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PubMed1998

[Significance of pontine high signal intensity lesions on magnetic resonance imaging in patients with cerebral infarction].

We reviewed MRI findings in a series of 211 patients with cerebral infarction. A high signal in the basis pontis bilaterally in T2 weighted images (Central Pontine Hyperintensity, CPH), with almost-normal T1 weighted images, was present in 29 cases (12.9%). CPH findings were present more frequently in elderly patients, and were significantly associated with a previous history of cerebrovascular accident, although not with other arteriosclerotic risk factors. In patients with CPH. periventricular hyperintensity was severe and the number of infarctions of the thalamus was higher. These results suggest that a) CPH may arise from ischemia in subcortical areas or in the territory of the vertebrobasilar system, and that b) chronic brain ischemia, which may be partially due to aging, may play a more important role in cerebral infarction than the usual arteriosclerotic risk factors.

Adult↗
PubMed2003

[Risk factors for intracerebral hemorrhage after intravenous thrombolysis in acute cerebral infarction].

OBJECTIVE: To identify risk factors of intracerebral hemorrhage (ICH) after intravenous thrombolysis in acute cerebral infarction. METHODS: Eighty-two patients with acute cerebral infarction were treated with intravenous urokinase within 12 hours from stroke onset. The data of clinic and laboratory were as readily available baseline factors and were analyzed to select potential contributors to ICH. RESULTS: ICH occurred in 15 patients (18.3%), including 6 hemorrhagic infarction (HI, 7.3%) and 9 Parenchyma hemorrhage (PH, 11.0%). Seven patients had symptomatic ICH, and 4 patients died. Patients with ICH had significantly lower European stroke scale (ESS) scores. Patients with ESS<60 scores, early ischemic changes (EIC) on cranial CT scans or artrial fibrillation had significantly higher risk of ICH. CONCLUSION: Risk factors associated with ICH are severity of neurological deficit, EIC and artrial fibrillation.

Adult↗
PubMedDate not supplied

[Antioxidant enzymes in acute cerebral infarction].

BACKGROUND AND PURPOSE: Oxidative modification of DNA, protein and lipids by reactive oxygen peroxides plays an important role in acute cerebral infarction. The biological antioxidant defence system against oxidative stress is an integrated array of enzymes such as superoxide dismutase (SOD), catalase (CAT) and glutathion peroxidase (GPx). The purpose of this work was: 1. To investigate the evolution of SOD and CAT activities as possible markers of oxidative activity in patients with acute cerebral infarction. 2. To establish the relationship between the type of stroke and the activity of these two enzymes. 3. To analyze the relationship between the degree of neurological deficits of patients with stroke and SOD and CAT activities. PATIENTS AND METHODS: This is a prospective study comprising 45 patients with acute cerebral infarction (24 females and 21 males), aged from 48 to 96. The infarcts were classified in atherotrombotics and cardioembolics. SOD and CAT activities were measured on days 1, 3, 6 and 15. RESULTS: Activities of SOD and CAT in patients on admission were lower than those of controls and showed a gradual increase over time. The activity mean of SOD was significantly higher in cardioembolic infarctions than in atherotrombotic infarctions (p < 0.05). SOD activity was significantly lower for Mathew score > 60, while CAT activity was higher. CONCLUSIONS: Our findings suggest that there is a progressive increase in SOD and CAT activity during ictus evolution, a different activity of SOD and CAT in cardioembolic and atherotrombotic infarctions, and that there is a relationship between activity of antioxidant enzymes and Mathew's score.

Acute Disease↗
PubMed1991

[Multiple cerebral infarctions during a migraine attack].

Two cases of migraine complicated with ischemic cerebral infarct are reported. Both met the established criteria for the diagnosis: definite history of classical or common migraine, development of an ischemic infarct during the crisis, duration of deficit lasting more than 24 hours and absence of other causes of cerebrovascular disease. Several laboratory examinations were carried out: routine blood tests, coagulation study, immunological study, serological tests for syphilis, ECG, echocardiogram, cerebral CT, and nuclear magnetic resonance imaging and angiography. The most remarkable finding in these two patients were multiple cerebral infarcts in different vascular territories. This fact is exceptionally reported in the literature. The clinical outcome of the patients was characterized by the virtually complete reversal of neurological deficit.

