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PubMed1989

[Anesthetic management of elderly patients in open heart surgery].

In the National Cardiovascular Center, 46 patients whose ages were above 70 underwent open heart surgery from 1977 to 1986. Twenty of them received AC bypass and 5 had repair of the rupture of ventricular septum or left ventricular aneurysm. Among them 2 had also insertion of left ventricular assist device because of acute myocardial infarction (MI). Eighteen underwent mitral and/or aortic valve replacement. The other 3 were operated on because of atrial myxoma etc. Preoperatively, in ischemic heart disease group, due to resultant heart failure, one third of the patients were given catecholamines. In valvular heart disease group, angina pectoris and old MI were also common. Beside arrhythmias, respiratory complications, renal dysfunction and diabetes mellitus, neurological complications such as brain infarction were prominent in both groups. Hospital mortality was 15% in AC bypass group, 40% in acute MI group and 11.1% in VHD group. In 36 patients who left hospital, mean NYHA class improved after operation. The mortality rate and symptomatic improvement demonstrate that cardiac surgery can be performed with acceptable risk in elderly patients. Anesthesiologists should manage them carefully, considering the problems stated above.

Aged↗
PubMed1998

Myelin degeneration in multiple system atrophy detected by unique antibodies.

A rabbit antiserum (anti-EP), induced against a synthetic peptide corresponding to residues 68 to 86 of guinea pig myelin basic protein, powerfully immunostained abnormal-appearing oligodendrocytic processes and cell bodies in demyelinating areas associated with multiple system atrophy (MSA). However, as we reported previously, the antiserum, which is highly specific for the sequence QDENPVV corresponding to human myelin basic protein residues 82 to 88, failed to recognize any structures in normal human brain. QD-9, a mouse monoclonal antibody raised against human myelin basic protein residues 69 to 88, which also recognizes specifically the epitope QDENPVV, gave the same results as did anti-EP. The unusual epitope recognized by anti-EP/QD-9 antibodies appears to be accessible in areas of myelin degeneration, and the antibodies have been shown to detect such areas in multiple sclerosis and infarcted brains. These antibodies detect myelin degeneration more widely than previous conventional methods. The present study emphasizes the importance of myelin degeneration in the pathogenesis of multiple system atrophy.

Aged↗
PubMed2003

Poly(ADP-ribose) polymerase as a key player in excitotoxicity and post-ischemic brain damage.

Poly(ADP-ribose) polymerases (PARPs) are a group of protein-modifying and nucleotide-polymerizing enzymes able to catalyze the transfer of multiple ADP-ribose units from NAD to substrate proteins. In the human genome, 16 different genes encoding for members of this emerging family of enzymes have been identified. Known family members are PARP-1, PARP-2, PARP-3, vPARP, tankyrase 1 and tankyrase 2, each of them with a possible specific role in cell biology. The most studied member of the family is PARP-1, which is abundantly present in the nucleus and is involved in the maintenance of genomic stability. In pathological conditions, highly reactive radical species may cause DNA damage and PARP-1 hyperactivation. This may lead to necrotic cell death through massive NAD consumption. We show that following middle cerebral artery occlusion, rats treated with PARP inhibitors displayed reduced brain infarct volumes. Similarly, PARP inhibitors reduced neuronal death induced by oxygen-glucose deprivation (OGD) or excitotoxins in primary cultures of murine cortical cells. On the contrary, PARP inhibitors did not attenuate the OGD-induced selective loss of CA1 pyramidal cells in rat organotypic hippocampal slices. In addition, they were not neuroprotective against transient bilateral carotid occlusion in gerbils. We observed that post-ischemic brain damage was predominally necrotic in cultured cortical cells, whereas a caspase-dependent apoptotic process was responsible for the CA1 pyramidal cell loss in hippocampal slices. Hence, it appears reasonable to propose PARP inhibitors as useful therapeutic agents in pathological brain conditions were necrosis predominates.

Animals↗
PubMed1986

[Ergotism with cerebral complications. Case report and review of the literature].

