1603

Lacunar Infarction as an Embolic
Complication of Cardiac and
Arch Angiography
Anh Cacciatore, MD, and Louis S. Russo Jr., MD
Background: Lacunar infarcts are small, deep cerebral infarcts resulting from occlusion of
small, penetrating cerebral arteries. They are most commonly associated with hypertension.
Cardiac sources of embolization are sometimes present in patients with lacunes, but direct
proof of a causal relationship is lacking. This report attempts to support the contention that
emboli can cause lacunar syndromes and lacunar infarction.
Case Descriptions: We report two cases of pure motor hemiplegia, each of which developed
while the patient was undergoing cardiac or aortic arch angiography. Neither patient had a
history of previous transient ischemic attack or stroke. Initial computed tomography of the
brain was normal in each. Repeat computed tomography in one confirmed a small, low-density
lesion in the posterior limb of the internal capsule on the side appropriate to the patient's
symptoms and remained normal in the second patient.
Conclusions: These two cases offer evidence that the classic lacunar stroke syndrome of pure
motor hemiplegia can occur on an embolic basis. (Stroke 1991;22:1603-1605)

L

acunes are small, deep infarcts found almost
exclusively in the lenticular nucleus, caudate,
thalamus, pons, and internal capsule. In the
mid 1960s, the classical theory of lacunes was developed from the detailed works of Fisher and colleagues.1"4 Fisher described several lacunar syndromes2 and provided pathological evidence of an
underlying microvascular disorder, lipohyalinosis.3
Fisher himself, however, questioned whether emboli
could give rise to lacunes.3 Subsequent pathological
and radiological studies have suggested,5"7 but not
proven, the relationship between embolic stroke and
lacunar syndromes. We present two cases of pure
motor hemiplegia, which occurred during cardiac and
arch angiography, as supporting evidence that emboli
can cause lacunar infarction.
Case Reports
Case 1

A 48-year-old hypertensive male with non-insulindependent diabetes was admitted following an acute
myocardial infarction. He was without neurological
symptoms on admission. He was treated with tissue
From the Departments of Internal Medicine (A.C.) and Neurology (L.S.R.), University of Florida Health Science Center/
Jacksonville, Fla.
Address for correspondence: Louis S. Russo Jr., MD, Department of Neurology, UFHSC/Jacksonville, 655 West 8th Street,
Jacksonville, FL 32209.
Received June 4, 1991; accepted August 23, 1991.

plasminogen activator and was stable for the first 24
hours of hospitalization, at which point cardiac catheterization was performed. No mural thrombus was
seen in the left ventricle. During the left ventricular
injection, the patient experienced the sudden onset
of left-sided weakness. There was no evidence of
transient cardiac arrhythmia, hypotension, or hypertension. He was examined by one of us within minutes of onset.
The patient's blood pressure was 158/86 mm Hg,
pulse rate 96 and regular, respiration rate of 20
breaths/min, and temperature of 98.8°F. General
physical exam was unchanged from that before catheterization. Neurological examination revealed an
alert man who was oriented to time, place, and
person. His memory for recent and remote events
was normal. He recalled three of three objects at 5
minutes. Spontaneous speech, comprehension, repetition, and naming were normal. He showed no signs
of denial of illness or hemispatial neglect. Mapping
ability was normal. No errors were made in a line
cancellation task. Cranial nerve function was intact
except for a moderate left,central facial paresis.
Motor exam was normal in the right-sided extremities. The left arm and leg showed no volitional
movement, flaccid tone, and hypoactive tendon reflexes. Sensory exam showed normal appreciation of
pin, touch, joint-position sense, vibration, graphesthesia, stereognosis, and two-point discrimination.
He did not extinguish the left side on double simul-

