[What was behind the brain infarctions?].
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Brain Infarction↗
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The Ginkgo biloba extract, EGb 761, fails to reduce brain infarct size in rats after transient, middle cerebral artery occlusion in conditions of unprevented, ischemia-induced fever.
There is much biochemical evidence, but very few studies in animal models of stroke in vivo, to suggest that Ginkgo biloba (EGb 761) may offer neuroprotection against regional, ischemic brain damage; additional investigations are needed to ensure future clinical trials. This study reports the effects of EGb 761 given acutely or chronically before ischemia. Rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h and the brain infarct size was assessed 24 h later. Dipyrone (100 mg/kg, i.p.) was injected 30 min before ischemia, and 2.5 and 5.5 h after ischemia, to reduce ischemia-induced fever. EGb 761 (Tebonin) was given acutely (200 mg/kg, p.o., 60 min before ischemia) or chronically (100 mg/kg, p.o., once daily, for 14 days before ischemia). Acute or chronic treatment with EGb 761, either alone or in combination with dipyrone, did not reduce the infarct size compared with saline alone (p > 0.05). Dipyrone failed to prevent ischemia-induced fever during the intra-ischemic period (p > 0.05 vs saline; p < 0.001 vs sham). In the reperfusion phase, dipyrone reduced fever to normothermic levels in the group treated acutely with EGb 761 (p < 0.01 vs saline, p > 0.05 vs sham) but not after chronic EGb 761 (p < 0.01 vs sham), indicating possible pharmacokinetic interaction. In conclusion, within the context of unprevented, ischemia-induced fever, the present results demonstrate that EGb 761 has no significant effect on brain infarct size.
Animals↗
Correlation between proto-oncogene, fibroblast growth factor and adaptive response in brain infarct.
Ischemia/hypoxia rapidly induce ischemic changes in vulnerable neurons: cortical neurons in layers II-III and V, hippocampal neurons, cerebellar Purkinje cells and certain basal ganglia and brainstem neurons. The ischemic changes are manifested histologically by nuclear pyknosis, cytoplasmic shrinkage and basophilia. These neurons exhibit strong and persistent expression of immediate early genes (IEGs): c-fos and c-jun. The onset of IEG expression is followed within a day by enhanced bFGF expression in non-ischemic neurons in the same general regions. The appearance of bFGF is followed within another day by proliferation of blood vessels, macrophages and glial cells around the infarct. The newly-formed blood vessels and macrophages migrate into the necrotic infarct aiming at disposal of the necrotic debris. The gliosis although concentrated around the infarct spreads to involve remote regions of both hemispheres. Based on the spatiotemporal correlation between cell proliferation and bFGF and the known mitogenic properties of bFGF, we believe that this molecule may be responsible for the late response in brain infarct including angiogenesis, gliosis and macrophage proliferation. The physiological roles of IEGs in the chain of adaptive response following brain infarction and its relationship with bFGF are subjects pending future investigations.
Adaptation, Physiological↗
Brain infarction in children with diabetic ketoacidosis.
During the last 10 years, five children were treated at Childrens Hospital Los Angeles for acute, persistent neurologic loss during diabetic ketoacidosis (DKA). Four were transferred from local hospitals after the neurologic crisis. Computed tomography (CT) studies showed one or more areas of brain infarction in each patient, and none had evidence of diffuse cerebral edema. As three of the five patients had been treated for cerebral edema before their CT, brain edema may have been present initially. Our findings emphasize the importance of brain infarction as a cause of persistent neurologic loss in children with DKA.
Cerebral Infarction↗
[Studies of the experimental brain infarction produced with lesion generator as a brain edema model (author's transl)].
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Animals↗
Renin-angiotensin-aldosterone system in brain infarction and vascular death.
