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PubMed2001

[Swallowing rehabilitation in two elderly patients with cerebral infarction].

We report two cases of cerebral infarction in which swallowing function improved following swallowing rehabilitation. Patient 1 was an 82-year-old man, who was admitted due to rheumatoid arthritis and multiple cerebral infarction, suffering from aspiration pneumonia. The abnormality of swallowing was assessed by the water swallowing test and videofluorography. It has been reported that videofluorography is useful in the diagnosis of aspiration. Three weeks after the start of swallowing rehabilitation, the serum level of inflammatory markers and the chest X-ray had returned to normal. His score on the water swallowing test had improved. Patient 2 was a 68-year-old [correction of 62] man, who was admitted with severe hemiplegia, dysphagia and dysarthria. One month after the swallowing rehabilitation, videofluorography showed that the magnitude of aspiration into the trachea had decreased and the pooling of barium in the piriform sinus had disappeared. The patient could begin taking a little food by mouth. These results suggest that swallowing rehabilitation will be affect the clinical improvement of swallowing function and help preventing aspiration pneumonia in our hospital.

Activities of Daily Living↗
PubMed1992

[Clinical study of correlation pre-senile, senile depressive state with silent cerebral infarction--MRI findings and its distribution].

We examined the relationship between the pre-senile/senile depressive state and silent cerebral infarction using MRI. The subjects studied were 56 patients 50 years of age or older with a depressive state who underwent MRI and who were hospitalized and treated at the Department of Psychiatry or the Department of Neurology of Hiroshima Prefectural Hospital. We made a diagnosis of depression in patients who fulfilled the criteria of DSM-III-R for major depression. Patients in whom apoplectic attacks had occurred, or who had local neurologic symptoms or a history of evident cerebrovascular disorders, were not included in the study. Silent cerebral infarction was observed with pre-senile onset in 60.3% of patients with a pre-senile depressive state, and the complication rate was significantly higher than for cases with juvenile onset (20%). For patients with a senile depressive state, the complication of silent cerebral infarction was found in 53.6% of cases of pre-senile onset and in 100% of cases of senile onset. These rates were remarkably higher than the age-related complication rate of silent cerebral infarction in normal persons reported hitherto, we therefore suspect that nearly half of patients with depressive state of pre-senile onset and most of patients with that of senile onset might have an organic-depressive state complicated by silent cerebral infarction. Both perforating-type infarcts and cortical-type infarcts were found, suggesting that infarct-related foci of depressive states were polyphyletic. When we divided the depressive states complicated by cerebral infarction into 2 subtypes, those complicated by a perforating-type infarct and those by a cortical-type infarct, and compared the 2 types, we found possible differences in clinical symptoms and course between the subtypes. These differences seem worthy of further study. Among cortical-type lesions, parietal lesions were predominant, followed by frontal and then temporal lesions in incidence. There were significantly more left frontal lesions than right frontal lesions. Infarcts of both the parietal lobe and left frontal lobe may be related to the depressive state. Compared with cases not complicated by cerebral infarction, those with perforating- and mixed-type cerebral infarction were complicated with PVH significantly more frequently, similarity in risk factors and pathology between perforating-type cerebral infarction and PVH was suggested by these results.

Age Factors↗
PubMed1989

Predisposing factors for cerebral infarction: the Oxfordshire community stroke project.

The frequency of known causative factors of cerebral infarction was studied in 244 cases of first ever stroke due to cerebral infarction proved by computed tomography or at necropsy who were registered in the first two years of a prospective community based study. Risk factors for cerebral infarction were present in 196 (80%) cases; hypertension in 126 (52%); ischaemic heart disease in 92 (38%); peripheral vascular disease in 60 (25%); a cardiac lesion that was a major potential source of embolism to the brain in 50 (20%); transient ischaemic attacks in 35 (14%); cervical arterial bruit in 33 (14%); and diabetes mellitus in 24 (10%). Thirty one patients (13%) were in atrial fibrillation. Of the 48 patients who were free of risk factors or a major potential cardiac source of embolism at the time of the stroke, 18 were found to have hypertension after the stroke and 10 to have non-atheromatous non-embolic conditions (migrainous cerebral infarction (three), arteritis (two), inflammatory bowel disease (one), arterial trauma (one), autoimmune disease (one), carcinoma of the thyroid (one), and major operation (one). In 20 patients no causative factors could be identified. In this unselected series of patients with first ever stroke due to cerebral infarction most of the strokes were presumed to be due to either atheromatous arterial disease or embolism from the heart, and only 4% (95% confidence interval 2 to 7%) were probably due to non-atheromatous non-embolic causes. This has implications for research into strokes and allocation of public health expenditure.

