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PubMed2000

Changes in coagulation and tissue plasminogen activator after the treatment of cerebral infarction with lumbrokinase.

This paper aimed to investigate the effect of lumbrokinase on the anticoagulation and fibrinolysis in treating cerebral infarction. Lumbrokinase was used in patients with cerebral infarction. Patients were randomly divided into treatment group (n = 31) and control group (n = 20). Single blind method was used in this investigation. The Chinese stroke score was used to evaluate the results of treatment before and after administration of lumbrokinase. Kaolin partial thromboplastin time (KPTT), prothrombin time (PT), fibrinogen content, vWF content were analyzed, and tissue plasminogen activator (t-PA) activity, plasminogen activator inhibitor (PAI) activity, D-dimer level were assayed. In both groups, the stroke score decreased after administration, but in the treatment group, it was more obvious. In the treatment group, KPTT was prolonged, t-PA activity and D-dimer level increased, while the content of fibrinogen decreased significantly. There were no significant changes of PT and PAI activity in both groups. It is concluded that lumbrokinase is beneficial to the treatment of cerebral infarction. The effect of lumbrokinase is related to the inhibition of intrinsic coagulation pathway and the activation of fibrinolysis via an increase of t-PA activity.

Aged↗
PubMed1994

Leukocyte involvement in cerebral infarct generation after ischemia and reperfusion.

White blood cell involvement in the generation of cerebral infarcts was evaluated following ischemia and reperfusion injury in the rat. Control and leukopenic rats (induced by vinblastine, WBC counts < 1500/mm3) were compared in a global forebrain ischemic model after 1 h of ischemia and 1 h 15 min of reperfusion. Cerebral infarcts were defined on coronal brain sections using Triphenyl tetrazolium chloride (TTC) staining. Electroencephalographic activity (EEG) and somatosensory evoked potentials (SSEP) were also compared. Results indicate that the area infarcted in leukopenic rats was significantly less than infarcts generated in corresponding controls (21 +/- 16% vs. 70 +/- 16%). In addition, EEG was preserved in all leukopenic animals when compared to controls, both during ischemia and after reperfusion. The cortical peak component of the SSEP was also better preserved in the leukopenic animals both during ischemia and at 60 min of reperfusion. These results indicate white blood cell participation in the generation of cerebral damage in a model of global forebrain ischemia and reperfusion as indicated by TTC staining of cerebral infarcts.

Animals↗
PubMed1998

[Cerebral infarction: a diagnostic and therapeutic emergency].

Emergency management of cerebral infarct aims to confirm the diagnosis, determine the mechanism and the cause (on which depend the prognosis and treatment), prevent and treat immediate, general and neurologic complications and to begin as early as possible the appropriate treatment. A first progressive step was made with the creation of hospital units devoted to management of cerebrovascular accidents. Various studies showed that patients hospitalised in such units have not only better survival and functional prognosis, but also that the length of hospitalisation and the number of patients requiring subsequent hospitalisation in rehabilitation centres are significantly reduced. More recently, clinical trials suggested that thrombolytic treatment, although comprising a risk of severe cerebral haemorrhage, can clearly improve patient prognosis if it is given in the first hours. Cerebral infarct should henceforth be considered as a medical emergency, and our health care system should be adapted to give patients the best chance of cure.

Cerebral Infarction↗
PubMed2006

Pharmacoeconomic analysis of cilostazol for the secondary prevention of cerebral infarction.

BACKGROUND: The antiplatelet agent, cilostazol, is known to reduce the risk of subsequent cerebral infarction. However, the cost effectiveness of such treatment in comparison to aspirin has not been studied. METHODS AND RESULTS: A Markov model was developed to calculate the health outcomes and associated costs for 65-year-old patients with cerebral infarction who were treated with 200 mg/day cilostazol or 81 mg/day aspirin. Cilostazol was more effective, but also more expensive than aspirin. Cilostazol would extend quality-adjusted life years (QALY) by 0.64, while increasing life-time costs by approximately Yen 1.1 million. The incremental cost-effectiveness ratio of cilostazol in comparison with aspirin was estimated to be Yen 1.8 million per QALY. CONCLUSIONS: The use of cilostazol to prevent recurrence of cerebral infarction appears to be cost effective.

