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PubMed2004

[Experimental study on the proliferation and plasticity of neural stem cells in situ in adult rats after cerebral infarction].

OBJECTIVE: To investigate the proliferation and plasticity of neural stem cells in situ in adult rats after cerebral infarction. METHODS: Cerebral infarction models of rats were made and the dynamic expression of bromodeoxyuridine (BrdU) and BrdU/polysialylated neural cell adhesion molecule (PSA-NCAM) were determined by immunohistochemistry and immunofluorescence staining. RESULTS: Compared with the controls, the number of BrdU-positive cells in the subventricular zone (SVZ) and hippocampus increased strikingly at day 1 (P < 0.05), reached maximum at day 7, and decreased markedly at day 14, but it was still elevated compared with that of the controls (P < 0.05); The number of BrdU-labeled with PSA-NCAM-positive cells increased strikingly at day 7 (P < 0.05), reached maximum at day 14, and markedly decreased at day 28, but it was still elevated compared with that of the controls (P < 0.05), and was equal to 60% of the number of BrdU-positive cells in the same period. CONCLUSIONS: Our results indicate that cerebral infarction stimulate the proliferation of inherent neural stem cells in situ and most proliferated neural stem cells represent neural plasticity.

Animals↗
PubMed2003

[Lipoprotein (a) and cerebral infarction in young adults].

OBJECTIVE: To investigate the relation between lipoprotein (a) (LP(a)) and cerebral infarction in young adults. METHODS: Serum LP(a) of 90 young adults (age below 45 years) with cerebral infarction was measured. Serum lipids include triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein A-I (ApoA-I) and apolipoprotein B (ApoB) were also measured. Other possible risk factors such as hypertension, smoking, drinking and family stroke history were reviewed. RESULTS: There was no significant difference of serum LP(a) value between stroke patients and controls. TG (P < 0.01) and ApoB (P < 0.01) values in patients with cerebral infarction were significant higher than those in controls. Lipoprotein (a) was correlated with total cholesterol and low density lipoprotein cholesterol, with the values of correlation coefficient (r) 0.28 and 0.23 (both P < 0.01). After adjustment for age, sex, hypertension, smoking, drinking alcohol, family stroke history and other serum lipids, the odd radio for LP(a) and cerebral infarction was 0.74 (95% CI: 0.27 - 1.98). The odd radio for elevated TG was 3.57 (95% CI: 1.34 - 9.49); The odd ratios for hypertension, heart diseases and smoking as risk factors for cerebral infarction in young patients showed as: hypertension OR = 8.18, 95% CI: 2.54 - 26.33; heart diseases: OR = 8.51, 95% CI: 2.27 - 31.85; smoking: OR = 3.21, 95% CI: 1.27 - 8.13. CONCLUSION: LP(a) might not be a risk factor for cerebral infarction in young patients while elevated triglyceride, hypertension, heart diseases and smoking were important risk factors in young adults with cerebral infarction.

Adult↗
PubMed2005

[The use of magnetic resonance and MR angiography in the detection of cerebral infarction--a complication of pediatric bacterial meningitis].

BACKGROUND: Association of both cerebral infarction and acute bacterial meningitis is more common in younger patients than in the elderly. The rate of mortality and the frequency of sequela are very high inspite of the use of modern antibiotic therapy. In more than 30% of the cases of childhood bacterial meningitis, both arterial and venous infarctions can occur. The aim of this study was to present the role of the use of magnetic resonance (MRI), and MR angiography (MRA) in the detection of bacterial meningitis in children complicated with cerebral infarctions. METHOD: In the Centre for MR, the Clinical Centre of Serbia, 25 patients with the diagnosis of bacterial meningitis, of which 9 children with cerebral infarction whose clinical condition deteriorated acutely, despite the antibiotic therapy, underwent MRI and MR angiography examination on a 1T scanner. Examination included the conventional spin-echo techniques with T1-weighted saggital and coronal, and T2- weighted axial and coronal images. Coronal fluid attenuated inversion recovery (FLAIR) and the postcontrast T1-weighted images in three orthogonal planes were also used. The use MR angiography was accomplished by the three-dimensional time-of-flight (3D TOF) technique. RESULTS: The findings included: multiple hemorrhagic infarction in 4 patients, multiple infarctions in 3 patients, focal infarction in 1 patient and diffuse infarction (1 patient). Common sites of involvement were: the frontal lobes, temporal lobes and basal ganglia. The majority of infarctions were bilateral. In 3 of the patients empyema was found, and in 1 patient bitemporal abscess was detected. In 8 of the patients MR angiography confirmed inflammatory vasculitis. CONCLUSION: Infarction is the most common sequela of severe meningitis in children. Since the complication of cerebral infarction influences the prognosis of meningitis, repetitive MRI examinations are very significant for the evaluation of the time course of vascular involvement. The use of MRI, especially FLAIR imaging, confirmed its value in the detection and determination of the site and the extent of cerebral infarction. Non-invasive technique of examination, 3D TOF MR angiography clearly shoud show the presence of inflammatory vasculitis.

