Cause Of Cerebral Ischemia Research Articles

Neurological aspects of patent foramen ovale: in search of the optimal treatment.

Although paradoxical embolism through a patent foramen ovale (PFO) has become an established cause of cerebral ischemia in younger patients without other obvious causes of stroke, the therapeutic options have not been investigated satisfactorily. There are still uncertainties about the natural history of PFO patients after suffering a stroke, and diagnostic criteria proving a causal and not incidental relation to the embolic event are not established. The stroke recurrence has been evaluated in several studies in a heterogeneous population and seems as low as 1.9% per year. Secondary prophylactic treatment has become a matter of discussion since efforts were made to close the PFO either surgically or by percutaneous transcatheter methods. Foramen closure seems to be effective in eliminating the mechanism of paradoxical embolism but its benefit-risk ratio has yet to be established. Following the goals of evidence-based medicine, none of the therapeutic options can be recommended. Fortunately, the issue has gone to trial and there are two studies underway to compare foramen closure to medical therapy.

“NEWER” CARDIAC SOURCES OF EMBOLIC STROKE

BACKGROUND- Although cardiac embolism has long been recognized as a cause of cerebral ischemia, relatively “new” potential sources of embolism have been recently documented, particularly with the advent of transesophageal echocardiography. REVIEW SUMMARY- In this review, we explore the data and controversies concerning patent foramen ovale and paradoxical embolism, aortic arch atheroma, atrial septal aneurysm, spontaneous echo contrast, valvular strands, and valvular calcification. CONCLUSIONS- Although much has been learned about these potential causes of stroke, considerable uncertainty remains as to underlying mechanism leading to stroke as well as optimal therapy.

Fibromuscular Dysplasia of the Internal Carotid Artery. Personal Experience with 13 Cases and Literature Review

SummaryFrom January 1990 to December 1997, the authors observed 13 cases of fibromuscular dysplasia of the internal carotid artery. Four patients presented transient ischemic attacks, one amaurosis fugax, two suffered from a minor stroke, four had non-focalized ischemic cerebral symptoms and two were asymptomatic. At angiography, all patients showed a typical image of “string of beads”.Seven patients were operated on. Six had endoluminal graduated dilatation, with rigid dilators up to 4.5 mm, associated with thrombendarterectomy of the bifurcation in three and to correction of a kink in one case. In one case a venous interposition graft was done to exclude a saccular microaneurysm of the dysplasic internal carotid artery. In another case, backflow was insufficient after endoluminal dilatation, and a long venous patch allowed to restitute a normal vascular lumen. There was neither postoperative mortality nor stroke.Six patients, asymptomatic or with non focalized symptoms, were treated medically.During a mean follow-up of 47 months, only one of the 13 patients developed a transient ischemic attack; the patient had not been operated on and received only medical treatment.Prevalence, etiopathology, diagnosis and management of fibromuscular dysplasia of the internal carotid artery are discussed. Fibromuscular dysplasia is a rare cause of cerebral ischemia. For asymptomatic lesions, a conservative approach seems appropriate. Surgery is only to be considered for symptomatic lesions. Surgical graduated endoluminal dilatation, where necessary combined with standard endarterectomy of the carotid bifurcation, is a safe, efficient and durable operation. Some complex cases of fibromuscular dysplasia may necessitate patch insertion or excision and graft interposition.

Hemodynamic evaluation by using near infrared spectroscopy during carotid endarterectomy

