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PubMed1995

Computer-assisted carotid plaque characterisation.

OBJECTIVE: To determine the relationship between plaque echogenicity as measured by computer and the incidence of cerebral brain infarction. PATIENTS AND METHODS: Eighty-seven patients with 148 plaques producing more than 50% internal carotid artery stenosis were studied. Sixty-nine plaques were in asymptomatic patients, 35 were associated with amaurosis fugax, 19 with transient ischaemic attacks and 25 with stroke. All patients had a CT brain scan and the presence of ipsilateral cerebral infarction was noted. Images of the plaques obtained with an ATL Ultramark-4 Duplex scanner (7.5 MHz high resolution probe) were transferred to a computer. Using an image analysis program a histogram for each plaque was obtained with the number of pixels plotted against the grey scale (0-225). The median of the grey scale was used as a measure of echogenicity. RESULTS: Fifty-three (36%) of the 148 plaques were associated with ipsilateral CT brain infarction. Plaques with a grey scale median more than 32 (echogenic) were associated with an incidence of 11% (7/64) CT infarction. In contrast, plaques with grey scale median below or equal to 32 (echolucent) were associated with 55% (46/84) incidence of CT infarction (chi 2 = 30.35, p < 0.001, relative risk = 22, 95% confidence interval from 4.7 to 108). CONCLUSION: This study indicates that computer analysis of carotid plaque can identify high-risk carotid plaques. The potential of such analysis in the identification of asymptomatic high-risk patients should be explored in further studies.

Arteriosclerosis↗
PubMed1981

Cerebral infarction in childhood bacterial meningitis.

Forty-nine children with complicated bacterial meningitis were studied. Thirteen had abnormalities on computed tomography compatible with the diagnosis of brain infarction; one had a brain biopsy with the histological appearance of infarction. Factors exist in childhood bacterial meningitis which are associated with the development of brain infraction.

Biopsy↗
PubMed2003

Neuroprotection of naloxone against ischemic injury in rats: role of mu receptor antagonism.

Naloxone has been advanced as a potential neuroprotectant against ischemic injury. This study examined the involvement of classical opioid receptors in the reduction of middle cerebral arterial ligation-induced cortical infarction in rats. The infarct volume was significantly reduced after infusion of (-)-naloxone, but not its inert stereoisomer (+)-naloxone. Beta-funaltrexamine (beta-FNA), a mu opioid antagonist, also reduced ischemic infarct volume. Both (-)-naloxone and beta-FNA attenuated cerebral ischemia/reperfusion (I/R)-induced increases in neutrophil-associated myeloperoxidase activity and chemokine mRNA expression, including macrophage inflammatory protein-1 alpha and -2. However, (-)-naloxone and beta-FNA failed to decrease cerebral I/R-induced brain edema. The findings suggest that naloxone, acting through a blockade of mu opioid receptor activation, is beneficial to cerebral I/R insult in terms of reducing brain infarction, neutrophil accumulation, and chemokine expression.

Animals↗
PubMedDate not supplied

Platelet thrombi in experimental cerebral infarction.

Cerebral infarction was produced in paralyzed, ventilated rats by a 30 min period of right common carotid artery occlusion combined with systemic hypoxia (Pao2 21-25 mm Hg). After 30 min the arterial clamp was removed and the animals were reoxygenated and allowed to survive for 1 min (6 animals), 30 min (12 animals), or 1 1/2 to 2 h (6 animals). The animals were reanesthetized and sacrificed by perfusion-fixation with paraformaldehyde-glutaraldehyde. Light and electron microscopy revealed ischemic cell change in neurons in the ipsilateral cerebral cortex, striatum and hippocampus. These changes were mild to moderate in the early post-ischemic period and severe in the post-ischemic period. Cerebral infarction was present in one of the 30 min survivors and in all of the 1 1/2 to 2 h survivors. Electron microscopy showed platelet thrombi in the infarcted brain in 3 of the 7 animals with infarcts, and in an area of very severe ischemic cell change in a fourth animal. They were not present in areas of brain showing only mild to moderate ischemic cell change. These findings showed that platelet thrombi form in association with cerebral infarcts and suggested that they are induced by tissue necrosis rather than by neuronal ischemic cell change alone.

