Cerebral Infarction of the Basal Ganglia Due to
Embolism from the Heart
JOAN SANTAMARIA, M . D . ,
FRANCESC G R A U S , M . D . ,
TXOMIN ARBIZU, M . D . ,
FRANCISCO RUBIO,
A N D JAUME PERES,
M.D.,
M.D.
SUMMARY We studied 8 patients with cerebral infarction in the deep territory of the middle cerebral
artery (MCA). All patients had a definite cardiac source of emboli and no known factors for thrombosis.
Mixed sensory and motor deficit was found in all but one patient and CT scan showed larger lesions than
usually reported in lacunar infarcts. Contrast enhancement was seen in all cases in which CT scan was
performed in the second or third week. It is concluded that embolic infarcts in deep cerebral territory of
MCA from a cardiac source are more frequent than previously reported. This diagnosis has to be consid­
ered when CT scan demonstrates a deep cerebral infarct.
Stroke Vol 14, No 6, 1983
DEEP CEREBRAL INFARCTS located in the basal
ganglia and internal capsule are usually caused by
thrombosis of the small penetrating arteries affected by
lipohyalinosis or microscopic atherosclerosis. The
most frequent clinical presentation is a pure motor
deficit but it is sometimes, accompanied by dysar­
thria, sensory impairment or cerebellar deficit. The
size of the infarct is usually small, with a diameter of 6
to 10 m m , but larger infarcts have been described in
computed tomography (CT) - *• and pathologic stud­
ies.
Although a source of emboli in patients with deep
cerebral infarcts is almost never considered, a few
experimental and pathologic studies suggest that
some may be embolic. Recently, Pullicino et al found
a possible cardiac source of emboli in 12% of 42 pa­
tients with small deep infarcts diagnosed by CT.
This report analyzes the clinical and CT findings of
eight patients with a definite cardiac source of emboli
and deep cerebral infarcts diagnosed by CT.
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Patients and Methods
We reviewed records of all patients with deep cere­
bral infarcts confirmed by CT seen during the period
1979-1981. Patients with hypertension (blood pres­
sure equal or more than 160/95 mm Hg in several
determinations) diabetes, blood hematocrit greater
than 45%, heavy cigarette smoking or vasculitis were
excluded. This review yielded 8 patients without
known risk factors for a thrombotic disease and with a
definite heart disease with high probability of cerebral
embolization. Six patients had rheumatic heart disease
and mitral valve stenosis, five of them with atrial fi­
brillation. The disease was diagnosed by clinical histo­
ry and auscultation. In three cases it was confirmed at
surgery. One patient had an aortic prosthetic valve
(Starr-Edwards) and anticoagulation had been stopped
one year before the stroke because of gastrointestinal
bleeding. Another patient had a subacute bacterial en­
docarditis with blood cultures positive for Streptococ-
From the Department of Neurology, C.S. "Principes de Espana"
Hospitalet de Llobregat, Barcelona, Catalonia, Spain.
Address correspondence to: Dr. Jaume Peres, Department of Neurol­
ogy, C.S. "Principe de Espana," Hospitalet de Llobregat, Barcelona,
Catalonia, Spain.
Received May 28, 1982: revision accepted May 24, 1983.
cus salivarius and infected vegetations were confirmed
at surgery.
Results
Clinical and CT findings are summarized in table 1.
The clinical deficit had an abrupt onset, reaching its
peak in a few minutes in half of the patients. In two
patients, the deficit progressed during the next 3 hours;
and in the remaining 2 , a fluctuating course over sever­
al hours was seen before stabilization occurred. Neuro­
logical examination showed a complete (5 cases) or
incomplete (3 cases) hemiplegia, accompanied by hypesthesia in 6 patients. A pure motor hemiplegia was
only seen in one case. In three of them, a transitory
anosognosia was clearly observed. In a further patient
(case 8), the motor hemiplegia was accompanied by an
expressive dysphasia. Her language disorder was char­
acterized by nonfluent conversational speech, naming
and reading difficulties, dysgraphia and a normal audi­
tory comprehension. She was almost normal one year
after the stroke. Recovery of the motor and sensory
deficit was complete in two patients, moderate in four,
and poor in two.
