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PubMed1996

[A case of cerebral infarction due to dissection in a branch of the middle cerebral artery].

A 65-year-old man developed left drop hand, dysarthria and emotional incontinence. Brain CT and MRI revealed multiple cerebral infarctions in the cortex and subcortical white matter of the right temporal and parietal lobes which were in the distribution of the right middle cerebral artery. Cerebral angiography disclosed segmental narrowing (string sign) and two pseudoaneurysms in the right angular artery which were diagnosed as dissecting aneurysm of a branch of the middle cerebral artery. In this case, cerebral angiography was more useful than MRI in diagnosis of dissecting aneurysm of a branch of the middle cerebral artery. This was a very rare case of dissecting aneurysm of the middle cerebral artery localized in one of its branches.

Aged↗
PubMed2000

[Diagnosis of acute cerebral infarction using diffusion-weighted imaging by low field (0.2 T) magnetic resonance image].

The purpose of this study is to confirm the diagnosis of acute cerebral infarction on diffusion-weighted imaging using low field (0.2 T) magnetic resonance image(MRI). Acute cerebral infarctions in 51 patients were examined on diffusion-weighted imaging using low field MRI within 48 hours after clinical symptoms. Diffusion-weighted imaging was examined using line scan method. Twenty-four cases were cortical infarction, and twenty-two cases were perforating infarction. In five cases out of 51 cases, ischemic regions were not detected as abnormal high signal intensity area on diffusion-weighted imaging. Four cases of no abnormal detection were transient ischemic attack, and the other one was a perforating infarction. The earliest detection time in cortical infarction cases was 1 hour and 20 minutes. On the other hand, the earliest detection time in perforating infarction cases was 3 hours. Detective ability for acute cerebral infarction on diffusion-weighted imaging by low field MRI was depending on both size and lesion of infarction. That is to say, either small size or brain stem infarction was hard to detect. Thin slice and vertical slice examination for the infarction may improve to diagnose in low field MRI. Our conclusion is acute cerebral infarction was able to be diagnosed on diffusion-weighted imaging by low field as well as high field MRI.

Acute Disease↗
PubMed2001

[Study on endothelial dysfunction and platelet activation in elderly hypertensive patients complicated with cerebral infarction].

OBJECTIVE: The aim of this paper was to investigate endothelial dysfunction, platelet activation, and inflammation in elderly hypertensive patients and those complicated with cerebral infarction. METHODS: Twenty-eight elderly hypertensive patients complicated with cerebral infarction(within 72 hours after onset of neurological symptoms), thirty-one Stage I-II elderly hypertensive patients and twenty-eight elderly healthy individuals were selected as subjects. Their plasma concentrations of von Willebrand factor(vWF), alpha granule membrane protein-140(GMP-140), and serum concentrations of C-reaction protein(CRP) were examined. RESULTS: Elderly hypertensive patients complicated with cerebral infarction had significantly higher plasma vWF, GMP-140, and serum CRP than elderly hypertensive patients and elderly healthy individuals. Plasma vWF and GMP-140 were higher in elderly hypertensive patients than elderly healthy individuals, whereas serum CRP was increased slightly and there was no significant difference between elderly hypertensive patients and elderly healthy individuals. CONCLUSION: This study suggests that elderly hypertensive patients complicated with cerebral infarction have obvious endothelial dysfunction, platelet activation, and inflammatory change. Stage I-II elderly hypertensive patients have obvious endothelial dysfunction and platelet activation as well.

Aged↗
PubMedDate not supplied

Cerebral infarctions and the relationship of depression symptoms to level of cognitive functioning in older persons.

OBJECTIVE: Recent studies report an association between depressive symptoms and cognitive impairment in old age. The neurobiologic basis of this association is unknown. The authors examined whether cerebral infarcts (present in 55 persons) accounted for the association of depressive symptoms with cognitive impairment in a group of 153 older Catholic nuns, priests, and brothers (67 with dementia and 86 without dementia). METHODS: Subjects underwent detailed clinical evaluations and brain autopsy at death. RESULTS: Mean values for depressive symptoms during the time of participation were associated with level of cognitive functioning proximate to death in analyses that controlled for age, sex, education, and Alzheimer disease (AD) pathology. The association of depressive symptoms with cognitive functioning was essentially unchanged after controlling for cerebral infarctions, which suggests that depressive symptoms, cerebral infarctions, and AD pathology were independently related to cognitive function. Similar results were found in analyses with episodic memory, semantic memory, working memory, perceptual speed, and visual-spatial ability. The results did not change in analyses examining the volume or location of cerebral infarctions. CONCLUSIONS: These data suggest that cerebral infarctions do not account for the association of depressive symptoms with level of cognitive functioning. The neurobiologic basis for this association remains to be elucidated.

