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.     

New England Medical Center Posterior Circulation Stroke Registry: I. Methods, Data Base, Distribution of Brain Lesions, Stroke Mechanisms, and Outcomes

Among 407 New England Medical Center Posterior Circulation Registry (NEMC-PCR) patients, 59% had strokes without transient ischemic attacks (TIAs), 24% had TIAs before strokes, and 16% had only posterior circulation TIAs. Embolism was the commonest stroke mechanism accounting for 40% of cases (24% cardiac origin, 14% arterial origin, 2% had potential cardiac and arterial sources). In 32%, large artery occlusive lesions caused hemodynamic brain infarction. Stroke mechanisms in the posterior and anterior circulation are very similar. Infarcts most often included the distal posterior circulation territory (rostral brainstem, superior cerebellum and occipital and temporal lobes), while the proximal (medulla and posterior inferior cerebellum) and middle (pons and anterior inferior cerebellum) territories were equally involved. Infarcts that included the distal territory were twice as common as those that included the proximal or middle territories. Most distal territory infarcts were attributable to embolism. Thirty day mortality was low (3.6%). Embolic stroke mechanism, distal territory location, and basilar artery occlusive disease conveyed the worst prognosis.     

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.     

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.     

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)     

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.     

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.     

Lateral thalamic infarcts

A patient with occlusion of the proximal posterior cerebral artery (PCA), a lateral thalamic infarct, and hemisensory loss later developed hemianopia and hemiparesis and had extensive PCA territory infarction in the midbrain, the lateral portion of the thalamus, and the occipital lobe noted at necropsy. Two other patients had lateral thalamic infarcts on computed tomography, normal angiographic findings, and presumed thalamogeniculate artery branch occlusion. There are three clinical syndromes associated with lateral thalamic infarction: (1) hemisensory loss, hemiataxia, and involuntary movements; (2) pure sensory stroke; and (3) sensory-motor stroke. Ataxia, adventitious movements, and sensory loss are due to infarction of the lateral, posterolateral, and posteromedial ventral nuclei caused by occlusion of the PCA proximal to the thalamogeniculate artery branches or by occlusion of large thalamogeniculate arteries. Pure sensory and sensory-motor strokes are due to smaller infarcts in the posterolateral-posteromedial ventral complex and adjacent internal capsule caused by occlusion of penetrating artery branches of the thalamogeniculate arteries.     

The intracranial vertebral artery: a neglected species. The Johann jacob wepfer award 2012

Among posterior circulation arteries, the intracranial vertebral artery (ICVA) has been given the least attention, especially concerning treatment of occlusive lesions. Early clinicopathological studies showed that the ICVA was often occluded in patients with lateral medullary and posterior inferior cerebellar infarcts. Severe stenosis or occlusion of the ICVA was the most common arterial lesion among the 408 patients in the New England Medical Center Posterior Circulation Registry (NEMC-PCR). In this registry, the distal portion of the artery was most often involved, sometimes with spread into the basilar artery. ICVA occlusive lesions were often bilateral and very often accompanied by basilar and cervical vertebral artery occlusive lesions. Patients with bilateral ICVA occlusions often had attacks of dizziness, blurred vision, and ataxia during months and years but rarely later developed disabling infarction. Most posterior circulation infarcts in patients with ICVA occlusive lesions were located in the middle and distal posterior circulation territories and were rostral to the medulla and inferior cerebellum. Although diagnostic techniques now image the ICVA and its lesions well, the optimal treatment of patients with various ICVA occlusive lesions has very rarely been analyzed or reported. The therapeutics of patients with ICVA disease is uncharted territory and begs for attention and clarification.     

