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Cerebral blood flow determination within the first 8 hours of cerebral infarction using stable xenon-enhanced computed tomography.

Cerebral blood flow mapping with stable xenon-enhanced computed tomography (Xe/CT) was performed in conjunction with conventional computed tomography (CT) within the first 8 hours after the onset of symptoms in seven patients with cerebral infarction. Six patients had hemispheric infarctions, and one had a progressive brainstem infarction. Three patients with very low (less than 10 ml/100 g/min) blood flow in an anatomic area appropriate for the neurologic deficit had no clinical improvement by the time of discharge from the hospital; follow-up CT scans of these three patients confirmed infarction in the area of very low blood flow. Three patients with moderate blood flow reductions (15-45 ml/100 g/min) in the appropriate anatomic area had significant clinical improvement from their initial deficits and had normal follow-up CT scans. One patient studied 8 hours after stroke had increased blood flow (hyperemia) in the appropriate anatomic area and made no clinical recovery.

Aged↗

[A case of delayed cerebral infarction occurring in puerperium preceded by herpes zoster ophthalmicus in late pregnancy].

Delayed central neurological symptoms following herpes zoster ophthalmicus (HZO) such as "herpes zoster ophthalmicus and delayed contralateral hemiparesis" are considered to be due to ipsilateral intracranial vasculopathy. We experienced a rare case with cerebral infarction occurred in puerperium following HZO in late pregnancy. A healthy 30-year-old woman had left HZO at weeks 35 of gestation. She was given acyclovir (ACV) for external use and improved with small pigmentation on the left eye-lid. Seven weeks after the onset of HZO, she suddenly developed aphasia and right hemiparesis. Cerebral angiogram showed narrowing on M 1 segment of the ipsilateral middle cerebral artery. The occlusion was seen on peripheral portion of the angular artery on the same side. In cerebrospinal fluid (CSF), cell count was slightly elevated, but concentration of protein and sugar were normal. Varicella-zoster titer was increased in both serum and CSF. She was treated with intravenous ACV (1500 mg/day) for 10 days. On the next day after the treatment, the cell count was normalized and on 18th day, varicella-zoster titer was decreased in CSF. Higher brain function improved and no relapses occurred. This is a first case of delayed cerebral infarction occurring in puerperium preceded by herpes zoster ophthalmicus in late pregnancy, as far as we searched. We should treat carefully pregnant or lactating patients with HZO, considering delayed cerebral infarction.

Acyclovir↗

Correlations between proton nuclear magnetic resonance imaging and retrospective histochemical images in experimental cerebral infarction.

Evaluation of ischemic brain injury in experimental cerebral infarction in gerbils and rats was performed by means of both proton nuclear magnetic resonance imaging ([1H]NMR-CT) and various histochemical analyses. In vivo nuclear magnetic resonance (NMR) imaging was carried out employing saturation recovery, inversion recovery, and spin echo pulse sequences. Spatial resolution of the images was excellent. The ischemic lesions were detected with a remarkable contrast in inversion recovery and spin echo images within a few hours after insult. Those changes in NMR images consistently corresponded with the various retrospective histochemical observations, especially with methods related to brain edema (K+ staining) rather than structural (enzymatic) studies. Calculated T1 and T2 relaxation times indicated the evolution of the edema state in the brain in situ. They correlated excellently with the retrospective water content measurement. As a result, detailed characterization of the edema state induced by cerebral ischemia was possible in vivo using [1H]NMR imaging.

Adenosine Triphosphatases↗

Improved image quality and detection of acute cerebral infarction with PROPELLER diffusion-weighted MR imaging.