Animals↗
PubMed2000

[A six year follow-up study on the influence of silent ischemic brain lesions on cognitive function and brain atrophy in elderly people].

METHODS: To investigate the influence of silent ischemic brain lesions (silent brain infarction (SBI) and periventricular hyperintensity (PVH) on cognitive function and brain atrophy, we studied MRI and cognitive tests in 27 healthy elderly people (above 65 years old) for 6 years. We examined Okabe's Scale for verbal intelligence, Koh's Block Design Test for performance intelligence and Zung's Self-rating Depression Scale (SDS). On MRI, lesions with high intensity on T2-weighted image and low intensity on T1-weighted image, and which were larger than 3 mm were diagnosed as SBI. The PVH was classified into 5 grades (0-4), and we divided the subjects into the PVH 0-1 group and the PVH 2-4 group. We evaluated brain atrophy using the ventricular area index (VAI) (the ratio of ventricular area to intracranial area at the level of lateral ventricle) on MRI by NIH image 1.55 (Macintosh). RESULTS: The SBI group and the PVH 2-4 group showed significant decline in Okabe's Score, and Koh's IQ, increase in SDS and VAI during six years. On the other hand, the non-SBI and the PVH 0-1 group showed a decline only in Okabe's score, and an increase in VAI. The rate of change in VAI was significantly higher in the subjects with SBI than those without it. However, there was no significant difference in the VAI change rate between the PVH 2-4 group and the PVH 0-1 group. CONCLUSION: Silent ischemic brain lesions such as SBI and PVH may have significant influence on decline of cognitive functions and progression of brain atrophy even in healthy elderly people.

Aged↗
PubMed2005

Intracranial arterial and arteriovenous malformations presenting with infarction. Lausanne Stroke Registry study.

Cerebral aneurysms and arteriovenous malformations (AVMs) are well-known sources of intracranial hemorrhage, but can also manifest as other clinical symptoms or remain clinically asymptomatic. The aim was to document and analyze cases of aneurysm or AVM with brain infarction. Survey on 4804 stroke patients treated at the Department of Neurology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland between 1978 and 2000 using the Lausanne Stroke Registry. Twenty patients presented with cerebral aneurysm and 21 with cerebral AVM. Hemorrhage was present in 100% of the AVM and in 75% of the aneurysm patients; in one (5%) of the remaining aneurysm patients, aneurysm and infarction were located in different territories. Infarction associated with Sylvian artery aneurysm was found in three (15%), vertebrobasilar ischemia because of fusiform left vertebral artery aneurysm in one (5%), and dural fistula draining to the distal transversal and left sigmoid sinus associated with a stroke in the territory of the left anterior inferior cerebellar artery in one patient. Ischemic stroke is infrequent, but important, complication in unruptured intracranial aneurysms and AVMs. The early recognition and therapy of these vascular malformations in selected patients can avoid a major neurological deficit or death caused by their rupture.

Adult↗
PubMed1993

A reproducible model of reversible, focal, neocortical ischemia in Sprague-Dawley rat.

A reproducible model of reversible, focal ischemia was developed for use with the normotensive, Sprague-Dawley rat. Blood flow to the left cerebral hemisphere was interrupted by occluding simultaneously the left middle cerebral artery and both carotid arteries (CCA). The arterial occlusion lasted for 1, 2 or 3 hours after which animals survived for 3 days. The volume of brain infarction was determined utilizing computer-assisted measurements of serial brain sections stained with triphenyltetrazolium. Tissue infarctions of variable size were observed following arterial occlusions which persisted 1 or 2 hours. In contrast, remarkably-consistent infarction size was obtained following a three hours period of occlusion. Tissue edema was also estimated by measuring the volumes of the two hemispheres and expressing these values as a ratio for each animal. The volume ratio was significantly greater in the 3 hour ischemic group, indicating the occurrence of edema in the infarcted hemisphere. These results demonstrate that reversible vascular occlusion in the normal, Sprague-Dawley rat results in consistent amounts of tissue infarction. This approach represents an attractive model system for studying the pathophysiological effects of transient, focal ischemia and for testing the effects of putative, therapeutic strategies.

Animals↗
PubMed1997

Effect of delayed albumin hemodilution on infarction volume and brain edema after transient middle cerebral artery occlusion in rats.