EEG was performed on 7 patients. In all but one
case, EEG showed a discrete focal slowing. The most
common CT abnormality, seen in four cases, was a
well-defined low density area placed in caudate, putamen and anterior limb of internal capsule (fig. 1). In a
further 3 cases, CT showed a posterior extension (fig.
2). The patient with aphasia had a small lesion circum­
scribed to putamen and anterior limb of the internal
capsule (fig. 3). In six cases, several CT scans were
performed during the first two weeks, giving the evi­
dence that the infarct was recent. Contrast enhance­
ment was observed in all cases in which CT were
performed during the second or third week. In one
case, the infarct was hemorrhagic (fig. 4).
Discussion
Although the clinical diagnostic criteria for cerebral
embolism are not universally agreed upon, in our cases
the absence of risk factors for thrombosis and the pres­
ence of a definite cardiac source of emboli suggest
embolism as the cause of the cerebral infarction. The
mean age and the female preponderance are similar to
those reported in studies of cerebral embolism secon­
dary to rheumatic heart disease. '
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TABLE
Clinical
Patient/
age/sex
and CT
Type of
heart disease*
1 44 F
R H D with MS
AF
2/37/F
R H D with MS
and A R , A F
3/53/F
1HSS and S B E
4/59/F
R H D with MS
5/34/M aortic prosthetic
valve (StarrEdwards)
6/65/F RHD with MS
AF
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7/49/F
R H D with MS
AF
8/37/F
R H D with M S
Findings
Clinical
presentation
Neurologic
findings
abrupt onset
m a x i m u m deficit
immediately
abrupt onset and
gradual progres­
sion during 3
hours
abrupt onset
m a x i m u m deficit
immediately
abrupt onset and
fluctuation during
5 hours
abrupt onset, maxi­
m u m deficit im­
mediately
abrupt onset and
gradual progres­
sion during 3
hours
abrupt onset
m a x i m u m deficit
immediately
abrupt onset and
fluctuation during
6 hours
Clinical course
C T findings
hemiplegia ( L )
hypesthesia
anosognosia
pure motor
hemiplegia ( L )
moderate recovery
anosognosia disap­
peared in 2 days
moderate recovery
hemiplegia (L)
hypesthesia
dysarthria
hemiplegia (L)
hypesthesia
poor recovery
capsulo-lenticular
and caudate
total recovery
caudate, putamen
and AL of IC
hemiplegia (L)
hypesthesia
moderate recovery
caudate, putamen
and A L of IC
hemiparesia (L)
hypesthesia
anosognosia
moderate recovery
anosognosia disap­
peared in few
days
poor recovery
head of caudate
AL of IC and
putamen
hemiplegia (L)
hypesthesia
anosognosia
hemiparesia (R)
aphasia
total recovery
head of caudate
ALof IC and putamen
hemorrhagic
capsulo-lenticular
and caudate
head of caudate
AL of IC and
putamen
putamen and
AL of IC
*Confirmed at surgery in cases 1, 2, 3 and 8.
RHD = rheumatic heart disease; MS = mitral stenosis; A F = atrial fibrillation; AR = aortic regurgitation; IHSS =
idiopathic hypertrophic subaortic stenosis; S B E = subacute bacterial endocarditis; L = left; R = right; AL = anterior
limb; IC = internal capsule.
All but one patient manifested clinical patterns dif­
ferent from those associated with lacunar infarcts and
the size of the lesions found by CT scan was usually
larger than those described pathologically by Fisher et
al. The deficit fluctuated or had a gradual progression
in four patients, this temporal profile more suggestive
of a thrombotic stroke has been described in cerebral
embolism as well." In addition the Harvard Cooper­
ative Stroke Registry reported this profile in 2 1 % of
the patients diagnosed of cerebral embolism.
2
The presence of anosognosia (a lack of recognition
of their hemiplegia or hemianesthesia) and aphasia in
four of our patients could suggest a concomitant lesion
in cortical areas. In the absence of pathological verifi­
cation this assumption cannot be ruled out definitively
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FIGURE 1.
capsule
(Case
A. Enhanced
and putamen
6).
