Cause Of Cerebral Infarction Research Articles

Internal carotid artery dissection: an update

Carotid artery dissection is a major cause of cerebral infarction in the young. The extracranial portion of the internal carotid artery is much more frequently involved that the intracranial portion. In up to 20% of cases it is bilateral or associated with vertebral artery dissection. It is mainly characterised by local signs such as headache or facial pain, Horner's syndrome, lower cranial nerve palsies and pulsatile tinnitus, followed a few hours or days later by signs of cerebral or retinal ischemia. Ultrasound investigations show signs of distal stenosis or occlusion, highly suggestive of dissection, but the best diagnostic tool is presently the association of magnetic resonance imaging (MRI) and MR angiography which tend to replace intra-arterial angiography. The prognosis is highly variable: excellent in cases limited to local signs, but very poor leading to death or major sequelae in about 15% of cases. Various treatments have been suggested but no controlled trial has ever been performed in this condition. Heparin in the acute stage followed by warfarin or aspirin for 3 to 6 months is most commonly used.

Frequency of cerebral arteritis in subarachnoid cysticercosis: an angiographic study.

Subarachnoid cysticercosis is a well-recognized cause of cerebral infarction. However, few patients with this infection develop cerebral infarction, and the reason for this is not known. The aim of this study was to determine the frequency of cerebral arteritis in these patients. Using cerebral arteriography, we studied 28 patients with subarachnoid cysticercosis admitted to our hospital from July 1993 to February 1996. All patients underwent MRI to detect the presence of basal arachnoiditis. We analyzed demographic data, time to cysticercosis since the first symptom onset, mode of onset, stroke syndromes, neuroimaging features of cysticercosis and cerebral infarction, and arteriographic findings for each patient. Of the 28 patients (mean age, 37 years), 15 patients had angiographic evidence of cerebral arteritis (53%); 12 of the 15 had a stroke syndrome (P=.02). Eight of the 15 patients (53%) with cerebral arteritis had evidence of cerebral infarction on MRI, whereas only one patient without cerebral arteritis had cerebral infarction (P=.05). The most commonly involved vessels were the middle cerebral artery and the posterior cerebral artery. The frequency of cerebral arteritis in subarachnoid cysticercosis is higher than previously reported, and middle-size vessel involvement is a common finding, even in those patients without clinical evidence of cerebral ischemia.

American Heart Association Prevention Conference. IV. Prevention and Rehabilitation of Stroke. Etiology of stroke.

The diagnosis of arterial stroke differentiates ischemia from hemorrhage. The former may be due to arterial occlusion or stenosis, the latter to leakage or rupture of an artery. Computed tomography (CT) and magnetic resonance imaging (MRI) have shown that this basic differentiation cannot be reliably made from the history and clinical examination alone. Of the clinical stroke syndromes, only Wallenberg’s syndrome has not been reported to be due to hemorrhage. When CT or MRI is not available for diagnosis, spinal tap is reliably positive only when the aneurysm or arteriovenous malformation has ruptured into the subarachnoid space; the results are often normal when a small hemorrhage occurs in the parenchyma. For some therapies, notably neuroprotective agents, the potential benefits for ischemia do not seem to be offset by potential harm in the case of hemorrhage. However, because fibrinolytics, antithrombotic agents, or surgery are treatment options, diagnostic certainty is essential to avoid harming the patient. Most—but not all—strokes have a sudden or rapidly evolving onset. Differential diagnosis of sudden change in focal neurological status includes seizures or postepileptic paralysis, hemorrhage into a tumor (itself a form of stroke), and migraine. Neuroimaging helps to differentiate between these and the cause of short-lived symptoms (transient ischemic attack [TIA]) usually presumed due to ischemia but possibly due to new-onset infarction or hemorrhage. More precise classification of stroke into a pathogenic subtype (embolism, thrombosis, decreased perfusion or “lacunar” infarction, leakage, or rupture) evades the best clinical skills. The classification of stroke mechanism depends on the presence of risk factors for stroke (preexisting condition or circumstance epidemiologically related to stroke) and etiologies (disease directly causing the mechanism) that implicate the cause of stroke in a given patient. However, more than one risk factor and etiology are frequently present in the same patient and may be related …

Expanded Spectrum of Coagulopathy in the Etiology of Cerebral Infarction in Younger Adults in Japan

To clarify the role of coagulopathy in cerebral infarction (CI) in adults with onset before age 45, we performed comprehensive and repeated hemostatic analyses in 77 consecutive young adult patients with CI. Coagulopathy was found in 24% (9% in older adults, n = 241); inherited coagulopathy was observed in 14 patients, including protein-S deficiency in 6, abnormal plasminogen (genetically confirmed) in 5, and protein-C deficiency in 2. Acquired coagulopathy confined to the acute stage was observed in 6 patients, including siently present anticardiolipin antibody in 3, and transiently present lupus anticoagulant in 2. Of 20 patients who did not have any risk factor for atherosclerosis, acquired coagulopathy was observed in 6. We conclude that protein-S deficiency and abnormal plasminogen are frequent and might be critical causes of CI in younger adults; transient coagulopathy is also a possible cause.

