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PubMed1987

[Brain infarct caused by trauma-induced intracranial pressure elevation. Clinical and computerized x-ray tomography findings].

Of 327 patients admitted to hospital with signs of trauma-induced raised intracranial pressure 41 had infarcts demonstrated by computed tomography (CT). The most common site was the area supplied by the posterior cerebral artery, usually ipsilaterally. Experience so far indicates that the infarcts are most commonly caused by transient, dynamically produced occlusion of the artery, more rarely by venous congestion, resulting from the raised intracranial pressure. Comparison of the morbidity and mortality rate of patients with and without infarction after trauma with signs of raised intracranial pressure indicates that an infarct clearly worsens prognosis. Infarcts can be easily distinguished from contusional foci by CT, although both have decreased density, because the former spread within the supply area of a vessel and, similarly to embolic or arteriosclerotic infarcts, produce contrast enhancement after administration of contrast media as an expression of a disturbed blood-brain barrier.

Adolescent↗
PubMed2003

3-Aminobenzamide reduces brain infarction and neutrophil infiltration after transient focal cerebral ischemia in mice.

Poly(ADP-ribose) polymerase (PARP) was shown to be detrimental in cerebral ischemia but the mechanisms whereby PARP is deleterious have yet to be determined. They may include a role in neutrophil infiltration known to aggravate ischemic damage. In this context, we investigated the effect of 3-aminobenzamide (3-AB), a PARP inhibitor, on brain damage and neutrophil infiltration after transient focal cerebral ischemia in mice. Ischemia was induced in male Swiss mice, anaesthetized with chloral hydrate (400 mg/kg, i.p.), by a 15-min-occlusion of the left middle cerebral artery using an intraluminal suture. Treatments with 3-AB were first administered intraperitoneally 15 min before reperfusion and endpoints measured at 24 h. Among the range of dosages studied (20-320 mg/kg), 40 mg/kg gave the maximal neuroprotection with a 30% decrease in the infarct volume and tended to improve the neurological score evaluated by a grip test. The same dosage was, however, devoid of effect when injection was delayed 2 or 6 h after reperfusion. Myeloperoxidase (MPO) activity used as an index of neutrophil infiltration showed that infiltration peaked 48 h after reperfusion in our model. At this time point, 3-AB (40 mg/kg given 15 min before reperfusion) markedly reduced the neutrophil infiltration, as evidenced by a 72%-decrease in MPO activity, and was still neuroprotective. Our results confirm that 3-AB reduces brain damage. Moreover, for the first time, a quantitative study shows that 3-AB decreases neutrophil infiltration elicited by cerebral ischemia.

Animals↗
PubMed1992

[Computerized tomography markers of morphologically confirmed hemorrhagic brain infarct].

Radiological differentiation between hemorrhagic infarction and intracerebral hemorrhage is important for patient management. To ascertain CT features of hemorrhagic infarction, we studied the findings in 19 cases with autopsy-proven hemorrhagic infarction. Most cases had multiple, mainly cortically located, small hyperdensities. However, some presented with a single hyperdensity, deeply located, that could be mistaken for primary intracerebral hematoma. Hemorrhagic infarctions usually present as multiple, small hyperdensities within a hypodense area compatible with an arterial territory. The shape can be round, slitlike, curvilinear, or spotted. Most often the hyperdensities are located cortically; however, some larger, deeply located hyperdensities may falsely suggest primary intracerebral hematoma. Some guidelines for a more reliable radiological separation between hemorrhagic infarctions and intracerebral hematomas are suggested.

Aged↗
PubMed2004

Multiple microembolic borderzone brain infarctions and endomyocardial fibrosis in idiopathic hypereosinophilic syndrome and in Schistosoma mansoni infestation.

We report two cases of multiple distal borderzone ischaemic strokes associated with hypereosinophilia due to idiopathic hypereosinophilic syndrome in one patient and to acute Schistosoma mansoni infestation in the other. Endomyocardial fibrosis (EMF) was documented pathologically, in one case at autopsy and in the other after cardiac surgery; and by cardiac CT, with initially negative echocardiography, in one patient. These observations suggest that so called borderzone infarcts may be due to microembolisms and that, in the context of hypereosinophilia, EMF diagnosis warrants complete cardiac investigation including cardiac CT and repeat echocardiography.

Adult↗
PubMed2004

Effects of combined estrogen and progesterone on brain infarction in reproductively senescent female rats.

