Cerebellar infarction in the territory of the superior cerebellar artery: a clinicopathologic study of 33 cases

We reviewed the clinical and pathologic findings in 33 patients with infarcts in the territory of the superior cerebellar artery (SCA). The clinical manifestations included the rostral basilar artery syndrome (8); coma at onset, often with tetraplegia (11); cerebellar and vestibular signs (9, with delayed coma due to cerebellar swelling in 6); and, in only 1 patient, the "classic" syndrome of the SCA. Clinical features were overshadowed by an infarct in the territory of the middle cerebral artery in 3 other patients, and the diagnosis was made only at autopsy in a fourth. Pathologically, SCA infarcts occurred in isolation in 7 patients. The most striking finding was the high frequency of associated infarcts in the territory of the rostral part of the basilar artery (73%). One-third of patients also had an infarct in the territory of the posterior inferior cerebellar artery, sometimes associated with infarction of the anterior inferior cerebellar artery. Tonsillar herniation was observed in 15 patients, 8 of whom had no infarcts in other cerebellar territories. Occlusions occurred mainly in the distal basilar artery and distal vertebral artery. The infarcts were mostly caused by cardiac and artery-to-artery emboli.     

Recent Advances in Cerebellar Ischemic Stroke Syndromes Causing Vertigo and Hearing Loss

Cerebellar ischemic stroke is one of the common causes of vascular vertigo. It usually accompanies other neurological symptoms or signs, but a small infarct in the cerebellum can present with vertigo without other localizing symptoms. Approximately 11 % of the patients with isolated cerebellar infarction simulated acute peripheral vestibulopathy, and most patients had an infarct in the territory of the medial branch of the posterior inferior cerebellar artery (PICA). A head impulse test can differentiate acute isolated vertigo associated with PICA territory cerebellar infarction from more benign disorders involving the inner ear. Acute hearing loss (AHL) of a vascular cause is mostly associated with cerebellar infarction in the territory of the anterior inferior cerebellar artery (AICA), but PICA territory cerebellar infarction rarely causes AHL. To date, at least eight subgroups of AICA territory infarction have been identified according to the pattern of neurotological presentations, among which the most common pattern of audiovestibular dysfunction is the combined loss of auditory and vestibular functions. Sometimes acute isolated audiovestibular loss can be the initial symptom of impending posterior circulation ischemic stroke (particularly within the territory of the AICA). Audiovestibular loss from cerebellar infarction has a good long-term outcome than previously thought. Approximately half of patients with superior cerebellar artery territory (SCA) cerebellar infarction experienced true vertigo, suggesting that the vertigo and nystagmus in the SCA territory cerebellar infarctions are more common than previously thought. In this article, recent findings on clinical features of vertigo and hearing loss from cerebellar ischemic stroke syndrome are summarized.     

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.     

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.     

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.     

双侧小脑梗死模式的探讨

目的探寻双侧小脑梗死的模式和机制。方法经MRI弥散成像(DWI)证实急性期小脑梗死的患者,根据梗死灶的分布将患者分为单侧小脑梗死组(UCI)和双侧小脑梗死组(BCI),并对两组的人口学特征、血管分布、小脑以外梗死灶以及病因进行了比较。结果因急性卒中入院的115例后循环脑梗死患者中,56例为小脑梗死或小脑合并其它部位梗死,其中单侧小脑梗死36例(64.3%),双侧小脑梗死20例(35.7%)。基线资料比较显示,脑卒中史(P=0.002)、纤维蛋白元水平(P=0.036)和入院时NIHSS评分(P=0.001)在双侧小脑梗死组明显高于单侧小脑梗死组。按血管分布区划分,小脑后下动脉(PICA)供血区小脑梗死发生率最高,且更多发生单侧小脑梗死(P=0.006);而双侧小脑梗死更常见于PICA+小脑上动脉(SCA)供血区(P=0.004)。双侧小脑梗死组合并小脑以外梗死灶的发生率明显高于单侧小脑梗死组(P=0.002),特别是合并幕下梗死灶常见(P=0.022)。在卒中机制上,双侧小脑梗死以大动脉粥样硬化性病变更多见(P=0.041),责任动脉病变主要是在椎动脉V4段、V4段与BA接合处的重度狭窄或闭塞。结论双侧小脑梗死并不少见,常见于PICA+SCA供血区;大动脉粥样硬化所致动脉源性栓塞是其卒中重要机制之一。     

Cerebellar lesions in the PICA but not SCA territory impair cognition

The authors sought to clarify whether lesions in different parts of the cerebellum result in differential cognitive and affective impairment. Six subjects with cerebellar lesions due to posterior inferior cerebellar artery (PICA) infarction, five subjects with lesions in the SCA vascular territory, and 11 matched controls were administered a battery of standard neuropsychological tests. PICA lesions but not SCA lesions resulted in cognitive and affective deficits pointing to a dominant role of posterior cerebellar regions in cognitive and affective processing.     

