11/84. Clinically unidentified dissection of vertebral artery as a cause of cerebellar infarction.BACKGROUND AND PURPOSE: dissection of vertebral arteries has been reported in association with minor neck movements without signs of trauma on the surface of the neck. In addition, injury of a vertebral artery can cause brain infarctions. However, few cases have been reported in which fatal brain infarction was due to nonocclusive, clinically undetected, traumatic thrombus formation in a vertebral artery. CASE DESCRIPTION: A 62-year-old man was hit by a car, and a right cerebellar infarction was found the day after the accident. The cause of the infarction could not be detected by angiography. Although the patient recovered favorably after surgical removal of the right lateral hemisphere of the cerebellum, he died suddenly 2 weeks after the accident. An autopsy and a microscopic study revealed pulmonary thromboembolism and organizing traumatic lesions of the right vertebral artery without occlusion or noteworthy stenosis of the artery. CONCLUSIONS: We concluded that the patient sustained traumatic lesions of the right vertebral artery during the traffic accident 2 weeks before death and that his cerebellar infarction was due to a thrombus resulting from these traumatic lesions.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
12/84. Bilateral symmetrical basal ganglia infarction after intravenous use of cocaine and heroin.A case is reported of a young man who developed bilateral symmetrical basal ganglia infarcts after intravenous use of cocaine and heroin. Ischemic infarcts of the brain are a known complication of to cocaine use, alone or in combination with heroin (speed balling). This symmetrical occurrence of infarction, however, is unusual and has not been reported after cocaine use.- - - - - - - - - - ranking = 0.5keywords = brain (Clic here for more details about this article) |
13/84. perfusion magnetic resonance imaging maps in hyperacute stroke: relative cerebral blood flow most accurately identifies tissue destined to infarct.BACKGROUND AND PURPOSE: In ischemic stroke, perfusion-weighted imaging (PWI) and diffusion-weighted imaging (DWI) provide important pathophysiological information. A PWI>DWI mismatch pattern suggests the presence of salvageable tissue. However, improved methods for distinguishing PWI>DWI mismatch tissue that is critically hypoperfused from benign oligemia are required. methods: We investigated the usefulness of maps of relative cerebral blood flow (rCBF), volume (rCBV), and mean transit time (rMTT) to predict transition to infarction in hyperacute (<6 hours) stroke patients with PWI>DWI mismatch patterns. Semiquantitative color-thresholded analysis was used to measure hypoperfusion volumes, including increasing color signal intensity thresholds of rMTT delay, which were compared with infarct expansion, outcome infarct size, and clinical status. RESULTS: Acute rCBF lesion volume had the strongest correlation with final infarct size (r=0.91, P<0.001) and clinical outcome (r=0.67, P<0.01). There was a trend for acute rCBF>DWI mismatch volume to overestimate infarct expansion between the acute and outcome study (P=0.06). Infarct expansion was underestimated by acute rCBV>DWI mismatch (P<0.001). When rMTT lesions included tissue with moderately prolonged transit times (mean delay 4.3 seconds, signal intensity values 50% to 70%), infarct expansion was overestimated. In contrast, when rMTT lesions were restricted to more severely prolonged transit times (mean delay 6.1 seconds, signal intensity >70%), these regions progressed to infarction in all except 1 patient, but infarct expansion was underestimated (P<0.001). CONCLUSIONS: The acute rCBF lesion most accurately identified tissue in the PWI>DWI mismatch region at risk of infarction. color-thresholded PWI maps show potential for use in an acute clinical setting to prospectively predict tissue outcome.- - - - - - - - - - ranking = 31.36638481163keywords = cerebral (Clic here for more details about this article) |
14/84. Bilateral sudden deafness as a prodrome of anterior inferior cerebellar artery infarction.BACKGROUND: Acute ischemic stroke in the distribution of the anterior inferior cerebellar artery is known to be associated with hearing loss, facial weakness, ataxia, nystagmus, and hypalgesia. There have been few reports on bilateral deafness and vertebrobasilar occlusive disease. Furthermore, previous reports have not emphasized the inner ear as a localization of bilateral deafness. OBJECTIVE: To describe the presentation of acute ischemic stroke in the distribution of the anterior inferior cerebellar artery as sudden bilateral hearing loss with minimal associated signs. DESIGN AND SETTING: Case report and tertiary care hospital. PATIENT: A 66-year-old man with diabetes mellitus developed sudden bilateral deafness, unilateral tinnitus, and vertigo 7 days before the onset of dysarthria, facial weakness, and ataxia. T2-weighted magnetic resonance imaging scans showed hyperintensities in the right lateral pons and right middle cerebral peduncle and a possible abnormality of the left middle cerebellar peduncle. A magnetic resonance angiogram showed moderately severe stenosis of the distal vertebral artery and middle third of the basilar artery. The patient's right limb coordination and gait improved steadily over several weeks, but there was no improvement in hearing in his right ear. CONCLUSIONS: The relatively isolated onset of deafness as well as the severity and persistence of the hearing loss led us to conclude that the hearing loss in this case was likely due to prominent hypoperfusion of the internal auditory artery, with labyrinthine infarction as the earliest event. Vertebrobasilar occlusive disease should be considered in the differential diagnosis of sudden bilateral deafness.- - - - - - - - - - ranking = 6.273276962326keywords = cerebral (Clic here for more details about this article) |