Recent data from the Women's Health Initiative have highlighted many fundamental issues about the utility and safety of long-term estrogen use in women. Current hormone replacement therapy for postmenopausal women incorporates progestin with estrogen, but it is uncertain if combined therapy provides major cerebrovascular risks or benefits to these women. No experimental animal stroke studies have examined combined hormone administration. The authors tested the hypothesis that combined hormone treatment reduces ischemic injury in middle-aged female rat brain. Reproductively senescent female rats underwent 2-hour middle cerebral artery occlusion (MCAO) followed by 22 hours reperfusion. Estrogen implants were placed subcutaneously at least 7 days before MCAO, and progesterone intraperitoneal injections were given 30 minutes before MCAO, at initiation, and at 6 hours of reperfusion. Rats received no hormone, a 25-microg estrogen implant, a 25-microg estrogen implant plus 5 mg/kg intraperitoneal progesterone, or 5 mg/kg intraperitoneal progesterone. Cortical, caudoputamen, and total infarct volumes were assessed by 2,3,5-triphenyltetrazolium chloride staining and digital image analysis at 22 hours reperfusion. Cortical and total infarct volumes, except in the acute progesterone-treated group, were significantly attenuated in all estrogen-alone and combined hormone-treated groups. There were no significant differences in caudoputamen infarct volumes in all hormone-treated groups as compared with untreated rats. These data have potential clinical implications relative to stroke for postmenopausal women taking combined hormone replacement therapy.

Age Factors↗
PubMed2002

[A case of hemodynamic brain infarction with postprandial hypotension].

A 76-year-old man with left internal carotid artery occlusion developed a progressing right hemiparesis. Brain MRI presented reinfarctions in the left anterior border zone and terminal zone in the left deep white matter. Ambulatory blood pressure monitoring showed a decrease in systolic blood pressure by more than 20 mmHg one hour after starting meals, which is considered as postprandial hypotension. The recurrent stroke occurred probably by a hemodynamic mechanism with the presence of internal carotid artery occlusion and postprandial hypotension. Administration of voglibose, an alpha-glucosidase inhibitor, improved postprandial hypotension. In patients with severe carotid or intracranial artery disease, the postprandial hypotension should be carefully monitored for prevention of hemodynamic brain ischemia.

Aged↗
PubMed2003

Electrical stimulation of the dorsal periaqueductal gray decreases volume of the brain infarction independently of accompanying hypertension and cerebrovasodilation.

We investigated whether selective stimulation of neurons of the sympathoinhibitory ventral periaqueductal gray (VPAG), or sympathoexcitatory dorsal periaqueductal gray (DPAG), differentially modulates CBF and EEG and exerts neuroprotection. Electrical stimulation of either regions of PAG comparably elevated AP and CBF, whereas chemical stimulation with the D,L-homocysteine produced either sympathoinhibition accompanied by decrease in CBF from ventral region or sympathoexcitation accompanied by increase in CBF from dorsal region in nonspinalized rats. The CBF effects evoked from DPAG and VPAG by chemical stimulation were preserved in spinalized rats supporting that the evoked CBF responses result directly from stimulation and are not secondary to AP changes. Stimulation of either region, whether chemical or electrical, synchronized the EEG. To explore whether PAG stimulation might protect the brain against ischemic injury, in other rats the VPAG or DPAG were stimulated for 1 h (50 Hz, 1 s on/1 s off, 75-100 microA) and the middle cerebral artery occluded 72 h later. Stimulation of the DPAG, but not VPAG, significantly reduced infarction volumes relative to sham-stimulated controls as determined 24 h after occlusion. Elevations of AP and CBF did not differ between groups. We conclude: (a). intrinsic neurons of D- and VPAG differentially regulate CBF; (b). neurons of DPAG are neuroprotective independently of changes in CBF and/or AP. The DPAG effect on infarct volume may be related to the central neuroprotective pathway evoked by stimulation of the cerebellar FN.

Analysis of Variance↗
PubMed2004

[Juvenile ischemic brain infarction. Clinical aspects, etiology spectrum, diagnosis and therapy].

Ischemic stroke in the young (age: 18-45 years) constitutes a diagnostic and therapeutic challenge. A broad spectrum of potential causes of juvenile strokes exists. Above all, nonatherosclerotic arteriopathies with dissections as their main proponent, paradoxical embolism, and thrombophilias have to be considered. Transient brief episodes with neurological deficits are difficult to discriminate from migrainous aura, epileptic seizure, psychogenic disorder. Therefore, the diagnostic work-up of juvenile stroke patients usually exceeds the amount of compulsory tests recommended in official guidelines. Various therapeutic modalities are not based on randomized large-scale studies and have to be selected on an individual basis. Despite good compliance, the annual risk of stroke recurrence is 2-3% and 1% for myocardial infarction.