Aged↗
PubMed1996

[Usefulness of MRA in an infant with cerebral infarction due to streptococcal meningitis].

We described a 4-month-old boy with cerebral infarction due to streptococcal meningitis. He complained of cough and high fever for 2 days. On the next day he admitted to our hospital because of bad humor, drowsiness, and vomiting associated with high fever, respiratory failure and loss of consciousness. On admission, he had opisthotonic posturing, anisocoria and elevated deep tendon reflexes with left side dominance. The cerebrospinal fluid showed increased cells (564/mm3), protein (295 mg/dl), and decreased sugar (1 mg/dl). Streptococcus pneumoniae was detected in the cerebrospinal fluid. Despite intensive treatment by antibiotics, glycerol, and dexamethasone, general condition was worsened, MRI showed a high intense area along the territory of bilateral anterior cerebral arteries and left middle cerebral artery 3-D time-of-flight MRA revealed a decreased signal of these arteries, confirming cerebral infarction. Recanalization of the arteries were observed 17 days after the first MRA examination. Since complication of cerebral infarction influences the prognosis of meningitis, repetitive MRA is very beneficial in patients with bacterial meningitis in order to evaluate the vascular lesion.

Cerebral Infarction↗
PubMed1998

Temporal pattern of blood volume change in cerebral infarction: evaluation with dynamic contrast-enhanced T2*-weighted MR imaging.

OBJECTIVE: The purposes of this study were to evaluate the temporal pattern of blood volume change in cerebral infarction and to provide a guideline in the interpretation of blood volume data, which are known to vary according to the stage of infarction. SUBJECTS AND METHODS: Thirty-three patients with large middle cerebral infarctions were examined one to three times (one time in 20 patients, two times in eight patients, and three times in five patients) after the onset of stroke by dynamic contrast-enhanced T2*-weighted MR imaging and MR angiography. A total of 54 infarctions (29 in an acute stage [up to 7 days], 15 in a subacute stage [8-21 days], and 10 in a chronic stage [22-35 days]) were included. After blood volume maps were created, blood volume ratios (blood volume of the infarcted region divided by blood volume of corresponding contralateral region) were compared at different stages. Likewise, findings on MR angiography were compared at different stages. RESULTS: Mean blood volume ratios in each stage of infarction were 0.46 in the acute stage, 1.48 in the subacute stage, and 0.73 in the chronic stage (p < .001). Recanalization of occluded arteries occurred in 21% of infarctions in the acute stage and 80% in the subacute stage. Infarctions with recanalization had higher blood volume ratios than did those without recanalization (p < .001). A biphasic pattern of blood volume ratios was found in 13 patients who underwent at least two MR examinations: increased blood volume in the subacute stage and decreased blood volume in the chronic stage, regardless of recanalization (p < .01). CONCLUSION: Blood volume that initially decreases in cerebral infarction increases in the subacute stage, reflecting reperfusion hyperemia. Blood volume decreases again in the chronic stage. The time interval between onset of stroke and MR examination must be considered for correct interpretation of blood volume data in cerebral infarction at various stages.

Adolescent↗
PubMed1999

Late epileptic seizures after cerebral infarction.

OBJECTIVES: To determine the profile of late epileptic seizures following cerebral infarcts and the predictive clinical and radiological factors associated with their development. METHODS: We compared 86 patients who developed late seizures after cerebral infarction with 285 similar patients who did not develop seizures for at least 1 year after their stroke. Patients who had seizures only at the onset of the stroke were excluded. Odds' ratios were used for statistical analysis. RESULTS: Simple partial, and mainly motor seizures, with or without secondary generalization, accounted for 80% of the classifiable seizures but it was not possible to determine the seizure type in half of the cases. Factors that appeared to be predictive of seizure development were the presence of large cortical infarcts and the presence of apparently preserved cerebral tissue within the infarcted area. Seizures were rare in patients with lacunar infarction but the presence of associated leukoaraiosis increased the risk. The risk was also increased in patients with other medical problems known to lower seizure threshold, such as renal failure.

