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PubMed1975

Evidence for disordered cyclic amp metabolism in patients with cerebral infarction.

Systemic blood cyclic AMP levels were elevated but urinary excretion was unaltered in patients with recent cerebral infarction. Cerebral venous levels for cyclic AMP were significantly higher than arterial levels. CSF cyclic AMP levels were also elevated. After intravenous 10% glycerol, CSF cyclic AMP levels decreased and cerebral A-V differences were reduced. Elevation of cyclic AMP levels in plasma may be due to alteration of neuroendocrinal function after cerebral infraction and contributed to in part by release from infarcted brain. Cyclic AMP release into cerebral venous blood and CSF suggests (1) blood brain barrier damage and (2) extracellular cyclic AMP accumulation in infarcted brain secondary to abnormal neurotransmitter release and/or impaired cellular function which appears to be partially reversed by glycerol.

Cyclic AMP↗
PubMed1990

Platelet count, mean platelet volume and their relation to prognosis in cerebral infarction.

The study was performed on patients with ischaemic cerebral infarction in order to obtain information on serial changes of some platelet parameters and to test their prognostic significance. Platelet count, obtained within 48 h after cerebral infarction, was significantly lower than in the control group (213,611 +/- 65,652 mm-3 vs. 299,525 +/- 60,611 mm-3, P less than 0.001), reaching the normal level on the ninth day and thereafter. The mean platelet volume was significantly greater than in the controls (11.26 +/- 1.29 fl vs. 8.93 +/- 0.93 fl, P less than 0.001), and normalization generally occurred on the forty-fifth day. The mean platelet count was significantly lower in the patients who died than in those who survived (P less than 0.025 and P less than 0.05 respectively on the first to second and fourth day after infarction). The reduction of platelet count and the increase of mean volume appear to be related to an increased platelet consumption in the infarction area, associated with an in vivo platelet activation, as larger platelets are more responsive to platelet activity and aggregability tests. The lower mean platelet count observed in the patients who died suggests that the platelet value might be considered as a prognostic index of cerebral infarction.

Aged↗
PubMed2006

Hyperglycemia in acute cerebral infarction.

OBJECTIVE: Report the results of hyperglycemia in the patients with acute cerebral infarction. MATERIAL AND METHOD: A retrospective review of 231 patients who presented with the syndrome of acute cerebral infarction at Ratchaburi Hospital from January 1, 2000 to December 31, 2004. Patients data, diagnosis, blood glucose, and underlying disease were collected from medical records (n = 231). RESULTS: Hyperglycemia is defined as the blood glucose level of more than 140 mg/dl. Odd ratio for 1 year mortality was calculated using multivariable Cox regression models. Admission hyperglycemia was present in 43.7 % of patients with acute cerebral infarction. 61% of these patients received oral hypoglycemic drugs during their hospital admission. Hyperglycemic patients had a longer hospital stay than normoglycemics (6.91 vs 4.60, p < 0.001) and increased risk for death at 1 year (odd ratio = 1.004, p < 0.01). CONCLUSION: Hyperglycemia can predict mortality of acute cerebral infarction.

Acute Disease↗
PubMed1986

Cerebral infarction in term neonates: diagnosis by cerebral ultrasound.

Cranial ultrasound (US) through the newborn's open fontanelle can diagnose not only intracerebral hemorrhages but also diffuse and localized hypoxic-ischemic encephalopathies. Sonographically, it was possible to distinguish between different courses of cerebral ischemia in seven neonates: ischemic infarction, usually in the area of the middle cerebral artery: borderline infarction; transient ischemia. The patients showed lateralized seizures during the first days of life with a corresponding focus in the electroencephalogram (EEG). Computed tomography showed areas of partially reduced density corresponding to the regions of increased echogenicity in ultrasound. The course was various; prognosis was good except in one patient. Etiologically, embolism, thromboses or hypoxemia were responsible for cerebral infarction. In some cases secondary bleeding ensued. The prognostic value of cerebral lesions was dependent on the involved area, gestational age, and any concurrent hypoxic cerebral damage.

