256

Computed Tomography in Patients

Presenting with Lacunar Syndromes
R. F. NELSON, M.D., F.R.C.P (C), P. PULLICINO, M.R.C.P.,
B. E. KENDALL, F.R.C.P., D.M.R.D., F.R.C.R., AND
JOHN MARSHALL, M.D., F.R.C.P., D.P.M.

SUMMARY Of 312 stroke patients who bad a CT scan, 37 had presented clinically with a lacunar syn-
drome. In 18 of the 37, lacunar sized infarcts were demonstrated on the scan, 13 had normal scans and in 6
large infarcts were found. Of these 6, 5 had a pure motor hemiplegia and one a pure sensory stroke.
Clinical evidence and anglography revealed a potential and treatable source of eraboli in both the lacunar
sized and the large infarcts. Two conclusions are drawn: a clinical lacunar syndrome may be associated with a
large infarct; demonstration of a lacunar infarct on CT scan does not exdude the need for angiography in ap-
propriate cases to discover a possible source of eraboli.
Stroke, Vo! 11, No. 3, 1980

T H E D E T E R M I N A T I O N of the anatomical Methods

localization and pathology of cerebral infarctions is of Among 312 stroke patients who had been studied by
more than academic importance. Fisher,1 Caplan2 and CT scanning at the National Hospital, London, on
others have emphasized that patients with lacunes EMI 1010 or 5005 machines, there were 37 who
have a good prognosis and should not be submitted to presented with one of 4 syndromes known to be
potentially hazardous investigations and needless associated with lacunar infarction. All the patients un-
therapy. derwent detailed neurological examination during the
The word lacune is a neuropathological term refer- acute stage of their stroke and fitted into one of the 4
ring to a small area of softening usually situated in the following groups;
distribution of the basal perforating arteries. Such
lesions may, however, occur elsewhere such as, for ex- 1. Pure motor hemiplegia (involving face, arm
ample, in the brain stem. The pathological features of and leg);4
lacunes have been studied by Fisher who also reviewed 2. Pure sensory stroke involving the face, arm
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the history. 1 '' In addition, he has delineated a number and leg;8

of clinical syndromes4"7 which, by subsequent autopsy 3. The dysarthria-clumsy hand syndrome;7 and
examination of the brain, he identified with lacunes in 4. Homolateral ataxia with crural paresis."
specific sites. Thus the term lacunar infarct or lacunar
In deciding that a patient was hypertensive, the
stroke has come into use as a clinical term, the
patient's history and blood pressure readings were
pathological and etiological basis being assumed from
considered. When these were not available, the
the clinical features. These include a specific
presence of hypertension was judged by serial read-
neurological deficit, the frequent association of
ings after the acute stage. Initial admission blood
arterial hypertension and marked tendency to
pressure readings were not used.
recovery. The Harvard Stroke Registry project, for
The CT scans of these patients, which were done at
example, includes lacunar stroke among the
various times after the onset of symptoms, were
cerebrovascular conditions to be recognized.'
reviewed and the anatomical localization and es-
The clinical diagnosis of lacunar stroke could only timated size of the lesions were recorded.
be confirmed if there were some imaging method
The size of the lesion was estimated by measuring
which would consistently demonstrate the path-
the longest dimension and the greatest dimension at
ological lesion. Computed tomography (CT) can show
right angles to it and multiplying them. This was cor-
the larger lacunes. The value of CT in recognizing the
rected for the method of display, i.e. polaroid,
smaller ones is limited and varies with the scanning
transparency, etc, and multiplied by the depth of the
system. It plays an important part in the diagnostic
lesion calculated by the number and depth of con-
study of strokes, mainly by excluding other types of
tiguous sections in which it was seen. This gave, in
pathology and it will reveal most infarcts which are
fact, the volume of the cuboid containing the lesion
too large or superficial to be termed lacunar.
and was thus the maximum possible size of the lesion
The present study was undertaken to determine the having the dimensions measured. Most infarcts
CT scan findings in patients presenting with the probably occupy approximately half this total volume
clinical syndromes which have been considered to be and so an arbitary estimate of the actual size was ob-
diagnostic of lacunar infarction. tained by dividing the size of the cuboid by two.
Despite the difficulties in obtaining an accurate assess-
ment of the size of an irregular lesion involving several
sections, it was considered better to use such a
From the Institute of Neurology and National Hospitals for Ner-
vous Diseases, Queen Square, London, WC1N 3BG, United measured approximation than merely to grade by eye.
Kingdom. The site of lesion was classified as being superficial or
 CT IN LACUNAR SYNDROMES/Nelson el al. 257