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.     

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.     

Hemi- and Monoataxia in Cerebellar Hemispheres and Peduncles Stroke Lesions: Topographical Correlations

Limb ataxia of sudden onset is due to a vascular lesion in either the cerebellum or the brainstem (posterior circulation, PC, territory). This sign can involve both the upper and the lower limb (hemiataxia) or only one limb (monoataxia). The topographical correlates of limb ataxia have been studied only in brainstem strokes. Therefore, it is not yet known whether this sign is useful to localize the lesion within the entire cerebellar system, both the cerebellar hemisphere and the cerebellar brainstem pathways. Limb ataxia was semi-quantified according to the International Cooperative Ataxia Rating Scale in 92 consecutive patients with acute PC stroke. Limb ataxia was present in 70 patients. Four topographical patterns based on magnetic resonance imaging findings were identified: picaCH pattern (posterior inferior cerebellar artery infarct); scaCH pattern (superior cerebellar artery infarct); CH/CP pattern (infarct involving both the cerebellum and the brainstem cerebellar pathways); and CP pattern (infarct involving the brainstem cerebellar pathways). Hemiataxia was present in (47/70; 67.1%) and monoataxia in (23/70; 32.9%) of patients. Monoataxia involved the upper limb in (19/70; 27.1%) and the lower limb in (4/70; 5.7%) of patients. Limb ataxia usually localized the lesion ipsilaterally (picaCH, scaCH, CH/CP, and CP patterns involving the medulla and sometimes the pons) (53/70; 75.7%), but it might be due also to contralateral (CP pattern involving the pons or midbrain) (16/70; 22.9%) or bilateral lesions (1/70). Limb ataxia usually localizes the lesion ipsilaterally but the infarct might be sometimes contralateral. The occurrence of monoataxia may suggest that the cerebellar system is somatotopically organized.     

Limb ataxia and proximal intracranial territory brain infarcts: clinical and topographical correlations

Background

Limb ataxia is classically attributed to cerebellar hemispheric lesions, although isolated lesions of the inferior cerebellar peduncle (ICP) in the medulla may also cause this sign. It is still unclear why only some patients with acute cerebellar infarcts in the posterior inferior cerebellar artery (PICA) territory present with limb ataxia. The proximal intracranial posterior circulation (P‐PC) territory includes structures fed by the intracranial vertebral arteries (ICVAs): the medulla, supplied by small ICVAs branches, and posterior inferior portion of the cerebellum, fed by PICA. ICP and PICA territory cerebellar infarcts most often occur independently but occasionally occur together.

Objective

To identify structures responsible for limb ataxia in acute P‐PC brain infarcts, correlating clinical and topographical findings.

Methods

Sixteen patients (8 women) were included, aged 30–82 years (mean 62 years), with isolated acute strokes in the P‐PC territory.

Results

The cases reported here indicate that limb ataxia in acute P‐PC territory infarcts may be associated with damage to the ICP in the dorsolateral medulla, regardless of a hemispheric cerebellar lesion. In fact, among the nine patients with PICA stroke, limb ataxia was observed only in the two patients who also presented damage to the dorsolateral medulla involving the ICP. Of the seven patients with isolated dorsolateral medullary infarct, only five patients with ICP damage had limb ataxia.

