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PubMedDate not supplied

Brain ischemia as a potential target of gene therapy.

Brain infarction is one of the most important age-associated medical conditions, and the age-related neuronal vulnerability to brain ischemia is suggested to play an important role. Recent advancements in gene transfer techniques have provided promising approaches to the treatment of brain ischemia. In experimental studies, the ischemic penumbra area can be targeted by gene transfer even after ischemic insult, and post-ischemic gene therapy seems effective in attenuation of ischemic damage in both global and focal brain ischemia. Perivascular approaches of gene transfer to the cerebral blood vessels through the subarachnoid space may lead to prevention of brain ischemia caused by vasospasm after subarachnoid hemorrhage. Gene transfer to cerebral blood vessels and ischemic brain tissue may offer future therapeutic approaches to stroke.

Adenoviridae↗
PubMed2002

Neuroprotective effects of lithium in cultured cells and animal models of diseases.

Lithium, the major drug used to treat manic depressive illness, robustly protects cultured rat brain neurons from glutamate excitotoxicity mediated by N-methyl-D-aspartate (NMDA) receptors. The lithium neuroprotection against glutamate excitotoxiciy is long-lasting, requires long-term pretreatment and occurs at therapeutic concentrations of this drug. The neuroprotective mcchanisms involve inactivation of NMDA receptors, decreased expression of pro-apoptotic proteins, p53 and Bax, enhanced expression of the cytoprotective protein, Bcl-2, and activation of the cell survival kinase, Akt. In addition, lithium pretreatment suppresses glutamate-induced loss of the activities of Akt, cyclic AMP-response element binding protein (CREB), c-Jun - N-terminal kinase (JNK) and p38 kinase. Lithium also reduces brain damage in animal models of neurodegenerative diseases in which excitotoxicity has been implicated. In the rat model of stroke using middle cerebral artery occlusion, lithium markedly reduces neurologic deficits and decreases brain infarct volume even when administered after the onset of ischemia. In a rat Huntington's disease model, lithium significantly reduces brain lesions resulting from intrastriatal infusion of quinolinic acid, an excitotoxin. Our results suggest that lithium might have utility in the treatment of neurodegenerative disorders in addition to its common use for the treatment of bipolar depressive patients.

Animals↗
PubMed2003

Diffusion imaging may predict reversible brain lesions in eclampsia and severe preeclampsia: initial experience.

OBJECTIVE: The purpose of this study was to validate diffusion-weighted magnetic resonance imaging in the prediction of the evolutive course of brain edema and to establish its pathophysiologic presence in patients with eclampsia/severe preeclampsia. STUDY DESIGN: Seventeen patients with a clinical diagnosis of severe eclampsia/preeclampsia and T2 hyperintense brain lesions on routine magnetic resonance imaging were evaluated at hospital admission and 8 weeks later. RESULTS: Brain edema was reversible in 13 patients and irreversible in 4 patients, as indicated on follow-up magnetic resonance imaging. Sixteen of 17 patients were differentiated accurately into reversible and irreversible groups on the basis of diffusion imaging on hospital admission. Diffusion-weighted magnetic resonance imaging demonstrated a significant increase in water mobility in abnormal regions compared with normal-appearing brains in patients in the reversible group (1.34+/-0.10 mm(2) vs 0.79+/-0.08 mm(2)/s x 10(-3), P<.001). In the irreversible group, restricted water diffusion was present, which was consistent with cytotoxic edema and early brain infarction in 3 of 4 patients. CONCLUSION: Diffusion-weighted magnetic resonance imaging can predict successfully the evolutive course of brain edema in an acute setting in these patients. Our findings indicate that brain edema is vasogenic, although ischemic/cytotoxic edema was observed less commonly.

Adolescent↗
PubMed2004

Macrophage imaging in central nervous system and in carotid atherosclerotic plaque using ultrasmall superparamagnetic iron oxide in magnetic resonance imaging.

