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(Stroke. 1997;28:1022-1027.)
© 1997 American Heart Association, Inc.

Articles

Cerebral Infarcts Related to Isolated Middle Cerebral Artery Stenosis

P. A. Lyrer, MD; S. Engelter, MD; E. W. Radü, MD; A. J. Steck, MD

From the Department of Neurology and Division of Neuroradiology (E.W.R.), University Hospital Basel (Switzerland).

Correspondence to P.A. Lyrer, MD, Department of Neurology, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland. E-mail LYRER{at}ubaclu.unibas.ch

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose The clinical presentation of middle cerebral artery (MCA) stenosis, a rarely diagnosed condition, is not well known. The aim of this study was to analyze the stroke patterns of patients with isolated MCA stenosis.

Methods Twenty-two patients with cerebral infarcts due to isolated MCA stenosis were analyzed with respect to their clinical syndrome, and cerebral lesions were assessed by neuroimaging. MCA stenosis was diagnosed by transcranial Doppler sonography (TCD) in 16, by TCD and digital subtraction angiography (DSA) in 4, and by DSA alone in 2 patients.

Results Ten patients (45.5%) had lacunar syndromes, suggesting small-vessel disease, and 12 patients (55.5%) showed signs and symptoms of cortical dysfunction. Cerebral CT or MRI showed no lesion in 2 patients, small deep infarcts in 10, large striatocapsular infarcts in 2, combined piomedullary and striatocapsular infarcts in 4, piomedullary branch infarcts in 3, and MCA trunk infarct in 1.

Conclusions The results suggest an association between MCA stenosis and (1) lacunar infarcts and (2) the occurrence of piomedullary MCA branch infarcts alone or in combination with subcortical infarcts. The clinical syndromes and the radiological findings correspond in most cases.

Key Words: cerebral infarction • lacunar infarction • middle cerebral artery • ultrasonics

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
The presence of an isolated atherosclerotic disease of the MCA is considered an infrequent cause of stroke.^{1 2 3 4} It has been increasingly recognized in patients with strokes or transient ischemic attacks since noninvasive evaluation by TCD has been performed more systematically.² Former reports regarding the clinical syndrome mentioned cortical involvement,^{5 6 7 8 9} but pure subcortical syndromes were also described.^{5 10 11} The published data primarily consist of small numbers of patients, and isolated MCA stenosis is mentioned only as a subgroup within series, including patients with complete MCA occlusion of unknown origin⁹ or concomitant ipsilateral internal carotid artery pathology.⁵ Embolic obstruction of the MCA is frequent and could mimic atherosclerotic stenosis in ultrasound studies as well as in imaging studies, when recanalization has started.¹ However, information about presumed cardiogenic or arterioarterial embolism is not given in detail in the previous reports.^{8 9 12}

TCD is an established diagnostic method to ascertain MCA stenosis and correlates well with angiographic studies.^{2 13 14 15 16 17 18} It may be difficult to show a stenosis of the MCA stem in standard anteroposterior and lateral pro-jections by angiography, and its quantification may be uncertain.^{2 18} With the use of TCD, local increases in MFV and peak flow velocity, low frequency signals, disturbed flow phenomena, and arterial wall covibrations are considered typical findings in stenotic intracranial vessels.¹⁵ A circumscribed unilateral MFV >80 to 90 cm/s or MFV side difference of >30 cm/s is considered the cutoff by many authors.^{14 15 18}

Small-vessel disease is considered the most common etiology of small deep infarcts,¹⁹ whereas piomedullary branch infarct may be caused by cardiac or arterial embolism²⁰ of various origins. MCA stenosis could cause ischemia of supplied distal territories, including the cerebral cortex, by the release of emboli²¹ and by impairment of distal perfusion.⁶ Alternatively, silent atherosclerosis of the MCA stem might become apparent by blockage of the orifices of deep penetrating lenticulostriate arteries,^{10 11 22} causing small deep infarcts.