PURPOSE: To compare periodically rotated overlapping parallel lines with enhanced reconstruction (PROPELLER) multishot fast spin-echo diffusion-weighted magnetic resonance (MR) imaging with single-shot echo-planar diffusion-weighted MR imaging for image quality and visualization of acute cerebral infarction. MATERIALS AND METHODS: Seventy subjects (35 men, 35 women; mean age, 55 years +/- 24 [SD]) who were suspected of having acute cerebral infarction (symptom duration, 2.8 days +/- 2.7) underwent PROPELLER and echo-planar MR imaging (b = 1,000 sec/mm(2)). Two neuroradiologists compared unlabeled images for presence of artifacts, visualization of infarction, and their preference of images. Interobserver agreement and image comparison were assessed by using the kappa statistic and the chi(2) test, respectively. RESULTS: PROPELLER MR imaging reduced susceptibility artifacts (n = 70 subjects), which limited visualization of temporal (echo-planar, n = 64; PROPELLER, n = 0; P <.01, chi(2) test), frontal (echo-planar, n = 58; PROPELLER, n = 1; P <.01), and parietal lobes (echo-planar, n = 5; PROPELLER, n = 0; P <.05) and cerebellum (echo-planar, n = 36; PROPELLER, n = 0; P <.01) and brainstem (echo-planar, n = 23; PROPELLER, n = 0; P <.01). Acute infarction (n = 31 subjects) was better demonstrated at PROPELLER MR imaging (PROPELLER better, n = 18; echo-planar better, n = 1; PROPELLER and echo-planar equal, n = 12; P <.01, chi(2) test). PROPELLER MR imaging was preferred in all (n = 70) but one case in which the lesion lay within the intersection gap (PROPELLER preferred, n = 69; echo-planar preferred, n = 1; P <.01, chi(2) test). CONCLUSION: With a short increase in imaging time, PROPELLER MR imaging offers better image quality and detection of acute cerebral infarction than does echo-planar MR imaging.

Acute Disease↗

Anticardiolipin response and its association with infections in young and middle-aged patients with cerebral infarction.

Antibodies binding to solid-phase cardiolipin (anticardiolipin antibodies, ACA), which are closely associated with lupus anticoagulant activity, have been found in patients with thrombosis. ACA are often seen also in patients after acute infections. To study further our recent observation on the association between infection and cerebral infarction in young and middle-aged patients we measured anticardiolipin response (IgG, IgM, IgA) in paired sera from 54 consecutive patients with cerebral infarction under 50 years of age and in 54 community controls matched for sex and age. An elevated IgG-class ACA level or a significant change in level as observed in 2 serial samples occurred in 15 (28%) patients, but in only 4 (7%) controls (P less than 0.02). These ACA levels were only slightly elevated, and there were no patients with levels approaching values commonly seen in lupus anticoagulant-positive patients. Neither were there any patients with systemic lupus erythematosus (SLE) as an underlying disease. The combination of IgG-class ACA positivity and preceding probable bacterial infection (based on clinical, cultural or serologic data) was found in 10 patients (18%) but in only 2 controls (4%) (P less than 0.05). There were no significant differences in IgM- or IgA-class ACA between the patients and their controls. These results suggest that IgG-class ACA response associated with preceding probable bacterial infection is more common in patients with cerebral infarction than in their community controls. However, slightly elevated ACA are probably only indirect indicators of preceding infection and not directly involved in the pathogenesis of thrombosis itself.

Adolescent↗

Neuroprotective effect of donepezil, a nicotinic acetylcholine-receptor activator, on cerebral infarction in rats.

This study evaluated the potential effect of donepezil, which is known as an acetylcholinesterase inhibitor used for treatment of Alzheimer's disease, against cerebral infarction induced by permanent left middle cerebral artery (MCA) occlusion. Donepezil was given orally in various regimens, prior to MCA occlusion in rats. Pretreatment with a single oral dose of donepezil (12 mg/kg), 2 h before ischemia, significantly attenuated cerebral infarction volume (165.5 +/- 105.3 vs. 377.1 +/- 48.5 mm(3); P < 0.05). These neuroprotective effects were prevented by coinjection with mecamylamine, a nicotinic acetylcholine-receptor (nAChR) antagonist, indicating that protection was mediated by nAChR activation.

Animals↗

A comparison of fast spin-echo, fluid-attenuated inversion-recovery, and diffusion-weighted MR imaging in the first 10 days after cerebral infarction.