The long blood circulating time and the progressive macrophage uptake in inflammatory tissues of ultrasmall superparamagnetic iron oxide (USPIO) particles are 2 properties of major importance for magnetic resonance imaging (MRI) pathologic tissue characterization. This article reviews the proof of principle of applications such as imaging of carotid atherosclerotic plaque, stroke, brain tumor characterization, or multiple sclerosis. In the human carotid artery, USPIO accumulation in activated macrophages induced a focal drop in signal intensity compared with preinfusion MRI. The USPIO signal alterations observed in ischemic areas of stroke patients is probably related to the visualization of inflammatory macrophage recruitment into human brain infarction since animal experiments in such models demonstrated the internalization of USPIO into the macrophages localized in these areas. In brain tumors, USPIO particles which do not pass the ruptured blood-brain barrier at early times postinjection can be used to assess tumoral microvascular heterogeneity. Twenty-four hours after injection, when the cellular phase of USPIO takes place, the USPIO tumoral contrast enhancement was higher in high-grade than in low-grade tumors. Several experimental studies and a pilot multiple sclerosis clinical trial in 10 patients have shown that USPIO contrast agents can reveal the presence of inflammatory multiple sclerosis lesions. The enhancement with USPIO does not completely overlap with the gadolinium chelate enhancement. While the proof of concept that USPIO can visualize macrophage infiltrations has been confirmed in animals and patients in several applications (carotid atherosclerotic lesions, stroke, brain tumors and multiple sclerosis), larger prospective clinical studies are needed to demonstrate the clinical benefit of using USPIO as an MRI in vivo surrogate marker for brain inflammatory diseases.

Arteriosclerosis↗
PubMedDate not supplied

[Level of monohydroxyeicosatetraenoic acid in the blood of patients with cerebral blood circulation disorders].

Content of 5-, 8-, 11-, 12- and 15-monohydroxyeicosatetraenoic acids was markedly increased in blood of patients with cerebral atherosclerosis accompanied by discirculatory encephalopathy and brain infarction. These values were lower in the patients with infarction as compared with healthy people. After tourniquet ischemia of limbs concentration of the eicosatetraenoic acids was altered in blood of patients: in one group the concentration of all the lipoxygenase metabolites of arachidonic acid was increased, in the other group of patients it was decreased. Development of atherosclerosis appears to be related to activation of lipoxygenases and production of monohydroxyeicosatetraenoic acids.

Adult↗
PubMed1985

Magnetic resonance with marked T2-weighted images: improved demonstration of brain lesions, tumor, and edema.

The object of this study was to determine the sensitivity of magnetic resonance (MR) for imaging intracranial lesions with heavily T2-weighted images compared with that of computed tomographic (CT) and T1-weighted images. Fifty-five patients with known intracranial pathology consisting of primary neurogenic tumors, brain infarcts, demyelinating disease, and metastases were studied by MR and CT. Patients were studied with either 0.6 or 1.5 T systems with T1- and T2-weighted radiofrequency pulse sequences. The heavily T2-weighted images were found to be superior to the T1-weighted images in terms of sensitivity, with 168 lesions found versus 86 by CT and 104 by T1-weighted imaging.

Brain Edema↗
PubMed2006

Investigating the association between Notch3 polymorphism and migraine.

OBJECTIVE: The aim of the present study was to evaluate whether the functional Notch3 polymorphism T6746C, which is not causative for cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), might be a risk factor for migraine. BACKGROUND: It has been recently demonstrated that migraine is characterized by subclinical brain infarctions and white matter lesions. Several genetic risk factors have been associated with migraine, but no study has unraveled a possible relationship between migraine and Notch3, which is involved in vascular damage. Mutations in Notch3 gene have been demonstrated to be pathogenetic for CADASIL, a small vessel disease of the brain characterized by migraine. METHODS: A total of 156 migraine patients and 128 nonheadache healthy volunteers entered the study. Demographic and clinical characteristics were carefully recorded, and a neurological work-up was performed. Moreover, each subject underwent a blood sampling for Notch3 genotype determination. RESULTS: Notch3 genotypes as well as allele frequencies did not differ in migraine patients compared to controls, even adjusting for the presence of possible confounds. No difference has been found either in migraine patients with aura or in those without aura. CONCLUSIONS: These findings support the view that functional polymorphism T6746C in Notch3 gene is not involved in increasing the risk of migraine or migraine subtypes.

Adult↗
PubMed2003

Inhibition of apoptosis by hyperbaric oxygen in a rat focal cerebral ischemic model.