Aged↗
PubMed2003

[Serum levels of soluble intercellular adhesion molecule-1 in patients with cerebral infarct].

OBJECTIVE: To observe the changes of the levels of soluble intercellular adhesion molecule-1(sICAM-1) in serum of patients with cerebral infarct and to explore the effect of sICAM-1 on cerebral infarct. METHODS: The serum levels of sICAM-1 in 55 patients with cerebral infarct both in acute stage(within 2 days) and convalescence(2 weeks after attack) were detected by using ELISA. At the same time, we compare the results with those of 32 patients having other neurologic diseases(20 patients with sciatica, 12 with trigeminal neuralgia) and 30 healthy subjects. RESULTS: (1) The serum levels of sICAM-1 of patients with cerebral infarct (acute stage: 766+/-179 microgram/L, convalescence: 602+/-155 microgram/L, respectively) were significantly higher than those of the control groups(530+/-77 microgram/L and 521+/-116 microgram/L, respectively, P<0.01). (2)There was a positive correlation of SICAM levels with the amount of leukocytes in acute stage(r=0.285,P<0.05), but negative correlation to clinical severity of cerebral infarct(r= 0.333,P<0.05). And there was no significant correlation between the level of sICAM-1 and the levels of cholesterol and triglyceride in serum(r= 0.042 and r=0.061, respectively, P>0.05). (3)There was no significant difference between sICAM levels of patients of cerebral cortex infarct and those of patients with basal ganglia infarct(773+/-178 microgram/L and 758+/-183 microgram/L, respectively, P>0.05). (4)The levels of sICAM-1 between patients of cerebral infarct with or without hypertension were no significant difference(774+/-189 microgram/L and 754+/-165 microgram/L, respectively, P>0.05). CONCLUSION: The levels of sICAM-1 increase significantly in patients with cerebral infarct. sICAM-1 may participate in the pathophysiologic process through inflammatory mechanism.

Aged↗
PubMed2002

[Association of estrogen receptor gene polymorphism with cerebral infarction, a case-control study].

OBJECTIVE: To explore the association between estrogen receptor (ER) gene PvuII and XbaI polymorphisms and cerebral infarction among Chinese Han people. METHODS: Samples of peripheral blood white cell were extracted among 234 patients with cerebral infarction, aged 63.9 +/- 10.3, and 259 controls without cerebrovascular disease, aged 59.2 +/- 9.2, all of Chinese Han nationality. PCR-RFLP and genotyping of ER PvuII and XbaI polymorphisms were performed. Multiple Logistic regression analysis was made to explore the risk factors for cerebral infarction. RESULTS: After adjustment for major confounders including age, gender, smoking, alcohol drinking, education, history of hypertension, diabetes mellitus, coronary artery disease and hyperlipoidemia, multiple Logistic regression analysis showed that: (1) The Pp genotype of ER PvuII polymorphism increased the risk of cerebral infarction significantly (OR = 1.97, 95% CI: 1.21 - 3.21); (2) The ER XbaI polymorphism was not in association with cerebral infarction significantly; (3) The PPXx/Ppxx genotypes increased the risk of cerebral infarction significantly (OR = 1.67, 2.52 and 2.18 respectively, P < 0.05) before or after all subjects were stratified by the history of hypertension or hyperlipoidemia; and (4) The positive interaction between the ER PvuII polymorphism and the presence of hypertension or diabetes or hyperlipoidemia could increase the risk of cerebral infarction significantly. CONCLUSION: ER gene may be one of the genetic candidate genes for cerebral infarction among Chinese Han population.

