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[The effect of mannitol in preventing the development of cerebral infarction--an electron microscopical investigation (author's transl)].

We have undertaken an electron microscopical investigation of the effects of mannitol on the development of cerebral infarction using an experimental model for thalamic infarction in dogs. 1) It was found that administration of 20% mannitol (2 g/kg) prior to arterial occlusion had significantly suppressive effects upon the formation of cerebral infarction following occlusion. 2) In the control group, only one animal with 30 minutes occlusion showed no pathological changes, but, in the mannitol group, dogs with normal brain tissue were seen even after 120 minutes occlusion. 3) All of the control animals with 60 minutes occlusion showed nerve cell shrinkage, but none of the mannitol treated animals showed such changes. 4) After 180 minutes of arterial occlusion, no notable differences were found between the control and mannitol groups. In one of the mannitol treated animals, cerebral infarction was more severe than in the control group.

Animals↗

Visualization of blood-brain barrier disruption on MR images of cats with acute cerebral infarction: value of administering a high dose of contrast material.

OBJECTIVE: The detection of blood-brain barrier disruption in patients with cerebral infarction by means of contrast-enhanced MR images improves the specificity of diagnosis, enables lesion dating, and on occasion improves lesion detection. Accordingly, we performed a study to determine the extent of visualization of disruption of the blood-brain barrier on contrast-enhanced MR images, with specific attention to contrast dose, in a cat model of acute cerebral infarction. We used doses of 0.1 and 0.3 mmol/kg of a gadolinium chelate, gadoteridol, which is characterized by extracellular distribution and renal excretion, and was approved by the Food and Drug Administration for clinical use at these doses. MATERIALS AND METHODS: Blood flow in the middle cerebral artery was occluded unilaterally in seven cats for 1 hr, followed by 4 hr of reperfusion. T2- and T1-weighted MR images were obtained before the injection of contrast material. After injection, the time course of enhancement was observed for 1 hr by repeated sequential acquisition of T1-weighted images. Five cats received an initial injection of 0.1 mmol/kg of contrast material, supplemented 33 min later by 0.2 mmol/kg (cumulative dose, 0.3 mmol/kg). Two cats received a single injection of contrast material, either 0.1 or 0.3 mmol/kg. The images were reviewed in a prospective fashion by a single observer, who was blinded to the dose of contrast material and the timing of image acquisition, in order to detect abnormal contrast enhancement. Changes in single intensity were quantified by region-of-interest measurements. RESULTS: Enhancement at 4 and 13 min, respectively, after injection of contrast material was 25 +/- 10% and 38 +/- 7% with 0.1 mmol/kg, vs 80 +/- 12% and 100 +/- 15% with 0.3 mmol/kg (n = 5). The difference between doses was statistically significant (p < .002) for all time points. Abnormal contrast enhancement was visible in three of six cats that received 0.1 mmol/kg and in all cats that received 0.3 mmol/kg. By 13 min after injection, enhancement had peaked with a dose of 0.1 mmol/kg and was within 20% of maximum with a dose of 0.3 mmol/kg. CONCLUSION: Detection of disruption of the blood-brain barrier in acute cerebral infarction in cats is improved when high doses (0.3 mmol/kg) of contrast material are used. Disruption may not be visualized when 0.1 mmol/kg, the currently accepted standard dose, is used.

Animals↗

[Photochemically induced focal cerebral infarction in rat and its pathological observation].

Cerebral infarction in Wistar rats was induced by photochemical method. A photochemical reaction was produced by the photosensitive agent rose bengal under the effects of green light (560 +/- 60 nm). This reaction released free radicals which may damage the endothelium of cerebral vessels and induce platelet aggregation, and then may cause thrombosis in cerebral parenchymal vessels. There were typical changes of thrombosis and ischemic necrosis in the irradiated region of the cerebrum under light and electron microscopy. Serial pathologic findings suggested that the critical phase of progressive necrosis lies at the time of 1-6 hours after cerebral ischemia induced photochemically. Therefore, effective protection of the brain is important in the early stage of cerebral ischemia.

