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Results for “Brain Infarction”

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At least 469 records · Page 26Linked to original sources
PubMed1995

[Atrial septal aneurysm and brain infarct: a causal connection?].

In four patients, 2 women aged 24 and 35 and 2 men aged 37 and 47 years, an ischaemic stroke was observed and an atrial septal aneurysm was found as a possible cardiac source of embolism to the brain. Atrial septal aneurysm is a bulging of the fossa ovalis region, that can be visualised by (preferably transoesophageal) echocardiography. In the four patients there were only few other risk factors for ischaemic stroke (migraine, smoking, oral contraceptives). Cerebral angiography was normal in all cases. Recent literature suggests that a causal relationship exists between atrial septal aneurysm and ischaemic stroke. It is still uncertain what treatment is best.

Adult↗
PubMed1989

Migraine-related stroke: brain infarction in superior cerebellar artery territory demonstrated by nuclear magnetic resonance.

We report 4 cases of migraine-related stroke in young females. Two patients were taking oral contraceptives and one was pregnant. The results of the computerized tomography of the brain were negative in 3 patients and partially positive in one, while NMR showed ischemic lesions in the posterior fossa in each case. We would like to highlight the value of NMR in the assessment of migraine associated with prolonged focal neurologic deficiencies when the clinical examination revealed brain stem or cerebellar signs and the peculiar localization of the ischemic lesion that corresponded in all 4 cases to the area irrigated by the superior cerebellar artery. An hormonal factor is suspected as the precipitating event of this complication in 3 of these patients.

Adult↗
PubMed1988

Closed cervicocranial trauma, "false aneurysm" of the internal carotid artery and brain infarction.

A 17-year-old man developed acute hemiparesis 6 months after a motor cycle accident. In the accident he had a closed trauma on the contralateral side of the head and the neck, with multiple bone fractures. Aortocervical angiography, performed after the infarction, revealed a 2.5 cm long aneurysmatic dilatation in the internal carotid artery, the presumably source of embolic infarction. This and the 24 other cases gathered from the literature support the notion that closed neck trauma may create "false aneurysm" which again may cause neurological deficits.

Accidents, Traffic↗
PubMed1998

Bilateral borderzone brain infarctions in association with heroin abuse.

A 25-year-old drug abuser who developed an unusual pattern of cerebral ischemic lesions is presented. Cerebral magnetic resonance imaging revealed bilateral borderzone infarctions which were attributed to a heroin-associated vasculitis of the basal cerebral arteries. Under probatory corticosteroid medication the mild neurological deficits completely disappeared.

Adult↗
PubMed2005

Imaging in acute brain infarction.

Imaging in a patient suspected of having suffered an acute stroke is used primarily to clear the patient for thrombolytic therapy, by excluding intracranial hemorrhage and nonstroke causes of the patient's symptoms, within a critical 3-hour window. Noncontrast CT of the brain is the imaging test of choice for the initial evaluation of a patient with suspected acute ischemic stroke. It is rapid and readily available and has a high sensitivity for intracranial hemorrhage. Contrast-enhanced CT angiography and perfusion imaging may provide additional information with only a minimal increase in scanning time. Finally, diffusion-weighted magnetic resonance sequences have a high sensitivity for acute stroke and, with magnetic resonance perfusion imaging, may play an increasing role in the future treatment of stroke.

Aged↗
PubMedDate not supplied

[Brain infarct due to non-bacterial thrombotic valvular vegetation associated with primary antiphospholipid antibodies--a case report].

A 50-year-old woman with antiphospholipid antibody syndrome (APAS) awoke in a morning to notice dizziness, so she came to our hospital. Several hours later she developed left oculomotor paralysis. Further two hours later she developed right oculomotor paralysis and could not stand. Brain MRI showed high signal intensity lesion of paramedian thalamic and midbrain on the T2-weighted image. Cerebral angiography did not reveal any occlusion. Transesophageal echocardiography disclosed mitral valvular vegetation. We thought this valvular abnormality was non-bacterial thrombotic vegetation associated with APAS and this suggests that cerebral infarction was due to emboli from this vegetation.