To evaluate the hemodynamic changes during carotid endarterectomy, we compared changes in oxyhemoglobin levels with changes in the internal carotid artery flow and the somatosensory evoked potential (SEP). In 40 of 42 patients, the oxyhemoglobin level, measured in the frontal area on the operated side using near infrared spectroscopy (NIRS), decreased immediately after cross-clamping the internal carotid artery and returned to the preclamping level after the clamp was removed. There was no linear relationship between the internal carotid flow and the decrement in the oxyhemoglobin level after carotid clamping. Nineteen patients (45%) had a large internal carotid flow (> or =90 mL/min), but a small decrease in the oxyhemoglobin level (<0.04 in index); presumably these patients had adequate collateral circulation. Eight patients (19%) had a large internal carotid flow and a marked decrease in the oxyhemoglobin level (> or =0.04); presumably these patients had insufficient collateral circulation. The changes in oxyhemoglobin and SEP after carotid clamping agreed in 77.5% of the patients; however, in the other 22.5%, the disparity between the two factors indicated different causes of cerebral ischemia following carotid clamping. A marked decrease in oxyhemoglobin without a significant change in SEP suggests ischemia predominantly in the frontal area, whereas a small decrease in oxyhemoglobin and a significant change in SEP suggest ischemia predominantly in the somatosensory pathway or cortex. In conclusion, the relationship between the internal carotid flow and the change in HbO(2) provides information about the collateral circulation. Simultaneous monitoring of NIRS and SEP is useful for assessing of the pattern of cerebral ischemia during carotid clamping.

Stroke in the developing world

Stroke is the third most common cause of death in most western populations after coronary-heart disease and cancer? It is thus the commonest life-threatening neurological disorder, and the resulting disability is the most important single cause of severe disability among western people living in their own homes) The burden of stroke on patients, their families, and society is, correctly, publicised in most developed countries. Stroke in the developing world is less well documented, and some data are not retrievable because of the language barrier or the limited dissemination of data collected. However, more than two-thirds of the world's population live in developing countries, and one of the consensus statements from the Asia-Pacific Consensus Forum on Stroke Management predicts that "In the next 30 years the burden of stroke will grow most in developing countries rather than in developed countries"? Thus stroke in developing countries ought to be examined further--in particular, the similarities and differences in stroke between developed and developing countries.

Spontaneous dissection of the internal carotid artery presenting with pulsatile tinnitus

Spontaneous dissection of the internal carotid artery (ICA) is an uncommon event but is increasingly recognized as a cause of cerebral ischemia in relatively young adults.1-4 Pulsatile tinnitus is often associated with dissections of the ICA, a fact well described in the neurology and vascular surgery literature.1-3,5,6 However, this entity has received little attention in discussions of pulsatile tinnitus in the otolaryngology literature.

Estados protrombóticos e isquemia cerebral

Hematological disorders per se represent unusual causes of cerebral ischemia, explaining in young people 4% of strokes. Hematological disorders that induce a thrombotic tendency contribute to overall ischemic stroke risk and may directly cause cerebral ischemia in patients without other risk factors. The frequency of cerebral infarctions caused by prothrombotic states is not known. This review will focus on disorders such as prothrombotic coagulopaties, including resistance to activated protein C and antiphospholipid syndrome as cause of cerebral infarction. Cerebral venous thrombosis and cerebral infarction from arterial origin are the most common form of neurological involvement. Pathophysiological mechanism of stroke in these patients are multiple and can include as in antiphospholipid syndrome embolism from valves abnormalities related to hematological disturbance, as well as thrombosis of extracranial or intracranial vessels. Is clear, however, that prothrombotic states could explains a high percentage of cases of those so called cryptogenic cerebral infarction in young people.

Race and sex differences in the distribution of cerebral atherosclerosis.

The purpose of this study was to assess the influence of race, sex, and other risk factors on the location of atherosclerotic occlusive lesions in cerebral vessels. Previous angiographic studies of patients with stroke or transient ischemic attack (TIA) suggest that extracranial atherosclerosis is more common in whites and intracranial disease is more common in blacks. Noninvasive techniques such as duplex ultrasound, transcranial Doppler (TCD), and magnetic resonance angiography (MRA) allow vascular assessment of a more representative proportion of patients than does conventional angiography alone. Consecutive patients evaluated at a community hospital for stroke or TIA over a 2-year period were reviewed. Lesions were defined as a 50% or greater atherosclerotic stenosis by angiography, duplex ultrasound, or TCD, or a moderate stenosis by MRA. Whites were more likely than blacks to have extracranial carotid artery lesions (33% versus 15%, P = .001), but the proportion of patients with intracranial lesions was similar (24% versus 22%). Men were more likely to have intracranial lesions than women (29% versus 14%, P = .03). When multivariate logistic regression analysis was used, white race was the only predictor for extracranial carotid artery lesions, and male sex was the only predictor for intracranial lesions. The cause of stroke/TIA was extracranial carotid artery disease in 8% and intracranial disease in 8% of all patients in the study. The distribution of cerebral atherosclerosis is influenced by race and sex but not by other vascular risk factors. In our patient population, intracranial disease is as common a cause of cerebral ischemia as extracranial carotid disease.