Aged↗
PubMed2000

Is decompressive craniectomy for acute cerebral infarction of any benefit?

BACKGROUND: Acute occlusion of the major cerebral arteries results in ischaemic changes to the brain, without time for reperfusion by the collateral circulation. The subsequent cellular events lead to a breakdown of the blood-brain barrier, causing malignant cerebral edema manifested clinically by a rapid neurological deterioration. The aim of this study was to determine the value of surgical decompression in patients who present with acute cerebral infarction. METHODS: Retrospective review of patients with deteriorating consciousness level from massive cerebral ischemia and secondary edema, treated by decompressive craniectomy. RESULTSThere were 10 patients over a 2-year period from 1997-99, consisting of seven male and three female patients (mean age 47.56 years) with a mean preoperative Glasgow Coma Scale (GCS) score of 6/15. Three patients had dominant middle cerebral artery (MCA) infarction, four had nondominant MCA infarction, one had posterior cerebral artery infarction, and the remaining two had cerebellar infarction. At a mean follow-up period of 7 months, two patients had died (20% mortality), four patients (40%) were vegetative or severely disabled, and the remaining four patients (40%) had mild disability or good outcome. Favorable prognostic factors were younger age (less than 50 years) and good initial GCS score (14 or better). CONCLUSION: Decompressive craniectomy in the setting of acute brain swelling from cerebral infarction is a life-saving procedure and should be considered in younger patients who have a rapidly deteriorating neurologic status.

Adult↗
PubMed2002

[Clinical curative effect of dengzhanhua injection on acute cerebral infarction: a report of 100 cases].

OBJECTIVE: To observe the clinical curative effect of dengzhanhua injection on acute cerebral infarction. METHODS: One hundred cases of acute cerebral infarction were treated with dengzhanhua injection (Group A) and 62 treated with fufangdanshen injection (Group B). The curative effects and the patients' hemorrheology and lipemia before and after the treatment were compared. RESULTS: The total effective rate and evidently effective rate of Group A were significantly higher than those of Group B (92.0% vs. 75.8%, 44.0 vs. 29.0%, P < 0.01). The levels of hemorrheology and lipemia in 72 hyperviscosityemia patients and 76 hyperlipidemia patients in Group A were significantly improved after the treatment. The integral difference of nerve function injury and the obsorbed situation of infarct focus in Group A were significantly higher than those in Group B. Group A had no adverse reaction during the treatment. CONCLUSION: Dengzhanhua injection in the treatment of acute cerebral infarction is safe and effective.

Adult↗
PubMed1997

[Diffusion-weighted magnetic resonance imaging in the diagnosis of cerebral infarct].

Forty-one patients demonstrating clinical symptoms for cerebral infarction were investigated by magnetic resonance imaging with diffusion-weighted echo-planar imaging (DWI) and T2-weighted imaging (T2WI). In 8 patients only DWI showed the cerebral lesions clearly. One patient with positive DWI and T2WI suffered from HSV encephalitis. DWI is superior to T2WI in assessment of small cortical infarcts and cerebral infarction in patients with preexisting vascular lesions. DWI is not specific, so other causes like cerebral hematoma and encephalitis have to be considered.

Adult↗
PubMed1983

Evaluation of anticoagulants in patients with cerebral infarction with slight to moderate neurological deficit.

In a non-randomized controlled study carried out on 238 hospitalized patients with cerebral infarction, anticoagulant treatment (AC) was compared with the natural course in the prevention of transient ischemic attacks (TIA), cerebral infarction, stroke, stroke or death. 137 patients were allocated to AC, mean follow-up 30.5 months, and 101 patients were allocated to the controls (untreated group), mean follow-up 25.2 months. There were no statistically significant differences among the patients in the group who had suffered TIA (AC treated group 10.2%, untreated group 5.9%), cerebral infarction (AC treated group 10.2%, untreated group 11.9%), stroke (AC treated group 14.6%, untreated group 12.9%), stroke or death (AC treated group 22.6%, untreated group 19.8%). Minor bleedings occurred significantly more frequently (P less than 0.01) in the treated group. Severe bleedings occurred in 8 patients in the treated group (5.8%) compared to 1 of the controls (1%). It is concluded from the trial that AC can only seldom be recommended as prophylactic against new strokes in patients with cerebral infarction due to arterial thromboembolism.

