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PubMed2001

Dual effect of HBO on cerebral infarction in MCAO rats.

Various reports in the literature have shown that hyperbaric oxygen (HBO) reduces cerebral infarction both in animals and humans. After the initial ischemic insult, however, initiating HBO treatment at different intervals has yielded conflicting results. The present study was undertaken to determine the optimal therapeutic window in which to start HBO treatment for cerebral infarction after transient focal ischemia. In this study, the operator occluded the middle cerebral artery (MCA) of anesthetized rats by introducing a blunted nylon filament into the proximal MCA from the dissected external carotid artery. When the operator removed the filament after 2 h, focal ischemia and reperfusion occurred. The operator then placed the rat in the HBO chamber and administered 3 atm absolute HBO for 1 h according to the protocol. The rat was killed 24 h after reperfusion, and the percentage of infarction (infarct ratio) was calculated by dividing the infarction area by the total area of the ipsilateral hemisphere. The results showed that the percentage of infarcted area decreased significantly (P < 0.05) both in the 3- (7.59%) and 6-h (5.35%) HBO-treatment groups compared with the control (no treatment) group (11.34%). However, the percentage of infarcted area increased significantly (P < 0.01 and P < 0.05, respectively) both in the 12- (23%) and 23-h (20%) treatment groups. The results of this study suggest that applying HBO within 6 h of ischemia-reperfusion injury could benefit the patient but that applying HBO 12 h or more after injury could harm the patient.

Animals↗
PubMed2006

Cognitive screening for silent cerebral infarction in children with sickle cell disease.

Silent cerebral infarctions have been shown to cause major morbidity in children with sickle cell disease, suggesting that silent infarctions are not as "silent" as once thought. The current definition of silent infarction includes signal changes on magnetic resonance imaging, the absence of overt abnormalities on neurologic examination, and no history of focal neurologic event. Using a decision tree algorithm, we identified a cognitive profile distinguishing children with (n=16) and without (n=49) silent infarctions. The best model combined learning slope from the California Verbal Learning Test-Children's Version and Block Design from the Wechsler Abbreviated Scale of Intelligence. Accuracy was 75%, with 75% sensitivity and 76% specificity. Administration of a brief cognitive battery may be the most feasible approach to screen for silent infarctions in children with sickle cell disease.

Adolescent↗
PubMedDate not supplied

Anticoagulant vs anti-platelet therapy as prophylactic against cerebral infarction in transient ischemic attacks.

156 patients with transient ischemic attacks (TIA) or reversible ischemic neurological deficit (RIND) were given prophylactic anticoagulant (AC) treatment against cerebral infarction in a prospective multicenter study from 5 hospitals in southern Sweden. After 2 months of AC treatment, 135 patients remained in the study and were randomized into 2 groups; one continued with AC treatment and one changed to anti-platelet therapy. The patients were followed for 12 months. No significant difference was seen between the 2 groups but 3 completed cerebral infarctions occurred during anti-platelet therapy against one during AC treatment. One cerebral hemorrhage was seen during AC treatment. All completed strokes occurred in men who initially had carotid symptoms. The number of patients with TIA/RIND was somewhat higher in the anti-platelet group whereas myocardial infarctions occurred more often during AC treatment. Compared to the natural history of untreated TIA/RIND both treatments were found to have a prophylactic effect against cerebral infarction.

Aged↗
PubMed2000

Isoflurane delays but does not prevent cerebral infarction in rats subjected to focal ischemia.