The renin-angiotensin-aldosterone system has functions that may contribute to brain infarction (BI). In 459 matched pairs of white patients and control subjects, we measured plasma angiotensin-converting enzyme (ACE) levels, seven polymorphisms (angiotensinogen T174M and M235T, ACE I/D and 4656 2/3CT repeat [rpt], angiotensin II type 1 receptor A1166C and A153G, and aldosterone synthase CYP11B2), and evaluated 5-year poststroke mortality. Mean plasma ACE levels (+/-standard error) were significantly greater in patients than control subjects (37.5 +/- 0.9 vs 33.9 +/- 0.9), in patients with lacunar stroke, and in patients with no previous vascular (cerebrovascular or cardiovascular) history. The risk for BI increased with tertiles of plasma ACE, without an interaction with hypertension. After adjustments, the association disappeared except among patients with cardioembolic BI and those without previous vascular events. Among the polymorphisms, there was a weak association of BI with angiotensin II type 1 receptor 1166C, a weak protective effect with angiotensinogen 174M, and a strong association of angiotensinogen 235T with 5-year vascular mortality. These results suggest that renin-angiotensin-aldosterone system activity and genes contribute to cerebrovascular disease and poststroke vascular death in white patients.
Adolescent↗
Blood lipids in brain infarction subtypes.
BACKGROUND: Little is known about the relationship between hypercholesterolaemia and specific aetiological subtypes of brain infarction (BI). METHODS: In a cross-sectional study of 492 pairs of patients with a BI proven by MRI and matched hospital controls, we determined the blood levels of triglycerides, total, HDL and LDL cholesterol, and apolipoprotein A(1) and B, in the same centralized laboratory. We performed aetiological BI subtype classification. RESULTS: Except for triglycerides, the risk of BI increased continuously with the lipid levels, without any heterogeneity between the main BI subtypes or the group on lipid-lowering therapy. The adjusted odds ratio per standard deviation in LDL cholesterol (0.93 mmol/l) was 1.74 (95% confidence interval, 1.02-2.98) in atherothrombotic strokes (n = 109) and 2.71 (95% confidence interval, 1.60-4.55) in lacunar strokes (n = 105). Eighty percent of patients were above the ATP-III guideline threshold LDL cholesterol of 2.59 mmol/l (100 mg/dl), with a major contribution of both atherothrombotic and lacunar stroke subtypes to this group. CONCLUSIONS: These findings suggest that blood lipids, particularly total and LDL cholesterol levels, are associated with all subtypes of BI, and that LDL above 2.59 mmol/l is highly prevalent.
Aged↗
Changes of circadian blood pressure patterns and cardiovascular parameters indicate lateralization of sympathetic activation following hemispheric brain infarction.
The effects of left- and right-sided hemispheric brain infarction on variability in circadian blood pressure and cardiovascular measures were investigated in 35 patients to test for asymmetry of the sympathetic consequences of stroke. No significant differences regarding age, size of infarction or extent and frequency of damage to the insular cortex could be detected between the two groups. Patients with right-sided infarction showed a significantly reduced circadian blood pressure variability [diastolic: -1% (95% CI -4 to 1) vs -6% (-9 to -2); P < 0.05] and a higher frequency of nocturnal blood pressure increase (47% vs 35%; P < 0.05) as compared with patients with left-sided infarction. Right-sided infarction was also associated with higher serum noradrenaline concentrations [546 pg/ml (95% CI 415-677) vs 405 pg/ml (266-544); P < 0.05], and ECG more frequently showed QT prolongation (53% vs 35%; P < 0.05) and cardiac arrhythmias (67% vs 20%; P < 0.005). However, irrespective of the hemisphere damaged, patients with insular infarction showed the most pronounced changes of these parameters. In addition, two patients with right-sided strokes (13%) involving the insula, but none with a left-sided infarction, developed myocardial infarction. These findings suggest lateralization of sympathetic activation with right-sided dominance for sympathetic effects following hemispheric stroke.
Aged↗
Plasma lipids and lipoproteins in young patients with brain infarction.
Thirty-two patients aged 60 or less with brain infarction were examined with regard to possible changes in lipoprotein pattern as compared with a reference group. Except for a lower concentration of total lipids, cholesterol and high-density lipoproteins in the female patients, no difference was demonstrated in the two groups. In all patients a significant reduction in total lipids, cholesterol, triglyceride and all lipoproteins was demonstrated after the acute cerebrovascular accident presumedly due to the stress situation.
Adult↗
Extracorporeal double filtration plasmapheresis in acute atherothrombotic brain infarction caused by major artery occlusive lesion.