Conclusions

When correlating limb ataxia and acute P‐PC infarcts, it is important to take into account the entire ICVA territory.Limb ataxia is characterised by dysmetria, dyssynergia and intention tremor, and is clinically assessed by the finger‐to‐nose and heel‐to‐knee tests.¹ It is classically associated with hemispheric cerebellar lesions² and rarely with brainstem lesions.³ Previous reports on cerebellar strokes focused on the frequency of neurological signs in patients with different cerebellar arterial territory infarcts.^4,5 Limb ataxia was reported in only approximately 50% of cases of posterior inferior cerebellar artery (PICA) infarcts but it was not related to the histological or neuroradiological findings.^4,5 A very recent clinical and MRI study⁶ reported limb ataxia in only 4 of 13 patients with acute PICA stroke. The authors correlated this finding with impairment of the intermediate and lateral cerebellar cortex or of the cerebellar nuclei, which are involved in the control of limb coordination. However, it is well known that lesions of the inferior cerebellar peduncle (ICP) without involvement of the cerebellar hemisphere may also cause limb ataxia.⁷The proximal intracranial posterior circulation (P‐PC) territory includes structures fed by the intracranial vertebral arteries (ICVAs), the medulla and the posterior inferior portion of the cerebellum. The blood supply of the posterior inferior cerebellum and the ICP derive from different branches of the ICVAs. The lateral medulla is supplied by small branches that originate from the ICVA and course through the lateral medullary fossa to supply the ICP and the dorsolateral medulla. The ICVA also gives rise to the PICA. The medial branch of the PICA supplies a small portion of the dorsal medulla but not the ICP. ICP and PICA territory cerebellar infarcts most often occur independently but occasionally occur together. Only 1 in 5 proximal territory infarcts include both the lateral medulla and the PICA territory cerebellum.⁸ When both occur together it is usually caused by a long occlusion of the ICVA which blocks flow in both the PICA and lateral medullary penetrators.Here we describe 16 patients with acute infarcts in the ICVA territory in order to understand the role of the cerebellum and of the ICP in the occurrence of limb ataxia.     

Combination of infarctions in the posterior inferior cerebellar artery and anterior spinal artery territories

After an episode of vasodilator-induced systemic hypotension, a 75-year-old man developed ocular lateropulsion to the right, left-side-dominant quadriparesis, loss of superficial sensation below C4 dermatome level, and anuresis. Magnetic resonance imaging (MRI) showed infarcts in the right cerebellar hemisphere (posterior inferior cerebellar artery territory) and the upper cervical cord (anterior spinal artery territory); the combination of posterior inferior cerebellar artery (PICA) and anterior spinal artery (ASA) infarcts has not been reported previously. Angiography revealed severe stenosis in the bilateral vertebral arteries. Hemodynamic hypoperfusion of the stenotic vertebral arteries may cause this unusual combination.     

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.     

The anterior inferior cerebellar artery infarcts: a clinical-magnetic resonance imaging study

Acute infarcts of the anterior inferior cerebellar artery (AICA) are unusual. We report 15 cases of AICA infarcts and their correlation with the topography of the lesion by brain MRI. During 2 years we prospectively identified 7 cases of AICA infarcts among 770 acute strokes (0.9% of the acute strokes seen in our department). We studied these cases and also another 8 that we found retrospectively. Most patients (8/15) had a unilateral affeétation of both middle cerebellar peduncle (MCP) and inferior lateral pontine area (ILP), in these cases the main symptoms were vertigo, ataxia, peripheral facial palsy and hypoacusia. Two other patients had isolated MCP infarcts and were characterized by peripheral vertigo and ataxia, without hypoacusia or facial palsy. Another 2 patients had isolated ILP territory infarct characterized by vertigo, left peripheral facial palsy without hypoacusia and mild or no ataxia. One patient had a Gasperini syndrome. Finally 3 patients had bilateral AICA infarcts due to basilar thrombosis. The etiology was atherosclerosis in 9 patients, lacunar due to hypertension in 1, cardiac embolism in 1, migraine in 1 and unknown in 3. Among the 15 patients only 2 died, both with AICA plus infarcts. In the remaining patients a follow-up during a mean of 31 months (3 months to 12 years) showed no recurrences.     

Clinical and radiologic features and their relationships with neurofunctional scores in patients with acute cerebellar infarct

Background:Cerebellar infarct is a rare condition with very nonspecific clinical features. The aim of this study was to assess the full spectrum of the clinical characteristics, neuroimaging findings and neurofunctional analyses of cerebellar infarction, and the relationship between them.Results:The mean age in our series was 65.2 years, with most being male (57.6%). The posterior inferior cerebellar (PICA) artery was the most commonly affected territory at 62.7%. There was concomitant lesion outside the cerebellum in 45.7%. The main etiology in PICA was cardioembolism. While mean National Institutes of Health Stroke Scale on admission was 2.08 ± 1.67 in study group, modified Rankin Scale (mRS) on admission was detected to be mRS1 (n: 44, 74.5%) and mRS2 (n: 12, 20.3%) most frequently. Fourteen (35%) patients were detected to be in Fazekas stage 0; 11 (27.5%) patients in Fazekas stage 1; 6 (15%) patients in Fazekas stage 2; and 9 (22.5%) patients in Fazekas stage 3.Conclusion:Cerebellar infarct is very heterogeneous. The other cerebral area infarcts which accompany ACI negatively affect neurologic functional scores. Although it is difficult to detect the relationship between WMLs and neurologic functional severity, timely detection of risk factors and their modulation may be associated with prevention and treatability of WMLs, and this may be one of the important points for prevention of stroke-related disability.     

