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PubMed1997

Inhibition of tumor necrosis factor and amelioration of brain infarction in mice.

Tumor necrosis factor alpha (TNF-alpha) is expressed in the ischemic brain; however, its precise role is not fully understood. We studied the effect of the dimeric form of the type I soluble TNF receptor linked to polyethylene glycol (TNFbp) on focal cerebral ischemia in mice using a permanent middle cerebral arterial occlusion (MCAO) model. TNFbp was applied topically, intravenously, or intraperitoneally. TNFbp binds and inhibits TNF-alpha. The volume of cortical ischemic lesions was measured by means of 2,3,5-triphenyltetrazolium chloride 24 h after MCAO. TNFbp produced a significant reduction in the cortical infarct volume of vehicle-treated animals (p < 0.001). The reduction in the volume of brain damage was 26% in animals that received 3 mg/kg of TNFbp topically. Further analysis of TNF-alpha inhibition following acute brain ischemia is indicated.

Animals↗
PubMed2005

Thrombosed unruptured cerebral aneurysm causing brain infarction followed by subarachnoid hemorrhage--case report--.

A 71-year-old man presented with right hemiparesis and aphasia due to cerebral infarction in the frontal lobe. Computed tomography (CT) revealed a high-density mass, 12 mm in diameter, in the stem of the left sylvian fissure. Carotid angiography demonstrated occlusion of the left ascending frontal artery complex and retention of contrast medium at the bifurcation of the left middle cerebral artery (MCA). The diagnosis was cerebral infarction caused by occlusion of the ascending frontal artery complex resulting from thrombosed left MCA aneurysm. The patient was managed conservatively and his neurological symptoms gradually improved. One month later, he lapsed into a coma. CT revealed subarachnoid hemorrhage. Carotid angiography showed a large left MCA aneurysm with branch occlusion of the left ascending frontal artery complex. A left frontotemporal craniotomy was performed. The MCA aneurysm was opened and the intramural thrombi removed, and finally neck clipping was performed. The patient made a good postoperative recovery.

Aged↗
PubMed2001

Patent foramen ovale complicated by paradoxical embolism and brain infarct in a patient with advanced ovarian cancer.

BACKGROUND: Recent investigations of patients with cerebral and peripheral arterial emboli of unknown cause suggest that paradoxical embolism through a patent foramen ovale might be responsible for more arterial embolic events than previously realized. CASE: A 60-year-old woman with advanced ovarian cancer presented with sudden onset of expressive aphasia and right upper hemiplegia postoperatively. A patent foramen ovale diagnosed by echocardiography with contrast combined with the presence of thrombosis in her right femoral vein leads us to speculate that her stroke was secondary to a paradoxical embolism. CONCLUSION: Paradoxical embolism should be considered in the differential diagnosis of ovarian cancer patients with embolic stroke and it may be appropriate to include a cardiac echo as part of the diagnostic evaluation.

Brain Infarction↗
PubMed2004

Functional and cellular effects of environmental enrichment after experimental brain infarcts.

Our genes interact with environmental stimuli throughout our lives. The attitude and reaction to an acute cerebral trauma or stroke, as well as the pre-lesion life event and activities, can influence functional outcome. Although difficult to separate in adult human beings, genetic and environmental factors can be selectively evaluated in animal studies. Post-ischemic housing in an enriched environment, i.e. larger cages which allow both social interaction and various activities improves functional outcome, modifies gene activation, and increases dendrite branching and number of dendritic spines in pyramidal neurons in layers II-III in the contra-lateral cortex. Furthermore, it alters lesion-induced progenitor cell differentiation and interacts with neocortical transplantation, drug treatment and training. It is proposed that the interaction between environment and specific treatment needs more clinical attention, and that a general stimulating and positive environment is the optimal base for specific interventions in neurological rehabilitation.

Animals↗
PubMed2000

[Brain infarct from a paradoxical embolism following a varices operation].