Abuse of ergotamine-containing suppositories was followed by generalized vessel stenoses in a pregnant 29-year-old migraine patient and led to a space-occupying great brain infarction in the area supplied by the right internal carotid artery. Impressive improvement of clinical, computed tomography and ultrasound findings was observed during treatment with nimodipine. The literature about cerebral symptoms of ergotism is reviewed.

Adult↗
PubMed2005

Ischemic preconditioning procedure induces behavioral deficits in the absence of brain injury?

Preconditioning describes a phenomenon whereby a sub-injury inducing insult can protect against a later larger injury. Thus, short-term cerebral ischemia can protect against a prolonged ischemia (ischemic preconditioning). This study examines rats undergoing ischemic preconditioning to test whether preconditioning may cause changes in behavior even though they do not cause an identifiable brain lesion. Rats had a transient (15 minutes) middle cerebral artery occlusion or a sham occlusion. Forelimb placing and forelimb use asymmetry tests were used to assess behavioral deficits. Brain histology, microglia activation, heat shock protein and ferritin levels were also examined. Ischemic preconditioning did not cause brain infarction, but induced behavioral changes. There were no significant differences between ischemic preconditioning and sham rats in the two behavioral tests at day one. However, the ischemic preconditioning group showed impaired forelimb placing at days 3, 7 and 14 (p<0.05). That group also had a significant (p<0.05) behavioral deficit in the forelimb use asymmetry test at days 3 and 7 (but not 14). Our present study demonstrated that a behavioral deficit occurred in ischemic preconditioning. This raises the question of whether induction of protective mechanisms by preconditioning stimuli necessarily involves some form of brain injury, detectable by changes in behavior though not by a lesion. This would be consistent with data suggesting that brain injury can initiate mechanisms potentially favorable to neuroplasticity and neuroprotection.

Animals↗
PubMed2000

[Hemiparesis as a sequela of traumatic pseudoaneurysm of the carotid bifurcation].

HISTORY AND CLINICAL FINDINGS: A 20-year-old patient was referred to our clinic after sudden onset of a left-sided hemiparesis. His past history revealed a severe trauma 4 years ago, including multiple bone fractures, rupture of the spleen, as well as renal failure, and an acute respiratory distress syndrome, from which he showed good recovery. At that time no central-nervous symptoms could be found. However, eighteen months ago, he complained about a transient weakness of his left arm and leg. INVESTIGATIONS: Examination of the cerebral arteries by duplex-sonography showed an aneurysm on the bifurcation of the right carotid artery with a peripheral flow-reduction. This could be confirmed by CT- and MR-based angiography, which also revealed a reopened embolic occlusion of the M1-segment of the right middle cerebral artery. On CT and diffusion weighted imaging there was evidence of an ischemic infarction pattern. TREATMENT AND COURSE: Under anticoagulation therapy with heparin the patient showed complete recovery from his symptoms. Duplex-sonography as well as MR-angiography documented a complete reopening of the primarily occluded middle cerebral artery. Finally, surgical reconstruction of the aneurysmatic part of the vessel was done. CONCLUSION: This case illustrates the potential risk of a traumatic aneurysm as a potential source of ischemic brain infarctions. We emphasize the importance of imaging the cerebral arteries in traumatic patients, even in the absence of initial neurological symptom.

Adult↗
PubMed1984

Influence of blood pressure on blood-brain barrier function in brain ischemia.

The influence of systemic blood pressure on blood-brain barrier leakage and hemorrhage in brain ischemia was evaluated in Sprague-Dawley rats with blood pressures at the lower and upper limit normally found in these animals when anesthetized on 70% N2O:30% O2. 24 h after unilateral cerebral microembolization - when significant increases in water content and barrier permeability and decrease in blood flow is present - the extravasation of Evans Blue-albumin and inulin as well as hemorrhage in the infarcted brain area was considerably more prominent in animals with the higher blood pressure. The findings imply that attempts to elevate pressure, as well as subacute surgical circulatory reconstruction to increase perfusion of an ischemic area, may be potentially harmful.