Animals↗

Topography of cerebral infarction associated with carotid artery dissection.

Because the pathogenesis of cerebral ischaemia in internal carotid artery dissection (ICAD) is controversial we studied the topography of cerebral infarction that results from ICAD according to pathophysiology of embolic and haemodynamic stroke. Sixty-four patients with 67 ICADs diagnosed by angiography, Doppler duplex sonography and magnetic resonance imaging (MRI) were studied prospectively during the past decade. According to current pathophysiological concepts, cortical territorial infarcts and large subcortical lenticulostriate infarcts revealed by CT or MRI were classified as embolic, while smaller infarcts in the subcortical junctional zone and infarcts in the cortical borderzone between the middle (MCA) and anterior cerebral artery were interpreted as haemodynamic infarcts. Of the 67 dissections 37 (55%) were associated with brain infarcts, of which territorial MCA infarcts of variable size accounted for 60%. These were combined with infarcts of the anterior and posterior cerebral artery in 5%; 8% of the patients had complete MCA infarction. Large lenticulostriate infarcts were present in 11%. Haemodynamic infarcts involved the subcortical junctional zone in 16% but never the anterior cortical borderzone. Although different abnormal Doppler findings indicated haemodynamically significant carotid obstruction in all symptomatic ICADs, only the characteristic high-resistance Doppler signal was significantly associated with the occurrence of brain infarction (in 66%, P < 0.01). The angiographic features of ICAD did not correlate with the incidence or with the topography of cerebral infarction. Patterns of infarction in ICAD indicate a predominantly embolic causation probably due to thrombus formation in the dissected carotid artery in the presence of severe haemodynamic obstruction, as demonstrated by Doppler sonography.

Adolescent↗

Frequency and patterns of abnormality detected by iodine-123 amine emission CT after cerebral infarction.

Single photon emission computed tomography (SPECT) was performed in 31 patients with cerebral infarction and 13 who had had transient ischemic attacks, using iodine-123-labeled N,N,N'-trimethyl-N'-(2-hydroxyl-3-methyl-5-iodobenzyl)-1,3-propanediamin e (I-123-HIPDM) as the radiopharmaceutical. SPECT scans were compared with computed tomographic (CT) scans. SPECT was as sensitive as CT in detecting cerebral infarction (94% vs. 84%). The abnormalities were larger on the SPECT scans than on the CT scans in 19 cases, equal in seven, and smaller in five (SPECT abnormalities greater than or equal to CT abnormalities in 86% of cases). Fifteen of 30 patients with hemispheric infarction had decreased perfusion (decreased uptake of I-123-HIPDM) to the cerebellar hemisphere contralateral to the cerebral hemisphere involved by the infarction (crossed cerebellar diaschisis). Nine of these 15 patients had major motor deficits, while only one of the 15 without crossed cerebellar diaschisis had a major motor deficit.

Cerebral Infarction↗

MR imaging of middle cerebral artery occlusion without cerebral infarction.

Magnetic resonance (MR) images of 12 patients with angiographically proven middle cerebral artery (MCA) occlusion were analyzed, retrospectively. In three of the 12 patients, cerebral infarctions related to the MCA occlusions were not evident. Two of the three patients were cases of atherosclerotic occlusion and the remaining patient had an acute thromboembolism. In all of the occluded M1 portions of the MCA the flow void was absent and there were isointense linear structures, with or without a hyperintense component in the Sylvian vallecula, on T1-weighted images. For nine of the 12 patients, the absence of flow void in the ipsilateral Sylvian fissure was evident on the T2-weighted images. Therefore, even in cases with no evidence of a cerebral infarction, the presence of flow void in the Sylvian vallecula and Sylvian fissure must be searched for in routine reviews of MR images. If MR imaging can be obtained on an emergency basis, appropriate interventional therapy may be immediately initiated.

Adult↗

[Analysis on the interaction among agents in arteriosclerotic cerebral infarction].