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1604

Stroke Vol 22, No 12 December 1991

speech was normal, as were comprehension and
repetition. There was no difficulty with naming, calculation, finger recognition, or left-right orientation.
Cranial nerve function was normal except for a mild
right,central facial paresis. Motor function was normal on the left side. The right-sided extremities
showed a dense hemiplegia, with flaccid tone and
hypoactive tendon reflexes. A Babinski sign was
present on the right. Pin, touch, joint-position sense,
and vibration were normally appreciated throughout.
Graphesthesia, stereognosis, and two-point discrimination were normal. There was no extinction of
either side on double simultaneous testing with pin.
No cranial or carotid bruits were heard.
A CT scan of the brain done within the initial 6
hours was normal, as was one repeated 10 days later.
She was treated with aspirin and antihypertensive
medication. Strength began to return on the right
side within 96 hours; significant improvement was
apparent within 3 weeks. Three months after the
event, she was left with minimal weakness in the right
side and was ambulatory without assistance.

FIGURE 1. Unenhanced computed tomographic scan of the
brain in case 1 on day 7.

taneous stimulation with pin. No cranial or carotid
bruits were heard.
A computed tomographic (CT) scan of the brain
done within the first 4 hours was normal. Carotid
ultrasound revealed minimal atherosclerotic disease
at the origin of both internal carotid arteries. He was
treated with aspirin and antihypertensive medication.
He began to regain strength within the first week and
was ambulating with a cane and ankle-foot orthosis
within 3 weeks. A repeat CT scan done on day 14
(Figure 1) revealed a well-defined, low-density lesion
in the posterior limb of the right internal capsule.
Case 2
A 61-year-old hypertensive female with non-insulin-dependent diabetes was admitted for evaluation
of a suspected thoracic aortic aneurysm. No neurological symptoms were present on admission. Admission physical examination was normal. While undergoing arch aortography, she experienced the sudden
onset of right-sided weakness. This was unaccompanied by change in vital signs or mental status.
Initial neurological examination was performed
within 1 hour of onset. The patient's blood pressure
was 170/100 mm Hg, pulse rate 82 and regular,
respiration rate 14 breaths/min, and temperature
99°F. General physical examination was unchanged
from admission. Neurological examination revealed
an alert woman who was fully oriented. Memory for
remote and recent events was normal. She recalled
three of three objects at 5 minutes. Spontaneous

Discussion
In 1965, Fisher and Curry4 described detailed
autopsies of nine cases of pure motor hemiplegia and
established the clinicopathologic relationship between this syndrome and lacunar infarction. Hypertension was present in 96-98% of patients with these
infarcts, and Fisher postulated that hypertension
produced a specific intracerebral arteriolar lesion,
lipohyalinosis, that caused lacunes. More than 10
years later, he provided the pathological evidence to
support this theory, with extensive reports on 11
cases of capsular infarcts.3 Of these 11 patients with
infarcts, nine were shown to have underlying microvascular disease. Only one, however, had lipohyalinosis. Embolism was mentioned as a possible explanation for the remaining two cases because the
penetrating arteries in the distribution of the infarct
showed no pathologic change.
In a subsequent pathologic review of 169 patients
with 327 lacunar infarcts, Tuszynski et al5 demonstrated a source of emboli in more than 30% of those
cases with no hypertension or disease in the perforating arteries at the base of the brain. This high
prevalence was derived by using liberal criteria in
denning possible embolic sources; in addition to
known rheumatic heart disease with atrial fibrillation, they included generalized atherosclerosis and
presumed nonbacterial thrombotic endocarditis not
persisting at autopsy. Demonstration of a source of
emboli, however, does not prove a cause-effect relationship between embolic stroke and lacunes.
More recent clinical studies, using CT scans in the
diagnosis of lacunes, have also raised the possibility
that microemboli can obstruct deep penetrating arteries and produce lacunes.67 Pullicino et al6 reported possible cardiac and carotid sources of emboli
in 33% of 38 cases with small, deep lesions found on
CT. Only two (5%) were considered to have a highly

