Neuro-Otological Aspects of Cerebellar Stroke Syndrome

Cerebellar stroke is a common cause of a vascular vestibular syndrome. Although vertigo ascribed to cerebellar stroke is usually associated with other neurological symptoms or signs, it may mimic acute peripheral vestibulopathy (APV), so called pseudo-APV. The most common pseudo-APV is a cerebellar infarction in the territory of the medial branch of the posterior inferior cerebellar artery (PICA). Recent studies have shown that a normal head impulse result can differentiate acute medial PICA infarction from APV. Therefore, physicians who evaluate stroke patients should be trained to perform and interpret the results of the head impulse test. Cerebellar infarction in the territory of the anterior inferior cerebellar artery (AICA) can produce a unique stroke syndrome in that it is typically accompanied by unilateral hearing loss, which could easily go unnoticed by patients. The low incidence of vertigo associated with infarction involving the superior cerebellar artery distribution may be a useful way of distinguishing it clinically from PICA or AICA cerebellar infarction in patients with acute vertigo and limb ataxia. For the purpose of prompt diagnosis and adequate treatment, it is imperative to recognize the characteristic patterns of the clinical presentation of each cerebellar stroke syndrome. This paper provides a concise review of the key features of cerebellar stroke syndromes from the neuro-otology viewpoint.     

The clinical and topographic spectrum of cerebellar infarcts: A clinical—magnetic resonance imaging correlation study

We studied 34 consecutive patients with non–mass-producing cerebellar infarcts using a standard protocol of investigations including magnetic resonance imaging (MRI). We analyzed the topography of infarcts to determine the involved arterial territories and we correlated the findings with neurological dysfunction and potential causes of stroke. Sixteen patients had an infarct in the territory of the posterior inferior cerebellar artery (PICA); 2, in the territory of the anterior inferior cerebellar artery (AICA); 13, in the territory of the superior cerebellar artery (SCA); and 8 had junctional infarcts between the territories of the medial and lateral branches of the PICA or PICA/SCA territories. PICA or medial PICA territory infarcts were manifested by acute vertigo and truncal ataxia, while the patients with lateral PICA territory infarcts presented with unsteadiness, limb ataxia and dysmetria without dysarthria. Patients with infarcts in the AICA territory were characterized by limb and trunk ataxia associated with signs of lateropontine involvement. Patients with SCA territory infarcts presented with dysarthria, unsteadiness and/or vertigo, limb ataxia, and dysmetria. Cardiac embolism was the main cause of large infarcts in the territories of the PICA (8/16) or SCA (4/7). Multiple small infarcts were associated with vertebrobasilar atherosclerosis (8/12). These clinical–MRI correlations allow better definition of the topographic and etiological spectrum of cerebellar infarction, which was previously based on pathological studies in subjects with severe infarction.     

以眩晕为首发症状的小脑梗死临床类型及供血区分布

目的:探讨以眩晕为首发症状的小脑梗死临床类型及病灶供血区分布特征。方法:对26例经MRI确诊、以眩晕为首发症状的小脑梗死患者的临床资料进行回顾性分析。结果:将眩晕为首发症状的小脑梗死分为2种临床类型:①稳定型:单纯自发性持续性眩晕伴平衡失调(19/26例,73.1%);②进展型:以持续性眩晕、平衡失调为首发症状,起病2d后伴有延迟神经功能受累症状(7/26例,26.9%)。梗死病灶以小脑后下动脉内侧支(16/26例,61.5%)受累最为常见;其次为小脑前下动脉区(6/26例,23.1%)及小脑上动脉区(2/26例,7.7%)。未见多发小脑供血动脉区梗死患者以单纯眩晕为首发症状。结论:以眩晕为首发症状的小脑梗死以小脑后下动脉内侧支受累最为常见,绝大多数患者呈良性病程,但需警惕可能出现的延迟神经功能受累症状和体征。     