The aim of the present study was to detect the presence of specific stroke syndromes and neuroradiological findings related to isolated MCA stenosis.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
We studied 20 patients with stroke in whom MCA stenosis was diagnosed by TCD. The patients were recruited during a 4-year period (June 1991 to July 1995) from a total of 4382 investigations by the neurosonology unit when repeated TCD examinations showed persisting flow acceleration of the MCA. Another 11 patients with signs of ipsilateral carotid pathology on TCD and 3 patients with transient ischemic attacks were not included. Two patients in whom transtemporal insonation was not possible were also included after detection of MCA stenosis by cerebral angiography. Of these 22 patients, 3 had a transient ischemic attack in the affected MCA territory before the stroke occurred (patients 8, 13, and 17). The symptoms were similar to the later stroke symptoms in all cases. The symptoms preceded stroke onset by <12 hours in 2 patients and by 3 weeks in 1 patient. Nineteen patients had no preceding symptoms. Age (mean±SD, 62.3±12.1 years) and sex distribution data are presented in Table 1.

View this table: [in this window] [in a new window]   Table 1. Demographic Data, Risk Factors, and TCD Data

The following risk factors were evaluated in all patients. Patients taking prescribed antihypertensive medication or with blood pressure >165/95 mm Hg persisting for >3 weeks were considered hypertensive. Hypercholesterolemia was assumed at fasting serum cholesterol levels >6.5 mmol/L. Patients taking prescribed antidiabetic drugs or with fasting glucose levels >6.7 mmol/L were considered diabetic. Patients were classified as smokers when they reported regular daily cigarette use.

In addition to the neurological examination, all patients had an unremarkable cardiovascular history, a normal clinical cardiac examination, and normal electrocardiography and chest roentgenography. The majority of patients (72%) were treated in the neurology department or the general medical ward. Additional examinations were requested by the treating physician when appropriate. After introduction of a stroke unit in March 1995, four patients were initially treated in the intensive care monitoring unit. Nine patients underwent 24-hour electrocardiographic monitoring or cardiovascular monitoring in the intensive care unit (patients 3, 5, 6, 10, 11, 16, 17, 19, and 20). Transthoracic echocardiography was performed in 1 patient (patient 20), and transesophageal echocardiography was performed in 7 patients (patients 6, 10, 11, 13, 16, 18, and 22). Five patients were excluded because of presumed cardioembolic etiology based on their cardiovascular history and examination or pathological test results.

We performed TCD studies using an EME TC2-64B or EME Pioneer TC 2020 device (2-MHz pulsed-wave device) with transtemporal insonation depth of 45 to 55 mm. TCD was performed after a mean time of 55.5 (range, 2 to 540) days after stroke onset. TCD diagnosis was established within 30 days after stroke onset in 17 patients and >30 days after stroke onset in 3 patients.

In selected patients, DSA (patients 8, 10, 13, 14, 16, and 22) or MR angiography (patients 3, 5, 8, 13, 15, 18, and 19) was additionally performed, confirming the TCD diagnosis in every case. DSA or MR angiography was indicated by the treating physician to confirm the diagnosis, mainly in patients at the beginning of the observation period. The criteria for diagnosis of MCA stem stenosis were as follows: circumscribed increased MFV >90 cm/s at an insonation depth of 50 to 55 mm, a side-to-side difference of >30 cm/s, and a poststenotic reduced flow signal at an insonation depth of 45 mm. In patients with MFV >90 cm/s in both MCAs, bilateral MCA stenosis was assumed.

Five patients also had clinically asymptomatic contralateral MCA stenosis.

The following clinical syndromes were distinguished as lacunar syndromes^{19 23 24 25} : pure motor hemiparesis, sensorimotor deficits, pure sensory deficits, and movement disorders such as ataxic hemiparesis, hemichorea, or hemiballism. Nonlacunar syndromes were recognized when we observed signs of dysphasia, visual field deficit, visuospatial problems, neglect, apraxia, or forced gaze alone or together with unilateral motor or sensory deficit.^{5 25 26} Thirteen patients were investigated by cranial MRI with T1- and T2-weighted images and 9 by cranial CT. The lesions were drawn on tracing paper; the slice showing the largest infarct extension was used. We analyzed the infarcts according to their anatomic localization, using templates showing the anatomic structure and vascular territories of lenticulostriate arteries arising from the MCA in cases of small deep infarcts.²⁷ The lesions of the white matter and the cortical areas were analyzed according to their presumed pial MCA branch territories.^{3 4} Furthermore, the correspondence of clinical features with radiological results was investigated.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
All but one patient had at least one cerebrovascular risk factor. Hypertension was present in 59.1%, smoking in 63.6%, hypercholesterolemia in 31.8%, and diabetes mellitus in 4.5% of the patients. The MFV on the asymptomatic MCA was 69.5±36.5 cm/s and on the symptomatic stenotic MCA was 153.8±56.7 cm/s (P<.0001). The right and the left MCA were each involved in 11 patients.