The authors examined the effect of delayed high-concentration albumin therapy on ischemic injury in a highly reproducible model of middle cerebral artery (MCA) occlusion in rats. Male Sprague-Dawley rats weighing 270 to 320 g were anesthetized with halothane and subjected to 120 minutes of temporary MCA occlusion induced by means of a poly-L-lysine-coated intraluminal nylon suture inserted retrograde via the external carotid artery into the internal carotid artery and MCA. The agent (20% human serum albumin [HSA]) or control solution (sodium chloride 0.9%) was administered intravenously at a dosage of 1% of body weight immediately after suture removal following a 2-hour period of MCA occlusion. The animals' neurological status was evaluated during MCA occlusion (at 60 minutes) and daily for 3 days thereafter. The brains were perfusion-fixed, and infarct volumes and brain edema were determined. The HSA significantly improved the neurological score compared with saline at 24 hours after MCA occlusion. The rats treated with HSA also had significantly reduced total infarct volume (by 34%) and brain edema (by 81%) compared with saline-treated rats. There was a strong correlation between hematocrit level and brain edema (p < 0.01), and between total infarct volume or brain edema and neurological score at 24, 48, and 72 hours postinjury (p < 0.0002). These results strongly support the beneficial effect of delayed albumin therapy in transient focal ischemia and indicate its possible usefulness in treating patients with acute ischemic stroke.

Anesthetics, Inhalation↗
PubMed2004

FK506 reduces infarct volume due to permanent focal cerebral ischemia by maintaining BAD turnover and inhibiting cytochrome c release.

It has been reported that immunosuppressant FK506 inhibited ischemic neuronal injury in forebrain ischemia or transient focal cerebral ischemia, but the mechanisms of the neuroprotective effect have not been clarified. In permanent focal cerebral ischemia, we investigated whether FK506 caused remission of brain infarction, and how mechanism was concerned. Male Balb/c mice were subjected to permanent middle cerebral artery (MCA) occlusion. They were treated with 1.0 or 3.0 mg/kg FK506 or vehicle 30 min before ischemia. Infarct volume was assessed by 2,3,5-triphenyltetrazolium chloride (TTC) method after 24 h. Cytochrome c release from mitochondria was evaluated by Western blotting and immunocytochemistry after ischemia. Simultaneously, the immunoreactivity of total and phosphorylated BAD was also studied using immunocytochemistry. We demonstrated that pretreatment with 3.0 mg/kg FK506 salvaged the tissue damage in the infarct rim and significantly reduced infarct volume to 75.5% (P<0.05), and FK506 inhibited cytochrome c release on 6 h after ischemia for Western blot analysis (P<0.05). Immunocytochemical study showed that permanent MCA occlusion increased the amount of cytochrome c and total BAD in the cytosol, but not phosphorylated BAD, in the ischemic core and the infarct rim as early as 1 h after ischemia, and FK506 inhibited the increases in the infarct rim. The results suggest that FK506 may, at least in part, ameliorate tissue damage due to permanent focal cerebral ischemia in the infarct rim through maintaining BAD turnover and inhibiting cytochrome c release from mitochondria.

Analysis of Variance↗
PubMed2005

Intracranial arterial dolichoectasia and small-vessel disease in stroke patients.

Two studies found that stroke patients with intracranial arterial dolichoectasia (IADE) had lacunar infarction more often than the control subjects. The relation between IADE and other manifestations of small-vessel disease (multilacunar state, leukoaraiosis, and état criblé) was not investigated. The magnetic resonance images of 510 patients with brain infarction in the Etude du Profil Genetique de l'Infarctus Cerebral (GENIC) study were evaluated for the diagnosis of multilacunar infarction (>1 lacunar infarct), leukoaraiosis (assessed in periventricular and subcortical regions according to Scheltens and colleagues' scale, with severe leukoaraiosis defined as a score > 8), état criblé (using a semiquantitative score ranging from 0-8, with severe EC > 4), and IADE (using the consensus method). By comparison with stroke patients without IADE (n = 447), IADE(+) stroke patients (n = 63) had significantly more frequent multilacunar state (51 vs 33%), severe leukoaraiosis (34 vs 19%), and severe état criblé (32 vs 12%). After adjustment for potential confounding factors, the odds ratios (95% confidence interval) for the presence of IADE were 2.05 (1.08-3.87) for multilacunar state, 2.40 (1.11-5.20) for severe leukoaraiosis, and 3.60 (1.43-9.08) for severe état criblé. The factors significantly associated with état criblé were older age and a familial history of stroke. IADE in stroke patients was independently associated with parenchymal manifestations of small-vessel disease. These conditions may have in common underlying pathophysiological processes.