Spontaneous cerebral embolus from a calcified aortic valve.

E mboli are a known cause of cerebrovascular infarct or transient ischemic attack. Causes of emboli include atheromatous carotid arteries. calcifled ascending aorta. and cardiac mural thrombus, or the cause may be unknown L 1. 2]. Spontaneous embolus from a calcified aortic valve is a rare cause of cerebral ischemia [I, 3, 41. In published reports. most calcific emboli are reported to occur after invasive procedures such as valvuloplasty. valvular surgery, or cardiac catheterization [3, 5, 6]. We report a middle-aged patient with a calcifled embolus to the right middle cerebral artery that originated spontaneously from a calcified bicuspid aortic valve.

Problems in the recognition of aortoembolic stroke

Recent reports suggest aortoembolism is an important cause of stroke. Although transesophageal echocardiography visualizes the aortic arch, diagnosis of aortoembolism stroke is not common. We investigated reasons for this discrepancy at our institution. We reviewed charts and transesophageal echocardiography videotapes of 16 patients with recent ischemic stroke or transient ischemic attack who had undergone transesophageal echocardiography. For each patient, we determined the most likely cause of cerebral ischemia, and we compared the official transesophageal echocardiography report to our interpretation of the videotape. In our videotape review, 13 patients had good visualization of the aortic arch. Of 6 patients with atherosclerosis in the arch, 1 had high-grade carotid stenosis, 1 had atrial fibrillation, 1 had "small-vessel disease," and 3 had cerebral ischemia of unknown cause. The official reports did not mention aortic arch disease in 4 of 6 patients. A possible cause of cerebral ischemia was identified in 6 of 7 patients with normal aortic arches. Of 3 patients who had poor visualization of the aortic arch, one had "small-vessel disease," and 2 had ischemic stroke of unknown cause despite extensive workups. We conclude that aortic arch disease is common in patients with ischemic stroke and transient ischemic attack and may be a cause of cerebral ischemia, especially in patients with stroke or transient ischemic attack due to small-vessel occlusion or of unknown cause. Aortic arch disease may not be identified as the cause of stroke or transient ischemic attack because (a) transesophageal echocardiography is not done, (b) transesophageal echocardiography is done but the aortic arch is not visualized, (c) transesophageal echocardiography is done, the aortic arch is visualized, but the examiner does not comment on aortic arch disease, or (d) despite transesophageal echocardiography identification of arotic arch disease, the treating physician does not consider the aorta to be a potential source of embolization.

Optic-disc hemorrhages: Cause or result of ischemia?

Visual-field defects may develop after optic-disc hemorrhages. The question whether blood may be a major damaging agent for the optic nerve head will be discussed. A female patient with an optic-disc hemorrhage in the left eye was followed with frequent disc photography and computerized perimetry for a period of two months. This patient presented, subsequently to an optic-disc hemorrhage of unknown cause, a delayed progression of the visual-field defect. The fact that the visual-field defect developed after the hemorrhage and was progressive in the next few days indicates that the hemorrhage may not be the result of an infarct, but rather provokes further damage. The case raises the question whether blood components may be involved in the pathophysiologic process of optic-nerve-head atrophy. In analogy of cerebral vasospasm after subarachnoid hemorrhage as an important cause of cerebral ischemia, the potential involvement of blood-related injury to the optic disc should be considered in such patients.

Etiopathogenesis and prognosis of cerebral ischemia in young adults.