Animals↗
PubMed2003

A lignocaine infusion worsens the leukoencephalopathy due to a carbon monoxide exposure in sheep.

Poisoning by carbon monoxide (CO) is common and conventional treatment of affected people is frequently unsuccessful. Lignocaine was identified as a potential therapy in this context because of the benefit shown for it in other brain injuries for which the received toxic mechanisms are similar. Twelve Romney ewes were exposed to 1% CO for 120 min were then infused intravenously with either lignocaine (N=6) or saline for 72 h, and were killed 5 days after the exposure for histological and immunohistochemical examination. This dose of CO was narcotic and caused white matter brain infarcts, with associated glial cell activation, axonal dysfunction and induction of both neuronal and glial haeme oxygenase and nitric oxide synthetase. The frequency of the white matter infarcts was significantly greater in the lignocaine-treated group. The mechanism of this adverse interaction is neither established here nor is it deducible from other published data; alternative antidotes to CO clearly need to be tested.

Animals↗
PubMed1991

MR imaging of intracranial hemorrhage in neonates and infants at 2.35 Tesla.

The variations of the relative signal intensity and the time dependent changing contrast of intracranial hemorrhages on high-field spin-echo magnetic resonance images (MRI) were studied in 28 pediatric patients. For T1-weighted images, a repetition time (TR) of 500 ms and an echo time (TE) of 30 or 23 ms was used. The corresponding times for T2-weighted images were TR 3000 ms and TE 120 ms. Intracranial hematomas, less than 3 days old, were iso- to mildly hypointense on short TR/TE scans and markedly hypointense on long TR/TE scans (acute stage). In the following four days the signal of the hematomas became hyperintense on short TR/TE scans, beginning in the periphery and proceeding towards the center. On long TR/TE scans the signal remained markedly hypointense (early subacute stage). 7-14 days old hematomas were of high signal intensity on short TR/TE scans. On long TR/TE scans they appeared hypointense in the center and hyperintense in the periphery (late subacute stage). By the end of the second week the hematomas were of high signal intensity on all pulse sequences (chronic stage). Chronic hematomas were surrounded by a parenchymal rim of hypointensity on long TR/TE scans. 28 neonates and infants (with 11 follow-up examinations) of 31.5-70.6 weeks postconceptional age (PCA), with an intracranial hemorrhage were examined. The etiologies of the hemorrhages were: asphyxia (17 cases), brain infarct (2), thrombocytopenia (1), clotting disorder (1) and unknown origin (7). The aim of this study was to describe the appearance of intracranial hemorrhages in neonates and infants with MRI at 2.35 Tesla using spine-cho sequences.

Acute Disease↗
PubMedDate not supplied

Vascular pathology in galactosialidosis.

This article immunohistochemically and ultrastructurally examines a brain with galactosialidosis, focusing on the structure of blood vessel endothelium. Lysosomes were observed in the expanded cytoplasm of the endothelial cells, which were vacuolated by light microscopy. Immunoreactivity for CD31, one of the vascular cell adhesion molecules, was minimal to faint in endothelial cells with vacuolations. The loss of CD31 immunoreactivity and breakdown of vascular cell adhesion molecules in vacuolated endothelial cells seem to promote the development of brain infarctions. Moreover, diffuse and various degrees of axonal damage, most likely caused by vascular disorder in cerebral or cerebellar white matter, was reported using the amyloid precursor protein (APP) immunohistochemical method.

Amyloid beta-Protein Precursor↗
PubMed2000

Linguistic ability in early life and the neuropathology of Alzheimer's disease and cerebrovascular disease. Findings from the Nun Study.