An 1:1 matched case-control study including 105 arteriosclerotic cerebral infarction cases and 105 controls was carried out to estimate the etiologic interaction, in Yi-xing city, March 1997. Results showed that the major risk factors were high levels of serum TG, Lp(a) and BMI while serum level of HDL-C was the only protective factor. When several levels were divided on Lp(a) and BMI, a significantly dose response relation was found. Considering the correlation among serum concentration of lipids, we analysed the interaction of different factors, using Log-Linear models. Results showed that there were significant interactions between arteriosclerotic cerebral infarction and TC, TG, HDL-C and Lp(a). There were also interactions between TC, TG, HDL-C and LDL-C. However, the strongest interaction is expected to happen at what level remains further investigations.

Aged↗

Effect of nicergoline on platelet aggregation, plasma viscosity and erythrocyte deformability in geriatric patients with cerebral infarction. Preliminary report.

The effects of nicergoline (Sermion) on platelet aggregation, plasma viscosity and erythrocyte deformability were evaluated in 11 geriatric patients with cerebral infarction, 2 men and 9 women (ages 61-78, mean age 71.6). Nicergoline was given orally at a dose of 5 mg 3 times daily after meals for 8 weeks. Hematological variables were determined twice prior to the administration and at 4 and 8 weeks after the administration. The platelet aggregation in vitro was determined by the turbidimetric method and the level of circulating platelet aggregates was determined according to the method of Wu-Hoak. Erythrocyte deformability was determined according to the method based on the examination of passing erythrocytes through a filter containing pores smaller than the undeformed cells. Collagen-, arachidonic acid- and PAF-induced platelet aggregation was decreased after nicergoline administration. Erythrocyte deformability was increased and plasma viscosity was also decreased after the administration. Thus the improvement of platelet aggregation, plasma viscosity and erythrocyte deformability in cerebral infarction may prevent disturbing blood flow and may contribute to prevention of formation and progression of thrombosis and atherosclerosis in geriatric patients with cerebral infarction.

Aged↗

Cerebral infarction in a young male following viper envenomation.

Neurological deficits can occur following viper bite. It is usually due to intracerebral or subarachnoid bleed as a result of depletion of clotting factors. A healthy 21-year old male developed motor aphasia and right hemiplegia within two hours of being bit by a viper. Brain CT scan revealed a left frontal lobe infarction. The possible mechanisms for cerebral infarction in this patient are hypotension, endothelial injury, hypercoagulability and vascular.

Adult↗

Cerebral infarction in an adult with disseminated varicella.

A 26-year-old patient with disseminated varicella developed a cerebral infarction 11 days into the illness. Cerebral infarction, typically delayed, is primarily reported in association with zoster with only one previous report in primary varicella. The mechanism is speculative and thrombosed vessels with and without vasculitis have been demonstrated. Our patient showed mild evidence of systemic alteration in immune function, suggesting the possibility of vasculitis.

Adult↗

[A case of agraphia due to cerebral infarction in the left parietal lobe].

A case of agraphia due to cerebral infarction in the left parietal lobe was reported. A 63-year-old right-handed man was admitted to our hospital with writing disturbance. His spontaneous speech was fluent, and object naming, word fluency, repetition, verbal comprehension, and reading were fully preserved. However, his writing was slow and required effort. He showed hesitation in spontaneous writing and dictation. His power to copy was better than his power to write spontaneously or to take dictation, but he had some difficulty in copying letters and complex figures. The patient showed abnormal sequences of strokes and completed his strokes by piecing out of several fragments. CT scan and MRI showed a cerebral infarction in the left parietal lobe which included the superior parietal lobule. The amytal (Wada) test, which was performed via the left internal carotid artery, revealed that the left hemisphere was dominant for language. The characteristics of his agraphia much more closely resembled "apractic agraphia", as reported by Alexander et al (1992), than spatial agraphia or pure agraphia. Agraphia in this patient might result partially from the loss or unavailability of the memory of motor patterns necessary for writing letters.

