bluuebunny/crossref_metadata_2025 huggingface dataset:
Rupture of atheromatous plaque as a cause of thrombotic occlusion of stenotic internal carotid artery.
Authors: Ogata J , Masuda J , Yutani C , Yamaguchi T
Published: June 2011

We analyzed the clinical profiles and autopsy findings of five patients who died shortly after developing cerebral infarction following thrombotic occlusion of the internal carotid artery. In all five cases, thrombotic occlusion was caused by rupture of the fibrous lining over the gruel of atheroma at the origin of the internal carotid artery showing tight stenosis of the lumen. The mean +/- SD shorter diameter of the lumen at the site of occlusion was 1.5 +/- 0.4 mm. Our results show that an internal carotid artery with tight stenosis of the lumen by atheroma containing gruel harbors a risk of thrombotic occlusion, which may give rise to cerebral infarction by artery-to-artery embolism or by reduced cerebral perfusion.
Pontine supranuclear facial palsy.
Authors: Hopf H C , Tettenborn B , Krämer G
Published: June 2011

Two patients presented with a unilateral supranuclear facial palsy. Additional dysarthria was attributed to the pontine origin documented by magnetic resonance imaging on the contralateral side. The pontine disorder also was indicated by an isolated delay of the blink reflex R1 component or of the masseter reflex. We attribute the facial palsy to a lesion of a supranuclear fiber bundle supplying the facial nucleus. The location of the lesions favors these fibers taking a separate course from the main pyramidal tract at the mid- to upper pontine level.
Geometric factors of the bifurcation in carotid atherogenesis.
Authors: Fisher M , Fieman S
Published: June 2011

In vitro studies have demonstrated that geometry of the carotid bifurcation predicts blood flow alterations associated with atherosclerotic plaque formation. We investigated intraindividual asymmetry of carotid atherosclerosis by measuring geometric aspects of the carotid bifurcation. We measured diameter stenosis, the internal carotid artery/common carotid artery area ratio, and the angle of the carotid bifurcation on 40 arteriograms. Stenosis asymmetry was significantly associated with area ratio asymmetry (r = 0.355, p less than 0.025); there was no such association between stenosis asymmetry and bifurcation angle asymmetry. Geometric factors of the carotid bifurcation, particularly the area ratio, may help explain intraindividual asymmetry in carotid atherosclerosis.
Effects of hypoxia-ischemia and MK-801 treatment on the binding of a phencyclidine analogue in the developing rat brain.
Authors: Silverstein F S , McDonald J W , Bommarito M , Johnston M V
Published: June 2011

The phencyclidine analogue [3H](1-[2-thienyl]cyclohexyl)piperidine (3H-TCP) binds to the ion channel associated with the N-methyl-D-aspartate receptor channel complex. In vitro autoradiography indicates that the distribution of 3H-TCP binding in brain closely parallels that of [3H]glutamate binding to the N-methyl-D-aspartate receptor. In nine 7-day-old rats, an acute focal hypoxic-ischemic insult produced by unilateral carotid artery ligation and subsequent exposure to 8% oxygen acutely reduced 3H-TCP binding ipsilateral to the ligation by 30% in the CA1, by 27% in the CA3, by 26% in the dentate gyrus, and by 17% in the striatum compared with values from the contralateral hemisphere. In 10 littermates that received 1 mg/kg of the neuroprotective noncompetitive N-methyl-D-aspartate antagonist MK-801 immediately before hypoxic exposure, the regional distribution of 3H-TCP binding in hypoxic-ischemic brain was relatively preserved and there were no interhemispheric asymmetries in 3H-TCP binding densities. In addition, in three unoperated rats decapitated 24 hours after MK-801 treatment, 3H-TCP binding was reduced by 15-35%; similar bilateral suppression of 3H-TCP binding was detected in MK-801-treated ligates. Our data indicate that 3H-TCP autoradiography can be used to assay the efficacy of neuroprotective agents in this experimental model of perinatal stroke.
Circadian variation in the frequency of ischemic stroke.
Authors: Argentino C , Toni D , Rasura M , Violi F , Sacchetti M L , Allegretta A , Balsano F , Fieschi C
Published: June 2011