Brain↗
PubMed1995

Temperature extremes and mortality from coronary heart disease and cerebral infarction in elderly Chinese.

We studied the relation between outdoor temperature and mortality rates from cardiovascular disease in Taiwan from 1981 to 1991. In 11 years, there were 30,085, 21,750, and 39,818 deaths from coronary artery disease, cerebral infarction, and cerebral haemorrhage, respectively, among 7.6 million residents aged 25 and over in selected areas where climate was recorded. A temperature-mortality relation was especially apparent in the elderly. A U-shaped relation was observed between temperature and mortality from coronary artery disease and cerebral infarction. The range corresponding to least deaths from coronary artery disease (26-29 degrees C) and cerebral infarction (27-29 degrees C) was higher than that in countries with colder climates. In the elderly, the risk of cerebral infarction at 32 degrees C was 66% higher than that at 27-29 degrees C; the risk increased by 3.0% per 1 degree C reduction from 27-29 degrees C. The risk of coronary artery disease at 32 degrees C was 22% higher than that at 26-29 degrees C; below 26-29 degrees C, the risk increased by 2.8% per 1 degree C reduction. Mortality from cerebral haemorrhage decreased with increasing temperature at a rate of 3.3% per 1 degree C. These results imply a pathophysiological difference between thromboembolic and haemorrhagic cardiovascular diseases. Poor thermoregulation in older people may precipitate cardiovascular disease events.

Adult↗
PubMed1998

Effect of prostaglandin E1 on cerebral blood flow in patients with chronic cerebral infarction.

The effect of prostaglandin E1 (PGE1) on cerebral blood flow (CBF) was studied in 10 patients with chronic cerebral infarction. Regional cerebral blood flow (rCBF) was measured by single photon emission computed tomography before and after they received PGE1 120 microg daily for 2 weeks. The rCBF of the brainstem, cerebellum, and frontal, temporal, and parietal lobes increased significantly after PGE1 administration. PGE1 also significantly increased the rCBF of the non-infarcted area adjacent to infarction. The results indicate that PGE1 increases the CBF of patients with chronic cerebral infarction without causing the intracerebral steal phenomenon.

Aged↗
PubMed1995

Cerebral infarction in Alzheimer's disease is associated with severe amyloid angiopathy and hypertension.

OBJECTIVE: To determine if severe cerebral amyloid angiopathy (AA) in patients with Alzheimer's disease (AD) is associated with an increased prevalence of cerebral infarction diagnosed at autopsy. Amyloid angiopathy is increasingly recognized as a cause of ischemic infarcts, as well as cerebral hemorrhages. However, the relationship of AA to cerebral infarction in patients with AD is uncertain. DESIGN: Retrospective clinicopathological study of autopsy-confirmed cases of AD. PATIENTS: One hundred forty-five deceased patients with AD confirmed at autopsy. MAIN OUTCOME MEASURES: Semiquantitative scores of AA severity were done in four brain regions: midfrontal, inferior parietal, superior temporal, and hippocampal. The finding of cerebral infarction at autopsy was modeled as a function of AA severity, hypertension, age at death, AD severity, and sex in chi 2 and multiple logistic regression analyses. RESULTS: Severe AA was significantly associated with cerebral infarction at autopsy in patients with AD (odds ratio [OR], 3.5; 95% confidence interval [CI], 1.4 to 8.9). None of the other independent variables in the multiple logistic regression analysis were significant predictors. While hypertension was equally common in the severe and mild AA subgroups, the combination of both severe AA and hypertension interacted to increase the risk of infarction (OR, 14.2; 95% CI, 3.2 to 63.4) beyond that observed with hypertension (OR, 1.1; 95% CI, 0.4 to 3.2) or severe AA (OR, 1.3; 95% CI, 0.3 to 5.3) alone. CONCLUSIONS: Severe AA is associated with an increased frequency of cerebral infarction in patients with AD. This appears to be largely due to an interaction between severe AA and hypertension that may produce multiplicative injuries on the vasculature. Further study with regard as to how AA may cause ischemia and its role in the neuropathologic and clinical progression of AD is needed.