BACKGROUND: Several investigations have shown that volatile anesthetics can reduce ischemic cerebral injury. In these studies, however, neurologic injury was evaluated only after a short recovery period. Recent data suggest that injury caused by ischemia is a dynamic process characterized by continual neuronal loss for a prolonged period. Whether isoflurane-mediated neuroprotection is sustained after a longer recovery period is not known. The current study was conducted to compare the effect of isoflurane on brain injury after short (2-day) and long (14-day) recovery periods in rats subjected to focal ischemia. METHODS: Fasted Wistar-Kyoto rats were anesthetized with isoflurane and randomly allocated to an awake (n = 36) or an isoflurane (n = 34) group. Animals in both groups were subjected to focal ischemia by filament occlusion of the middle cerebral artery. Pericranial temperature was servocontrolled at 37 degrees C throughout the experiment. In the awake group, isoflurane was discontinued and the animals were allowed to awaken. In the isoflurane group, isoflurane anesthesia was maintained at 1.5 times the minimum alveolar concentration. After 70 min of focal ischemia, the filament was removed. Animals were killed 2 days (awake, n = 18; isoflurane, n = 17) and 14 days (awake, n = 18; isoflurane, n = 17) after ischemia. The volumes of cerebral infarction and selective neuronal necrosis in the animals were determined by image analysis of hematoxylin and eosin-stained coronal brain sections. RESULTS: Cortical and subcortical volumes of infarction were significantly less in the isoflurane 2-day group (26 +/- 23 mm3 and 17 +/- 6 mm3, respectively) than in the awake 2-day group (58 +/- 35 mm3, P < 0. 01; and 28 +/- 12 mm3, P < 0.01, respectively). By contrast, cortical and subcortical volumes of infarction in the awake (41 +/- 31 mm3 and 28 +/- 16 mm3, respectively) and isoflurane (41 +/- 35 mm3 and 19 +/- 8 mm3, respectively) 14-day groups were not different (cortex, P = 0.99; subcortex, P = 0.08). The volume of cortical tissue in which selective neuronal necrosis was observed, however, was significantly less in the isoflurane 14-day group (5 +/- 4 mm3) than in the awake 14-day group (17 +/- 9 mm3, P < 0.01). The total number of necrotic neurons in the region of selective neuronal necrosis was significantly smaller in the isoflurane 14-day group than in the awake 14-day group (P < 0.01). CONCLUSION: Compared with the awake state, isoflurane reduced the extent of infarction assessed 2 days after focal ischemia in rats. At 14 days, however, only selective neuronal necrosis, but not infarction, was reduced by isoflurane. These results suggest that isoflurane delays but does not prevent cerebral infarction caused by focal ischemia. Isoflurane may attenuate the delayed development of selective neuronal necrosis in periinfarct areas in this animal model.

Anesthetics, Inhalation↗
PubMedDate not supplied

Diffusion-weighted imaging of cerebral infarctions: are higher B values better?

PURPOSE: The purpose of this work is to determine whether high -value ( = 3,000 s/mm ) diffusion-weighted (DW) imaging is superior to low -value ( = 1,000 s/mm ) DW imaging for the detection of cerebral infarctions older than 6 h. METHOD: Echo planar DW imaging was performed at 1.5 T in 26 consecutive patients (mean age 66 years) referred for clinical diagnosis of definite acute/subacute cerebral infarction (6 h to 14 days old). The DW imaging sequences were performed using matched parameters (TR = 10,000 ms, TE (eff)= 97 ms, FOV = 24 cm, 128 x 192 matrix, slice = 5 mm, NEX = 2) with values of 1,000 and 3,000 s/mm. Areas of infarction were compared visually by two experienced neuroradiologists. Quantitative measures of MR signal and noise levels in the infarcted areas compared with contralateral normal brain were also obtained. RESULTS: The median time after infarction was 2.5 days (range 10 h to 14 days). By visual inspection, all infarctions were reliably identified on both the = 1,000 and the = 3,000 images. The gross signal ratio (infarct/normal brain) was approximately 33% higher in the = 3,000 images, but the = 3,000 images were rated as noticeably "noisier" by both observers in every case. This visual observation was confirmed quantitatively: The signal-to-noise (SNR) and contrast-to-noise (CNR) ratios were 70% and 51% higher in the = 1,000 than the = 3,000 images (p < 0.0005 for both). CONCLUSION: For the evaluation of late acute/subacute cerebral infarctions, high -value ( = 3,000 s/mm(2) ) DW imaging offers no apparent diagnostic advantages compared with = 1,000 images and is significantly inferior in terms of SNR and CNR.

Acute Disease↗
PubMed2004

Functional effects of NAD(P)H oxidase p22(phox) C242T mutation in human leukocytes and association with thrombotic cerebral infarction.

BACKGROUND: Previous study showed that polymorphism of the NAD(P)H oxidase p22(phox) gene is associated with atherosclerosis, although others could not confirm such association. We investigated the association between p22(phox) C242T polymorphism and thrombotic cerebral infarction and the role of this polymorphism on superoxide-production activity in human neutrophils and promyelocytic HL-60 cells as a model system. METHODS: PCR-RFLP analysis revealed that genotype and allele frequencies of C242T polymorphism in 120 patients with thrombotic cerebral infarction and 177 control subjects. The superoxide-production activity in neutrophils was determined by cytochrome c reduction assay. To clarify the role of p22(phox) C242T polymorphism on NAD(P)H oxidase activity, we used transgenic HL-60 cells transfected with expression plasmids carrying p22(phox) cDNAs with or without C242T polymorphism. RESULTS: Genotype and allele frequencies of C242T polymorphism in patients and control subjects were not significantly different. The superoxide-production activity in neutrophils with T allele was higher than in neutrophils without T allele. Moreover, expression analysis showed that superoxide-production activity in p22(phox) C242T-expressing HL-60 cells were significantly higher than in p22(phox)-expressing HL-60 cells. CONCLUSIONS: We conclude that C242T of p22(phox) gene is not involved in thrombotic cerebral infarction but more likely in increased NAD(P)H oxidase activity in phagocytes.