Cerebral Infarction↗
PubMed1998

Warfarin reduces silent cerebral infarction in elderly patients with atrial fibrillation.

BACKGROUND: Atrial fibrillation is reportedly one of the risk factors of silent cerebral infarction. The Shiga Atrial Fibrillation Trial was conducted in five medical centers, to test the hypothesis that warfarin can prevent silent cerebral infarction in patients with atrial fibrillation. METHODS: Magnetic resonance images (MRI) were taken at the time of the patient's entry to the study and 1 year later in 15 asymptomatic patients (74 +/- 4 years old) with atrial fibrillation who were randomly allocated to two treatment groups to receive or not receive warfarin. The frequency of hyperintensities on T2-weighted axis MRI was rated using a four-point scale in the periventricular and centrum semiovale areas. Total silent cerebral infarction scores were calculated at the sum of the scores on MRI. RESULTS: Silent cerebral infarction was seen in 14 (93%) of the 15 patients with atrial fibrillation and a total of 109 silent cerebral infarction lesions were detected. The number of hyperintensities in the periventricular and centrum semiovale areas increased over the 1 year of study (P < 0.01). The increase in total score over 1 year was less in the warfarin-treated group (1.6 +/- 0.7 compared with 5.4 +/- 0.9, P < 0.05). CONCLUSION: Anticoagulation therapy can be useful to prevent silent cerebral infarction in neurologically normal elderly patients with atrial fibrillation.

Aged↗
PubMed1993

Incidence of silent cerebral infarction in patients with major depression.

BACKGROUND AND PURPOSE: There have been few studies of the incidence of silent cerebral infarction detected by magnetic resonance imaging in patients with presenile or senile major depression. METHODS: We examined silent cerebral infarction in patients with presenile and senile major depression who were diagnosed at Hiroshima Prefectural Hospital. The diagnostic criteria of the American Psychiatric Association (DSM-III-R) were used. Patients with stroke or focal neurological symptoms were excluded. RESULTS: Silent cerebral infarction was observed in 51.4% of the patients with presenile-onset presenile depression, and the incidence was significantly higher than in patients with juvenile-onset presenile depression (P < .01). Among the patients with senile major depression, silent cerebral infarction was observed in 65.9% of those with presenile-onset depression and in 93.7% of those with senile-onset depression. CONCLUSIONS: Our findings suggest that half of presenile-onset major depression and the majority of senile-onset major depression might be organic depression related to silent cerebral infarction. Because major depression occurring for the first time during or after the presenile period may be related to silent cerebral infarction, it is important to keep this possibility in mind when treating such patients.

Age of Onset↗
PubMed2004

Polymorphisms of the coagulation factor VII gene and its plasma levels in relation to acute cerebral infarction differences in allelic frequencies between Chinese Han and European populations.

BACKGROUND: Coagulation factor VII (FVII) levels in plasma are usually related to ischemic heart disease (IHD) and cerebral infarction shares many of the risk factors related to IHD. Is there any relationship between factor VII and cerebral infarction? We investigated the relationship between FVII and acute cerebral infarction and reported genotype frequencies and allelic frequencies of FVII gene polymorphisms in the Chinese Han population. METHODS: We recruited 62 patients with acute cerebral infarction confirmed by magnetic resonance imaging (MRI) from Ruijin Hospital, and 149 age-matched patients clinically free of vascular disease to act as controls. All of them were unrelated, and were from the Chinese Han population. FVII coagulant activity (FVIIc) was determined using an clotting assay, activated FVII (FVIIa) and FVII Ag were assayed using enzyme immunoassay kits. The FVII gene polymorphisms to be detected included-401G/T, -402G/A, 5'F7A1/A2, IVS7 and R353Q. 5'F7 and IVS7 were revealed by means of a PCR and direct agarose gel electrophoresis. The rest were examined by a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: The results showed that FVIIc, FVIIAg and FVIIa were higher in the acute cerebral infarction group than in the control group (P < 0.01, P < 0.05, P < 0.05, respectively). There were no significant differences in the genotype frequencies of FVII gene polymorphisms between the two groups. The allelic frequencies in the Chinese Han population were as follows: -401G/T (96.64/3.36), -402G/A (52.01/47.99), 5'F7A1/A2 (96.64/3.36), IVS7 H5/H6/H7/H8 (0.34/52.35/46.98/0.34) and R353Q (95.64/4.36). There were significant differences (P < 0.01, P < 0.001, P < 0.001, P < 0.001, P < 0.001, respectively) in these allelic frequencies between the Chinese Han and European populations. CONCLUSIONS: The results indicate that increased plasma FVII levels may contribute to thrombosis in cerebral infarction. And there was no significant difference in genotype frequencies of these five FVII gene polymorphisms between the acute cerebral infarction and control groups. Moreover, these results showed that the frequencies of protective allele, including -401T, 5'F7 A2 and 353Q were lower, but that -402A, which was previously found to be associated with increased plasma FVII levels, is higher in Chinese Han population.