Aged↗
PubMed2000

[An autopsy case of catastrophic antiphospholipid syndrome presenting with recurrent multiple cerebral infarction associated with lung cancer].

We reported an autopsy case of cerebral infarction with primary lung cancer. The patient was a 50-year-old man. Despite having been treated with warfarin potassium and ticlopidine hydrochloride, he relapsed cerebral infarction. His laboratory data on admission showed that lupus anticoagulant was positive, together with a high value of beta-thromboglobulin, thrombin-antithrombin III complex, markers of platelet and coagulation activation, CEA and CA 19-9. The autopsy finding revealed a primary papillary adenocarcinoma in the right lower lung, multiple cerebral infarction, renal infarction, pulmonary infarction and splenic infarction. The atherosclerotic changes were mild in the whole tissues and findings of vasculitis were not observed. Recurrence of cerebral infarction was effectively suppressed with the addition of steroid therapy to antithrombotic therapy. This case was considered as catastrophic antiphospholipid syndrome. It is necessary to differentiate antiphospholipid syndrome in case of the abnormal coagulation and fibrinolytic factors with recurrent cerebral infarction. Moreover, systemic examinations are important, because malignant tumor may exist on the background of the case.

Adenocarcinoma, Papillary↗
PubMed2003

Raised plasma oxidised LDL in acute cerebral infarction.

BACKGROUND: The association between oxidised low density lipoprotein (OxLDL) and cerebral infarction is suspected but not established. OBJECTIVES: To determine whether plasma OxLDL is a useful marker for monitoring oxidative stress in stroke patients. METHODS: Plasma OxLDL concentrations were determined in 56 stroke patients with cerebral infarction (n = 45) or cerebral haemorrhage (n = 11), and in 19 age matched controls, using a novel sandwich enzyme linked immunosorbent assay. RESULTS: Compared with the controls (0.130 (0.007) ng/ micro g LDL, mean (SEM)), OxLDL was significantly raised in patients with cerebral infarction (0.245 (0.022); p < 0.0001) but not in those with haemorrhage (0.179 (0.023)). Patients with cortical ischaemic infarcts (n = 22) had higher OxLDL levels than either the controls (p < 0.0001) or the patients with non-cortical ischaemic infarcts (n = 23) (p < 0.001). Increased OxLDL concentrations in patients with cortical infarcts persisted until the third day after stroke onset. The National Institutes of Health stroke scales in patients with cortical infarction were higher than in those with non-cortical infarction (p < 0.01). CONCLUSIONS: There is a significant association between raised plasma OxLDL and acute cerebral infarction, especially cortical infarction. Plasma OxLDL may reflect oxidative stress in stroke patients.

Acute Disease↗
PubMed2001

Cerebroprotective action of a Na+/Ca2+ channel blocker NS-7. I. Effect on the cerebral infarction and edema at the acute stage of permanent middle cerebral artery occlusion in rats.

The effect of a novel Na+/Ca2+ channel blocker NS-7 [4-(4-fluorophenyl)-2-methyl-6-(5-piperidinopentyloxy)pyrimidine hydrochloride] on the cerebral infarction, edema and brain energy metabolism was investigated in rats after permanent middle cerebral artery occlusion (MCAO). The infarction and brain water content were evaluated at 48 h and 24 h after MCAO, respectively. A single bolus injection of NS-7 (0.03125-0.25 mg/kg) immediately after MCAO produced a dose-dependent reduction in the infarct volume as well as edema both in the cerebral cortex and striatum. Glycerol (4 g/kg) also decreased water content both in the occluded and non-occluded brain, but it did not reduce the size of cerebral infarction. Unlike glycerol, NS-7 did not change the water content in non-occluded brain. Moreover, a significant protective action was still observed even when NS-7 was injected once at 12 h after occlusion. In addition, NS-7 significantly reversed the decrease in tissue ATP content observed at 3 h but not at 0.5 h after MCAO. These findings suggest that a Na+/Ca2+ channel blocker NS-7 protects cerebral tissues against ischemic insults by improving the disturbance of cerebral energy metabolism and suppressing the cerebral edema.

Adenosine Diphosphate↗
PubMed1996

[Cerebral infarctions in a drug addict inhaling heroin].