BACKGROUND AND PURPOSE: Echo-planar diffusion-weighted and fluid-attenuated inversion-recovery (FLAIR) imaging have both proved valuable for detecting acute ischemic infarcts, but little is known about the value of diffusion-weighted imaging beyond the acute infarct period. Furthermore, no direct comparison of the techniques has been published. We compared the diagnostic utility of diffusion-weighted, FLAIR, and T2-weighted fast spin-echo (FSE) imaging for detecting cerebral infarctions up to 10 days old. METHODS: FSE, FLAIR, and diffusion-weighted MR sequences were obtained prospectively over a 6-month period in 212 patients with suspected cerebral infarctions. Seventy patients with nonhemorrhagic ischemic infarcts less than 10 days old whose symptoms lasted longer than 48 hours were identified. The three sequences were compared for detectability and conspicuity of abnormalities that correlated with the neurologic deficit. RESULTS: Seventy-two symptomatic infarcts were found in the 70 patients. Diffusion-weighted imaging detected 70 (97%), FLAIR, 69 (96%), and FSE, 64 (89%) of the 72 lesions. Only the difference between diffusion-weighted and FSE imaging approached statistical significance. There was no difference in the number of lesions detected in the patients imaged 48 hours or more after infarction. Lesion conspicuity on diffusion-weighted images was judged superior to that on FSE and FLAIR images in 55 (77%) and 47 (67%) of the cases, respectively. FLAIR images were judged superior to FSE in 34 (48%) of the cases. CONCLUSION: Diffusion-weighted images showed more infarcts than FLAIR and FSE images, and FLAIR images showed more than FSE images, but the differences were not statistically significant. Lesion conspicuity, however, was consistently better on diffusion-weighted images than on either FLAIR or FSE images throughout the 10-day period. Acquisition of diffusion-weighted images in the late acute and subacute periods after ischemic cerebral infarction appears to be beneficial.

Acute Disease↗

[MR diffusion-weighted imaging of cerebral infarction].

MR diffusion-weighted imaging was performed to investigate changes in water diffusion in patients with cerebral infarction, and diffusion-weighted images (DWI) were compared with T2-weighted images (T2WI). Acute and subacute infarcts were seen as areas of high intensity on DWI and showed lower apparent diffusion coefficients (ADCs), while chronic infarcts showed a relative increase in ADCs. The relative ADC increased progressively over time, becoming renormalized at 3 to 4 weeks, and was elevated in the chronic state. On DWI, infarcts as small as 5 to 6 mm in diameter and lesions adjacent to the ventricular or subarachnoid space could be readily identified. DWI was useful for distinguishing acute lesions from chronic lesions in patients with multiple cerebral infarction, and provided valuable pathophysiologic information on the course of ischemic stroke evolution.

Aged↗

Cerebral infarction: shortcomings of angiography in the evaluation of intracranial cerebrovascular disease in 25 cases.

We studied the utility and limitations of conventional cerebral angiography in 25 patients with cerebral infarction unassociated with extracranial cerebrovascular disease during a 7-year period. In only one-third of cases was the angiogram diagnostic, and in a single case it altered the pre-angiogram diagnosis by revealing a previously unsuspected embolus. Among the cases clinically diagnosed as cerebral emboli, the 2 confirmatory angiograms were performed early (within 48 hours), and demonstrated medium-large or large vessel filling defects. Two-thirds of the negative angiograms in the embolic clinical category were delayed, but there was no statistically relevant predilection for specific vessel size involvement. The category, primary cerebral vasculopathy, comprised the largest group, 10 in all, and one-half had angiographic confirmation despite time delays. Angiographic recognition was dependent on a characteristic picture of vascular involvement, and not on timing or vessel size predilection. Mitral valve prolapse figured prominently in the clinical cases of vasculopathy of uncertain etiology, which contained a total of 4 cases. The 3 cases with nondiagnostic angiograms were all delayed and demonstrated nonspecific radiographic changes. Clinically, these cases demonstrated signs or symptoms of autoimmune dysfunction, raising the specter of primary cerebral vasculopathy as a cause of cerebral infarction, in contrast to recurrent cerebral emboli.

Adult↗

Cerebral infarction does not occur typically at night.