Aged↗
PubMed1993

[The use of nimodipine in the acute period of a cerebral infarct].

Before and after intravenous administration of 1-1.5 mg nimotop 18 patients with acute brain infarction underwent EEG, integral body rheography, computed tomography and measurement of regional volumetric cerebral circulation (RVCC). Nimotop appeared to increase RVCC in the infarction zone, especially in low initial RVCC levels. The drug induced a shift to EEG normalization and a hypotensive effect, cerebral hemodynamics remaining without changes. Nimodipine-type calcium antagonists favourably affect brain perfusion and bioelectric activity which is promising for application in acute cerebral infarction.

Acute Disease↗
PubMed1995

Microglial localization of alpha-interferon receptor in human brain tissues.

The localization of the alpha-interferon receptor (alpha-IFNR) was examined in human brain tissues from neurologically normal, Alzheimer's disease (AD) and cerebral infarction cases, using one antibody (IFNaR3) which preferentially recognizes alpha 2-IFN receptor and a second antibody (anti-p40) which recognizes the soluble alpha-IFN alpha/beta receptor. In all cases, microglial cells were stained with the antibodies. In infarct brains, macrophages were intensely labeled for alpha-IFNR. The anti-p40 antibody also showed capillary staining which might be due to residual blood plasma. On Western blots, IFNaR3 recognized only a 210 kDa alpha-IFN/receptor complex, indicating its localization in microglial cells. The anti-p40 antibody recognized this complex as well as four other major materials of lower molecular weight. These results suggest that alpha-IFNR protein is constitutively expressed in microglial cells.

Aged↗
PubMed2006

Post-lesional cerebral reorganisation: evidence from functional neuroimaging and transcranial magnetic stimulation.

Reorganisation of cerebral representations has been hypothesised to underlie the recovery from ischaemic brain infarction. The mechanisms can be investigated non-invasively in the human brain using functional neuroimaging and transcranial magnetic stimulation (TMS). Functional neuroimaging showed that reorganisation is a dynamic process beginning after stroke manifestation. In the acute stage, the mismatch between a large perfusion deficit and a smaller area with impaired water diffusion signifies the brain tissue that potentially enables recovery subsequent to early reperfusion as in thrombolysis. Single-pulse TMS showed that the integrity of the cortico-spinal tract system was critical for motor recovery within the first four weeks, irrespective of a concomitant affection of the somatosensory system. Follow-up studies over several months revealed that ischaemia results in atrophy of brain tissue adjacent to and of brain areas remote from the infarct lesion. In patients with hemiparetic stroke activation of premotor cortical areas in both cerebral hemispheres was found to underlie recovery of finger movements with the affected hand. Paired-pulse TMS showed regression of perilesional inhibition as well as intracortical disinhibition of the motor cortex contralateral to the infarction as mechanisms related to recovery. Training strategies can employ post-lesional brain plasticity resulting in enhanced perilesional activations and modulation of large-scale bihemispheric circuits.

Animals↗
PubMed2003

Intracranial arterial dolichoectasia and its relation with atherosclerosis and stroke subtype.

OBJECTIVE: To investigate the relationship between intracranial arterial dolichoectasia (IADE) and vascular risk factors, atherosclerosis of the carotid arteries as measured by ultrasound scan, and stroke subtypes. METHODS: The sample consists of 510 consecutively recruited patients with brain infarction confirmed by MRI. The diagnosis of IADE was made by consensus between two neurologists based on MRI results. An independent reading of the 510 scans was made, with measurement of the diameter of the seven main intracranial arteries with a 16-diopter lens to validate the consensus and to better characterize patients with IADE. RESULTS: Sixty-three IADE(+) patients were identified by consensus (12%), of whom 59 (94%) had at least one intracranial artery in the fourth quartile of the distribution of diameters of intracranial arteries. Multivariate analyses found an association between IADE(+) and age (OR [95% CI] 1.04 [1.01-1.08]), male sex (3.31 [1.67-6.55]), hypertension (1.94 [1.01-3.72]), and previous myocardial infarction (2.68 [1.33-5.38]). There was no association between IADE and carotid atherosclerosis markers such as plaque or intima-media thickening. Lacunar infarct was more frequent in patients with IADE (36% versus 19%), with an adjusted OR of 2.89 (95% CI 1.29-6.46) compared with atherothrombotic infarct. CONCLUSIONS: IADE was associated with vascular risk factors such as age, male sex, hypertension, previous history of myocardial infarction, and lacunar infarct, but not with carotid atherosclerosis.