The frequency of myocardial infarction and sudden death is increased between 6 AM and noon. To determine whether the same is true for the onset of ischemic stroke, we studied 426 consecutive patients within 12 hours after the onset of their first hemispheric stroke. The frequency of onset of hemispheric stroke was significantly (p = 0.0001) higher from 6:01 AM to noon (56.1%) than from 12:01 PM to 6 PM (20.2%), from 6:01 PM to midnight (8.2%), and from 12:01 AM to 6 AM (15.5%). The identification of periods of high risk for vascular events may have important therapeutic implications, such as matching drug effects with vulnerability.
Epidemilogy of stroke in the Poznań district of Poland.
Authors: Wender M , Lenart-Jankowska D , Pruchnik D , Kowal P
Published: June 2011

The incidence of cerebrovascular disease was established in the Poznań district in Poland for 1985. Mortality from cerebrovascular disease during this year was compared with mortality during 1977. The autopsy material from the years 1925 to 1985 was analyzed to differentiate ischemic from hemorrhagic stroke. The incidence of stroke was 198.3 per 100,000 inhabitants greater than 20 years of age. Mortality from cerebrovascular disease decreased significantly in both males and females from 1977 to 1985. Analysis of the pattern of cerebrovascular disease in the autopsy material from 1925 to 1965 demonstrated an overwhelming percentage of hemorrhagic stroke. In the years that followed, an inversion was noticed in the ratio of ischemic to hemorrhagic stroke. It should be assumed that the growing efficacy of antihypertensive therapy largely explains the decreasing incidence of stroke-induced mortality.
Perivascular blood attenuates noradrenergic but not cholinergic effects on piglet pial arterioles.
Authors: Busija D W , Leffler C W
Published: June 2011

We examined the chronic and acute effects of perivascular blood on cerebrovascular responses to norepinephrine and acetylcholine in 35 piglets. In the chronic experiment, fresh autologous blood (n = 15) or cerebrospinal fluid (n = 14, control) was placed under the dura mater over the parietal cortex, and the piglets were allowed to recover from anesthesia. One to 4 days later, a closed cranial window was placed over the parietal cortex and baseline pial arteriolar responses and responses to topical application of the neurotransmitters norepinephrine (10(-6) and 10(-4) M) and acetylcholine (10(-4) M) were determined. We also sampled cerebrospinal fluid from under the window during baseline conditions and during application of the neurotransmitters, and we measured the concentrations of prostanoids (6-ketoprostaglandin F1 alpha, thromboxane B2, prostaglandin F2 alpha, and prostaglandin E2) via radioimmunoassay. Pial arterioles in the chronic control group (n = 13) constricted by 20 +/- 2% (mean +/- SEM) in response to 10(-4) M norepinephrine and by 28 +/- 2% in response to 10(-4) M acetylcholine. In the chronic blood group (n = 14), pial arterioles did not constrict significantly in response to 10(-4) M norepinephrine but constricted normally (23 +/- 4%) in response to 10(-4) M acetylcholine. In the acute experiment, six other piglets had blood placed on the brain surface for 30 minutes and then removed; pial arterioles constricted by 21 +/- 1% in response to 10(-4) M norepinephrine (n = 5) and by 28 +/- 4% in response to 10(-4) M acetylcholine (n = 3).(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of hyperglycemia on neuronal changes in a rabbit model of focal cerebral ischemia.
Authors: Kraft S A , Larson C P , Shuer L M , Steinberg G K , Benson G V , Pearl R G
Published: June 2011

