(Stroke. 1996;27:1679-1681.)
© 1996 American Heart Association, Inc.
Articles |
Infarction of Superior Cerebellar Artery Presenting as Cerebellar Symptoms
the Division of Neurology, Fourth Department of Internal Medicine, Aichi Medical University (S.T., M.I., T.M.); the Department of Neurology, Nagoya University School of Medicine (G.S.); and the Department of Neurology, Nagoya National Hospital (N.M., A.T.) (Japan).
Correspondence to Gen Sobue, MD, Department of Neurology, Nagoya University School of Medicine, Nagoya 466, Japan.
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Abstract |
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Background MRI of the brain has facilitated the diagnosis of cerebellar infarction in the territory of the superior cerebellar artery (SCA). We analyzed the data on patients with SCA infarction who presented with only cerebellar symptoms in an attempt to define its underlying pathophysiology.
Summary of Report Ten patients with SCA infarction who presented with cerebellar symptoms were studied by brain MRI, angiography, and underlying pathology. Brain MRI demonstrated an infarct in the SCA territory in the anterior rostral cerebellum of all patients. None had abnormalities in the brain stem. In four patients, a hemorrhagic infarct was present in the same region. Cerebral angiography revealed no obvious SCA occlusion or atherosclerotic vascular disease in any patient. Eight of the 10 patients had heart disease, such as atrial fibrillation or old myocardial infarction. The presumed diagnosis was occlusion of the SCA in its periphery due to cardiogenic embolism.
Conclusions When a patient presents with only cerebellar symptoms and has cerebellar infarction demonstrated by brain MRI, the SCA branch is probably occluded by cardiogenic embolism.
Key Words: cerebellar infarction • cerebral arteries • embolism • magnetic resonance imaging
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Introduction |
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Patients with a clinical diagnosis of superior cerebellar artery (SCA) infarction can be divided into two groups: one with diffuse brain stem signs in addition to unilateral cerebellar ataxia, who have an occlusion of the SCA at its origin,1 2 3 4 5 6 and the other presenting solely with cerebellar symptoms, due to peripheral occlusion.7 8 9 When the SCA is occluded at its origin, mainly ipsilateral cerebellar and brain stem signs are seen, and a contralateral dissociated sensory impairment is present. This is the classic presentation described by Mills,1 2 which has been considered a rare syndrome.3 4 5 6 It has recently become easy to demonstrate anterior rostral cerebellar infarcts in the territory of the medial and lateral branches of the SCA, even in patients without the typical findings of Mill's syndrome, by performing MRI of the brain.7 8 9 To clarify the underlying pathophysiology, we investigated the clinical characteristics of patients with anterior rostral cerebellar infarction who presented with only cerebellar symptoms.
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Subjects and Methods |
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Of 68 consecutive Japanese patients with cerebellar infarction admitted to our division at the Aichi Medical University between 1989 and 1995, the infarct areas included the SCA region in 12 (17.6%), the anterior inferior cerebellar artery region in 11 (16.2%), and the posterior inferior cerebellar artery region in 45 (66.2%). Ten patients (14.7%) who presented solely with cerebellar symptoms were the subject of our study. The subjects, all men, ranged in age from 50 to 72 years. They had abrupt onset of symptoms, and an infarct of the anterior rostral cerebellar part of the brain was demonstrated on MRI. No patients with anterior or posterior inferior cerebellar artery infarcts presented with cerebellar symptoms alone. We excluded patients with occlusion of the basilar artery, including the "top of the basilar" syndrome10 and the rostral basilar artery syndrome,11 as well as those with lesions at any site of the vertebrobasilar system other than the anterior rostral cerebellum. Clinical symptoms, cerebral angiographic findings, underlying diseases (particularly cardiac diseases), and background risk factors were evaluated. Examinations of brain MRI and angiography in each patient were performed at almost the same time, within a month after the onset. Brain MRI was performed within 3 weeks after the onset and obtained with T1- and T2-weighted sequences on both the axial and coronal planes. Cerebral angiography was performed 1 to 14 days after the onset. All patients received cardiac studies including electrocardiogram, transthoracic echocardiogram, and Holter monitoring.
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Results |
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Clinical findings are listed in the Table
. The lesion was on the left side in 5 patients, the right in 4, and bilateral in 1. Subjective symptoms at onset consisted of nausea and vomiting in 3 patients, dizziness in 8, tinnitus in 1, and headache in 3. These symptoms disappeared within a few days. All patients had cerebellar ataxia and dysarthria. No overt brain stem signs (eg, Horner's syndrome, facial palsy, hearing loss, involuntary movements, or contralateral dissociated sensory impairment) were noted. The underlying pathology included heart disease (7 cases of atrial fibrillation, 3 old myocardial infarctions), hypertension (4 cases), and diabetes mellitus (1 case). Transthoracic echocardiograms did not detect obvious ventricular thrombi in any patients. In all patients the cerebellar symptoms diminished within 1 week to 3 months, and their functional prognosis was generally good. No abnormal cerebral angiographic evidence, such as arteriogenic emboli, was found in any patient. On brain MRI, an infarct in the SCA territory was consistently noted in the upper surface of the cerebellar hemisphere (Figure). Hemorrhagic infarction in the same region was noted in 4 patients (patients 1, 4, 8, and 9). No abnormalities were seen in the brain stem.
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Discussion |
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As clinical manifestations of SCA infarction presenting with only cerebellar involvement, dysarthria and unsteady gait are of primary importance, whereas vestibular signs such as vertigo are far less frequent and of minor importance.8 9 12 Clear visualization of the SCA on the diseased side on cerebral angiography suggests that the artery is occluded not at its origin but in the periphery of the lateral or medial branch.7 9 Eight of our patients had heart disease as a potential embolic source. Arterial occlusion or evidence of atherosclerotic vascular disease was not found on cerebral angiography. In 3 patients with underlying heart disease (patients 4, 8, and 9), hemorrhagic infarcts were seen on MRI. The patients with heart disease satisfied diagnostic criteria for cardiogenic brain embolism.13 The 2 patients without heart disease (patients 1 and 5) had abrupt onset of symptoms and absence of arterial occlusion or atherosclerotic vascular disease on cerebral angiography. Patient 1 also had hemorrhagic infarcts. We suggest that the cerebellar infarction in these patients was also due to the same pathogenetic mechanism. It is not known why the cerebellum in the SCA territory was selectively infarcted, with preservation of the posterior cerebral artery and its perforating branches to the thalamus. Recent reports on the underlying pathology of SCA infarcts emphasize the importance of an embolic mechanism, either originating from cardiac disease or derived from an atheromatous arterial lesion.5 6 7 8 9 14 15 Our results support this view regarding localized anterior rostral cerebellar infarctions. We suggest that when a patient presents solely with cerebellar symptoms and has such cerebellar infarction on brain MRI, the cause of the infarction is likely to be SCA branch occlusion caused by a cardiogenic embolism.
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Acknowledgments |
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This study was supported in part by grants from the Ministry of Welfare and Health of Japan and by a grant from the Aichi Health Promotion Foundation.
Received February 21, 1996; revision received May 6, 1996; accepted May 8, 1996.
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References |
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