Acute Disease↗
PubMed2001

Polymorphism of the angiotensin-converting enzyme gene in patients with cerebral infarction in Koreans.

The relationship between cerebrovascular disease and an insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene is still being debated. The frequency of the DD genotype of the ACE gene was significantly higher in subjects with than those without cerebral infarction in Japan. The aim of the present study was to assess the relationship between ACE gene polymorphism and the development of cerebral infarction in a population from Korea. We examined its possible role as a risk factor in patients with cerebral infarction. The association between ACE gene polymorphism and cerebral infarction was examined in 106 patients with cerebral infarction and 498 controls without cerebral infarction. Frequencies of the genotypes and alleles of the ACE gene were investigated. The ACE genotype was analyzed by the polymerase chain reaction (PCR). The frequency of D allele was 37.7% in patients and 39.1% in controls (chi2 = 0.128, p = 0.720). The frequencies of the genotypes of the ACE gene were II: 39.6%, ID: 45.3%, and DD: 15.1% in patients, and II: 37.1%, ID: 47.6%, and DD: 15.3% in controls (chi2 = 0.127, p = 0.721). There was no significant difference in the frequency of the DD genotype of the ACE gene, and we did not find any association between ACE polymorphism and cerebral infarction. These results indicate that ACE polymorphism is not a risk factor for the development of cerebral infarction in a Korean population.

Adult↗
PubMed2001

[Curative effect of soybean lecithin on cerebral infarction].

OBJECTIVE: To investigate the clinical curative effect of soybean lecithin on cerebral infarction. METHODS: 542 patients with cerebral infarction within 48 h after the onset with the nervous function defect scores of 31-35 were divided into 3 groups: basic treatment group, 60 cases, with conventional treatment; citicoline group, 122 patients, with conventional treatment and citicoline; and soybean lecithin group, 360 patients, with conventional treatment and soybean lecithin 10 g tid. For all patients, treatment began sometime within 48 hours after the onset. The treatment course lasted 28 days. RESULTS: When the course was over, the infarct volumes in basic group citicoline group, and soybean lecithin group, were 7.6 cm3 +/- 2.9 cm3, 7.3 cm3 +/- 3.1 cm3, and 6.4 cm3 +/- 2.7 cm3 respectively (F = 7.371, P = 0.0007). The basic group and citicoline group being compared with the soybean group by Dunnett test, t = 4.387 and 3.969 respectively, P < 0.01. The nervous function defect integral in the 3 groups decreased 14.2 +/- 10.93, 15.0 +/- 9.0, and 18.5 +/- 10.9 respectively. Two-way analysis of variance of drug kind and beginning time of treatment showed the value of F in drugs as 6.250, P = 0.0021, and value of F in times as 0.9417, P = 0.4201. In the order of death,deterioration, no improvement, improvement, significant improvement, and recovery, the Ridit values for the comprehensive curative effect in the 3 groups were 0.4003, 0.4118, and 0.54 5 respectively; chi2 = 27.89, P < 0.001. CONCLUSION: Soybean lecithin is effective in treatment of acute cerebral infarction. The mechanism may be that soybean lecithin lowers the decrease of brain phospholipid content in brain ischemia.

