Chronic subdural hematoma simulating
transient cerebral ischemic attacks
Case report
ELDAD MELAMED, M.D., SLVAN LAVY, M.D.,

AVlNOAM RECHES, M.D., AND ABRAHAM SAHAR M . D .

Department of Neurology and Department of Neurosurgery, Hadassah University
Hospital and Hebrew University-Hadassah Medical school, Jerusalem, Israel

~" A patient is presented in whom chronic subdural hematoma simulated transient
ischemic attacks. The neurological manifestations were those of recurrent, transient
episodes of expressive dysphasia preceded by focal sensory deficit. Various
pathophysiological mechanisms which could have caused the unusual clinical picture
are briefly considered.
KEYWORDS

chronic subdural hematoma
transient cerebral isehemia
9 dysphasia
~

S a slowly expanding intracranial mass,
chronic subdural hematoma usually
has the typical symptomatology of a
progressive neurological deficit. In the following report we present an unusual case in
which chronic subdural hematoma gave rise
to recurrent transient, focal neurological
phenomena.

A

Case Report

A 59-year-old male was transferred as an
emergency to the Department of Neurology
of the Hadassah University Hospital in
Jerusalem. Until September, 1973, the
patient had enjoyed good general health, with
no history of hypertension, coronary or
peripheral vascular disease or diabetes
mellitus. On September 14 he developed a
dull left frontoparietal headache, which was
constant and unrelieved by analgesics. Two
J. Neurosurg. / Volume 42 / January, 1975

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days later he experienced transient, recurrent
sensations of numbness in his right hand, involving mainly the thumb and index, but with
no weakness. On the following day he
developed transient episodes of speech disturbances in which he could not express
himself properly, had difficulties in formulating words, confused letters within words, and
mixed two languages in the same sentence.
On the whole, he had about 15 attacks ofdysphasia, each lasting 10 to 15 minutes, often
preceded by numbness of the right hand. In
between the increasingly frequent attacks, the
patient felt quite well except for the headache
and, later on, an occasional difficulty in finding the appropriate word while speaking. No
clear-cut history of head trauma could be
determined.
Examination. On admission the general
physical examination was normal. The blood
pressure was 120/80 mm Hg. The pulse rate
]0]

E. M e l a m e d , S. L a v y , A. R e c h e s a n d A. S a h a r
was 72/min and regular. Good pulses were
palpated over both carotid arteries, and there
was no bruit. There were no positive neurological findings except for speech disturbances, observed during two attacks, each
lasting 10 minutes. Routine laboratory examinations were within normal limits. Skull
films were normal. Electroencephalographic
(EEG) recordings were repeatedly normal. A
left carotid angiogram (Fig. 1) disclosed an
avascular, crescent, space-occupying mass
over the left hemispheric convexity.
Operation. A liquified, chronic subdural
hematoma, encapsulated in an old and thick
membrane, was removed through two leftsided burr holes. Exploration through a rightsided burr hole was negative. The patient
made an uneventful recovery following the
operation; no recurrence of his previous
symptoms and signs was found in follow-up
examinations during the next 6 months.
Discussion

Recurrent, transient episodes of expressive
dysphasia preceded by focal sensory deficit
are often produced by cerebrovascular disease
in patients this age. The true nature of the lesion in this case was demonstrated by routine
angiographic investigation. The clinical picture is usually that of progressive, though
sometimes fluctuating, neurological phenomena? ,7,8 Unlike most patients with subdural hematoma, our patient presented with
the unusual symptomatology of short, frequently recurrent and transient episodes of
neurological deficit, which had a striking
similarity to transient ischemic attacks.
Although rare, intermittent neurological
phenomena that mimic transient ischemic attacks have been reported in other intracranial mass lesions such as meningioma, I'2
metastatic brain tumor, and brain abscess.
The literature is rather scanty concerning
chronic subdural hematoma. Groch, et a/., 4
describe a case with a sudden appearance of
hemiplegia and aphasia which had been
preceded by transient hemiparesis. Okihiro,
et al.,6 report a case quite similar to ours, with
intermittent aphasia and numbness of the
right hand.
Several pathophysiological mechanisms by
which the chronic subdural hematoma could
have produced these unusual manifestations
can be offered, although none seems to be cer102

tain. The mechanical pressure of the mass on
the neighboring cerebral vessels could cause
impairment of flow, leading to cerebral
ischemia and paralysis of function. The intermittent nature of the attacks could be attributed to a rise and fall in the pressure exerted by the hematoma during changes of
head position or performance of the Valsalva
maneuver.
Also, hematoma can act as an irritative lesion, producing epileptic discharges. Thus,
the intermittent dysphasia could be looked
upon as a form of post-ictal paralysis of cortical function and the focal sensory deficit as a
kind of an aura. In our patient there was,
however, no further spread of symptoms;
there were no convulsions nor loss of consciousness, and the EEG failed to show
evidence of ictal etiology. Another possible
mechanism suggested by Daly, et al., ~ is
based on the phenomenon of spreading cortical depression 5 whereby the mechanical
stimulation of the cortex by the lesion causes
a depression of spontaneous electrical activity
that spreads over the cortex; the cortex then
becomes inexcitable to electrical stimulation.
On the whole, there is obviously no one
satisfactory explanation for the appearance of
recurrent episodes in this chronic expanding
lesion.

F,~. 1. Left carotid angiogram, anteroposterior projection, showing an avascular space between the vessels on the left cerebral convexity and
the inner table of the skull.
J. Neurosurg. / Volume 42 / January, 1975

Subdural hematoma simulating transient ischemia
It is worthwhile to remember that on rare
occasions intracranial mass lesions such as
chronic subdural hematoma may simulate
cerebrovascular insufficiency. Our experience
stresses the importance of a complete and
detailed workup, including carotid angiography, of every patient with clinical symptoms suggesting transient ischemic attacks.
References

1. Daly DD, Svien H J, Yoss RE: Intermittent
cerebral symptoms with meningiomas. Arch
Neurol 5:287-293, 1961
2. Fowler GW: Meningioma and intermittent
aphasia of 44 years' duration. J Neurosurg
33:100-102
3. Gardner W J: Traumatic subdural hematoma
with particular reference to the latent interval.
Arch Nenrol Psychiat 27:847-858, 1932

J. Neurosurg. / Volume 42 /January, 1975

4. Groch SN, Hurvitz LJ, Wright IS, McDowell
F: Intracranial lesions simulating cerebral
thrombosis. JAMA 172:1469-1472, 1960
5. Leao AAP: Spreading depression of activity in
the cerebral cortex. J Neurophysiol 7:359-390,
1944
6. Okihiro MM, Daly DD, Yoss RE: Intermittent
aphasia due to mass intracranial lesions. Proc
Staff Meet Mayo Clin 36:525-529, 1961
7. Zollinger R, Gross RE: Traumatic subdural
hematoma, an explanation of the late onset of
pressure symptoms. JAMA 103:245-249, 1934
8. Zulch KJ: Neuropathology of intracranial
haemorrhage. Prog Brain Res 30:151-165, 1968

Address reprint requests to: Eldad Melamed,
M.D., Department of Neurology, Haddassah University Hospital, Jerusalem, Israel.

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