Adolescent↗
PubMed1995

Habitual snoring as a risk factor for brain infarction.

The association of habitual snoring with cerebral ischaemia was studied, in a case control-study, in 133 patients aged 45-75 years (103 men and 30 women) and 133 controls matched for sex and age. Ischaemic stroke was confirmed by brain computed tomography or magnetic resonance imaging. History of risk factors, especially of snoring and sleeping habits was recorded with structured questionnaire during interview. Prevalence of habitual snoring significantly differs between patients with stroke and controls: 31/133 (23.3%) vs 11/133 (8.3%) (Odds ratio 3.4, 95% confidence interval 1.5 to 7.6, p < 0.001). Even after adjusting for matching variables and confounding risk factors (arterial hypertension, cardiac arrhythmia, and obesity), habitual snoring carries a significant risk factor for stroke (odds ratio: 2.9, 95% confidence interval 1.3 to 6.8 (p = 0.01)). The risk of ischaemic stroke was higher among older male patients with arterial hypertension who always snored. Habitual snoring was not significantly linked with sleep-related stroke nor with the pathophysiology of strokes. Inquiring about habitual snoring should become a routine practice, especially among older male patients with arterial hypertension, and specific preventive measures should be instituted at an earlier stage.

Adult↗
PubMed2006

Delayed treatment with nicotinamide inhibits brain energy depletion, improves cerebral microperfusion, reduces brain infarct volume, but does not alter neurobehavioral outcome following permanent focal cerebral ischemia in Sprague Dawley rats.

Delayed treatment with nicotinamide (NAm) reduces infarction induced by middle cerebral artery occlusion (MCAO) in rats. This study explored some potential mechanisms by which delayed NAm treatment may confer protection in the brain of Sprague-Dawley rats following permanent MCAO (pMCAO). NAm (500 mg/kg) or vehicle was given 2 h after the onset of pMCAO. Cortical microperfusion, brain and rectal temperature were serially measured. Neurobehavioral examinations were performed at 24 h post-ischemia followed by sacrifice for histologic assessment. Some rats were also sacrificed at 4 h post-ischemia for analyses of ATP, ADP, AMP, and adenosine. Permanent MCAO induced spontaneous hyperthermia and a sharp decrease in cortical microperfusion, ATP concentration, and the sum of adenine nucleotides (p < 0.05). At 4 h post-ischemia, NAm improved ATP recovery, the sum of adenine nucleotides (p < 0.05) and attenuated the ischemia-induced systemic hyperthermia (p < 0.05) without affecting brain temperature or cortical microperfusion. At 24 h, NAm improved cortical microperfusion in the ischemic hemisphere and reduced total infarct volume (p < 0.05), but did not affect behavioral scores. The data suggest that NAm attenuated brain damage following pMCAo initially by improving cerebral bioenergetic metabolism during the sub-acute phase of ischemia, followed by a delayed improvement in microvascular perfusion.

Adenine↗
PubMed2004

[Multiple brain infarctions in a young patient with Buerger's disease. A case report of cerebral thromboangiitis obliterans].

We report a 46-year-old woman with Buerger's disease who presented vascular dementia. In her early thirties, she began to feel cold sensation and pain in the lower extremities and later developed Raynaud's phenomenon in the upper extremities. The diagnosis of Buerger's disease was established on the basis of angiographic findings which showed the obstruction of peripheral vessels in both anterior tibial arteries. She was admitted to our hospital because of a transient attack of left brachial monoparesis and two episodes of epileptic seizure with progressive cognitive impairment for preceding five years. Neurological examination revealed acalculia, constructional apraxia, recent memory disturbance, and hyperreflexia of the left limbs without motor disturbance. Brain MRI revealed multiple infarctions mainly located in the border zone territories of the major cerebral arteries. Conventional angiography failed to detect abnormalities of cerebral vessels. She had no cardiovascular abnormality or coagulopathy. Cerebrovascular complications, so-called cerebral thoromboangiitis obliterans (CTAO), occur approximately in 2% of patients with Buerger's disease. CTAO has two types. Type 1 is associated with large artery changes and type 2 is associated with medium and small artery changes. Patients with type 2 CTAO usually have multiple infarcts in the cerebral arterial border zones and may develop progressive cognitive decline without motor deficit. Her clinical features are compatible with type 2 CTAO. While CTAO is a relatively rare manifestation of Buerger's disease, it should be suspected in cases of Buerger's disease in association with cognitive impairment of unknown onset.

