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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary progressive aphasia is a neurodegenerative variant of frontotemporal lobe degeneration presenting with isolated selective impairment of language domain, not secondarily due to stroke. We present a case of middle-aged female patient who underwent F-FDG PET of the brain for evaluating progressively declining speaking ability associated with altered fluency of speech and occasional mutism. F-FDG PET revealed asymmetric hypometabolism involving the left inferior frontal gyrus along with left anterior cingulate gyrus suggestive of Broca's aphasia.
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PMID:18F-FDG PET/CT Brain in a Case of Agrammatic/Nonfluent Variant of Primary Progressive Aphasia (Broca's Aphasia). 3220 83

Enriched environment (EE) is an effective rehabilitative protocol designed to enhance sensorimotor, cognitive and social stimulation. Current understanding of neuronal remodeling after EE intervention mainly derived from conventional histological methods. The efficacy of EE treatment on post-stroke brain reorganization still needed to be elucidated in vivo. This study aimed to examine the effects of post-ischemic EE treatment on the brain remodeling using magnetic resonance imaging (MRI) and 18F-FDG positron emission tomography (PET). Male Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (MCAO) and housed in standard environment (SE) or EE for consecutive 30 days. Cognitive testing was performed using the Morris water maze. White matter structural modifications were detected by MRI combined with histological analysis. In addition, PET scanning with 18F-FDG as a molecular probe was conducted to detect brain energy metabolism. Our results showed that EE significantly mitigated MCAO-induced impairments in spatial learning and memory, attenuated brain atrophy, protected white matter integrity, and enhanced white matter reorganization coupled with promoting oligodendrogenesis. In parallel to these findings, PET-MRI fused images showed that EE remarkably elevated regional cerebral metabolic rates of glucose in the lesioned sensorimotor cortex, striatum and corpus callosum/external capsule. More importantly, a strong correlation was demonstrated between glucose utilization and diffusion tensor imaging indices in the corresponding brain regions. The data herein indicated that improved global metabolism of glucose was a critical step in the reorganization of the white matter following post-stroke EE intervention. Although EE did not produce beneficial effects on restoring brain infarct volume, the broad range of structural and functional benefits observed in the present study raised the interesting possibility that EE might be an effective rehabilitative strategy for ischemic stroke.
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PMID:Enhanced white matter reorganization and activated brain glucose metabolism by enriched environment following ischemic stroke: Micro PET/CT and MRI study. 3261 89

Stroke-like episodes (SLEs) are a hallmark of mitochondrial encephalopathy, lactic acidosis, and stroke-like episode (MELAS) syndrome but occur in other mitochondrial disorders (MIDs) as well. The morphological equivalent of the SLE is the stroke-like lesion (SLL) on magnetic resonance imaging (MRI). The pathophysiology of SLLs is under debate, but several hypotheses have been raised to explain the phenomenon. Of these, the metabolic, epileptogenic, and vascular hypotheses are the most frequently discussed. There are several arguments for and against these hypotheses, but a consensus has not been reached which of them provides the correct explanation. A recent consensus statement generated by a panel of experts applying the Delphi method, favoured the epileptogenic hypothesis and recommended treatment of SLEs with antiepileptic drugs, irrespective if the patient presented with a seizure or epileptiform discharges on electroencephalography (EEG) or not. We disagree with this general procedure and provide the following arguments against the epileptogenic hypothesis: 1. not each SLE is associated with seizures. 2. epileptiform discharges may be absent on EEG during a SLE. 3. SLLs are not restricted to the cortex. 4. antiseizure-drugs (ASDs) may not prevent the progression or recurrence of a SLL. 5. ASDs may terminate seizures but no other phenotypic feature of a SLE. 6. patients already under ASDs are not immune from developing a SLL. 7. SLLs usually last longer than seizures. 8. no animal model supports the epileptogenic hypothesis. The strongest arguments for the metabolic hypothesis are that SLLs are not confined to a vascular territory, that the oxygen-extraction fraction within a SLL is reduced, and that there is hypometabolism within a SLL on FDG-PET. SLLs may respond to antioxidants, NO-precursors, steroids, or the ketogenic diet. ASDs should be applied only if there is clinical or electrophysiological evidence of seizure-activity.
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PMID:The metabolic hypothesis is more likely than the epileptogenic hypothesis to explain stroke-like lesions. 3264 51

