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PubMed1998

Influence of aerobic exercise training on brain natriuretic peptide secretion in patients in the chronic phase of myocardial infarction.

Brain natriuretic peptide (BNP) secretion increases after myocardial infarction (MI); its plasma level may reflect the degree of left ventricular dysfunction. This study examines how aerobic exercise therapy for MI influences BNP secretion. Subjects included 70 patients (mean age, 62.0+/-11.3 years) who were divided into four groups: (1) 20 patients with an anterior MI and exercise training; (2) 20 patients with an anterior MI and no exercise training; (3) 15 patients with an inferior MI and exercise training; and (4) 15 patients with an inferior MI and no exercise training. The training groups performed aerobic exercise 3 times a week for 2 months. Exercise intensity was defined as a heart rate of anaerobic threshold (AT), derived from the treadmill cardiopulmonary exercise testing at 1 month after the onset of MI. The subjects underwent cardiopulmonary exercise testing again at 3 months after the onset of MI. To measure BNP, blood samples were obtained in the resting state and immediately after the peak exercise. AT and peak oxygen uptake increased in the training group with anterior MI and in both the training and nontraining groups with inferior MI. Significant serial change in plasma BNP level was not observed in the inferior MI groups. Plasma BNP level decreased longitudinally only in the nontraining anterior MI group. It was concluded that exercise training in patients with an anterior MI could delay the recovery of left ventricular function, but will increase exercise tolerance.

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PubMed2004

Signal characteristics of FLAIR related to water content: comparison with conventional spin echo imaging in infarcted rat brain.

To examine the correlation between tissue water content and signal intensity on fluid-attenuated inversion recovery (FLAIR) images, we analyzed infarcted rat brain, verified the results by theoretical simulation, and compared them with conventional spin-echo images. We produced brain infarction with cavitation in five rats by middle cerebral artery occlusion. After in vivo MRI, histologic sections of the MRI plane were obtained. We measured the signal intensity of regions on FLAIR and spin-echo images, and measured the area of cavitation on histologic sections. We plotted curves of cavity percentage to signal intensity. Theoretical values were calculated using a two-compartment model. On the curve of cavity area to signal intensity, the signal on FLAIR images peaked in tissues with 20% to 30% area of cavitation. On the theoretical curve, the signal on FLAIR images peaked at 90% tissue water content. These results seem to be characteristic of FLAIR.

Animals↗
PubMed1994

Immunohistochemical localization of glutathione peroxidase in infarcted human brain.

This is the first report which demonstrates the presence of glutathione peroxidase in the autopsied brain of 5 patients without cerebral infarction and 21 patients with cerebral infarction by the indirect enzyme-labeled antibody technique with monoclonal antibody to human glutathione peroxidase. In 2 out of 5 patients without cerebral infarction, a weak reaction for glutathione peroxidase was demonstrated both in neurons and glia. In 6 patients who had died within 5 days after stroke, no staining was observed in infarcted brain tissue except in macrophages. In all 15 patients who had died more than 6 days after stroke, however, a reaction for glutathione peroxidase was demonstrated in the cytoplasm of glial cells in the marginal area around the infarction, and there was a patchy reaction in the cytoplasm of macrophages in the core lesion. These results suggest that glutathione peroxidase in glial cells of the marginal area around the infarction may play a protective role against lipid peroxidation after cerebral infarction, or alternatively, may be involved in the healing process after ischemia.

Adult↗
PubMed1979

[Production of infarction model in dogs by several brain arteries occlusion. Part 1: Production of hemispheric non blood supply model (author's transl)].