In clinical medicine, cerebral ischemia is frequently due to a focal, rather than global, insult. The effect of hyperglycemia in focal cerebral ischemia is not well defined. We studied the effect of hyperglycemia on neuropathologic changes in a rabbit model of focal cerebral ischemia. Rabbits were randomized to receive saline (n = 12) or glucose (n = 12) infusions. The left anterior cerebral and left internal carotid arteries were clipped after the infusion began. After 6 hours of occlusion, the area of severe ischemic neuronal damage in the left neocortex and striatum on two standard sections of brain was calculated and expressed as a percentage of the total area of the left cortex or striatum. The mean +/- SEM cortical area of severe ischemic neuronal damage was 22.1 +/- 2.8% in the glucose-treated rabbits and 34.0 +/- 4.6% in the saline-treated rabbits (p less than 0.05). The cortical area of severe ischemic neuronal damage was inversely correlated with plasma glucose concentration at the time of arterial clipping (p less than 0.05). We conclude that hyperglycemia is associated with decreased histologic neuronal injury in this model of focal cerebral ischemia and may be protective when cerebral ischemia occurs from a focal insult.
Long-term follow-up of occlusive cervical carotid dissection.
Authors: Pozzati E , Giuliani G , Acciarri N , Nuzzo G
Published: June 2011

We retrospectively studied 19 cases of occlusive cervical carotid dissection encountered at our hospital between 1974 and 1984 and followed for 5-13 (mean 8.2) years to assess the long-term prognosis of the disease. Five patients had transient ischemic attacks, seven had minor stroke, six had major stroke, and one had epileptic seizures. Angiography demonstrated the typical string sign in 17 cases, a double lumen with occlusion in one, and multiple scalloped narrowings with distal occlusion in the other. Three patients died within 1 month and three remain severely disabled (overall mortality and major morbidity 32%), five have permanent deficits, and seven are neurologically intact; the remaining patient was lost to follow-up. Five patients were treated surgically (two had extracranial-intracranial bypass and three had cervical carotid exploration), and the other 14 were treated medically. The overall rate of reopening was 47% with eight of 10 patients demonstrating recanalization on control angiography and another patient demonstrating recanalization at surgery. These nine patients remain clinically stable on follow-up evaluations. However, vascular abnormalities in the healed arteries were notable and include kinking, fibromuscular dysplasia, dissecting aneurysms, intracranial occlusion, and a residual mural defect.
Focal headache during balloon inflation in the internal carotid and middle cerebral arteries.
Authors: Nichols F T , Mawad M , Mohr J P , Stein B , Hilal S , Michelsen W J
Published: June 2011

Although a number of reports are available on the occurrence of headache in patients with ischemic cerebrovascular disease, most studies have recorded the frequency but not the specific sites of the pain. We report 18 patients who underwent balloon inflation in the distal internal carotid artery and middle cerebral artery stem during embolization therapy for intracerebral arteriovenous malformations. Eleven patients had reproducible patterns of headache during balloon inflation. Inflation in the proximal middle cerebral artery stem produced pain primarily in the ipsilateral temple, that in the middle of the middle cerebral artery stem produced pain referred primarily retro-orbitally, and inflation in the distal middle cerebral artery stem produced pain referred primarily to the forehead. Experimental studies have demonstrated similar patterns of referred pain. The fact that these areas of referred pain are so reproducible is of potentially great clinical importance in the approach to management of patients with cerebrovascular disease.
Hemorrhagic transformation following tissue plasminogen activator in experimental cerebral infarction.
Authors: del Zoppo G J , Copeland B R , Anderchek K , Hacke W , Koziol J A
Published: June 2011