Multiple large and small cerebellar infarcts

To assess the clinical, topographical, and aetiological features of multiple cerebellar infarcts,18 patients (16.5% of patients with cerebellar infarction) were collected from a prospective acute stroke registry, using a standard investigation protocol including MRI and magnetic resonance angiography. Infarcts in the posterior inferior cerebellar artery (PICA)+superior cerebellar artery (SCA) territory were most common (9/18; 50%), followed by PICA+anterior inferior cerebellar artery (AICA)+SCA territory infarcts (6/18; 33%). One patient had bilateral AICA infarcts. No infarct involved the PICA+AICA combined territory. Other infarcts in the posterior circulation were present in half of the patients and the clinical presentation largely depended on them. Large artery disease was the main aetiology. Our findings emphasised the common occurrence of very small multiple cerebellar infarcts (<2 cm diameter).These very small multiple cerebellar infarcts may occur with (13 patients/18; 72%) or without (3/18; 22%) territorial cerebellar infarcts. Unlike previous series, they could not all be considered junctional infarcts (between two main cerebellar artery territories: 51/91), but also small territorial infarcts (40/91). It is suggested that these very small territorial infarcts may be endzone infarcts, due to the involvement of small distal arterial branches. It is possible that some very small territorial infarcts may be due to a microembolic process, but this hypothesis needs pathological confirmation.     

Acute bilateral hearing loss as a “worsening sign” in a patient with critical basilar artery stenosis

We report a patient who presented with an acute-onset transient vertigo and unsteady gait with bilateral hearing loss. Brain MRI revealed a critical basilar artery (BA) stenosis at the lower pons and infarction in various areas on both sides in the territories of the posterior inferior cerebellar arteries (PICA). Further, we could not visualize the right anterior inferior cerebellar artery (AICA). The bilateral hearing loss may be ascribed to stroke due to the critical BA stenosis, causing hypoperfusion injury extending from the PICA to the AICA on both sides. Local intra-arterial thrombolytic therapy with the administration of 1 × 10⁶ IU of urokinase aided partial recanalization of the BA, after which the right AICA reappeared. The neurological function of the patient recovered to normal, and no hemorrhagic complications were observed. Therefore, practitioners should be alert when treating patients with acute bilateral hearing loss, which may be related to an underlying catastrophic stroke.     

Recurrent audiovestibular disturbance initially mimicking Ménière’s disease in a patient with anterior inferior cerebellar infarction

An anterior inferior cerebellar artery (AICA) stroke is characterized by vertigo, tinnitus, and deafness in addition to facial weakness, hemiataxia, and hypalgesia. Sometimes, it can present as sudden deafness with vertigo, without brainstem or cerebellar signs. We report a 55-year-old woman with hypertension and diabetes, showing recurrent audiovestibular disturbance before a typical pattern of AICA infarction, which was initially diagnosed as Ménière’s disease. In elderly patients with recurrent hearing loss and vertigo lasting several minutes, lack classic brainstem or cerebellar signs, if they have vascular risk factors, physicians may also consider the potential symptom of AICA infarction.     

Infarcts in the territory of the lateral branch of the posterior inferior cerebellar artery.

The territory of the lateral branch of the posterior inferior cerebellar artery (1PICA) supplies the anterolateral region of the caudal part of the cerebellar hemisphere. Because infarcts in the territory of the 1PICA have rarely been studied specifically, 10 patients with this type of infarct are reported. An 1PICA infarct was isolated in only three patients, whereas it was associated with brainstem infarct in four, with occipital infarct in one, and with multiple infarcts in two patients. The most common symptom at onset was acute unsteadiness and gait ataxia without rotatory vertigo (six patients). Unilateral cerebellar dysfunction was found in all patients, with limb ataxia (nine patients), dysdiadochokinesia (five patients), and ipsilateral body sway (four patients), but dysarthria and primary position nystagmus were notably absent. In the patients with a coexisting infarct in the brainstem, cranial nerve and sensorimotor dysfunction was prominent and often masked the signs of cerebellar dysfunction. Unlike other infarcts in the PICA territory, 1PICA territory infarcts were mainly associated with vertebral artery atherosclerosis (six patients), whereas cardiac embolism was less common (three patients). Unilateral limb ataxia without dysarthria or vestibular signs suggests isolated 1PICA territory infarction and should allow its differentiation from other cerebellar infarcts.     