Experimental brain infarction in model animals should most ideally be constant in the site of occurrence, be of severity that is controllable by the occlusion time of blood flow and, moreover, be reproducible at a high rate to desired extent and severity. However, among infarction models elaborated in animals so far, only thalamus infarction model in dogs which were reported by us previously have been proven to satisfy almost all of these requirements. In experiments with these model dogs we found that an extensive infarction can be produced at a high frequency in the involved hemisphere by a transient occlusion of blood flow at such intracranial levels as the internal carotid artery, the junction of the anterior cerebral artery and ophthalmic artery, the middle cerebral artery, the origin of the segment A2 of the anterior cerebral artery, and the junction of the posterior communicating artery and posterior cerebral artery. During about one hour following the releasing of the arteries approximately 2 hours occlusion, the development of severe brain edema resulted involving the whole hemisphere on the affected side invariably in all cases. This method for experimental production of brain infarction permits to control the degree of resultant brain edema by changing the duration of occlusion of blood flow, requires simple manipulations only and ensures production of a constant lesion. With these advantage it can be anticipated to prove of great benefit in the study of postischemic brain edema.

Animals↗
PubMed1997

[Clinical and image diagnostics of brain stem infarction].

Clinical features and image diagnostic characteristics of brain stem infarction were studied in 28 patients to facilitate early diagnosis. Crossed hemiparesis was found in all the patients with medulla oblongata and midbrain infarction. Pontine infarction had a variety of clinical syndromes as follows: (1) crossed-hemiparesis in 8 cases (44.4%) and ipsilateral hemiataxia in one case. (2) tetraplegia in 3 cases (16.7%). (3) pure hemiparesthesia in 4 cases. (4) hemiparesis and hemiparesthesia without cranial nerve palsy in 3 cases (16.7%). MRI was found to be a very useful diagnostic measure for brain stem infarction with a positive rate of 82.6%. However, brain stem infarction was sometimes not revealed by MRI. Brain stem infarction could not be diagnosed by CT, but brainstem hemorrhage might be excluded by CT.

Adult↗
PubMed1995

Prognosis for patients following a transient ischemic attack with and without a cerebral infarction on brain CT. North American Symptomatic Carotid Endarterectomy Trial (NASCET) Group.

BACKGROUND: Although cerebral infarctions are commonly observed on brain CTs of patients with TIAs, their prognostic importance is unknown. METHOD: The association between appropriately sited brain infarctions (ie, lesions located in the anterior circulation of the brain and ipsilateral to the symptomatic stenosed carotid artery) visualized on CT and the risk of subsequent stroke was assessed by Cox proportional hazards regression in 164 patients presenting with TIA (and no history of previous stroke) and severe angiographically defined carotid stenosis (70 to 99%) from the North American Symptomatic Carotid Endarterectomy Trial. RESULTS: Patients with a TIA and CT-verified brain lesions were older and were more likely to have higher degrees of carotid stenosis and carotid plaque ulceration, a longer duration of symptoms, and a history of hypertension. With regard to prognosis, after adjusting for all known risk factors (patient characteristics) in a regression analysis, the presence of ischemic lesions observed on CT was not associated with an increased risk of ipsilateral stroke at 2 years (adjusted hazard ratio = 1.00; 95% CI: 0.39 to 2.58; p value = 0.99). CONCLUSION: Considered in combination with other patient characteristics, the mere presence of an appropriately sited cerebral infarction on CT does not alter the prognosis (risk of ipsilateral strokes) of severely stenosed patients with TIA. Therefore, there is no clinical rationale in differentiating patients with TIA on the basis of CT findings alone.

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PubMed2000

Prevalence of renal artery stenosis in autopsy patients with stroke.

BACKGROUND AND PURPOSE: Atherosclerotic renal artery stenosis commonly exists as one manifestation of more generalized atherosclerosis. It is a progressive but potentially curable disorder. Thus, information on renal artery involvement in atherosclerotic diseases could be important. We investigated the prevalence of renal artery stenosis in autopsied patients with stroke over 40 years of age. METHODS: From 2167 consecutive autopsy patients who died between 1980 and 1997, we studied 346 cases of mean age of 69+/-11 years with clinical evidence of stroke. RESULTS: Atherosclerotic renal artery stenosis (>/=75% luminal area narrowing) was found in 36 patients (10.4%). Patients with renal artery stenosis were older and had worse renal function. Renal artery stenosis was found in 14.7%, 28.6%, and 23.9% of patients with hypertension, renal insufficiency, and aortic aneurysm, respectively. Extracranial carotid artery stenosis (>50% luminal area narrowing) was found in 101 patients (29.2%). Of the 346 stroke patients, 256 had a history of brain infarction. In patients with brain infarction, renal artery stenosis was found in 31 (12.1%) and carotid stenosis was found in 81 (33.6%). Patients with carotid artery stenosis were more likely to have renal artery stenosis than patients without carotid artery stenosis (24.4% versus 5.9%, P<0.0001). Multiple logistic regression analysis identified renal insufficiency, hypertension, female gender, and presence of carotid artery stenosis as independent predictors of renal artery stenosis in patients with brain infarction. CONCLUSIONS: These data reveal that atherosclerotic renal artery stenosis is common in patients with stroke, especially in those with brain infarction.