The effect of an intravenous infusion of recombinant tissue plasminogen activator on hemorrhagic transformation early after middle cerebral artery territory ischemia was studied in an established awake nonhuman primate (baboon) model. Following 3 hours' occlusion of the middle cerebral artery and 30 minutes' reperfusion in each of 30 baboons, a 60-minute infusion of recombinant tissue plasminogen activator (at three doses: Group A, 0.3 mg/kg, n = 6; Group B, 1.5 mg/kg, n = 6; Group C, 10 mg/kg, n = 6) or normal saline (n = 12) was undertaken. The frequency and volume of intracerebral hemorrhage, the volume of infarction, and clinical alterations were determined by computed tomography at 24 hours and 10 days, neuropathology at 14 days, and serial daily neurologic evaluations, respectively. Peripheral (nonintracranial) hemorrhage (Group A, p = 0.46; Group B, p = 0.015; Group C, p = 0.002) and peak plasma tissue plasminogen activator levels varied directly with the dose of recombinant tissue plasminogen activator. Petechial hemorrhagic infarction was a common finding among the 30 baboons. No significant differences in the incidences or volumes of infarction-related hemorrhage were apparent in any group compared with the respective saline-treated baboons. In pooled data, no significant relation between the volume of hemorrhage and the volume of infarction could be established. We conclude that the incidence and severity of hemorrhagic transformation are not related to infarction size and that recombinant tissue plasminogen activator does not increase the incidence or severity (volume) of hemorrhage when given early (less than or equal to 3.5 hours) after the onset of focal cerebral ischemia in this model.
Delayed treatment with a t-PA analogue and streptokinase in a rabbit embolic stroke model.
Authors: Phillips D A , Fisher M , Davis M A , Smith T W , Pang R H
Published: June 2011

Fibrinolytic therapy may be effective in the treatment of ischemic stroke, and clinical trials are under way. We evaluated two fibrinolytic agents, an analogue of tissue plasminogen activator (Fb-Fb-CF, the catalytic fragment of the tissue plasminogen activator molecule with a prolonged serum half-life, n = 10) and streptokinase (n = 7), in a rabbit model of embolic stroke. Both agents were given 3 hours after stroke onset, a time relevant to the clinical setting. Fb-Fb-CF was significantly better (p less than 0.04) than saline (n = 7) in restoring blood flow to previously occluded intracranial arteries, but streptokinase was ineffective. Neither fibrinolytic agent was associated with a substantial risk for intracerebral hemorrhagic side effects. Our study demonstrates that Fb-Fb-CF can safely and effectively reperfuse rabbit intracranial arteries 3 hours after occlusion, while streptokinase does not.
Three cases of spontaneous extracranial vertebral artery dissection.
Authors: Youl B D , Coutellier A , Dubois B , Leger J M , Bousser M G
Published: June 2011

We describe three cases of extracranial vertebral artery dissection that are unusual in both their modes of presentation and their associations with other pathologic conditions. The first patient had Marfan's syndrome and migraine; his dissection was asymptomatic and was diagnosed by chance at the time of repeat angiography following a previous internal carotid artery dissection. The second patient had systemic lupus erythematosus and presented with a subarachnoid hemorrhage attributed to an intracranial vertebral artery dissection by the demonstration of an extracranial dissection. The third patient had a minor basilar artery stroke in which dissection had occurred beside a congenital hemivertebra deformity.
Superior sagittal sinus thrombosis in a patient with protein S deficiency.
Authors: Cros D , Comp P C , Beltran G , Gum G
Published: June 2011

A 30-year-old man presented with sagittal sinus thrombosis. He had a history of multiple thrombotic events since adolescence, and his father had had a similar history. Laboratory studies revealed the complete absence of free protein S in his plasma. Protein S deficiency, an autosomal dominant disorder, is an identifiable cause of cerebral thrombosis. The literature and our experience with this case suggest that long-term anticoagulant therapy may prevent thrombotic episodes in patients with this disorder.
Alcohol consumption and carotid atherosclerosis in the Lausanne Stroke Registry.
Authors: Bogousslavsky J , Van Melle G , Despland P A , Regli F
Published: June 2011

We evaluated the association between alcohol consumption and carotid atherosclerosis in 261 consecutive patients greater than 50 years old admitted to our community-based primary-care center with first ischemic stroke; their characteristics were entered into a computerized data bank (Lausanne Stroke Registry). Reported regular alcohol consumption was compared with the presence and severity of internal carotid artery disease as assessed by duplex scanning with spectral analysis of the Doppler signal and real-time B-mode imaging at the level of the carotid bifurcation. We found an inverse linear relation between light-to-moderate alcohol intake (less than or equal to 4 standard drinks/day) and severity of internal carotid artery stenosis. No conclusion could be drawn for heavier drinkers because there were too few. A logistic regression model showed that hypertension, cigarette smoking, and age in men and diabetes mellitus and cigarette smoking in women strongly counterbalanced the potential benefit of alcohol consumption. Although regular alcohol drinking cannot be advocated on the basis of our findings, light-to-moderate consumption of alcohol is the first factor to be inversely associated with extracranial carotid atherosclerosis in symptomatic patients with cerebrovascular disease.
Neural damage in the rat thalamus after cortical infarcts.
Authors: Iizuka H , Sakatani K , Young W
Published: June 2011