New England Medical Center Posterior Circulation registry

Among 407 New England Medical Center Posterior Circulation registry patients, 59% had strokes without transient ischemic attacks (TIAs), 24% had TIAs then strokes, and 16% had only TIAs. Embolism was the commonest stroke mechanism (40% of patients including 24% cardiac origin, 14% intraarterial, 2% cardiac and arterial sources). In 32% large artery occlusive lesions caused hemodynamic brain ischemia. Infarcts most often included the distal posterior circulation territory (rostral brainstem, superior cerebellum and occipital and temporal lobes); the proximal (medulla and posterior inferior cerebellum) and middle (pons and anterior inferior cerebellum) territories were equally involved. Severe occlusive lesions (>50% stenosis) involved more than one large artery in 148 patients; 134 had one artery site involved unilaterally or bilaterally. The commonest occlusive sites were: extracranial vertebral artery (52 patients, 15 bilateral) intracranial vertebral artery (40 patients, 12 bilateral), basilar artery (46 patients). Intraarterial embolism was the commonest mechanism of brain infarction in patients with vertebral artery occlusive disease. Thirty-day mortality was 3.6%. Embolic mechanism, distal territory location, and basilar artery occlusive disease carried the poorest prognosis. The best outcome was in patients who had multiple arterial occlusive sites; they had position-sensitive TIAs during months to years.     

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.     

Anterior and posterior inferior cerebellar artery infarction with sudden deafness and vertigo

We report a patient with anterior and posterior inferior cerebellar artery infarction, which manifested as profound deafness, transient vertigo, and minimal cerebellar signs. We suspect that ischaemia of the left internal auditory artery, which originates from the anterior inferior cerebellar artery, caused the deafness and transient vertigo. A small lesion in the middle cerebellar peduncle in the anterior inferior cerebellar artery territory and no lesion in the dentate nucleus in the posterior inferior cerebellar artery territory are thought to explain the minimal cerebellar signs despite the relatively large size of the infarction. Thus a relatively large infarction of the vertebral-basilar territory can manifest as sudden deafness with vertigo. Neuroimaging, including magnetic resonance imaging, is strongly recommended for patients with sudden deafness and vertigo to exclude infarction of the vertebral-basilar artery territory.     

Bilateral intracranial vertebral artery disease in the New England Medical Center, Posterior Circulation Registry.

BACKGROUND: Previous studies of patients with bilateral intracranial vertebral artery (ICVA) disease were selective and retrospective. METHODS: We studied risk factors, vascular lesions, symptoms, signs, and outcomes in patients with bilateral ICVA disease among 430 patients in the New England Medical Center Posterior Circulation Registry. RESULTS: Forty-two patients had bilateral ICVA occlusive disease (18 had bilateral stenosis; 16, unilateral occlusion and contralateral stenosis; and 8, bilateral occlusion). The most common risk factors were hypertension (32/42 [76%]) and hyperlipidemia (22/42 [52%]). Sixteen patients (38%) had transient ischemic attacks (TIAs) only; 18 (43%), TIAs before stroke. Occlusive vascular disease also involved the basilar artery in 29 patients (69%), the extracranial vertebral arteries in 18 (43%), and the internal carotid arteries in 11 (26%). Only 6 patients had no other major vascular lesion. Cerebellar symptoms were common. Among 30 patients with infarction, 21 (70%) had proximal intracranial territory involvement, and 15 (50%) had distal territory involvement. The location of occlusive lesions in relation to posterior inferior cerebellar artery origins did not significantly influence prognosis. During follow-up, 31 patients had no symptoms or slight disability, 2 had progression, and 7 died. Among 7 patients with poor outcome, 6 also had basilar artery stenosis or occlusion and 5 had proximal and distal intracranial territory infarcts. CONCLUSIONS: Most patients with bilateral ICVA occlusive disease have hypertension, other major occlusive lesions, and TIAs before stroke. Short- and long-term outcomes are usually favorable, but patients with bilateral ICVA and basilar artery-occlusive lesions often have poor outcomes.     

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.     