Adult↗
PubMed2005

[Optimum selection of acupuncture treatment programs of cerebral infarction and its effects on insulin resistance].

OBJECTIVE: To study the optimum acupuncture treatment program and the mechanism for treatment of cerebral infarction. METHODS: Sixty-three cases were randomly divided into 9 groups. The four factors, times of manipulation, the retaining time of the needle, acupuncture instrument and acupoints,and their corresponding three levels were adopted respectively in treatment of each group. Then nerve function defect score and insulin resistance were observed before and after treatment. RESULTS: The acupoints, the times of manipulation and the retaining time of the needle have significant effects on nerve function defect and insulin resistance (P < 0.01 or P < 0.05), and the acupuncture instrument has a significant effect on insulin resistance (P < 0.01). The choice of acupoints was the most important factor for acupuncture treatment of cerebral infarction. CONCLUSION: Acupuncture for regulating The Governor Vessel with twice manipulations and retaining the needle for 60 min is optimum treatment program for cerebral infarction. The good regulating effect of acupuncture on insulin resistance is one of the mechanisms of achieving the therapeutic results.

Acupuncture Points↗
PubMed2006

Correlation between fibrinogen level and cerebral infarction.

OBJECTIVE: To investigate the correlation between plasma fibrinogen level and cerebral infarction (CI) as well as the difference of fibrinogen among subtypes of CI. METHODS: A case-controlled study was conducted with 131 cases of CI and 148 controls. Plasma fibrinogen levels were detected by the Clauss method. RESULTS: High fibrinogen level (3.09 +/- 0.94 g/L) was correlated with CI (OR = 2.47, 95% CI: 1.51-4.04, P < 0.005) at the onset stage of the disease. Persistent high fibrinogen level (3.14 +/- 0.81 g/L) at 6-month after stroke onset was detected and correlated with CI (OR = 4.34, 95% CI: 1.80-10.51, P = 0.001). Higher fibrinogen level was correlated with total anterior circulation infarction (TACI), partial anterior circulation infarction (PACI), and posterior circulation infarction (POCI) (OR = 4.008, P < 0.001). Higher fibrinogen level was correlated with extracranial atherosclerosis (OR = 3.220, P < 0.05, but not with intracranial atherosclerosis. CONCLUSION: Fibrinogen level may be a risk factor of CI and probably correlates with subtypes of CI and distributions of atherosclerosis.

Aged↗
PubMed1995

Lipoprotein(a) and other risk factors for cerebral infarction.

The serum concentration of lipoprotein(a) [Lp(a)], lipids, lipoproteins, apolipoprotein A-I, and apolipoprotein B were determined in 228 patients with cerebral infarction, composed of 87 cases of asymptomatic lacunar infarction, 99 cases of lacunar infarction, and 42 cases of atherothrombotic infarction, and in a control group of 138 healthy subjects with normal MRI. Observations were made on the distribution of Lp(a), Lp(a) and other risk factors for cerebral infarction and these were statistically analyzed, primarily by multiple logistic regression analysis. The diagnosis of these cases was based on the Classification of Cerebrovascular Diseases III of the National Institute of Neurological Disorders and Stroke. The following results were obtained. 1) Lipoprotein (a) (1) Lp(a) did not show a normal distribution with the curve showing a gradual declining slope to the right. It was therefore considered not appropriate in our analysis to use as a means or standard deviation. (2) The 25th percentile, 50th percentile, and 75th percentile of the control group were 5.0 mg/dl, 11.0 mg/dl, and 22.4 mg/dl, respectively. In studying the distribution in these percentile ranges by subtypes of infarction, an increase in cases showing values greater than the median of the control group was observed in asymptomatic lacunar infarction, lacunar infarction, and atherothrombotic infarction, when compared to the control group. In asymptomatic lacunar infarction and lacunar infarction in particular, Lp(a) showed a significantly higher value compared to the control group. (3) However, by multiple logistic regression analysis to adjust for age and sex, Lp(a) did not show a significant odds ratio for asymptomatic lacunar infarction, lacunar infarction and atherothrombotic infarction. 2) Various serum lipids and other parameters (1) The various serum lipids did not show any involvement in asymptomatic lacunar infarction. However, involvement of HDLC and Apo A-I in lacunar infarction and atherothrombotic infarction was observed with the odds ratios in lacunar infarction being 4.2 with a confidence interval of 2.9-9.4 and 4.7 with a confidence interval of 2.2-10.1, and the odds ratios in atherothrombotic infarction being 3.1 with a confidence interval of 1.1-9.0 and 9.6 with a confidence interval of 3.0-30.5, respectively. (2) Involvement of diabetes mellitus in asymptomatic lacunar infarction and lacunar infarction was small, but a strong involvement in atherothrombotic infarction was observed with the odds ratio being 4.3 with a confidence interval of 1.2-16.2. (3) Involvement of hypertension in asymptomatic lacunar infarction and lacunar infarction was observed with the odds ratios being 2.6 with a confidence interval of 1.4-5.2 and 5.6 with a confidence interval of 2.4-13.0, respectively, but the involvement in atherothrombotic infarction was low. The foregoing results indicated that there was no involvement of Lp(a) as a risk factor for any type of cerebral infarction, unlike its involvement in coronary heart diseases. Only blood pressure was involved as a risk factor for asymptomatic lacunar infarction, but for lacunar infarction not only blood pressure but also HDLC and Apo A-I were involved as risk factors. HDLC, Apo A-I, and diabetes mellitus were involved as risk factors for atherothrombotic infarction, but the involvement of hypertension was minimal.

