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PubMed2003

Hypoxic preconditioning prevents cortical infarction by transient focal ischemia-reperfusion.

One of the proposed pathologic actions underlying brain infarction is excess free radicals resulting from reoxygenation. In this paper we report an investigation of the neuroprotective effect of hypoxic preconditioning on transient focal ischemia-reperfusion injuries in rat brain. Female Wistar rats were subjected to 380 mmHg in an altitude chamber for 15 hours/day. Our ex vivo studies showed that auto-oxidation and iron-induced lipid peroxidation of brain homogenates of the four-week hypoxia-preconditioned rats were significantly lower than those of the normoxic rats. A focal infarction in the cerebral cortex of normoxic rats was consistently observed 24 hours after a 60-minute transient ischemic occlusion of the right middle cerebral artery and bilateral common carotid arteries. Hypoxic preconditioning in fact attenuated cortical infarction in a duration-dependent manner. Induction of the neuroprotection required two weeks of hypoxic preconditioning. Four weeks of hypoxic preconditioning significantly reduced the cortical infarcted area, the elevated lipid peroxidation, and resulted in an acute increase in cytosolic cytochrome c in the infarcted cortex of normoxic rats. The protective effect of four weeks of hypoxic preconditioning lasted seven days under a renormoxic condition. Our data suggest that oxidative stress may result in apoptosis in the transient focal ischemia-reperfusion injuries. Furthermore, hypoxic preconditioning attenuated cortical infarction in the rat brain. Although supplementation of antioxidants may encounter difficulty at the blood-brain barrier, hypoxic preconditioning is very likely to protect CNS targets from oxidative injuries without any barrier.

Animals↗
PubMedDate not supplied

Imaging of leukocytic infiltration in human cerebral infarcts.

The circulating white blood cells of patients with brain infarction were labelled in vitro with Indium-111 tropolonate; the cells were reinjected to study the inflammatory process by gamma camera imaging. Eight patients with acute cerebral ischemic infarct were studied during the first two weeks after the onset of neurological symptoms. In seven cases a well defined area of increased radioactivity was revealed in the infarcted hemisphere indicating active migration and tracking of labelled leukocytes in cerebral infarct. This method allows monitoring of the cellular inflammatory response in human cerebral infarcts and adds another imaging technique.

Acute Disease↗
PubMed1996

[Cerebral infarct in chronic acetylsalicylic acid poisoning].

Salicylates increase the risk of hemorrhage. An ischemic brain infarct has not previously been described following intoxication with salicylates. Case report. A 58-year-old comatose patient was admitted with symptoms of a basilar artery thrombosis. A diagnostic angiography was impossible because laboratory results showed a prothrombin time (Quick) of 9% and a toxic salicylate level of 528 mg/l. During the next few days CCT and MRI scans revealed ischemic infarctions within the brain stem. Discussion. Salicylates can induce hemorrhage both by inhibiting platelet aggregation and - especially in higher doses - by vitamin K antagonism, leading to severe coagulopathy. The occurrence of an ischemic infarction, as presented in this case report, can be explained by a reduction of the vitamin K-dependent protein C level.

Aspirin↗
PubMed2003

Neuropsychological manifestations in a case of bilateral thalamic infarction.

Neuropsychological manifestation has been reported with lesions of the anterior and non-specific thalamic nuclei and mammilothalamic tract (MMT). These have been reported in the setting of arterial infarction and/or haemorrhage. Cerebral venous sinus thrombosis (CVT) is a rare cause of brain infarction. It occurs in the setting of oral contraceptive administration or pregnancy. Inherited thrombophilias are documented risk factors. The most frequent being heterozygous factor V Leiden mutation. We report a single case of bilateral thalamic infarction due to cerebral vein and sinus thrombosis. Clinically the case manifested with memory impairment and dysexecutive symptoms. Predisposing factor for venous thrombosis was a homozygous factor V Leiden mutation. The patient was treated with anticoagulation and made a good recovery.

Adult↗
PubMed2006

Postischemic gene transfer of soluble Flt-1 protects against brain ischemia with marked attenuation of blood-brain barrier permeability.

