Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Brain Infarction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources
PubMedDate not supplied

Noninvasive measurement of brain temperature after stroke.

BACKGROUND AND PURPOSE: Brain temperature may be an important factor governing the extent of neuronal injury associated with stroke. The goal of this study was to develop a noninvasive method for measuring brain temperature, both to characterize the extent to which temperature changes after stroke and to test protocols designed to reduce brain temperature. We used an animal model to test the ability of 1H MR spectroscopy to measure temperature from infarcted brain tissue at 24 hours after insult. METHODS: Unilateral permanent focal ischemia in the middle cerebral artery territory was induced in adult dogs by intravascular delivery of microfibrillar collagen. MR imaging performed at 24 hours after insult was used to guide the implantation of temperature probes into the basal ganglia infarct and into the same anatomic location on the contralateral side. Serial non-water-suppressed 1H MR spectra were obtained from 1.3-cm3 voxels using an echo time of 136 and 272 ms, alternately, from the infarcted and contralateral non-infarcted tissue during a period when brain temperature was raised and lowered by whole-body heating and cooling. RESULTS: The chemical shift difference between the 1H MR spectroscopy signal of water and N-acetylaspartate or water and trimethylamines was plotted against brain temperature for two voxel locations. The slope and intercept of the plots obtained for infarcted and non-infarcted brain were not significantly different (P < .05, t test), and there was no difference between the slope and intercept of plots made from data collected with an echo time of 136 or 272 ms. CONCLUSION: The results of this study indicate that brain temperature can be measured from regions of brain containing infarcted tissue, at least up to 24 hours after ischemia. It should be possible to apply the 1H MR spectroscopy method used in the present study to measure brain temperature after stroke.

Animals↗
PubMed1995

Prospective CT confirms differences between vascular and Alzheimer's dementia.

BACKGROUND AND PURPOSE: Cognitive test performances were correlated prospectively with changes in cerebral CT measurements of atrophy, infarct volume, ventricular enlargement, local tissue density, and local perfusion to contrast annual rates of changes among patients with ischemic vascular dementia (IVD) or dementia of the Alzheimer type (DAT). METHODS: The cerebral atrophic index (ATI; ratio of cerebrospinal fluid or infarcted brain to intracranial volume), infarct volume ratio, ventricular volume ratio (VVR; ventricular volume/intracranial volume), cortical and subcortical gray and white matter local perfusion (local cerebral blood flow [LCBF]), and local Hounsfield unit (HU) density were measured concurrently and compared longitudinally with Cognitive Capacity Screening Examinations (CCSE) scores among 24 treated IVD (age, 68.2 +/- 9.7 years; follow-up, 42 +/- 27 months) and 24 DAT patients (age, 74.2 +/- 6.2 years; follow-up, 30 +/- 19 months). RESULTS: IVD annual changes were as follows: CCSE, +1.2 +/- 5.9; ATI, +2.1%/y; VVR, +3.2%/y; and LCBF in the subcortical basal ganglia, -0.74 mL.100 g-1.min-1.y-1 (-1.8%/y). DAT annual changes were as follows: CCSE, -1.8/y; ATI, +8.1%/y; VVR, +9.6%/y; cortical LCBF, -2.0 mL.100 g-1.min-1.y-1 (-5.2%/y); LCBF in the basal ganglia, -3.0 mL.100 g-1.min-1.y-1 (-6.7%/y); white matter LCBF, -0.75 mL.100 g-1.min-1.y-1 (-4.1%/y); and all cortical tissue densities, -0.83 HU/y (-2.1%/y). In IVD, multiple regression analyses correlated cognitive changes directly with (1) recurrent silent infarctions and (2) bidirectional changes of perfusions within frontal white matter, thalamus, and internal capsules. In DAT, cognitive declines correlated with cerebral atrophy and cortical hypoperfusion related to frontotemporal and parietal cortical polioaraiosis (decreased gray matter tissue densities). CONCLUSIONS: In IVD, recurrent strokes were not observed clinically during risk factor control, and antiplatelet therapy and cognitive impairments improved or stabilized. In DAT, cognitive performance relentlessly declined. Ischemic pathogenesis for vascular dementia is supported by the following: (1) cognitive declines correlate directly with recurrent "silent" strokes, and (2) bidirectional cognitive changes correlate directly with frontal white matter, thalamic, and internal capsular perfusional changes.

Aged↗
PubMed1999

The role of diaschisis in stroke recovery.

