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 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical features of the anterior inferior cerebellar artery (AICA) territory infarcts were investigated in ten patients, ranging in age from 38 to 76 years. In all patients, there were MR images of infarction located in the area supplied by the AICA. The lesion was on the left side in 6 patients and right side in 4. The lesion of brain stem including the middle cerebellar peduncle was found in 7 patients and that extended to the cerebellum was in 3 patients. The main ipsilateral neurological signs were the VII and VIII cranial nerves palsy and cerebellar ataxia. The V and VI cranial nerves palsy. Horner's syndrome, and dysphagia were also present. The main contralateral sign was superficial sensory disturbance, but no hemiplegia. The underlying pathology included chiefly hyperlipidemia, hypertension, and diabetes mellitus. Cerebral angiography was performed in 8 patients, most of which was observed severe arteriosclerosis suggesting poor hemodynamics in the vertebral and basilar arteries. The prognosis was relatively good, but the VII, VIII, and V cranial nerves palsy and contralateral superficial sensory disturbance remained as the sequelae. As mentioned above, there were various neurological findings and MR images in AICA territory infarcts. Especially there were some patients whose lesion extended to the upper medulla and neurological findings were similar to the Wallenberg syndrome. It is important that one investigates not only axial slices but also coronal slices of MR image to estimate the extension of AICA territory infarct.
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PMID:[Clinical features of anterior inferior cerebellar artery territory infarcts--a study of ten patients]. 904 27

A 52-year-old man with diabetes mellitus, hyperlipidemia and smoking habit, experienced transient ischemic attacks (TIAs) with symptoms of left orbital pain, left blepharoptosis and hoarseness lasting for five minutes on March 10, 1997. Subsequently, the same symptoms repeated once or twice daily. On March 28, he had dysphagia, numbness and disturbance of pain and temperature sensation (segmental dissociated sensory disturbance) on the right side of the body above the level of the Th10, the right upper limb and face. The deficits persisted for more than 24 hours. Angiographic studies revealed an occlusion of the left vertebral artery immediately after branching of the posterior inferior cerebellar artery. MRI demonstrated a hyperintense lesion on MRI T2 weighted image in the left lateral medulla. About three months after the completed stroke, he had six episodes of TIAs of left Horner's sign and hoarseness. To our knowledge, this is the rare case that had frequent TIAs presenting the Wallenberg syndrome before and after the onset of lateral medullary infarction. We speculate that the TIAs resulted from microembolism from the proximal end of occluted left vertebral artery and failure of the microcirculation in and around the lateral portion of the medulla oblongata.
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PMID:[A case with frequent episodes of transient ischemic attack presenting the Wallenberg syndrome before and after the onset of brain infarction]. 1042 53

From 1990 to 1997, June, 296 patients (156 males and 140 females), aged 16 to 45 years, admitted in the Neurology Department of the University Hospital of Nancy (F) for ischemic stroke, were prospectively evaluated according to a standardized analysis of anamnestic and clinical data, angiography (90 p. 100 of cases), TEE (78 p. 100), hemostasis. Women were younger (mean age = 34.82 y) than men (36.87 y; p = 0.003), with a peak in the 4th decade. Clinical event was a TIA in 14.2 p. 100, a stroke in 51.7 p. 100; it concerned the anterior circulation in 64.5 p. 100, posterior circulation in 25 p. 100, multiple territories in 10.5 p. 100. History of TIA, cervical-cranial pain or Horner syndrome suggestive of dissection, pregnancy or post-partum were found respectively in 60 (20.3 p. 100), 34 (11.1 p. 100) and 13 (9.3 p. 100) cases. Risk factors concerned 87.2 p. 100 of patients, mainly smoking (55.1 p. 100), oral contraceptive (53 p. 100), hyperlipemia (35 p. 100), and were more frequent in case of atheroma and lacunar stroke (p < 0.0000). Etiology, according to TOAST classification, was: atheroma (8.4 p. 100), cardioembolism (8.7 p. 100), small-artery disease (7.1 p. 100), dissection (15.5 p. 100), other determined causes (11.1 p. 100), multiple causes (5.7 p. 100), undetermined cause (34.8 p. 100). Septal pathology was found 34 times. Patients whose stroke remained unexplained were younger (33.7 y vs 37.7, p = 0.002), had less risk factors (p < 0.0000), had more TIA (p = 0.005), more often in the carotid territory (p = 0.008), had a better prognosis (p = 0.01), and showed more often emboli at angiography (p = 0.001). During a mean follow-up of 33 months (median = 19), 21 recurrent strokes occurred and 6 patients died. 134 (46 p. 100) patients had no sequelae, 101 (34.7 p. 100) minor disability, 42 (14.4 p. 100) major sequelae. These results, compared to the main studies of the literature, suggest the interest of common definition criteria and classification of etiologies. In practice, hierarchisation of investigations may be proposed, and vascular risk factors should be tracked in young patients. In patients whose stroke remains unexplained, further studies, as atrial vulnerability, are needed.
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PMID:[Cerebral ischemic accidents in young subjects. A prospective study of 296 patients aged 16 to 45 years]. 1048 47

OBJECTIVE Dissection of the carotid and vertebral arteries can result in the development of aneurysmal dilations. These dissecting pseudoaneurysms can enlarge and cause symptoms. The objective of this study is to provide insight into the progression of dissecting pseudoaneurysms and the treatments required to manage them. METHODS A review of the electronic medical records was conducted to detect patients with carotid and vertebral artery dissection. An imaging review was conducted to identify patients with dissecting pseudoaneurysms. One hundred twelve patients with 120 dissecting pseudoaneurysms were identified. Univariate and multivariate analyses were conducted to assess the factors associated with undergoing further interventions other than medical treatment, pseudoaneurysm enlargement, pseudoaneurysms resulting in ischemic and nonischemic symptoms, and clinical outcome. RESULTS Overall, 18.3% of pseudoaneurysms were intracranial and 81.7% were extracranial, and the average size was 7.3 mm. The mean follow-up time was 29.3 months; 3.3% of patients had a recurrent transient ischemic attack, no patients had a recurrent stroke, and 14.2% of patients had recurrence of nonischemic symptoms (headache, neck pain, Horner syndrome, or cranial nerve palsy). Follow-up imaging demonstrated that 13.8% of pseudoaneurysms had enlarged, 30.2% had healed, and 56% had remained stable. In total, 20.8% of patients had an intervention other than medical treatment. Interventions included stenting, coiling, flow diversion, and clipping. Predictors of intervention included increasing size, size > 10 mm, location in the C2 (petrous) segment of the internal carotid artery (ICA), younger age, hyperlipidemia, pseudoaneurysm enlargement, and any symptom development. Significant predictors of enlargement included smoking, history of trauma, C2 location, hyperlipidemia, and larger initial pseudoaneurysm size. Predictors of pseudoaneurysm resulting in recurrent ischemic and nonischemic symptoms included increasing size and location in the petrous segment of the ICA. Smoking was a predictor of unfavorable outcome. CONCLUSIONS Dissecting pseudoaneurysms have a benign course and most will not cause symptoms or enlarge on follow-up. Medical treatment can be a sufficient, initial treatment for dissecting pseudoaneurysms.
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PMID:Dissecting pseudoaneurysms: predictors of symptom occurrence, enlargement, clinical outcome, and treatment. 2682 74