, or

TABLE I Pathology and Clinical Features of Ataxic-hemiparesis in Literature

Localisation Pathology Sensation Nystagmus Others

Fisher 1978

Sakai et al 1981

Schnapper 1982

Bendheim & Berg 1981

Perman & Racy 1980

Ichikawa et al 1982

Iragui & McCutchenPresent report (1)

(2)

(3)

(4)

(5)

pons

pons

pons

pons

pons

midbrain

internal capsule

internal capsule

internal capsuleinternal capsule

internal capsule

corona radiata

internal capsule

no lesion seen

infarct

infarct

infarct

infarct

haemorrhage

tumour

infarct

infarct

infarctinfarct

infarct

infarct

infarct

normal

normal

normal

normal

normal

normal

1 P, T? 4 vibration position

1 P . T

normal1 P, TI propioception

1 vibration

I propioception

4 P . T

normal

+ transient ischaemic attackdysarthria

+ progression in defect

+ progression in defect

- dysarthriatrigeminal weakness

+ —

- widebased gait

— sensory TIA attacks

— progression in defect

— progression in defect— progression in defect

—

— progression in defect

—

— progression in defecthoarseness of voice

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366 STROKE VOL 15, No 2, MARCH-APRIL 1984

as large vessel disease with small vessel embolisation.The anatomical basis of the lesions causing ataxic-

hemiparesis have been previously discussed. It is like-ly that interruption of pontocerebellar fibres from pon-tine nuclei plus corticospinal tracts in the basis pontis,is responsible for pontine ataxic-hemiparesis.2 Inter-ruption of cerebral peduncle and the superior cerebel-lar pednucle after it has crossed the midbrain, in theventral spect of the midbrain may be responsive for amidbrain ataxic-hemiparesis. '•5 Capsular ataxic-hemi-paresis will cause the syndrome by involving the corti-cospinal tract as well as the frontopontine fibres in theposterior limb of the internal capsule. Although cap-sule ataxia hemiparesis seems frequently to be associ-ated with sensory loss, sensory loss is not essential forataxia to be present, as in Iragui and McCutchen'scase, and our case 4. Involvement of cerebellar projec-tion to the cortex appears also possible,1-8 and underlie

perhaps the ataxic hemiparesis when the lesion isabove the internal capsule.

References1 Fisher CM and Cole M: Homolateral Ataxia and Crural Paresis: A

Vascular Syndrome. J Neural Neurosurg Psychiat 28: 48-55, 19652. Fisher CM: Ataxic Hemiparesis A Pathologic Study. Arch Neurol

35: 126-128, 19783 Sakai T, Murakami S and Ito K: Ataxic Hemiparesis with Tnge-

minal Weakness. Neurology (Ny) 31: 635-636, 19814. SchnapperRA: Pontine Hemorhage Presenting as Ataxic Hemipare-

sis. Stroke 13: 518-519, 19825. Bendheim PE and Berg BO: Ataxic Hemiparesis from a Midbrain

Mass. Annals of Neurology 9: 405-406, 19816. Perman GP and Racy A: Homolateral Ataxia and Crural Paresis:

Case Report. Neurology 30: 1013-1015, 19807. IchikawaK.Tsutsumishita A and Fujioka A: Capsular Ataxic Hemi-

paresis: A Case Report Arch Neurol 39: 585-586, 19828. Iragui VJ and McCutchen CB: Capsular Ataxic Hemiparesis Arch

Neurol 39: 528-529, 1982

The Isolated Occlusion of the Angular Gyri ArteryA Correlative Neurological and Anatomical Study —

Case ReportSLOBODAN V. MARINKOVIC, M.D. ,* MIROSLAV S. KOVACEVIC, M . D . , t

AND VLADIMIR S. KOSTIC, M.D.

SUMMARY We examined a patient who had signs of a cerebral hemisphere lesion: right hemiparesis,facial weakness, right hemianopsy, acustico-mnestic dysphasia, "empty speech," acalculia, visuo-spatialagnosia and constructional apraxia, but without changes in consciousness. Taking into account clinicalsigns, computed tomography and carotid angiography findings, we concluded that our patient had aninfarction zone in the left temporo-parieto-occipital region, as a consequence of the isolated angular gyriartery (ANG) occlusion. Some clinical signs were a direct effect of the ANG's occlusion. Namely, this arterysupplies the cortical regions of great functional significance: the planum polare and temporale, the trans-verse temporal gyri, the superior and middle temporal gyri, the angular and supramarginal gyri, as well asthe superior, middle and inferior occipital gyri. But the other symptoms and signs could be explained by thepathophysiological effect of the cerebral edema on regions supplied by the non-occluded branches of themiddle cerebral artery.

Stroke Vol 15, No 2, 1984

IN THE COURSE of our clinical work we registered acase of an angular gyri artery occlusion. Numerousauthors have studied complete or partial occlusion ofthe middle cerebral artery.1"6 However, the isolatedocclusion of its single pial branches has rarely beenreported.78 That is the reason that made us examinethis case in detail. We carried out two groups ofexaminations: clinical and anatomical. We studied andcompared the collected results in order to find the

From the Departments of Anatomy,* and Neurology and Psychia-try,t Medical School of University, Beograd, Yugoslavia.

Dr. Marinkovic is Associate Professor of Anatomy, and Drs. Kova-cevic and Kostic are Assistant Professors of Neurology and Psychiatry.

Address correspondence to: Dr. Miroslav S. Kovacevic, Departmentof Neurology and Psychiatry, Medical School of University, Suboticeva6, 11000 Beograd, Yugoslavia

Received April 25, 1983; revision #1 accepted September 22, 1983.

corresponding correlation among the clinical, neuro-anatomical and functional facts.

Material and MethodsWe used the available neurophysiological, neuro-

radiological, neuroophthalmological and laboratorymethods of examinations.

Thirty-four forebrain hemispheres were used foranatomical study. The hemispheres were fixed for atleast two weeks in 10% formaldehyde solution. Themain stem and all pial (cortical) branches of the middlecerebral artery of each hemisphere were microdissect-ed, with complete angular gyri artery examination.

Case ReportThe patient M. B., aged 29, a farmer, was admitted

into hospital with acute right hemiparesis, facial weak-

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C Y Huang and F S LuiAtaxic-hemiparesis, localization and clinical features.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1984 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.15.2.363

1984;15:363-366Stroke. 

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