Cerebral infarcts complicating heroin abuse have been seldom reported and only clinically and radiologically documented. We report a pathological case of cerebral infarct in a heroin sniffer. A 31 year old, male, heroin sniffing addict for several years, with no known past neurological history, was found dead one morning. The evening before, he had presented the usual signs of recent heroin intake. Opiates were found in large amounts in blood and urine. Post mortem HIV serology was negative. Post mortem examination revealed the usual signs of heroin addiction, but no cutaneous signs of IV drug use. Myocardial ischemic lesions of various ages involved the anterolateral part of the left ventricle; coronary arteries were normal. Neuropathological study revealed, partly cystic infarcts involving both cerebral hemispheres. They were mostly cortical with an intralaminar pattern and a watershed distribution at the boundaries between the territories of the anterior and middle cerebral arteries and the middle posterior cerebral arteries. Intracerebral vessels, large intracranial and cervical arteries were normal.

Administration, Inhalation↗
PubMed1997

Inhibition of collagen-induced platelet aggregation by argatroban in patients with acute cerebral infarction.

Platelet aggregation induced by collagen is enhanced in patients with cerebral thrombosis [1], and platelet aggregates and activation products such as beta-thromboglobulin appear in the circulation, particularly during the acute phase [2]. It is known that the presence of activated platelets markedly amplifies thrombin generation by the prothrombinase complex. Platelet aggregation, for which thrombin is the most potent stimulator, is effected by the activation of the thrombin receptor. Activated platelets likely provide the principal surfaces on which intrinsic coagulation factors and prothrombinase assemble in vivo. Moreover, the blood coagulation cascade is simultaneously enhanced during the acute phase of cerebral infarction, resulting in thrombin production and fibrin formation [3]. Cerebral arterial thrombosis is thought to be initiated by rupture of atherosclerotic plaque. Platelets adhere to the constituents of the plaque, and platelet aggregation and the formation of thrombin occur rapidly. The presence of activated platelets involving thrombin generation in cerebral infarction remains to be further clarified. The present study in patients with acute cerebral infarction was undertaken to determine whether argatroban, a direct thrombin inhibitor, is effective in inhibiting collagen-induced platelet aggregation. It is well known that argatroban inhibits not only thrombin cleavage of fibrinogen with a Ki of 19 nM, but also thrombin-mediated platelet activation with a Ki of 40 nM [4]. We evaluated whether the sensitivity of platelets to collagen is increased in the presence of a trace amount of thrombin associated on platelets, at a concentration that does not induce platelet aggregation in acute cerebral infarction. The study also measured the inhibitory effect, if any, of the addition of argatroban during platelet hyperactivation induced by collagen.

Acute Disease↗
PubMed2003

[Expression of urokinase-type plasminogen activator and its receptor in plasma of patients with cerebral infarction].

OBJECTIVE: To measure the urokinase-type plasminogen activator (UPA) and its receptor (UPAR) in the plasma of patients with cerebral infarction and to study the effects of UPA and UPAR on cerebral infarction. METHODS: ELISA sandwich method was used to measure the plasma levels of UPA and UPAR in 89 patients with acute cerebral infarction, subdivided into mild, moderate and severe subgroups according to the modified Edinburgh-Scandinavia stroke scale (mESSS), and 30 patients with other disease and 30 healthy persons as controls. RESULTS: Within 2 days after the onset of cerebral infarction the UPA and UPAR levels were (1663.7 +/- 384.2) ng/L and (1 375.3 +/- 303.0) ng/L respectively, both significantly higher than those of the patients with other diseases [(1 033.0 +/- 122.7) ng/L and (978.3 +/- 120.0) ng/L respectively (P = 0.038 and P = 0.000)] and those of the normal control group [(1 005.0 +/- 128.9) ng/L and (904.7 +/- 158.6) ng/L respectively, both P = 0.000]. Two weeks after the onset of stroke, the plasma UPA level was (1 185.5 +/- 384.6) ng/L, not significantly different from those of the 2 control groups (both P > 0.05); while the plasma UPAR level in the cerebral infarction was (1 159.3 +/- 261.2) ng/L, significantly higher than those in the 2 control groups (P < 0.01). Within 2 days after the onset of infarction the plasma UPA and UPAR levels of the severe subgroup were (1 938.9 +/- 256.5) ng/L and (1 510.8 +/- 378.7) ng/L respectively, both significantly higher than those of the moderate subgroup [(1 593.7 +/- 204.8) ng/L and (1 296.6 +/- 151.2) ng/L respectively, both P < 0.01] and those of the mild subgroup [1 358.5 +/- 175.9] ng/L and (1 226.8 +/- 98.3) ng/L respectively, both P < 0.01], Two weeks after the onset of stroke,the plasma UPA and uPAR levels of the severe subgroup remained significantly higher than those of the mild subgroup [(1 152.6 +/- 170.3) ng/L vs (1 041.9 +/- 187.0) ng/L, (P < 0.05)] and [(1 186.4 +/- 158.3) ng/L vs (1 053.9 +/- 109.4) ng/L, (P < 0.01)]. In addition, the plasma UPA and UPAR levels of the patients who died from cerebral infarction at last were the highest among all the groups. CONCLUSION: The plasma levels pf UPA and UPAR increase in patients with cerebral infarction and may be related with the severity of disease. The UPA and UPAR genes may play an important role via proteolytic degradation of the extracellular matrix and basement membrane during the development of cerebral infarction.