Brain edema is a major and often mortal complication of brain ischemia. Vascular endothelial growth factor (VEGF) is also known as a potent vascular permeability factor and may play detrimental roles at the acute stage of brain infarction. Our goal in this study was to explore protective effects of gene transfer of soluble flt-1 (sFlt-1), a natural inhibitor of VEGF, on focal brain ischemia. Adenoviral vector encoding sFlt-1 or beta-galactosidase as control was injected into the lateral ventricle 90 mins after photochemical distal middle cerebral artery occlusion in male spontaneously hypertensive rats. The transduced sFlt-1 was released to the cerebrospinal fluid from the ventricular wall and significantly increased 6 h, 1 and 7 days after sFlt-1 transfection. One day after brain ischemia, sFlt-1 gene transfer significantly reduced infarct volume (by 35%), brain edema (by 35%), and blood-brain barrier permeability (Evans blue extravasation; by 69%) with diminished phosphorylation of focal adhesion kinase (FAKtyr397 and FAKtyr861) in the ischemic vessels. Seven days after ischemia, sFlt-1 gene transfer also significantly attenuated infarct volume (by 29%) and monocyte/macrophage infiltration (by 27%), although there were no reductions in angiogenesis by sFlt-1 overexpression. These results suggest that sFlt-1 gene therapy targeting brain edema in acute stage of brain ischemia may be useful for brain infarction.

Animals↗
PubMed1991

Rebound alkalosis and persistent lactate: multinuclear (1H, 13C, 31P) NMR spectroscopic studies in rats.

Intracellular pH levels of infarcted brain determined by phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy disclosed a notable phenomenon. The acidotic brain pH seen in the acute stage of infarction was observed to rebound into the alkalotic range in the subacute phase before returning to the normal range in the chronic phase. This "rebound alkalosis" which was usually observed between the 24th and the 48th hour after experimental induction of infarction in rats was accompanied by significant lactate levels as detected by proton NMR spectroscopy. Analysis of the satellite methyl resonance of 13C-lactate using high-resolution proton NMR spectroscopy after 13C-glucose infusion indicated that no lactate was produced in the subacute phase of infarction and that the lactate detected during this phase must have been generated prior to this phase of infarction.

Alkalosis↗
PubMed1994

Comparison of triphenyltetrazolium dye with light microscopic evaluation in a rabbit model of acute cerebral ischaemia.

The present study was performed to compare brain infarct size assessment by routine histology (haematoxylin and eosin) and by 2,3,5-triphenyltetrazolium chloride staining techniques. New Zealand white rabbits were subjected to autologous clot embolization to the anterior circulation of the brain. After a study period of 7-8 h the brains were harvested and serially sectioned in the coronal plane. Brain slices were then immersed in a 1% triphenyltetrazolium chloride dye. Following visualization of the infarcted region, the brains were immediately placed in 10% formalin and later prepared for histologic evaluation by routine haematoxylin and eosin. The two methods were compared for their ability to estimate infarct size by an independent observer. There was excellent correlation between the two methodologies; infarct sizes of 57.4 +/- 5.0% versus 55.9 +/- 5.4% (mean +/- SEM, p < 0.007, r = 0.73, n = 12; expressed as percentage of the hemisphere infarcted) were noted for light microscopic evaluation versus triphenyltetrazolium chloride staining, respectively. It is concluded that triphenyltetrazolium chloride staining is an acceptable method for delineating brain infarct size in this rabbit model of thromboembolic stroke. The relative ease of infarct size determination with this technique suggests its more widespread use in similar models.

Animals↗
PubMedDate not supplied

Hyperbaric oxygen in the treatment of patients with cerebral stroke, brain trauma, and neurologic disease.