The hypothesis was tested that hyperbaric oxygen therapy (HBO) reduced brain infarction by preventing apoptotic death in ischemic cortex in a rat model of focal cerebral ischemia. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) and subsequently were exposed to HBO (2.5 atmospheres absolute) for 2 h, at 6 h after reperfusion. Rats were killed and brain samples were collected at 24, 48, 72 h, and 7 days after reperfusion. Neurologic deficits, infarction area, and apoptotic changes were evaluated by clinical scores, 2,3,7-triphenyltetrazolium chloride staining, caspase-3 expression, DNA fragmentation assay, and terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling (TUNEL)-hematoxylin and eosin (H&E) costaining. In MCAO/R without HBO treatment animals, DNA fragmentation was observed in injured cortex at 24, 48, and 72 h but not in samples at 7 days after reperfusion. Double labeling of brain slides with NeuN and caspase-3 demonstrated neurons in the injured cortex labeled with caspase-3. TUNEL+H&E costaining revealed morphologic apoptotic changes at 24, 48, and 72 h after reperfusion. Hyperbaric oxygen therapy abolished DNA fragmentation and reduced the number of TUNEL-positive cells. Hyperbaric oxygen therapy reduced infarct area and improved neurologic scores at 7 days after reperfusion. One of the molecular mechanisms of HBO-induced brain protection is to prevent apoptosis, and this effect of HBO might preserve more brain tissues and promote neurologic functional recovery.

Animals↗
PubMed1978

Transient paralytic attacks of obscure nature: the question of non-convulsive seizure paralysis.

Eleven patients with transient paralytic attacks of obscure nature are described. Paralysis could involve face or leg alone, face and hand, or face, arm and leg. The duration varied from two minutes to one day. Four patients had brain tumors, six probably had brain infarcts, and one a degenerative process. The differential diagnosis included TIAs, migraine accompaniments, and seizures. In the absence of good evidence for the first two, the cases are discussed from the standpoint of possibly representing nonconvulsive seizure paralysis (ictal paralysis, inhibitory seizure paralysis or somatic inhibitory seizure). Because of the difficulty in defining seizures as well as TIAs and migraine in their atypical variations, a firm conclusion concerning the mechanisms of the spells was not attained. Two cases of the hypertensive amaurosis-seizure syndrome have been added as further examples of ictal deficits.

Adult↗
PubMed1999

Combined diffusion and perfusion MRI with correlation to single-photon emission CT in acute ischemic stroke. Ischemic penumbra predicts infarct growth.

BACKGROUND AND PURPOSE: More effective imaging methods are needed to overcome the limitations of CT in the investigation of treatments for acute ischemic stroke. Diffusion-weighted MRI (DWI) is sensitive in detecting infarcted brain tissue, whereas perfusion-weighted MRI (PWI) can detect brain perfusion in the same imaging session. Combining these methods may help in identifying the ischemic penumbra, which is an important concept in the hemodynamics of acute stroke. The purpose of this study was to determine whether combined DWI and PWI in acute (<24 hours) ischemic stroke can predict infarct growth and final size. METHODS: Forty-six patients with acute ischemic stroke underwent DWI and PWI on days 1, 2, and 8. No patient received thrombolysis. Twenty-three patients underwent single-photon emission CT in the acute phase. Lesion volumes were measured from DWI, SPECT, and maps of relative cerebral blood flow calculated from PWI. RESULTS: The mean volume of infarcted tissue detected by DWI increased from 46.1 to 75.6 cm(3) between days 1 and 2 (P<0.001; n=46) and to 78.5 cm(3) after 1 week (P<0.001; n=42). The perfusion-diffusion mismatch correlated with infarct growth (r=0. 699, P<0.001). The volume of hypoperfusion on the initial PWI correlated with final infarct size (r=0.827, P<0.001). The hypoperfusion volumes detected by PWI and SPECT correlated significantly (r=0.824, P<0.001). CONCLUSIONS: Combined DWI and PWI can predict infarct enlargement in acute stroke. PWI can detect hypoperfused brain tissue in good agreement with SPECT in acute stroke.

Acute Disease↗
PubMedDate not supplied

Cerebral blood volume maps with dynamic contrast-enhanced T1-weighted FLASH imaging: normal values and preliminary clinical results.

PURPOSE: In this article we investigate the application of a method that uses the relaxation effect of bolus-like injected Gd-DTPA to quantify regional cerebral blood volume (rCBV). The aim of the study was to determine if the method provides correct rCBV values in healthy subjects as well as to obtain additional diagnostic information for patients with a glioma or stroke. METHOD: Twenty healthy subjects, 12 patients with brain infarctions, and 18 patients with gliomas were examined. A series of 64 sequential images of one slice was recorded during bolus transit with a FLASH sequence. The measured signal intensity-time curves were converted pixel-wise to concentration-time curves from which the rCBV images were calculated applying the indicator dilution method. RESULTS: An average value for gray and white matter of 4.4 +/- 1.6 vol% was obtained for the group of healthy subjects. The grading of the tumors could be classified according to the differences of their corresponding rCBV values. Fifty percent of the infarct patients had to be excluded from the analysis in the acute phase due to mispositioning of the slice and data degradation by gross motion artifact. Different rCBV values were found for areas that develop later into gliotic scars or cystic necrosis. CONCLUSION: The proposed method is easy to apply in clinical routine MR investigations and provides valuable information for noninvasive, preoperative assessment of tumor grading. It can also provide additional criteria for estimating the histological outcome and with it the degree of ischemia in stroke patients.

