Incomplete Brain Infarction (original) (raw)
Related papers
SPECT and MRI in posterior cerebral artery infarction and related visual field defects
Journal of Nuclear Medicine, 1993
nation disclosed a dense left homonymous hemianopia and slightlyhesitant gait. A serologicaltest for syphilis, urine analysis, complete blood count, sedimentation rate, antinuclear antibody, B12, folate and Lyme titer were all within normal limits or negative. Rheumatoid factor and anti-cardiolipin antibod ies were normal. Electrolytes were within normal limits exceptfora slightincrease inglucose to 146mg/dl.Thyroid function and liver function tests were within normal limits except for a slight elevation in gamma-glutaryltransferase to 62. EEG showed asymmetric slowing of the alpha rhythm on the right. Carotid ultrasonography and transc ranial doppler studies were normal. Neuro-ophthalmologic examination on October 29, 1991 recorded a visual acuity of 20/20 bilaterally. There was a dense left homonymous hemianopia and 1+ temporal pal br on the left optic nerveheadwith a mild left afferent pupillary defect. On December 17, 1991, the patient was seen in the cognitiveneurologyclinic. Psychomotor retardationand sadness were indicativeof hiscontinueddepression. The examinationwas significantfor perceptually-relatederrors in describing the colors of complex pictures despite normal color naming and color matching. He also demonstrated impairedvisualmemoryfor simpledesigns andthe inabil ity to recognizeandlearnnew faces,althoughhe had no difficulty recognizing and naming geometric shapes and black-and-white line drawings. The patient also com plained of becoming lost in relatively familiarlocations. MRI on June 6, 1991 disclosed an area of low intensity onprotonimages andhighintensity onT2-weighted images in the right PCA distribution with mild dilatation of the posterior horn of the ventricle adjacent to this area (Fig. . This abnormalitywas consistent with a large right posterior temporal-occipital lobe infarction. The lesion ex tended to the medial temporal lobe adjacent to the pons . Also, subtle white matter lesions were noted in the vicinity of the occipital horn of the left lateral ventricle . On November 7, 1991, a SPEC!' scan of the brain was acquiredwith a dedicatedtriple-headedsystem(Prism 3000, Picker International Inc., Cleveland, OH) 1 hr after A 48-yr-oldright-handed malewith a historyof hyper tensionand depression was evaluatedfor complaintsof â€oesnow blindness― anddifficultyrecognizing familiarfaces (prosopagnosia).
Confirmation of CT Criteria to Distinguish Pathophysiologic Subtypes of Cerebral Infarction
American Journal of Neuroradiology
To determine whether cerebral infarctions classified as embolic or hemodynamic by their appearance on CT scans reflect distinct pathophysiologic entities. METHODS: Cerebral infarctions were retrospectively classified into two groups according to their morphologic appearance on CT scans: territorial infarctions and watershed, or terminal supply area, infarctions. Specific CO 2 reactivity for both groups of patients was determined with the xenon-133 method and 32 stationary detectors. Twenty-one patients with unilateral, supratentorial, ischemic cerebral infarctions were selected. CT findings were highly suggestive of a territorial infarction in 14 patients (mean age, 56 years) and of a watershed infarction in seven patients (mean age, 52 years).
