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Chronic subdural hematoma with transient neurological deficits A review of 15 cases.

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Chronic Subdural Hematoma
with Transient Neurologcal Deficits:
A Review of 15 Cases
Mark L. Moster, MD," David E. Johnston, M D , and Oscar M. Reinmuth, MD
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Fifteen patients with chronic subdural hematomas had transient neurological deficits. The important clinical features
were aphasia i n 9 patients, absence of headache i n 8, and head injury in 8. Computed tomographic scan correctly
identified all 15 cases of chronic subdural hematoma and should be considered mandatory before initiating anticoagulation in patients w i t h transient ischemic attacks.
Moster ML, Johnston DE, Reinmuth OM: Chronic subdural hematoma with transient neurological deficits:
a review of 15 cases. Ann Neurol 14:539-542, 1983
Most patients with chronic subdural hematoma ( C S H )
have headache, depression of consciousness, and a fluctuating but persistent neurological deficit. Nevertheless, CSH can present as transient neurological
deficits ( T N D s ) , simulating a transient ischemia attack
(TIA) 13, 4 , 9, 11, 13, 14, 16-18], This phenomenon
has b e e n considered rare. I n t h e course of o n e year
(July 1, 1981 to June 30, 1982), we cared for 3 patients
with CSH who presented with T N D . I n a review of
130 cases of CSH at t h e University Health Center of
Pittsburgh (hospitals in this center include Presbyterian-University Hospital, Montefiore Hospital, and
Pittsburgh Veterans Administration Medical Center)
between 1976 and 1980, we identified 12 additional
cases (9%) producing similar clinical characteristics.
Case Reports
Patient 1
An 82-year-old right-handed man had four episodes of
speech arrest and right upper extremity numbness and weakness lasting 30 minutes each over a 4-day period. H e denied
headaches or head trauma. H e had had mild hypertension
of six years' duration and chronic obstructive pulmonary
disease.
Initial assessment of his speech and motor function revealed no abnormality. During the examination, however,
while lying supine he became drowsy and developed a global
aphasia over a period of 5 minutes. The signs resolved within
15 minutes after the patient assumed a sitting position and
recurred in the recumbent position one hour later. The patient was thereafter kept semisitting.
A computed tomographic (CT) scan revealed a subdural
collection on the left, and midline shift. Angiography demonstrated bilateral subdural collections, greater on the left side,
with a 5 mm shift of the internal cerebral veins to the right.
Superficial intimal ulcerations were noted at the origin of the
internal carotid arteries bilaterally, with a 25% stenosis of the
right internal carotid artery.
The CSH on the left was evacuated surgically. The patient
was asymptomatic 18 months later without medical treatment.
Patient 2
A 61-year-old right-handed man experienced two 10-minute
episodes of numbness of the right hand and right side of the
face two weeks before admission. He was treated with dipyridamole. Four similar episodes occurred over the next
two weeks. He had been in an automobile accident 2
months before admission and had experienced transient
loss of consciousness; afterward he complained of daytime
headaches. His medical history was otherwise normal.
Examination revealed a right arm drift, impaired rapid alternating movements, and a slight left hyperreflexia.
A C T scan showed compression of the left lateral ventricle
consistent with an isodense left parietal CSH. Carotid angiography outlined a large left parietal CSH producing subfalcial
herniation of the cingulate gyrus. The extracranial carotid
arteries were normal.
The CSH was evacuated and the patient has been asymptomatic for two years.
Patient 3
A 50-year-old woman had two 5-minute episodes of right
arm numbness and left frontal headache in the week before
From the Department of Neurology, 322 Scaife Hall, University of
Pittsburgh School of Medicine, Pittsburgh, PA 15261.
Received Jan 17, 1983, and in revised form Mar 22, 1983. Accepted
for publication Mar 25, 1983.
*Present address: Neuro-Ophthalmology Unit, Wills Eye Hospital,
9th and Walnut Sts, Philadelphia, PA 19107.
Address reprint requests to Dr Mosrer at his present address.
5 39
admission. O n the day before admission, right arm numbness
recurred and persisted. She also complained of difficulty in
“getting words cut” during the 2 days before admission. Her
medical history was abnormal only for glaucoma.
Examination revealed a mild global aphasia. She could
name objects well and repeat with slight difficulty. There
were some paraphasic errors, more prominent with writing
than with speech. The remainder of the neurological findings
were normal.
A CT scan revealed a left convexity CSH with moderate
shift of the midline and compression of the left lateral ventricle.