Auditory disturbance as a prodrome of anterior inferior cerebellar artery infarction

OBJECTIVES: To investigate the clinical and radiological features of patients presenting with an acute auditory syndrome as a prodromal symptom of anterior inferior cerebellar artery (AICA) infarction. METHODS: 16 consecutive cases of AICA infarction diagnosed by brain magnetic resonance imaging completed a standardised audiovestibular questionnaire and underwent a neuro-otological evaluation by an experienced neuro-otologist. RESULTS: Five patients (31%) had an acute auditory syndrome as a prodrome of AICA infarction one to 10 days before onset of other brain stem or cerebellar symptoms. Two types of acute auditory syndrome were found: recurrent transient hearing loss with or without tinnitus (n = 3), and a single episode of prolonged hearing loss with or without tinnitus (n = 2). The episodic symptoms were brief, lasting only minutes. The tinnitus preceding the infarction was identical to the tinnitus experienced at the time of infarction. At the time of infarction, all patients developed hearing loss, tinnitus, vertigo, and ipsilateral hemiataxia. The most commonly affected site was the middle cerebellar peduncle (n = 5). Four of the five patients had incomplete hearing loss and all had absence of vestibular function to caloric stimulation on the affected side. CONCLUSIONS: Acute auditory syndrome may be a warning sign of impending pontocerebellar infarction in the distribution of the AICA. The acute auditory syndrome preceding an AICA infarct may result from ischaemia of the inner ear or the vestibulocochlear nerve.     

Lesion patterns and etiology of ischemia in the anterior inferior cerebellar artery territory involvement: a clinical – diffusion weighted – MRI study

The topography and mechanism of stroke in the anterior inferior cerebellar artery (AICA) territory are delineated before, but the detailed clinical spectrum of lesions involving AICA territory was not studied by diffusion weighted imaging (DWI). We reviewed 1350 patients with posterior circulation ischemic stroke in our registry. We included patients if the diagnosis of AICA territory involvement was confirmed, and DWI, and magnetic resonance angiography were obtained in the 3 days of symptoms onset. The potential feeding arteries of the AICA territory were evaluated on magnetic resonance imaging (MRI) using a three-dimensional rotating cineoangiographic method. There were 23 consecutive patients with lesion involving AICA territory, six with isolated lesion in the AICA territory, six with posterior inferior cerebellar artery, 11 with multiple posterior circulation infarcts (MPCIs). The clinical feature of isolated AICA infarct was vertigo, tinnitus, dysmetria, ataxia, facial weakness, facial sensory deficits, lateral gaze palsy, and sensory-motor deficits in patients with pontine involvement. Patients with largest lesion extending to the anterior and inferolateral cerebellum showed mixed symptomatology of the lateral medullary (Wallenberg's syndrome) and AICA territory involvement. Patients with MPCIs presented various clinical pictures with consciousness disturbances and diverse clinical signs because of involvement of different anatomical structures. Large-artery atherosclerotic disease in the vertebrobasilar system was the main cause of stroke in 12 (52%) patients, cardioembolism (CE) in one (4%), and coexisting large-artery disease and a source of CE in four (17%). The main cause of stroke was atheromatous vertebrobasilar artery disease either in the distal vertebral or proximal basilar artery. The outcome was usually good except those with multiple lesions. The new MRI techniques and clinical correlations allow better definition of the diverse topographical and etiological spectrum of AICA territory involvement and associated infarcts which was previously based on pathological and conventional MRI studies.     