Findings from the Nun Study indicate that low linguistic ability in early life has a strong association with dementia and premature death in late life. In the present study, we investigated the relationship of linguistic ability in early life to the neuropathology of Alzheimer's disease and cerebrovascular disease. The analyses were done on a subset of 74 participants in the Nun Study for whom we had handwritten autobiographies completed some time between the ages of 19 and 37 (mean = 23 years). An average of 62 years after writing the autobiographies, when the participants were 78 to 97 years old, they died and their brains were removed for our neuropathologic studies. Linguistic ability in early life was measured by the idea (proposition) density of the autobiographies, i.e., a standard measure of the content of ideas in text samples. Idea density scores from early life had strong inverse correlations with the severity of Alzheimer's disease pathology in the neocortex: Correlations between idea density scores and neurofibrillary tangle counts were -0.59 for the frontal lobe, -0.48 for the temporal lobe, and -0.49 for the parietal lobe (all p values < 0.0001). Idea density scores were unrelated to the severity of atherosclerosis of the major arteries at the base of the brain and to the presence of lacunar and large brain infarcts. Low linguistic ability in early life may reflect suboptimal neurological and cognitive development, which might increase susceptibility to the development of Alzheimer's disease pathology in late life.

Adult↗
PubMed2005

Quantitative measures of gait characteristics indicate prevalence of underlying subclinical structural brain abnormalities in high-functioning older adults.

Abnormal gait in high-functioning older adults may indicate underlying subtle structural brain abnormalities. We tested the hypothesis that temporal and spatial parameters of gait, including speed, stride length and double support time, are cross-sectionally associated with white matter hyperintensity, subcortical infarcts or brain atrophy on brain MRI. We examined 321 men and women (mean age = 78.3) participating to the Cardiovascular Health Study who were free of dementia or stroke at the time of the gait assessment. Analyses were set with gait as independent variable and brain MRIs as dependent variables. Gait measures were determined from the footfalls recorded on a 4-meter-long instrumented walking surface, the GaitMat II. Brain MRIs were examined for the presence of white matter hyperintensity (WMG, graded from 0 to 9), brain infarcts (predominantly subcortical) and ventricular enlargement (graded from 0 to 9). Slower gait, shorter stride length and longer double support times were associated with greater prevalence of white matter grade > or =3 (p = 0.02), and at least 1 brain infarct (p = 0.04) independent of age. In multivariate logistic regression models adjusted for demographics and clinical cardiovascular diseases, those with gait speed <1.02 m/s were more likely to have WMG > or =3 and at least 1 brain infarct, compared with those with faster gait - odds ratio (OR): 2.85, 95% confidence interval (95% CI): 1.35, 6.02, and OR: 2.09, 95% CI: 1.04, 4.19. Shorter stride length was also associated with greater probability of having at least 1 brain infarct (gait stride <0.88 vs. >1.10 m: OR: 3.20, 95% CI: 1.49, 6.88), while longer double support times were associated with a greater probability of having WMG > or =3 (double support time >0.19 vs. <0.14 s: OR: 2.3, 95% CI: 1.1, 4.7) independent of demographics and clinical cardiovascular diseases. Gait parameters were not significantly associated with ventricular grade. In summary, in this group of high-functioning older adults, poorer gait speed, shorter stride and longer double support time are associated with high white matter disease and subclinical strokes.

Aged↗
PubMed2004

Delayed treatment with melatonin enhances electrophysiological recovery following transient focal cerebral ischemia in rats.

