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PubMed2003

Greater impact of coexistence of hypertension and diabetes on silent cerebral infarcts.

BACKGROUND AND PURPOSE: Silent cerebral infarcts (SCIs), often found in the elderly and hypertensives, have been proposed as an indicator of poorer cerebrovascular prognosis. The aim of this study was to evaluate the prevalence and determinants of SCI in hypertensives with or without diabetes mellitus (DM). METHODS: We studied 360 asymptomatic hypertensive subjects with or without DM (mean age, 67.4 years; range, 41 to 88 years). We performed 24-hour ambulatory blood pressure (BP) monitoring and brain MRI. The subjects were classified into a diabetic hypertension group with DM (DHT, n=159) or a non-DM hypertension group (non-DHT, n=201). RESULTS: SCIs (presence of > or =1) were found in 82% of the DHT and 58% of the non-DHT (P<0.001) group; multiple SCIs (the presence of > or =3) were found in 62% of the DHT and 35% of the non-DHT group (P<0.001); and 24-hour ambulatory BP levels were comparable between groups. DM was a powerful determinant of both SCIs (odds ratio [OR], 2.95; P<0.01) and multiple SCIs (OR, 3.05; P<0.001) independently of age and 24-hour systolic BP, whereas only multiple SCIs were associated with 24-hour systolic BP. When patients were subclassified by ambulatory BP and the presence of DM (sustained hypertension [SHT]+DM, white-coat hypertension [WCHT]+DM, SHT, and WCHT groups), the prevalence of SCI and multiple SCIs was higher in the SHT+DM than in the SHT group, and only multiple SCIs were higher in the WCHT+DM than the WCHT group. CONCLUSIONS: Diabetes was the major determinant of SCIs in both SHT and WCHT.

Adult↗
PubMed1994

[A case of occipital lobe epilepsy following cerebral infarction].

We report a rare case of occipital lobe epilepsy following cerebral infarction in bilateral occipital lobes. The patient is a seventeen-year-old female, who had cerebral infarction in bilateral occipital regions a few days after an open-heart surgery at 15 years of age. Thereafter she sometimes complained of visual field defects and ictal amaurosis. Seventeen months later, she developed a tonic seizure with ictal amaurosis, visual field defects and head deviation. On admission, results of the neurological examinations were all normal with the exception of peripheral visual field defects. Scalp electroencephalographic (EEG) findings showed paroxysmal discharges that were more prominent in the frontal to parietal leads than in the occipital leads. Sometimes the laterality of paroxysmal discharges changed. Her visual defects were diagnosed as psychogenic activity by the ophthalmological visual fields test. Simultaneous recordings of pattern reversal visual evoked potential (VEP) and electroretinograms (ERG) showed normal in 15 minute checks, but prolongation of bilateral P100 latency in 30 minute checks. These findings suggested that peripheral visual fields were disturbed. In this case, EEG findings and the initial symptoms of amaurosis and visual fields defect suggested occipital epilepsy following cerebral infarction in bilateral occipital lobes. We wish to emphasize that simultaneous VEP and ERG recording is a useful diagnostic tool for estimating visual functions.

Adolescent↗
PubMed2004

[Influence of Jieyu Huoxue Decoction on rehabilitation of patients with depression after cerebral infarction].

OBJECTIVE: To study the influence of Jieyu Huoxue Decoction on rehabilitation of patients with depression after cerebral infarction. METHODS: Fifty four patients suffered from the depression after acute cerebral infarction were randomly divided into three groups: depression control group, fluoxetine treated group and Jieyu Huoxue Decoction treated group. Eighteen patients of cerebral infarction without depression were enrolled in the no depression control group randomly. The Zung self-rating depression scale (SDS), the modified Edinburgh-Scandinavia stroke scale (MESSS) and the activities of daily living (ADL) were evaluated before treatment, 30 and 60 days after treatment. RESULTS: After 30 and 60 days of treatment, SDS evaluation of the Jieyu Huoxue Decoction treated group showed significant difference as compared with the condition before treatment and that of the depression control group (P < 0.05 or P < 0.01), MESSS evaluation and ADL evaluation also showed significant difference as compared with the condition before treatment and that of the depression control group (P < 0.05 or P < 0.01); there was no obvious difference between the fluoxetine treated group and the Jieyu Huoxue Decoction treated group, but the Jieyu Huoxue Decoction treated group showed fewer symptoms and less side effect. CONCLUSION: Jieyu Huoxue Decoction can not only relieve depression after cerebral infarction, but also improve neurological functions.