Aged↗
PubMed1979

Unresponsiveness to hypoglycemia of centers controlling epinephrine release in cerebral infarct patients.

Urinary excretion of catecholamines under insulin hypoglycemia was studied in cerebral infarct patients as well as in patients with Parkinson's disease and subjects with lumbar discopathy (control group). While in the last two categories of subjects a normal response to hypoglycemia, i.e., an increase in urinary excretion of epinephrine was noticed, no such increase was found in patients with cerebral infarction. The disorder is attributed to the unresponsiveness to hypoglycemia of the brain stem centers controlling epinephrine secretion.

Blood Glucose↗
PubMedDate not supplied

Functional recovery and social outcome after cerebral infarction in young adults.

This study was designed to assess the return to work, the poststroke depression and the quality of life after a cerebral infarction in young adults and was conducted on 71 consecutive young patients (aged 15-45 years) affected by a cerebral infarct who were hospitalized for the first time and discharged at least 1 year before the study. Data about risk factors, etiology, side and territory of stroke, social characteristics of the patient (age, sex, profession, educational level, family situation), poststroke seizures, recurrent stroke, other vascular events, and deaths were collected. Neurological deficits were graded with the National Institutes of Health (NIH) Stroke Scale. Poststroke depression (PSD) was quantified using the DSM-IIIR criteria and the Montgomery Asberg Depression Rating Scale. Outcomes were rated with the Ranking Scale, the Barthel Index and the Glasgow Outcome Scale. Quality of life was assessed with the Sickness Impact Profile. Follow-up information was obtained by interview and neurological examination. Follow-up information was obtained in 65 patients at a mean of 31.7 +/- 13.0 (range 12-59) months, as 2 patients died and 4 were lost to follow-up and were thus excluded from this study. Poststroke seizures occurred in 7 patients (10.8%) and recurrent strokes in 4 patients (6.2%), but none were fatal. The outcome after stroke among survivors was usually good, since more than two-thirds of the patients (69.8%) reported no problem, 11.1% moderate handicap and one-fifth major handicap. Forty-six patients (73%) returned to work: the time period ranging from several days after stroke to 40 months, with a mean of 8 months. However, adjustments in their occupation were necessary for 12 patients (26.1%). PSD was common, since 48.31% of the patients were classified as depressed. PSD was associated with the localization of the infarct (carotid territory), a severe disability, a bad general outcome, and an absence of return to work. Their opinion about their quality of life was negative among approximately 30% of the patients, especially in emotional and alertness behaviors. social interaction, recreation and pastimes. The general outcome after cerebral infarct in young adults is usually good. However, the risk of a PSD is high, and only half of the patients had returned to their previous work. A remaining psychosocial handicap and depression of sexual activity impaired the quality of life. In multivariate analysis, a low NIH score at admission is a significant predictor for return to work, the absence of PSD, and a good quality of life.