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

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

Cerebral infarction due to moyamoya disease in an 18 year old female

Moyamoya disease was diagnosed as the cause of cerebral infarction in an 18 year old white female. The clinical features, pathology and treatment of this occlusive cerebrovascular disorder are discussed.

Childhood stroke associated with protein C or S deficiency and primary antiphospholipid syndrome

Two girls, 22 months and 12 years of age, presented with repeated cerebral infarctions in association with primary antiphospholipid syndrome. The younger patient also suffered from protein C deficiency, while the other one had protein S and complement C 4 deficiencies. All other causes of cerebral infarction were excluded; however, vasculitis remains a possibility in one patient. Both girls developed spastic tetraparesis as a sequela of the previous infarctions. The two patients were treated with aspirin and prednisone, with remission of the infarctions during the next 8 months of observation. A primary deficiency of protein C or S is proposed which would produce cerebral thrombosis with exposure of phospholipids; this thrombosis then, like antigens, would generate antibodies acting on the thrombin-thrombomodulin complex, exacerbating the thrombotic process. The association of complement C 4 deficiency is an additional risk factor.

The cause of cerebral infarction: prevalence of ulcerated plaques in the aortic arch

The cause of cerebral infarction: prevalence of ulcerated plaques in the aortic arch

Hypertension and the brain. The National High Blood Pressure Education Program

Neurogenic mechanisms are important in the maintenance of most forms of hypertension, yet the brain is highly vulnerable to the deleterious effects of elevated blood pressure. Hypertensive encephalopathy results from a sudden, sustained rise in blood pressure sufficient to exceed the upper limit of cerebral blood flow autoregulation. The cerebral circulation adapts to chronic less severe hypertension but at the expense of changes that predispose to stroke due to arterial occlusion or rupture. Stroke is a generic term for a clinical syndrome that includes focal infarction or hemorrhage in the brain, or subarachnoid hemorrhage. Atherothromboembolism and thrombotic occlusion of lipohyalinotic small-diameter end arteries are the principal causes of cerebral infarction. Microaneurysm rupture is the usual cause of hypertension-associated intracerebral hemorrhage. Rupture of aneurysms on the circle of Willis is the most common cause of nontraumatic subarachnoid hemorrhage. Stroke is a major cause of morbidity and mortality, particularly among persons aged 65 years or older. Treatment of diastolic hypertension reduces the incidence of stroke by about 40%. Treatment of isolated systolic hypertension in persons aged 60 years and older reduces the incidence of stroke by more than one third. Blood pressure management in the setting of acute stroke and the role of antihypertensive therapy in the prevention of multi-infarct dementia require further study.

Hypertension and the Brain

Neurogenic mechanisms are important in the maintenance of most forms of hypertension, yet the brain is highly vulnerable to the deleterious effects of elevated blood pressure. Hypertensive encephalopathy results from a sudden, sustained rise in blood pressure sufficient to exceed the upper limit of cerebral blood flow autoregulation. The cerebral circulation adapts to chronic less severe hypertension but at the expense of changes that predispose to stroke due to arterial occlusion or rupture.<i>Stroke</i>is a generic term for a clinical syndrome that includes focal infarction or hemorrhage in the brain, or subarachnoid hemorrhage. Atherothromboembolism and thrombotic occlusion of lipohyalinotic small-diameter end arteries are the principal causes of cerebral infarction. Microaneurysm rupture is the usual cause of hypertension-associated intracerebral hemorrhage. Rupture of aneurysms on the circle of Willis is the most common cause of nontraumatic subarachnoid hemorrhage. Stroke is a major cause of morbidity and mortality, particularly among persons aged 65 years or older. Treatment of diastolic hypertension reduces the incidence of stroke by about 40%. Treatment of isolated systolic hypertension in persons aged 60 years and older reduces the incidence of stroke by more than one third. Blood pressure management in the setting of acute stroke and the role of antihypertensive therapy in the prevention of multi-infarct dementia require further study. (<i>Arch Intern Med</i>. 1992;152:938-945)