Cerebral Infarction↗
PubMed1998

Effects of MK-801 on bladder overactivity in rats with cerebral infarction.

PURPOSE: Our objective was to evaluate the underlying mechanisms of neurogenic voiding dysfunction following cerebral infarction. MATERIALS AND METHODS: The left middle cerebral artery (MCA) was occluded using 4-0 monofilament nylon thread in male S-D rats. Cystometric examination was performed in unanesthetized and urethane-anesthetized rats through a catheter chronically implanted in the dome of the bladder. RESULTS: Bladder capacity of unanesthetized or urethane anesthetized rats was significantly reduced just after occlusion of the left MCA; 2 weeks after the occlusion, the capacity was less than half that in sham-operated rats. Intravenous administration of N-methyl-d-aspartate (NMDA) receptor antagonist MK-801 to the unanesthetized sham-operated rats led to a marked dose-dependent decrease in bladder capacity. Its administration to unanesthetized rats with cerebral infarction resulted in a slight decrease in bladder capacity. In the urethane-anesthetized state, the bladder capacity of the rats with cerebral infarction was significantly increased by MK-801, 0.1 mg./kg., without inhibiting the contraction pressure or increasing the amount of residual urine. A high dose (1 mg./kg.) of MK-801 was required to increase the bladder capacity of sham-operated rats. This led to an inhibition of contraction pressure and an increase in residual urine. CONCLUSION: Results in urethane anesthetized rats indicate that NMDA glutamatergic transmission is important in the overactivity of the bladder following a cerebral infarction. This model is useful in studying the neurogenic voiding dysfunction observed in patients with cerebrovascular disease.

Anesthesia↗
PubMed1993

Prediction of cerebral infarction due to vasospasm following aneurysmal subarachnoid haemorrhage using acetazolamide-activated 123I-IMP SPECT.

Prediction of cerebral infarction due to vasospasm (VS) following aneurysmal subarachnoid haemorrhage (SAH) was investigated using acetazolamide-activated (A-A) N-isopropyl-p-[123I]iodoamphetamine (123I-IMP) single photon emission computed tomography (SPECT) in 79 SAH patients. A-A SPECT was undertaken twice or more for one each patient by Day 18. Fifty-six (71%) of the 79 patients presented with reduction of cerebral vasodilatory capacity (CVC) on SPECT due to VS by Day 18. Of the 56 patients, 29 showed CVC by Day 8 (Group A), while the other 27 first showed CVC reduction between Day 9 and 18 (Group B). Cerebral infarction on CT was revealed by Day 18 in 15 patients (52%) of Group A and 3 (11%) of Group B. Of the 56 patients, 20 showed reduced CVC in watershed[s] (Type 1), 12 in a sole territory of the intracranial major arterial trunk (Type 2), and 24 in several territories or in a sole territory with distant watershed[s] (Type 3). Cerebral infarction on CT by Day 18 was revealed in one patient (5%) in Type 1, 3 (25%) in Type 2, and 14 (58%) in Type 3. Twelve (71%) of 17 patients belonging to both Group A and Type 3 resulted in cerebral infarction. These results suggest that early and extensive CVC reduction are significant factors responsible for cerebral infarction due to VS following SAH. Cerebral infarction can be reasonably predicted using A-A SPECT in SAH patients.

Acetazolamide↗
PubMed1994

Background factors and clinical symptoms of major depression with silent cerebral infarction.