Adolescent↗
PubMed1979

Hypercapnic alteration of visual evoked responses in acute cerebral infarction.

To determine the effect of inhaled carbon dioxide on acute ischemic cerebral injury, we have compared occipital visual evoked responses (VER) at baseline and during hypercapnia in 20 patients with acute unilateral cerebral infarction (ten with and ten without homonymous hemianopsia) and in ten normal controls. Visual evoked responses were judged on the basis of interhemispheral symmetry. In eight of ten controls and six of 20 patients, baseline VERs were symmetrical and remained unchanged during hypercapnia. In 14 patients with asymmetrical baseline VERs, hypercapnia caused improvement of symmetry in five, worsening in three, and no change in six. Hypercapnic vasodilation may be either beneficial or deleterious to cerebral function in patients with acute cerebral infarction.

Acute Disease↗
PubMed1989

Cerebral infarction due to disseminated intravascular coagulation with thromboexclusion for dissecting aortic aneurysma.

Cerebral infarction due to chronic disseminated intravascular coagulation (DIC) after thromboexclusion for thoracic dissecting aortic aneurysma is described. Chronic DIC may be caused by the delay of thrombus formation at the site of thromboexclusion, and local DIC occurred at that site. It is difficult to find chronic DIC. This case shows that DIC after thromboexclusion for dissecting aortic aneurysma may be one of the causes of recurrent cerebral infarction.

Aortic Dissection↗
PubMed1994

Magnetic resonance contrast enhancement in cerebral infarction.

Contrast enhancement may aid significantly in the diagnosis, dating, and grading of cerebral infarctions. On MR imaging, four patterns of contrast enhancement may be distinguished: intravascular, meningeal, transitional, and parenchymal. Each pattern has a different appearance, time course, and clinical significance. The anatomic and physiologic mechanisms that give rise to these distinct types of contrast enhancement in cerebral infarction are discussed.

Brain↗
PubMed1997

[Motor function outcome and changes in motor impairment level of the upper limbs and fingers in patients with acute carotid-system cerebral infarction].

Early diagnosis of motor function status and changes in motor impairment level of the upper limbs and fingers in patients with acute cerebral infarction is important in establishing a treatment plan. This study investigated a method of predicting motor function outcome and changes in motor impairment based on the characteristics of symptoms on admission and severity according to the CT classification. The subjects were 309 patients with carotid-system cerebral infarction admitted on the day of onset of symptoms and who exhibited a low density area in the territory of the middle cerebral artery on CT images within 5 day of the onset of symptoms. The motor function level was evaluated according to Brunnstrom's stage. The findings were as follows: 1) The motor function level of the upper limbs and fingers improved to stage 3 or more in patients without unilateral neglect. 2) Complete recovery of motor impairment of the upper limbs and fingers was observed in 163 patients (54.7%). Motor impairment of the upper limbs recovered within 3 weeks after the onset in 121 patients, and from 22 days to 3 months after the onset in the remaining 42 patients. Similarly, motor impairment of the fingers recovered within 3 weeks after the onset in 113 patients, and between 22 days and 3 months after the onset in the remaining 50 patients. 3) Stage 4 or higher motor impairment grade on admission was seen in 107 (88.4%) of the patients with recovery of impaired motor function in the upper limbs within 3 weeks after the onset. Similarly, stage 4 or higher was seen in 101 (89.4%) patients with recovery of impaired motor function of the fingers within 3 weeks after the onset. 4) Of the 44 patients with recovery of impaired motor function of the upper limbs between 22 days and 3 months after the onset, 30 improved to stage 4 by 2 weeks after the onset and to stage 6 by one month. The remaining 12 patients improved to stage 5 by one month after the onset and to stage 6 by 3 months. Of the 50 patients with recovery of impaired motor function of the fingers between 22 days and 3 months after the onset, 44 improved to stage 4 by 2 weeks after the onset and to stage 6 by one month. The remaining 6 patients improved to stage 5 by one month after the onset and to stage 6 by 3 months. 5) Progressive stroke was observed in 60 patients (20.1%). All patients with progressive stroke showed unilateral neglect on admission. 6) Completed stroke, excludise of progressive stroke, was seen in 75 patients (24.3%). In the patients with completed stroke, there was clearly no improvement in the motor impairment of the limbs and fingers over 3 months after onset. 7) It was difficult to predict motor function level at the time of discharge based on the evaluation of stage on admission and the location of the low density area on CT. 8) Our CT classification was closely correlated with the motor function outcome of the upper limbs and fingers. Therefore, this classification and assessment of whether unilateral neglect is present on admission may be useful in predicting motor function outcome and changes in motor impairment of the upper limbs and fingers early after the onset of acute cerebral infarction.