Histopathologic changes in the thalamus of 23 rats after somatosensory cortical infarction produced by middle cerebral artery occlusion were examined using the Fink-Heimer silver staining method, immunohistochemistry with antibodies against glial fibrillary acidic protein and laminin, and conventional stains. Middle cerebral artery occlusion produced cortical infarcts in the lateral parietal region, with variable involvement of the frontoparietal parasagittal sensorimotor cortex. Within 3 days after occlusion, massive terminal degeneration but no neuronal changes were apparent in the ipsilateral thalamus. By 1 week after occlusion, abnormal neurons with darkly stained, shrunken nuclei and atrophic perikarya were present in the ipsilateral thalamic nuclei. These neurons were densely argyrophilic in Fink-Heimer sections. Rats with small lateral parietal cortical lesions had degenerating neurons limited to the medial ventroposteromedial nucleus. Large lesions involving the parasagittal sensorimotor cortex resulted in widespread neuronal damage in the ventroposteromedial, ventroposterolateral, intralaminar, and posterior nuclear regions but nowhere else. Immunoreactivity to laminin antibody decreased, and astrocytic proliferation was abundant in affected thalamic areas. These findings are consistent with retrograde neuronal degeneration due to thalamocortical fiber damage in ischemic cortical regions. Such lesions remote from the infarct may influence functional recovery in patients with stroke.
Anesthetic modulation of cerebral hemodynamic and evoked responses to transient middle cerebral artery occlusion in cats.
Authors: Helfaer M A , Kirsch J R , Traystman R J
Published: June 2011

We measured cerebral blood flow and somatosensory evoked potentials during transient focal cerebral ischemia in cats to compare the effects of four commonly used anesthetic regimens: ketamine/fentanyl/N2O (fentanyl), pentobarbital, ketamine/alpha-chloralose (alpha-chloralose), and ketamine/halothane/N2O (halothane). Six cats in each group were subjected to 60 minutes of left middle cerebral artery occlusion followed by 120 minutes of reperfusion. Although the amplitude of the initial somatosensory evoked potential wave complex was highest in the alpha-chloralose group (58.6 +/- 16.5 microV) and smallest in the halothane group (27.5 +/- 5.7 microV), amplitude fell by 75% in all groups upon occlusion. Baseline cerebral blood flow varied substantially between groups (e.g., in the right intersylvian gyrus: fentanyl, 96 +/- 12; pentobarbital, 30 +/- 5; alpha-chloralose, 24 +/- 3; and halothane, 76 +/- 11 ml/min/100 g). Occlusion decreased cerebral blood flow to subcortical (e.g., left caudate) structures in all groups (fentanyl, 29 +/- 11%; pentobabital, 45 +/- 12%; alpha-chloralose, 27 +/- 13%; and halothane, 18 +/- 5% of baseline). Postischemic hyperemia occurred in the cortical regions of cats anesthetized with pentobarbital or alpha-chloralose that had reduced cerebral blood flows during occlusion but not in cats anesthetized with fentanyl (cerebral blood flow during occlusion not different from that of cats anesthetized with pentobarbital or alpha-chloralose) or halothane. After 120 minutes of reperfusion, cerebral blood flow had returned to baseline values in all groups. Recovery of cerebral blood flow and somatosensory evoked potential amplitude at that time did not differ among groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Local cerebral blood flow during and after bilateral carotid artery occlusion in unanesthetized gerbils.
Authors: Nadasy G L , Greenberg J H , Reivich M , Kovach A G
Published: June 2011

