OBSERVATION

Acute Aphasia in Multiple Sclerosis
Todd R. Devere, MD; John L. Trotter, MD; Anne H. Cross, MD

A

cute aphasia is rare in multiple sclerosis. We describe 3 patients with multiple sclerosis who had acute exacerbations presenting as aphasias. One patient had a mixed
transcortical aphasia, 1 had a transcortical motor aphasia, and 1 had a Broca aphasia.
Magnetic resonance imaging scans of the brain with contrast enhancement revealed
new white matter lesions in the left hemisphere in all 3 patients. Two of the 3 patients had a good
response to treatment with methylprednisolone sodium succinate.
Arch Neurol. 2000;57:1207-1209
Multiple sclerosis (MS) primarily affects the
white matter of the brain and spinal cord.1,2
Aphasia rarely occurs as a clinical manifestation of MS.2 Since aphasia is usually associated with diseases of the gray matter,
it is not an expected presentation of MS.
Only a handful of case reports in the literature describe this entity.3-6 We describe
3 patients with acute MS exacerbations presenting as aphasias with lesions compatible with their new symptoms demonstrated on magnetic resonance imaging
(MRI) scans (Table). The patients were followed up at the Washington University
Multiple Sclerosis Clinic, St Louis, Mo. The
clinic provides care to more than 1300 patients with MS. All 3 patients were diagnosed as having clinically definite MS.2,7
REPORT OF CASES

CASE 1
A 24-year-old left-handed woman with relapsing-remitting MS had a history of exacerbations that included left hypesthesia, dysarthria, poor coordination, and
weakness. She was admitted with a 5-day
history of right leg weakness and a 1-day
history of “trouble getting words out.” On
examination, her speech was slightly dysFrom the Department of Neurology, Washington University School of Medicine,
St Louis, Mo.

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arthric and her language was nonfluent.
Naming was impaired, and she had difficulty following complex commands. Her
sentences consisted of only 3 to 4 words,
and her reading was impaired. Repetition
was intact. She had a new right-sided hemiparesis, along with bilateral hypesthesia
and dysmetria.
An MRI scan of the brain revealed interval formation of large confluent foci in
the deep white matter of both cerebral
hemispheres, with extensive involvement of the periventricular white matter
adjacent to the frontal and occipital horns
on fluid attentuation inversion recovery
images and T2-weighted sequences. Postgadolinium T1-weighted images demonstrated a small area of contrast enhancement in the left frontal area corresponding
to a 233-cm area of hyperintensity on T2weighted images.
The patient was treated with 5 g of
intravenous methylprednisolone sodium
succinate over 5 days. Her aphasia and
right-sided hemiparesis gradually improved over several months. At a follow-up visit more than 1 year later, she reported only occasional word-finding
difficulty when speaking quickly.
CASE 2
A 45-year-old right-handed woman with an
8-year history of relapsing-remitting MS had

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Data on 3 Patients With Relapsing-Remitting Multiple Sclerosis
Patient No./
Age, y/Sex

Type of Aphasia

White Matter Finding on MRI*

1/24/F
2/45/F
3/25/M

Mixed transcortical
Broca
Transcortical motor

3 3 2-cm Lesion with small area of contrast enhancement in left frontal lobe
3 3 2-cm Lesion with trace contrast enhancement in left temporal lobe
5 3 3-cm Foci with contrast enhancement in left parietal lobe

*MRI indicates magnetic resonance imaging.

Patient 3. Magnetic resonance imaging scans of the brain. Left, T2-weighted sequence with a large left parietal lesion. Right, T1-weighted postgadolinium
sequence with contrast enhancement in the left parietal lesion.