Adult↗
PubMed2000

[Study of platelet membrane glycoproteins and its fibrinogen binding reaction in patients with cerebral infarction and diabetes mellitus].

OBJECTIVE: To investigate the change of platelet membrane glycoproteins and its fibrinogen binding reaction in patients with cerebral infarction and type II diabetes mellitus (DM), and assess their value in the study of thrombosis and pro-thrombosis state. METHODS: By flow cytometry, the platelet glycoprotein (GP) I b, GP II b, GP III a, GP II b- III a complex and P-selectin expression as well as fibrinogen binding reaction were analyzed in 85 patients with type II DM and 28 with cerebral infarction, and compared with that in 30 normal subjects. RESULTS: The platelet membrane GP II b- III a complex, P-selectin expression and fibrinogen binding reaction were higher, while the platelet surface GP I b was lower in the patients with cerebral infarction and type II DM with vascular disease than those in normal group. The GP II b and GP III a were not significantly changed. There was no difference of these parameters between the type II DM without vascular disease patients and normal group. CONCLUSION: The platelet fibrinogen binding reaction, P-selectin and GP II b- III a complex expression were increased while the GP I b decreased in patients with cerebral infarction and type II DM with vascular disease.

Adult↗
PubMed1991

[Thrombolytic agents in cerebral infarctions].

Thrombolytic agents are aimed at restoring arterial patency thus reducing the risk of cerebral infarction in case of arterial occlusion by blood thrombus or embolus. A review of data from the literature is presented, and the authors have tried to answer the following questions: 1) What are the probabilities of early mortality (first 30 days) and of morbidity due to untreated or medically (thrombolysis excluded) treated cerebral infarction? 2) What are the morbidity and mortality rates after systemic thrombolysis or selective intraarterial thrombolysis? 3) Are the results of thrombolysis affected by the site of arterial occlusion (carotid or vertebrobasilar system)? 4) Does thrombolysis increase the risk of cerebral haemorrhage? 5) Can thrombolysis be regarded as an effective treatment and, if so, in which cases? This study of systemic thrombolysis yielded a mean mortality rate of 22.2%, with satisfactory functional outcome in 58.2% of the survivors. The corresponding figures for selective intraarterial thrombolysis were 29.7% and 84.5% respectively. However when the arterial territories occluded were taken into account, they became 10.4% and 84.4% respectively in the carotid system and 61.5% and 85.00% in the vertebrobasilar system. Comparisons between the natural history of cerebral infarctions, as far as it is known, and the results of thrombolysis suggest that thrombolytic agents are: 1) probably justified by the selective intraarterial route when the occlusion lies in the carotid system; 2) not indicated by the systemic route with urokinase or streptokinase but trials with tPA are being performed. These conclusions, however, must be interpreted with caution as they rest on general data leaving out a number of factors that are often neglected in reports particularly the exact site of arterial occlusion, chiefly in the vertebrobasilar system. From 3 limited cohorts it was possible to evaluate at about 14% the mortality rate in thrombolysis for basilar artery occlusion. This figure, compared with the 70-80% estimate found in the literature for untreated occlusions, suggests that the selective intraarterial thrombolysis may perhaps be indicated also in basilar artery occlusions. It must be noted that selective intraarterial thrombolysis is still an exceptional treatment which requires sophisticated techniques, highly qualified neuroradiologists and prompt application i.e. emergency stroke units.

Cerebral Infarction↗
PubMed1993

[Two elderly cases of megacolon associated with cerebral infarction and diabetes mellitus].

