Cerebral Infarction of the Basal Ganglia Due to Embolism from the Heart

JOAN SANTAMARIA, M.D. , FRANCESC GRAUS, M.D. , FRANCISCO RUBIO, M.D. ,

TXOMIN ARBIZU, M.D. , AND JAUME PERES, 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 consid­ered 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.1 The most frequent clinical presentation is a pure motor deficit2 3 but it is sometimes, accompanied by dysar­thria, sensory impairment4 or cerebellar deficit.5 The size of the infarct is usually small, with a diameter of 6 to 10 mm, 2 but larger infarcts have been described in computed tomography (CT)3- *•7 and pathologic stud­ies. 2

Although a source of emboli in patients with deep cerebral infarcts is almost never considered, a few experimental8 and pathologic1 studies suggest that some may be embolic. Recently, Pullicino et al 6 found a possible cardiac source of emboli in 12% of 42 pa­tients 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.

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 pres­sure 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 fi­brillation. The disease was diagnosed by clinical histo­ry 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 en­docarditis 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 Neurol­ogy, 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 sever­al hours was seen before stabilization occurred. Neuro­logical examination showed a complete (5 cases) or incomplete (3 cases) hemiplegia, accompanied by hy-pesthesia 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 char­acterized by nonfluent conversational speech, naming and reading difficulties, dysgraphia and a normal audi­tory 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, puta-men 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 circum­scribed 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 evi­dence that the infarct was recent. Contrast enhance­ment 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 pres­ence 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 secon­dary to rheumatic heart disease. 9 ' 1 0

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TABLE Clinical and CT Findings

Patient/ Type of Clinical Neurologic age/sex heart disease* presentation findings Clinical course C T findings

1 44 F RHD with MS abrupt onset hemiplegia ( L ) moderate recovery head of caudate AF maximum deficit hypesthesia anosognosia disap­ ALof IC and putamen

immediately anosognosia peared in 2 days 2/37/F RHD with MS abrupt onset and pure motor moderate recovery hemorrhagic

and AR, AF gradual progres­ hemiplegia ( L ) capsulo-lenticular sion during 3 and caudate hours

3/53/F 1HSS and SBE abrupt onset hemiplegia (L) poor recovery capsulo-lenticular maximum deficit hypesthesia and caudate

immediately dysarthria 4/59/F RHD with MS abrupt onset and hemiplegia (L) total recovery caudate, putamen

fluctuation during hypesthesia and AL of IC 5 hours

hypesthesia

5/34/M aortic prosthetic abrupt onset, maxi­ hemiplegia (L) moderate recovery caudate, putamen valve (Starr- mum deficit im­ hypesthesia and AL of IC Edwards) mediately

6/65/F RHD with MS abrupt onset and hemiparesia (L) moderate recovery head of caudate AF gradual progres­ hypesthesia anosognosia disap­ AL of IC and

sion during 3 anosognosia peared in few putamen hours days

7/49/F RHD with MS abrupt onset hemiplegia (L) poor recovery head of caudate AF maximum deficit hypesthesia AL of IC and

immediately anosognosia putamen 8/37/F RHD with MS abrupt onset and hemiparesia (R) total recovery putamen and

fluctuation during aphasia AL of IC 6 hours

*Confirmed at surgery in cases 1, 2 , 3 and 8. RHD = rheumatic heart disease; MS = mitral stenosis; AF = atrial fibrillation; AR = aortic regurgitation; IHSS =

idiopathic hypertrophic subaortic stenosis; SBE = subacute bacterial endocarditis; L = left; R = right; AL = anterior limb; IC = internal capsule.

All but one patient manifested clinical patterns dif­ferent 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 . 2 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 wel l ." 1 2 In addition the Harvard Cooper­ative Stroke Registry reported this profile in 2 1 % of the patients diagnosed of cerebral embolism. 1 1

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 verifi­cation this assumption cannot be ruled out definitively

FIGURE 1. A. Enhanced CT scan showing an infarct involving the right caudate head nucleus, anterior limb of internal capsule and putamen <Case 4). B. CT scan showing a right caudate and lenticular nuclei enhancement and a discrete atrophy (Case 6).

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FIGURE 2. Unenhanced (A) and enhanced (B) CT scan of case 3, showing a low attenuation area involving right lenticular, and both limbs of internal capsule.

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 1 4 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 in­volving the right thalamus 1 5 or in basal ganglia hemor­

rhages. 1 6 Recently Healton et a l 1 7 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 usu­ally caused by thrombosis of the lenticulostriated arter­ies 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 3 . Enhanced CT scan of case 8. A small infarct in­volving left putamen and anterior limb of internal capsule is demonstrated.

FIGURE 4 . Unenhanced CT scan showing a right lenticular hemorrhagic infarction with a patent mass effect (Case 2).