BACKGROUND AND PURPOSE: Recovery from hemiparesis after stroke has been shown to involve reorganization in motor and premotor cortical areas. However, whether poststroke recovery also depends on changes in remote brain structures, ie, diaschisis, is as yet unresolved. To address this question, we studied regional cerebral blood flow in 7 patients (mean+/-SD age, 54+/-8 years) after their first hemiparetic stroke. METHODS: We analyzed imaging data voxel by voxel using a principal component analysis by which coherent changes in functional networks could be disclosed. Performance was assessed by a motor score and by the finger movement rate during the regional cerebral blood flow measurements. RESULTS: The patients had recovered (P<0. 001) from severe hemiparesis after on average 6 months and were able to perform sequential finger movements with the recovered hand. Regional cerebral blood flow at rest differentiated patients and controls (P<0.05) by a network that was affected by the stroke lesion. During blindfolded performance of sequential finger movements, patients were differentiated from controls (P<0.05) by a recovery-related network and a movement-control network. These networks were spatially incongruent, involving motor, sensory, and visual cortex of both cerebral hemispheres, the basal ganglia, thalamus, and cerebellum. The lesion-affected and recovery-related networks overlapped in the contralesional thalamus and extrastriate occipital cortex. CONCLUSIONS: Motor recovery after hemiparetic brain infarction is subserved by brain structures in locations remote from the stroke lesion. The topographic overlap of the lesion-affected and recovery-related networks suggests that diaschisis may play a critical role in stroke recovery.

Adult↗
PubMed1999

[Two cases of fluent aphasia with selective difficulty of syllable identification].

We report two aphasic patients who could discriminate Japanese syllables but could not identify them. Case 1 was a 51-year-old right handed woman with 12-year education. Case 2 was a 50-year-old right handed man with 9-year education. They developed fluent aphasia after a cerebral infarction. Brain MRI of case 1 revealed widely distributed lesions including inferior frontal, superior temporal, angular and supramarginal gyri. Lesions revealed by Brain CT in case 2 included the left superior and middle temporal, angular and supramarginal gyri. Both showed severe impairment of repetition and confrontation naming. No difference of performance was present between repetition of single syllables and polysyllabic words. On the contrary, oral reading of Kana characters were preserved. We examined their ability to perceive syllables in detail. In the discrimination task, they judged whether a pair of heard syllables was same or different. Case 1 was correct in 85% of the tasks and case 2 in 98%. In an identification task, they heard a syllable and chose a corresponding Kana, Kanji, or picture out of 10 respective candidates. Case 1 was correct only in 30% and case 2 in 50% of these tasks. On the other hand, selection of a correct target in response to a polysyllabic word was much better, i.e. 70% in case 1 and 90% in case 2. Based on these data we concluded that (1) syllabic identification is a different process from syllabic discrimination, and (2) comprehension of a polysyllabic word can be achieved even when the precise phonological analysis of continuent syllables are impaired.

Aphasia, Wernicke↗
PubMed2000

[Coronary arterial revascularization in dialysis patients].

It is recently reported that among chronic renal dialysis patients myocardial infarction accounts 7.4% of all the cause of death in Japan. In order to improve the mortality of dialysis patients the treatment of ischemic heart disease (IHD) is a major problem. We review previous reports and discuss about the treatment of IHD in dialysis patients. The collected data from the previous reports written about CABG in dialysis patients shows that the mortality of CABG is 7.8% (30/387), the probability of perioperative myocardial infarction (PMI) 8.6% (21/243), brain infarction 1.6% (4/243) and major infection 5.8% (14/243). 3-year and 5-year mortality rate after CABG is reported to be 69-80% and 48-56%, respectively. The result of CABG is excellent and shows that this procedure improves the mortality of dialysis patients with IHD. The procedural mortality of PTCA is 5.6% (8/143), the probability of PMI is 7% (10/143). Many reports shows the high probability of the recurrence of chest pain (60-86%). This procedure when performed in dialysis patients is incomplete because of the calcification of the coronary artery. Even among the dialysis patients it is preferable to perform CABG positively.

Coronary Artery Bypass↗
PubMed2001

Blood-brain barrier disturbances and morphological changes in rat brain after photochemically induced focal ischaemia.