Stroke-like episodes (SLEs) are a hallmark of mitochondrial encephalopathy, lactic acidosis, and stroke-like episode (MELAS) syndrome but occur in other mitochondrial disorders (MIDs) as well. The morphological equivalent of the SLE is the stroke-like lesion (SLL) on magnetic resonance imaging (MRI). The pathophysiology of SLLs is under debate, but several hypotheses have been raised to explain the phenomenon. Of these, the metabolic, epileptogenic, and vascular hypotheses are the most frequently discussed. There are several arguments for and against these hypotheses, but a consensus has not been reached which of them provides the correct explanation. A recent consensus statement generated by a panel of experts applying the Delphi method, favoured the epileptogenic hypothesis and recommended treatment of SLEs with antiepileptic drugs, irrespective if the patient presented with a seizure or epileptiform discharges on electroencephalography (EEG) or not. We disagree with this general procedure and provide the following arguments against the epileptogenic hypothesis: 1. not each SLE is associated with seizures. 2. epileptiform discharges may be absent on EEG during a SLE. 3. SLLs are not restricted to the cortex. 4. antiseizure-drugs (ASDs) may not prevent the progression or recurrence of a SLL. 5. ASDs may terminate seizures but no other phenotypic feature of a SLE. 6. patients already under ASDs are not immune from developing a SLL. 7. SLLs usually last longer than seizures. 8. no animal model supports the epileptogenic hypothesis. The strongest arguments for the metabolic hypothesis are that SLLs are not confined to a vascular territory, that the oxygen-extraction fraction within a SLL is reduced, and that there is hypometabolism within a SLL on FDG-PET. SLLs may respond to antioxidants, NO-precursors, steroids, or the ketogenic diet. ASDs should be applied only if there is clinical or electrophysiological evidence of seizure-activity.
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PMID:The metabolic hypothesis is more likely than the epileptogenic hypothesis to explain stroke-like lesions. 0

Giant cell arteritis (GCA) is a rare form of large and medium vessel vasculitis affecting about 20 cases per 100,000 persons older than the age of 50 years. GCA results in inflammation and constriction of the temporal arteries, cranial arteries, the aorta, and its major branches. Patients often present with vague constitutional symptoms and fever of unknown origin. GCA is a medical emergency requiring prompt diagnosis and early treatment with glucocorticoids which is essential to avoid irreversible end organ damage such as loss of vision, stroke and aneurysm formation. We report a case of a 63-year-old male patient presenting to our healthcare facility with sudden loss of vision and an ischemic brain infarct to be finally diagnosed as a case of giant cell arteritis with positron emission tomography-computed tomography imaging used to evaluate the full extent of the involved vasculature. Diagnostic imaging with FDG positron emission tomography-computed tomography can play a crucial role in the diagnosis, evaluation of the full burden of the disease and follow up to the response of therapy.
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PMID:Large vessel vasculitis and the rising role of FDG PET-CT: A case report and review of literature. 3296 62

Carotid atherosclerotic plaques represent a risk for ischemic stroke. The data indicate that the risk for distal embolization from atherosclerotic lesions in internal carotid arteries is not related only to the degree of stenosis but also to the composition of plaques. The stability of atherosclerotic plaque depends on the thickness of the fibrous cap and plaque hemorrhage. Recent research indicated that the inflammatory activity of atherosclerotic lesions is pivotal in the progression of atherosclerotic plaques. It also promotes the development of unstable atherosclerotic lesions and is related to thromboembolic cerebrovascular complications. Inflammation destabilizes atherosclerotic plaques through the degradation of their fibrotic structure. Inflammation of atherosclerotic plaques was confirmed by histopathologic findings and levels of circulating inflammatory markers which were correlated to the intensity of the inflammation in atherosclerotic lesions. Recently, new techniques like fluorodeoxyglucose positron emission tomography (18-FDG PET) were developed for the identification of inflammation of atherosclerotic lesions in the vessel wall in vivo. Systemic inflammatory markers, particularly interleukins, tumor necrosis factor-alpha and metalloproteinases were shown to be related to the intensity of the inflammatory process in atherosclerotic lesions and the cerebrovascular events. Identification of inflamed atherosclerotic plaques may help to identify unstable atherosclerotic lesions and subjects at high risk for cerebrovascular incidents who need intensive preventive measures including anti-inflammatory medication.
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PMID:Inflammation of carotid plaques and risk of cerebrovascular events. 3317 13


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