Aged↗
PubMed2004

Regional angiographic grading system for collateral flow: correlation with cerebral infarction in patients with middle cerebral artery occlusion.

BACKGROUND AND PURPOSE: Collateral flow plays an important role in maintaining tissue viability in proximal large vessel occlusion. We developed and tested a regional angiographic collateral grading system for patients with angiographically confirmed acute symptomatic middle cerebral artery occlusion to predict regional infarction. METHODS: A subset of 42 patients was selected from 180 patients enrolled in the Prolyse in Acute Cerebral Thromboembolism II (PROACT II) trial. Readers evaluated baseline cerebral angiograms in a blinded fashion for the degree of regional collateral circulation, which was graded on a 4-point scale in each of 15 anatomic regions. Regional and total collateral flow scores were compared with the presence or absence of infarction on 7- to 10-day follow-up computed tomography (CT), as well as clinical outcome as assessed by National Institute of Health Stroke Scale (NIHSS) scores. RESULTS: The collateral flow score on baseline angiography accurately predicted infarction, demonstrating a receiver operating characteristic curve of 0.87 (95% CI: 0.83 to 0.91) for all regions. Collateral grades on baseline angiography correlated moderately with infarct volume on follow-up CT scan at 7 to 10 days (R=0.61; P=0.0001). Collateral grades also correlated with follow-up NIHSS scores for patients who received thrombolysis (R=0.36 to 0.49, P<0.05), but not for control patients. CONCLUSIONS: An angiographic grading system for regional collateral flow accurately predicts the extent and location of cerebral infarction. This study corroborates the correlation between the presence of collateral flow, infarction volume, and clinical outcome, and it reinforces the need to control for collateral flow in clinical trials.

Cerebral Angiography↗
PubMed2001

Aggressive decompressive surgery in patients with massive hemispheric embolic cerebral infarction associated with severe brain swelling.

Massive hemispheric cerebral infarction, also known as malignant infarction, is characterized by rapid clinical deterioration due to brain swelling and downward transtentorial herniation, and is associated with a mortality of 80%. Early patient selection and establishment of the optimum therapeutic modality are important to improve the outcome. Early clinical, computed tomography (CT), and angiographic characteristics were analysed to identify patients with malignant infarction and external and internal decompression was performed, with unco-parahippocampectomy if needed, and the outcomes were compared with those of conservative treatment. Thirty-four of 55 patients admitted with large cerebral infarctions due to embolism showed rapid clinical deterioration due to brain swelling and herniation. These 34 patients were treated under a diagnosis of malignant infarction by decompressive surgical treatment (19 cases) or conservative treatment (15 cases). CT showed significantly higher infarction volume in patients with malignant infarction (288 +/- 62 cm3) compared to patients with non-malignant infarction (200 + 57 cm3, P < 0.001) and angiography showed a higher incidence of recanalization of the occluded vessels in patients with malignant infarction (58%) compared to patients with non-malignant infarction (15%, P < 0.05). Discriminant analysis revealed that an infarction volume of more than 240 cm3 was predictive of malignant infarction with 76.4% accuracy. Basic clinical characteristics on admission and deterioration were not statistically different between the surgically treated and conservatively treated groups of patients with malignant infarction. The shift of midline structures was significantly improved (14 +/- 3.5 to 10 +/- 4.7 mm) after surgical treatment (P < 0.05). compared to deterioration (12 +/- 5.8 to 15 +/- 4.5 mm) after conservative treatment. The mortality was 67% in the conservative group and 16% in the surgical group. Surgical treatment significantly improved the mortality and Glasgow Outcome Scale score (P < 0.01). However, the mean Barthel Index scores of the survivors were not significantly different. An infarct volume of more than 240 cm3 on CT and angiographic recanalization of the occluded artery are predictors of fatal brain swelling after massive cerebral infarction. Decompressive surgical treatment dramatically improves the mortality of massive hemispheric infarction.

Aged↗
PubMed1992

[Cerebral infarctions in elderly patients with anemia].