The disturbances in cerebral circulation lead to focal brain ischaemia and brain infarcts. The pathogenesis of brain ischaemia has been a subject of numerous experimental studies employing different models and focusing on the anatomy of collateral circulation. The aim of this study was the evaluation of our own model of focatcerebral damage caused by a photodynamic reaction, and determination of its utility as a model of brain necrosis and blood-brain barrier damage in the rat. Wistar rats were used for the experiments. The animals were anaesthetised with 3% chloral hydrate (325 mg/kg) and injected intravenously with 40 mg/kg of 3% solution of rose bengal. After removal of the periostium the brain was irradiated through the skull for 30 min with a 250 W halogen, air-cooled light source. The material for morphologic studies was sampled 24 h, 4 days and 7 days after irradiation. The brains were fixed by perfusion, embedded in paraffin, and stained with haematoxilin-eosin (HE), acid vanadium fuchsin, cresyl violet, and GFAP. The results document the usefulness of this method for studying focal brain ischaemia in rats. The observed morphological changes and disturbances in blood-brain barrier provided information about the dynamics of the formation of gliosis, the formation of necrotic foci, and the quality and extent of brain damage in the surrounding tissue.

Anesthetics, Intravenous↗
PubMed1992

[Evaluation of cerebral blood circulation using fast magnetic resonance imaging (turbo-FLASH)].

In its initial stage of development, poor time resolution was supposed to be inevitable for magnetic resonance imaging (MRI). The development of the gradient echo technique, however, has made an opening for a breakthrough to a fast MRI technique. However, conventional gradient echo technique is not fast enough to disclose the cerebral blood circulation. A new technique (turbo-FLASH), which combines gradient echo and preparation pulse, has opened the door to a true dynamic (high time resolution) MRI. The authors performed a basic study of this new fast imaging technique (Turbo-FLASH) for the evaluation of cerebral blood circulation. Using this dynamic MRI, the conventional Gd-DTPA administration (0.1mmol/kg, intravenous manual administration) has produced sufficient contrast to reveal a difference of the extent of enhancement between normal gray matter and white matter. In patients of cerebral infarction, the infarcted brain does not show any significant increase of signal intensity after the administration of contrast medium, whereas the normal brain shows a sharp increase of signal intensity after the administration of contrast medium. Indeed, many puzzling questions remain to be solved for clinical application of this new dynamic MRI. For example, the optimal quantity of contrast medium and optimal parameters for this sequence (T1 weighted or T2 weighted?) are still unknown. But, in any case, this dynamic MRI is expected to be a clinically powerful tool for the evaluation of cerebral blood flow.

Brain↗
PubMed1994

Cerebral blood flow and effects of cerebrospinal fluid on calcium transport in patients with cerebral infarction.

BACKGROUND AND PURPOSE: In this study we investigated whether cerebrospinal fluid in patients with brain infarction possesses an activity that contributes to the evolution of brain ischemia. As a test, the effect of cerebrospinal fluid on Ca2+ influx into the intracellular space was chosen because this process is a mechanism for vasospasm, platelet aggregation as thrombi, and neuron damage. METHODS: Effects of cerebrospinal fluid taken from 48 patients with cerebral hemispheric infarction on the concentration of cytosolic free Ca2+ in platelets were studied using the fluorescent probe quin-2. Hemispheric cerebral blood flow was measured using 133Xe intravenous injection. RESULTS: Cerebrospinal fluid in 19 of 48 patients with cerebral hemispheric infarction increased the level of cytosolic free Ca2+ in platelets. The course of the disease in the patients who showed a positive effect of cerebrospinal fluid on Ca2+, when compared with that of patients who showed a negative effect, was characterized by a more severe clinical manifestation and mortality. The decrease in hemispheric cerebral blood flow was more marked in both ischemic and contralateral hemispheres in patients with positive effects of cerebrospinal fluid on the level of Ca2+. CONCLUSIONS: These data suggest that the ability of cerebrospinal fluid to evoke Ca2+ influx into the intracellular space in patients with brain infarction is a factor that aggravates ischemic brain damage.

Biological Transport↗
PubMed2004

Acute aortic dissection with new massive cerebral infarction - a successful repair with ligature of the right common carotid artery.

It remains unclear whether or not the infarcted brain caused by aortic dissection should be reperfused when an emergency operation is needed for aortic arch dissection. A 64-year-old woman presented with severe back pain and syncope with a sudden left hemiplegia. CT scan demonstrated an aortic dissection of the entire aorta, obstruction of the right common carotid artery by extended aortic dissection, cerebral infarction of the right middle cerebral artery territory, brain edema and pericardial effusion. Though she was unable to communicate with us, she underwent an emergent aortic arch replacement and ligature of the right common carotid artery nine hours after the onset of stroke, when massive cerebral infarction was established. She survived the operation and regained full consciousness. When brain infarction was established by extended aortic dissection in emergent aortic surgery, concomitant ligature of the responsible artery to the brain infarction may be allowed for avoiding cerebral damage leading to brain death.