Adult↗
PubMed2004

Neuroprotective effect of gamma-glutamylethylamide (theanine) on cerebral infarction in mice.

In the present study, we examined the neuroprotective effect of gamma-glutamylethylamide (theanine) on the ischemic brain damage in a middle cerebral artery occlusion model in mice. Theanine was injected i.p. 3 h after the occlusion or immediately before and 3 h after the occlusion. Theanine (1 mg/kg) significantly decreased the size of the cerebral infarcts 1 day after the occlusion. In contrast, theanine did not affect the cerebral blood flow, brain temperature and physiological variables (pH, pCO(2), pO(2) and hematocrit) in this model. These results suggest that theanine directly provides neuroprotection against focal cerebral ischemia and may be clinically useful for preventing cerebral infarction.

Analysis of Variance↗
PubMed1993

[Mortality of cerebral infarction with auricular fibrillation. Results of a population study].

To evaluate the relationship between atrial fibrillation (AF) and mortality of the cerebral infarction, we have studied in a population survey, 540 cerebral infarctions, whose 162 were with AF (30%) and 378 without AF (70%). The group with AF differs significantly from that without AF, by the higher frequency of women (62% versus 35%), older subjects (75.4 +/- 10.2 years old versus 69.1 +/- 9.7 years old), a severe loss of consciousness, a more frequent subcortical infarction on CT-Scan. During a period of 24 months, 139 patients died, 64 among the 162 patients with AF (40%), 75 among the 378 patients without AF (20%). Rates of death are different in the 2 groups with, in the group with AF, at 1, 6, 18 and 24 months a rate of 20, 24, 37 and 40 percent. To the opposite, in the group without AF, the rates are 8, 12, 16 and 20 percent. The authors try to research the factors that may explain the mortality linked to AF, and they insist on the necessity to look for AF on admission for a stroke, to identify a subgroup of stroke patients with a high risk of death.

Aged↗
PubMed1998

[A study on the relationship between Lp(a) and arteriosclerotic cerebral infarction].

Using a 1:1 matched case control study, we analysed the data of 105 arteriosclerotic cerebral infarction cases and controls to detect the levels of TC, TG, HDL-C, LDL-C and Lp(a). The results showed that the average level of Lp(a) in cases was (238.38 mg/L), significantly higher than that of controls (149.98 mg/L t = 3.96, P < 0.001). Comparing the levels of different age groups and sex, no significant difference, except the group over 70 years, which was higher than that in other groups was found. Dose-response analysis also showed that the OR value was positively correlated with the Lp(a). Multi-variable logistic regression model indicated that Lp(a) was an independent risk factor with OR = 1.93. Another risk factor was TG. However, LDL-C, HDL-C were found to be the protective factors of arteriosclerotic cerebral infarction, with an OR = 0.32.

Aged↗
PubMed2004

Human cerebral infarct: a proposed histopathologic classification based on 137 cases.

We studied the microscopic features of 137 cases of human cerebral infarct. In each case, the age of the lesion was determined by measuring the time elapsed between initial clinical presentation and date of surgery or death. Multiple microscopic variables were analyzed on hematoxylin and eosin-stained sections. There were 104 (76%) male and 33 (24%) female patients with a median age of 64 years. The location of the infarcts included 129 cerebral, 5 cerebellar, and 1 each in the pons, midbrain and medulla. The age of the lesions ranged from 1 day to 53 years. All lesions were single and varied from lacunes to large infarcts in the distribution of one or more cerebral arteries. Key histologic features of the proposed classification are as follows: (1) phase of acute neuronal injury (11 cases studied), age 1-2 days, characterized by the presence of neuronal changes, and spongiosis of the neuropil and absence of neuronal ferrugination, chronic inflammation, macrophages, neo-vascularization and cavitation; (2) phase of organization subdivided into: (a) phase of acute inflammation (31 cases), age 3-37 days, characterized by coagulative necrosis, and frequent acute inflammation, and (b) phase of chronic inflammation (57 cases), age 10 days-53 years, characterized by the presence or absence of coagulative necrosis, neuronal injury, red neurons, macrophages, mononuclear inflammatory cells, perivascular cuffing, cavitation, gliosis, spheroids; absence of neutrophils; and (3) phase of resorption (38 cases), age 26 days-23 years, characterized by absence of an inflammatory response. Neuronophagia is not a feature of cerebral infarcts.