been stable since her last hospitalization for right leg weakness 1 year earlier. She presented with a 2-week history of
poor memory and language impairment. On examination, her language was nonfluent, with paraphasic errors
and prominent anomia. Repetition was mildly impaired.
Comprehension was intact. She had poor recall on memory
testing. The findings of the rest of her neurologic examination were remarkable for patchy hypesthesia, spasticity, and an unsteady gait.
An MRI scan of the brain revealed extensive periventricular white matter disease, including a 332-cm area
in the white matter of the left temporal lobe on T2weighted images. Postgadolinium T1-weighted images revealed a trace amount of contrast enhancement in the left
temporal lobe lesion.
The patient was treated with 5 g of intravenous methylprednisolone sodium succinate over 5 days. She had
incomplete improvement in her aphasia and was transferred to a rehabilitation unit. The course of her MS later
became progressive, and she is now in a nursing home,
with marked cognitive impairment.
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CASE 3
A 25-year-old right-handed man with a 4-year history of
relapsing-remitting MS presented with an acute exacerbation associated with aphasia. Six weeks before admission, he developed right hand weakness and right foot
drop. These symptoms resolved spontaneously after 1
week. Two weeks later, he developed paresthesias in the
right side of his face and in his right arm and leg. Four
days before admission, his speech became slurred and he
began to have difficulty “finding words.” On examination, he demonstated dysarthria, impaired fluency with
word-finding difficulty, paraphasic errors, and rightsided hemiparesis with bilateral spasticity and hypesthesia. Comprehension and repetition were intact.
An MRI scan of the brain (Figure) revealed multiple white matter lesions in the periventricular areas and
the pons. There was also a new 5 3 3-cm left frontoparietal subcortical lesion that was most prominent on T2weighted images and demonstrated contrast enhancement on T1-weighted postgadolinium sequences.
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The patient was treated with 5 g of intravenous methylprednisolone sodium succinate over 5 days. Examination a few months later demonstrated complete resolution of his aphasia.
COMMENT

Patients with MS often develop cognitive abnormalities
that have been reported to occur with a frequency of up
to 65%.2,8 These abnormalities include memory deficits,
psychomotor slowing, visual spatial impairment, and poor
conceptional reasoning. Language deficits are relatively
uncommon. Moreover, cognitive deficits in MS typically develop progressively over time. The unusual
aspect of our 3 cases is the development of acute
language impairment.
Although cortical lesions produce most cases of aphasia, a variety of subcortical white matter lesions may cause
similar clinical syndromes. Subcortical strokes and intraparenchymal hemorrhages involving the putamen, internal capsule, caudate nucleus, and thalamus have been
associated with a variety of aphasias.9-11 The concept of
diaschisis, whereby impaired function occurs in one area
of the brain secondary to an acute focal lesion in a more
distant part of the brain, has been cited as one explanation for subcortical lesions causing aphasias.12,13 According to this concept, lesions of the white matter tracts that
are anatomically connected to the cortical language centers could produce aphasias that are sometimes difficult
to distinguish from aphasias that are associated with cortical lesions. Several studies have demonstrated cortical
hypoperfusion in aphasic patients with acute strokes in
the subcortical regions.12,13 However, the type of aphasia produced by a subcortical lesion may not always be
predicted from the location of the lesion.12
All 3 of our patients presented with primarily motor aphasias as part of an acute MS exacerbation. Patient
1 had a mixed transcortical aphasia with more motor than
sensory involvement; patient 2 had a Broca aphasia; and
patient 3 had a transcortical motor aphasia. Friedman et
al5 reported a case of global aphasia and Arnett et al6 reported a case of conduction aphasia in MS. However, the
majority of previously reported cases of aphasia in MS
have described motor aphasias.3,4,6 Achiron et al4 performed serial MRI scans on 2 patients with MS who developed acute motor aphasias. Each of their patients had
interval development of a large plaque (.5 cm) located
in the white matter of the dominant hemisphere. One
patient had a 6-cm plaque in the left frontotemporal
region. The other patient had a 5-cm plaque in the left
centrum semiovale.
In our series, all 3 patients had MRI scans that demonstrated bilateral disease associated with 2- to 5-cm lesions in the left hemisphere and showed contrast en-

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hancement on postgadolinium T1-weighted images. The
MRI lesions in each patient occurred only in the white
matter, with sparing of the gray matter. All 3 patients had
relapsing-remitting MS at the time of their exacerbations. Two of our 3 patients had significant improvement in their aphasia after treatment with intravenous
methylprednisolone. However, it is unclear if the clinical improvement was the result of treatment with methylprednisolone, or simply spontaneous recovery.
The experience in our center with acute aphasia in
MS is consistent with the paucity of reported cases in
the literature. We have identified only 3 cases in our MS
clinic population during a period of more than 7 years.
Despite the possibility that acute aphasia in patients
with MS can represent an exacerbation of the disease,
the clinician must always exclude cerebrovascular
events, seizures, and infectious origins. This report provides further evidence that aphasia may present as an
acute exacerbation in MS and is often associated with
some recovery.
Accepted for publication December 27, 1999.
Reprints: Todd R. Devere, MD, Barnes Jewish Hospital, Campus Box 8111, 660 S Euclid Ave, St Louis, MO 63110.
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