Extracorporeal double filtration plasmapheresis (EDFP) can quickly lower plasma viscosity and fibrinogen concentration. EDFP has the potential to improve cerebral microcirculation in acute ischemic stroke and ultimately to salvage penumbral tissue. However, no evidence is available to show that EDFP can increase cerebra blood flow (CBF). Therefore, we investigated whether EDFP could increase CBF by quantitative CBF measurements and documented the clinical effects of EDFP in acute ischemic stroke. EDFP was performed ten times in seven patients diagnosed as having acute atherothrombotic brain infarction caused by major artery occlusive lesion. They also fulfilled one of the following entry criteria: 1) diffusion/perfusion mismatch demonstrated by MRI on admission; 2) a hemispheric syndrome, but only a small lesion on diffusion weighted MRI (<25% of MCA territory); or 3) progressing stroke. Exclusion criteria were 1) contraindication of heparin or 2) spontaneous improvement of symptoms. Time from stroke onset to EDFP varied from 5 hr to 7 days. Plasma viscosity was quickly lowered by EDFP without affecting RBC counts, Hb, or Hct in all patients. Positron emission tomography (PET) with 15-O labeled H2O measurements revealed a significant CBF increase from 36.4 +/- 8.3 ml/100 g/min to 40.7 +/- 6.8 ml/100 g/min in the affected hemisphere (P=0.048). Definite CBF improvement was also demonstrated by single photon emission computed tomography (SPECT) in one of two patients who had severe stenosis of the middle cerebral artery. Furthermore, this patient showed remarkable improvement of hemiplegia immediately following EDFP (NIHSS score: 18 to 13). In conclusion, EDFP can increase CBF in ischemic brain tissue in acute atherothrombotic brain infarction. Further clinical studies should focus on the efficacy of EDFP on outcome of patients with this stroke subtype.
Aged↗
Carotid plaque texture analysis can predict the incidence of silent brain infarcts among patients undergoing carotid endarterectomy.
OBJECTIVE: To evaluate the correlation between microembolism (ME) and incidence of silent brain infarcts during carotid endarterectomy. MATERIALS AND METHODS: Patients were assessed using transcranial Doppler, carotid ultrasound and pre- and postoperative magnetic resonance imaging (MRIs). The clinical status, need for shunt insertion and significant decrease in the blood flow in the middle cerebral artery were recorded. All data were analysed using multivariate regression models. RESULTS: Out of the 76 patients examined, 17 (22%) had new postoperative lesions seen on MRI. Three of them (4%) were symptomatic, 14 (18%) were asymptomatic. The multivariate regression models showed that ME is a potent predictor of "silent" ischemic brain lesions, at p<0.001 (OR [95% CI]-1.1 [1.05, 1.2]). Digital plaque texture analysis predicted ME (p=0.028; OR [95% CI]-0.32 [0.12, 0.89]). The risk of ME increases steadily with the decrease in the echogenicity of the plaque. CONCLUSIONS: ME is a potent predictor of "silent" ischemic brain lesions among patients with carotid stenosis. An analysis of plaque texture can predict the degree of ME during endarterectomy and is more precise than the standard GSM.
Brain Infarction↗
Hyperhidrosis as a reflection of autonomic failure in patients with acute hemispheral brain infarction. An evaporimetric study.
BACKGROUND AND PURPOSE: Sweating dysfunction is one of the most frequently encountered symptoms of autonomic failure but has received scant attention in patients with cerebrovascular diseases. Our purpose was to evaluate the prevalence, pathogenesis, and clinical correlates of sweating dysfunction in stroke. METHODS: We studied sweating at baseline and after a heating stimulus in 53 patients with acute hemispheral brain infarction and in 40 healthy control subjects by using a quantitative evaporimetric method. RESULTS: Significant hyperhidrosis on the paretic side of the body was verified in 55% of the patients at baseline, in 74% after 5 minutes of heating, and in 77% after 10 minutes of heating. Hyperhidrosis was established throughout the body and correlated with the severity of paresis, the presence of reduced muscle tone, and the extensor plantar response. CONCLUSIONS: The phenomenon of hyperhidrosis in hemiparetic patients reflecting autonomic dysfunction seems to be a common manifestation that should be listed among the expected consequences of brain infarction. This sweating disturbance might be attributed to a lesion of a putative sympathoinhibitory pathway controlling sweating. The failure of this pathway could also be related to other manifestations of sympathetic hyperfunction, e.g., cardiac complications. Therefore, assessment of sweating may provide a new, important aspect in the evaluation of stroke patients.