Etiology and long-term prognosis were prospectively investigated in 155 consecutive patients (96 men and 59 women), aged 16 to 45 years, referred to our Neurosurgical Unit with cerebral transient ischemic attacks or infarction during the period 1978-1988. All patients underwent neurological and medical-cardiological evaluation, cerebral computerized tomography scanning, electrocardiogram, and laboratory tests. Two-dimensional echocardiography was performed in 123 cases (79%), cerebral angiography in 147 (95%). Atherosclerosis was the leading etiology occurring in 48 patients (31%). A cardioembolic disorder was considered the probable cause of ischemia in 8 cases (5.1%). Further possible etiologies were contraceptive pill assumption (5.8% of the total, but 15.3% within the female group), spontaneous arterial dissection (4.5%), migraine (4%), puerperium (2.6%), cervical trauma (2.6%), and other, more uncommon conditions. Despite extensive evaluation, the cause of cerebral ischemia remained unknown in 40% of cases. All patients received antiplatelet medication and 16 underwent surgery. The long-term outcome at a mean follow-up of 5.8 years was favorable: 91% of subjects resumed their work on a full or part-time basis.

Autosomal dominant syndrome with strokelike episodes and leukoencephalopathy.

We conducted a prospective survey of a family presenting a new syndrome characterized mainly by recurrent strokelike episodes and neuroimaging evidence of leukoencephalopathy. Forty-five members of a single family were studied clinically and with magnetic resonance imaging. Nine had strokelike episodes, including transient ischemic attacks, and minor or major strokes starting between the fourth and sixth decades, with neuroimaging evidence of small, deep infarcts and a widespread white matter disorder. Other symptoms included migraine (three), dementia (two), epilepsy (one), and hearing loss (one). In some patients, we found various immunologic anomalies and muscular lipidosis without ragged-red fibers. Eight other family members were clinically normal, but had identical neuroimaging signs of leukoencephalopathy. No abnormality was detected in the 28 other members of the family examined. Extensive investigations failed to reveal any known cause of cerebral ischemia. There appears to be a new syndrome in this family that is characterized by recurrent subcortical strokelike episodes, leukoencephalopathy, immunologic anomalies, muscular lipidosis, and an autosomal dominant pattern of transmission.

Investigation of the Patient with Ischemic Stroke

Evaluation of a patient with recent stroke is divided into studies that confirm the diagnosis of an ischemic event and those that determine the most likely etiology. While clinical manifestations of hemorrhagic and ischemic stroke overlap, imaging studies (computed tomography, CT, or magnetic resonance imaging, MRI) effectively differentiate these disorders. Imaging studies also define the site and extent of the stroke and provide evidence towards its etiology and prognosis. Imaging also detects complications of stroke or therapy including edema, hydrocephalus or hemorrhagic infarction. MRI also detects very acute, small or posterior fossa infarctions that can be missed by CT. MRI can also detect arterial-flow abnormalities. The role of transcranial Doppler or Duplex imaging in acute ischemic stroke has not been defined. While atherosclerosis is the most common cause of cerebral ischemia, a number of diseases present with or are complicated by stroke. Investigation for the etiology of stroke is justified particularly in patients with atypical presentations. Arteriography is warranted in most patients but may, in the future, be replaced by MRI angiography. Specialized hematologic studies for evaluation of hypercoagulable states are indicated. Transthoracic echocardiography can be supplemented by Doppler or contrast techniques. Transesophageal echocardiography effectively visualizes the left atrium and atrial appendage. Ultrafast CT imaging of the heart may add valuable information in screening patients with stroke.

Isolated supraclinoid occlusive disease of the internal carotid artery.

Isolated supraclinoid occlusive disease of the internal carotid artery is a rare cause of cerebral ischemia. The authors of the only review of this subject concluded that it is caused predominantly by factors other than atherosclerosis. We examined 6 patients with isolated supraclinoid occlusive lesions. Five of them had one or more risk factors for atherosclerosis. Thus, the isolated stenosis of that part of the internal carotid artery does not seem to represent a particular pathologic entity.

Cerebral ischemic accidents of cardiac origin.

The cardiac causes of cerebral ischemia, particularly the origins and etiology of embolism, are described in some detail.