Aged↗
PubMed2004

[The status of carotid arteries and the main vascular risk factors in cerebral infarctions of "anterior circulation"].

The aim of the work was to examine the degree of carotid stenosis, the structure of atherosclerotic plaques, and the predominance of the main vascular risk factors in patients with multiple lacunar and comparatively large "non-lacunar" cerebral infarctions. A study WAS made of the data on 110 patients (mean age 62.5 years) with multiple cerebral infarctions revealed by MRT and with stenoses of the internal carotid artery (ICA) of varying degrees of severity. Minor lacunar infarctions (LI) were present in 62 cases whereas comparatively large "non-lacunar" infarctions (NLI) in 48 cases. All the patients underwent standard neurologic examination, laboratory analyses, MRT of the brain with angiography (MRA) of the extra-intrecrania1 vessels, transcranial Doppler (TCD), and examination of the heart for revealing the cardioembolic nature of cerebral infarctions. Among patients with both LI and NLI, arterial hypertension was the most frequently occurring risk factor in 53 (85%) and 35 (73%) patients respectively. In the study groups, there were no appreciable differences in the incidence of high hematocrit, hyperfibrinogenemia, tobacco-smoking, and diabetes mellitus. Patients with NLI demonstrated hypercholesterolemia, CAD and atherosclerosis of the peripheral vessels significantly more often (p<0.05). In the patient group with NLI, hemodynamically significant stenoses of the ICA were predominant: in 18 (37.5%) patients, they were moderate, in 12 (25%) critical, and 7 (14.6%) patients had occlusions whereas in LI, the portion of critical stenoses and ICA occlusions was cooperatively low - in 11 (17.7%) and in 5 (8.1%) patients respectively. Both groups showed the thickening of the complex of the medial CCA layer. Ultrasonopraphy of the vessels has revealed that in patients with NLI and LI, there predominated potentially embologenic plaques, namely in 69% and in 53% of cases, respectively. Our investigations allow to assume that arterial hypertension is the most frequently occurring risk factor of cerebral infarction (both minor lacunar and large "non-lacunar"). Factors such as CAD, hypercholesterolemia, DM, hemorheological disorders, end tobacco-smoking are likely to have an unfavorable impact on both general and cerebral hemodynamics as well as on the microcirculatory bed whereby being on the whole important risk factors of cerebral infarction. Hemodynamically significant stenoses, especially critical ones, occlusions, and embologenic plaques of the ICA are pathogenetically closely linked with the development of "non-lacunar" cerebral infarctions. At the same time they, under certain conditions, may become the cause of multiple lacunar cerebral infarctions.

Aged↗
PubMed1987

Cerebral infarction due to presumed haemodynamic factors in ambulant hypertensive patients.

The role of haemodynamic factors in the pathogenesis of cerebral infarction is unclear. Watershed or distal field infarction is most often caused by haemodynamic mechanisms. Watershed cerebral infarcts can now be identified in stroke survivors using CT scanning. The clinical findings are presented of 14 patients with cerebral infarction in whom haemodynamic factors contributed to the stroke. Evidence for this diagnosis includes (i) a history of posture-related or exercise-induced syncopal attacks or neurological deficits before and in some cases after the stroke, (ii) the demonstration of watershed or distal field infarction on CT scan, (iii) commencement of symptoms after increase in antihypertensive medications, and (iv) improvement following reduction of treatment. Regional cerebral hypoperfusion may be a more common cause of cerebral infarction than is generally thought. Particular care should be exercised when potent antihypertensive medication is prescribed for elderly hypertensive patients.