Neurological Symptomatology
Table 2 summarizes clinical symptomatology in patients with MCA stenosis. Ten patients (45.5%) suffered from lacunar syndromes: Pure motor hemiparesis, the most common symptom, was present in 6 patients (27.3%). Two patients (9.1%) had movement disorders with hemichorea and hemiballisms. One patient (4.5%) had pure sensory deficits, and another had sensorimotor deficits alone without cortical dysfunction. Twelve patients (54.5%) had nonlacunar syndromes with hemiparesis of different degrees of severity and signs and symptoms of cortical dysfunction.

View this table: [in this window] [in a new window]   Table 2. Clinical Symptomatology in Patients With MCA Stenosis

Neuroradiological Data
Table 3 summarizes neuroimaging in patients with symptomatic MCA stenosis. CT scans showed no lesions in 2 patients (9.1%), and small deep infarcts of the basal ganglia were disclosed in 10 patients (45.5%). Large striatocapsular infarcts were found in 2 patients (9.1%). Pial MCA branch infarcts were present in 3 patients (13.6%), combined striatocapsular and pial branch infarcts were present in 4 (18.2%), and 1 patient (4.5%) had a large MCA trunk infarct (Fig 1). In 20 of the 22 patients (90.9%) the clinical syndrome corresponded to the neuroradiological findings. Eight of the 10 patients with lacunar syndrome had a corresponding small deep infarct on CT or MRI. Two patients had no lesion on CT scan, and MRI was not performed. Eight of the 12 patients with nonlacunar syndromes showed cortical infarcts (Fig 2; see also Table 3). Of the remaining 4 patients, 1 had an internal border zone infarct, 1 had a large striatocapsular infarct, and 2 had small deep infarcts on neuroimaging.

View this table: [in this window] [in a new window]   Table 3. Neuroimaging in Patients With Symptomatic MCA Stenosis

View larger version (32K): [in this window] [in a new window]   Figure 1. Patients 1 through 10. Topography of infarcts in MCA stenosis in patients with different types of lacunar syndromes.

View larger version (42K): [in this window] [in a new window]   Figure 2. Patients 11 through 22. Topography of infarcts in MCA stenosis in patients with nonlacunar syndromes.

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
We analyzed 22 consecutive patients with ultrasonographic or angiographic evidence of isolated MCA stenosis to detect specific clinical and radiological stroke patterns. Hypertension and smoking were the most common risk factors.^{5 6 7} However, frequency did not differ from that in other types of stroke.^{6 27 28} Elevated blood cholesterol was present in 32%, which was within the published range of 11%⁵ to 61%.⁷ Diabetes mellitus was present in only one patient (4.5%), although an incidence of 16% to 40% was reported in populations of stroke patients, and diabetes mellitus is considered a risk factor for lacunar strokes.^{5 6 7} The association of MCA stenosis with diabetes remains questionable in our series.

Two main groups of clinical syndromes were found in association with MCA stenosis. Lacunar syndromes caused by small deep infarcts were found in almost half of the patients. The others had various types of nonlacunar syndromes with signs and symptoms of cortical dysfunction suggesting MCA pial branch infarct in most cases.

Lacunar Syndromes
Forty-five percent of the patients had lacunar syndromes. Pure motor hemiparesis, the most common feature in lacunar syndromes, was present in 27.3% of our patients, similar to other studies of lacunar syndromes.^{23 28 29} In an extracranial-intracranial bypass study,⁵ pure motor hemiparesis occurred in 15% of the patients with MCA occlusion or stenosis, while pure sensory deficits were detected in only 2%. The basal ganglia and the internal capsule are thought to be primarily involved in pure motor hemiparesis.^{29 30} Of patients with pure motor hemiparesis, 4 had a corresponding small deep infarct on CT or MRI and 2 had no visible lesions. Pure sensory deficit and sensorimotor deficit were each noted in 1 patient. For pure sensory deficit due to MCA stenosis, a lesion in the thalamo-striatal pathway is likely; for sensorimotor deficit, involvement of the internal capsule or the basal ganglia is likely.²⁹ Our patients had visible lesions of the anterior limb of the internal capsule (pure sensory deficit) and of the rostral putamen (sensorimotor deficit). Eight of 10 patients with lacunar syndromes had a corresponding lesion that could be visualized by neuroimaging, which agrees with published data, although half of the patients were investigated by CT scan alone.^{29 30 31 32 33} Two patients had predominant signs of hemichorea and hemiballism. Disturbance of the basal ganglia, particularly the putamen and the globus pallidus, is known to cause contralateral movement disorders^{34 35} and can also be classified as lacunar syndrome.¹⁹ An ischemic etiology that could be related to the MCA territory²³ has been established in similar cases.³⁴

