Superior Cerebellar Artery Infarction and Vertebral...
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1431 Superior Cerebellar Artery Infarction and Vertebral Artery Dissection Steven R. Levine, MD, and K.M.A. Welch, MD Isolated superior cerebellar artery infarction is rare, and the mechanism is often not readily apparent. We describe a patient with an isolated superior cerebellar artery infarction resulting from an ipsilateral vertebral artery dissection. Angiography demonstrated intraluminal clot in the superior cerebellar artery, suggesting artery-to-artery embolus as a mechanism of this uncommon stroke syndrome. (Stroke 1988;19:1431-1434) I solated superior cerebellar artery (SCA) infarc- tion is rare, 1 - 8 and the mechanism is often not readily apparent. 4 We report the case of a young man with vertebral artery (VA) dissection associated with ipsilateral SCA territory infarction diagnosed clinically and by computed tomography (CT). Cere- bral angiography demonstrated intraluminal clot in the SCA, suggesting that artery-to-artery embolus may be a mechanism of SCA infarction. Case Report A 40-year-old man awoke one morning, turned, and abruptly experienced dizziness and double vision. He felt off-balance, noted left-sided weak- ness and clumsiness, and vomited. These symp- toms were severe for 5-6 hours and then gradually resolved except for the left-sided weakness and clumsiness. Several days previous he had noted transient pain "between his ears" and periodic nausea. There was no history of neck manipulation, trauma, or pain. Medical history was unremarkable. Findings of the general physical examination including cardiac auscultation were normal. Neuro- logic examination revealed anisocoria, with the left pupil 1 mm larger, and vertical diplopia that was worse on gaze to the right; pursuits were saccadic but there was no ocular dysmetria. Palatal myo- clonus was present. A mild hypotonic left hemipa- resis was present as was left-sided dysmetria and hyperreflexia; he fell to the left. Findings of the sensory examination were normal. Results of hematologic and coagulation testing were normal, and there was no laboratory evidence From the Center for Stroke Research, Department of Neurol- ogy, Henry Ford Hospital, Detroit, Michigan. Supported in part by National Institutes of Health Grant NS23393 and research funds from Henry Ford Hospital. Address for correspondence: Steven R. Levine, MD, Center for Stroke Research, Department of Neurology, K-ll, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI 48202. Received March 10, 1988; accepted June 29, 1988. of vasculitis. Electrocardiogram and chest x-ray were normal. On the day of admission, head CT revealed an early infarction in the medial left supe- rior cerebellar hemisphere (Figure 1). Cerebral angi- ography demonstrated an irregular 70% narrowing of the left VA 1.5 cm long at the level of the atlas (Figure 2). Intraluminal clot was present in the left proximal ipsilateral SCA at its bifurcation along the anterolateral margin of the left mesencephalon (Fig- ures 2 and 3). Echocardiography demonstrated min- imal intermittent mitral valve prolapse. The patient was placed on intravenous heparin, discharged on warfarin sodium (Coumadin), and has gradually improved during 3 years of follow-up. Repeat cere- bral angiography 1 year later demonstrated resolu- tion of both the VA and the SCA lesions. Discussion SCA territory infarction is much less commonly diagnosed clinically, radiographically, and postmor- tem than the posterior inferior cerebellar artery (PICA) syndrome of Wallenberg. 1 - 10 Although the SCA is the largest and most consistent branch of the vertebrobasilar tree, relatively few reports have documented isolated SCA infarcts and their mech- anisms. 1 - 8 Our patient had an angiographically doc- umented distal extracranial VA dissection with ipsi- lateral SCA intraluminal clot. Clinical examination and CT supported an isolated SCA syndrome. Our patient had a mild hypotonic hemiparesis ipsilateral to the infarct. Limb weakness has been described with cerebellar lesions, 11 although it is generally due to organizational and coordination deficits of mus- cle activity. Given the variability of supply of the SCA, it is conceivable that ischemia in the right brainstem may explain our patient's weakness as hemiparesis is generally not a feature of the SCA syndrome. An extensive search failed to reveal evidence of hypercoagulability, and minimal mitral valve pro- by guest on June 18, 2018 http://stroke.ahajournals.org/ Downloaded from
Transcript of Superior Cerebellar Artery Infarction and Vertebral...