Adult↗
PubMed1998

Angiotensin-Converting Enzyme Gene Polymorphism and Plasminogen Activator Inhibitor 1 Levels in Subjects with Cerebral Infarction.

It has been suggested that the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene is an independent risk factor for coronary artery disease, but its relation to cerebral infarction is still controversial. Plasminogen activator inhibitor 1 (PAI-1) is also a predictor of risk of atherothrombotic disease. In this study we investigated the association of the ACE gene polymorphism and plasma PAI-1 levels in subjects with cerebral infarction. We evaluated the genotype of the ACE gene in 26 subjects with and 28 subjects without a history of ischemic stroke. The ACE genotype was analyzed by the polymerase chain reaction. Plasma PAI-1 antigen levels were measured by ELISA. There were no differences in accepted risk factors between the groups with or without cerebral infarction. However, the frequency of the D allele was significantly higher in subjects with cerebral infarction (0.63) than in those without infarction (0.39) (chi(2) = 6.306, P = 0.012). The frequency of the DD genotype of the ACE gene was also significantly higher in subjects with than in those without cerebral infarction (DD: 46.2%, ID: 34.6%, II: 19.2% vs. DD: 14.3%, ID: 50.0%, II: 35.7%, chi(2) = 6.689, P = 0.035). Plasma PAI-1 levels were not significantly different between groups with and without cerebral infarction. There was no association between the ACE genotype and PAI-1 levels. The DD genotype of the ACE gene is associated with cerebral infarction, which is independent of plasma PAI-1 level.

Journal Article↗
PubMedDate not supplied

Cerebral infarction associated with possible enteroviral infection in an infant.

Enterovirus infection has been rarely reported to cause cerebral infarction in infants. We describe a 2-month-old boy with right focal seizure and right hemiparesis associated with enterovirus infection during an epidemic of enterovirus 71 infection in Taiwan in 1998. Magnetic resonance imaging and angiography showed vasculitis in the left anterior cerebral artery with cerebral infarction. In the unclarified pathogenesis of cerebral disease in enterovirus infection, this case suggests focal vasculitis with subsequent cerebral infarction. Enterovirus-related vasculitis of the central nervous system is thus another consideration when facing a child with focal seizure, acute hemiplegia and cerebral infarction.

Anticonvulsants↗
PubMed1998

Cerebral infarction in young women: analysis of 130 cases.

UNLABELLED: The aim of this study was to determine the risk factors and mechanism of cerebral infarction in young women. METHODS: We evaluated 130 consecutive women younger than 41 years of age with cerebral infarction and compared the risk factors with a control group of 122 healthy, age-matched women. RESULTS: The leading risk factors in patients with cerebral infarction were migraine (15%), tobacco use (15%), and oral contraceptive (OC) use (12%). Cerebral arteriograms were abnormal in 59% of patients (57 of 96). The causes of cerebral infarction were cardiac embolism in 36%, nonatherosclerotic vasculopathy in 25%, hematologic disorders in 8%, and migraine in 8%. The etiology could not be determined in 23% of patients. CONCLUSION: Migraine and OCs are independent risk factors for cerebral infarction in young women. The leading etiologies were rheumatic valve disease and nonatherosclerotic vasculopathy, hematologic disturbances, and migraine were responsible for a few cases.

Adolescent↗
PubMed1996

[Experimental study of voiding dysfunction induced by cerebral infarction in rats].