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and no occlusion in the appropriate lenticulostriated artery, although neither of them had a clear source of emboli. 1 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.1 Recently Pullicino et al reported the pres­ence of a source of emboli in 33% of their patients with small deep infarcts diagnosed by CT scan, 6 and the same was found by Rascol et al in 13% of their cases of pure motor hemiplegia. 1 8

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 lenticulo­striated arteries. A deep infarction is produced whereas the superficial territory is spared by the collateral cir­culation.2' 1 9 In this way two of the deep infarcts associ­ated with an embolic cardiac source described by Blackwood et a l , 2 0 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 stud­ies.6- 2 1 Crowell et al 2 1 reported deep infarcts in 17 of 27 monkeys subjected to temporary MCA occlusion. The infarcts involved the anterior limb of the internal cap­sule, the caudate nucleus and the anterior portion of putamen. This high incidence may be due to the vari­ations of meningocortical anastomoses between man and animals. It is our impression, however, that cere­bral 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.

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 lenticu­lostriate artery — and the clinical presentation indi­cates also a much bigger lesion. The differentiation between these two types of deep cerebral infarcts is useful in order to establish an appropriate therapy.

References 1. Fisher CM: Capsular infarcts: the underlying vascular lesions.

Arch Neurol 36: 65-73, 1979 2. Fisher CM, Curry HB: Pure motor hemiplegia of vascular origin.

Arch Neurol 13: 30-44, 1965 3. Donnan GA, Tress BM, Bladin PF: A prospective study of lacunar

infarction using computerized tomography. Neurology (Ny) 32: 49-56, 1982

4. Mohr JP, Kase CS, Meckler RJ, Fisher CM: Sensorimotor stroke due to thalamocapsular ischemia. Arch Neurol 34: 739-741, 1977

5. Perman GP, Racy A: Homolateral ataxia and crural paresis: Case report. Neurology (Ny) 30: 1013-1015, 1980

6. Pullicino P, Nelson RF, Kendall BE, Marshall J: Small deep in­farcts diagnosed on computed tomography. Neurology (Ny) 30: 1090-1096, 1980

7. Weisberg LA: Lacunar infarcts. Clinical and computed tomo­graphic correlations. Arch Neurol 39: 37-40, 1982

8. Moiinari GF: Experimental cerebral infarction. II Clinicopatholog-ical model of deep cerebral infarction. Stroke 1: 232-244, 1970

9. Rowe JC, Bland EF, Sprague HW, White PD: The course of mitral stenosis without surgery: Ten- and twenty-year perspectives. Ann Int Med 52: 741-749, 1960

10. Daley R, Mattingly TW, Holt CL, Bland EF, White PD: Systemic arterial embolism in rheumatic heart disease. Am Heart J 4 2 : 5 6 6 -581, 1951

11. Fisher CM, Pearlman A: The nonsudden onset of cerebral embo­lism. Neurology (Minneap) 17: 1025-1032, 1967

12. Wells CE: Cerebral embolism. The natural history, prognostic signs and effects of anticoagulation. Arch Neurol 1:667-677, 1959

13. Mohr JP, Caplan LR, Melski JW, Goldstein RJ, Duncan GW, Kistler JP, Pessin S, Bleich HL: The Harvard Cooperative Stroke Registry: A prospective registry. Neurology (Ny) 28: 754-762, 1978

14. Damasio AR, Damasio H, Rizzo M, Vamey N, Gersh F: Aphasia with non-hemorrhagic lesions in the basal ganglia and internal capsule. Arch Neurol 39: 15-20, 1982

15. Watson RT, Heilman KM: Thalamic neglect. Neurology (Ny) 29: 690-694, 1979

16. Hier DB, Davis KR, Richardson EP Jr, Mohr JP: Hypertensive putaminal hemorrhage. Ann Neurol 1: 152-159, 1977

17. Healton EB, Nacarro C, Bressman S, Brust JCM: Subcortical neglect. Neurology (Ny) (Abstract) 31 (2): 62, 1981

18. Rascol A, Clanet M, Manelfe C, Guiraud B, Bonafe A: Pure motor hemiplegia: CT study of 30 cases. Stroke 13: 11-17, 1982

19. Mohr JP: Lacunes. Stroke 13: 1-11, 1982 20. Blackwood W, Hallpike JF, Kocen RS, Mair WGP: Atheromatous

disease of the carotid arterial system and embolism from the heart in cerebral infarction: A morbid anatomical study. Brain 92: 897-910, 1969

21. Crowell RM, Marcoux FW, De Girolami U: Variability and revers­ibility of focal cerebral ischemia in unanesthesized monkeys. Neu­rology (Ny) 31: 1295-1302, 1981

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J Santamaria, F Graus, F Rubio, T Arbizu and J PeresCerebral infarction of the basal ganglia due to embolism from the heart.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1983 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.14.6.911

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