Adult↗
PubMed1996

Cerebral infarcts associated with migraine: clinical features, risk factors and follow-up.

There have been few reports concerning the characteristics of cerebral infarction associated with migraine (CIAM), and especially about the subsequent fate of these patients. We studied 14 patients (9 female) with CIAM. In all these patients the onset of cerebral infarction was accompanied by a unilateral throbbing headache, in 8 also with a gradual build-up of neurological deficits. No other cause of cerebral infarction could be found in these patients. Twelve patients had had previous attacks of migraine, with auras in 6. The nature of the neurological deficit was similar to previous auras in only 3 of these patients. The 2 patients without a history of migraine both developed migraine attacks afterwards. During the same period we also studied 14 patients (8 female) with a cerebral infarct of unknown origin (CIUO). The infarct involved the occipital lobe in 11 of the 14 patients with CIAM, whereas this occurred in 4 patients with CIUO [relative risk (RR): 2.8; 95% confidence interval (CI): 1.2-6.6]. Patients with CIAM had risk factors for atherosclerosis significantly less often than patients with CIUO (RR: 0.1; 95% CI: 0.02-0.9). The functional outcome of patients with CIAM was better than in patients with CIUO: all 14 patients with CIAM were independent in their daily activities, compared with 9 patients with CIUO (RR: 1.6; 95% CI: 1.1-2.3). No patient in either group had a recurrent stroke during a median follow-up period of 5.8 years. In conclusion, CIAM is a stroke entity causing mostly infarcts in the occipital lobe; vascular risk factors are uncommon and prognosis is generally good.

Adolescent↗
PubMed1982

High frequency CT findings within 24 hours after cerebral infarction.

Twenty-six patients with clinically documented acute cerebral infarction were evaluated by computed tomography within the first 24 hr. In 21 patients, subtle mass effects and/or focal areas of decreased attenuation corresponding to areas of clinical deficit were demonstrated. Enhancement occurred in only five of 15 infarctions rescanned after contrast administration. In three of these, the region of infarction became isodense after contrast administration. In a patient with multifocal infarcts, enhancement was the only clue to infarction in one focus. The improved spatial and contrast resolution of current generation scanners appears to have significantly increased the sensitivity of computed tomography in demonstrating acute cerebral infarction and has important clinical application.

Acute Disease↗
PubMed2000

Out-of-hospital diagnosis of cerebral infarction versus intracranial hemorrhage.

OBJECTIVE: To establish a model based on clinical and anamnestic data easily available in the out-of-hospital setting, which facilitates the differential diagnosis between cerebral infarction and intracranial hemorrhage. DESIGN: Retrospective study that simulates a prospective approach. SETTING: Emergency Department of the University Hospital in Vienna, Austria. PATIENTS AND PARTICIPANTS: Data of 224 patients with either intracranial hemorrhage or cerebral infarction were prospectively collected. Uni-and multivariate analysis was performed to identify neurological symptoms and anamnestic data, which were associated with either intracranial hemorrhage or cerebral infarction. MEASUREMENTS AND RESULTS: Unilateral weakness or sensory loss was observed more frequently in patients with infarction compared to hemorrhage (69.8 % vs 11.9 %, P < 0.001). The frequency of patients with impaired level of consciousness was significantly higher in the hemorrhage group compared to the infarction group (59.3 % vs 3.8 %, P < 0.001). A multivariate logistic regression analysis showed that hypertension (OR = 0.31, 95 % CI = 0.12-0.76, P = 0.01), diabetes (OR = 0.17, 95% CI = 0.04-0.68, P = 0.01), and unilateral weakness or sensory loss (OR = 0.10, 95 % CI = 0.04-0.26, P < 0.001) were significantly associated with cerebral infarction. Impaired level of consciousness was significantly related to hemorrhage (OR = 13.41, 95 % CI = 3.92-45.91, P < 0.001). On the basis of the logistic regression analysis, we generated a scoring system for the out-of-hospital diagnosis between infarction and hemorrhage. The values of the score lay between -3 and +3. The probability of infarction increases when the score becomes negative, and the probability for hemorrhage increases when the score becomes positive. CONCLUSION: Our model is a useful guideline for the differential diagnosis between cerebral infarction and intracranial hemorrhage in the out-of-hospital setting, as it is based on easily available clinical and anamnestic parameters.

Aged↗
PubMed1995

[A case of successful operation for chronic aortic dissection (DeBakey 1 type) complicated with cerebral infarction].