The Usefulness of the TOAST Classification and Prognostic Significance of Pyramidal Symptoms During the Acute Phase of Cerebellar Ischemic Stroke

Cerebellar stroke is a rare condition with very nonspecific clinical features. The symptoms in the acute phase could imitate acute peripheral vestibular disorders or a brainstem lesion. The aim of this study was to assess the usefulness of the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification in cerebellar stroke and the impact of clinical features on the prognosis. We retrospectively analyzed 107 patients with diagnosed ischemic cerebellar infarction. We studied the clinical features and compared them based on the location of the ischemic lesion and its distribution in the posterior interior cerebellar artery (PICA), superior cerebellar artery (SCA), and anterior inferior cerebellar artery (AICA) territories. According to the TOAST classification, stroke was more prevalent in atrial fibrillation (26/107) and when the lesion was in the PICA territory (39/107). Pyramidal signs occurred in 29/107 of patients and were more prevalent when the lesion was distributed in more than two vascular regions (p?=?0.00640). Mortality was higher among patients with ischemic lesion caused by cardiac sources (p?=?0.00094) and with pyramidal signs (p?=?0.00640). The TOAST classification is less useful in assessing supratentorial ischemic infarcts. Cardioembolic etiology, location of the ischemic lesion, and pyramidal signs support a negative prognosis.     

Sudden deafness in vertebrobasilar ischemia: clinical features, vascular topographical patterns and long-term outcome

BACKGROUND AND PURPOSE: The aim of this study is to document the clinical features and natural history of sudden deafness associated with vertebrobasilar ischemia (VBI) and to describe the vascular topographic patterns of ischemic lesions on brain MRI associated with sudden deafness based on data collected from a prospective acute stroke registry. METHODS: From 364 consecutive cases of VBI diagnosed by clinical features and brain MRI between January 2000 and September 2003, 29 patients were identified as having sudden deafness as a symptom of VBI. RESULTS: In our series, the incidence of sudden deafness following VBI is 8.0% (29/364). Hearing loss occurred unilaterally (n=27) or bilaterally (n=2). All but one had vertigo as an associated symptom. Nine patients (31%) presented with an isolated audiovestibular loss initially and subsequently had delayed neurological deficits. Nearly a half of patients (14/29: 48%) showed cochlear features of hearing loss. Seventeen (81%) of 21 patients who were followed for at least 1 year after onset of sudden deafness had a recovery of hearing partially (n=10) or completely (n=7). The improvement rate of hearing loss in patients with profound hearing loss was significantly lower than that in patients with less than profound hearing loss (40% vs. 89%, P<0.01). In addition to infarction in the territory of anterior inferior cerebellar artery (n=23), cerebellar infarction in the territory of the medial branch of posterior inferior cerebellar artery (n=4) or an isolated brainstem infarction (n=2) was also associated with sudden deafness. CONCLUSION: An isolated sudden deafness with cochlear audiometric features can be the initial presentation of VBI. Sudden deafness due to VBI often has a good outcome. There is topographic heterogeneity of ischemic lesions on brain MRI in patients with sudden deafness due to VBI.     

Ocular torsion associated with infarction in the territory of the anterior inferior cerebellar artery: frequency, pattern, and a major determinant

BACKGROUND: Acute ischemic stroke in the distribution of the anterior inferior cerebellar artery (AICA) can cause the vestibular dysfunction in the roll plane of the vestibuloocular reflex with abnormal ocular torsion (OT). There has been no systemic study that carefully investigates the nature of OT that occurs with AICA infarction. OBJECTIVES: To investigate the frequency, the characteristic patterns of OT associated with AICA territory infarction, and the crucial site for determining the direction of OT in AICA territory infarction. METHODS: We studied 12 consecutive cases of infarction in the territory of the AICA diagnosed by brain MRI. Fundus photography, prism cover test, and subjective visual vertical tilting test were performed to evaluate the function of the otolith system. Pure tone audiogram was also performed to evaluate the function of the auditory system. RESULTS: Nine (75%) of 12 patients exhibited pathological ocular torsion (OT). Two types of pathological OT were found: ipsiversive OT accompanying skew deviation (n=6), and contraversive OT only (n=3). Six patients with ipsiversive OT with skew deviation showed an audiovestibular loss with canal paresis and hearing loss ipsilaterally whereas three patients with contraversive OT without skew deviation had a normal audiovestibular response. In all cases with pathological OT, the direction of the subjective visual vertical tilt corresponded to the direction of the OT. CONCLUSIONS: Our findings emphasize that the peripheral vestibular structure with inner ear probably plays a crucial role in determining the direction of OT associated with AICA territory infarction.     