Hyperbaric oxygen (HBO) therapy has been used to treat patients with numerous disorders, including stroke. This treatment has been shown to decrease cerebral edema, normalize water content in the brain, decrease the severity of brain infarction, and maintain blood-brain barrier integrity. In addition, HBO therapy attenuates motor deficits, decreases the risks of sequelae, and prevents recurrent cerebral circulatory disorders, thereby leading to improved outcomes and survival. Hyperbaric oxygen also accelerates the regression of atherosclerotic lesions, promotes antioxidant defenses, and suppresses the proliferation of macrophages and foam cells in atherosclerotic lesions. Although no medical treatment is available for patients with cerebral palsy, in some studies, HBO therapy has improved the function of damaged cells, attenuated the effects of hypoxia on the neonatal brain, enhanced gross motor function and fine motor control, and alleviated spasticity. In the treatment of patients with migraine, HBO therapy has been shown to reduce intracranial pressure significantly and abort acute attacks of migraine, reduce migraine headache pain, and prevent cluster headache. In studies that investigated the effects of HBO therapy on the damaged brain, the treatment was found to inhibit neuronal death, arrest the progression of radiation-induced neurologic necrosis, improve blood flow in regions affected by chronic neurologic disease as well as aerobic metabolism in brain injury, and accelerate the resolution of clinical symptoms. Hyperbaric oxygen has also been reported to accelerate neurologic recovery after spinal cord injury by ameliorating mitochondrial dysfunction in the motor cortex and spinal cord, arresting the spread of hemorrhage, reversing hypoxia, and reducing edema. HBO has enhanced wound healing in patients with chronic osteomyelitis. The results of HBO therapy in the treatment of patients with stroke, atherosclerosis, cerebral palsy, intracranial pressure, headache, and brain and spinal cord injury are promising and warrant further investigation.

Animals↗
PubMed2006

PET Imaging of cerebral astrocytoma with 13N-ammonia.

UNLABELLED: We performed this study in order to assess the clinical potential of (13)N-ammonia PET in patients with cerebral astrocytoma. METHODS: Dynamic 13N-ammonia PET was performed in 25 patients with suspected cerebral gliomas or recurrent cerebral astrocytomas (19 male and 6 female patients; age range 18-64 years) detected by MRI. The histopathological diagnoses were made for all cases either by biopsy or craniotomy, except for one patient with brain infarction and one patient with brain radiation necrosis confirmed by repeated MRI imaging. PET images were visually inspected, and the tumor-to-white matter count (T/W) ratios and the perfusion index (PI) of the tumors were determined. RESULTS: Six out of nine cases of low-grade gliomas were detected with 13N-ammonia PET, and three non-astrocytoma low-grade gliomas were not detected with 13N-ammonia PET. All 11 high-grade astrocytomas exhibited markedly increased uptake of 13N-ammonia. The five non-neoplastic lesions exhibited low uptake, low T/W ratios and low PI. The significant differences were observed between high-grade and low-grade gliomas with respect to both the T/W ratios and PI (T/W ratios: 5.92+/-2.27, n=11 vs. 1.66+/-0.61, n=9, P<0.01; PI: 5.22+/-1.67, n=11 vs. 1.60+/-0.54, n=9, P<0.01). There were the significant differences between the T/W ratios and PI in low-grade astrocytomas and that in non-neoplastic lesions (T/W ratios: 2.00+/-0.42, n=6 vs. 0.97+/-0.11, n=5, P<0.01; PI: 1.89+/-0.37, n=6 vs. 0.99+/-0.03, n=5, P<0.01). CONCLUSIONS: There is a substantial uptake of 13N-ammonia in cerebral astrocytomas. 13N-ammonia PET may enable differentiation between low- and high-grade astrocytomas, and has the potential to enable differentiation between low-grade astrocytomas and non-neoplastic lesions.

Adult↗
PubMed1994

Cardiac anesthesia risk management. Multicenter outcome research.

Perioperative cardiovascular morbidity represents a major health-care challenge. Morbidity after coronary artery surgery annually consumes $750 million in health-care resources in-hospital and about $500 million in posthospitalization care. Of the 25 million patients who undergo noncardiac surgery annually in the United States, more than 1 million suffer postsurgical cardiovascular morbidity. The annual in-hospital cost of this morbidity is $10 billion, with posthospitalization care costing $12 billion more. Early efforts to reduce perioperative cardiovascular and central nervous system morbidity focused largely on the development and use of technologies designed to achieve earlier detection of end-point surrogates. However, despite advances in the early detection of infarction surrogates, perioperative heart and brain infarctions remain urgent problems. Future advances in perioperative care will require large-scale therapeutic trials of agents intended to alter outcome. The McSPI Research Group is a unique international, multicenter research organization focused on the problems of heart attack and stroke, with the goals of identifying not only effective therapies, but also developing the academic careers of clinical investigators.

Cardiac Surgical Procedures↗
PubMed1999

[Multiple renal infarction associated with lupus anticoagulant in a patient with systemic lupus erythematosus].