Agraphia↗

Serum neurone specific enolase (NSE) levels as an indicator of neuronal damage in patients with cerebral infarction.

A radioimmunoassay has been developed and used to measure serum neurone specific enolase (NSE) concentrations in 24 patients, following cerebral infarction. A significant correlation between cerebral infarct volume and maximum serum NSE concentration was observed (P = 0.047). Serum NSE was also assayed at times 24, 48, 72 and 96 h post ictus. At 72 h a significant correlation existed between serum NSE levels and infarct volume (P = 0.012), and levels appeared to be approaching statistical significance at 48 h (P = 0.067). No correlation existed at 24 and 96 h. In addition serum concentrations of NSE were compared to clinical outcome as determined by the Glasgow Outcome Score. Using the Mann-Whitney U test, there was no significant difference in maximum NSE level between patients graded 1-3 on the Glasgow Outcome Score and those graded 4 and 5. However, further studies are required on a larger population to more completely assess this. NSE may prove to be a useful marker of neuronal damage in the study of stroke, with particular application in the assessment of treatment.

Adult↗

Prolonged hyperglycemia in the early subacute period after cerebral infarction: effects on short term prognosis.

Although the adverse effect of admission hyperglycemia in cerebral infarction on prognosis is well known, studies generally have not questioned the effect of hyperglycemia in the early subacute period on prognosis after a stroke. Forty-six patients with acute ischemic stroke were seperated into 3 groups: Group 1) Known diabetes or admission blood glucose (ABG) > or = 140 mg/dl and HbA1c > or = 8,0%); Group 2) ABG > or = 140 mg/dl and HbA1c < 8,0%; and Group 3) ABG < 140 mg/dl and HbA1c < 8,0%. Blood glucose was followed-up 4 times a day for 10 days after the stroke and the mean of these measurements was calculated as the mean of glycemic regulation (MGR). Neurological evaluation was done at presentation and on day 10 and 30 with the National Institute of Health (NIH) scale. Oedema, lesion size and presence of hemorrhagic transformation were evaluated using CT. The MGR was significantly higher in group 1 compared to the other two groups (p < 0,001 and p < 0,01) and in group 2 compared to group 3 (p < 0,001). Patients with clinical worsening had a significantly higher MGR (p < 0,05). Patients with marked cerebral edema had a significantly higher MGR (p < 0,01) compared to patients with lesser edema. No correlation was found between MGR and lesion size or hemorrhagic transformation. Our results show that hyperglycemia in the early subacute period after cerebral infarction is associated with more pronounced cerebral edema and has an adverse effect on short term prognosis. We suggest that studies investigating the effect of insulin infusion on stroke prognosis should also consider infusions for a longer period than 24 hours.

Aged↗

Semiquantitative dynamic computed tomography to predict response to anti-platelet therapy in acute cerebral infarction.

We investigated whether dynamic computed tomography (CT) in patients with acute cerebral infarction could identify patients likely to respond to anti-platelet therapy. Seventy patients underwent semiquantitative dynamic CT within 6 h as well as cerebral angiography. All then received anti-platelet therapy with a thromboxane A2 synthetase inhibitor. Peak value (pv) and time-to-peak (tp) (time-density curves) for the Sylvian fissure were extracted from dynamic CT data and standardizing interpatient data, two indices, PV/TP index and TP index, were prepared following a standard semiquantitative manner. Both PV/TP index and TP index were effective in discriminating between 48 responders (modified Rankin scale (mRS): 0 to 2) and 22 non-responders (mRS: 3 to 5, or death: 6; both P<0.0001). High PV/TP index (>or=0.8) was a strong indicator of favorable response. Most of these patients maintained regional cerebral blood flow (rCBF) via anterograde flow or collaterals, with a TP index 1.1) and non-compensated rCBF. Intermediate PV/TP values could not predict outcome. Dynamic CT prior to therapy can identify patients with acute cerebral infarction who are treatable with anti-platelet therapy alone.