BACKGROUND: Although clinical reports concerning voiding dysfunction after cerebrovascular disease are observed, no experimental studies have been carried out using an animal model. This study was performed to establish an animal model to evaluate neurogenic voiding dysfunction associated with cerebral infarctions. METHODS: Male Sprague-Dawley (S-D) rats weighing between 250 to 350 g were used. To induce regional cerebral infarction in rats, 4-0 monofilament nylon thread was introduced through the left internal carotid artery into the origin of the left middle cerebral artery. Cystometric examination was performed in conscious rats through a catheter chronically implanted into the bladder dome. Changes in body weight and bladder capacity were studied. The effects of intravenous oxybutynin hydrochloride, atropine and nifedipine on the conscious rat bladder were examined. By measuring the contractile response to field stimulation with added atropine and alpha, beta-methylene-ATP, the proportion of muscarinergic and purinergic innervation was compared between them. RESULTS: Bladder capacity in cerebral infarcted rats was significantly decreased just after middle cerebral artery occlusion, and 14, 21 and 28 days after occlusion reached less than half that in sham operated and untreated rats. Bladder capacity correlated with the area of infarcted lesion determined by triphenyltetrazolium chloride staining. In the cerebral infarcted rats, bladder capacity significantly increased at low concentrations of oxybutynin hydrochloride, while in the sham operated rats bladder capacity did not increase. Although an increase in bladder capacity was observed after administration of atropine both in cerebral infarcted and sham operated rats, a significant increase of residual urine was found and considered to be caused by decreased detrusor contraction pressure. Nifedipine increased bladder capacity in the cerebral infarcted rats without increasing residual urine. There was no significant difference in the proportion of muscarinergic and purinergic innervation between the cerebral infarcted and sham operated rats. CONCLUSION: These results indicate that calcium channel blocking agents may operate especially on the central nervous system rather than peripheral neuromuscular system, resulting in augmentation of the bladder capacity in the cerebral infarcted rats. Hitherto, the action of oxybutynin hydrochloride on the peripheral neuromuscular system is considered to be the most important, but in the cerebral infarcted rats its action on the central nervous system should also be considered. This type of animal model is believed to be useful to study neurogenic voiding dysfunction of human subjects with cerebrovascular disease.

Animals↗
PubMed1982

Qualitative measurement of cerebral infarction using ultraviolet fluorescence.

A reliable method of macroscopically determining the volume of cerebral infarction using ultraviolet fluorescence was developed in an animal model. Cerebral infarction was induced in 40 dogs by occluding the distal internal carotid and middle cerebral arteries. No barbiturates were administered. Intravenous sodium fluorescein was given before the animal was killed. Following fixation, 1 cm coronal sections were evaluated with ultraviolet light of 366 nm wavelength. The area of induced fluorescence for each section was determined using a grid overlay. Microscopic examination revealed that the areas of ischemic cell necrosis corresponded to areas of maximal fluorescence. This is an easily reproducible method to determine the volume of cerebral infarction.

Animals↗
PubMed1988

Cerebral infarction due to moyamoya disease in young adults.

Moyamoya disease was diagnosed as the cause of cerebral infarction in eight young adults (seven women, one man), aged 17-40 (mean 33) years. All had angiographic abnormalities characteristic of moyamoya disease. Single-photon emission tomography showed bilateral carotid circulation hypoperfusion and posterior circulation hyperemia in all seven patients with regional cerebral blood flow studies. All seven women had used oral contraceptives before cerebral infarction. Four patients were treated medically; one died of a second cerebral infarction 9 months after diagnosis. Four patients underwent superficial temporal-to-middle cerebral artery anastomosis; they did well. Moyamoya disease should be included in the differential diagnosis of cerebral infarction as well as intracranial hemorrhage in young adults, particularly women. A possible relation between moyamoya disease and oral contraceptive use deserves investigation.

Adolescent↗
PubMed1992

Early clinical differentiation of cerebral infarction from severe atherosclerotic stenosis and cardioembolism.