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。     

New England Medical Center Posterior Circulation Stroke Registry II. Vascular Lesions

Among 407 New England Medical Center Posterior Circulation Registry (NEMC-PCR) patients, the extracranial (ECVA) and intracranial vertebral arteries (ICVA) were the commonest sites of severe occlusive disease followed by the basilar artery (BA). Severe occlusive lesions were found in >1 large artery in 148 patients; 134 had unilateral or bilateral severe disease at one arterial location. Single arterial site occlusive disease occurred most often in the ECVA (52 patients, 15 bilateral) followed by the ICVA (40 patients, 12 bilateral) and the BA (46 patients). Involvement of the ICVAs and the BA was very common and some patients also had ECVA lesions. Hypertension, smoking, and coronary and peripheral vascular disease were most prevalent in patients with extracranial disease while diabetes and hyperlipidemia were more common when occlusive lesions were only intracranial. Intra-arterial embolism was the most common mechanism of brain infarction in patients with ECVA and ICVA occlusive disease. ICVA occlusive lesions infrequently caused infarction limited to the proximal territory (medulla and posterior inferior cerebellum). BA lesions most often caused infarcts limited to the middle posterior circulation territory (pons and anterior inferior cerebellum). Posterior cerebral artery occlusive lesions were predominantly embolic. Penetrating artery disease caused mostly pontine and thalamic infarcts. Prognosis was poorest in patients with BA disease. The best prognosis surprisingly was in patients who had multiple arterial occlusive lesions; they often had position-sensitive transient ischemic attacks during months or years.     

Neurovascular territory involved in different etiological subtypes of ischemic stroke in the Perugia Stroke Registry

We studied the correlation between the potential causes of stroke (TOAST etiological groups) and the involvement of different vascular territories seen on computed tomography (CT) scans in patients with ischemic stroke. Information from consecutive patients with a first-ever stroke have been prospectively coded and entered into a computerized data bank (Perugia Stroke Registry). A population of 1,719 patients were evaluated: 1,284 patients (74.7%) had ischemic stroke. Large artery disease was the main cause of entire middle cerebral artery (MCA) territory infarcts (40.9%), superficial MCA territory infarcts (35.7%), and watershed infarcts (68.2%). The highest presence of emboligenic heart disease was found in the entire MCA territory infarcts (28.8%) or superficial (29.4%) supratentorial infarcts and in cerebellar infarcts (36.8%). Small artery disease was the most common presumed cause of deep MCA infarcts (75.0%) and posterior cerebral artery (PCA) territory infarcts (52.1%). In conclusion: stroke location could depend on its etiology. Lacunar infarcts are the most prevalent (36.7%), being mostly localized in the deep MCA territory; large artery disease includes more than two-thirds of watershed infarcts; the most prevalent territories involved in cardioembolic stroke are the entire MCA and posterior fossa.     

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.     

Role of impaired CO2 reactivity in the diagnosis of cerebral low flow infarcts.

Previous studies on CO2 reactivity in cerebral low flow infarcts (LFIs) included patients with lesions in the frontoparasagittal area, supraganglionic white matter, and temporoparieto-occipital zone. Supraganglionic white matter LFIs are, however, difficult to separate from non-low flow induced infarcts of the lacunar type, and temporoparieto-occipital LFIs from infarcts in the territory of the inferior stem of the middle cerebral artery. The CO2 reactivity of the middle cerebral artery was studied in 56 patients with high grade stenoses and occlusions of the internal carotid artery and LFIs (n = 9) in the frontoparasagittal border zone, territorial infarcts (n = 26), no infarcts (n = 21), and normal subjects (n = 25) by means of transcranial Doppler sonography. The aim was to investigate whether patients with LFIs have significantly lower CO2 reactivity than patients with territorial infarcts, no infarcts, and normal subjects. Patients with LFIs had the most severely reduced CO2 reactivity on the symptomatic side and CO2 reactivity was significantly lower than on the asymptomatic side. It was also lower than in patients with unilateral and bilateral internal carotid artery obstructions and territorial infarcts, asymptomatic patients, and healthy volunteers. It is concluded that LFIs are associated with significantly reduced CO2 reactivity.     

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.