Journal of the Neurological Sciences 197 (2002) 85 – 87
www.elsevier.com/locate/jns

Short communication

Multiple sclerosis presenting as ataxic hemiparesis
Mark J. Gorman*
Department of Neurology, Wayne State University, 4201 St. Antoine 8D UHC, Detroit, MI 48201, USA
Received 23 July 2001; received in revised form 3 January 2002; accepted 11 February 2002

Abstract
Multiple sclerosis (MS) can present with many clinical pictures, but only rarely as a lacunar syndrome. The following case presentation is
of multiple sclerosis with initial presentation as ataxic hemiparesis (AH), indistinguishable from the vascular syndrome. This case serves to
illustrate that even classic lacunar syndromes can actually be the initial manifestation of multiple sclerosis and that other etiologies besides
ischemic stroke need to remain in the differential diagnosis until a definitive has been concluded. D 2002 Elsevier Science B.V. All rights
reserved.
Keywords: Multiple sclerosis; Stroke; Lacunar syndrome; Ataxic hemiparesis

1. Introduction
Despite a propensity for focal or multifocal neurological
deficits that present insidiously, multiple sclerosis (MS) has
been documented to present with initial episodes that
resemble stroke, including a lacunar syndrome [1 – 3],
although this is distinctly unusual. Other unusual presentations include paroxysmal attacks of brainstem dysfunction
lasting just seconds or minutes without concomitant neurological findings. Transient dystonias and acute vertiginous
attacks have also been reported [4]. The following is a case
of MS that initially presented as an ataxic hemiparesis (AH),
indistinguishable from the vascular syndrome.

2. Case report
A 42-year-old right-handed female presented to the
emergency department, 11 days after onset of flu-like symptoms (malaise, lightheadedness and anorexia), with complaints of lightheadedness, incoordination and difficulty in
walking. She never had prior neurological symptoms and
was released after an examination revealed no abnormalities.
Two days later, she noted right-sided incoordination and a
tendency to bite the right side of her tongue and cheek.
Although no headache was noted, she did admit to fatigue
and watery stools. She was taking no medications and stroke
*

Tel.: +1-313-577-1242; fax: +1-313-745-4216.
E-mail address: mgorman@moose.med.wayne.edu (M.J. Gorman).

factors were absent, save for a strong family history of
atherosclerosis, including a brother who had myocardial infarction at the age of 30.
General examination revealed an obese, but normotensive female. Mental status was normal and there was no
dysarthria. Cranial nerve examination revealed saccadic
pursuits to the left, diminished pinprick sensibility on the
right side of the face, with accompanying increase in the
right palpebral fissure and nasolabial fold flattening. Increased tone as well as mild weakness was noted in the right
hand and finger extensors, triceps and grip. A right downward drift and increased checking response were noted.
Mildly diminished pinprick sensation was found in a patchy
distribution in the right leg. Increased right-sided deep
tendon reflexes along with slowed and clumsy right hand
movements. Dysmetria was found on right-sided finger-tonose testing. Her gait was wide-based and unsteady and she
was unable to perform tandem walking. Some circumduction
was noted, along with a tendency to hold the right arm in a
flexed posture while ambulating.
Extensive hypercoagulable work-up was unremarkable.
MRI of the head revealed an area of increased signal on the
proton density and T2-weighted images (Fig. 1) in the
posterior limb of the left internal capsule and a smaller
lesion adjacent to the right lateral ventricle, as well as a
similar lesion in the right periventricular white matter (Fig.
2). MRA of the circle of Willis was normal. Slight gadolinium enhancement of the left thalamus and internal capsule
was noted, indicating an acute lesion, and confirming its
likelihood of causing the patient’s symptoms (Fig. 3). CSF

0022-510X/02/$ - see front matter D 2002 Elsevier Science B.V. All rights reserved.
PII: S 0 0 2 2 - 5 1 0 X ( 0 2 ) 0 0 0 4 5 - X

86

M.J. Gorman / Journal of the Neurological Sciences 197 (2002) 85–87

Fig. 1. Transverse MRI, T2-weighted, showing a large high signal intensity
lesion involving left thalamus and posterior limb of the internal capsule. A
small lesion is also found adjacent to the posterior horn of the right lateral
ventricle.

had normal glucose, protein and white blood count, but an
IgG index of 1.3 (normal 0.3 – 0.7) and four oligoclonal
bands were noted. Visual evoked potentials were normal.
Transthoracic echocardiogram revealed mild left ventricular
hypertrophy and Holter monitoring for 24 h did not find any
significant abnormalities. Serological testing found a posi-

Fig. 3. T1-weighted MRI with gadolinium enhancement at the same level as
that in Fig. 1. Enhancement can be seen in the area of the left thalamus and
posterior limb of the internal capsule.

tive antinuclear antibody (1:320– 1:640), but negative rheumatoid factor and an erythrocyte sedimentation rate of 12
(normal 1 –20).
A diagnosis of laboratory-supported definite multiple
sclerosis was made. Treatment with high dose intravenous
corticosteroids was initiated and then converted to oral after
5 days. Clinical improvement ensued and at 6 weeks followup, she had a return of normal strength, but mild residual
dysmetria, hyperreflexia and clumsiness remained. Extended follow-up revealed intermittent symptoms of fatigue and
hand numbness, without neurological findings. The patient
has done well a year on interferon.