Adult↗
PubMed1998

[Cerebral infarction associated with nephrotic syndrome in a young adult: a case report].

We report a 19-year-old man who developed a cerebral infarction in the territory of the anterior choroidal artery and showed a hypercoagulable state and nephrotic syndrome after diarrhea and appetite loss. He had suffered from nephrotic syndrome from the age of three and had been treated for five years. MR-angiography showed an occlusion originating in the right internal carotid artery. The right anterior and middle cerebral arteries were imaged from the left internal carotid artery via the anterior communication artery. He showed symptoms of left hemiparesis, agnosia, loss of activity, anasarca and left hypacusis following his clinical course, but had recovered from all but left hemiparesis following medical treatments including steroid therapy. The histologic finding by a renal biopsy revealed focal glomerulosclerosis. In this case, we considered that when he was in a hypercoagulable state and had a second attack of nephrotic syndrome because of inflammation and dehydration due to diarrhea and appetite loss, his hypercoagulable state grew worse, and he then developed a cerebral infarction. When one see a patient with nephrotic syndrome, one should be attentive to the possibility of a complication of cerebral infarction.

Adult↗
PubMedDate not supplied

Cholesterol crystal embolization in rat brain: a model for atheroembolic cerebral infarction.

Acute and delayed effects of embolizing cerebral surface vessels with cholesterol crystals were studied by direct observation in anesthetized rats and rabbits, using an open-skull technique, and by histological examination of brains at intervals of one day and one week following embolization. The number and size spectrum of crystals, which were infused into the ipsilateral internal carotid artery, were believed to approximate those released by a rupturing large atheromatous plaque in man, but the other lipid materials contained in such plaques were intentionally excluded. It was found that cholesterol crystals had only limited ability to impede blood flow in the 20--80 mu diameter arteries in view. They were also inert within the lumen, causing no vessel wall reaction even after a week; nor was any evidence seen of a thrombogenic effect. Local caliber changes in the containing artery were reproducibly seen, with dilatation of the arterial segment proximal to the embolus and narrowing of the segment in front. These changes appeared to represent an active response of the vessel wall, rather than a passive response to alterations in intraluminal pressure. The difficulty in subsequently locating cholesterol emboli histologically was confirmed. Possible therapeutic implications for atheroembolic cerebral infarction in man were discussed.

Animals↗
PubMed1989

Determinants of early recurrence of cerebral infarction. The Stroke Data Bank.

We studied 1,273 patients with ischemic cerebral infarction who were entered into the Stroke Data Bank, a prospective, observational study involving four university hospitals and the Biometry and Field Studies Branch of the National Institute of Neurological Disorders and Stroke. Forty patients had noniatrogenic recurrent stroke within 30 days after the index cerebral infarction. Using life tables, the 30-day cumulative +/- SE risk of early recurrence for all infarctions was 3.3 +/- 0.4%. The risk of early recurrence was greatest for atherothrombotic infarction (7.9 +/- 2.2%, eight of 113 patients) and least for lacunar infarction (2.2 +/- 1.2%, eight of 337 patients). Both cardioembolic infarction (4.3 +/- 0.9%, 10 of 246 patients) and infarction of undetermined cause (3.0 +/- 0.5%, 14 of 508 patients) had intermediate risks. History of hypertension and diabetes mellitus, as well as diastolic hypertension and elevated blood sugar concentration at admission, were associated with early recurrence. Logistic regression analysis estimated the risk of early recurrence to be 8.56% in those with coexisting hypertension and a glucose concentration of 300 mg/dl versus 0.77% in the absence of these two abnormalities. Early recurrence was associated with longer median duration of initial hospital stay (27 vs. 14 days) and a higher 30-day case-fatality rate (20% vs. 7.4%). Increased weakness scores were associated with early recurrent stroke. Identification of the determinants of early recurrent stroke may lead to better secondary prevention and may help select high-risk patients for further study.