Acute Disease↗
[Thrombolytic therapy of brain infarct: the end of beginning].
Thrombolysis by intravenous application of thrombolytic drugs may improve the outcome of patients with a brain infarct, but it also entails risks. The effect of recombinant tissue plasminogen activator (rtPA) was compared with placebo in three medium-sized randomized controlled clinical trials. One study, performed in North America, showed a clear benefit of rtPA administered within 3 hours after the onset of symptoms. Two European trials showed a less strong effect, but the number of patients who were independent after 3 months' follow-up was also larger after treatment with rtPA within 6 hours. A meta-analysis of all three trials demonstrates a significant advantage of rtPA over placebo for all the usual outcome measures, without significant excess mortality in the rtPA group. The chance of being able to live independently increases by about 8% after treatment with rtPA. In conclusion there is now sufficient evidence to start with thrombolytic treatment for cerebral infarcts in hospitals with a stroke unit, if a number of additional quality standards for the acute diagnosis and treatment of stroke patients are met.
Acute Disease↗
Decreased severity of brain infarct can in part explain the decreasing case fatality rate of stroke.
BACKGROUND AND PURPOSE: Case fatality rates for stroke has declined in most Western industrialized countries during recent decades. One possible explanation for this is a decrease in the severity of stroke symptoms. We therefore sought evidence for a change in stroke severity and its relationship with case fatality rates. METHODS: We compared the severity of symptoms among first-ever stroke patients in 2 population-based prospective stroke registers maintained during 1972 to 1973 and 1989 to 1991 in Finland. Patients who were evaluated by study assistants or the investigator during the first week after the onset of symptoms were included in the study, and their severity of symptoms was assessed with the use of comparable scales modified from the Scandinavian Stroke Scale. RESULTS: A total of 244 and 594 patients were registered, and a portion of them (155 [63.5%] and 360 [60.6%]) were included in the analyses in the registers for Espoo-Kauniainen from 1972 to 1973 and for 4 separate districts in Finland from 1989 to 1991, respectively. The death rates during the first week among those who were not included did not differ between the registers. The severity of symptoms decreased significantly between the registers in both patients with brain infarct or intracerebral hemorrhage but not in those with subarachnoid hemorrhage. The severity of symptoms was an independent factor of case fatality at 1 month. CONCLUSIONS: The severity of symptoms of brain infarcts has decreased and can in part explain the decreased case fatality rate of stroke in Finland. However, the change in patients with intracerebral hemorrhage may be overestimated due to undiagnosed intracerebral hemorrhages in the first register resulting from the lack of brain CT.
Aged↗
Serum cortisol and outcome of ischemic brain infarction.
The predictive value of serum cortisol level on the prognosis in acute brain infarction of the carotid circulation territory was studied in 101 patients younger than 70 years. The levels of 7 a.m. and 7 p.m. serum cortisol were measured initially and at 1 week. All patients underwent a computed cerebral tomography (CT) within 2 days of the onset of symptoms, and a second CT 3 weeks or 3 month later. Serum cortisol values predicted the stroke outcome. Both the 7 a.m. and the 7 p.m. values in the initial and 1-week samples correlated positively with the severity of hemiparesis on the corresponding days. The 7 p.m. values predicted better than the 7 a.m. values the functional outcome and case fatality during the 3 month follow-up. Initially and at 1 week, the median 7 p.m. serum cortisol values were statistically significantly higher in those with frontally extending infarcts than in those with non-frontal infarcts. Both 7 a.m. fasting blood glucose and glycosylated hemoglobin (HbA1c) measurements were taken within 3 days of the onset in 95 cases. The patients were diagnosed to have prestroke normoglycemia (n = 73) and hyperglycemia (n = 22) on the basis of the HbA1c level. A highly significant (P = 0.0001) correlation was demonstrated between the initial 7 p.m. cortisol and 7 a.m. fasting blood glucose values in those with prestroke normoglycemia, suggesting that hyperglycemia during the acute phase of stroke is a stress response.