CT scan
showing
an infarct
<Case 4). B. CT scan showing
involving
a right caudate
the right caudate
and lenticular
head
nuclei
nucleus,
enhancement
anterior
limb
of
and a discrete
internal
atrophy
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FIGURE 2.
Unenhanced
and both limbs
(A) and enhanced
of internal
(B) CT scan of case 3, showing
but the serial CT scans performed in all patients did not
show a cortical lesion in any case. On the other hand
these symptoms have been described in patients with
deep cerebral infarctions or hemorrhages. Damasio et
al reported atypical aphasia syndromes in six patients
with infarctions that involved the left anterior limb of
the internal capsule, the head of caudate and putamen.
Anosognosia has usually been reported in lesions in­
volving the right thalamus or in basal ganglia hemor­
14
15
FIGURE 3 .
volving
Enhanced
left putamen
demonstrated.
a low attenuation
area involving
right
lenticular,
capsule.
CT scan of case 8. A small
and anterior
limb
of internal
infarct
in­
capsule
is
16
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rhages. Recently Healton et a l described a patient
with anosognosia and a pathologically verificated right
hemorrhagic infarct restricted to putamen, caudate and
genu and posterior limb of the internal capsule.
When an embolism involves the deep cerebral areas
it is usually in the context of a large infarct that extends
to the cortical territory. Deep cerebral infarcts are usu­
ally caused by thrombosis of the lenticulostriated arter­
ies or internal carotid artery and the possibility of an
embolic origin has been hardly ever considered in the
literature.
Fisher, in a detailed pathologic study, suggested an
embolic mechanism in two cases with lacunar infarcts
FIGURE 4 .
Unenhanced
hemorrhagic
infarction
CT scan showing
with a patent
mass
a right
effect
(Case
lenticular
2).
and no occlusion in the appropriate lenticulostriated
artery, although neither of them had a clear source of
emboli. The possibility of an embolic occlusion of a
lenticulostriated artery would be supported by the
demonstration of small emboli in the retinal arteries of
patients with amaurosis fugax and ulcerated carotid
atheromas. Recently Pullicino et al reported the pres­
ence of a source of emboli in 33% of their patients with
small deep infarcts diagnosed by CT scan, and the
same was found by Rascol et al in 13% of their cases of
pure motor hemiplegia.
Another way in which an embolic infarction can be
restricted to a deep cerebral territory is when a large
embolus is arrested in the trunk of the middle cerebral
artery (MCA) occluding the mouths of the lenticulo­
striated arteries. A deep infarction is produced whereas
the superficial territory is spared by the collateral cir­
culation. ' In this way two of the deep infarcts associ­
ated with an embolic cardiac source described by
Blackwood et a l , although not specially commented
by these authors, had a pathologically demonstrated
occlusion of the trunk of the MCA. Deep cerebral
infarcts have also been produced in experimental stud­
ies. - Crowell et al reported deep infarcts in 17 of 27
monkeys subjected to temporary MCA occlusion. The
infarcts involved the anterior limb of the internal cap­
sule, the caudate nucleus and the anterior portion of
putamen. This high incidence may be due to the vari­
ations of meningocortical anastomoses between man
and animals. It is our impression, however, that cere­
bral embolism in the deep territory of the MCA is more
frequent than is reported and its better prognosis has
prevented the possibility of more pathological studies.
With the use of CT scan this diagnosis will probably
increase.
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It is worth noting that our cases are not the same as
Fisher's lacunar stroke patients. The patients described
here have much larger lesions than Fisher described
pathologically — the location is similar but they are
not usually restricted to the territory of a single lenticu­
lostriate artery — and the clinical presentation indi­
cates also a much bigger lesion. The differentiation
between these two types of deep cerebral infarcts is
useful in order to establish an appropriate therapy.
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Cerebral infarction of the basal ganglia due to embolism from the heart.
J Santamaria, F Graus, F Rubio, T Arbizu and J Peres
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Stroke. 1983;14:911-914
doi: 10.1161/01.STR.14.6.911
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