BACKGROUND AND PURPOSE: Hyperacute cerebral infarction trials require early differentiation of infarction subtype. Our aim was to determine clinical factors predictive of infarction subtype from data collected in the early hours of admission. METHODS: Using the 1,273 patients enrolled in the Stroke Data Bank, stroke risk factors and demographic, clinical, and radiological features were compared between the 246 cardioembolic and 113 large-vessel atherosclerotic cerebral infarcts. RESULTS: Stroke Data Bank definitions ensured more transient ischemic attacks in atherosclerotic infarcts and more cardiac disease in cardioembolic infarcts, but the diagnosis was distinguished further using a logistic regression model. Fractional arm weakness (shoulder different from hand) (odds ratio 3.1, 95% confidence interval [CI] 1.6-5.8), hypertension (odds ratio 2.8, CI 1.4-5.3), diabetes (odds ratio 2.5, CI 1.2-5.1) and male gender (odds ratio = 2.2, CI 1.2-4.1) occurred more frequently in patients with atherosclerotic than cardioembolic infarcts. Reduced consciousness (odds ratio = 3.2, CI 1.4-7.3) was more frequent in cardioembolism. For a male patient with hypertension, diabetes, and fractional arm weakness, the estimated odds of an atherosclerotic infarction were 47-fold that of a cardioembolic infarction. Patients with atherosclerotic infarcts were more likely to have a fractional arm weakness regardless of infarct size, whereas, for those with cardioembolic infarctions, fractional weakness was more frequent in infarcts less than 20 cc in volume. CONCLUSIONS: Clinical features that are observed at stroke onset can help distinguish cerebral infarction subtypes and may allow for early stratification in therapeutic trials.

Aged↗
PubMed1994

[Epidemiology of cerebral infarction].

The annual incidence of strokes (all types) is estimated to be between two and four per thousand in the 55 to 64 year age-group and reaches about 15 per thousand over the age of 75 years. Population registries and hospital registries show that cerebral infarcts represent about 80% of all strokes and indicate the respective roles of the principal causes. A significant reduction in mortality related stroke in general and cerebral infarction in particular has been observed in many countries over recent decades. Hypertension constitutes the principal risk factor for ischaemic and haemorrhagic stroke. This risk varies by about 40% when the mean diastolic blood pressure varies from 5 to 10 mmHg, even in normotensive subjects. Several studies have demonstrated that treatment of moderate or severe hypertension lowers the incidence of stroke. Smoking, diabetes, chronic alcoholism (> 3 standard glasses per day), hypercholesterolaemia and raised plasma fibrinogen also constitute independent risk factors for cerebral infarction. Of the emboligenic heart diseases, non-valvular atrial fibrillation (80% of all cases of atrial fibrillation) is the most potent risk factor for cerebral infarction: subjects with this disease have a risk of cerebral infarction of approximately 5% per year. The presence of asymptomatic carotid artery stenosis is associated with an annual risk of cerebral infarction generally estimated to be between 1 and 2% which, in reality, increases with the degree of stenosis. Even in the case of tight stenosis, the risk of ipsilateral cerebral infarction remains low (< 3% per year for stenosis > 75%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2003

[Changes of serum cholesterol, high-density lipoprotein and serum lipoprotein electrophoretogram in senior patients with cerebral infarction].

OBJECTIVE: To investigate the changes in the levels of serum cholesterol and high-density lipoprotein and in serum lipoprotein electrophoretogram in elderly patients with cerebral infarction. METHODS: Serum lipoprotein electrophoretograms (SLPG) of 118 elderly patients with cerebral infarction and 60 healthy elderly subjects were measured by means of double gradient polyacrylamide gel electrophoresis, and the serum concentrations of total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) were determined by enzymatic method. RESULTS: Compared with the control group, the serum level of HDL-C was significantly increased in the patients (1.0+/-0.3 mmol/L), who also had decreased TC/HDL-C ratio (5.3+/-1.4), but no significant difference occurred in terms of TC concentration between these two groups. Among the patients with cerebral infarction, 86.4% had abnormalities of SLPG, especially in the alpha-lipoprotein electrophoretogram (P<0.001-0.05) regardless of HDL-C elevations. CONCLUSIONS: Decreased HDL-C, elevated TC/HDL-C ratio and abnormal SLPG may be the risk factors for the onset of cerebral infarction in senior patients, for which alpha-lipoprotein electrophoretogram can be more sensitive than serum HDL-C level. TC levels is of little value in predicting cerebral infarction.

Aged↗
PubMed1991

One-year outcome after cerebral infarction in whites, blacks, and Hispanics.

