Spectrum of the Posterior Inferior Cerebellar Artery Territory Infarcts

Background: Pathologic investigations showed that lacunar infarction could develop in the deep cerebellar region. However, the etiology of small deep cerebellar ischemic lesions (SDCI) has not been adequately studied. The aim of this study was to investigate the relationship between SDCI and small-vessel disease. Methods: We studied 100 consecutive patients who had both (1) acute ischemic stroke (index stroke) confirmed by diffusion-weighted MRI and (2) evidence of a chronic small cerebellar ischemic lesion (<15 mm). Small-vessel-related MRI findings, risk factors and subtype of index stroke were compared between the patients with SDCI and those with small cortical cerebellar ischemic lesions (SCCI). Results: Eighty patients had SCCI, and 20 patients had SDCI. Cardioembolic sources (38.8 vs. 5%, p = 0.003) and vertebrobasilar artery stenosis (61.3 vs. 35%, p = 0.034) were more frequent in patients with SCCI. In a multivariate model including traditional risk factors, patients with SDCI had significantly more lacunar infarcts (odds ratio, 1.18; 95% confidence interval, 1.02–1.37) and cerebral microbleeds (odds ratio, 10.92; 95% confidence interval, 2.16–55.32) than those with SCCI. Patients with SDCI frequently had the small-artery disease subtype of index stroke (odds ratio, 5.84; 95% confidence interval, 1.71–19.9). Conclusions: The results suggest that SDCI are frequently associated with small-vessel disease.

Section: Discussionmentioning

confidence: 99%

“…It is well known that embolism from an arterial or cardiac source is the most common cause of territorial cerebellar infarcts [1,2,3,4,5,6,7]. Previous studies showed that small nonterritorial cerebellar infarcts usually have the same embolic mechanism as territorial infarcts, and they sometimes have a hemodynamic mechanism [8,9,10,11].…”

Section: Introductionmentioning

confidence: 99%

Association between Small Deep Cerebellar Ischemic Lesion and Small-Vessel Disease

Park

Chung²,

Kim³

et al. 2009

“…We also observed dysarthria in a patient with concomitant AICA and PICA lesions. Dysarthria was reported in different frequencies in individuals with infarcts in the AICA and PICA territories [43,44,45,46,47]. These differences may be due to the retrospective study design, different frequencies of brainstem involvement and the absence of a standardized evaluation of dysarthria.…”

Section: Discussionmentioning

confidence: 99%

Dysarthria due to Supratentorial and Infratentorial Ischemic Stroke: A Diffusion-Weighted Imaging Study

Kumral

Çelebisoy²,

Çelebisoy³

et al. 2007

Self Cite

Background and Purpose: Dysarthria characterized by slurring with imprecise articulation without evidence of aphasia is a frequent symptom in the acute phase of cerebral ischemia, although there is little knowledge on its anatomic specificity and spectrum of associated clinical characteristics regarding diffusion-weighted imaging (DWI). Methods: An investigation of 101 consecutive patients with sudden-onset dysarthria due to a single or multiple lesions on DWI, corresponding to 8.7% of 1,160 patients with ischemic stroke, was made. The presence of lesions of the cranial arteries was sought by magnetic resonance angiography and reviewed with a three-dimensional rotating cineangiographic method. Results: Dysarthria was mostly associated with a supratentorial lesion (63%) and with a classic lacunar stroke syndrome in 45% of patients. Lacunar lesions on DWI were found in 69 (68%) patients, while only 45 of the patients (65%) with a lacunar infarct presented a classic lacunar syndrome with dysarthria. Pure dysarthria occurred in 15% of patients, dysarthria + pure motor hemiparesis in 14%, dysarthria + ataxic hemiparesis in 11%, dysarthria + clumsy hand syndrome in 7%, dysarthria + pure sensory stroke in 3%, dysarthria + central facial paresis in 8% and lingual paresis occurred in 2%. The lesions were due to small-artery disease in 41%, large-artery disease in 15%, cardioembolism in 10% and a mixed etiology in 3%. The cause of stroke was not identified in 17 patients. Lesions on DWI were found mainly in the corona radiata (n = 18), middle cerebral artery territory, including the motor cortex and/or insular cortex (n = 13), striatocaudate nuclei (n = 11), primary motor cortex (n = 10), internal capsule (n = 7), pons (n = 25), pontobulbar junction (n = 5) and the thalamomesencephalic junction (n = 4). Isolated cerebellar infarctions (n = 6) or associated brainstem lesions (n = 6) affected mostly the superior cerebellar artery or the posterior inferior cerebellar artery territory. Conclusion: Cortical involvement was more frequent in patients with pure dysarthria than those with dysarthria and additional neurological signs, while the frequency of pontine involvement was higher in patients with additional neurological signs than those with pure dysarthria. One third of the patients with dysarthria had multiple lesions on DWI, and the most common cause of stroke was small-artery disease. Pure dysarthria, dysarthria with lingual paresis, dysarthria with clumsy hand and dysarthria with facial paresis had predictive value for lacunar lesions.

“…In the ischemic cases, the prognosis of PICA infarction is generally good [18, 19] except for patients with multiple brainstem lesions [20]; in the SAH cases, the prognosis of vertebrobasilar dissections is usually poor with regard to the initial state, and there is a high risk of rebleeding [21, 22]. Dissecting aneurysm of the PICA carries a 24% risk of rebleeding in the acute phase, associated with a high mortality rate [23].…”

Section: Discussionmentioning

confidence: 99%

Dissection of the Posteroinferior Cerebellar Artery: Clinical Characteristics and Long-Term Follow-Up in Five Cases

Sédat

Chau²,

Mahagne³

et al. 2007

Background and Purpose: Spontaneous isolated posteroinferior cerebellar artery (PICA) dissection is very rare. The aim of the study was to investigate the clinical manifestations, the neuroradiological aspects and the treatment of 5 cases collected in 5 years. Methods and Results: From 1999 to 2003, five patients (40–71 years old) were hospitalized for PICA dissection. Two patients presented symptoms after cervical manipulation. No predisposing factor or traumatic cause was described in the other cases. The diagnosis was carried out by cerebral angiography in all the cases: in 4, angiography showed focal stenosis with saccular or fusiform dilatation of the artery at the site of the dissection; in 1 a double lumen aspect was described. One patient presented ischemic manifestations; he was treated with heparin. The others presented subarachnoid hemorrhage (SAH) and were treated by embolization (endovascular sacrifice of the PICA). No ischemic complication and no rebleeding were observed after sacrifice of the PICA. Three patients presented acute hydrocephalus and were treated with surgical derivation. The angiographic and clinical follow-up lasted more than 3 years. We assessed the long-term results with the Glasgow Outcome Score and the modified Rankin Score. A good recovery was achieved for 4 patients (modified Rankin Score 0); one patient who presented SAH and who was in bad clinical state on admission had a Glasgow Outcome Score of 3 and a modified Rankin Score of 4 three years later. Conclusion: Clinical course and prognosis are variable in PICA dissections. The treatment depends on the existence of a hemorrhagic event. In the group of patients presenting SAH, endovascular treatment was safe and effective. The long-term clinical results depend mainly on the clinical status on admission.