Language function returned to normal within a few days of
surgical evacuation of the CSH.
Clinical Featura in 15 Caes of Chronic Subduraf Hematom
with Transient Neurdogical DeJEcits
Symptom
No. of Patients
HISTORY
Aphasia
Headache
Weakness
Numbness
Head injury
Dysarthria
Visual loss
NEUROLOGICAL EXAM
Clinical Features of All 15 Patients
The clinical features of the 15 patients are summarized
in the Table. The group comprised 10 men and 5
women, ranging in age from 49 to 84 years (mean age,
71 years). They exhibited an average of five TNDs
(range, one to twenty). The total duration of the history
of TND ranged from 1 to 90 days and averaged 21
days; the duration of deficit averaged 30 minutes and
ranged from 4 minutes to three hours. The most common symptom was a disturbance of language. The patients’ descriptions were not of sufficient detail to determine the particular type of aphasia, however. The
only patient with a persistent language deficit subjected
to exmination had global aphasia. Patient 1 had transient global aphasia during the examination. Two other
patients had persistent anomia when examined.
The next most common complaint was a hemiparesis
or hemisensory defect. Four patients had weakness of
the right face, arm, and leg, and 3 of these were
aphasic; 2 had “numbness” of the right face and arm,
and 1 of these was aphasic; 2 had “numbness” of the
right arm, associated with aphasia in both cases; 1 had
“numbness”of the right arm and leg; 1 had weakness of
the right arm; 1 had “numbness” on the right side of
the face and dysarthria; and 1 had left facial and arm
weakness, left hand numbness, and dysarthria. One patient had “numbness” and weakness of the left arm and
leg and had a bilateral CSH larger on the right side.
After evacuation of the bilateral CSH, this patient developed transient episodes of right arm weakness and
aphasia that resolved spontaneously.
Headache affected only 8 patients, and in 4 it was
mild.
One patient was receiving warfarin sodium for an
aortic valve replacement but had a prothrombin time of
14112 (patiendcontrol) on admission. Another patient
had received a ventriculoperitoneal shunt 5 months
earlier to treat normal pressure hydrocephalus. Head
injury was recalled in only 7 patients. In the remaining
6 patients, no precipitating cause for CSH could be
found.
CT scans identified the CSH in this group of patients. Angiography was performed in 7 patients and
540 Annals of Neurology Vol 14 No 5
.-
6
Weakness
Dysarthria
Anomia
Aphasia
Hemianopsia
Visual neglect
Lethargy
Coma
Sensory loss
2
2
1
1
1
1
1
0
CT SCAN FINDINGS
11
CSH, left
CSH, right
CSH, bilateral
CT
=
computed tomographic; CSH
2
2
=
chronic subdural hematoma.
revealed the CSH in all 7. Three patients had coexisting extracranial carotid artery disease.
In 14 patients the CSH was evacuated surgically.
One was transferred to another hospital before operation and we lack information on her subsequent clinical
course. Of the 14 who were operated on, the 1 patient
who was comatose preoperatively died.
TNDs persisted in 3 patients postoperatively for as
long as eleven days. Thirteen patients were followed
for between 2 and 65 months (mean, 20 months); all
became asymptomatic.
Two of our patients had had previous CSHs that
were evacuated within 2 months before they presented
with TND. The initial symptoms with their first CSH
were typical: headache, depression of consciousness,
and hemiparesis. With reaccumulation of the CSH,
however, they had only TNDs.
Discussion
In 1960 Groch and colleagues 131 described a 59-yearold man with right hemiparesis and aphasia accompanying CSH. They emphasized both the rarity of the association and that patients with CSH forget imporrant
details of their history, such as head trauma. Okihiro
November 1983
and associates [ 131 in the following year reported a 44year-old patient who had transient right hand numbness and aphasia and was treated with anticoagulants
for presumed cerebrovascular disease until the diagnosis of CSH was made. Welsh and co-workers [17} in
1979 described 4 of their patients with TND in CSH
and reviewed prior cases reported in the literature.
We prefer the term transient neurological deficit to
transient ischemic attack because, without having directly examined many of the patients, we are not
confident that their examinations between attacks were
normal and that the symptoms would therefore conform to the strict definition of TIA E12).
The incidence of CSH presenting with TND has not
been defined clearly. Luxon and Harrison {9Jreported
that only 2 of 174 patients with CSH (1%) presented
with TIA-like symptoms. Most other reviews of CSH
describe no patients with accompanying TIA-like disorders {l, 2, 8, lo}. We found our 12 patients with
TNDs (7%) among 130 with CSH.