Multiple acute infarcts in the posterior circulation.

OBJECTIVE--to evaluate clinical, radiological, and prognostic features of patients with multiple acute infarcts in remote arterial territories of the posterior circulation. DESIGN--Data analysis from a prospective acute stroke registry in a community based primary care centre using a standard protocol including MRI and MRA. RESULTS--In three and a half years, 27 of the 236 patients (11%) with posterior circulation stroke had multiple acute infarcts in the posterior circulation as shown by gadolinium enhancement on MRI. Eighteen patients had multiple infratentorial and supratentorial infarcts including the cerebellum and posterior cerebral artery territory, with coexisting brainstem involvement in seven patients. Fourteen patients had a rostral basilar artery syndrome and cerebellar signs; four patients had a visual field defect with cerebellar signs. Causes were vertebral (six) or basilar (four) artery atheromatosis, and cardioembolism (four). Seven patients had multiple acute infarcts in the posterior circulation of the cerebellum and lower brainstem. Brainstem and cerebellar signs were found in most patients (five); aetiologies were small vessel disease (four), cardioembolism (one), and vertebral artery dissection (one). Two patients with large artery atheromatosis had multiple acute infarcts in the posterior circulation in the brainstem and posterior cerebral artery territory. One month after stroke more than 25% of the patients were dependent or had died. There was no difference in the outcome between the three groups, and recovery was linked to the size of infarcts rather than to a high number of infarcts. CONCLUSIONS--multiple acute infarcts in the posterior circulation usually involve the cerebellum. Simultaneous brainstem and posterior cerebral artery territory infarcts sparing the cerebellum are uncommon. They can be suspected clinically before neuroimaging, mainly when supratentorial and infratentorial infarcts coexist. This may be important, because different patterns of infarction are associated with different causes of stroke.     

Midbrain infarction: associations and aetiologies in the New England Medical Center Posterior Circulation Registry

Most reports of midbrain infarction have describedclinicoanatomical correlations rather than associations andaetiologies. Thirty nine patients with midbrain infarction (9.4%) aredescribed out of a series of 415 patients with vertebrobasilarischaemic lesions in the New England Medical Center PosteriorCirculation Registry. Patients were categorised according to therostral-caudal extent of infarction. The "proximal" vertebrobasilarterritory includes the medulla and posterior inferior cerebellar artery territory. The "middle" territory includes the pons and anterior inferior cerebellar artery territory. The "distal" territoryincludes the rostral midbrain, thalami, superior cerebellum, and medial temporal and occipital lobes. Midbrain infarction was accompanied by"proximal" territory infarcts in four patients, and by "middle" territory infarction in 19 patients. Thirteen patients had associated "distal" territory infarcts, three of whom had occipital ortemporal lobe infarcts. Only three patients had isolated midbraininfarcts. Cardioembolism (n=11), in situ thrombosis (n=9), large artery to artery embolism (n=7), and intrinsic branch penetrator disease (n=5)were the most common aetiologies. Bilateral infarction and accompanyingpontine infarction were associated with the most extensivevertebrobasilar occlusive disease. Midbrain infarction was 10-fold morelikely to be accompanied by ischaemia of neighbouring structures thanit was to occur in isolation. Recognition of the different patterns ofinfarction may act as a guide to the underlying aetiology and vascular lesions.

     

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.     

椎动脉优势对基底动脉弯曲及椎基底动脉连接部脑梗死的影响

目的 探讨椎动脉优势对基底动脉弯曲及椎基底动脉连接部脑桥和小脑梗死的影响. 方法 回顾性分析郑州人民医院神经内三科自2009年1月至2011年1月收治的91例单侧脑桥或小脑后下动脉脑梗死患者的影像学资料,包括梗死侧别、椎动脉优势、基底动脉弯曲及其方向性关系等,应用多元logistic回归分析寻找基底动脉弯曲的预测因素. 结果 旁正中动脉供血区的脑桥中央是脑桥梗死最多的受累部位,右侧小脑内下部是小脑后下动脉梗死最多的受累部位.椎动脉优势常发生于左侧(69.2％,63/91).91例患者中有76例在椎动脉优势和基底动脉弯曲之间存在相反方向的关系.椎动脉内径是基底动脉中重度弯曲的唯一预测因素,其OR值为2.70,95％CI为1.22～5.98. 结论 椎动脉优势是基底动脉弯曲的重要预测因素,且弯曲多朝向优势椎动脉的对侧.椎动脉优势及其造成的基底动脉弯曲增加了椎基底动脉连接部脑梗死的发生率.     

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)