Adult↗
Angiographic evaluation of brain infarction limited to the anterior cerebral artery territory.
BACKGROUND AND PURPOSE: Brain infarction localized in the anterior cerebral artery territory is rather uncommon, and its etiology has not yet been fully elucidated. METHODS: Based on computed tomographic findings, 17 patients with solitary anterior cerebral artery territory infarction were selected from among 3,619 patients admitted consecutively to our institute. Patients without angiographic examinations were excluded. The angiographic findings and clinical category of stroke were analyzed in each patient. RESULTS: Angiographic abnormalities were revealed in all patients. These consisted of occlusive changes (n = 10) or reversible segmental dilatation (n = 3) of the anterior cerebral artery, A1 hypoplasia (n = 5), and occlusive changes of the carotid artery (n = 3). In one patient with anterior cerebral artery occlusion, the occluded artery was reopened and subsequently became reoccluded. The clinical category of stroke was classified as atherothrombotic in 10 patients, cardioembolic in three, and undetermined in the remaining four. In eight of the 10 patients with atherothrombotic infarction, the anterior cerebral artery was narrowed or occluded. In all patients with cardioembolic infarction, the A1 segment contralateral to the infarction was hypoplastic. CONCLUSIONS: In our series, solitary anterior cerebral artery territory infarction was attributable most commonly to local atherothrombosis and occasionally to cardiogenic embolism. A hypoplastic A1 segment may facilitate the occurrence of embolism in the anterior cerebral artery. Reversible dilatatory and occlusive changes of this artery may be another important cause of infarction.
Adult↗
Lipoprotein disorder in brain infarction and hemorrhage.
The cholesterol, triglyceride, and apolipoprotein B content of very low-, intermediate-, low-, and high-density lipoprotein fractions (separated by ultracentrifugation) and plasma were measured in healthy controls and patients with atherothrombotic infarction (26), lacunar infarction (26), and brain hemorrhage (14). In both atherothrombotic and lacunar infarction, increased plasma and low-density lipoprotein apolipoprotein B and a decreased low-density lipoprotein cholesterol/apolipoprotein B ratio were noted. In brain hemorrhage patients, a decreased ratio was also observed. These findings suggest that increased small dense low-density lipoprotein is a characteristic risk factor for atherothrombotic and lacunar infarction.
Adult↗
Influx of leukocytes and platelets in an evolving brain infarct (Wistar rat).
The results of several experimental studies of focal ischemia and anecdotal observations suggest that leukocytes may contribute to the injury initiated by an arterial occlusion. The timing and the nature of leukocyte responses in evolving brain infarcts (either human or experimental) are incompletely characterized. This is a study of experimental brain lesions in 96 Wistar rats that underwent occlusion of a large intracranial artery for variable intervals ranging between 30 minutes and 7 days. The experimental model, based on the occlusion of a middle cerebral artery ostium via the insertion of a nylon monofilament through the external carotid artery, does not require opening the skull; therefore, the inflammatory response is not influenced by the effects of craniotomy and changes in intracranial pressure are only those induced by the ischemic lesion. All 96 animals having the same type of arterial occlusion developed an ischemic brain lesion (limited to the territory of the corresponding artery) that evolved into an area of extensive neuronal necrosis over a period of 6 to 12 hours followed by pan-necrosis (infarct) approximately 60 hours later. In this study, leukocytes (in particular polymorphonuclear cells) were detected in the microvessels (capillaries and venules) of the ischemic hemisphere as early as 30 minutes after the arterial occlusion. Numbers of intravascular neutrophils peaked at 12 hours, whereas intraparenchymal granulocytes were most numerous at 24 hours; a few granulocytes were visible in the brain infarct as late as day 7. Circulating monocytes were first detected within the capillaries/venules of the ischemic area after 4 to 6 hours. Platelet aggregates were more abundant in the arterial than the venous side of the circulation, and luminal obstruction of arteries by platelet aggregates became noticeable only 48 hours after the arterial occlusion. Fibrin thrombi were conspicuous for their absence. These observations provide the background for studies that will attempt to unravel the relationship between the biological responses of leukocytes and neuronal necrosis secondary to focal ischemia.
Animals↗