Aged↗
PubMed2006

Different additional risk factors for cerebral infarctions associated with the factor V Leiden mutation in a family.

Several cases with cerebral infarctions associated with the factor V Leiden mutation have been reported. However, bearing in mind the large number of asymptomatic individuals with the factor V Leiden mutation, additional risk factors for cerebral infarctions should be considered. In this report, two siblings with cerebral infarctions associated with a combination of heterozygous factor V Leiden mutation and different additional exogenous and endogenous thrombogenic risk factors are described. Respiratory problems in the perinatal period and increased lipoprotein (a) concentrations in the first patient and an episode of gastroenteritis from Shigella infection and persistent high titers of serum anticardiolipin and beta(2)-glycoprotein I antibodies in the second patient were recorded as additional thrombogenic risk factors. Furthermore, both patients were found to be heterozygous for the methylenetetrahydrofolate reductase gene C677T mutation. These findings suggest that even in the same family, different additional thrombogenic risk factors can be present in infants with cerebral infarctions associated with the factor V Leiden mutation. An extensive search of additional circumstantial and genetic thrombogenic risk factors should be useful for prophylaxis and prognosis of these infants with cerebral infarctions associated with the factor V Leiden mutation and of their related family members. To our knowledge, the second patient in this study is the first patient reported to have cerebral infarctions associated with the combination of the factor V Leiden mutation and persistent high titers of serum beta(2)-glycoprotein I antibodies.

Adult↗
PubMed1997

[Change of serum soluble vascular cell adhesion molecule-1 in patients with acute cerebral infarction and its clinical significance].

The aim of this study is to characterize the pattern of release of soluble vascular cell adhesion molecule-1 (sVCAM-1) in patients with acute cerebral infarction. The level of serum sVCAM-1 was measured serially with two-layer antibody sandwich enzyme-linked immunosorbent assay (ELISA) in 89 patients with acute cerebral infarction, 43 patients with cerebral haemorrhage and 30 normal controls. It is shown that the level of serum sVCAM-1 in patients with cerebral infarction 24 hours after the onset was higher than that in patients with cerebral haemorrhage and normal controls (P < 0.01). The level of serum sVCAM-1 was significantly higher in the patients with large cerebral infarction than that in patients with medium and small cerebral infarctions (P < 0.01). The level of serum sVCAM-1 in patients with cerebral infarction increased from 24 hours to 7 days and decreased from 7 days to 14 days, but it was still higher than that in patients with cerebral haemorrhage and normal controls on the 14th day. The level of serum sVCAM-1 was higher in patients with infection as compared with those without. These findings suggested that sVCAM-1 is closely related to the development of acute cerebral infarction. It is essential to have further study on the change of serumsVCAM-1 in cerebral infarction.

Aged↗
PubMed2002

Experience with 123I-iomazenil SPECT in acute cerebral infarction.