Adolescent↗
PubMed1996

Extent of autonomic activation following cerebral ischemia is different in hypertensive and normotensive humans.

OBJECTIVES: To evaluate whether the extent of autonomic activation following brain infarction differs between hypertensive and normotensive humans, and to investigate the role of the insular cortex for this sympathetic activation. DESIGN: Prospective, hospital-based study. SETTING: Department of Neurology of a university medical center. SUBJECTS: Forty-two patients with essential hypertension and 45 patients who were normotensive. MAIN OUTCOME MEASURES: Extent of autonomic activation following stroke as indicated by circadian blood pressure patterns, serum norepinephrine levels, and cardiovascular variables. RESULTS: Normotensive patients with insular infarction showed a significantly reduced circadian blood pressure variation and a higher frequency of nocturnal blood pressure increase compared with patients suffering from essential hypertension and insular stroke. These findings were also associated with higher serum norepinephrine concentrations and more frequent electrocardiographic abnormalities. No significant changes in these variables were seen between normotensive and hypertensive patients without insular involvement. CONCLUSIONS: Our findings suggest a difference in cortical control of autonomic function between hypertensive and normotensive patients after stroke and point to a possible role of the insular cortex in the pathogenesis of essential hypertension.

Aged↗
PubMed2005

Characterization of a novel thrombotic middle cerebral artery occlusion model in monkeys that exhibits progressive hypoperfusion and robust cortical infarction.

In an attempt to establish a thrombotic middle cerebral artery (MCA) occlusion model using cynomolgus monkeys, we measured the blood flow in the main MCA tract and cerebral cortex, brain damage, and neurological deficits, and compared them with those of mechanical MCA occlusion model. Thrombotic occlusion was induced photochemically by green light application on the MCA following rose bengal treatment; mechanical occlusion was induced by MCA clipping for 3h. Patency of the main MCA tract showed two patterns in the thrombotic model: permanent occlusion or cyclical flow reduction (CFR). Regional cerebral blood flow (rCBF) decreased during occlusion followed by post-ischemic hyperperfusion in the clipping model, whereas rCBF reduction expanded time-dependently in the thrombotic occlusion model. Brain infarction and neurological scores in the thrombotic occlusion model were significantly larger than those in the clipping occlusion model. In histological assessment, microthrombi containing myeloperoxidase- and fibrinogen-positive cells were observed in the cortex following the thrombotic but not clipping occlusion. These results collectively suggest that this thrombotic MCA occlusion model, because it shows impairment of cerebral microcirculation, could provide a vital platform for understanding progressive ischemia as well as for evaluating potential therapeutic drugs.

Animals↗
PubMed2004

Gene deletion of cystatin C aggravates brain damage following focal ischemia but mitigates the neuronal injury after global ischemia in the mouse.

Cystatin C is distributed in all human tissues and fluids with a particular abundance in the cerebrospinal fluid. Cystatin C is a strong endogenous inhibitor of lysosomal cysteine proteases, such as cathepsin B, L, H and S, that are involved in various biological processes such as degradation of cellular proteins and regulation of enzymes, as well as in pathological processes. Pharmacological inhibition of cathepsins has been shown to reduce neuronal damage after brain ischemia, suggesting that cystatin C is an endogenous neuroprotectant. Cystatin C has also amyloidogenic properties and is co-localized with beta-amyloid in degenerated neurons in Alzheimer's disease, suggesting a role in neuronal degeneration. To test the hypothesis that endogenous cystatin C is neuroprotective during brain ischemia, global and focal brain ischemia was induced in mice with the cystatin C gene knocked out. Following focal ischemia, larger brain infarcts were found in cystatin C knockout mice, probably due to a reduced inhibition of the cathepsins during ischemia. In contrast, brain damage after global ischemia was diminished in cystatin C knockout mice, suggesting that cystatin C has an aggravating effect on selective neuronal damage after global ischemia.

Animals↗
PubMed1992

Repeated negative DC deflections in rat cortex following middle cerebral artery occlusion are abolished by MK-801: effect on volume of ischemic injury.