In a hospital-based series of 66 consecutive patients with non-progressive cerebral infarction, the time of onset and the type of infarction on computed tomography were studied retrospectively. Forty-six (78%) patients suffered cerebral infarction between 6 am and 6 pm. Only five patients (8%) had their infarct between midnight and 6 am. Only three patients had a watershed-infarct, and these occurred during the daytime. Our results do not support the belief that atherothrombotic brain infarction is largely determined by haemodynamic factors.

Cerebral Arteries↗

The arterial patterns associated with internal carotid disease and cerebral infarcts.

In 20 necropsies with 15 stenosed and 17 thrombotic occluded internal carotid arteries there were 46 cerebral infarcts larger than 1 cm diameter. Using portmortem arteriographic and pathological techniques the patterns of the neck and brain artery systems were correlated with the situation and extent of the brain infarcts. Massive infarcts involving two major cerebral artery territories were associated with distal internal carotid artery occlusion and grossly ineffective cervical and circle of Willis anastomoses. Isolated middle cerebral artery territory infarcts were associated with internal carotid occlusion or stenosis and impairment of the circle of Willis anastomoses, perhaps with middle cerebral artery stenosis. The pattern of adequate size arteries determined if these infarcts were total, deep central, anterior, medium or posterior partial territory infarcts. Boundary zone infarcts were associated with internal carotid artery disease and limitation of anterior or posterior circle of Willis anastomoses. These limitations determined which boundary zones were affected. Isolated anterior cerebral artery territory infarcts were associated with bilateral internal carotid disease and an anterior cerebral artery stenosis or small caliber anterior communicating artery. Isolated posterior cerebral artery territory infarcts were associated with internal carotid disease and a direct impairment of the ipsilateral posterior cerebral artery capability.

Adult↗

Clinical features and treatment response of patients with major depression and silent cerebral infarction.

Previously, we reported a relationship between silent cerebral infarction (SCI), as detected by magnetic resonance imaging (MRI), and late onset major depression. In the present study, we clarify the clinical features of the depressive phase of patients with major depression and SCI, and their response to antidepressant pharmacotherapy. Using clinical charts, we retrospectively examined patients with depression, who were first admitted for antidepressant pharmacotherapy. All patients were classified according to the MRI findings and the age on admission (older or younger than 50 years) into either the young SCI(-) group (n = 23), the elderly SCI(-) group (n = 27) or the elderly SCI(+) group (n = 20).The characteristics of the clinical features were evaluated at the time of admission, after 2 weeks of treatment and at the time of discharge using the Hamilton rating scale for depression (HAMD). These data were compared between each patient group. No differences in the clinical features, as evaluated by HAMD, were observed between the three groups at the time of admission. However, the mean length of treatment was significantly longer and the treatment response, as evaluated by the total HAMD score, was significantly worse in the elderly SCI(+) group than in the other two groups, when examined after 2 weeks of treatment and at the time of discharge. The elderly SCI(+) group demonstrated higher scores in feelings of guilt, suicide, retardation and hypochondriasis than the young SCI(-) group and the elderly SCI(-) group after two weeks of treatment, and higher scores in early insomnia, late insomnia, somatic anxiety and hypochondriasis at the time of discharge. Our findings suggest that while the presence of SCI does not affect the clinical features observed at the time of admission, it does affect the treatment response to antidepressant pharmacotherapy.

Adult↗

Recurrent cerebral infarction during anticoagulation therapy in patients with mitral valve prolapse.

Mitral valve prolapse has been associated with an increased risk of transient or lasting ischemic events. Recurrence is uncommon after initiation of antiplatelet or anticoagulant therapy. In this communication we report two patients, both female, who had mitral valve prolapse as the major risk factor for cerebrovascular disease and who developed cerebral infarction despite anticoagulation. The cerebral infarctions were bilateral and extensive in one patient and led to the patient's death. In the second case, three infarctions resulted in moderate disability.

Adult↗

[Clinical evaluation of the diagnosis of neuronal reversibility with acute cerebral infarction using ADC by diffusion weighted echo planar imaging].