Neuronal cells are susceptible to cerebral ischaemia. As gamma-aminobutyric acid(A) (GABA(A)) receptors are specific for neurones, functional receptor imaging using I-iomazenil (IMZ), a ligand to the GABA benzodiazepine receptor, has been proposed as an imaging modality for the assessment of neuronal integrity. However, there is only limited experience with IMZ in patients with acute cerebral infarction. Therefore, the aim of this study was to evaluate IMZ single photon emission computed tomography (SPECT) in patients with acute cerebral ischaemia. IMZ SPECT was performed in 21 patients with acute cerebral infarction 7-10 days after stroke onset. Eleven patients underwent systemic thrombolysis within 6 h after symptom onset (group 1), whereas 10 patients were treated conservatively (group 2). IMZ (150-200 MBq) was injected intravenously and imaging was performed using a dedicated four-head SPECT camera at 5 min (perfusion) and 90 min (receptor distribution) post-injection, with an acquisition time of 50 min each. Images were analysed by visual inspection. Four patients showed normal IMZ distribution, and 17 patients showed abnormalities of IMZ uptake on both early and late images. In six patients with regional uptake deficits, a crossed cerebellar diaschisis was observed on early images. Cerebellar inhomogeneity of tracer uptake was absent at the time of late images in all six patients. In eight patients, areas of hypoperfusion corresponded exactly to the regions of receptor deficiency (match). In five patients, preserved neuronal integrity was present in hypoperfused areas (mismatch). In four patients, normally or even hyperperfused areas exhibited regional receptor deficiency (inverse mismatch). In conclusion, IMZ SPECT demonstrated differences between regional perfusion and receptor distribution in about one-half of patients 7-10 days after acute cerebral ischaemia. Interesting patterns between the early phase (perfusion) and the late phase (receptor distribution) were found. These patterns are indicative of the heterogeneous development of cerebral ischaemia where, even days after stroke onset, areas of hypoperfusion but preserved neuronal integrity may be present. However, the evaluation of the potential clinical and therapeutic impact of individual IMZ distribution patterns requires further investigation.

Adult↗
PubMed2003

RNA synthesis in pons necessary for maintenance of bladder overactivity after cerebral infarction in rat.

PURPOSE: The maintenance of long lasting bladder overactivity caused by cerebral infarction is believed to require transcription in the pontine micturition center. Therefore, we examined the influence of the RNA synthesis inhibitor actinomycin D (Banyu Pharmaceutical Co., Ltd., Tokyo, Japan) on bladder overactivity induced by left middle cerebral artery occlusion. MATERIALS AND METHODS: Rats under halothane anesthesia were injected with actinomycin D or vehicle (mannitol) into the bilateral dorsal pontine tegmentum, followed by middle cerebral artery occlusion. Awake rats were cystometrically examined for 12 hours. The expression of c-fos and zif268 mRNA in the dorsal pontine tegmentum was monitored with real-time polymerase chain reaction. RESULTS: Injection of actinomycin D produced a significant decrease in bladder capacity in sham operated rats but bladder capacity returned to control levels before sham operation within 6 hours. In cerebral infarcted rats pretreated with vehicle bladder capacity was significantly decreased after middle cerebral artery occlusion and it remained consistently below half of pre-occlusion capacity. Actinomycin D blocked the decrease in bladder capacity in cerebral infarcted rats. In actinomycin D treated cerebral infarcted rats bladder capacity gradually recovered and returned to the control level before middle cerebral artery occlusion within 10 hours. Actinomycin D suppressed an increase in c-fos mRNA expression 1 hour after middle cerebral artery occlusion as well as in zif268 3 hours after occlusion. Administering actinomycin D 0.5 or 1 hour after middle cerebral artery occlusion also suppressed bladder overactivity until at least 10 hours after occlusion but injection 3 hours after occlusion did not. CONCLUSIONS: These results indicate that an RNA synthesis inhibitor can prevent a late stage of bladder overactivity. Transcription in the dorsal pontine tegmentum was found to be necessary to maintain the long lasting bladder overactivity caused by cerebral infarction.

Animals↗
PubMedDate not supplied

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

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

Animals↗
PubMed1997

Large cerebral infarction during praziquantel therapy in neurocysticercosis.

BACKGROUND: Large cerebral infarction is a rare complication of neurocysticercosis. Endarteritis by inflammation of the leptomeninges is known to be its cause. CASE DESCRIPTION: A 59-year-old man with known neurocysticercosis developed a large cerebral infarction during praziquantel therapy. A follow-up MRI obtained immediately after his cerebral infarction demonstrated notable decrease in the size of the cysts and more prominent enhancement around the peripheral margins of the cysts and the major vessels in comparison with the initial MRI. Cerebral angiography disclosed occlusions and narrowing of both internal carotid arteries at the supraclinoid portions, where multiple cysts were found on the MRI. CONCLUSIONS: Findings in our patient strongly suggest that a secondary inflammation reaction caused by the destruction of the cysts might have enhanced the process of endarteritis. The possible deleterious effects of praziquantel therapy should be considered in the treatment of patients with subarachnoid cysticerci.

Antiplatyhelmintic Agents↗