3. Discussion

Fig. 2. Transverse T2-weighted MRI revealing a similar lesion in the right
periventricular white matter.

Ataxic hemiparesis is a well-known lacunar syndrome,
usually associated with small, deep infarction in the posterior limb of the internal capsule or in the basis pons
(although other localizations have reported [3– 6]). Localization to the thalamocapsular region is more likely, in this
case, on clinical grounds because of the sensory changes [5],
and also based on the enhancement noted on the MR scan.
Initial descriptions attributed this syndrome predominantly
to arteriolar lipohyalinosis and atheromatous plaque [8], but
the syndrome has been well documented to be caused by
atheroma of the parent artery overlying the mouth of the
penetrating arteriole [8]. Although debate continues, there
seems ample evidence that at least some lacunar syndromes
are caused by cardioembolism [9] and large artery disease

M.J. Gorman / Journal of the Neurological Sciences 197 (2002) 85–87

[10]. Rare etiologies have included cerebral cysticercosis
[11], trauma [6], hemorrhage [12] and tumor [7].
While there have been a few reported cases of ataxic
hemiparesis due to a demyelinating lesion of multiple sclerosis [2], the clinical details of such a case have not been
presented. It is possible that this case could be one of acute
disseminated encephalomyelitis (ADEM), although the clinical picture of ADEM is usually more severe and involves
headache, fever, nausea, vomiting, confusion, delirium and
even coma [13]. Multiple sclerosis, while generally thought
of as a ‘‘white matter’’ disease, actually involves some gray
matter in the large majority of cases. Since myelin surrounds
the axons throughout their extent except for the most proximal segment, myelin pathological changes can be found
within collections of neurons in gray matter structure [14].
Acute multiple sclerosis can present as a ‘‘gray matter’’
syndrome. It is usually distinguishable from acute stroke by
a slightly slower onset and a detailed exam may reveal
subtle signs of dysfunction correlating to other locations,
reflecting ‘‘silent’’ lesions of multiple sclerosis. This case
serves to demonstrate that while infarction can explain the
majority of cases of ataxic hemiparesis, demyelinating
disease, as well as other causes in the differential should
remain in consideration until appropriate clinical and laboratory determinations have been completed.

Acknowledgements
I wish to thank Steven R Levine, MD for his assistance in
reviewing this manuscript.

87

References
[1] Anzalone N, Landi G. Non ischaemic causes of lacunar syndromes:
prevalence and clinical findings. J Neurol Neurosurg Psychiatry
1989;52:1188 – 90.
[2] Lazzarino LG, Martinelli A, Nicolai A. Lacunar syndromes due to non
ischaemic causes: prevalence and clinical findings. Acta Neurol
1993;15:401 – 8.
[3] Luijckx G-J, Spaans F, Boiten J, Lodder J. Ataxic hemiparesis caused
by infarction of the cerebral peduncle. Cerebrovasc Dis 1997;7:183 –
4.
[4] Kelly R. Clinical aspects of multiple sclerosis. In: Koetsier JC, editor.
Handbook of Clinical Neurology. Demyelinating Diseases, vol. 3 (47).
Amsterdam: Elsevier; 1985. p. 49 – 78.
[5] Helgason CM, Wilbur AC. Capsular hypesthetic ataxic hemiparesis.
Stroke 1990;21:24 – 33.
[6] Hershkowitz N, Bergey GK, Joslyn J, Evans D. Isolated midbrain
lesion resulting from closed head injury. A unique presentation of
ataxic hemiparesis. Neurology 1989;39:452 – 3.
[7] Biller J, Scardigli K. Ataxic hemiparesis from lesion of the corona
radiata [letter]. Arch Neurol 1984;41:136 – 7.
[8] Fisher CM. Capsular infarcts. The underlying vascular lesions. Arch
Neurol 1979;36:65 – 73.
[9] Fisher CM. Lacunar strokes and infarcts: a review. Neurology
1982;32:871 – 6.
[10] Mohr JP. Lacunes. Stroke 1982;13:3 – 11.
[11] Barinagarrementeria F, Del Brutto OH, Otero E. Ataxic hemiparesis
from cysticercosis. Arch Neurol 1988;45:246.
[12] Mori E, Yamadori A, Kudo Y, Tabuchi M. Ataxic hemiparesis from
small capsular hemorrhage. Computed tomography and somatosensory evoked potentials. Arch Neurol 1984;41:1050 – 3.
[13] Tselis AC, Lisak RP. Acute disseminated encephalomyelitis. In: Antel
J, Birnbaum G, Hartung H-P, editors. Clinical neuroimmunology.
Malden: Blackwell; 1998. p. 116 – 47.
[14] Moore GRW. Neuropathology and pathophysiology of the multiple
sclerosis lesion. In: Paty DW, Ebers GC, editors. Multiple Sclerosis.
Philadelphia: FA Davis Company; 1998. p. 257 – 327.