The authors investigated the cause of cerebral infarctions in elderly patients with anemia. Among 411 patients with acute cerebral infarctions, eight patients showed anemia (Hb < 10 g/dl) at the time of stroke. Only 2 patients had strokes during hospitalization were aware of their anemias before stroke. They were classified into two groups. One was the sudden onset group (4 patients) of whom 3 had malignant tumors, and 2 showed disseminated intravascular coagulations (DIC). There were no patients with atrial fibrillation or cardiac disease. All patients showed cortical infarction, and two died soon after stroke. Autopsy revealed verruca formation of the mitral valve in one patient and thrombus in the right ventricle in another. We thought that non-bacterial thrombotic endocarditis (NBTE) was the major cause of cerebral infarctions in this group. The other group consisted of 4 cases of thrombotic stroke. Their neurological symptoms appeared to be progressive. They also showed cortical infarctions except for one case of pontine infarction. Severe stenosis of the cerebral arteries was revealed by angiography in two patients and by autopsy in one. We concluded that cerebral infarctions in elderly patients with anemia can be important signs of underlying malignant tumors in sudden onset strokes or cases of severe cerebral artery stenosis with thrombotic strokes.

Aged↗
PubMed2006

[Protective effects of Denghuang injection on cerebral infarction in animal].

OBJECTIVE: To observe the protective effects of Denghuang injection on cerebral infarction in animal. METHOD: The study evaluated the protective effects of Denghuang injection on cerebral infarction through 3 experiments: 1. ligating the arteria cerebri media of dog; 2. blocking the internal carotid artery of rat; 3. ligating the common carotiol artery of gerbil. RESULT: The results showed Denghuang injection could reduce the cerebral infarction area after the dog's arteria cerebri media was ligated, and also could restrain the AKP&CK increase. The injection could reduce the cerebral infarction area of rat after the internal carotid artery was bloked by thrombus, and the mark of behavior and nerve symptom was better than that in the control group. Denghuang injection could obviously reduce the water content in pallium of gerbil after the common carotiol artery was ligated, and also could increase the amount of living pyramidal neuron in hippocampus, and reduce the MDA&LDH increase in pallium slurry. CONCLUSION: Denghuang injection can obviously protect animal on cerebral infarction.

Alkaline Phosphatase↗
PubMed1994

Carotid artery and heart disease in subtypes of cerebral infarction.

BACKGROUND AND PURPOSE: The aim of the study was to determine the prevalences of carotid artery disease and major and minor potential cardioembolic sources (1) in patients with cerebral infarction and age-matched control subjects and (2) in different clinical subtypes of cerebral infarction. METHODS: A series of 166 consecutive patients with cerebral infarction and 59 control subjects was examined. The study protocol included clinical subtyping of the cerebral infarctions, ultrasonography of the carotid arteries, transthoracic echocardiography (TTE), transesophageal echocardiography (TEE), ECG, and examination of the brain with computed tomography, magnetic resonance imaging, or autopsy. RESULTS: Carotid artery stenosis > or = 80% or occlusion was present in 35 (21%) patients but in no control subjects (P < .001; chi 2 test). A major potential cardioembolic source was detected in 65 (39%) patients and 3 (5%) control subjects. Atrial fibrillation was present in 35 (21%) patients and 3 (5%) control subjects at initial ECG (P < .01) and in 47 (28%) patients at repeat examination; 17 patients had paroxysmal atrial fibrillation. Sinus rhythm and a major potential cardioembolic source were detected in 18 (11%) patients but in no control subjects (P < .01) at TTE (all patients and control subjects examined) or TEE (118 patients and 52 control subjects examined). The frequency of a minor potential cardioembolic source detectable at TTE or TEE was similar in the patient and control groups (51% and 53%, respectively [NS]) and increased significantly with age. A finding of carotid artery stenosis > or = 80% or occlusion, atrial fibrillation, or a major cardioembolic source detected at TTE or TEE was more frequent among patients with cortical symptoms from anterior or middle cerebral artery territories than among those with lacunar syndromes (66% versus 22%, respectively). The probable source of cerebral infarction was identified in most of the 166 patients: cardiac embolism in 28% of cases (n = 46), carotid artery disease in 8% (n = 14), both cardiac embolism and carotid artery disease in 7% (n = 11), and lacunar infarction in 23% (n = 38). In 57 (34%) of the patients no unequivocal cause of the cerebral infarction was found. CONCLUSIONS: The prevalences of carotid artery and heart disease differ significantly between clinical subtypes of cerebral infarction. The cause of cerebral infarction remains uncertain in one third of patients. Because a minor potential cardioembolic source occurs in about 50% of both patients and control subjects, this finding is of questionable value as a risk factor for stroke in the elderly.