Adolescent↗
PubMed2004

Neuroprotection against transient cerebral ischemia by exercise pre-conditioning in rats.

There is increasing evidence that physical activity is associated with decreased stroke risk and incidence. The purpose of this study was to determine whether increased levels of physical activity could reduce brain damage in rats subjected to transient or permanent middle cerebral artery (MCA) occlusion. Adult male Sprague-Dawley rats (three months old, n=36) exercised on a treadmill, which required repetitive locomotor movement, for 30 min each day for three weeks. Then, using an intraluminal filament, stroke was induced by either 2-h MCA occlusion followed by two days of reperfusion or by MCA occlusion for two days without reperfusion. Brain damage was determined by evaluating neurologic deficits and brain infarction. In rat with transient MCA occlusion, pre-ischemic motor activity significantly (p<0.01) reduced neurologic deficits and infarct volume in the frontoparietal cortex and the dorsolateral striatum. In contrast, the same exercise procedure did not produce neuroprotection in the permanently MCA-occluded stroke. In addition to decreasing stroke risk and incidence, physical activity also reduces brain damage after stroke. Although we cannot completely rule out a neuroprotective effect on ischemic episode, our study suggests that a major neuroprotection is conferred during reperfusion for rats that have undergone exercise pre-conditioning. This exercise-induced endogenous neuroprotection may be an effective strategy to ameliorate ischemia/reperfusion brain injury from stroke.

Analysis of Variance↗
PubMed1986

[Hypertonic central nervous system complications from the viewpoint of the pathologist].

Based on 2130 autopsies with a hypertension it is reported on the hypertensive CNS-lesions. The frequency of encephalomalacia was 12%. By 9.7% was founded brain haemorrhages. The relapse rate of haemorrhages was about 5%. The encephalomalacia existed by way of secondary finding in 24.7%, and the haemorrhage in 2.2%. The investigations showed an important arteriosclerosis by 39.8% in haemorrhages and by 51.6% in brain infarct. It was remarkable by the hypertensive brain haemorrhages a dominant right hemisphere.

Adolescent↗
PubMedDate not supplied

[Lacunar cerebral infarct: its etiology, pathogenesis, clinical picture and treatment].

The present article focuses on lacunar brain infarction--that of acute or gradually progressive ischemic cerebral circulatory disorder under arterial hypertension. Major risk factors are described as are pathogenesis, pathomorphology, location of the lesion, clinical picture together with principle symptoms of manifestation, diagnosis, treatment and prophylaxis of the condition.

Acute Disease↗
PubMed2005

Novel alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor antagonists of 2,3-benzodiazepine type: chemical synthesis, in vitro characterization, and in vivo prevention of acute neurodegeneration.

Under pathophysiological conditions, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor activation is considered to play a key role in several disorders of the central nervous system. In the search for AMPA receptor antagonists, the synthesis and pharmacological characterization of a series of novel compounds that are structurally related to GYKI 52466 (1), a well-known selective noncompetitive AMPA receptor antagonist, was performed. In vitro, 2,3-dimethyl-6-phenyl-12H-[1,3]dioxolo[4,5-h]imidazo[1,2-c][2,3]benzodiazepine (ZK 187638, 14a) antagonized the kainate-induced currents in cultured hippocampal neurons with an IC(50) of 3.4 microM in a noncompetitive fashion. When tested in a clinically predictive rat model of acute ischemic stroke, this noncompetitive AMPA receptor antagonist significantly reduced brain infarction, indicating that it is neuroprotective after permanent focal cerebral ischemia.

Acute Disease↗