Several mechanisms have been proposed to explain
transient neurological dysfunction in CSH, including
(1) intermittent mechanical pressure by CSH on neighboring vessels [l 11, (2) transient increase in parenchymal swelling causing vascular displacement and ischemia 1171, (3) seizure activity with postictal deficits
[ l l ] , and (4)spreading cortical depression, as described by Lea0 { 7 , 111.
While being examined, patient 1 developed aphasia
and weakness while supine that resolved promptly
upon the patient’s sitting up. This finding suggests that
a transient increase in intracranial pressure was instrumental in producing his symptoms, because in most
patients with mass lesions, intracranial pressure increases while the patient is supine El>}.A shift of the
CSH within the subdural space with change in position
may also increase pressure on leptomeningeal and cortical vessels or on the parenchyma. Although this
explanation might seem reasonable in this case, it is
unlikely that it would apply to all the other reported
patients.
It is unlikely that seizure activity was responsible for
the symptoms in our patients, for a number of reasons.
The symptoms in our patients, such as weakness and
aphasia, were not of the jacksonian type, with no evidence of active seizures before or during the development of the deficit. Furthermore, the average duration
of the deficits was 30 minutes, much longer than the
average focal seizure and more consistent with the time
course of TIA [12). A recent report of CSH with jacksonian seizures reports symptoms of less than 60 seconds’ duration [j l.
A mechanism not previously proposed is that small
repeated hemorrhages within the subdural space and
the granulation tissue (membranes) encapsulating the
hematoma may be responsible for the TNDs. Indeed,
the increase in size of CSH is now considered by many
to be caused by repeated episodes of bleeding into the
subdural space [bl.
The possibility that CSH and TIAs coexist in the
same patient has been considered [17) and is supported further by the continued TNDs after evacuation of the CSH in 3 of our patients. The absence of
any TNDs beyond 11 days after operation, however,
and the consistency of the symptoms in relation to the
location of the CSH do not favor this explanation.
CSH symptoms occasionally persist after operation,
and it is known that reexpansion of brain parenchyma
and normal intracranial pressure do not occur immediately postoperatively.
Although aphasia usually is considered a rare manifestation of CSH, recent reviews estimate its occurrence in up to 20% of patients with CSH [I, 9, lo].
Aphasia was the most common symptom in our patients and occurred in 9 of 13 patients with CSH on the
left side. Of previously reported patients, 11 of 13 with
TNDs had aphasia {3,4, 11, 13, 14, 17, IS]. Aphasia is
therefore the most common symptom of TNDs associated with CSH.
The increased incidence of left hemisphere over
right hemisphere CSH [S) is supported by our study.
Because headache often is emphasized as a symptom
of CSH, its absence may be erroneously assumed to
diminish the likelihood of that disorder. In this series
only 7 of 15 patients complained of headache.
CSH may occur in the absence of recognized head
injury. Recent reviews report that 30 to 50% of patients deny any history of head trauma 11, 2, 7, lo].
Although it is important to ask about trauma in all
patients with a characteristic history of TIA, a history
of head injury could be elicited retrospectively in only
7 of our patients.
In 2 of our patients, TND was the signal of recurrent
CSH after operation for the initial CSH. Therefore, in
patients with CSH postoperative T N D should suggest
the recurrence of CSH.
Our findings in these 15 patients demonstrate that
patients with CSH may have the characteristic symptoms of TIA, including language disturbances. This
mode of presentation may be more common than previously suspected. Head injury, headache, hemiparesis,
and depression of consciousness, all common with
CSH as it often presents, may be absent. To detect
those cases of CSH with T N D resembling TIA, a CT
scan prior to anticoagulation is mandatory.
Supported in part by the regional center of the National Foundation
for Cancer Research, University of Pittsburgh.
Presented in part at the 107th Annual Meeting of the American
Neurological Association, Washington, DC, Sept 30 to Oct 2, 1982.
The authors thank Drs John Moossy, Benjamin H. Eidelman, and
Percy N. Karanjia for their review of the manuscript and helpful
suggestions.
Moster et al: CSH with TND
541
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1975
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I S . Ropper A H , O’Rourke D, Kennedy SK Head position, intr‘icranial pressure, and compliance. Neurology tNY) 32.1288 1291, 1982
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N o v c m b c r 1983
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