Academic Medical Centers↗
PubMed2006

Risk-factor profile for the incidence of subarachnoid and intracerebral haemorrhage, cerebral infarction, and unspecified stroke during 21 years' follow-up in men.

AIMS: To study the risk-factor profile for the incidence of non-fatal and fatal stroke among middle-aged men according to the stroke subtypes subarachnoid or intracerebral haemorrhage, cerebral infarction, and unspecified stroke. METHODS: The study design is a prospective cohort study. A total of 16,209 men aged 40-49 years resident in Oslo were screened for cardiovascular disease risk factors in 1972-73. Of these, 14,403 men had no cardiovascular symptoms or diseases or diabetes. The incidence of stroke after 21 years of follow-up of all men was extracted from hospital records and linkage to Statistics Norway. RESULTS: A total of 429 non-fatal and 107 fatal stroke events were registered. Case fatality within 28 days (number and percentage of cases) was 51% (41, 7.7%) for subarachnoid haemorrhage, 39% (67, 12.6%) for cerebral haemorrhage, 10% (246, 46.3%) for cerebral infarct, and 19% (177, 33.4%) for unspecified stroke. Risk of stroke (not subarachnoid haemorrhage) increased with the presence of symptoms or a history of cardiovascular disease or diabetes. In multivariate analysis of men without CVD or diabetes, high blood pressure was a risk factor for all subtypes of stroke; furthermore, daily smoking was a risk factor for all subtypes except subarachnoid haemorrhage. Serum cholesterol and glucose concentrations and height (inverse association) were independently associated with cerebral infarction. Smoking was a significantly stronger predictor of fatal than non-fatal events. CONCLUSIONS: The risk-factor profile differed according to the underlying subtype of stroke. Cerebral infarction clearly shared with myocardial infarction the classical risk factors, including non-fasting glucose concentration.

Adult↗
PubMed1993

Risk factors for dementia associated with multiple cerebral infarcts. A case-control analysis in predominantly African-American hospital-based patients.

OBJECTIVE: To clarify risk factors for dementia associated with cerebral infarction. DESIGN: Case-control study. SETTING: The study was conducted in a hospital setting. PATIENTS: The subjects were consecutive patients with acute stroke with multiple cerebral infarctions who were admitted to the hospital between November 1, 1987, and December 1, 1990. They were predominantly elderly African Americans. Index cases met criteria of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, for multi-infarct dementia, whereas control subjects were patients with multiple infarcts who did not have dementia. There were 61 multi-infarct disease index cases and 86 controls without cognitive impairment. MAIN OUTCOME MEASURES: Demographic and cardiovascular disease risk factor variables. RESULTS: Index cases were older (mean [+/- SD] age, 75.5 +/- 9.7 vs 69.6 +/- 9.1 years), were less well educated (odds ratio, 4.37; confidence interval, 2.12 to 9.04), had lower annual incomes (odds ratio, 8.82; confidence interval, 2.38 to 32.70), more frequently had a family history of dementia (odds ratio, 3.61; confidence interval, 1.09 to 11.96) and laboratory evidence of proteinuria (odds ratio, 3.66; confidence interval, 1.54 to 8.71), had lower scores on neuropsychological tests, had more neurologic signs and symptoms, and were more functionally impaired in activities of daily living. Multiple logistic regression analysis showed that advanced age, lower educational attainment, history of myocardial infarction, and recent cigarette smoking were positively associated with case status and systolic blood pressure level was negatively associated with case status. CONCLUSIONS: Cardiovascular disease risk factors may be modifiable predictors of dementia associated with cerebral infarction. Additional well-designed epidemiologic studies are needed to clarify these associations.

Black or African American↗