HISTORY AND CLINICAL FINDINGS: A 70-year-old woman developed an acute right-sided hemiparesis and global aphasia 10 days after saphenous vein stripping of varicosities. Initially, she presented with somnolence, conjugated to the left, flexor synergism of the right extremities, exaggeration of knee and ankle jerks and extensor plantar responses on the right side. INVESTIGATIONS: The initial cranial computed tomography one hour after the onset of symptoms did not show reliable signs of cerebral ischaemia but a "dense artery sign" of the left middle cerebral artery. Repeat computed tomography then revealed a partial, mainly subcortical, infarction of the left middle cerebral artery territory. Doppler sonography revealed an occlusion of the left internal carotid artery. In duplex sonography there was no evidence of arteriosclerosis. Transesophageal echocardiography revealed a patent foramen ovale with right-to-left shunt. TREATMENT AND COURSE: Immediately after admission intravenous anticoagulation was initiated because of the suspected cardioembolic origin of the stroke. During hospitalization the global aphasia regressed and a continuing mobilization was achieved while the right-sided hemiparesis persisted. The neurological rehabilitation was initiated and continuous oral anticoagulation was planned. CONCLUSION: This case suggests a causal relationship between previously performed vein stripping and paradoxical embolism resulting in a stroke. For patients with patent foramen ovale, vein stripping may be associated with an increased stroke risk.

Aged↗
PubMed2002

CADASIL: a common form of hereditary arteriopathy causing brain infarcts and dementia.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary cerebrovascular disease leading to cognitive decline and dementia. CADASIL usually begins with migraine in about one third of the patients. More severe manifestations, transient ischemic attacks or recurrent strokes, appear between 30 and 50 years of age. CADASIL, however, may be diagnosed well before the first stroke on the basis of characteristic white matter hyperintensities upon magnetic resonance imaging and presence of pathognomonic granular osmiophilic material in arterial walls, including dermal arteries, since the arteriopathy is generalized. Gradual destruction of vascular smooth muscle cells (VSMC) leads to progressive wall thickening and fibrosis and luminal narrowing in small and medium-sized penetrating arteries. The reduced cerebral blood flow finally causes lacunar infarcts, mainly in the basal ganglia and fronto-temporal white matter, which lead to cognitive deficits and dementia of the subcortical vascular type. CADASIL is caused by single missense mutations or small deletions in Notch3 gene encoding a transmembrane receptor Notch3, of which upon ligand binding a nuclear signaling protein is generated by regulated intramembrane proteolysis. Notch signaling is essential during development, regulating cellular differentiation. In adults Notch3 is expressed only in VSMCs and it may promote cell survival by inhibiting apoptosis, but its exact function is unknown. Mutations result in either a gain or loss of one (or rarely, 3) cysteine residue(s) in one of the 34 epidermal growth factor-like repeats in the extracellular amino-terminal region of Notch3. It is as yet unclear which disturbance in the Notch signaling pathway leads to the characteristic vascular pathology of CADASIL.

Arteries↗
PubMed2005

Cognitive and functional outcome after intravenous recombinant tissue plasminogen activator treatment in patients with a first symptomatic brain infarct.

OBJECTIVE: To examine whether intravenous recombinant tissue plasminogen activator (rt-PA) treatment given in the acute phase of ischaemic stroke has a favourable effect on cognitive and functional outcome at six months post-stroke. METHODS: The present study included 92 patients with a first-ever symptomatic infarct, of whom 25 (27%) were subjected to rt-PA treatment in the first three hours post-stroke. Multivariate logistic regression analyses adjusted for stroke severity, education, age, and sex were performed to examine whether rt-PA treatment influenced cognitive outcome (assessed with a neuropsychological examination covering 7 cognitive domains), basic ADL independence (modified Barthel Index > or = 19), and instrumental ADL independence (Frenchay Activities Index > or = 15) after six months. RESULTS: The adjusted odds ratio for intact cognition was 1.0 (95% CI 0.2 to 4.3), that for basic ADL outcome 13.5 (95 % CI 1.4 to 129.4) and for instrumental ADL 7.1 (95 % CI 1.2 to 42.2). CONCLUSION: Our findings suggest that rt-PA treatment is associated with a favourable basic and instrumental ADL outcome, but not with a beneficial cognitive outcome after 6 months.

Activities of Daily Living↗
PubMed2006

Etiology of young adult onset brain infarction in Iran.