We report a rare case with multiple renal infarction associated with lupus anticoagulant and SLE. A 20-year old woman presented with remitent fever, butterfly rash and, abdominal pain. Laboratory findings showed leukopenia, positive antinuclear and anti-DNA antibodies, and biological false positive for syphilis. Despite a therapy with prednisolone 25 mg/day, the patient showed hypocomplementemia, high titer of anti-DNA antibody and a development of proteinuria and an elevation of serum creatinine. Renal biopsy revealed no abnormalities. She presented abdominal pain with an elevation of serum LDH. Abdominal dynamic computed tomography demonstrated multiple perfusion defects in both kidneys indicating multiple renal infarction. Brain MRI showed multiple micro infarction in the anterior lobes. She was treated with 80 mg of aspirin and have been in remission for two years. Although there have been reported 18 cases with renal infarction associated with antiphospholipid syndrome, this is the first report in Japan. Renal infarction should be differentiated from renal involvement in patients with SLE who have antiphospholipid antibodies.

Adult↗
PubMedDate not supplied

Bifrontal decompressive craniotomy in a 6-month-old infant with posttraumatic refractory intracranial hypertension.

OBJECTIVE: To document the outcome of bifrontal decompressive craniotomy (BDC) in an infant who developed refractory intracranial hypertension (IH) and massive brain infarction following severe head injury. CLINICAL PRESENTATION: A 6-month-old girl sustained a severe closed head injury in a car accident. Her Glasgow coma score dropped from 10 to 6/15 within 6 h after admission, and her pupils became dilated and fixed. CT brain scans showed severe brain swelling and extensive infarction in both cerebral hemispheres with no grey-white mater differentiation. She developed a state of refractory IH despite maximal medical treatment. INTERVENTION: She had BDC and duraplasty carried out 8 h after admission. She made a quick recovery to Glasgow outcome score 3, and her total hospital stay was 10 weeks. CONCLUSION: BDC can be a life-saving procedure for infants with refractory IH and massive brain infarction.

Accidents, Traffic↗
PubMedDate not supplied

[Epilepsy in the adult. A prospective study of 100 cases].

INTRODUCTION: The onset of epileptic seizures after 20 years old (late onset epilepsy) explains 20 to 25% of epileptic patients. The etiology is diverse and includes neurocysticercosis, brain tumors, brain infarcts, etc. Approximately 50% of these patients will have structural brain damage as a cause of the disease. MATERIALS AND METHODS: Prospective study of 130 adult patients with adult onset of epilepsy after 20 years old, studies since February 1989 to June 1997. All the patients had CT scan of brain, and when necessary brain magnetic resonance imaging. RESULTS: We found structural brain lesion in 51% of patients. The most frequent cause of seizures was neurocysticercosis (28%) followed by cerebral infarct (11%) and brain atrophy (11%). CONCLUSIONS: In our area the most frequent cause of adult onset epilepsy is neurocysticercosis. Due to the high probability of structural brain lesion, all the patients with late onset epilepsy must have brain CT scan examination.

Adult↗
PubMed2003

Increased prevalence of platelet glycoprotein IIb/IIIa PLA2 allele in ischaemic stroke associated with large vessel pathology.

INTRODUCTION: Platelet glycoprotein IIb/IIIa is a membrane receptor with a central function in the platelet adhesion and ultimately in the thrombus formation. Two major variants of the gene encoding the IIIa subunit, called PLA1 (A1) and PLA2 (A2), have been identified in the general population. There are indications that the A2 allele can also be associated with acute thrombosis or stroke. The purpose of this study was to study the distribution of the A2 allele in different vascular subtypes of stroke disease. MATERIALS AND METHODS: A total of 638 consecutive patients were analyzed and classified as having large vessel pathology (n=168) or a small vessel infarct (n=210). Localization of the vascular occlusions was deducted from analysis of the magnetic resonance imaging (MRI) scan results in stroke patients. The remainder patients were listed into a mixed vascular pathology group (n=167). Patients with other or poorly characterized stroke etiology were excluded from the study (n=93). RESULTS: In the small vessel and mixed vascular pathology groups, the PLA2 allele frequency was similar to that in the controls. By contrast, PLA2 allele frequency was approximately two-fold higher in patients with large vessel pathology (23.3%) than in the stroke-free control subjects (11.7%, p<0.0005). Multivariate logistic regression analysis of data confirmed this association with an odds ratio (OR) of 2.9 (95% confidence interval [CI]: 1.6-4.9, p<0.0005). CONCLUSIONS: These data suggest that the PLA2 allele is more frequent in brain infarcts associated with large-vessel occlusion.