Little is known about outcome after cerebral infarction for different ethnic groups. Of 590 stroke patients hospitalized from 1983 to 1986 at the Neurological Institute, cerebral infarction over age 39 years occurred in 135 whites, 177 blacks, and 82 Hispanics. Outcome after cerebral infarction differed by ethnicity. The 1-month mortality rate was similar in whites and blacks and least in Hispanics. Whites had a slightly greater risk of recurrent stroke or death than blacks or Hispanics until 6 months after infarction, when their risk stabilized, while the risk in blacks and Hispanics continued to rise for the entire year of follow-up. By 1 year, the rate of recurrent stroke or death was 34.8 +/- 4.2% in whites, 31.1 +/- 3.6% in blacks, and 21.4 +/- 4.8% in Hispanics (p = 0.04). Differences were found in the distribution of various stroke risk factors in the three ethnic groups. A Cox proportional hazards model demonstrated that the ethnic differences in stroke risk factors and infarct subtype were responsible for the ethnic differences in outcome. An abnormal first electrocardiogram was a risk factor for stroke recurrence or death in all three ethnic groups, while a nonlacunar infarct subtype and a history of diabetes were significant only in Hispanics. Understanding the associations of stroke determinants with ethnicity may lead to more focused secondary prevention of recurrent stroke.

Aged↗
PubMed2005

Cerebral infarction: incidence and risk factors after diagnostic and interventional cardiac catheterization--prospective evaluation at diffusion-weighted MR imaging.

PURPOSE: To prospectively evaluate incidence of clinically silent and clinically apparent embolic cerebral infarction following diagnostic and interventional coronary angiography and associated risk factors. MATERIALS AND METHODS: Written informed consent was obtained from all patients, and the study was approved by the research ethics committee of University of Heidelberg, Germany. Fifty-two patients, including 37 men (mean age, 66.1 years +/- 11.9 [standard deviation]) and 15 women (mean age, 65.3 years +/- 10.3), undergoing elective cardiac catheterization were examined 3-26 hours (mean, 15.3 hours +/- 6) before and 12-48 hours (mean, 25.9 hours +/- 10.4) after cardiac catheterization. Magnetic resonance imaging protocol included isotropic and anisotropic diffusion-weighted single-shot echo-planar sequences. T2-weighted turbo spin-echo and T1-weighted spin-echo sequences also were performed. Apparent diffusion coefficient maps were calculated to exclude false-positive reading results on diffusion-weighted images because of T2 shine-through effect. Images were assessed by two experienced radiologists blinded to clinical data. Cardiac catheterization was performed by 11 experienced cardiologists to exclude operator-related risk. A neurologic examination according to the National Institutes of Health Stroke Scale and Barthel index was performed by a senior cardiologist before acquisition of each image. Sixteen clinical and angiographic variables were analyzed with univariate analysis for ability to predict occurrence of cerebral infarction. RESULTS: No embolic cerebral lesions could be detected at diffusion-weighted imaging before catheterization. After coronary angiography, seven (15%) of 48 patients demonstrated nine focal cerebral infarcts affecting anterior and posterior circulation. Patients remained asymptomatic. Of all tested variables, only duration of the procedure was identified as an independent predictor of occurrence of cerebral infarction (P < .05). CONCLUSION: In this prospective study, asymptomatic cerebral infarction following cardiac catheterization occurred in 15% of patients in whom duration of the procedure was significantly longer than in those without infarction (P = .017).

Aged↗
PubMed1978

[Experimental cerebral infarction. Part 1: Production of thalamus infarction model in dogs (author's transl)].

Difficulties in producing temporary cerebral ischemia in experimental animals have delayed the study on the prevention and treatment of cerebral infarction. Although occlusion of the middle cerebral artery in dog proved to be fruitless, we eventually succeeded in producing focal cerebral infarction by temporary occlusions of brain arteries. Infarction confined to the anterior portion of the thalamus was obtained by simultaneous occlusion of four arteries for 60 or 120 minutes: internal carotid, anterior cerebral, middle cerebral and posterior communicating arteries. This experimental model in dogs is unique, since a marked infarction can be seen in high frequency, and the dogs can be managed for sufficient periods after temporary clipping. Consequently, it is possible to investigate cerebral infarction not only from the pathophysiological viewpoint, but also for its prevention and treatment.

Animals↗