deep and according to the distribution of the supply- 15 of our 18 patients were within this limit. However,
ing artery. Fisher extended the concept to include what he termed
giant lacunes,1 the largest having a volume of less than
Results 3 ml and one of 3.8 ml. Twelve of our patients had a
Out of 312 patients with stroke who were in- single small lesion and 5 had at least 2; one had both a
vestigated by CT scan, 37 were identified as having a small and a large lesion. Six patients had large infarc-
clinical presentation compatible with a known lacunar tions only, ranging in size from 5.8 to 23.0 ml.
syndrome. Twenty-six patients had a pure motor
hemiplegia, 4 a pure sensory stroke, 6 a dysarthria- Pure Motor Hemiplegia
clumsy hand syndrome and one a crural paralysis with The 26 patients with pure motor deficit had no im-
ataxia. paired visual field defect or speech difficulties on ex-
Twenty-nine were male, 8 female, (mean ages 58.5 amination. In 14 patients, there was hemiplegia, in-
years and 45.5 years respectively). Ten patients were volving face, arm and leg, while in 12 patients there
normotensive (8 male, 2 female). Twenty-seven had was only a paresis of face, arm and leg, the severity of
elevated blood pressure with systolic over 150 or involvement often being greater in one part than
diastolic over 110 mm Hg (23 of these were males). another. One patient had 3 episodes of paresis of one
Three patients were diabetic and 5 had elevated blood arm separated by months but paresis of the face, arm
lipids. and leg in one of these attacks.
Each of the patients had at least one scan. Thirteen The clinical course was benign in most patients with
had normal scans; 2 others had a normal scan within pure motor hemiplegia, 18 making almost complete
24 hours of the acute episode, but an abnormal scan recovery. Twelve patients had more than one distinct
after one week. Among the patients with abnormal episode. The tendency was for less recovery with each
scans, 18 had small deep lesions of less than 4 ml es- succeeding stroke. One patient had a subsequent brain
timated volume. Fisher initially limited the term stem stroke to which he succumbed.
lacune to lesions of less than 15 mm diameter which Ten of the patients had an appropriate lacunar le-
by our method of calculation gives a volume of 1.7 ml; sion on the scan (fig. 1), 10 had normal scans but 5 had
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FIGURE 1A and B Contiguous CT sections after intravenous contrast medium showing a

large lacunar infarct involving posterior limb of left internal capsule and extending into len-
tiform nucleus and corona radiata in a hypertensive man with pure right hemiplegia which
recovered completely.
 258 STROKE VOL 11, N o 3, MAY-JUNE 1980

FIGURE 2A and B Contiguous CT sections showing a large superficial infarct in right middle
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cerebral artery distribution in a hypertensive man with pure motor hemiplegia with complete
recovery.

large superficial infarcts at sites appropriate to the In summary of 37 patients presenting with a clinical
clinical deficit (fig. 2). These results are recorded in the syndrome usually associated with a lacunar infarct, 18
table. (48%) had the lesion confirmed by CT scan. Thirteen
patients had normal scans but these may have in-
Pure Sensory Stroke cluded lacunes which were too small to be identified.
However, there were 6 examples of large superficial
Four patients had pure sensory stroke. All had sen- lesions accounting for the neurological deficit; 5 oc-
sory symptoms involving the left face, arm and leg curring in the pure motor hemiplegia group, and one
without motor findings, visual field abnormality or in the pure sensory deficit group.
speech disturbance. One had a normal scan, one The sites of lesions considered as lacunes were all
diffuse cerebral atrophy, one showed bilateral lacunar localized to the internal capsule or adjacent lentiform
infarcts, and one had an infarct of 5.8 mis which is nucleus or corona radiata (fig. 3). Five lesions were
larger than the accepted range for lacunes. considered to be in the genu, 3 in the posterior limb
and 3 in adjacent trigone area. Five lesions were
Dysarthria-Clumsy Hand Syndrome
Six patients had symptoms compatible with the
dysarthria-clumsy hand syndrome. Five had involve- TABLE CT Scan Results
ment of the left hand, one the right. One patient had a Number of Large
motor hemiplegia involving the other side with com- patients Normal Lacunes lesions
plete recovery 20 years previously. The scans in all six i Pure motor
patients showed small deep lesions in the capsular hemiplegia 26 10 ii 5
region; one had, in addition, an equivocal lesion in the ii Pure sensory
pons. In 2 patients, 4 distinct lesions were seen. stroke 4 2 i 1
iii Clumsy hand-
Homolateral Ataxia with Crural Paresis dysarthria 6 0 6 0
One patient, a 60 year old hypertensive man, had a iv Crural paresis 1 1 0 0
crural paralysis with mild ataxia of the same side. His 37 13 18 6
scan was normal.
 CT IN LACUNAR SYNDROMES/Nelson el al. 259