Cerebellar infarction in the area of the posterior cerebellar artery. Clinicopathology of 28 cases

We report a neuropathological study of cerebellar infarctions involving the territory of the posterior inferior cerebellar artery (PICA) in 28 cases. Fifteen cases involved the PICA territory only. In 13 cases infarctions in the anterior inferior cerebellar artery (AICA) territory and/or in the superior cerebellar artery (SCA) territory were also present. A thorough post-mortem study of the arterial supply of the brain from the heart up to the cerebellar arteries, including the cervical spine segment of the vertebral arteries was performed in 27 cases. The territory of the cerebellar infarcts has been ascertained. In 15/28 cases (54 percent), infarction involved the PICA territory only (17 infarcts). All of these cases had a benign outcome and death was due to another cause. Six of these were recent infarctions. None had evidence of swelling and tonsillar herniation. Infarcts were generally of small size and involved the entire PICA territory in only 2 cases. Most of these cases were unexpected discovered at autopsy. Cerebellar infarction in the territory of the medial branch of the PICA (9/17 infarcts) drew grossly a set square with a dorsal base and a ventral top headed for the IVth ventricle. Five out of these cases were associated with infarction in the dorsal and lateral medullary territories. Retrospective clinical study showed that they had been unnoticed or overshadowed by other neurological disorders (4 cases), or presented as Wallenberg's syndromes (4 cases), or as a pure vestibular syndrome (due to an infarction involving only the cerebellum) mimicking an acute labyrinthine disorder (1 case). Infarctions in the territory of the lateral branch of the PICA (5/17 infarcts) always occurred without medullary involvement. All of them were unexpectedly discovered at autopsy, and were unnoticed during the life (3 infarcts) or were overshadowed by other neurological disorders (2 infarcts). That was also the case in 2 cases of infarction in the whole PICA territory (3/17 infarcts). Thus infarctions strictly localized to the entire PICA territory only were rare. Thirteen/28 cases (46 p. 100) of infarction in the whole PICA territory were associated with infarction in the AICA and/or the SCA territories. This resulted from an association with other infarctions and not from an abnormally large territory of the PICA. Cerebellar swelling with brain stem compression and tonsillar herniation occurred 8/13 cases (62 p. 100). There were other massive median and paramedian brain stem infarctions involving midbrain, pons or medulla in 55 p. 100 of 13 cases.(ABSTRACT TRUNCATED AT 400 WORDS)     

Spectrum of the posterior inferior cerebellar artery territory infarcts. Clinical-diffusion-weighted imaging correlates

BACKGROUND AND PURPOSE: The clinical, etiological and stroke mechanisms are defined well before but the detailed clinical and etiologic mechanisms regarding to all clinical spectrum of posterior inferior cerebellar artery (PICA) infarcts were not systematically studied by diffusion-weighted imaging (DWI). METHODS: Seventy-four patients with PICA territory ischemic lesion proved by DWI with decreased apparent diffusion coefficient and FLAIR (fluid attenuation inversion recovery) included in our Registry, corresponding to 2% of 3,650 patients with ischemic stroke, were studied. The presence of steno-occlusive lesions in the posterior circulation were sought by magnetic resonance angiography, and reviewed with a three-dimensional rotating cineangiographic method. RESULTS: We found six subgroups of PICA territory infarcts according clinico-topographical relationship: (1) 9 patients with lesion in the territory lateral branch of PICA; (2) 23 patients with an infarct in the territory of medial branch of PICA; (3) 9 patients with a lesion involving both medial and lateral branches of the PICA; (4) 9 patients with cortical infarcts at the boundary zones either between medial and lateral branches of the PICA or between PICA and m/l superior cerebellar artery (SCA); (5) 10 patients with a lesion at the deep boundary zones either between medial and lateral PICA, or between PICA and medial/lateral SCA; (6)14 patients with concomitant multiple lesions in the PICA and in other vertebrobasilar artery territories. The main cause of PICA infarcts was extracranial large-artery disease in 30 patients (41%) patients, cardioembolism and in situ branch disease in 15 patients (20%) each. CONCLUSIONS: Multiple PICA territory lesions on DWI were not uncommon and could be caused by multiple emboli originating from break-up of atherosclerotic plaque in the subclavian/innominate-vertebral arterial system. DWI findings of single or multiple small lesions could account for some cases with transient and subtle cerebellar symptoms which have been considered before as 'vertebrobasilar insufficiency' without morphologic lesion. Different clinical-DWI correlations allow us to determine better definition of the topographical and etiological spectrum of acute PICA territory lesions, which was previously defined by pathological and conventional MRI studies.     