Acute Disease↗

[Why cerebral infarction is an emergency].

The three main criteria for a medical emergency: sudden onset, poor prognosis and possibility of an effective medical treatment apply to cerebral infarction which is the end result of a focal ischemia, occurring all the more rapidly than perfusion pressure is low. Studies devoted to experimental cerebral infarction as well as to thrombolysis in human have shown that the therapeutic window to save the penumbral tissue is very short, presently 3 hours in human for intra venous thrombolysis but with considerable individual variations best assessed by MRI diffusion-perfusion. Caring for the patient who has a cerebral infarction is an emergency because it is necessary, in the very first hours, to properly diagnose the infarct and its etiopathogenesis, to detect the vital manifestations to prevent the general complications, to start an antithrombotic treatment, to establish a vital and functional prognosis, to apply in due time the rare surgical or intra-arterial thrombolytic treatments and to start secondary prevention in patients with transient ischemic attacks.

Animals↗

Prediction of language and neurologic recovery after cerebral infarction with SPECT imaging using N-isopropyl-p-(I 123) iodoamphetamine.

Fourteen patients (10 with left-sided and 4 with right-sided cerebral infarction) were prospectively studied with single-photon emission computed tomography (SPECT) using N-isopropyl-p-(I 123) iodoamphetamine (IMP, SPECTamine) to determine its usefulness in predicting neurologic/language recovery after cerebral infarction. All neuro-SPECT imaging was performed within 30 days after infarction. Detailed assessment of neurologic and/or language recovery (after 3 months) was carried out prospectively in each patient. Patients with smaller volume IMP defects in the region of infarction demonstrated significantly better neurologic and language recovery than patients with large IMP defects. Analysis of the IMP "redistribution" phenomenon failed to demonstrate definitively a relationship with clinical recovery. It was concluded that the volume of the IMP defect can aid in predicting recovery potential after cerebral infarction.

Aged↗

Cocaine-induced ischemic cerebral infarction mistaken for a psychiatric syndrome.

We present the case of a 39-year-old woman who developed an ischemic cerebral infarction after using cocaine. Initially the patient was thought to suffer from a psychiatric disorder, and a computed tomography (CT) scan at the time of admission was entirely normal. Further evaluation of the patient by staff on the Psychiatric Unit led to the suspicion that she had suffered a stroke. A repeat CT scan on the third hospital day showed a large infarction in the left middle cerebral artery territory. We discuss the diagnosis of cerebral infarction with subtle presentations due to cocaine use.

Adult↗

Nitric oxide deficiency contributes to large cerebral infarct size.

The purpose of this study was to examine the role played by a deficit in nitric oxide (NO) in contributing to the large cerebral infarcts seen in hypertension. Cerebral infarction was produced in rats by occlusion of the middle cerebral artery (MCA). Studies were performed in Sprague-Dawley (SD) rats subjected to NO synthase blockade (N(G)-nitro-L-arginine [L-NNA], 20 mg x kg(-1) x d(-1) in drinking water) and in spontaneously hypertensive stroke-prone rats (SHRSP). NO released in the brain in response to MCA occlusion was monitored with a porphyrinic microsensor in Wistar-Kyoto rats. The increment in NO released with MCA occlusion was 1.31+/-0.05 micromol/L in L-NNA-treated rats, 1.25+/-0.04 micromol/L in SHRSP, 2. 24+/-0.07 micromol/L in control SD rats, and 2.25+/-0.06 micromol/L in Wistar-Kyoto rats (P<0.0001 for control versus the other groups). Infarct sizes in the L-NNA-treated and control SD rats were 8.50+/-0. 8% and 5.22+/-0.7% of the brain weights, respectively (P<0.05). The basilar arterial wall was significantly thicker in L-NNA-treated rats compared with their controls. We conclude that both the deficit in NO and the greater wall thickness contribute to the larger infarct size resulting from MCA occlusion in SHRSP and in L-NNA-treated rats compared with their respective controls.

Animals↗