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Cacciatore and Russo Lacunar Infarction

probable source of emboli, however. In a later study
of the relationship between embolism and infarction
in the basal ganglia, Santamaria et al7 reported eight
cases of radiologically confirmed deep subcortical
lesions with clear evidence of emboli. Only one
patient had a classic lacunar syndrome, and this
patient's CT revealed a large hemorrhagic lesion in
the capsulolenticular region and caudate rather than
a lacune. Hart et al,8 in reporting strokes in patients
with infective endocarditis, mentioned three cases of
small subcortical infarcts. These infarctions, occurring in young patients during an acute illness known
to produce embolic cerebral lesions, strengthen the
association between emboli and lacunes. Unfortunately, clinical and radiological details are lacking.
In the two cases presented here, both patients had
abrupt onset of pure motor hemiplegia shortly after
the injection of radiographic contrast material. In
each case, the patient was actively being monitored
and there was no transient arrhythmia or change in
blood pressure. The acuteness of the development of
symptoms, the presence of maximal deficit immediately upon onset, and the rapid resolution speak for
an embolic etiology. The clinical feature of pure
motor hemiplegia is consistent with a lacunar syndrome in each case. In one, CT confirmed a small,
deep infarct in the posterior limb of the internal
capsule. Although hypertension was present in both
cases, it is difficult to refute the temporal relationship
between the injection of angiographic contrast and
the onset of neurological symptoms.
One may question the ability of emboli to lodge in
an individual small, penetrating artery as opposed to
the proximal middle cerebral artery. In an animal
study, Futrell et al9 produced a model for embolic
cerebral infarction by laser irradiation of the common carotid artery in rats. This induced a nidus for

1605

platelet aggregation and secondary embolism. Several of the animals developed basal ganglia infarctions with the pathologic characteristics of lacunes.
In summary, our two cases provide the clinical
hallmarks of embolic disease, the clinical characteristics of a known lacunar syndrome, and radiological
proof of a small infarction in the posterior limb of the
appropriate internal capsule. These two cases, although lacking angiographic or pathological proof,
provide further evidence that lacunar infarction and
pure motor hemiplegia can be caused by emboli. An
embolic source, therefore, should be sought in patients with lacunar infarcts, especially those who lack
the classic presence of hypertension.
References
1. Fisher CM: Lacunes: Small, deep cerebral infarcts. Neurology
(Minneap) 1965;15:774-784
2. Fisher CM: Lacunar strokes and infarcts: A review. Neurology
1982;32:871-876
3. Fisher CM: Capsular infarcts: The underlying vascular lesions.
Arch Neurol 1979;36:65-73
4. Fisher CM, Curry H: Pure motor hemiplegia of vascular origin.
Arch Neurol 1965;13:30-45
5. Tuszynski M, Petito C, Levy D: Risk factors and clinical
manifestations of pathologically verified lacunar infarctions.
Stroke 1982;20:990-999
6. Pullicino P, Nelson R, Kendall B, Marshall J: Small deep
infarcts diagnosed on computed tomography. Neurology 1980;
30:1090-1096
7. Santamaria J, Graus F, Rubio F, Arbizu T, Peres J: Cerebral
infarction of the basal ganglia due to embolism from the heart.
Stroke 1983;14:911-914
8. Hart R, Foster J, Luther M, Kanter M: Stroke in infective
endocarditis. Stroke 1990;21:695-700
9. Futrell N, Millikan C, Watson BD, Dietrich WD, Ginsberg M:
Embolic stroke from a carotid arterial source in the rat:
Pathology and clinical implications. Neurology 1989;39:
1050-1056
KEY WORDS • cerebral infarction
• lacunar infarction

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embolism • hemiplegia

Lacunar infarction as an embolic complication of cardiac and arch angiography.
A Cacciatore and L S Russo, Jr
Stroke. 1991;22:1603-1605
doi: 10.1161/01.STR.22.12.1603
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1991 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628

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