The authors experienced two elderly patients of megacolon associated with cerebral infarction and diabetes mellitus. The first patient was a 66-year-old female who was admitted to our hospital for rehabilitation with a complaint of knee pain. She had suffered from diabetes mellitus since she was 30 years old and multiple cerebral infarction since age 62. Two months after admission, she had an episode of abdominal distension and obstructive symptoms. The roentgenograms of her abdomen showed diffuse dilatation of the colon. The second patient was a 78-year-old female admitted to our hospital with complaints of abdominal pain, distension of the abdomen and vomiting. Her abdomen was severely distended and plain roentgenograms of the abdomen, X-ray studies of the colon with the aid of contrast medium and CT scan of the abdomen showed striking dilatation of the colon. Megacolon may be congenital or acquired, and in acquired forms the conditions are secondary to organic diseases, smooth muscle atrophy, metabolic and neurological diseases, ulcerative colitis or psychogenic origin (idiopathic). The two patients in this series were suffered from cerebral infarction and diabetes mellitus. The mechanisms of megacolon seen in these two patients are not known, but involvement of the visceral autonomic innervation is presumed. Some elderly patients have chronic constipation, and dilatation of the colon may not be uncommon due to underlying diseases or drugs. Therefore, when examining elderly patients, careful attention should be paid to their bowel movement.

Aged↗
PubMed2001

Interaction between D2 dopaminergic and glutamatergic excitatory influences on lower urinary tract function in normal and cerebral-infarcted rats.

Previous studies showed that bladder hyperactivity after cerebral infarction in Sprague-Dawley (SD) rats was mediated in part by D2 dopaminergic and NMDA glutamatergic mechanisms. In the present experiments, the interaction between dopaminergic and glutamatergic excitatory mechanisms in the control of bladder and external urethral sphincter (EUS) reflexes was investigated in urethane-anesthetized sham-operated (SO) and cerebral-infarcted (CI) SD rats. Occlusion of the left middle cerebral artery or a sham operation was performed under halothane anesthesia. Two hours after either of the two procedures, rats were anesthetized with urethane. Dizocilpine, an N-methyl-d-aspartate (NMDA) glutamatergic antagonist, was administered intravenously in doses of 0.3 or 3 mg/kg to CI rats and 3 mg/kg to SO rats. These doses completely inhibited bladder and EUS activity. The effects of apomorphine (a dopamine agonist with greater efficacy at D2 than D1 receptors) or quinpirole (a selective D2 dopamine receptor agonist) were examined on the dizocilpine-induced depression of bladder contractions and EUS EMG activity. Apomorphine did not antagonize the dizocilpine depression of EUS activity, but it did reestablish the micturition reflex after dizocilpine blockade and did increase the amplitude of bladder contractions and voided volume in a dose-dependent manner (0.0001-10 mg/kg, iv), in both CI rats and SO rats pretreated with dizocilpine. There were no differences between SO rats and CI rats in the apomorphine responses in rats pretreated with doses of 0.3 or 3 mg/kg dizocilpine. A larger dose of dizocilpine (10 mg/kg) did not affect the bladder contractions after apomorphine administration. Quinpirole (0.001-1 mg/kg, iv) also partially reversed the dizocilpine depression of bladder activity in SO and CI rats. These results indicate that NMDA glutamatergic and D2 dopaminergic mechanisms exert independent excitatory influences on bladder activity in both SO and CI rats. D2 dopamine receptor agonists can reverse the effect of NMDA receptor blockade on bladder activity but were ineffective in reversing the block of sphincter activity.

Anesthesia↗
PubMed2000

Effects of aniracetam on bladder overactivity in rats with cerebral infarction.