Lesion patterns and etiology of ischemia in superior cerebellar artery territory infarcts

BACKGROUND AND PURPOSE: Infarcts in the territory of superior cerebellar artery (SCA) are uncommon. The clinical, and etiological mechanisms of different infarct patterns of SCA are not well known. Diffusion-weighted imaging (DWI) is superior to conventional magnetic resonance imaging for detecting acute small and multiple ischemic lesions. METHODS: We studied 60 patients with lesions involving SCA territory proved by DWI, which have been selected from 3,800 patients with first ischemic stroke consecutively admitted to our stroke unit over a period of 5 years. RESULTS: There are 7 distinctive SCA lesion patterns: (1) a lesion was found in the medial (m) branch territory of SCA (mSCA) in 14 patients; (2) a lesion in the lateral (l) branch territory of SCA (lSCA) was seen in 9 patients; (3) a coexisting lesion involving mSCA and lSCA was found in 9 patients; (4) a lesion in cortical borderzones between SCA and m/l branches of the posterior inferior cerebellar artery (PICA) was observed in 6 patients; (5) a lesion in deep borderzones between lSCA and mSCA, and lPICA and mPICA was present in 8 patients; (6) a lesion involving the medial rostral cerebellum between the right and left SCA was found in 4 patients; (7) multiple lesions involving SCA and other vertebrobasilar artery territories were present in 10 patients. The main cause was possible artery-to-artery embolism from atherosclerotic vertebrobasilar arteries to distal branches of SCA in 20 patients (33%). Fourteen patients had a source of cardioembolism (23%), and 6 patients (8%) had concomitant atherosclerotic vertebrobasilar artery disease and a source of cardioembolism. CONCLUSIONS: An acute ischemic lesion in the SCA territory is mainly multiple. The lSCA territory was the most involved area. Small territorial infarcts were frequently associated with large territorial SCA infarcts. Borderzone SCA infarcts occurred in one third of the patients with transient benign symptoms. Mass effects are unusual despite the large amount of SCA involvement. Our results supported the fact that embolism is the predominant stroke mechanism in the SCA territory infarction.     

Anatomy of the cerebellar arteries

Origin, course and distribution of the cerebellar arteries and of their branches are described. Anatomical drawings of the territory of these arteries are presented. They are based on a neuropathological study of 64 cases of cerebellar infarctions, the detailed study of which is reported elsewhere. The superior cerebellar artery (SCA) supplies a small brain stem territory, located on the dorsal tegmentum and the tectum of the upper part of the pons. The superior part of the cerebellum supplied by this artery includes the following lobules: lobulus anterior, lobulus simplex, lobulus semilunaris superior, and, in the vermis, lobulus centralis, culmen and clivus. The dentate nucleus belongs to this territory. The anterior inferior cerebellar artery (AICA) irrigates a ponto-cerebellar territory. It usually supplies the lateral territory of the lower part of the pons, the middle cerebellar peduncle, the flocculus and the neighbouring lobules of cerebellum. When the posterior inferior cerebellar artery (PICA) is hypoplastic, AICA takes over the territory usually supplied by the lateral branch of the PICA. The PICA always gives rami to the group of arteries supplying the dorsal medullary territory, but rarely participates to the supply of the lateral medullary territory. It supplies the lobulus semilunaris inferior, the lobulus gracilis, the lobulus biventer, the tonsilla cerebelli, and, in the vermis, the clivus, the tuber, the pyramis, the uvula and the nodulus. PICA never supplies the dentate nucleus. The flocculo-nodular lobe is usually supplied by 2 arteries: the flocculus is supplied by the AICA and the nodulus is supplied by the PICA.     