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Superior Cerebellar Artery Infarction andVertebral Artery Dissection
Steven R. Levine, MD, and K.M.A. Welch, MD
Isolated superior cerebellar artery infarction is rare, and the mechanism is often not readilyapparent. We describe a patient with an isolated superior cerebellar artery infarction resultingfrom an ipsilateral vertebral artery dissection. Angiography demonstrated intraluminal clot inthe superior cerebellar artery, suggesting artery-to-artery embolus as a mechanism of thisuncommon stroke syndrome. (Stroke 1988;19:1431-1434)
Isolated superior cerebellar artery (SCA) infarc-tion is rare,1-8 and the mechanism is often notreadily apparent.4 We report the case of a young
man with vertebral artery (VA) dissection associatedwith ipsilateral SCA territory infarction diagnosedclinically and by computed tomography (CT). Cere-bral angiography demonstrated intraluminal clot inthe SCA, suggesting that artery-to-artery embolusmay be a mechanism of SCA infarction.
Case ReportA 40-year-old man awoke one morning, turned,
and abruptly experienced dizziness and doublevision. He felt off-balance, noted left-sided weak-ness and clumsiness, and vomited. These symp-toms were severe for 5-6 hours and then graduallyresolved except for the left-sided weakness andclumsiness. Several days previous he had notedtransient pain "between his ears" and periodicnausea. There was no history of neck manipulation,trauma, or pain. Medical history was unremarkable.
Findings of the general physical examinationincluding cardiac auscultation were normal. Neuro-logic examination revealed anisocoria, with the leftpupil 1 mm larger, and vertical diplopia that wasworse on gaze to the right; pursuits were saccadicbut there was no ocular dysmetria. Palatal myo-clonus was present. A mild hypotonic left hemipa-resis was present as was left-sided dysmetria andhyperreflexia; he fell to the left. Findings of thesensory examination were normal.
Results of hematologic and coagulation testingwere normal, and there was no laboratory evidence
From the Center for Stroke Research, Department of Neurol-ogy, Henry Ford Hospital, Detroit, Michigan.
Supported in part by National Institutes of Health GrantNS23393 and research funds from Henry Ford Hospital.
Address for correspondence: Steven R. Levine, MD, Centerfor Stroke Research, Department of Neurology, K-ll, HenryFord Hospital, 2799 West Grand Boulevard, Detroit, MI 48202.
Received March 10, 1988; accepted June 29, 1988.
of vasculitis. Electrocardiogram and chest x-raywere normal. On the day of admission, head CTrevealed an early infarction in the medial left supe-rior cerebellar hemisphere (Figure 1). Cerebral angi-ography demonstrated an irregular 70% narrowingof the left VA 1.5 cm long at the level of the atlas(Figure 2). Intraluminal clot was present in the leftproximal ipsilateral SCA at its bifurcation along theanterolateral margin of the left mesencephalon (Fig-ures 2 and 3). Echocardiography demonstrated min-imal intermittent mitral valve prolapse. The patientwas placed on intravenous heparin, discharged onwarfarin sodium (Coumadin), and has graduallyimproved during 3 years of follow-up. Repeat cere-bral angiography 1 year later demonstrated resolu-tion of both the VA and the SCA lesions.
DiscussionSCA territory infarction is much less commonly
diagnosed clinically, radiographically, and postmor-tem than the posterior inferior cerebellar artery(PICA) syndrome of Wallenberg.1-10 Although theSCA is the largest and most consistent branch of thevertebrobasilar tree, relatively few reports havedocumented isolated SCA infarcts and their mech-anisms.1-8 Our patient had an angiographically doc-umented distal extracranial VA dissection with ipsi-lateral SCA intraluminal clot. Clinical examinationand CT supported an isolated SCA syndrome. Ourpatient had a mild hypotonic hemiparesis ipsilateralto the infarct. Limb weakness has been describedwith cerebellar lesions,11 although it is generally dueto organizational and coordination deficits of mus-cle activity. Given the variability of supply of theSCA, it is conceivable that ischemia in the rightbrainstem may explain our patient's weakness ashemiparesis is generally not a feature of the SCAsyndrome.
An extensive search failed to reveal evidence ofhypercoagulability, and minimal mitral valve pro-
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1432 Stroke Vol 19, No 11, November 1988
FIGURE 1. Head computed tomogram of 40-year-oldman on day of admission demonstrating early ischemicchanges in medial left superior cerebellar hemisphere.
lapse detected by echocardiography was probablynot responsible for the irregular appearance of theVA on angiography. There was no clinical or angio-graphic evidence of a congenital or acquired diffusesystemic or cerebral arteriopathy.