BACKGROUND: Stroke in young adults causes morbidity in this socioeconomically-active age group. Etiologic frequency of ischemic stroke in young adults is different around the world. This study was conducted to determine the causes of stroke in Iranian young adults. METHODS: The study population consisted of 314,000 young adult residents in the Southern Khorasan Province, East of Iran. All the patients with stroke, admitted to Vali-e-Asr Tertiary Care Hospital, entered this study. Demographic data, clinical presentation, and investigations of consecutive patients aged 15 - 45 years, presented with ischemic stroke, were registered in Southern Khorasan Stroke Database between 2000 and 2005. All the patients underwent a standard battery of diagnostic investigations by a stroke neurologist. Etiologic classification of stroke in the patients was made based on the Practical Iranian Criteria. RESULTS: One hundred and twenty-four patients (60 females and 64 males) were prospectively investigated during a 5-year period. The incidence of ischemic stroke in young adults was 8/100,000 per year. Cardioembolic mechanism constituted 54% of all stroke etiologies in young adults. Rheumatic valvular heart disease was present in 32% of the patients and caused 2.5 preventable stroke cases per 100,000 young adults per year. CONCLUSION: Rheumatic valvular heart disease is the most common cause and a preventable etiology of stroke in Iranian young adults.

Adolescent↗
PubMed2001

Hypercholesterolemia, lipid-lowering agents, and the risk for brain infarction.

Clinical trials in the 1990s using HMG-CoA reductase inhibitors (statins) showed that cholesterol-lowering treatment significantly reduces cardiovascular events including strokes in the primary and secondary prevention of myocardial infarction (MI). Paradoxically, the link between serum cholesterol level and the incidence of stroke remains to be fully established. This is largely due to conflicting evidence from a series of observational cohort studies and a suggestion that lowering serum cholesterol increased the risk for hemorrhagic stroke. These findings have tended to influence the treatment of stroke, despite alternative interpretations for the failure of these studies to find a clear association between cholesterol levels and stroke. The statin trials present a strong argument for a reappraisal of the link between cholesterol and stroke. Three meta-analyses have all shown a relative risk reduction in stroke of 12 to 48% in patients with coronary heart disease (CHD) after MI. There was no statistically significant increase in hemorrhagic stroke. Recently, gemfibrozil has also been shown to reduce the relative risk for stroke (25%), which contradicts the findings of previous fibrate trials. It is becoming clear that the clinical action of many cholesterol-lowering drugs is the result of pleiotropic/antiatherogenic effects rather than simply a reduction in cholesterol. There is also evidence that these agents exert direct effects that promote atherosclerotic plaque stability. After these observations, it is now generally accepted that lipid-lowering treatment should be considered in all stroke patients with a history of CHD/MI. However, for the remaining patients with ischemic stroke, there is no proven therapeutic approach, and several large randomized, placebo-controlled trials are under way or planned for this indication.

Anticholesteremic Agents↗
PubMed2001

Mannitol bolus preferentially shrinks non-infarcted brain in patients with ischemic stroke.

Changes in brain tissue volume in six patients who had acute complete middle cerebral artery (MCA) infarctions and CT evidence of midline shift were measured using the brain boundary shift integral (BBSI) on sequential T1-weighted MR images acquired before and after a 1.5-g/kg bolus infusion of mannitol. At 50 to 55 minutes after the baseline scan, total brain volume decreased by 8.1 +/- 2.8 mL (0.6%, p < 0.005). Brain in the noninfarcted hemisphere shrank more (0.8 +/- 0.4%) than in the infarcted hemisphere (0.0 +/- 0.5%, p < 0.05).

Adult↗
PubMed1992

The breakdown process of human brain infarction in middle-aged and senile cases.

The material comprised 15 cases of ischemic brain stroke at the age of 45 to 101 years. Six brain of subjects deceased at the age of 45 to 57 years and 9 brains of those deceased at the age of 80 to 101 years were studied. Phagocytic cell immunoreactivity in both age groups during the first 5 days and on the 11th and 12th were compared. Phagocytic reactivity in cases of patients who died on the 6th, 15th and 35th days after stroke onset was also estimated. Colliquative necrosis with cavitation was observed in middle-aged cases from the 3rd infarction day. In the senile group the beginning of tissue breakdown was noted on the 5th day, but colliquative necrosis with cavitation was found on the 11th infarction day. Senile alterations in the biochemical components in various brain tissue elements are probably the cause of the different course and dynamics of the pathological process.

Aged↗
PubMed1994

Tumour-like thallium-201 accumulation in brain infarcts, an unexpected finding on single-photon emission tomography.