The etiology of small deep infarcts due to small-artery disease in association with MCA arteriosclerosis^{19 23 29 32} may be explained by the occlusion of the small perforating arteries at their origin.^{10 22} This explanation may be supported by the fact that neuroimaging showed no evidence for other sites of small-vessel disease in the patients with lacunar syndromes. The same mechanism has been observed in the basilar artery when atherosclerotic plaques obstruct the mouth of perforating pontine branches, while pathological studies have failed to detect these findings in the MCA thus far.^{22 23 36} However, local MCA atherosclerosis might be underestimated as the etiology of small deep infarcts.^{10 22 36} The lenticulostriate arteries originate primarily from the proximal MCA stem,^{37 38} a location that is preferentially involved in atherosclerotic MCA disease.^{6 8} The lateral lenticulostriate arteries supply the lateral third of the globus pallidus, the caudate nucleus, and most of the putamen and internal capsule. The medial globus pallidus is supplied by the medial lenticulostriate arteries.^{6 26 37 38} Reduced flow within a single lenticulostriate artery might cause small ischemic lesions of parts of the basal ganglia or the internal capsule, leading to the aforementioned clinical syndromes and mimicking small-vessel disease.

Nonlacunar Syndromes
Twelve patients exhibited signs and symptoms suggestive of cortical dysfunction.^{5 6 8 9} Seven patients had piomedullary MCA branch infarcts of various localizations, 4 in combination with striatocapsular infarcts. One additional patient had an MCA trunk infarct, 2 had large striatocapsular infarcts, 1 had a small subcortical infarct, and 1 had a small deep infarct. The presence of cognitive dysfunction suggesting cortical infarct has already been reported in pure striatocapsular infarcts.^{39 40} Since our patients recovered rapidly from aphasia, sufficient leptomeningeal collaterals may have prevented these patients from experiencing additional cortical infarction.^{6 36 40} It is believed that large striatocapsular infarcts are caused by blockage of multiple perforating lenticulostriate arteries.^{23 35} In most cases embolism with occlusion of the MCA stem but occasionally in situ MCA thrombosis was mentioned as the pathogenetic mechanism.^{6 23 36} Our data suggest that MCA atherosclerosis could cause striatocapsular infarcts by occlusion of several lenticulostriate arteries. Another pathogenetic mechanism of territorial piomedullary branch infarcts might be distal embolism from the MCA stem^{21 41} or, alternatively, impaired distal perfusion.⁶

We have found that MCA stenosis can cause lacunar syndromes as well as hemiparesis with circumscribed cortical dysfunction. By neuroimaging, three main types of MCA territory infarcts could be distinguished: small deep infarcts, larger lenticulostriate infarcts, and piomedullary MCA branch infarcts. Only one patient had an MCA trunk infarct, and no patient had a complete MCA infarct. Correspondence between the clinical symptomatology and the neuroradiological findings was high. To our knowledge this distribution of lesions has not previously been reported. Few reports have focused on clinical symptomatology with respect to the course of the disease.^{8 41} We suggest that in patients with piomedullary MCA branch infarcts as well as small deep infarcts, the MCA territory should be evaluated noninvasively by TCD. This may be important in patients in whom no extracranial source of embolism is evident and also in patients with risk factors for small-artery disease.

	Selected Abbreviations and Acronyms

 

DSA = digital subtraction angiography MCA = middle cerebral artery MFV = mean flow velocity TCD = transcranial Doppler sonography

Received November 21, 1996; revision received January 9, 1997; accepted February 14, 1997.

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lyrer, P. A. Articles by Steck, A. J. Search for Related Content PubMed PubMed Citation Articles by Lyrer, P. A. Articles by Steck, A. J.