Aorta, Thoracic↗
PubMed1997

[Hemodynamically induced cerebral infarcts. Clinical significance of infarct pattern and angiomorphology].

Classification of brain infarcts based on the location, size and shape of parenchymal damage alone can be difficult and misleading. This is particularly true in subcortical infarctions and infarcts in so-called watershed areas between neighboring territories of the main hemispheric arteries. Pathogenetic mechanisms, signs and symptoms, lesion patterns in CT and MRI are discussed as well as angiomorphological conditions. Hemodynamically induced low-flow infarcts are rare and show typical, but not pathognomic lesion patterns on CT and MRI. Characteristic subcortical chainlike and confluent lesions are located in the supra- and paraventricular white matter, representing the core of a hemodynamically induced infarction. Definite diagnosis of low-flow infarcts requires information on the underlying complex vascular compromise of the extra- and intracranial arterial circulation. A noncompetent circle of Willis is the main predisposing condition in hemispheric low-flow infarcts even in severe occlusive disease of the internal carotid arteries.

Cerebral Infarction↗
PubMedDate not supplied

Production of various models of cerebral infarction in the dog by means of occlusion of intracranial trunk arteries.

Using the dog, which has been believed unsuitable for research on brain infarction because of an extensive collateral cerebral circulation, we have succeeded in producing at will ischemic foci, as determined from post-occlusion carbon perfusion, in the thalamus, cerebral mantle or entire cerebral hemisphere. This has been achieved by occlusion of various combinations of cerebral vessels at the base of the brain. A unilateral temporal approach has been used in identifying and occluding all of the bilateral trunk arteries. The following models of cerebral infarction have been made: 1) unilateral or bilateral complete cerebral hemisphere infarction, 2) unilateral or bilateral cerebral mantle infarction, 3) unilateral or bilateral thalamic infarction, 4) unilateral hemispheric and contralateral cerebral mantle infarction, 5) unilateral cerebral mantle and contralateral thalamic infarction, and 6) unilateral complete cerebral hemisphere and contralateral cerebral mantle infarction. These models of infarction in the dog can be produced with a high degree of success, and the amount of infarction can be controlled by the duration of vessel occlusion. The pathophysiology of brain infarction and brain edema following recirculation can be hemodynamically, electroencephalographically and biochemically studied using these models of cerebral infarction.

Animals↗
PubMed2004

Is cerebral angiography redundant in undetermined cause of stroke in patients below 50 years when the stroke is lacunar?

BACKGROUND: In the diagnostic work-up of young stroke patients angiography is still considered as mandatory to identify otherwise undetected causes of stroke. We hypothesized that stroke cause is more heterogeneous among patients with a territorial infarct, whereas in lacunar stroke it is generally small vessel disease. Therefore, angiography yields more often a specific stroke cause in territorial than in lacunar infarct patients. METHODS: Angiograms of 39 lacunar and 41 territorial brain infarct patients, aged between 14 and 51 years, and who had unexplained stroke cause, were evaluated. RESULTS: 1 of the 39 lacunar (3%), and 18 of the 41 territorial stroke patients (44%) had abnormal angiogram: odds ratio 0.03, 95% confidence interval: 0.01-0.017. The predictive value of lacunar stroke for a normal angiogram was 97%. CONCLUSION: When undetermined cause of stroke in young patients is lacunar, it is highly predictive for a normal angiogram. Our data may be of value in deciding on performing angiography in individual young stroke patients, depending on whether the stroke is territorial or lacunar.

Adolescent↗
PubMed2004

An optimized triphenyltetrazolium chloride method for identification of cerebral infarcts.