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PubMed1989

Transcranial Doppler in acute brain stem infarction.

Two patients with acute brain stem infarctions were examined angiographically and with the transcranial Doppler. One patient had a patent basilar artery but worsened clinically. The second patient had a thrombosis of the left vertebral artery which was dislodged with the angiographic catheter. Thrombolytic therapy was initiated. Serial transcranial Doppler examinations showed persistent patency of the vertebrobasilar system although the patient failed to improve. The usefulness of the transcranial Doppler in the management of acute stroke is discussed in the context of these patients.

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PubMed2005

Effects of blood pressure levels on case fatality after acute stroke.

OBJECTIVE: We evaluated the relationship between admission blood pressure (BP) and early prognosis in patients with acute stroke in a single cohort. DESIGN: The subjects comprised 1004 cases of brain infarction and 1097 cases of brain hemorrhage, who were admitted to hospitals on the day of stroke onset. Death within 30 days after onset was evaluated in relation to admission BP levels. RESULTS: In brain infarction, a U-shaped relationship was found between BP levels and mortality rate, with a nadir at systolic blood pressure (SBP) of 150-169 mmHg and at diastolic blood pressure (DBP) of 100-110 mmHg. After adjustments for age and sex, the highest relative risks (RR) was observed in the lowest BP levels compared with nadir groups, and were 2.69 [95% confidence interval (CI), 1.43-5.07] in SBP and 3.49 (95% CI, 1.58-7.74) in DBP. In subjects with previous hypertension, the relationship between prognosis and SBP level shifted significantly toward higher pressure by about 10 mmHg compared with those without previous hypertension. In subjects with brain hemorrhage, the relationship between BP levels and mortality rate showed a J-shape in SBP and a U-shape in DBP. Highest BP levels had the poorest prognoses (>/= 230 mmHg in SBP, RR = 4.13, 95% CI = 2.45-6.94; >/= 120 mmHg in DBP, RR = 1.83, 95% CI = 1.11-3.04). CONCLUSION: Lower and higher BP after brain infarction and higher BP after brain hemorrhage were predictors for poor early prognosis. In subjects with brain infarction, patients with previous hypertension had better outcomes at higher admission BP level than did normotensive patients.

Acute Disease↗
PubMed1989

Neurotransmitter deficits in a non-multi-infarct category of vascular dementia.

Brain tissue from 9 severely demented patients cared for in psychiatric long-term wards and with records of stroke episodes, macroscopic signs of brain infarcts and with no clinical evidence of senile dementia of the Alzheimer type was investigated and compared with control material. The mean volume of the brain infarcts in this vascular dementia group was only 6.8 ml. Pronounced disturbances of the serotoninergic and cholingergic systems were found in subcortical and cortical grey matter. These widespread neurotransmitter changes can hardly be explained by the localized brain infarcts per se, but suggest the existence of another category of vascular dementia. Since the neurotransmitter disturbances were found to be similar to those of Alzheimer's disease and senile dementia of the Alzheimer type, it seems more likely that they indicate a common pathway for dementia disorders than that they serve as markers of different dementia categories.

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PubMed2004

[Protective effect of ONO-1078, a leukotriene receptor antagonist, on focal cerebral ischemia induced by endothelin-1 in rats].