Aniracetam has been used to improve the mental condition of patients with cerebrovascular disease. Previous studies have demonstrated that aniracetam activates the residual functions of cholinergic neurons in damaged brain areas. In this study, the effects of aniracetam on bladder overactivity after left middle cerebral artery occlusion were assessed through oral or i.c.v. administration in sham-operated and cerebral infarcted rats. Oral administration of aniracetam (100 and 300 mg/kg) resulted in a significant and dose-dependent increase in bladder capacity in cerebral infarcted rats but had no effect on bladder capacity in sham-operated rats. Intracerebroventricular administration of aniracetam (0.25 and 2.5 microg/rat) resulted in a significant and dose-dependent increase in bladder capacity in cerebral infarcted rats but not in sham-operated rats. Aniracetam had no significant effect on bladder contraction pressure or micturition threshold pressure in either sham-operated or cerebral infarcted rats. Furthermore, i.c.v. administration of atropine (1 microg/rat), a muscarinic acetylcholine receptor antagonist, completely inhibited the enhancing effects of aniracetam on bladder capacity in cerebral infarcted rats. The effects of aniracetam on bladder overactivity are thought to be mediated in part by activation of cholinergic inhibitory mechanisms in the brain. These results indicate that aniracetam may improve the neurogenic voiding dysfunction observed in patients with cerebrovascular disease.

Animals↗
PubMedDate not supplied

Cerebral infarction due to giant cell arteritis-three case reports.

The objective of this report was to explore the clinical features of patients with cerebral infarction due to giant cell (temporal) arteritis (GCA) and its characteristic changes in pathology, and on computed tomography (CT) and magnetic resonance imaging (MRI). Three cases of cerebral infarction due to GCA, treated during the past 2 years, were analyzed. Their clinical manifestations were observed carefully, their temporal artery biopsies were performed, their immunohistochemistries were done, and CT as well as MRI were used. The results showed that all the patients had new-onset headache and temporal artery abnormality when the disease began, and there was tremor on the right limbs of 1 patient; temporal artery biopsies revealed evidence of inflammatory cell infiltration in the arterial wall, mainly including T-lymphocytes and macrophages; small cerebral infarction foci were found on CT and MRI; and the responses to corticosteroid therapies were good. The results suggest that it is important to recognize the clinical features of cerebral infarction due to GCA, including the changes of pathology and on CT and MRI. In some cases, special attention is paid to differentiating between atherosclerotic infarction and infections to avoid misdiagnosis.

Aged↗
PubMed1999

Influence of treated blood pressure on progression of silent cerebral infarction.

PURPOSE AND METHODS: To examine whether treatment for hypertensive patients prevents the progression of cerebral infarction, we performed magnetic resonance imaging (MRI) repeatedly at mean intervals of 22 months on 117 Japanese subjects aged 65-89 (mean 74 years), including 84 hypertensive patients. The patients were given various anti-hypertensive agents, and the blood pressure of each patient was monitored periodically during the observation period. Depending on the average blood pressure at the end of the follow-up period, hypertensive patients were classified into three subgroups: normotension (N), borderline (B) and hypertension (H). None had a prior history of symptomatic cerebral infarction and neurological abnormalities. The number of infarcted lesions were determined on brain MRI by two independent observers. RESULTS: Silent cerebral infarction (SCI) lesions were observed in 42 hypertensive subjects (50.0%) and in eight control subjects (24.2%) on enrollment. The numbers of SCI lesions increased in 33 hypertensive subjects (39.3%) and three control subjects (9.1%) during the observation period. In the hypertensive subjects, an increased number of infarcted lesions was found in six of 28 subjects in group N (21.4%), 17 of 44 in group B (38.6%), and 10 of 12 in group H (83.3%). Thus, blood pressure controlled to the normal level appears to result in a lower incidence of progression of infarcted areas in patients with hypertension (N versus H, P < 0.001). CONCLUSION: Our data indicate that an appropriate anti-hypertensive treatment reduces the risk of a cerebrovascular accident in hypertensive patients.

Aged↗
PubMed1991

[A case of cerebral infarction with circulating anticoagulant to Fletcher factor].