The Prevalence of Ulcerated Plaques in the Aortic Arch in Patients with Stroke

The cause of cerebral infarction is obscure in up to 40 percent of patients with this disorder who are studied prospectively. In this investigation, we determined the frequency of ulcerated plaques in the aortic arch and explored the part they may play in the formation of cerebral emboli. Using an autopsy data bank, we studied the prevalence of ulcerated plaques in the aortic arch in 500 consecutive patients with cerebrovascular and other neurologic diseases who were studied at autopsy. Ulcerated plaques were present in 26 percent of the 239 patients with cerebrovascular disease but in only 5 percent of the 261 patients with other neurologic diseases (P less than 0.001). After we controlled for age and heart weight, the adjusted rates were 16.9 percent and 5.1 percent, respectively (adjusted odds ratio, 4.0; 95 percent confidence interval, 2.1 to 7.8; P less than 0.001). Among the patients with cerebrovascular disease, the prevalence of ulcerated plaques in the aortic arch was 28 percent in the 183 patients with cerebral infarcts and 20 percent in the 56 patients with brain hemorrhage. The prevalence of ulcerated plaques was 61 percent among the 28 patients with no known cause of cerebral infarction, as compared with 22 percent among the 155 patients with a known cause of cerebral infarction (P less than 0.001). After adjustment for covariates, the prevalence was 57.8 percent among patients with no known cause of cerebral infarction and 20.2 percent among those with a known cause (adjusted odds ratio, 5.7; 95 percent confidence interval, 2.4 to 13.6; P less than 0.001). The presence of ulcerated plaques in the aortic arch was not correlated with the presence of extracranial internal-carotid artery stenosis, suggesting that these were two independent risk factors for stroke. Ulcerated plaques in the aortic arch may play a part in causing cerebral infarction, especially in patients in whom cerebral infarction has no known cause.

Floating Thrombus in the Innominate Artery as a Cause of Cerebral Infarction in Young Adults

Intraluminal thrombi in the carotid circulation are uncommonly reported as a cause of stroke in young adults. We report two young women who suffered an embolic cerebral infarction from a floating thrombus in the innominate artery, without clotting abnormalities. Intraluminal thrombus at that level may have been previously overlooked as a cause of embolic cerebral infarction in young patients, because of the lack of a systematic assessment of the aortic arch and its proximal branches. Taking into account the fact that the evolution may be rapidly fatal, this possibility should be considered early in young patients without a clear etiology of stroke.

老年者の貧血下における脳梗塞の原因

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.

Medical Management of Acute Cerebral Ischemia in the Elderly

Stroke ranks third as a cause of death in much of the industrial world, surpassed only by heart disease and cancer. Thrombotic and embolic arterial occlusions are the leading causes of cerebral infarction. Once a major cerebral infarction has occurred, therapy is limited to the prevention of complications and rehabilitation. Identification and treatment of stroke-prone patients are now not a standard part of medical practice. However, the proper management of the patient with acute cerebral ischemic or progressing stroke is a subject of debate. Treatment of progressing or acute cerebral ischemia is aimed at prevention of infarction in areas of the brain that are still viable. A number of therapeutic strategies are currently being investigated in the management of ischemic stroke.

Mortality in Acute Cerebral Infarction in Young Adults—A Ten-Year Experience

We reviewed the one-month mortality among 213 patients aged fifteen to forty-five years (mean thirty-five) with acute cerebral infarction (CI) evaluated during the period July 1, 1977, to February 1, 1988. Atherosclerotic cerebral infarction (ACI) was diagnosed in 59 (27.7%) patients, 53 (24.9%) had non-atherosclerotic vasculopathies (NAV); 46 (21.6%) had cardioembolic infarcts (CEI). Hematologically related disorders were diagnosed in 30 (14.1%) patients; the cause of CI could not be established in 25 (11.7%) patients. Fourteen patients (9 men, 5 women, mean age 34.8 years), (6.6%) died within thirty days of their CI: 7 had CEI (7/46,15.2%); 4 had ACI (4/59, 6.7%); and 3 had NAV (3/53, 5.6%). Our data suggest that young patients with acute CI have a thirty-day mortality rate lower than older patients. Deaths were most common in patients with CEI. Brain edema and herniation accounted for 6 (43%) of the deaths.

Etiology of stroke in Broca's aphasia

We reviewed clinical and diagnostic data from 36 patients with Broca's aphasia due to stroke who were evaluated at the University of Iowa Hospitals and Clinics between 1982 and 1989. The group consisted of 20 women and 16 men, aged 28-80 (median, 63.5; mean, 57.5). The presumptive cause of cerebral infarction was embolism in 15 patients (42%), atherothrombosis in 9 (25%), undetermined in 9 (25%), and "other" in 3 (8%). The ratios of women to men were 8:7, 3:6, 7:2, and 2:1, respectively. A majority of emboli were of presumed cardiac origin: atrial fibrillation, 7; prosthetic cardiac valve, 3; and recent myocardial infarction, 2. Eight of nine patients with atherothrombotic infarction had complete occlusion of the left internal carotid artery by duplex scan and/or angiography. Our data demonstrate (a) Broca's aphasia is frequently caused by cerebral embolism, (b) carotid occlusion can result in selective infarction of anterior language areas; and (c) women outnumbered men in our Broca's aphasia group. The latter finding is in contrast to a similar study of 38 patients with Wernicke's aphasia due to cerebral infarction studied at our institution, in which men outnumbered women 25 to 13, with most of the difference in the embolic and undetermined groups. Gender differences in types of aphasia might be due to a predilection for middle cerebral artery emboli to result in infarction of anterior language areas in women and posterior language areas in men.