Adult↗
PubMed1979

Anticoagulant treatment to prevent cerebral infarction.

The indications for anticoagulant treatment to prevent cerebral infarction or progression of cerebral infarction are now clear. The indications are: (1) Prevention of recurrent embolization from a cardiac source (long-term anticoaguland treatment). (2) Transient ischemic attacks (particularly vertebrobasilar system) if a surgically accessible causative lesion, polycythemia, and thrombocytosis are not present (anticoagulants for a few months.) (3) Progressing stroke in either systme assuming that the neurological defect is partial and CT scan shows no evidence of bleeding (anticoagulants for a few months.) (4) Rarely, completed stroke (long-term).

Anticoagulants↗
PubMed1986

Brain SPECT imaging with 99Tcm-hexamethylpropyleneamine oxime in the early detection of cerebral infarction: comparison with transmission computed tomography.

A new cerebral blood flow agent, 99Tcm-hexamethylpropyleneamine oxime (HM-PAO), was evaluated for early detection of acute cerebral infarction in conjunction with the transmission computed tomographic (CT) studies. The data from 22 cases were analysed. Results reveal that 99Tcm-HM-PAO enables the early detection of acute cerebral infarction prior to CT with rather proper depiction of the extent of physiological abnormality in the majority of patients. This promising result together with the lack of logistical problems will make 99Tcm-HM-PAO a useful and practical agent worldwide for diagnosing and managing acute cerebral infarction.

Brain↗
PubMed1998

[Protective effect of hyperin on cerebral infarction in rats].

OBJECTIVE: To study the protective effect of hyperin (Hyp) on cerebral infarction. METHOD: The cerebral infarction in rats was made by ligating the right common carotid artery and the right middle cerebral artery. The infarction weight was determined by NBT stain. The cerebral cortex was taken to measure nitric oxide (NO) and malondialdehyde (MDA). The cerebral blood flow(CBF) was measured with H2 clearance method. RESULT: Hyp 6.25, 12.5, 25 mg.kg-1 markedly improved the abnormal nervous symptoms, and 12.5, 25 mg.kg-1 Hyp significantly reduced the infarction weight and inhibited the increase of MDA and NO in the cerebral cortex. Hyp(25, 12.5 mg.kg-1) could increase the CBF of the cerebral cortex. CONCLUSION: Hyp has a protective effect on cerebral infarction via attenuating lipid peroxidation and NO.

Animals↗
PubMed1990

Cognitive changes in patients with multiple cerebral infarcts.

Consensus has not been achieved regarding the impact of multiple cerebral infarcts on neurobehavioral status. To evaluate cognitive function in patients with multiple cerebral infarcts, we administered a comprehensive neuropsychological test battery to 23 consecutive male patients with clinical and brain computed tomographic findings consistent with at least two separate areas of cerebral infarction. Based on brain computed tomographic findings, patients were classified as having either mixed (n = 12) or lacunar (n = 11) infarcts. Results of these two groups were compared with those of 11 age-, sex-, and education-matched controls with no clinical or brain computed tomographic evidence of cerebrovascular disease. The mixed group had significantly lower mean scores than the controls for every cognitive domain tested. The lacune group showed cognitive impairment on most neuropsychological measures but did not differ from the controls in the attention domain. Although some degree of cognitive impairment was detected by the neuropsychological test battery in virtually every patient, only seven of 23 (30%) had Mini-Mental State Examination scores indicating dementia (less than 24). We conclude that virtually every patient with multiple cerebral infarcts has some degree of cognitive impairment but that only a minority can be classified as demented if the Mini-Mental State Examination is used as the primary defining examination.