Acute Cardioembolic Cerebral Infarction: Answers to Clinical Questions
Current Cardiology Reviews, 2012
Cardioembolic cerebral infarction (CI) is the most severe subtype of ischaemic stroke but some clinical aspects of this condition are still unclear. This article provides the reader with an overview and update of relevant aspects related to clinical features, specific cardiac disorders and prognosis of CI. CI accounts for 14 30% of ischemic strokes; patients with CI are prone to early and long-term stroke recurrence, although recurrences may be preventable by appropriate treatment during the acute phase and strict control at follow-up. Certain clinical features are suggestive of CI, including sudden onset to maximal deficit, decreased level of consciousness at onset, Wernicke's aphasia or global aphasia without hemiparesis, a Valsalva manoeuvre at the time of stroke onset, and co-occurrence of cerebral and systemic emboli. Lacunar clinical presentations, a lacunar infarct and especially multiple lacunar infarcts, make cardioembolic origin unlikely. The most common disorders associated with a high risk of cardioembolism include atrial fibrillation, recent myocardial infarction, mechanical prosthetic valve, dilated myocardiopathy and mitral rheumatic stenosis. Patent foramen ovale and complex atheromatosis of the aortic arch are potentially emerging sources of cardioembolic infarction. Mitral annular calcification can be a marker of complex aortic atheroma in stroke patients of unkown etiology. Transthoracic and transesophageal echocardiogram can disclose structural heart diseases. Paroxysmal atrial dysrhyhtmia can be detected by Holter monitoring. Magnetic resonance imaging, transcranial Doppler, and electrophysiological studies are useful to document the source of cardioembolism. In-hospital mortality in cardioembolic stroke (27.3%, in our series) is the highest as compared with other subtypes of cerebral infarction. Secondary prevention with anticoagulants should be started immediately if possible in patients at high risk for recurrent cardioembolic stroke in which contraindications, such as falls, poor compliance, uncontrolled epilepsy or gastrointestinal bleeding are absent. Dabigatran has been shown to be non-inferior to warfarin in the prevention of stroke or systemic embolism. All significant structural defects, such as atrial septal defects, vegetations on valve or severe aortic disease should be treated. Aspirin is recommended in stroke patients with a patent foramen ovale and indications of closure should be individualized. CI is an important topic in the frontier between cardiology and vascular neurology, occurs frequently in daily practice, has a high impact for patients, and health care systems and merits an update review of current clinical issues, advances and controversies.
Journal of Stroke and Cerebrovascular Diseases, 1992
The results of un enhanced computed tomography (CT) obtained in 105consecutive patients admitted with cerebral infarction were compared with the patients' clinical outcome and their Glasgow Outcome Scores upon discharge. Specific analysis of the findings in patients with early admission CT (within 12 h of onset) was carried out. The size of the infarction was calculated from delayed CT images (small ifIess than 50 mm 3 ; moderate if50-250 mm 3 ; large ifgreater than 250 mm'). Initial CT demonstration of the cerebral infarction was accomplished in 57 (54.3%) patients. Forty patients were studied early « 12 h) and, ofthese,20 (50%) showed abnormal admission CT. The size of the infarction correlated with its demonstration by admission CT. This correlation was found in all patients (p < 0.0001), as well as in those who had early CT (p = 0.015). Also, the size of the infarction correlated with the outcome of the patient (p < 0.001). The demonstration of the lesion by early CT, however, failed to correlate with the outcome of the patients. This finding, although at first surprising, is analogous to reports addressing the predictive value of other CT parameters.
Human cerebral infarct: a proposed histopathologic classification based on 137 cases
Acta Neuropathologica, 2004
We studied the microscopic features of 137 cases of human cerebral infarct. In each case, the age of the lesion was determined by measuring the time elapsed between initial clinical presentation and date of surgery or death. Multiple microscopic variables were analyzed on hematoxylin and eosin-stained sections. There were 104 (76%) male and 33 (24%) female patients with a median age of 64 years. The location of the infarcts included 129 cerebral, 5 cerebellar, and 1 each in the pons, midbrain and medulla. The age of the lesions ranged from 1 day to 53 years. All lesions were single and varied from lacunes to large infarcts in the distribution of one or more cerebral arteries. Key histologic features of the proposed classification are as follows: (1) phase of acute neuronal injury (11 cases studied), age 1-2 days, characterized by the presence of neuronal changes, and spongiosis of the neuropil and absence of neuronal ferrugination, chronic inflammation, macrophages, neo-vascularization and cavitation; (2) phase of organization subdivided into: (a) phase of acute inflammation (31 cases), age 3-37 days, characterized by coagulative necrosis, and frequent acute inflammation, and (b) phase of chronic inflammation (57 cases), age 10 days-53 years, characterized by the presence or absence of coagulative necrosis, neuronal injury, red neurons, macrophages, mononuclear inflammatory cells, perivascular cuffing, cavitation, gliosis, spheroids; absence of neutrophils; and (3) phase of resorption (38 cases), age 26 days-23 years, characterized by absence of an inflammatory response. Neuronophagia is not a feature of cerebral infarcts.
Computerized Tomography, 1977
Large confluent petechial hemorrhages and/or hemorrhage within infarcts may be seen on CT scan. Small petechial hemorrhages are not resolved by current equipment and techniques. Elevation of absorption values of an infarct following contrast media primarily occurs in the first month after onset, and may be occasionally confused with a tumor. Sequential CT changes in infarcts correlate well with established pathologic changes. Cerebral infarction may be seen on CT scan in some cases as early as 24-48 hr after its onset. Brain radiography Brain infarction diagnosis Cerebrovascular disease