Angiographic evidence of occlusion of the SCAwith a corresponding clinical syndrome has onlyrarely been documented.3812 Embolism isolated tothe SCA is also distinctly unusual.35-7 Other spe-cific etiologies for isolated SCA infarction includebasilar artery atherothrombosis,3-4 cardiac embo-lism,45 dissection associated with fibromusculardisplasia,13 and migraine associated with oral con-traceptive and cigarette use.12
Artery-to-artery embolism causing infarction inthe vertebrobasilar circulation is becoming morecommonly recognized as a specific mechanism ofstroke.1415 Infarction generally occurs within theterritory of one or both posterior cerebral arteries.15
Pessin et al15 described intraluminal clot in the SCAaccompanying a basilar artery clot resulting in aright pontine infarction. The source of embolus wasan occluded VA at the level of the second cervicalvertebral body; cause of the VA occlusion was notreadily apparent. Zimmerman et al16 reported a7-year-old boy who developed a right cerebellarinfarct after gymnastics and chiropractic treat-ments. Angiography revealed intraluminal clot inthe distal basilar artery. Artery-to-artery embolus
FIGURE 2. Selective left vertebral angiogram in 40-year-old man, lateral view. Irregular narrowing of left extra-dural vertebral artery (arrowhead) is seen at high cervicallevel. Intraluminal filling defect (arrow) is present inproximal left superior cerebellar artery at bifurcation.
from a traumatic thrombosis of the left VA to theright SCA was postulated to explain his ataxia andright-sided cerebellar signs. The boy also had a rightsuperior quadrantanopsia. In most angiographic stud-ies of artery-to-artery embolism in the vertebroba-silar circulation, the local embolus was not docu-mented by an intraluminal filling defect thatsubsequently cleared. This angiographic appear-ance in our case strongly supports embolism.1718
VA dissection is a well-known cause of vertebro-basilar stroke, generally within the PICA terri-tory.19-21 However, Kase and colleagues3 reportedthe case of a 49-year-old man with mild headacheand dysarthria, left hemiataxia, and normal powerand sensation. Four days later, CT demonstrated ananteromedial left cerebellar infarct, and the nextday angiography demonstrated a significant lesionof the left VA, suggestive of a dissection. A doubleSCA pattern was noted on the left. Proximal ste-
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Levine and Welch Superior Cerebellar Artery Stroke 1433
FIGURE 3. Selective vertebral angiogram in 40-year-oldman, anteroposterior view. Intraluminal filling defect(arrow) documented at first major bifurcation of leftsuperior cerebellar artery.
nosis of the upper SCA branch on the left (pre-sumed to be partially recanalized embolism) wasdemonstrated. Slow improvement with mild residuaoccurred while the patient was receiving intrave-nous heparin. Katirji et al22 reported the case of a57-year-old man with recurrent left occipitoparietalischemia following heavy lifting. CT of his head wasnormal; angiography demonstrated a long area ofarterial narrowing suggestive of a subintimal hema-toma. Intraluminal thrombus attached both to apedicle at the superior aspect of the subintimaldissection and in the left SCA was noted. Osteo-phytes were noted at C4-5 and at C5-6. Despitetransient symptoms on anticoagulation, no furtherstrokes occurred. Perez-Higueras et al23 recentlyreported the case of a 9-year-old boy who hadtransient recurrent episodes of loss of conscious-ness, myoclonus, and ocular deviation. He wasnoted to be somnolent with a right abducens palsy,general hypotonia, hyporeflexia, and gait ataxia. CTshowed a large right cerebellar hemispheric infarc-tion that led to obstructive hydrocephalus. Angiog-raphy demonstrated type I focal fibromuscular
dysplasia of the left VA. An adjacent dissectinganeurysm was also present; either lesion may havecaused distal embolism. Savoiardo et al9 publishedthe CT scan of a patient with a SCA territory infarctin a single paravermian branch and contralateralhemispheral branch caused by embolism from ananeurysm of the ipsilateral VA at the C-2 level. Masand colleagues24 could not demonstrate distal embo-lization from extracranial VA dissections in any oftheir 13 patients, even in those with early angio-grams, and they found only two such reported casesin the literature. These authors surmised that distalembolization from extracranial VA dissection maybe rare, but we believe that this stroke mechanismis probably underrecognized and not easily docu-mented. VA dissection (due to minor trauma orchiropractic manipulation or spontaneous) has beenreported to cause unilateral or bilateral cerebellarhemisphere infarction16-19-21 and should be consid-ered in the differential diagnoses of all posteriorcirculation ischemia.22
Our patient improved with anticoagulation, andfollow-up angiography revealed resolution of thearterial lesions. The limited number of similarcases in the literature suggests that anticoagula-tion in this setting may reduce ischemic complica-tions distal to the dissection.
AcknowledgmentHally Summers provided technical assistance in
the preparation of this manuscript.
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KEY WORDS • cerebral infarction • vertebral artery
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S R Levine and K M WelchSuperior cerebellar artery infarction and vertebral artery dissection.
Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1988 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.19.11.1431
1988;19:1431-1434Stroke.
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