AIM: To determine the protective effect of ONO-1078, a leukotriene receptor antagonist, on focal cerebral ischemia induced by endothelin-1 in rats. METHODS: Slow microinjection of endothelin-1 (120 pmol in 6 microL, for > 6 min) into the region near the middle cerebral artery was used to induce focal cerebral ischemia. ONO-1078 (0.1 mg.kg-1) was i.p. injected 1 h before endothelin-1 injection. Neurological symptoms, brain edema, brain infarction size, and the survival neurons in cortex and striatum were observed 24 h after ischemia. RESULTS: Intracerebral microinjection of endothelin-1 induced remarkable neurological symptoms, brain infarction, brain edema, and decrease of survival neurons in the cortex and striatum. In rats pretreated with ONO-1078, endothelin-1-induced brain edema and brain infarction size were decreased. The numbers of survival neurons in striatum and cortex were increased significantly. The neurological symptoms were improved but not significantly. CONCLUSION: ONO-1078 possesses neuroprotective effect against cerebral ischemic injury induced by endothelin-1, therefore, leukotrienes may play a role in the injury of cerebral ischemia.

Animals↗
PubMed1993

Plasma brain natriuretic peptide as an indicator for angiotensin-converting-enzyme inhibition after myocardial infarction.

Brain natriuretic peptide (BNP) is a cardiac ventricular hormone that may be a sensitive and specific marker of changes in ventricular function. In a prospective, randomised open trial with 16 patients followed for 6 months after first Q wave anterior myocardial infarction we set out to determine: whether BNP concentrations are raised acutely, the effect on circulating BNP of angiotensin-converting enzyme (ACE) inhibition, how BNP and atrial natriuretic peptide (ANP) concentrations compared as correlates of left-ventricular ejection fraction, and whether plasma BNP concentrations could distinguish patients with low (< 40%) and relatively preserved (> 40%) ejection fractions. Plasma concentrations of BNP measured on days 2, 7, 8, 42, and 180 postinfarction were significantly raised in patients compared with normal controls and to a proportionately greater degree than ANP concentrations. Treatment with placebo (n = 8) or oral captopril (n = 8) from day 8 resulted in significantly lower BNP concentrations at days 42 (p = 0.05) and 180 (p < 0.05) in the captopril-treated group. Compared with ANP, BNP concentrations were much more strongly correlated with radionuclide-measured left-ventricular ejection fraction at days 2, 42, and 180. All 8 patients with baseline (day 2) ejection fractions of 40% or above had plasma BNP concentrations less than 10 pmol/L, whereas the 8 patients with ejection fractions less than 40% had BNP concentrations greater than 10 pmol/L. Our findings suggest that measurements of circulating BNP may identify those patients with significant left-ventricular dysfunction who have been highlighted by the Survival and Ventricular Enlargement study as likely to benefit from long-term ACE inhibition after myocardial infarction.

Adult↗
PubMed2003

Enhanced expression of aquaporin 4 in human brain with infarction.

A series of human brains with cerebral infarction obtained at autopsy were investigated to clarify the possible contribution of aquaporin 4 (AQP4) to the development of brain edema. Cellular localization of AQP4 and its relation to ischemic foci were examined with double-labeling immunohistochemistry. AQP4 immunoreactivity (IR) was more intense at the periphery of ischemic foci than at their center. Double-labeling study demonstrated that AQP4 IR was restricted to astrocytes and was localized to their entire processes, including their end feet facing the outer surface of capillaries. Moreover, AQP4 IR, detectable in the subpial and subependymal zone in the normal condition, was more intense in the vicinity of ischemic foci. Accumulation of AQP4 IR may reflect its participation in the development of brain edema in human brains by playing a role in the transport of water not only through blood vessel walls but also through pial and ependymal surface of the brain.

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PubMed2005

Cerebral small-vessel disease and decline in information processing speed, executive function and memory.