We report a successful operation for a patient of chronic aortic dissection complicated with cerebral infarction. A 60-year-old woman has been treated suffering from cerebral infarction for 7 years. She was referred to our hospital for abnormal chest X-ray and complaint of dry cough. The enhanced CT scan and aortogram demonstrated chronic aortic dissection (DeBakey I) extending from ascending aorta to the abdominal aortic bifurcation with occlusion of right common carotid artery and dilated ascending aorta and aortic arch. The onset of aortic dissection seemed to be, from a clinical point of view, coincident with the onset of cerebral infarction seven years ago. The replacement of the ascending aorta and aortic arch with woven Dacron velour graft were performed under hypothermic and selective cerebral perfusion. The postoperative course was uneventful although complicated with transient recurrence nerve palsy and she has been doing well.

Aortic Aneurysm, Thoracic↗
PubMed1990

Cigarette smoking. A risk factor for cerebral infarction in young adults.

To assess the impact of cigarette smoking on stroke in young adults (15 to 45 years old), we compared smoking data from 181 patients with cerebral infarction with that of 307 control subjects matched for age, gender, geographic location, and hospital admission dates. While controlling for these matching variables and hypertension, an analysis based on a conditional logistic regression model indicated that a smoker was 1.6 times more likely to have a cerebral infarction than a non-smoker (95% confidence interval, 1.07 to 2.42). There was a cumulative dose effect with each additional pack-year causing a greater risk of having a cerebral infarction. In fact, after adjusting for all other risk factors, there was a significant quadratic component to the dose-response relationships, with the result that individuals with a larger number of pack-years were invariably the stroke patients. There was no significant difference in smoking status among the various subtypes of cerebral infarction (atherosclerotic, nonatherosclerotic vasculopathy, cardioembolic, hematologic related, undetermined). These data indicate that cigarette smoking is an important risk factor for cerebral infarction in young adults. Risk factor modification through cessation of smoking may reduce the risk of ischemic stroke in young adults.

Adolescent↗
PubMed2004

Association of the mitochondrial DNA 16189 T to C variant with lacunar cerebral infarction: evidence from a hospital-based case-control study.

A transition of T to C at nucleotide position 16189 in the hypervariable D-loop region of mitochondrial DNA (mtDNA) has attracted research interest for its probable correlation with increasing insulin resistance and development of diabetes mellitus (DM) in adult life. In this article, we present our observations of the positive relationship between this variant and cerebral infarction. Six hundred and one subjects in two groups-one with cerebral infarction (307 cases), the other with no cerebral infarction (294 cases)-were recruited. Their clinical features, fasting blood sugar and insulin levels, and insulin resistance index, were recorded. Patients with cerebral infarction were further categorized into four different subgroups according to the TOAST criteria for stroke classification. The results showed the occurrence of the mtDNA 16189 variant in 34.2% of patients with cerebral infarction and in 26.5% of normal controls. The difference in the occurrence rates between the two groups was statistically significant (P = 0.041). Further studies of the occurrence rate in each stroke subgroup revealed that the variant occurred at the highest frequency in the small vessel subgroup (41.5%). The difference in occurrence rate between this subgroup and the normal controls is highly significant (P = 0.006). These results correlated well with the findings of significantly increased levels of average fasting blood insulin and a higher index of average insulin resistance in the small vessel subgroup of patients harboring this mtDNA variant. Taken together, we suggest that the mtDNA 16189 variant is a predisposing genetic factor for the development of insulin resistance and may be related to various phenotypic expressions in adult life such as development of DM and vascular pathologies involved in stroke and cardiovascular diseases.

Adult↗
PubMed2004

Strong correlation between the prevalence of cerebral infarction and the presence of anti-cardiolipin/beta2-glycoprotein I and anti-phosphatidylserine/prothrombin antibodies--Co-existence of these antibodies enhances ADP-induced platelet activation in vitro.