Adolescent↗
PubMed1990

[Assessment of cerebral infarction by MRI--particularly fogging effect].

Fogging effect in cerebral infarction was studied by MRI in a 51-year-old male patient. Initial symptoms consisted of mild disturbance of consciousness and left hemiparesis. MRI examination was performed 2, 13 and 22 days after onset and the results were compared with CT findings during the same period. CT on day 2 revealed a wide of infarction in the region of the middle cerebral artery including the basal ganglia. The presence of a fogging effect was seen by CT on day 12 and MRI revealed a high signal intensity in the region of the basal ganglia in T 1 image, a high signal intensity in the peripheral region and a low signal intensity in the center in T 2 image. It was possible to define the lesion as the ordinary infarcted lesion by the subsequent CT and MRI. MRI indicated the infarct lesion was to be a high signal intensity in T1 image and a high signal intensity in the periphery and a low signal intensity in the center in T 2 image. It was concluded that these findings indicated hemorrhage, strongly suggesting that the cause of the fogging effect was hemorrhagic infarction.

Cerebral Hemorrhage↗
PubMed1998

[Clinical and experimental study on treatment of acute cerebral infarction with Acanthopanax Injection].

OBJECTIVE: To evaluate the effect of Radix Acanthopanacis Senticosi in treating acute cerebral infarction and its mechanism. METHODS: Clinical study using single-blind, control trial, in which 60-80 ml of Acanthopanax Injection (AI) added to 500 ml of 0.9% normal saline was given by intravenous drip once a day for 14 days in the AI group(34 patients), while 500 ml of dextra-40 was given by the same way in the control group(26 patients). In experimental study, rabbit model of acute incomplete cerebral ischemia was made by ligation of bilateral common carotid artery. 10 ml of AI were given once daily intravenously for 7 days to the AI group and 10 ml of normal saline was given to the control group in the same way. Clinical effects (in clinical study) and effect of AI on cerebral oxygen free radicals (OFR), superoxide dismutase (SOD), and serum concentration of ACTH and cortisone were observed (in experimental study). RESULTS: Clinical study showed that the total effective rate of AI group (86%) was higher than that of the control group (50%) while nervous functional deficit score was lower in AI group (9.96 +/- 4.66) than that in the control group (13.56 +/- 1.84) significantly. Experimental study showed that the cerebral level of OFR decreased while SOD increased and serum concentration of ACTH and cortisone decreased after treatment in AI group. CONCLUSIONS: AI was effective in treating acute cerebral infarction, the mechanism is probably by ameliorating peroxidation in brain and improving hypothalamic-pituitary-adrenocortical axis function.

Adrenocorticotropic Hormone↗
PubMed2005

[A case report of a patient who developed hemiparaplegia with multiple cerebral infarction during thoracoabdominal aortic aneurysm repair].

To protect the spinal cord during thoracoabdominal aortic aneurysm repair, motor evoked potentials (MEP) monitoring and cerebrospinal fluid drainage are often employed. Herein, we report a case, where intraoperative diminishment of motor evoked potentials was accompanied by multiple cerebral infarction. A 63-year-old man underwent elective surgery for both thoracoabdominal aortic aneurysm and abdominal aortic aneurysm. He had a past history of cerebral infarction, resulting in Wernicke aphasia but no paralysis. Preoperative magnetic resonance angiography and echocardiography revealed occlusion of the intercostal and lumbar arteries, mild aortic regurgitation, and atherosclerotic lesions at the aortic arch as well as descending aorta. Anesthesia and muscular relaxation were maintained with fentanyl, propofol, and continuous administration of vecuronium at 0.5 mg x kg(-1) x h(-1). The thoracoabdominal aortic aneurysm was repaired under distal aortic perfusion with femorofemoral bypass. After terminating the bypass, we found that the MEP at the lower limb had disappeared. Although we reconstructed intercostal arteries under mild hypothermia and partial bypass, the amplitude of MEP remained very low. Suspecting spinal cord ischemia, we performed cerebrospinal fluid drainage immediately after the operation. On the postoperative day 4, when we stopped the cerebrospinal fluid drainage and propofol administration, his level of consciousness was poor and brain CT revealed multiple cerebral infarction. On the postoperative day 30, he was discharged from an intensive care unit with complications of hemiplagia and paraplegia. Although cerebrospinal fluid drainage may be recommended to protect spinal cord during thoracoabdominal aortic aneurysm repair, we should consider performing brain CT to exclude a risk of brain herniation secondary to cerebrospinal fluid drainage if there is a possibility of cerebral incidents.