Melatonin has been reported to reduce infarct volumes induced by transient middle cerebral artery (MCA) occlusion. We examined whether melatonin could improve electrophysiological and neurobehavioral recoveries in rats after 72 hr of reperfusion following 1.5 hr of MCA occlusion. Melatonin (5 mg/kg) or vehicle was given intravenously at the commencement of reperfusion. Neurobehavioral outcome was serially examined, and somatosensory evoked potentials (SSEP) were recorded prior to ischemia and at 72 hr after the onset of reperfusion. Brain infarction was assessed upon killing. Before ischemia-reperfusion, stable SSEP waveforms were consistently recorded after individual fore- or hindpaw stimulation. The amplitude between the first positive (P1) and the first negative (N1) peaks and the P1 latency did not differ significantly between controls and melatonin-treated animals. At 72 hr of reperfusion, controls had severely depressant SSEPs recorded from ischemic fore- and hindpaw cortical fields, and the amplitudes decreased to 36 and 35% of baselines, respectively (P < 0.001). These animals also had transcallosal electrophysiological diaschisis in the SSEPs recorded at the contralateral hindpaw cortical field (P < 0.01). Relative to controls, melatonin-treated animals not only had significantly improved amplitudes of the SSEPs recorded from both ischemic fore- and hindpaw cortical fields, by 33 and 37% of baselines, respectively (P < 0.001), but also exhibited diminished transcallosal electrophysiological diaschisis following ischemia-reperfusion. In addition, melatonin improved sensory and motor neurobehavioral outcomes by 40 and 28%, respectively (P < 0.001), and reduced cortical and striatal infarct sizes by 32 and 40%, respectively (P < 0.05). Thus, delayed intravenous administration with melatonin both enhances electrophysiological and neurobehavioral recoveries and reduces cortical and striatal infarct sizes after cerebral ischemia and reperfusion injury.

Animals↗
PubMed1999

Idazoxan does not prevent but worsens focal hypoxic-ischemic brain damage in neonatal Wistar rats.

We examined the neuroprotective efficacy of a post-treatment with idazoxan (Idaz): an alpha2-adrenoceptor antagonist with activity at the I1- and I2-subtypes of the imidazoline receptor (I-receptor), in an experimental model of perinatal hypoxic-ischemic (HI) brain damage. Seventy-two, 7-day-old Wistar rats were subjected to permanent unilateral ligation of the common carotid artery and transient (2 hr) hypoxia (8% O(2)). The surviving animals were sub-divided into 3 groups: one "control" group received intraperitoneal (i.p.) injection of saline (Sigma; n = 21) and two "treated" groups received, 10 min post-HI, i.p. treatments with Idaz (I3: 3 mg/kg; n = 19) or (I8: 8 mg/kg; n = 20). Idaz effects were assessed by TTC-staining 72 hr post-HI for Sigma (n = 13), I3 (n = 11), and I8 (n = 12) groups and by MRI-examination 5 weeks post-HI for Sigma (n = 8), I3 (n = 8), and I8 (n = 6) groups. Total ratio of brain infarct areas were significantly (P < 0.01) different between Sigma and Idaz-treated rats: 20.9 +/- 4.0%, 35.6 +/- 5.9 % and 36.8 +/- 5.8% for Sigma, I3 and I8, respectively, when determined with TTC-staining and; 23.3 +/- 3.7%, 39.8 +/- 4.2%, and 43.2 +/- 10.1%, for Sigma, I3, and I8, respectively, when assessed by MRI. Our results suggest that Idaz, given as a post-HI treatment, does not exert neuroprotective effects but enhances the brain injury induced by focal neonatal cerebral HI. The deleterious mechanism may result from an overactivity of sympathetic tone and/or the immaturity of central I-receptors in newborn rats.

Animals↗
PubMed1998

[Invasive therapeutic strategies in the acute phase of ischemic arterial cerebral infarct].

BACKGROUND: Currently to an increasing extent aggressive therapeutic approaches in ischemic stroke are discussed. These approaches include intraarterial and systemic thrombolysis to reduce infarction size and also decompressive surgical measures to prevent from fatal consequences of elevated intracranial pressure. This report gives an overview over these strategies. Their specific values are discussed. STRATEGIES: In acute vertebrobasilar artery occlusion an attempt of intraarterial thrombolysis is indicated because of the mostly poor prognosis of large brainstem infarction. Acute artery occlusion in carotid territory has a better prognosis, so that the indication of intraarterial thrombolysis has to be regarded more critically. In view of recent reports systemic rt-PA-thrombolysis seems to be justified in well defined cases independently from site of occlusion. At present there is no longer doubt about the benefit of decompressive surgery in space occupying cerebellar stroke. The value of surgery in malignant brain infarction in carotid territory is not clear due to date. Further randomised studies are necessary to learn more about benefit, risks and required proceedings in space occupying supratentorial infarction. CONCLUSIONS: A well defined group of patients suffering from ischemic stroke seems to benefit from aggressive therapeutic approaches in ischemic stroke. Concerning the selection of patients and management of those approaches a close cooperation with an experienced center is required.