Cerebral infarction is the most common arterial thromboembolic complication in the anti-phospholipid antibodies (aPL) syndrome. In an effort to clarify the roles of aPL in the pathogenesis of cerebral infarction in patients with SLE, we examined the levels of anti-cardiolipin/2-glycoprotein I antibodies (anti-CL/beta2-GPI) and anti-phosphatidylserine/prothrombin anti-bodies (anti-PS/PT) in addition to lupus anticoagulant (LA) activity in 126 patients with SLE (35 with cerebral infarction and 91 without thrombosis). Both anti-CL/beta2-GPI and anti-PS/PT strongly correlated with the presence of LA activity. The prevalence of cerebral infarction was obviously higher in the patients who had both anti-CL/beta2-GPI and anti-PS/PT (76.5% [26/34 cases], p<0.0001) than in the other patients having anti-CL/beta2-GPI or anti-PS/PT alone or neither of them (9.8% [9/92 cases]). Furthermore, we studied the in vitro effects of anti-CL/beta2-GPI and/or anti-PS/PT on the enhancement of platelet activation induced by stimulation with a low concentration of adenosine diphosphate (ADP). The purified IgG containing both anti-CL/beta2-GPI and anti-PS/PT caused significant enhancement of platelet activation caused by ADP. However, the purified IgG containing either anti-CL/beta2-GPI or anti-PS/PT had no enhancing effects on it. Furthermore, platelet activation was generated by the mixture of anti-CL/beta2-GPI-IgG and anti-PS/PT-IgG prepared from individual patients, but not by each fraction alone. These results indicate that anti-CL/beta2-GPI and anti-PS/PT may cooperate to promote platelet activation, which may contribute to the risk of cerebral infarction in patients with SLE.

Adolescent↗
PubMed1989

[Brain abscess following cerebral infarction: a case report].

The authors report a case of brain abscess following cerebral infarction. A 73-year-old man was admitted to our clinic with symptoms of right hemiparesis and total aphasia. CT scan revealed abnormal low density area in the left fronto-temporo-parietal region. Cerebral angiography demonstrated occlusion of the left middle cerebral artery at the M1 portion. On the 16th hospital day, an episode of generalized seizure with high fever appeared, and intermittent high fever persisted thereafter. Two months after admission, CT scan revealed several cystic lesions with marked ring enhancement at the site of cerebral infarction, suggesting multiple abscesses. Aspirations of left frontal and parietal abscesses were accomplished and the cultures of the pus disclosed Proteus vulgaris. Due to progressive hydrocephalus, a ventriculoperitoneal shunt was constructed one month later. Repeated CT scans showed a gradual diminution of the abscesses. It is considered that the blood-brain barrier is broken and the local immunological system against bacteria may be weakened when the brain is damaged by ischemia. Brain abscess seems to be developed in such circumstances even under the influence of transient bacteremia which originates in other parts of the body. Therefore the possibility of cerebral abscess should be suspected if patients with cerebral infarction suffer from the symptoms such as fever, neck stiffness or disturbance of consciousness.

Aged↗
PubMed2002

Serial magnetic resonance angiography in cerebral infarction after varicella infection.

The case of a 1-year-8-month-old-boy with cerebral infarction after varicella infection is reported here. Brain magnetic resonance (MR) angiography revealed segmental narrowing of the left middle cerebral artery which became normal 8 months later. The MR angiography well demonstrated the time course of the vascular involvement in the present patient. In cerebral infarction after varicella infection, the proximal portion of the main cerebral arteries were frequently damaged therefore MR angiography is useful for diagnosis and therapeutic decision-making. Moreover, serial MR angiographic studies can clarify the natural course of vascular changes in varicella virus-related cerebral infarction.

Cerebral Infarction↗
PubMed1992

Urinary 11-dehydro-thromboxane B2: a quantitative index of platelet activation in cerebral infarction.

Thromboxane A2 (TXA2) biosynthesis was studied in healthy subjects, patients with chronic cerebral infarction, patients under chronic aspirin treatment and patients with atrial fibrillation. Urinary 11-dehydro-TXB2, as a major metabolite of TXA2, was measured by radioimmunoassay. The extent of carotid atherosclerosis was determined by B-mode ultrasonography. The mean +/- SD urinary excretion in patients with cerebral infarction and distinct carotid-atherosclerotic lesions (1,725 +/- 239 ng/g creatinine, n = 6) was significantly higher (p less than 0.01) than in healthy subjects (911 +/- 239 ng/g creatinine, n = 44) and patients with cerebral infarction who had no distinct carotid lesion (1,050 +/- 191 ng/g creatinine, n = 6). The urinary excretion of healthy subjects was higher (p less than 0.01) in smokers (1,063 +/- 244 ng/g creatinine, n = 17) than in non-smokers (815 +/- 183 ng/g creatinine, n = 27). Aspirin largely suppressed 11-dehydro-TXB2 excretion (266 +/- 114 ng/g creatinine, n = 7). Three of 5 patients with atrial fibrillation showed very high values. Our results indicated that platelet activation occurs in the atherosclerotic lesions, and that urinary 11-dehydro-TXB2 is the appropriate analytic target for detecting platelet activation.

Adult↗