15/84. Internuclear ophthalmoplegia and cerebellar ataxia: report of one case.Deep hemispheric or brainstem small infarcts can lead to atypical lacunar syndromes. Unilateral internuclear ophthalmoplegia (INO) and cerebellar ataxia has not been reported previously. A 57-year-old hypertensive female presented with bilateral appendicular and left truncal cerebellar ataxia and right INO. Cranial MRI showed a right paramedian infarct of lacunar size located in the tegmentum of caudal mesencephalon. At this level the involvement of medial longitudinal fascicle (MLF) led to right INO and the lesion of brachium conjunctivum caused the bilateral cerebellar ataxia. Ipsilateral involvement of both cerebellofugal fibers, before and after decussation, was responsible for bilateral cerebellar ataxia.- - - - - - - - - - ranking = 0.5keywords = brain (Clic here for more details about this article) |
16/84. Patent foramen ovale complicated by paradoxical embolism and brain infarct in a patient with advanced ovarian cancer.BACKGROUND: Recent investigations of patients with cerebral and peripheral arterial emboli of unknown cause suggest that paradoxical embolism through a patent foramen ovale might be responsible for more arterial embolic events than previously realized. CASE: A 60-year-old woman with advanced ovarian cancer presented with sudden onset of expressive aphasia and right upper hemiplegia postoperatively. A patent foramen ovale diagnosed by echocardiography with contrast combined with the presence of thrombosis in her right femoral vein leads us to speculate that her stroke was secondary to a paradoxical embolism. CONCLUSION: Paradoxical embolism should be considered in the differential diagnosis of ovarian cancer patients with embolic stroke and it may be appropriate to include a cardiac echo as part of the diagnostic evaluation.- - - - - - - - - - ranking = 8.273276962326keywords = cerebral, brain (Clic here for more details about this article) |
17/84. Haemorrhagic venous infarction following the posterior petrosal approach for acoustic neurinoma surgery: a report of two cases.The authors report two surgical cases with acoustic neurinoma in which haemorrhagic infarction occurred via a compromise in cerebral deep venous outflow. In both cases, surgery was performed via the posterior petrosal approach, and the neurinomas were completely removed. In the first case, the haemorrhagic infarction was considered to have resulted from transection of the tentorial sinus, the presence of which had not been predictable by preoperative angiography. In the second case, the haemorrhagic infarction was caused by a coagulation of the petrosal vein, which was firmly adherent to a tumour. With the posterior petrosal approach, meticulous care is necessary to preserve the deep anastomotic veins into and around the cerebellar tentorium. Thereby, catastrophic morbidity related to compromised deep cerebral venous outflow can be avoided.- - - - - - - - - - ranking = 12.546553924652keywords = cerebral (Clic here for more details about this article) |
18/84. Thalamic venous infarction as a cause of subacute dementia.The clinical picture of deep cerebral vein thromboses (DCVT) usually is acute, combining vigilance disorders, headaches, and focal neurologic deficit. The authors describe a patient who presented with isolated subacute dementia as the sole manifestation of DCVT. In the setting of subacute cognitive deficit, the diagnosis of DCVT must be considered when neuroimaging shows bilateral thalamic changes. Enhanced venous MR angiography is the noninvasive method of choice to ascertain the diagnosis.- - - - - - - - - - ranking = 6.273276962326keywords = cerebral (Clic here for more details about this article) |
19/84. Comparison of 1.5 and 8 tesla high-resolution magnetic resonance imaging of lacunar infarcts.PURPOSE: We present a case report comparing 1.5 fast spin-echo (FSE) and high-resolution 8 Tesla (T) gradient echo (GE) MRI of a patient with multiple lacunar infarcts. methods: A 51-year-old man with a history of previous lacunar infarctions was studied with two-dimensional Fourier transform axial 8 T GE MRI using the following parameters: 3 mm thick slices skip 3 mm, flip-angle approximately 20 degrees, TR 800 milliseconds, TE 12 milliseconds, 1024 x 1024 matrix, field of view (FOV) 20 cm, and bandwidth 50 kHz. These images were then compared with routine clinical 1.5 T T2-weighted FSE images with 5 mm thick sections, 256 x 256, FOV 20, TR 5650, TE 102, and 16 echo train length. RESULTS: The majority of the infarctions were seen as areas of high signal intensity on both the 1.5 and 8 T images. They were seen in the corona radiata or the basal ganglia. More lesions were seen on the 8 T images. Low intensity signal was best demonstrated on the 8 T images at segments of the periphery of a few of the larger infarcts. There were a few small punctate low signal intensity regions localized at the termination of some of the microvessels on the 8 T images only. The foci of decreased signal intensity in regions of chronic hemorrhage appeared larger on the 8 T images compared with the 1.5 T images. The 8 T images demonstrated direct visualization of many small vessels, primarily in the deep white matter, which were not visible on the 1.5 T images. On the 8 T images, some of the infarcts appeared to be located between the medullary veins of the deep white matter. CONCLUSION: This case report indicates that GE 8 T images demonstrate more infarctions compared with the FSE 1.5 T images. It is possible to simultaneously identify the microvessels of the brain, small foci of hemorrhage, and lacunar infarctions using 8 T MRI.- - - - - - - - - - ranking = 0.5keywords = brain (Clic here for more details about this article) |
20/84. Prominent matched hypoperfusion in an intact cerebellum after a solitary middle cerebellar peduncle infarct.We examined the cerebellar metabolism of a 61-year-old man with a small infarct in the left middle cerebellar peduncle and an intact cerebellum. Positron emission tomographic images obtained 28 days after onset showed prominent hypoperfusion and hypometabolism (almost 50% below the normal level) in the left cerebellar hemisphere. This case report shows that neural deafferentation may cause prominent hypometabolism without morphologic changes in the cerebellum. An arrest in synaptic activity may be the most important factor for the adaptive decrease in oxygen metabolism seen in ischemic brain.- - - - - - - - - - ranking = 0.5keywords = brain (Clic here for more details about this article) |
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