Bilateral Cerebellar Infarctions Caused by a Stenosis of a Congenitally Unpaired Posterior Inferior Cerebellar Artery

Bilateral symmetrical cerebellar infarcts in the territory supplied by the medial posterior inferior cerebellar artery (PICA) branches are extremely rare. In the few cases published, it has not been possible to clearly pinpoint the cause of this infarct pattern. The authors present the case history of a 58-year-old man who had acute headaches accompanied by pronounced rotatory vertigo with nausea and vomiting. The neurological examination revealed bilateral cerebellar signs. Cranial magnetic resonance imaging showed bilateral, nearly symmetrical infarcts in the territory of the medial branches of both PICAs. These bilateral PICA infarctions were caused by a stenosis of an unpaired PICA originating from the left vertebral artery supplying both cerebellar hemispheres.     

Atherothrombotic cerebellar infarction: vascular lesion-MRI correlation of 31 cases.

BACKGROUND AND PURPOSE: Correlation of MRI findings with atherosclerotic vascular lesions has rarely been attempted in patients with cerebellar infarction. The aim of this study was to correlate the MRI lesions with the vascular lesions seen on conventional cerebral angiography in cerebellar infarction. METHODS: The subjects included 31 patients with cerebellar infarcts who underwent both MRI and conventional cerebral angiography. We analyzed the risk factors, clinical findings, imaging study, and angiography results. We attempted to correlate MRI lesions with the vascular lesions shown in the angiograms. RESULTS: The vascular lesions seen on angiograms were subdivided into 3 groups: large-artery disease (n=22), in situ branch artery disease (n=6), and no angiographic disease with hypertension (n=3). The proximal segment (V1) lesions of vertebral artery were the most common angiographic features in patients with large-artery disease in which stroke most commonly involved the posterior inferior cerebellar artery (PICA) cerebellum. The V1 lesions with coexistent occlusive lesions of the intracranial vertebral and basilar arteries were correlated with cerebellar infarcts, which had no predilection for certain cerebellar territory. The intracranial occlusive disease without V1 lesion was usually correlated with small cerebellar lesions in PICA and superior cerebellar artery (SCA) cerebellum. The subclavian artery or brachiocephalic trunk lesion was associated with small cerebellar infarcts. The in situ branch artery disease was correlated with the PICA cerebellum lesions, which were territorial or nonterritorial infarct. No angiographic disease with hypertension was associated with small-sized cerebellar infarcts within the SCA, anterior inferior cerebellar artery, or SCA cerebellum. CONCLUSIONS: Our study indicates that the topographic heterogeneity of cerebellar infarcts are correlated with diverse angiographic findings. The result that large-artery disease, in which nonterritorial infarcts are more common than territorial infarcts, is more prevalent than in situ branch artery disease or small-artery disease, suggest that even a small cerebellar infarct can be a clue to the presence of large-artery disease.     

Sudden deafness with vertigo as a sole manifestation of anterior inferior cerebellar artery infarction

Sudden deafness without associated neurological symptoms and signs is typically attributed to a viral inflammation of the labyrinth. Although sudden deafness occurs with anterior inferior cerebellar artery (AICA) infarction, the deafness is usually associated with other brainstem or cerebellum signs such as crossed sensory loss, lateral gaze palsy, facial palsy, Horner syndrome or cerebellar dysmetria. An 84-year-old woman suddenly developed right-sided tinnitus, hearing loss, vertigo and vomiting. Audiometry and electronystagmography documented absent auditory and vestibular function on the right side. T2-weighted and diffusion-weighted MRI showed a tiny infarct in the right lateral inferior pontine tegmentum. AICA occlusion can cause sudden deafness and vertigo without brainstem or cerebellar signs.