Attention↗
PubMed1995

Silent cerebral infarction in patients with nonrheumatic atrial fibrillation. The Veterans Affairs Stroke Prevention in Nonrheumatic Atrial Fibrillation Investigators.

BACKGROUND: Cerebral infarction in patients with atrial fibrillation may vary from being clinically silent to catastrophic. The prevalence of silent cerebral infarction and its effect as a risk factor for symptomatic stroke are important considerations for the evaluation of patients with atrial fibrillation. METHODS AND RESULTS: This Veterans Affairs cooperative study was a double-blind controlled trial designed primarily to determine the efficacy of warfarin for the prevention of stroke in neurologically normal patients with nonrheumatic atrial fibrillation. It also was designed to evaluate patients with silent cerebral infarction. Computed tomography scans of the head were performed at entry, at the time of any subsequent stroke, and at termination of follow-up on all patients who completed the study without a neurological event. Of 516 evaluable scans performed at entry, 76 (14.7%) had evidence of one or more silent cerebral infarcts. Age (P = .011), a history of hypertension (P = .003), active angina (P = .012), and elevated mean systolic blood pressure (P < .001) were associated with the presence of this finding. Silent cerebral infarction occurred during the study at rates of 1.01% and 1.57% per year for the placebo and warfarin treatment groups, respectively (NS). Silent cerebral infarction at entry was not an independent predictor of later symptomatic stroke, but active angina was a significant predictor; 15% of the placebo-assigned patients with angina developed a stroke compared with 5% of the placebo-assigned patients without angina. CONCLUSIONS: Silent cerebral infarction is frequently seen in asymptomatic patients with atrial fibrillation. Age, history of hypertension, active angina, and elevated mean systolic blood pressure were associated with silent infarction at entry. The sample size was too small to determine whether warfarin had an effect on the incidence of silent infarction during the trial. Active angina at baseline was the only significant independent predictor for the later development of symptomatic stroke.

Aged↗
PubMed1989

Cerebral infarctions and transient neurologic deficits associated with acquired immunodeficiency syndrome.

PURPOSE: Little information is available concerning the clinical importance of cerebral infarction in patients with acquired immunodeficiency syndrome (AIDS). The purpose of this retrospective study was two-fold: (1) to determine the frequency and clinical characteristics of cerebral infarction and transient neurologic deficits (TNDs) among patients with AIDS; and (2) to identify specific patient subgroups at risk for such complications and whether there were underlying associated diseases requiring specific therapy. PATIENTS AND METHODS: Neurology inpatient and consult service records, neuropathology reports, and the University of California, San Francisco, AIDS computerized registry were used in identifying study cases. Information on demographic background, associated clinical diagnoses, presenting neurologic symptoms and signs, laboratory results, pathologic findings, and clinical follow-up was obtained from each patient's medical record. RESULTS: Twenty-five patients with AIDS (mean age, 38) having clinical or pathologic findings suggestive of focal cerebral ischemia or infarction were identified. Ten patients had non-hemorrhagic cerebral infarctions, 13 had acute TNDs, and two had both. Cerebral infarction was associated with central nervous system (CNS) infections (cryptococcus, four; tuberculosis, one; zoster vasculitis, one) and cardiogenic embolism (one). TNDs were associated with toxoplasmosis (four), cerebral infarction (two), cryptococcal meningitis (one), vasculitis (one), and CNS Kaposi's sarcoma (one). A presumptive cause was absent in five cases of cerebral infarction and eight of TND. All five patients with pathologically proven macroscopic cerebral infarcts were diagnosed clinically before death. CONCLUSIONS: We conclude the following: (1) AIDS patients, especially given their young age, appear to be increased risk for cerebral infarction and TND. (2) Cerebral infarction and TND may be the initial presentation of AIDS. (3) TND and cerebral infarction often signify treatable CNS infection among AIDS patients. (4) The causes of AIDS-related cerebral infarction and TND are unknown in many cases.

Acquired Immunodeficiency Syndrome↗