Adult↗
PubMedDate not supplied

The natural history of hemispheric and brainstem infarction in Rochester, Minnesota.

All cases of first episodes of brain infarction occurring in the population of Rochester, Minnesota, from 1960 through 1979 were categorized as hemispheric or brainstem (including cerebellar) on the basis of clinical criteria, autopsy evidence, and the results of computed tomography (from 1973 on). Hemispheric infarction was 5 times more frequent than infarction of the brainstem and/or cerebellum. The magnitude of the decline in incidence was the same in each group during the 20-year period of the study. Thirty-day case fatality was similar in each group, but patients with brainstem infarction had a better long-term survival. Functional outcome among survivors of brainstem infarction was also better, 35% having returned to independent living by 1 year after onset compared with 22% of survivors of hemispheric infarction. This may have been a consequence of the higher proportion of residual cognitive and sensory impairments present in survivors of hemispheric infarction.

Activities of Daily Living↗
PubMed2005

[Decompressive hemicraniectomy for malignant middle cerebral artery infarction. Report of two cases].

Malignant middle cerebral territory infarction represents 5 to 10% of all brain infarctions. Its mortality is 80%, due to brain herniation and it is not reduced by medical treatment. Decompressive hemicraniectomy reduces mortality to 12%, and the subsequent quality of life of patients is acceptable. We report two male patients aged 61 and 54 years, with a malignant middle cerebral territory infarction who were treated with decompressive hemicraniectomy. After two years of follow up, both patients are self-sufficient and live at home with their families.

Craniotomy↗
PubMed2005

Inhibition of nitric oxide production and protein tyrosine nitration contribute to neuroprotection by a novel calmodulin antagonist, DY-9760e, in the rat microsphere embolism.

Microsphere embolism (ME)-induced ischemia model in rat resembles to multiple brain embolism in human with several clinical features. We here tested whether nitric oxide (NO) production contributes to the neuronal injury in the ME model. A novel calmodulin antagonist, DY-9760e, having a potent inhibitory effect on neuronal nitric oxide synthase (nNOS), reduced brain infarct size in the ME-induced brain ischemia. Consistent with our previous observation with gerbil ischemia/reperfusion model, DY-9760e completely inhibited NO production immediately after and 24 or 48 h after ME. Unlike the gerbil ischemia/reperfusion model, protein tyrosine nitration markedly increased 6-48 h after ME. DY-9760e treatment completely inhibited the marked increase in the protein tyrosine nitration at 24 h after ME. These results suggest that the inhibition of NO production and protein tyrosine nitration by DY-9760e contribute to its neuroprotective action in the ME-induced brain damage.

Animals↗
PubMed1994

Ischemia-induced brain iron delocalization: effect of iron chelators.

Tissue damage in cerebral ischemia may be produced by acidosis-induced delocalization of intracellular iron which acts as a catalyst in oxidative reactions. Acidosis was induced either by homogenization and incubation of rat cortical homogenates in acidified buffers or by submitting hyperglycemic rats to complete ischemia, a procedure that leads to intracellular lactic acidosis. The level of low molecular weight species (LMWS) iron was measured after filtration of tissue homogenates through a 10,000 Mr ultrafiltration membrane. When cortical tissue was homogenized in buffer pH 7, the level of LMWS iron was equal to 0.21 microgram/g. It was significantly enhanced by acidification of the homogenization medium, reaching 0.34 microgram/g at pH 6 and 0.75 microgram/g at pH 5. When the tissue was homogenized in water, the LMWS iron level reached 0.17 microgram/g in normoglycemic rats and 0.38 microgram/g (p < .05) in hyperglycemic rats. Both aerobic incubation of homogenates for 1 h at 37 degrees C and inclusion of EDTA in the homogenization medium led to further increases in the iron level. In order to demonstrate the deleterious role of iron in brain ischemia, the effect of treatment with bipyridyl, an iron-chelating agent, was assessed by measuring regional brain edema by the specific gravity method, 24 h following induction of thrombotic brain infarction. The treatment significantly attenuated the development of brain edema, reducing the water content of the infarcted area by about 2.5%. Taken together, these results support the hypothesis that a significant component of brain ischemic injury involves an iron-dependent mechanism.

2,2'-Dipyridyl↗