FIGURE 3 A and B CT scan showing lacunar infarct in posterior limb of left internal capsule
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extending into lentiform nucleus in a hypertensive man with pure right motor hemiplegia which
recovered. There are also lacunes in the right thalamus and an ill-defined area of low density in
the right frontal lobe which had not caused clinical disturbance. (Bj Coronal section of the brain
showing lacunes in the right thalamus and left internal capsule and lentiform nucleus corre-
sponding with CT scan. The patient had died from a subsequent cerebral hemorrhage which is
also seen. The left and right hemispheres are respectively on the left and right of the picture.

mainly situated in the anterior limb, globus pallidus or tioned above in a patient who has a marked tendency
putamen. In 2 of the lesions in the capsular region, the to recover. The absence of hypertension in any patient
site could not be identified more specifically. Lesions does not exclude the diagnosis. The majority of our 37
were not identified with certainty in the brain stem but patients had pure motor hemiplegia and 5 of the 6
2 patients with capsular lesions also had cerebellar in- large infarcts were in this group. The diagnosis of a
farcts. lacunar infarction on the basis of pure motor
In view of the fact that clinical syndromes usually hemiplegia obviously entails exclusion of any
associated with lacunes were also shown in some in- dysphasic speech disturbance and, in minimally
stances to be caused by large superficial lesions, the affected cases, this may be difficult to distinguish from
histories of the patients were re-examined in the 3 non-dysphasic speech difficulties. It is also necessary
groups; those with normal scans, those with scans to exclude patients with even minor sensory distur-
showing lacunes and those with large infarctions. The bance. The care with which these exclusions are made
patients with large lesions had a lower incidence of will obviously depend on the individual clinician; the
hypertension with only 3 of 6 having elevated blood examinations in each patient in this series were per-
pressure compared with 14 of 18 patients with small formed by a competent neurologist and the findings at
lesions and 12 of 13 with normal scans. There were no the time of examination were consistent with the
significant differences in sex distribution but those lacunar syndrome. We excluded all patients with any
with large lesions were older (mean age 64 years com- speech disturbance, for the above reasons.
pared with 56 for those with lacunes and 58 for those Of 37 patients who presented with a clinical picture
with normal scans). compatible with lacunar infarction, 18 had the lesions
verified by CT scan. There are a number of possible
Discussion
reasons for the 13 with normal scans.
The clinical diagnosis of a lacunar syndrome entails Campbell et al.10 have noted that early scans may be
the recognition of one of the 4 known syndromes men- negative with a peak detection rate between the eighth
 260 STROKE VOL 11, No 3, MAY-JUNE 1980