Thallium-201 brain single-photon emission tomography (201Tl-SPET) is widely used to detect viable tumour tissue with increased metabolic activity. When reperfusion takes place early in cerebrovascular lesions of embolic origin, the presence of tissue areas with increased regional blood flow and preserved metabolic activity can also be assumed. In the present study our purpose was to investigate whether or not foci of 201Tl accumulation occur in reperfused areas with sustained morphological integrity indicated by computed tomography (CT) scans not showing hypodensity in the acute or subacute period. In 16 stroke patients with possible cortical embolic infarction, dual 201Tl and technetium-99m hexamethylpropylene amine oxime (99mTc-HMPAO) SPET was performed in both the acute and the subacute period. 99mTc-HMPAO SPET was performed to detect reperfusion. Follow-up CT scans from the same period were also available. In five cases 99mTc-HMPAO SPET ruled out reperfusion and 201Tl SPET was also negative. In four cases 99mTc-HMPAO studies indicated reperfusion early in the acute phase (24-72 h), and comparative CT, without showing hypodensity in the acute or subacute period, also favoured the possibility of sustained metabolic activity. In these cases 201Tl SPET was negative in both the acute and the subacute period. In seven cases CT already showed necrosis in 99mTc-HMPAO hypoperfused areas in the acute period, with negative results on corresponding 201Tl SPET. Later reperfusion occurred in the subacute period (8-14 days) as indicated by 99mTc-HMPAO SPET, at which time an unexpected focal accumulation of 201Tl was detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2004

How important is hyperglycemia during acute brain infarction?

BACKGROUND: Although well supported by animal studies, it remains unproven whether lowering hyperglycemia during acute cerebral infarction will improve outcomes. Further support for this therapeutic approach comes from clinical studies in acute myocardial infarction and in ventilated postsurgical patients, where lowering hyperglycemia improved outcomes. REVIEW SUMMARY: Animal studies support the hypothesis that hyperglycemia during acute brain ischemia augments the brain injury, but only in models with reperfusion. The available human studies to date are all observational and they usually find an association between hyperglycemia during acute cerebral infarction and worse outcome. Also, there is evidence that hyperglycemia during acute cerebral infarction is detrimental only with reperfusion. This association appears to be linear in the glucose ranges tested (normal to high). In addition, there is an association between admission hyperglycemia and hemorrhagic conversion of an acute cerebral infarct when thrombolytics are used. CONCLUSION: Sufficient evidence has accumulated to proceed to clinical efficacy trials to see if tight glycemic control compared with persistent hyperglycemia during acute cerebral infarction will improve outcomes. If such therapy proves beneficial, the increased cost, effort, and risk associated with tight glycemic control during acute cerebral infarction could be justified. Randomized clinical trials to test this hypothesis are currently in progress.

Acute Disease↗
PubMed2005

The broad-spectrum cation channel blocker pinokalant (LOE 908 MS) reduces brain infarct volume in rats: a temperature-controlled histological study.

Activation of cation channels conducting Ca2+, Na+ and K+ is involved in the pathogenesis of infarction in experimental focal cerebral ischaemia. Pinokalant (LOE 908 MS) is a novel broad-spectrum inhibitor of several subtypes of such channels and has previously been shown to improve the metabolic and electrophysiologic status of the ischemic penumbra and to reduce lesion size on magnetic resonance images in the acute phase following middle cerebral artery occlusion in rats. The purpose of the present study was to investigate whether these beneficial effects of pinokalant are translated into permanent neuroprotection in terms of a reduction in infarct size one week after middle cerebral artery occlusion in rats. Halothane-anaesthetized male Wistar rats subjected to permanent distal middle cerebral artery occlusion were randomly assigned to one of two treatment groups: 1) Control (vehicle intravenous loading dose followed by infusion); 2) Pinokalant (0.5 mg/kg intravenous loading dose followed by infusion of 1.25 mg/kg/hr). Infusions started 30 min. after middle cerebral artery occlusion and were continued for 24 hr. Body temperature and mean arterial blood pressure were monitored by telemetry during this period and the spontaneous temperature after course in control rats established in other experiments was imitated. Seven days later histological brain sections were prepared and the infarct volumes measured. Body temperature did not differ between the groups. Mean arterial blood pressure was slightly higher in the pinokalant group. Pinokalant treatment significantly reduced cortical infarct volume from 33.8+/-15.8 mm3 to 24.5+/-13.1 mm3 (control group versus pinokalant group, P=0.017, t-test). Taking the effective drug plasma concentration established in other experiments into account revealed that in rats with plasma concentrations within the therapeutic interval, infarct volumes were further reduced to 17.9+/-7.5 mm3 (P<0.005).

Acetamides↗