Cerebral Infarction↗
PubMed2001

A neuroprotective role for gap junctions.

Glial-neuronal interactions have been implicated in both normal information processing and neuroprotection. One pathway of cellular interactions involves gap junctional intercellular communication (GJIC). In astrocytes, gap junctions are composed primarily of the channel protein, connexin43 (Cx43), and provide a substrate for formation of a functional syncytium implicated in the process of spatial buffering in the CNS. Thus gap junctional communication may be neuroprotective following a CNS insult that entails glutamate cytotoxicity (i.e. ischemia). We have shown that blocking gap junctions during a glutamate insult to co-cultures of astrocytes and neurons results in increased neuronal injury. To assess the effect of reduced Cx43 and GJIC on neuroprotection, we examined brain infarct volume in wild type and Cx43 heterozygote null mice following focal ischemia. Cx43 heterozygous null mice exhibited a significantly larger infarct volume compared to wild type. At the cellular level, a significant increase in TUNEL positive cells was observed in the penumbral region of the Cx43 heterozygote mice. These results suggest that augmentation of GJIC in astrocytes may contribute to neuroprotection following ischemic injury. These findings support the hypothesis that gap junctions play a neuroprotective role against glutamate cytotoxicity.

Animals↗
PubMed1991

Cerebrovascular abnormalities in pediatric stroke: assessment using parenchymal and angiographic magnetic resonance imaging.

Three-dimensional (volume) magnetic resonance angiography is a noninvasive technique that images the intracranial and cervical arterial vasculature without contrast agents. Twenty-four children with strokes had combined parenchymal magnetic resonance imaging and magnetic resonance angiography 1 day to 4 years after acute presentation. Eight had had prior intra-arterial angiography. Eighteen magnetic resonance angiographic studies showed arterial stenosis or occlusion in the vascular distribution of magnetic resonance image-defined brain infarction and, in 7 children, in the same location as previously defined abnormalities on intra-arterial angiography. One child had a normal intra-arterial angiogram and magnetic resonance angiogram. The other 5 children with normal magnetic resonance angiographic studies included 3 with presumed embolic disease, 1 with meningitis, and 1 with Crohn's disease-related vasculitis. Collateral flow patterns could be determined in 4 children. Artifact presenting as filling defects in vessels was present in 10 studies, but did not interfere with interpretation of 8 studies. Combined magnetic resonance imaging/magnetic resonance angiography provides a screening technique to evaluate noninvasively brain parenchyma and vasculature in children with suspected large-vessel abnormalities, allowing selection for intra-arterial angiography and serial monitoring of vascular abnormalities over time and during therapeutic intervention.

Anemia, Sickle Cell↗
PubMed2004

Blood rheological properties and lipid peroxidation in cerebral and systemic circulation of neurocritical patients.

The present study was aimed at investigating the red blood cell (RBC) aggregation and the parameters of lipid peroxidation - malondialdehyde (MDA) and MDA + 4-hydroxyalkenals (HAE) - in the blood of critically deteriorated stroke patients (brain infarcts, parenchymatous and subarachnoid hemorrhages) and in the control group. Measurements were made in blood samples from the common carotid artery, the both internal jugular and cubital veins. The RBC aggregation index was found to increase by about 80 per cent in both the cerebral and systemic circulation as compared to the control blood samples. MDA content appeared also significantly higher in the blood flowing out of the damaged hemisphere of the neurocritical patients as compared to the control group. In the blood flowing out of the damaged hemisphere of the neurocritical patients MDA as well as MDA + HAE content significantly exceeded the values found in blood samples of the jugular vein of the contralateral hemisphere, carotid artery and the cubital vein. The results of this study suggest a certain interdependence between the blood plasma lipid peroxidation and the RBC aggregation in the brain vessels following its damage.

Adult↗