Stroke in young adults.

Strokes in young adults are uncommon and often a diagnostic challenge. A retrospective study of strokes due to intracerebral hemorrhage, subarachnoid hemorrhage, or cerebral infarction was undertaken. We reviewed the medical records of 113 young patients aged 15-45 years who were admitted to the Medical Center Hospital of Vermont with a diagnosis of stroke between 1982 and 1987. This group comprised 8.5% of patients of all ages admitted for stroke, 2.3 times the proportion observed in the National Survey of Stroke. Nontraumatic intracerebral hemorrhage was diagnosed in 46 young patients (41%); the main causes included aneurysms, arteriovenous malformations, hypertension, and tumors. Subarachnoid hemorrhage was found in 19 young patients (17%); the majority were due to aneurysms. The remaining 48 young patients (42%) had cerebral infarction, the majority due to cardiogenic emboli and premature atherosclerosis. Mitral valve prolapse, the use of oral contraceptives, alcohol drinking, and migraine were infrequent sole causes of cerebral infarction in the absence of other risk factors. The case-fatality rate for this group of young patients with stroke was 20.4% compared with 23.9% for the National Survey of Stroke. Young adults with stroke deserve an extensive but tailored evaluation, which should include angiography and echocardiography.

Cerebral infarction due to moyamoya disease in young adults.

Moyamoya disease was diagnosed as the cause of cerebral infarction in eight young adults (seven women, one man), aged 17-40 (mean 33) years. All had angiographic abnormalities characteristic of moyamoya disease. Single-photon emission tomography showed bilateral carotid circulation hypoperfusion and posterior circulation hyperemia in all seven patients with regional cerebral blood flow studies. All seven women had used oral contraceptives before cerebral infarction. Four patients were treated medically; one died of a second cerebral infarction 9 months after diagnosis. Four patients underwent superficial temporal-to-middle cerebral artery anastomosis; they did well. Moyamoya disease should be included in the differential diagnosis of cerebral infarction as well as intracranial hemorrhage in young adults, particularly women. A possible relation between moyamoya disease and oral contraceptive use deserves investigation.

Cerebral Infarction

We studied the utility and limitations of conventional cerebral angiography in 25 patients with cerebral infarction unassociated with extracranial cerebrovascular disease during a 7-year period. In only one-third of cases was the angiogram diagnostic, and in a single case it altered the pre-angiogram diagnosis by revealing a previously unsuspected embolus. Among the cases clinically diagnosed as cerebral emboli, the 2 confirmatory angiograms were performed early (within 48 hours), and demonstrated medium-large or large vessel filling defects. Two-thirds of the negative angiograms in the embolic clinical category were delayed, but there was no statistically relevant predilection for specific vessel size involvement. The category, primary cerebral vasculopathy, comprised the largest group, 10 in all, and one-half had angiographic confirmation despite time delays. Angiographic recognition was dependent on a characteristic picture of vascular involvement, and not on timing or vessel size predilection. Mitral valve prolapse figured prominently in the clinical cases of vasculopathy of uncertain etiology, which contained a total of 4 cases. The 3 cases with nondiagnostic angiograms were all delayed and demonstrated nonspecific radiographic changes. Clinically, these cases demonstrated signs or symptoms of autoimmune dysfunction, raising the specter of primary cerebral vasculopathy as a cause of cerebral infarction, in contrast to recurrent cerebral emboli.

Nonhemorrhagic cerebral infarction in young adults.

We evaluated 144 patients (81 males and 63 females) aged 15 to 45 years who had nonhemorrhagic cerebral infarction. Atherosclerotic cerebral infarction was diagnosed in 38 patients. Potential cardiac causes of cerebral embolism were found in 33 patients. Only three events could be attributed to mitral valve prolapse. Hematologically related disorders were diagnosed in 21 patients, while 38 patients had nonatherosclerotic vasculopathies. Young patients with cerebral infarction are a heterogeneous group. A potential cause can be found in most patients. We found more than 40 possible etiologies among our patients. Mitral valve prolapse apparently is not a common cause of cerebral infarction among young adults. Cerebral infarction should not be ascribed to oral contraceptives or migraine until other possible causes have been eliminated.