Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 61-year-old woman with a history of photosensitive dermatitis and recurrent mouth ulcers presented with progressive weakness typical of amyotrophic lateral sclerosis (ALS), and subsequently underwent extensive neurologic and rheumatologic testing. We investigated whether ALS-like motor neuron disease associated with a positive antinuclear antibody (ANA) is really ALS or rather neuropsychiatric systemic lupus erythematosus (NPSLE). On neurologic evaluation, she had prominent bulbar involvement with dysarthria and dysphagia associated with profound lingual fasciculations and a denervating pattern on electromyogram. MRI showed no evidence of cerebral ischemia. Laboratory studies revealed a positive ANA (1:2560 titer), positive antiphospholipid antibodies (GPL and MPL), circulating lupus anticoagulant, and depressed C3 and C4. Repeat MRI studies at 4 and 11 mo revealed an evolving infarct in the paramedian pons consistent with the presence of NPSLE. Therapy was initiated with corticosteroids and intravenous cyclophosphamide, and the neurologic condition did not improve, but also did not progress inexorably as would be expected with ALS. NPSLE, presumably through the mechanism of ischemic vasculopathy, may present as motor neuron disease clinically indistinguishable from ALS.
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PMID:Neuropsychiatric systemic lupus erythematosus presenting as amyotrophic lateral sclerosis. 1190 83

Acute cerebral ischemic injury can be rapidly detected on diffusion-weighted images. The apparent diffusion coefficient (ADC) depends on the stage of cytotoxic edema and water content in the infarcted parenchyma. The purpose of this study is to determine the time course of ADC during the first days of ischemic stroke. These data should make it possible to distinguish between multiple stroke and a single progressive infarction. Eight patients with clinically diagnosed acute cerebral ischemia were examined by diffusion-weighted MRI from 2 to 20 h after onset of symptoms. Daily control scans were performed for up to 10 days. ADC values were analyzed from 55 MRI studies. Furthermore, ADC was measured in the tissue which showed a hyperintense signal at the first examination and in the contralateral tissue. White and gray matter were analyzed separately. Data were expressed as the ratio ADC (rADC) of lesion to control region of interest. All patients showed a uniform reduction in rADC from the first hours of stroke and decreasing to the 3rd day. The rADC increased again from the 4th day up to the point of pseudo-normalization on day 9. The gray matter showed a slightly faster increase than the white matter. rADC shows significant changes in the first days after stroke, following a rather uniform time course. Together with T2-weighted MRI this makes it possible to differentiate between hyperacute, acute, and chronic stroke. Furthermore, the age of an ischemia can be determined and multiple strokes can be distinguished from a single progressive stroke.
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PMID:Serial analysis of the apparent diffusion coefficient time course in human stroke. 1191 3

The presence of a thrombus on initial arteriography is directly related to the baseline NIHSS score. Magnetic resonance angiography (MRA) offers a noninvasive and rapid assessment of large cerebral vessel patency. We aimed at evaluating (1) the baseline NIHSS score as a tool for predicting the likelihood of an occluded artery on MRA and (2) the course of stroke within the first week according to the presence of a cerebral arterial occlusion. Patients were enrolled in this prospective study according to the following criteria: (1) acute cerebral ischemia with a neurological deficit lasting >1 h, and (2) brain MRI performed within 24 h of stroke onset. The NIHSS score assessment was performed on admission and at day 1 and day 7. The MRI protocol included: (1) T2-weighted Turbo spin echo, (2) echo-planar imaging isotropic diffusion, (3) T2*-gradient echo sequence, and (4) time of flight MRA (3D TOF Turbo MRA). The presence of a symptomatic cerebral arterial occlusion on MRA was systematically screened. Fifty-four patients were studied. Median age was 60 years. Mean time from stroke onset to NIHSS assessment was 170 +/- 95 min. The mean baseline NIHSS score was 13.5 +/- 7.3. The mean time from stroke onset to MRI was 384 +/- 171 min. MRA was readable in 50 cases. An arterial occlusion was detected in 23 patients (46%). The median baseline NIHSS score was significantly higher in the group of patients with occlusion than in the group of patients without occlusion (18 vs. 7, p = 0.01). The predictive probability to demonstrate an arterial occlusion was related to the baseline NIHSS score. None of the patients with an NIHSS score of 1-6 (11 patients) had visible occlusion, whereas 9 (43%) out of 21 patients with an NIHSS score of 7-15 and 14 (78% ) out of 18 patients with an NIHSS score above 16 had an arterial occlusion. For an increase by one point in the NIHSS score, the odds ratio for the presence of occlusion was 1.28 (95% CI: 1.11-1.46). The course of the stroke as assessed by follow-up NIHSS score was significantly more severe if an occlusion was detected. Median day 0, day 1 and day 7 NIHSS score were, respectively, 18, 16 and 13 in patients who had an occlusion versus 7, 4 and 0 in patients who had no visible occlusion (p < 0.01). A direct relation between the baseline NIHSS score and the likelihood of the presence of an occlusion on initial MRA is demonstrated. The presence of a cerebral arterial occlusion on MRA is significantly linked to a poor neurological outcome.
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PMID:Early detection of cerebral arterial occlusion on magnetic resonance angiography: predictive value of the baseline NIHSS score and impact on neurological outcome. 1201 45