BACKGROUND AND PURPOSE: We previously reported that major depression developing during or after the presenile period is frequently combined with silent cerebral infarction and that these patients have a high risk of stroke. Therefore, we investigated whether the background factors and clinical symptoms of patients with major depression with silent cerebral infarction [SCI(+)] different from those in patients with major depression without silent cerebral infarction [SCI(-)] before medical treatment. METHODS: Patients with major depression with onset after 50 years of age were classified based on magnetic resonance imaging findings into the SCI(+) (n = 37) or SCI(-) (n = 20) group. The diagnostic criteria for major depression were those of the American Psychiatry Association (DSM-III-R). Patients with stroke or focal neurological symptoms were excluded. The SCI(+) group was subclassified according to whether the infarction area was perforating, cortical, or mixed artery. Family history of affective disorder, risk factors for stroke, and Zung's Self-rated Depression Scale (SDS) score before medical treatment of the group were compared. RESULTS: The SCI(+) group had a significantly lower (P < .05) frequency of family history of affective disorder but a significantly higher (P < .01) frequency of hypertension than did the SCI(-) group. The mean SDS score in the SCI(+) group was significantly higher than that in the SCI(-) group (P < .01). The mean SDS score of the mixed artery infarction group was higher than that of the perforating artery infarction group (P < .05). CONCLUSIONS: Patients with major depression with silent cerebral infarction present more marked neurological factors and more severe depressive symptoms than do those without silent cerebral infarction. Because these features were more prominent in the patients with mixed artery infarction with broad obstructions, we consider that the area of brain damage caused by cerebral infarction is positively related to the severity of depressive symptoms.

Aged↗
PubMedDate not supplied

Changing pattern of cerebral infarction: 1945--1974.

This study has identified all persons in the population of Rochester, Minnesota, who had a diagnosis of cerebral infarction during the period Jan. 1, 1970, through Dec. 31, 1974, and has confirmed the continuing decline in the incidence rate previously reported. The decline in the rate has been accelerating, with a relatively greater reduction occurring in women and in the more elderly age groups. There has been a decline in the prevalence rate in women which was not seen in men. The over-all impact of cerebral infarction was to reduce the proportion of those persons who were completely independent from 57% before cerebral infarction to 16% after infarction. Comparison of survival among patients with cerebral infarction occurring in the two quinquennia 1945--49 and 1970--74 showed only a 2% increased probability of survival at 30 days; the difference in survival increased progressively to 16% at 5 years. The reason for the declining incidence and increased survival in cerebral infarction in this population has not been established, but evidence of increased community surveillance and treatment of hypertension among persons before the onset of cerebral infarction is presented.

Age Factors↗
PubMed2006

Meta-analysis of defibrase in treatment of acute cerebral infarction.

BACKGROUND: Fibrinogen-depleting agents are promising in the treatment of cerebral ischemic disease. They were studied by many trials, and the outcomes were different because of different regimens and different doses. In this study, we assessed the efficacy and safety of defibrase on acute cerebral infarction in China. METHODS: A search using Chinese hospital knowledge database (CHKD) and MEDLINE database for randomized controlled trials was carried out. A CHKD (1994 June 2005) search was performed with the keyword "defibrase", then a second search for the keyword "acute cerebral infarction"; a MEDLINE search (1950 June 2005) was performed with the following keywords: [(cerebral ischemia), OR (acute cerebral infarction), OR (stroke)], AND [defibrase]. Meta-analysis was performed with RevMan software 4.2. RESULTS: Included were 14 studies comparing the efficiency and safety of defibrase with other drugs in the treatment of acute cerebral infarction. Patients' records were pooled (total 646 patients; defibrase, n = 328, no defibrase n = 318). Neurological deficit score (NDS) before treatment showed weighted mean differences (WMD) = 0.95, 95% confidence interval (CI) = (-0.60, 2.50), P = 0.23; NDS after treatment showed WMD = -2.20, 95% CI = (-4.21, -0.18), P = 0.03; Barthel index at 3 months showed WMD = 4.45, 95% CI = (-0.13, 9.03), P = 0.06; the plasma fibrinogen level before treatment showed WMD = 0.02, 95% CI = (-0.16, 0.19), P = 0.86; plasma fibrinogen level after treatment showed WMD = -1.51, 95% CI = (-1.88, -1.15), P < 0.00 001. CONCLUSIONS: With the given dose and regimen of defibrase in China, defibrase may play a role of anticoagulation. It might inhibit the progression of stroke and prevent the recurrence of stroke.

Acute Disease↗
PubMed2003

Early diagnosis of cerebral infarction with near-infrared spectroscopy: an experimental study.