Cerebral small-vessel disease is common in older people and may contribute to the development of dementia. The objective of the present study was to evaluate the relationship between measures of cerebral small-vessel disease on MRI and the rate of decline in specific cognitive domains in participants from the prospective, population-based Rotterdam Scan Study. Participants were 60-90 years of age and free from dementia at baseline in 1995-1996. White matter lesions (WML), cerebral infarcts and generalized brain atrophy were assessed on the baseline MRI. We performed neuropsychological testing at baseline and repeatedly in 1999-2000 and in 2001-2003. We used random-effects models for repeated measures to examine the association between quantitative MRI measures and rate of decline in measures of global cognitive function, information processing speed, executive function and memory. There were a total of 2266 assessments for the 832 participants in the study, with an average time from the initial to last assessment of 5.2 years. Increasing severity of periventricular WML and generalized brain atrophy and the presence of brain infarcts on MRI were associated with a steeper decline in cognitive function. These structural brain changes were specifically associated with decline in information processing speed and executive function. The associations between MRI measures of cerebral small-vessel disease and cognitive decline did not change after additional adjustment for vascular risk factors or depressed mood. After exclusion of participants with an incident stroke, some of the associations of periventricular WML, brain infarcts and generalized brain atrophy with measures of information processing speed and executive function were no longer significant. This may indicate that stroke plays an intermediate role in the relationship between cerebral small-vessel disease and cognitive decline. Our results suggest that in older people cerebral small-vessel disease may contribute to cognitive decline by affecting information processing speed and executive function.

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PubMed2003

MRI correlates of executive dysfunction in patients with ischaemic stroke.

Executive dysfunction (ED) may lead to problem behaviour and impaired activities of daily living in many neuropsychiatric disorders, but the neuroanatomical correlates of ED are still not well known. Different aspects of executive functions were studied by widely used neuropsychological tests in 214 elderly patients 3 months after ischaemic stroke, and a sum score of eight different measures was counted in each patient. The number and site of brain infarcts as well as severity and location of white matter lesions (WMLs) and brain atrophy on magnetic resonance imaging were recorded and compared between patients with and without ED. ED was present in 73 (34.1%) of the 214 patients. The mean frequency of brain infarcts in the brain and in the left hemisphere was higher in the patients with ED. Lesions affecting the frontal-subcortical circuits (e.g. pallidum, corona radiata or centrum semiovale) were more frequent in patients with ED than in those without. Also, patients with pontine brain infarcts frequently had ED, but this may have been due to more extensive ischaemic changes in these patients in general. Mean number of brain infarcts affecting the pons and posterior centrum semiovale on the left side, moderate to severe medial temporal atrophy, the Fazekas white matter score, the Mini-Mental State Examination score and low education were independent correlates of ED. Brain infarcts and WML affecting the frontal-subcortical circuits or the pons may increase risk for ED in stroke patients.

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PubMed2005

Poor surgical technique in cervical plating leading to vertebral artery injury and brain stem infarction--case report.

BACKGROUND: Lateral mass plating is a safe fixating system for lower cervical fractures. Brain stem infarction after cervical lateral mass screw plating has not been reported in previous literature. We report a case of poor surgical technique leading to vertebral artery injury and brain stem infarction after cervical lateral mass plating. CASE DESCRIPTION: A 41-year-old male patient was transferred to our hospital because of hemiparesis and dysarthria immediately after lateral mass plating for fracture and dislocation of the fifth and sixth cervical vertebrae. Brain magnetic resonance imaging showed infarction of the left posterior inferior cerebellar artery territory, and the vertebral artery angiography showed complete occlusion of the left vertebral artery. The cervical computed tomography revealed a left screw of the fifth and sixth cervical vertebrae penetrating the central portion of the transverse foramen. The patient was managed with anticoagulant and supportive therapy only, with subsequent improvement of hemiparesis and dysarthria. CONCLUSIONS: Poor surgical technique of lateral mass plating in the cervical spine could lead to vertebral artery injury and even brain stem infarction. Postoperative brain infarction in cervical fusion could be a complication of the usually safe lateral mass plating of the cervical spine.

Adult↗
PubMed1985

Megadolichobasilar anomaly associated with brain stem infarction: a case report.

A rare case of megadolichobasilar anomaly associated with localized brain stem infarction showing right hemiparesis and disturbance of consciousness is described. The etiologic mechanisms of brain stem infarction in this anomaly are discussed. The tortuosity and dilatation of the basilar artery were thought to play an important role in the pathogenesis of the brain stem infarction.

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