Antiphospholipid Syndrome↗
PubMed2005

[Ischemic brain infarction after an air embolism. Case report].

Ischemic stroke due to embolic air is uncommon. There are few reports of patients with air embolic stroke as a complication of endoscopic procedures. The temporal relationship between the stroke and this procedure is the most important clue for the diagnosis. CT scan and MRI of the brain are confirmatory tests. The morbidity and mortality is high. Patients should be hospitalized in a critical care service and treated as soon as possible with oxygen in a pressure camera. We report a 52 years old woman with an ovarian cancer that, during an upper gastrointestinal endoscopy, had a severe alteration of consciousness that did not respond to the use of Flumazenil. A CT scan showed multiple areas of air embolism in the watershed area between anterior and middle right cerebral arteries. A conservative treatment was decided and the patients died 48 hours later.

Anterior Cerebral Artery↗
PubMed1999

Decreased brain infarct following focal ischemia in mice lacking the transcription factor E2F1.

E2F1+/- mice subjected to 2 h middle cerebral artery occlusion developed an infarct of 77.0 +/- 3.2 mm3 (mean +/- s.e.m., n = 15) in the ischemic hemisphere after 24 h reperfusion. A significantly smaller infarct of 58.8 +/- 4.8 mm3 (n = 15; p < 0.01) was found in E2F1-/- animals. Both deficient and normal mice had similar cerebral angioarchitecture and intra-ischemic decreases in regional blood flow. Similar areas of hypoxia in both groups of ischemic animals were demonstrated directly by immunohistochemical detection of nitroimidazole adducts. It was concluded that all animals received the same ischemic insult, yet the subsequent damage was different in the mutant mice. This is the first indication that the E2F1 gene plays a role in ischemic death of post-mitotic neurons.

Animals↗
PubMedDate not supplied

Embolic brain infarction: a rare complication of thoracic outlet syndrome. A report of two cases.

The thoracic outlet syndrome is known to cause brachial neuropathy. Pressure on the subclavian artery causing post-stenotic dilatation with intraluminal thrombosis is not a common complication. This may lead to antegrade embolisation and ischemic changes in the upper limb. In right sided thoracic outlet syndrome the thrombus may extend retrogradely. From this an embolus may detach to the right hemisphere of the brain resulting in left sided hemiplegia. This is a rare but serious complication from a neglected, relatively benign, curable condition. This report describes two cases of a right sided thoracic outlet syndrome due to cervical rib compression with retrograde embolisation.

Adult↗
PubMed1993

Functional integration of cortical grafts placed in brain infarcts of rats.

Five to 6 days after a right middle cerebral artery occlusion, a cell suspension of fetal neocortex was grafted into the infarcted area of adult spontaneously hypertensive rats. Three to 17 months later, functional integration of the grafts into the afferent somatosensory pathway was tested using the 2-[14C]deoxyglucose method for estimation of glucose utilization. Grafted rats (n = 8) and control rats (n = 5) with no arterial occlusion were stimulated in the left vibrissal region resulting in an increased glucose utilization in the left trigeminal sensory nucleus and the right ventroposterior nucleus of the thalamus, whereas the same regions in a group (n = 5) of nonstimulated grafted rats were not activated. Glucose uptake in the right somatosensory cortex of control rats was 96 +/- 5 (mean +/- SEM) mumol/100 gm/min. Neocortical grafts consumed less glucose than cortex in control rats but the vibrissae-stimulated group displayed a 110% higher value than the nonstimulated grafted group (32 +/- 5 vs 15 +/- 2, p < 0.05). We conclude that graft glucose metabolism is increased following stimulation of the host somatosensory pathway, which demonstrates that transplanted neurons can be functionally integrated with neural circuitries of the host after an ischemic insult.

Animals↗
PubMed1997

Arthrogryposis multiplex congenita and bilateral mid-brain infarction following maternal overdose of co-proxamol.