OBJECTIVE: To monitor the changes in the blood flow and blood-oxygen content in rat cerebral tissue with focal cerebral infarction using near-infrared spectroscopy (NIRS), so as to verify the value of NIRS in early diagnosis of cerebral infarction. METHODS: Focal cerebral infarction models were established in 16 rats by injecting silk threads into the internal carotid artery. The bilateral blood flow and blood-oxygen content were monitored with NIRS in the models and also in 16 normal rats receiving saline injection to serve as blank control group. RESULTS: Focal cerebral infarction in rats caused the decrement in blood-oxygen content and the increase in blood flow. No changes were observed in the control group after saline injection (P >0.05). CONCLUSION: In the earlier stages of focal cerebral infarction, blood-oxygen decreases while blood flow increases in the infarcted area. NIRS provides real-time, non-invasive monitoring of blood volume and blood-oxygen content in the cerebral tissue.

Animals↗
PubMed1990

A prospective study of acute cerebrovascular disease in the community: the Oxfordshire Community Stroke Project--1981-86. 2. Incidence, case fatality rates and overall outcome at one year of cerebral infarction, primary intracerebral and subarachnoid haemorrhage.

The age and sex specific incidence rates for cerebral infarction, primary intracerebral haemorrhage and subarachnoid haemorrhage in a population of approximately 105,000 are presented. Over four years 675 patients with a first-ever stroke were registered with the Oxfordshire Community Stroke Project. The pathological diagnosis was confirmed by computerised tomography (CT) scan, necropsy or lumbar puncture (cases of subarachnoid haemorrhage only) in 78% of cases and a further 17% were diagnosed according to the Guy's Hospital Stroke Diagnostic Score. The proportion of all first-ever strokes by pathological type was: cerebral infarction 81% (95% confidence interval 78-84), primary intracerebral haemorrhage 10% (8-12), subarachnoid haemorrhage 5% (3-7) and uncertain type 5% (3-7). These proportions are similar to other community-based studies. The overall 30 day case fatality rate was 19% (16-22), that for cerebral infarction being 10% (7-13), primary intracerebral haemorrhage 50% (38-62) and subarachnoid haemorrhage 46% (29-63). One year post stroke 23% (19-27) with cerebral infarction were dead and 65% (60-70) of survivors were functionally independent. The figures for primary intracerebral haemorrhage were 62% (43-81) dead and 68% (50-86) of survivors functionally independent and for subarachnoid haemorrhage were 48% (24-72) dead and 76% (56-96) of survivors functionally independent. There are important differences between these rates and those from other sources possibly due to more complete case ascertainment in our study. Nevertheless, the generally more optimistic early prognosis in our study, particularly for cases of cerebral infarction, has important implications for the planning of clinical trials and for the expected impact that any treatment might have on the general population.

Adolescent↗
PubMed1980

Epilepsy in patients with cerebral infarcts.

Out of series of 240 patients, with proved cerebral infarcts at necropsy, 14 with a clinical history of epilepsy were selected. The possible etiology of seizures was analyzed by comparing the clinical and pathological data. It appeared from this series that epileptic spells, preceding for years the occurrence of a stroke, were due to other causes than to cerebrovascular insufficiency. It was also difficult to separate apoplectic seizures from those occurring due to scar formation after a cerebral infarct, as postapoplectic epilepsy was induced either by the occurrence of a new stroke or by hemodynamic disturbances. Severe generalized or local hemodynamic and metabolic disturbances were also noted in cases of convulsions resulting from a cerebral infarct.

Aged↗
PubMed1992

Cerebral infarction in a child. A case report.

Cerebral infarcts in children are rather rare and in most cases no precise etiology is established. The authors describe a case of cryptogenetic cerebral infarction in a 9-year-old boy. The child presented an acute onset of hemiplegia in the right arm and leg, central facial palsy, dysarthria and steppage. The infarction was proved by Computed Tomography (CT) and Magnetic Resonance Imaging (MRI). Laboratory and instrumental studies rule out all known causes of brain infarction. The only possible etiopathogenetic hypothesis was a varicella arteritis which occurred 45 days before the clinical manifestation.

Arteritis↗