The possibility of diagnosing neuronal reversibility with acute cerebral infarction was studied using ADC measured by diffusion weighted imaging (DWI). The subjects were eleven patients who underwent DWI within 24 hours of onset. The area of abnormal signal on DWI during the acute stage was visually compared with that on T2-WI in the subacute phase. ADC was calculated in the two different abnormal areas on DWI, which were differentiated by the presence or absence of abnormality on T2-WI in the subacute phase. The abnormal signals of three cases showed an obviously narrowed area on DWI in the acute phase compared with the abnormality on T2-WI in the sub-acute phase. ADCs of the ischemic areas in DWI abnormalities that showed no abnormality on subacute T2-WI were slightly higher than those of the infarct areas with remaining abnormal signals on T2-WI. However, no statistically significant difference was found between these two regions, because there were large variations within each pixel. We considered that the diagnosis of neuronal reversibility in acute cerebral infarction was difficult using ADC values only and that other parameters such as perfusion or blood volume will be necessary to improve diagnostic quality prior to determining therapy.

Acute Disease↗

Cerebral infarction and release of platelet thromboxane after subarachnoid hemorrhage.

Platelet aggregation induced by adenosine diphosphate and the release of thromboxane B2 were studied in 68 patients with subarachnoid hemorrhage during the second week after the hemorrhage, when delayed ischemic deterioration most often occurs. Follow-up computed tomographic scans were performed later than 1 month after subarachnoid hemorrhage to reveal permanent hypodense areas consistent with cerebral infarction. Occurrence of hypodense lesions on the follow-up computed tomographic scan was significantly associated with the presence of delayed ischemic deterioration (DID) (P less than 0.01). Patients with subcortical or cortical cerebral infarctions due to DID released more platelet thromboxane B2 than those with no evidence of a hypodense lesion on the computed tomographic scan (P less than 0.05). Hypodense areas caused by an intracerebral hematoma or small, deep-seated infarcts due to DID were not associated with significantly elevated release of thromboxane B2, but the lacunar type infarcts were associated with increased aggregation of platelets. The results suggest that augmented platelet function may be involved in the pathogenesis of cerebral infarction due to DID.

Adult↗

Cerebral infarction in sickle cell trait.

Sickle cell disease is known to predispose patients to the risk of cerebral infarction. However, only scattered reports exist of the neurological sequelae of the sickle cell trait. Only 8 cases are reported in the English literature, in some of which the sickle cell trait was not documented by hemoglobin electrophoresis. This report describes 2 men, age 35 and 24 years, who developed acute cerebral infarction. Investigation revealed no apparent cause for the lesion other than the sickle cell trait.

Adult↗

Postmortem MR imaging of lobar cerebral infarction with pathologic and in vivo correlation.

Postmortem magnetic resonance (MR) imaging features of different types of lobar cerebral infarction are correlated with the findings in gross and histologic specimens. The postmortem findings are also correlated with in vivo findings in similar cases selected from teaching files. In acute infarction, white matter vasogenic edema leads to high signal intensity on T2-weighted images and blurring of the gray-white matter junction. Petechial hemorrhage in the cortex results in inhomogeneous signal intensity on T2-weighted images. In laminar necrosis, the hyperintense cortex on T1-weighted images is due not to hemorrhage but possibly to necrosis and the presence of lipid-laden macrophages. In subacute infarction, cortical edema and necrosis may cause the gyral pattern of enhancement. Meningeal inflammation and early fibrosis are probably responsible for meningeal enhancement. In chronic infarction, gliosis and cystic malacia are responsible for the increased signal intensity of white matter on T2-weighted images. Knowledge of the pathologic features of cerebral infarction helps in understanding the MR imaging findings.

Acute Disease↗

Asymptomatic cerebral infarction in patients with chronic atrial fibrillation.

A retrospective analysis of 54 patients with atrial fibrillation presenting with symptoms of cerebral ischemia between 1980 and 1985 was performed. Seven patients (13%) had computed tomographic evidence of previous, clinically silent cerebral infarction. In a control group of 168 persons (studied prospectively) in sinus rhythm presenting with symptoms of cerebral ischemia, seven (4%) had computed tomographic evidence of previous, clinically silent cerebral infarction (p less than 0.05). In those patients with atrial fibrillation all infarcts were peripheral and consistent with embolism, while in three of the seven patients in sinus rhythm the asymptomatic infarcts were lacunes.

Atrial Fibrillation↗