Effects of hematocrit on brain metabolism in experimentally induced cerebral ischemia in spontaneously hypertensive rats (SHR).

Brain tissue lactate, pyruvate, and adenosine triphosphate (ATP) were measured 60 min after bilateral carotid ligation in spontaneously hypertensive rats, of which hematocrit (HCT) was varied by exchanging with isovolemic homologous red cells, plasma or whole blood. Supratentorial lactate of the ischemic brain was increased more in high HCT (greater than or equal to 50%) and less in low HCT (30-39%) compared with normal HCT (40-49%). In very low HCT (less than 30%), however, lactate was increased to further extent compared with any other group of HCT (ANOVA p less than 0.0001). Lactate/pyruvate (L/P) ratio of the ischemic brain showed similar changes, namely U-shaped correlation to HCT. In contrast, supratentorial ATP was decreased more markedly in very low HCT, followed by high and normal HCT, and minimally decreased in low HCT, demonstrating an inverse U-shaped relationship to HCT. Mean arterial pressure and arterial acid-base parameters in ischemic animals did not differ among HCT groups. There were no HCT-related changes of brain metabolites in non-ischemic control rats. These findings indicate that cerebral ischemia following carotid ligation is more severe in high HCT but less in low HCT, probably due to hemodynamic effects of HCT changes. When HCT is reduced to below 30%, however, insufficient oxygen supply to the brain or anemic hypoxia may superimpose on ischemia, resulting in more markedly impairment of brain metabolism. The role of HCT as a cause of cerebral ischemia and its severity is discussed.

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysm rupture. There are two definitions of cerebral vasospasm: angiographic and clinical. Care must be exercised to be certain that it is clear which entity is being addressed. The diagnosis of the clinical syndrome is one of exclusion and can rarely be made with absolute certainty. The pathogenesis of cerebral vasospasm is poorly understood. Most current theories focus on the release of factors from the subarachnoid clot. More attention must be given to the role of endothelial damage and alterations in the blood-arterial wall barrier. The application of modern techniques for studying vascular smooth muscle which have been developed as a result of research in the areas of hypertension and atherosclerosis must be applied to the problem of cerebral vasospasm. A stress test to select patients with angiographic arterial narrowing who have adequate cerebral vascular reserve to undergo surgery should be developed. The optimal treatment of vasospasm awaits development of agents for blocking or inactivating spasmogenic substances or blocking arterial smooth muscle contraction. Rheological or hemodynamic manipulations to prevent or reverse ischemic consequences of vasospasm are relatively effective, but complicated and hazardous, and should be viewed principally as interim measures awaiting development of more specific therapies for the arterial narrowing.

Mitral valve prolapse and cerebral ischemic events in young patients.

We evaluated 32 young patients with mitral valve prolapse (MVP) as the only recognized cause of cerebral ischemia. The mean follow-up from the time of the first ischemic event was 8 years. At the time of the follow-up evaluation, 24 patients (75%) had a normal cardiac examination, and 4 had midsystolic clicks; only 1 had the characteristic click-murmur. In 75%, the first ischemic event was stroke. When MVP-associated ischemia was recognized, 44% had recurrent ischemic events. In the mean 4-year period between diagnosis of MVP-associated ischemia and follow-up, 16% had recurrent ischemic events, but none had a new persistent deficit from these events. At the time of follow-up, 63% of patients were taking platelet antiaggregants or anticoagulants. These data suggest a good prognosis for recurrent ischemic events after diagnosis of MVP-associated ischemia.

Cerebral ischemia in young adults.

56 cerebral ischemia patients up to the age of 40 were investigated using a strict clinical and instrumental protocol in order to elicit the relative importance of the various iatrogenic factors involved. In addition to atherosclerosis risk factors (smoking, hypertension, ischemic heart disease, diabetes, dyslipidemia) other possible causes of cerebral ischemia were sought (arteritis, migraine, head injury, oral contraceptives, coagulation disorders, cardiogenic embolism, etc.). 50% of the patients examined had at least two atherosclerosis risk factors and 55% had other causes singly or in association with atherosclerosis.