The mouse is an excellent model for investigations of stroke and neural injury. However, there is a paucity of long term functional outcome measurements for the mouse. We, therefore, developed a sensorimotor functional test (corner test) and applied this test to a model of focal cerebral ischemia in the mouse. Male C57/6J mice (n=20) were subjected to embolic middle cerebral artery (MCA) occlusion. Reduction of cerebral blood flow (CBF) was measured by perfusion weighted MRI at 1 h after ischemia. The corner test, which is sensitive to chronic sensorimotor and postural symmetries, a general neurological test battery, and a foot fault test were performed between 2 and 90 days after ischemia. Infarct volume was measured at 90 days after ischemia. Multivariable analysis revealed that the corner test was highly predictive for infarct volume measured at 90 days after stroke, with R(2) values ranging from 0.73 to 0.93. The foot-fault test and neurological score did not detect chronic behavioral impairments. A significant (P<0.001) correlation between the infarct volume and the corner test was detected at 90 days after mild focal cerebral ischemia, whereas, there was no correlation between the infarct volume and neurological score or foot-fault. The data demonstrate that the corner test is a sensitive and objective test, which can be applied to evaluate long term functional outcome after stroke in the mouse.
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PMID:A test for detecting long-term sensorimotor dysfunction in the mouse after focal cerebral ischemia. 1210 Sep 87

Cerebral blood volume (CBV) provides information complementary to that of cerebral blood flow in cerebral ischemia, tumors, and other conditions. We have developed an alternative theory and method for measuring CBV based on dynamic imaging by MRI or CT during a short contrast infusion. This method avoids several limitations of traditional approaches that involve waiting for steady state or measuring the area under the curve (AUC) during bolus contrast injection. Anesthetized dogs were studied by T2*-weighted echo planar imaging during gadolinium-DTPA infusions lasting 30-60 sec. CBV was calculated from the ratio of the signal changes in tissue and artery. Method responsiveness was compared to AUC measurements using the vasodilator acepromazine. The ratio of signal change in tissue to that in artery rapidly approached an asymptotic value even while the amount of contrast in artery continued to increase. Using 30-sec infusions, the mean (+/- SD) of CBV for control animals was 3.6 +/- 0.9 ml blood/100 g tissue in gray matter and 2.3 +/- 0.8 ml blood/100 g tissue in white matter (ratio = 1.6). Acepromazine increased CBV to 5.7 +/- 1.5 ml blood/100 g tissue in gray matter and 3.1 +/- 0.8 ml blood/100 g tissue in white matter (ratio = 2.0). AUC measurements after bolus injection yielded similar values for control animals but failed to demonstrate any change after acepromazine. It is possible to measure CBV using dynamic MRI or CT during 30-60-sec contrast infusions. This method may be more sensitive to changes in CBV than traditional AUC methods.
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PMID:Cerebral blood volume measurements by rapid contrast infusion and T2*-weighted echo planar MRI. 1211 61

Cerebral ischemia provokes tissue damage by two major patho-physiological mechanisms. Direct cell necrosis is induced by diminished access of neurons and glia to essential nutrients such as glucose and oxygen leading to energy failure. A second factor of cellular loss is related to the activation of immune-competent cells within and around the primary infarct. While granulocytes and presumably monocytes are linked to the no-reflow phenomenon, activated microglia cells and monocytes can release cytotoxic substrates, which cause delayed cell death. As a consequence the infarct volume will increase, despite restoration of cerebral perfusion. In the past, visualization of immune competent cells was only possible by histological analysis of post-mortem tissue. However, contrast agents based on small particles of iron oxide are known to accumulate in organs rich in cells with phagocytotic function. These particles can be tracked in vivo by MRI methods based on their relaxation properties. In the present study, the spatio-temporal distribution of USPIO particles was monitored in a rat model of transient cerebral infarction using T1- and T2-weighted MRI sequences. USPIO were detected in vessels at 24 h after administration. At later time points specific accumulation of USPIO was observed within the infarcted hemisphere, with maximal signal enhancement on day 2. Their detectability based on T1-contrast disappeared between day 4 and day 7. Immuno-histochemically (IHC) stains confirmed the presence of macrophages, presumably blood-derived monocytes within areas of T1 signal enhancement. Direct visualization of iron-burdened macrophages by IHC was only possible later than day 3 after occlusion.
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PMID:In-vivo visualization of phagocytotic cells in rat brains after transient ischemia by USPIO. 1211 10