Cerebral Infarction↗
PubMed1996

Environmental influence on outcome after experiment brain infarction.

After permanent ligation of the middle cerebral artery the motor function of rats housed in an enriched environment, i.e. cages with opportunities for various activities but not forcing the rats to do any particular task, is significantly better than in rats housed in individual cages. Rats kept in an enriched environment before and after MCA ligation improved sooner and slightly more than those placed in the enriched environment after ischemia but with no lasting significant difference except for climbing. Preliminary studies suggest that social stimulation is more important than physical activity. Rats with fetal neocortical grafts implanted into the infarct cavity performed better if exposed to enriched environment than grafted control rats housed in standard laboratory cages with 5 rats in each cage. However, they did not perform better than non-grafted rats housed in the same enriched environment. The infarct size did not differ between rats housed in an enriched environment and control rats. There was no correlation between infarct size and performance in rats exposed to an enriched environment. The improved motor function suggest that a rich environment may stimulate mechanisms that enhance brain plasticity.

Animals↗
PubMed2000

Vasogenic oedema and brain infarction in an experimental penumbra model.

The aim of this study was to modify the photochemical stroke model of Watson et al. [23] so as to make possible microscopical investigation of the so-called penumbra, a tissue zone at risk that surrounds an infarction. The idea was to minimize photochemical challenge to endothelial membranes in such a way that thrombotic vascular obstruction is avoided but destabilization of the blood-brain barrier is still obtained. Morphological examination of the challenged area revealed open blood vessels, overt blood-brain barrier leakage over the entire area, severely swollen glial cells and structurally intact neurons. The lesion expanded over time due to progressive extravasation, formation of perivascular edema and consequent development of secondary ischemia through mechanical compression and microvascular congestion. In contrast to a photothrombotic infarct, in which the ischemic insult is more severe and blood vessels are completely congested by aggregated platelets, with this approach blood flow is partially preserved. In this way, an ischemic penumbra is created that mimics pathologic conditions secondary to stroke and trauma. The model may be useful in studying effects of drugs on pathologic phenomena that are characteristic of a penumbra, e.g. vasogenic and cellular edema, inflammation and infarction.

Animals↗
PubMed1995

Influence of an enriched environment and cortical grafting on functional outcome in brain infarcts of adult rats.

The purpose of this work was to study if enriched housing conditions and fetal neocortical transplantation could enhance the functional outcome after focal brain ischemia in adult rats. The right middle cerebral artery (MCA) was ligated in 34 inbred, spontaneously hypertensive male rats, which were then randomly divided into three groups. Groups A and B were transferred to an enriched environment, i.e., a large cage with opportunities for various activities but not forcing the rats to do any particular tasks; group C was kept in standard laboratory cages. Three weeks after the MCA occlusion blocks of fetal neocortical tissue (Embryonic Day 17) were transplanted to the infarct cavity in groups B and C. Rats in group A (n = 11) and group B (n = 11) performed equally well and significantly better than rats in group C (n = 10) when placed on an inclined plane and when traversing a rotating pole 6 and 9 weeks after the MCA occlusion and in a leg placement test at 9, but not 6 and 12 weeks. Skilled forelimb function did not differ between the groups. Infarct size and thalamic atrophy did not differ between the groups and graft size was similar in group B and C. There was no correlation between infarct size and motor function in any of the tests in rats housed in an enriched environment. Since the environment can significantly alter functional outcome without reducing infarct size we suggest that more attention should be given to the role of the laboratory environment and to long term behavioral outcome in experimental stroke.

Animals↗
PubMed1989

Computed tomographic patterns of proven embolic brain infarctions.

To define patterns of infarction on computed tomography that are characteristic of embolism, as opposed to hemodynamically or microangiopathically induced brain lesions, a consecutive series of 60 patients with acute brain embolism were studied. Strokes were embolic in origin; that is, hemodynamic and in situ thrombotic stroke mechanisms had been excluded. Embolically active, cardiac disease was proved in 42 and was clinically evident in 13 patients. Five patients had suffered a stroke due to catheter-related embolism. Computed tomography revealed pial artery territorial infarction in 55 patients (92%). In 5, the infarction had the size or location (or both) characteristic of lacunes, although shape and lack of multiplicity raised questions about this interpretation. No patient showed a low-flow type of infarction pattern. These findings strongly support the view that (1) except for in situ thrombosis, pial artery territorial infarctions are indicative of an embolic mechanism, and (2) that the mechanism underlying lacunes is hardly, if ever, embolic.

Adolescent↗