and eleventh day. This is unlikely to be the explana- than its size, should be the criterion for the term
tion in our patients in that all of the normal scans were lacune. However, he referred to lesions larger than 1
carried out at least 5 days after the acute episode. Two ml as giant lacunes. The pathogenesis of these lesions
patients who had had normal scans within 24 hours of appears to be similar to that of the smaller lesions
their acute episode had lacunar lesions demonstrated and involves atheroma or a degeneration termed
in the second week. Alcala et al.11 have studied possi- lipohyalanosis of the small penetrating thalamostriate
ble reasons for normal scans in the presence of infarc- arteries. Hughes,12 however, suggested that they are
tion. The most obvious explanation is that the lesion is due to kinking of these small vessels and Ross Rus-
too small to be picked up by the scan, particularly if it sell13 has demonstrated small aneurysms in relation
is in the brain stem. to them; Cole and Yates14 have shown that many are
It should be noted that almost half the normal scans due to small hemorrhages, probably from these same
occurred in patients with a paresis of one limb or the aneurysms. Prineas and Marshall,18 as well as Fisher,
face and minimal involvement of the other parts. This have emphasized the relationship to hypertension,
might suggest that the smallest lacunes may produce sion.
incomplete syndromes. Fisher* has stated that an in- While many of our patients were hypertensive,
farct of restricted size in the capsule may cause a pure several were not. Lesions with the same appearance on
motor monoplegia. However, he also points out that a scan could have been due to emboli, although a source
monoplegia is more likely to result from a small cor- of emboli was not obvious. Only one patient had a car-
tical lesion. One would have expected in the latter case diac arrhythmia, one had a history of myocardial in-
that the lesion would have been detected by the scan. farction, and a further 2 had angiographic abnor-
A third explanation for normal scans is that the malities of middle cerebral artery, delayed flow, and
lesions are in the brain stem which is a less favorable occlusion respectively. Both the patient with a cardiac
area for demonstration of lesions by scan. However, arrhythmia and the patient with delayed flow in the
there were no particular features pointing to the brain middle cerebral artery territory had lacunar infarcts.
stem as the site of the pathology in our patients. The neck vessels are an alternate source of emboli
It is evident from postmortem studies that patients and one patient had bilateral carotid atheroma and
may have multiple lacunes with little clinical evidence severe internal carotid stenosis with an infarct just
of neurological deficit. The lesions seen on CT scan outside the lacunar range. A further patient, however,
are not necessarily the only lacunes present and exact had bilateral carotid atheroma with a lacunar sized in-
clinico-pathological correlation is therefore difficult. farct on the side opposite the hemiplegia and a symp-
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In general, however, patients with pure motor tomless larger right frontal infarct. This patient un-
hemiplegia with positive scans had lesions appropriate derwent endarterectomy. Several other patients were
to the clinical picture. The highest incidence of treated with either aspirin or anticoagulants. On the
positive scans was found in patients with dysarthria- other hand, out of 7 patients with atheroma of neck
clumsy hand syndrome, where all of the patients had vessels, the 4 patients in whom the atheroma was
lacunar lesions in the contralateral internal capsule. regarded as minor, all had lacunar sized infarcts or
Fisher, however, incriminated a lesion in the pons as normal scans.
responsible for this syndrome. One of our patients had Four patients had carotid occlusions, all of them
a possible pontine infarct as well and two others had right-sided and on the side opposite the hemiparesis.
unilateral or bilateral deep cerebellar infarcts, one The scans were normal in one patient, 2 had lacunar
having a total of 5 lacunar infarcts. Pontine infarcts sized lesions on the same side as the occlusion and the
could have been present in other patients since they fourth had a large infarct. All 4 were normotensive.
are difficult to demonstrate and, therefore, are never Thus the demonstration of small deep infarcts on CT
excluded by scans. scan does not exclude the necessity for angiography.
The presence of 6 large infarcts — 5 of them with From this study, it is apparent that patients present-
pure motor hemiplegia and the sixth with a pure sen- ing clinically with the lacunar syndrome may have
sory stroke — suggests that the clinical diagnosis of a large and superficial infarcts as well as small deep
lacunar syndrome is not always accurate. The 5 ones, and that both may be associated with a potential
patients with pure motor hemiplegia were all males and treatable source of emboli. One benefit of CT
over 62 with a right-sided lesion. Three of them were scanning in these patients is to detect large lesions
normotensive and the other 2 were adequately con- producing the clinical picture usually associated with
trolled on antihypertensive agents. There was lacunes. Though cost effectiveness of CT scanning in
otherwise nothing remarkable about their histories. the practical management of cerebrovascular
The patient who had a large lesion causing a pure sen- problems has recently been called into question,18 it
sory stroke was a normotensive female of 26 on oral clearly has a part to play in clinicoanatomical correla-
contraceptives. tion in this difficult diagnostic field.
The size of lesions demonstrated by CT scan is
similar to those described by Fisher9 some of which Acknowledgment
were 25 X 25 X 10 mm when measured at autopsy; Dr. Nelson was supported by the Ontario Heart Foundation and
these he refers to as large lacunes. In an earlier paper, Dr. Pullicino by a grant from EMI Ltd. We wish to thank Miss
Fisher1 suggested that the nature of the lesion, rather Catherine Shevlin and Miss Beryl Laatz for secretarial assistance.
 Ca ANTAGONIST EFFECT ON CEREBRAL ARTERY/STiimizu et al. 261

References 9. Fisher CM: Capsular infarcts, the underlying vascular lesion.