Aortic Aneurysm, Abdominal↗
PubMed1995

Midkine is present in the early stage of cerebral infarct.

Expression of midkine (MK), a growth factor with neurotrophic activities, was examined immunohistochemically in experimental cerebral infarct of rats. From postoperative day 1 to day 7 after the onset of infarct, anti-MK immunoreactivity was observed in the surrounding ischemic zone of the infarct but not in the necrotic lesion. The immunoreactive material was identified to be MK by Western blotting. On day 14, anti-MK immunoreactivity became negative. Absence of MK in the normal brain was verified both by immunohistochemical staining and Western blotting. The induced expression of MK is an early event: increased expression of glial fibrillary acidic protein (GFAP), a marker of astrocytes, started on day 4 and continued to day 14. These findings suggest that MK is produced around the site of nerve damage and plays a role as a reparative neurotrophic factor during the early phase of cerebral infarct.

Animals↗
PubMed1991

An improved photochemical model of embolic cerebral infarction in rats.

To provide further evidence that the multiple cerebral infarcts found in rats following photochemical damage to the carotid artery are caused by emboli and to eliminate the systemic hypotension and heating of the blood reported with the previous photochemical embolic stroke model (rose bengal and a green laser), I have modified the photochemical technique. Brain pathology was studied in 18 Wistar rats following carotid artery irradiation with a red laser (632 nm) at powers ranging from 100 to 800 mW/cm2 for 10 or 20 minutes following the injection of the photosensitizing dye Photofrin II. Multiple cerebral arterioles were occluded by platelet aggregates containing frequent erythrocytes and leukocytes, identical to the thrombotic material in the carotid artery but different from the platelet aggregates seen in the carotid artery and the brain in the rose bengal model. Eighty infarcts were distributed randomly throughout the brain ipsilateral to the nonocclusive carotid thrombus. Significant heating (0.5 degree C or more) of the blood occurred only with laser powers higher (1,600 mW/cm2) or laser irradiations longer (25 minutes) than those used in the improved model of embolic stroke. This model mimics one mechanism of stroke in humans and provides a means to study systematically the morphological evolution of small cerebral infarcts.

Animals↗
PubMed1985

Factors influencing return to work following cerebral infarction.

A study of 379 patients, employed before cerebral infarction and living one year afterward, was undertaken to determine what factors had influenced their returning to work. We found age, occupation, degree of disability, race, and hemisphere infarcted to be significant. Younger patients with less disability were more likely to return to work. Patients employed in professional-managerial positions were more likely to return to work than patients in blue-collar or farming positions. Although there were no racial differences following a left-hemisphere infarct, white patients were more likely to return to work following a right-hemisphere infarct. Sex, blood pressure, severity of stroke, educational level, consciousness level at admission, maximum weakness in extremities, first v repeated stroke, care by a specially trained stroke team, rehabilitation therapy, and speech did not additionally influence the probability of returning to work.

Age Factors↗
PubMed1996

Aspirin improves the enhanced erythrocyte aggregability in patients with cerebral infarction.

We examined the effect of aspirin on the enhanced erythrocyte aggregability in 19 patients with cerebral infarction during the chronic phase. Aspirin (81 mg/day) was administered for 8 weeks. The rate of erythrocyte aggregation (aggregability) was measured using the whole-blood erythrocyte aggregometer developed by us (Am. J. Physiol. 251, H1205-H1210, 1986) before, and at 4 and 8 weeks after initiation of the aspirin administration. Concomitant measurements were made of certain blood factors such as the hematocrit, albumin-globulin (A/G) ratio and fibrinogen concentration. The erythrocyte aggregation rates before, and at 4 and 8 weeks were 0.154 +/- 0.019/s, 0.144 +/- 0.020/s, and 0.143 +/- 0.020/s, respectively. The erythrocyte aggregation rates at 4 and 8 weeks were significantly (P < 0.05, Bonferroni's modified t-test) lower than that before aspirin administration. Although the hematocrit value and A/G ratio were not changed at 4 and 8 weeks after the initiation of aspirin, the concentration of fibrinogen were significantly (P < 0.05) reduced at 4 weeks. The above results suggest that aspirin can improve the enhanced erythrocyte aggregability in patients with cerebral infarction during the chronic phase.

Adult↗