Following permanent occlusion of the left middle cerebral artery (MCA) in rats, electrophysiological and hemodynamic characteristics of the periinfarct border zone were investigated in sham-operated (n = 6), untreated (n = 6), and MK-801-treated (3.0 mg/kg; n = 6) animals. For this purpose, direct current potential (DC), EEG, and blood flow (laser-Doppler flowmetry) were recorded from the cortex in the periphery of the MCA territory. In sham-operated rats, a single negative cortical DC deflection was observed after electrocoagulation of the cortex, whereas in untreated MCA-occluded animals, three to eight transient DC deflections were monitored during the initial 3 h of ischemia. The duration of these cortical DC shifts gradually increased from 1.2 +/- 0.3 to 3.7 +/- 2.7 min (mean +/- SD; p less than 0.05) during this time. In animals treated intraperitoneally with MK-801 (3.0 mg/kg) immediately after MCA occlusion, the number of cortical DC shifts significantly declined to one to three deflections (p less than 0.005). The EEG of the treated animals revealed low-amplitude burst-suppression activity. In the untreated and treated experimental group, the reduction of cortical blood flow amounted to 69 +/- 25 and 49 +/- 13% of control, respectively. Despite the more pronounced cortical oligemia, MK-801 treatment resulted in a significant decrease of the volume of the ischemically injured tissue from 108 +/- 38.5 (untreated group) to 58 +/- 11.5 (p less than 0.05) mm3. Our results suggest that repetitive cortical DC deflections in the periinfarct border zone contribute to the expansion of ischemic brain infarcts.

Action Potentials↗
PubMed1989

Plasma lipoproteins in cortical versus lacunar infarction.

We investigated the relation of plasma lipids to the risk for ischemic stroke by comparing clinical and biochemical characteristics of survivors of cortical (n = 48) and lacunar (n = 36) brain infarction. By analysis of variance, no differences were observed in the concentrations of total cholesterol, triglycerides, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, or apoproteins A1 and B. Patients with lacunar infarction, however, had higher concentrations of high density lipoprotein (HDL)-cholesterol than patients with cortical stroke. This HDL-cholesterol difference was due primarily to a strikingly low HDL-cholesterol content in white patients with cortical stroke. These data suggest that previously demonstrated differences in HDL-cholesterol concentrations between patients with ischemic stroke and control subjects without stroke may apply to patients with cortical but not lacunar infarction. Separation of cerebral infarction into subtypes based on mechanism may help clarify lipid-related risk factors in cerebrovascular disease.

Age Factors↗
PubMed1986

Cerebral vasospasm evaluated by transcranial ultrasound correlated with clinical grade and CT-visualized subarachnoid hemorrhage.

In 39 patients with a proven subarachnoid hemorrhage (SAH), the clinical status, the amount of subarachnoid blood on a computerized tomography scan obtained within 5 days after SAH, and the flow velocities (FV's) in both middle cerebral arteries (MCA's) measured by transcranial Doppler sonography were recorded daily and correlated. All patients had pathological FV's over 80 cm/sec between Day 4 and Day 10 after SAH. The side of the ruptured aneurysm showed higher FV's than did the unaffected side in cases of laterally localized aneurysms. Increase in FV preceded clinical manifestation of ischemia. A step early increase of FV's portended severe ischemia and impending infarction. Maximum FV's in the range of 120 to 140 cm/sec were not critical and in no case led to brain infarction. Maximum FV's over 200 cm/sec were associated with a tendency for ischemia, but the patients may remain clinically asymptomatic. In cases of no or only a little blood in the basal cisterns, mean FV's in both MCA's increased only moderately whereas, with thick clots of subarachnoid blood, there was a steeper and higher increase of mean FV's.

Adult↗
PubMed2005

[Tooth loss and the incidence of ischemic stroke].

Chronic infectious diseases may increase the risk of stroke. We investigated whether periodontal disease was a risk factor for cerebral ischemia. A case-control study with 444 stroke patients, 194 hemorrhagic patients and 250 ischemic patients, and 164 hospital controls with nonvascular and noninflammatory neurological diseases, was performed. All subjects were evaluated by either a CT scan or MRI and their number of teeth was determined. The number of teeth in the patients with cerebral ischemia was found to be significantly fewer than for the cerebral hemorrhage group and a control group between 40 and 65 years of age. The degree of tooth loss was particularly remarkable in patients with atherothrombotic and cardioembolic brain infarction. As a result, tooth loss following severe periodontal disease may therefore be a risk factor for the onset of cerebral infarction in some patients.

Adult↗