Arch Neurol (Chicago) 36: 65-73, 1979
1. Fisher CM: Lacunes: small deep in fa rets. Neurology (Minneap) 10. Campbell JK, Houser OW, Stevens JC et al: Computerized
15: 774-784, 1965 tomography and radionuclide imaging in the evaluation of
2. Caplan LR: Lacunar infarction a neglected concept. Geriatrics ischaemic stroke. Radiology 126: 695-702, 1978
31: 71-75, 1976 11. Alcala H, Gado M, Torrack RM: The effect of size, histological
3. Fisher CM: The arterial lesions underlying lacunes. Acta elements and water content on the visualization of cerebral in-
Neuropathol (Berlin) 12: 1-15, 1969 farcts. Arch Neurol (Chicago) 35: 1-7, 1978
4. Fisher CM, Curry HB: Pure motor hemiplegia of vascular
12. Hughes W: Origin of lacunes. Lancet 2: 19, 1965
origin. Arch Neurol (Chicago) 13: 30-44, 1965
13. Ross Russell R: Observations on intraccrebral aneurysms.
5. Fisher CM: Pure sensory stroke involving face, arm and leg.
Brain 86: 425-442, 1963
Neurology (Minneap) 15: 76-80, 1965
6. Fisher CM, Cole H: Homolateral ataxia and crural paresis: a 14. Cole FM, Yates PO: Comparative incidence of cerebrovascular
vascular syndrome. J Neurol Neurosurg Psychiatry 28: 48-65, lesions in normotensive and hypertensive patients. Neurology
1965 (Minneap) 18: 265-269, 1968
7. Fisher CM: A lacunar stroke. The dysarthria clumsy-hand syn- 15. Prineas J, Marshall J: Hypertension and cerebral infarction. Br
drome. Neurology (Minneap) 17: 614-617, 1967 Med J 1: 14-17, 1966
8. Mohr JP, Caplan LR, Melski JW et al: The Harvard 16. Larson EB, Omena GS, Loop JW: Computerized tomography
Cooperative Stroke Registry: a prospective registry. Neurology in patients with cerebrovascular disease: impact of a new
(Minneap) 28: 754-762, 1978 technology on patient care. Am J Roentgen 131: 35-40, 1978

Evidence for Greater Susceptibility of Isolated

Dog Cerebral Arteries to Ca Antagonists
than Peripheral Arteries
KOICHIRO SHIMIZU, M . D . , TOMIO OHTA, M . D . , P H . D . ,

AND NOBORU TODA, M . D . , P H . D .

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SUMMARY In helically-cut strips of dog cerebral, coronary and mesenteric arteries, contracted with
prostaglandin (PG) F to or K+, tbe addition of verapamii caused a dose-related relaxation. Verapamil-induced
relaxations were greater in cerebral than in the other arteries when contracted with PGF*,, but did not
significantly differ in tbe arteries contracted with K+. Similar results were obtained with diltiazem and
nifedipine. The contractile response to PGF^ was attenuated by pretreatment with verapamii, the attenuation
being greater in cerebral than in mesenteric arteries. Nitrogiycerin and sodium nitroprusside relaxed cerebral,
coronary and mesenteric arteries contracted with PGF^ to a similar extent. It may be concluded that dog
cerebral arteries contracted with PGF*,, one of endogenous rasospastic substances, are more susceptible to
agents which interfere with the influx of Ca + + across cell membranes than coronary and mesenteric arteries;
these agents may thus be of value in the treatment and prophylaxis of cerebral vasospasm.
Stroke, Vol 11, No 3, 1980

ISOLATED CEREBRAL ARTERIES respond to Nitrogiycerin and sodium nitroprusside are potent
vasoconstricting and vasodilating agents differently vasodilators 9 ' 10 and cause rapid hypotension. These
from peripheral arteries. 1 ' 2 Cadmium ( C d ) + + an- agents are also expected to release cerebroarterial
tagonists, including verapamii, nifedipine, diltiazem spasm following subarachnoid hemorrhage.11 No in-
and C d + + , interfere with the influx of C a + + across cell formation is available concerning the response of
membranes of vascular smooth muscle,8"7 thereby cerebroarterial smooth muscle to these vasodilators.
resulting in vasodilatation. Contractile responses to The present study was thus undertaken to compare
C a + + of cerebral arteries exposed to Ca + + -free media quantitatively the response of isolated dog cerebral,
and depolarized by K + are attenuated to a greater ex- coronary and mesenteric arteries to C a + + antagonists,
tent by verapamii and C d + + than those of coronary nitrogiycerin and sodium nitroprusside. Verapamii
and mesenteric arteries." prevention of drug-induced contractions was also
compared in cerebral and mesenteric arteries.

From the Department of Pharmacology, Shiga University of

Medical Sciences, Seta, Ohtsu 520-21, and Department of Methods
Neurosurgery, Osaka Medical College, Takatsuki 569, Japan (Drs.
Shimizu and Ohta). Mongrel dogs of both sexes, weighing 7 to 15 kg,
Reprints: Dr. Toda, Dept. Pharmacology, Shiga University of were anesthetized with intraperitoneal injections of
Medical Sciences, Seta, Ohtsu 520-21, Japan. sodium pentobarbital 50 mg/kg, and sacrificed by