We report a case of arthrogryposis multiplex congenita secondary to fetal hypokinesia in a 41-week gestation infant following antenatal central nervous system injury. The mother's pregnancy was complicated by an episode of attempted self harm, with an overdose of co-proxamol at 22 weeks of gestational age, and by the use of cocaine in combination with excess alcohol intake. Magnetic resonance imaging showed bilateral mid-brain cysts and marked atrophy of the basal ganglia and thalami.

Acetaminophen↗
PubMed1986

Prostanoid concentrations in human CSF following acute ischaemic brain infarction.

Thromboxane A2 and prostacyclin are two compounds which have been implicated as important modulators of local cerebral blood flow. Concentrations of the stable metabolites of these two compounds, thromboxane B2 and 6-keto-PGF1 alpha, were measured in cerebrospinal fluid (CSF) from eight acute ischaemic stroke patients and 14 patients with no evidence of cerebrovascular disease. Concentrations of thromboxane B2 ranged from 0.15 to 4.0 pg/ml and were significantly higher (P = 0.025) in the ischaemic stroke group when compared with the control group (0.1-0.3 pg/ml). Simultaneously acquired concentrations of 6-keto-PGF1 alpha were not elevated in the stroke group when compared to normals. These clinical findings support evidence from animal studies that emphasizes the importance of cerebral prostaglandins in mediating the secondary vascular changes of cerebral infarction. In conclusion there is an aberration in CSF thromboxane B2 concentrations in patients who have had a stroke. This may be an acute or chronic phenomenon.

6-Ketoprostaglandin F1 alpha↗
PubMed2003

Alcohol misuse: a risk factor for putaminal damage by ischemic brain infarct?

The relationship between alcohol consumption and the risk of ischemic stroke has been widely studied, whereas the effect of alcohol use on stroke features is not well established. This study compared the clinical and stroke features of ischemic stroke in two groups of patients with ischemic stroke: those with a history of alcohol misuse and those with a history of more social drinking. DSM-IV criteria were used to diagnose alcohol use disorder (dependency or abuse) in 275 of 486 consecutive patients aged 55-85 years, 3-4 months after ischemic stroke. Magnetic resonance imaging of the head was performed 3 months after stroke. Alcohol use disorder was diagnosed in 37/275 (13.5%) of ischemic stroke patients. These patients had more frequently (70.3 vs. 34.5%; OR 4.5; 95% CI 2.2-9.1; p < 0.000) an infarct affecting the putamen compared with patients who indulged in more social drinking. Another predisposed area was the superior anterior cerebral artery area. The stroke due to large- artery atherosclerosis was more common in patients with alcohol use disorder. The misuse of alcohol seemed to be associated with cerebral infarct localization in the putamen and superior anterior cerebral artery area. Prospective studies are needed to verify our preliminary finding.

Aged↗
PubMed1977

[Brain infarctions during treatment with ovulation inhibitors (author's transl)].

392 cases of cerebrovascular disturbances in women while taking oral contraceptives are reported since 1962. There has been a remarkable change of the distribution of age among these women. Till 1970 were mostly women involved between the age of 30 and 34 years. Today this type of distribution is no more to be seen because of the growing number of reports about complications in other age-groups. Complications were till 1970 mostly reported in the period from ten days till six months after taking oral contraceptives. The publications of the last three years are showing that many women are involved, who had taken oral contraceptives more than two years. New publications and our own results are showing no changes of the clinical syndromes and of the prognosis. Our investigation shows no decrease in the number of young women suffering of thromboembolic cerebral disorders of unknown aetiology in the last years. In this group is the percentage of the women, which had taken ovulation inhibitors, no reduced. The conception, that there is a connection between oral contraceptives and cerebrovascular occlusions seems more possible as before. Especially attention in prescription of oral contraceptives should be given to the fact of a known predisposition. The rareness of these complications leads to the conclusion that one or more predisponating factors of a nature not yet known have to be existent.

Adult↗