2,3,5-Triphenyltetrazolium chloride (TTC) staining is a convenient procedure for detection of brain infarcts but no standardized procedure is available. We report here an optimized and economic procedure of staining with TTC. Rats were subjected to reversible middle cerebral artery (MCA) occlusion (2-h ischemia and 24-h reperfusion). At the end of reperfusion, brain was isolated and sliced rostro-caudally into serial 2-mm-thick slices. Sets of three serial slices from each brain were incubated for 30 min at 37 degrees C in three different concentrations of TTC-the first slice of the set in 1%, the second in 0.05% and the third in 0.1% TTC-in phosphate-buffered saline. Staining characteristics, optical density (OD) and infarct size were compared between juxtaposing cut surfaces of the slices stained with the three concentrations of TTC. After the first use, 0.05% TTC solution was stored at 4-8 degrees C and reused on the same day or on subsequent days. TTC at 0.05% concentration provided high contrast staining with clear demarcation between normal and infarct tissue. The infarct size in 0.05% TTC-stained slices correlated well with that in 0.1% TTC (r=0.92)- and 1% TTC (r=0.93)-stained preparations. 'Nonspecific' staining of corpus callosum and the anterior commissures was minimal with the method. Once-used 0.05% TTC solution could be stored at 4-8 degrees C and reused. In conclusion, staining with 0.05% TTC provided improved delineation of brain infarcts, reduced 'nonspecific' staining of white matter and the infarct size correlated well with that measured after 1% TTC staining; the method also reduces the costs to 1/20.

Animals↗
PubMed2002

Local carboxyfullerene protects cortical infarction in rat brain.

The neuroprotective effect of carboxyfullerene, a water-soluble derivative of fullerene, on the transient focal ischemia-reperfusion injury was investigated in rat brain. A focal infarction in the cerebral cortex was consistently observed 24 h after a 60-min transient ischemia by occlusion of the right middle cerebral artery and bilateral common carotid arteries. The fluorescent end products of lipid peroxidation were increased in the infarcted cortical area. Furthermore, the GSH level was decreased in the infarcted cortex. Carboxyfullerene was either intravenously (6 mg/kg) or intracerebroventricularly (0.1, 0.3 mg per rat) infused to the chloral hydrate-anesthetized Sprague-Dawley rats 30 min prior to transient ischemia-reperfusion. No protection of cortical infarction was observed after intravenous administration of carboxyfullerene. In contrast, intracerebroventricular infusion of carboxyfullerene not only attenuated cortical infarction but also prevented both the elevated lipid peroxidation and the depleted GSH level induced by transient ischemia-reperfusion. Adverse behavioral changes were simultaneously observed in rats receiving intracerebroventricular infusion of carboxyfullerene (0.3 mg per rat), including writhing accompanied by trunk stretch and even death. Our data suggest that intracerebroventricular infusion of carboxyfullerene may attenuate oxidative injuries by transient ischemia-reperfusion. Nevertheless, undesired side effects may limit the usefulness of carboxyfullerene in biological organisms.

Animals↗
PubMed2005

[Bilateral multiple border zone infarctions after massive bleeding: report of two cases].

We present two patients who developed bilateral border zone brain infarctions after massive bleeding. Patient 1 was a 46-year old woman who developed bilateral visual disturbance and left hand monoparesis after excessive menstruation with severe anemia. Diffusion-weighted MRI of brain showed multiple border zone infarcts bilaterally in cerebral and cerebellar hemispheres while brain MRA was normal. Patient 2 was a 67-year old man who developed disturbance of consciousness and right hemiplegia after upper gastrointestinal tract bleeding. Diffusion-weighted MRI of brain showed bilateral multiple border zone infarcts in cerebral hemispheres, although he had asymptomatic occlusion of the left internal carotid artery. The bilateral multiple border zone infarcts are one of the key findings suggesting the presence of anemic hypoxia as a result of global brain hypoperfusion caused by massive blood loss.

Aged↗
PubMed2003

[Acute cervical spinal epidural hematoma during antithrombotic therapy: dual warnings against antithrombotic therapy].

Two aged women suddenly suffered from severe cervical and back pain followed by ipsilateral hemiparesis sparing the face. One woman had taken anticoagulant for prosthetic mitral valve and another had taken antiplatelet for prevention of recurrent brain infarction. On admission, MRI did not document any definite lesions in the brain, and revealed epidural hematoma compressing the cervical spinal cord for both patients. We promptly stopped their anticoagulants and antiplatelets use, because the agents seemed to be the leading cause of hematoma. In addition, we performed emergent laminectomy and evacuation of hematoma for the former patient. These cases suggest dual warnings against recently prevalent antithrombotic therapy for patients with histories of thromboembolic accidents. First, we should be careful about spinal epidural hematoma as a hemorrhagic complication of antithrombotic therapy. Second, we should not misdiagnose spinal epidural hematoma as ischemic stroke nor select hyperacute thrombolytic therapy. Cervical pain and hemiparesis sparing face are important signs for distinction of spinal epidural hematoma from stroke.

Acute Disease↗