A 44-year-old woman with a history of cerebral infarction and hypertension developed sudden onset of speech and visual disturbance. On admission, her general physical examinations showed high blood pressure of 210/120 mmHg and Raynaud's phenomena. The neurological examinations revealed right upper quadratic hemianopsia, left oculomotor nerve paresis and left hyperreflexia. Laboratory findings showed that antinuclear and anti-DNA antibodies were positive. The activity of Fletcher factor was reduced to 50%, and the activated partial thromboplastin time (APTT) was prolonged to 82.6 seconds. And a 1:1 dilution with normal plasma failed to correct the prolonged APTT, indicative of circulating anticoagulant to Fletcher factor. Plasma fibrinogen increased to 500 mg/dl but FDP was normal. The CT scan demonstrated the recurrently developed cerebral infarction in the left occipital lobe. Cerebral angiogram revealed mild atherosclerosis of basilar and bilateral posterior cerebral arteries, but any occlusive lesions were not found. Although she had a history of hypertension, this case suggests the possibility that the disturbance in fibrinolytic system may have been caused by the circulating anticoagulant to Fletcher factor, and contributed to her cerebral infarctions.

Adult↗
PubMed2003

Cerebral infarction in a 24-year-old pilot.

Ischemic stroke is a rare event in young adults. We report on a 24-yr-old pilot with cerebral infarction of undetermined etiology, temporally associated with chain smoking. The patient exhibited dysphasia, stupor (confused consciousness), and right facial-nerve palsy. Computed-tomography revealed a low-density area in the left insular cortex. Cerebroangiography showed severe stenosis in a branch of the left middle cerebral artery. After admission, the patient made a rapid and uneventful recovery within 72 h. MRI showed an area of hyperintensity on T2-weighted images 2 mo after the attack. Based on the hyperintense area on FLAIR (fluid attenuated inversion recovery sequence) images obtained in MRI performed 10 mo after the attack, we diagnosed a cerebral infarction. In the Japan Air Self-Defense Force, cerebral infarction is an aeromedically disqualifying condition. However, in the evaluation 2 mo after the attack, differentiation from reversible ischemic neurological deficit was difficult. We discuss the criteria used for diagnosis and the risk factors for cerebral infarction in young adults, as well as the aeromedical disposition of young pilots.

Adult↗
PubMed1996

Collagen-encapsulated coagulation necrosis in cerebral infarcts: a pathological study.

Coagulation necrosis (CN)--a type of necrosis characterized by firm, eosinophilic parenchyma with recognizable cell outlines--is thought to be a result of rapid degeneration of tissue protein to a gel state and loss of water which prevents the necrotic tissue from undergoing autolysis and cellular digestion. In this study, we observed CN in cerebral infarcts of 11 of 150 consecutive autopsy cases of large cerebral infarction. Cerebral CN in patients who had survived for about 1 month had already started to be surrounded by newly formed vessels and type I collagen-positive tissue. In patients who had survived for more than 1 year, CN was deposited with calcium and cholesterin crystals and encapsulated by thick, dense collagenous tissue. Encapsulation, however, was not always complete, a finding that suggests that other factors, such as gel transformation at an early stage of CN and calcification at a later stage, are important for the persistence of CN in the infarct. The results of our study suggest that cerebral CN occurs more frequently than is generally believed.

Aged↗
PubMedDate not supplied

Spontaneous hemorrhage in previously ischemic (pale) cerebral infarcts.

Spontaneous bleeding into a pale cerebral infarct is documented in 2 patients. Neither patient had received anticoagulants or was hypertensive. The development of the hemorrhage was associated with neurological worsening. Initial CT scans showed a hypodense lesion in an arterial distribution representing infarction; subsequent CT scans showed multiple areas of hemorrhage within the hypodense lesion. The size of the hemorrhages and their location in gray and white matter differ from the pattern of hemorrhagic infarction and primary intracerebral hemorrhage as visualized on CT scan and at autopsy.

Aged↗