Cases reported "Brain Infarction"

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1/7. Apraxic agraphia due to thalamic infarction.

    The authors report a patient of pure apraxic agraphia with normal praxis due to left thalamic infarction. 15O-gas-PET showed reduced oxygen metabolism in the left thalamus and the left dorsolateral premotor area, while MRI and 11C-fulumazenil-PET showed no remarkable lesions in the frontal cortex. The patient's word imaging remained normal. The authors hypothesize that thalamic destruction causes pure apraxic agraphia by exerting a remote effect on left dorsolateral premotor area and blocking somewhere between graphemic area and motor programming.
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2/7. 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.
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3/7. 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.
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4/7. 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.
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5/7. Sudden deafness and anterior inferior cerebellar artery infarction.

    BACKGROUND AND PURPOSE: Acute ischemic stroke in the distribution of the anterior inferior cerebellar artery (AICA) is known to be associated with vertigo, nystagmus, facial weakness, and gait ataxia. Few reports have carefully examined the deafness associated with the AICA infarction. Furthermore, previous neurological reports have not emphasized the inner ear as a localization of sudden deafness. The aim of this study was to investigate the incidence of deafness associated with the AICA infarction and the sites predominantly involved in deafness. methods: Over 2 years, we prospectively identified 12 consecutive patients with unilateral AICA infarction diagnosed by brain MRI. Pure-tone audiogram, speech discrimination testing, stapedial reflex testing, and auditory brainstem response were performed to localize the site of lesion in the auditory pathways. electronystagmography was also performed to evaluate the function of the vestibular system. RESULTS: The most common affected site on brain MRI was the middle cerebellar peduncle (n=11). Four patients had vertigo and/or acute auditory symptoms such as hearing loss or tinnitus as an isolated manifestation from 1 day to 2 months before infarction. Audiological testings confirmed sensorineural hearing loss in 11 patients (92%), predominantly cochlear in 6 patients, retrocochlear in 1 patient, and combined on the affected side cochlear and retrocochlear in 4 patients. electronystagmography demonstrated no response to caloric stimulation in 10 patients (83%). CONCLUSIONS: In our series, sudden deafness was an important sign for the diagnosis of AICA infarction. Audiological examinations suggest that sudden deafness in AICA infarction is usually due to dysfunction of the cochlea resulting from ischemia to the inner ear.
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6/7. Panhemispheric infarction: a complication of cuffed catheter.

    The need for reliable vascular access remains the Achilles heel of hemodialysis. Complications of vascular access are a leading cause of morbidity and mortality in patients who undergo hemodialysis, especially in those patients with end-stage renal disease. Among methods of vascular access, arteriovenous fistulae have the lowest rate of infection and should be the access of choice when vascular anatomy permits. Also, the incidence of staphylococcal infections in patients infected with human immunodeficiency virus is increasing. To emphasize the need to use arteriovenous fistula access for hemodialysis whenever possible, we report the case of a patient with end-stage renal disease and human immunodeficiency virus infection who died as a result of panhemispheric infarction and uncal herniation as a result of fulminant staphylococcal bacteremia caused by central venous catheter sepsis.
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7/7. stroke and seizure following a recent laparoscopic Roux-en-Y gastric bypass.

    Laparoscopic Roux-en-Y gastric bypass (LRYGBP) has been an available operation for weight loss for the past decade, and bariatric surgery is increasing in the united states. Careful patient screening and follow-up have been the cornerstone for success against the complexities of morbid obesity. Neurologic complications have occurred, such as polyneuropathy and Wernicke-korsakoff syndrome. We report an 18-year-old female with morbid obesity, steatohepatitis, tobacco, recreational drug, and oral contraceptive use who at 4 months after LRYGBP experienced a generalized seizure and stroke. She was diagnosed with an acute ischemic stroke, possibly venous infarction. Her postoperative course had been complicated by malnutrition and dehydration, apparently related to nausea from chronic cholecystitis. She had a possible protein-S deficiency. Rare neurologic complications emphasize the importance of postoperative surveillance in these patients.
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