The aim of this survey is the characterization of the present value of multi-slice computed tomography (MSCT) for the assessment of hyperacute cerebral ischemia based on our experience and a review of the literature. MSCT is compared with single-slice CT (SSCT) as to the diagnostic value of standard cranial CT, CT angiography (CTA) and perfusion CT. CTA obtained with MSCT surpasses CTA obtained with SSCT. For perfusion CT, the value added by MSCT is small. With regard to standard cranial CT, MSCT and SSCT are considered equivalent. CTA and perfusion CT should be used in patients with acute stroke if the indication for thrombolysis is entertained but diffusion and perfusion weighted MRI cannot be carried out. This applies to both SSCT and MSCT. If advanced MRI and advanced CT are available, MRI continues to be the preferred imaging modality.
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PMID:[The value of multi-slice computed tomography for early diagnosis of focal cerebral ischemia]. 1222 65

We report a 78-year-old female presenting fluctuation of cerebral ischemic symptoms for a long time. Three weeks after transient ischemic attack of speech disturbance, she suffered right hemiparesis and motor dominant aphasia. The symptoms gradually progressed. Magnetic resonance angiography (MRA) showed a stenosis of branches of the left middle cerebral artery and single photon emission computed tomography (SPECT) did hypoperfusion of the same artery territory. Though antiplatelet and anticoagulant therapy was continued, the symptoms fluctuated. After 5 months, she recovered to mild deficit and MRI finally showed no responsible infarcted area. The pathophysiology of this course was considered to be progressing stroke based on a stenosis of the middle cerebral artery and the atrial fibrillation. Early diagnosis and treatment for cerebral ischemia may lead to the recovery from fluctuating symptoms.
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PMID:[A case of effective antithrombotic therapy for cerebral infarction presenting long-lasting fluctuation of symptoms]. 1235 79

MRI assessment of diffusion changes in acute cerebral ischaemia necessitates analysis of the apparent diffusion coefficient (ADC). We used the concept of relative weighted mean ADC (rwmADC) to obtain an accurate estimate of the extent of infarcted tissue. We studied ten patient with of acute ischaemic stroke, using diffusion- and perfusion- weighted MRI. The rwmADC was used to calculate a corrected ADC-lesion volume (DLVR), which was compared with the diffusion-lesion volume (DLV), initial perfusion lesion volumes and the follow-up infarct volume on T2-weighted images. We looked at correlations between the MRI and clinical findings. DLVR was closest to the final infarct size and had the best clinicoradiological correlation (r=0.77). Weighting the mean ADC within the ischaemic and normal parenchyma can give a more correct estimate of the volume of infarcted brain parenchyma, thus improving the definition of the penumbra.
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PMID:Apparent diffusion coefficient mapping of infarcted tissue and the ischaemic penumbra in acute stroke. 1238 28

In vivo monitoring of stem cells after grafting is essential for a better understanding of their migrational dynamics and differentiation processes and of their regeneration potential. Migration of endogenous or grafted stem cells and neurons has been described in vertebrate brain, both under normal conditions from the subventricular zone along the rostral migratory stream and under pathophysiological conditions, such as degeneration or focal cerebral ischemia. Those studies, however, relied on invasive analysis of brain sections in combination with appropriate staining techniques. Here, we demonstrate the observation of cell migration under in vivo conditions, allowing the monitoring of the cell dynamics within individual animals, and for a prolonged time. Embryonic stem (ES) cells, constitutively expressing the GFP, were labeled by a lipofection procedure with a MRI contrast agent and implanted into rat brains. Focal cerebral ischemia had been induced 2 weeks before implantation of ES cells into the healthy, contralateral hemisphere. MRI at 78-microm isotropic spatial resolution permitted the observation of the implanted cells with high contrast against the host tissue, and was confirmed by GFP registration. During 3 weeks, cells migrated along the corpus callosum to the ventricular walls, and massively populated the borderzone of the damaged brain tissue on the hemisphere opposite to the implantation sites. Our results indicate that ES cells have high migrational dynamics, targeted to the cerebral lesion area. The imaging approach is ideally suited for the noninvasive observation of cell migration, engraftment, and morphological differentiation at high spatial and temporal resolution.
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PMID:Monitoring of implanted stem cell migration in vivo: a highly resolved in vivo magnetic resonance imaging investigation of experimental stroke in rat. 1244 55


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