Using [14C]iodoantipyrine autoradiography, we measured regional cerebral blood flow in unanesthetized gerbils subjected to 2 (n = 5) or 30 (n = 6) minutes of bilateral carotid artery occlusion or 5 (n = 6), 30 (n = 6), or 120 (n = 5) minutes of reflow after 30 minutes of occlusion. Blood pressure, respiratory rate, and blood gases were recorded, and these and other gerbils were evaluated with periodic neurologic examinations. Blood flow to structures above the level of the diencephalon ceased almost totally during occlusion. The lateral thalamus, the rostral three quarters of the hypothalamus, and the superior colliculi were also markedly ischemic. Blood flow to the brainstem and cerebellum was only slightly affected. After release of the occlusion, blood flow was restored in some of the affected areas but to levels somewhat below that in eight sham-operated gerbils. In several areas, principally column-shaped areas in the cortex as well as patchy areas in other structures, blood flow did not recover. This inhomogeneous blood flow distribution lasted at least 30 minutes after release of the occlusion. Thereafter, the inhomogeneity slowly disappeared in such a manner that blood flow to originally well reperfused areas appeared to decrease while that to poorly reperfused areas increased. During reflow, blood flow in the brainstem and cerebellum slowly and continuously decreased. We show that there is an early no-reflow phenomenon that is inhomogeneous and appears to be of vascular origin and lasts approximately 30 minutes after release of the occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Functional impairment due to white matter ischemia after middle cerebral artery occlusion in cats.
Authors: Graf R , Kataoka K , Wakayama A , Rosner G , Hayakawa T , Heiss W D
Published: June 2011

We recorded regional cerebral blood flow, somatosensory evoked potentials, and auditory evoked potentials in the thalamic relay nuclei (ventral posterior lateral nucleus and medial geniculate body) and in the somatosensory and auditory cortices during and after 1 hour of transient left middle cerebral artery occlusion in nine cats. Regional cerebral blood flow was also measured in the thalamocortical tracts of five of these cats. Additionally, the integrity of thalamocortical connections was tested by retrograde labeling of the thalamic nuclei with horseradish peroxidase in eight cats (three of which experienced no ischemia). Regional cerebral blood flow was severely reduced during middle cerebral artery occlusion in the left primary auditory cortex (8.5 ml/100 g/min) and in white matter pathways (6.4-7.6 ml/100 g/min). In contrast, regional cerebral blood flow did not change significantly in the somatosensory cortex or in either thalamic nucleus. Evoked potentials were abolished in both cortices but remained unchanged in the thalamic nuclei. Cortical somatosensory evoked potentials disappeared 5-8 minutes later than auditory evoked potentials. Recirculation after 1 hour of ischemia resulted in rapid and almost complete recovery (94%) of somatosensory evoked potentials and little recovery (18.4%) of auditory evoked potentials. We conclude that in the auditory pathway both cortical and fiber tract ischemia are (perhaps synergistically) responsible for dysfunction, while in the somatosensory cortex evoked potentials are abolished due to white matter ischemia. The delayed disappearance and better recovery of somatosensory than of auditory evoked potentials indicate that ischemic tolerance is higher in fiber tracts than in cortex.
Relationship between plasma glucose, brain lactate, and intracellular pH during cerebral ischemia in gerbils.
Authors: Combs D J , Dempsey R J , Maley M , Donaldson D , Smith C
Published: June 2011

The dose-response relation between plasma glucose and brain lactate and the relation of these parameters to intracellular pH during severe cerebral ischemia have not been well characterized over a wide range of plasma glucose levels. Experiments to delineate these relations in the gerbil model of global ischemia were performed by using phosphorus-31 nuclear magnetic resonance spectroscopy to measure intracellular pH and a new method to measure brain lactate. Ischemia increased final brain lactate linearly 4 mumol/g for every 100 mg/dl increase in plasma glucose up to 650 mg/dl (p = 0.0001, r2 = 0.9); beyond 650 mg/dl, saturation of the glucose transport-glycolysis system occurred. Plasma glucose correlated better with ischemic intracellular pH than did brain lactate. However, when brain lactate levels are compared with intracellular pH during ischemia, the relation may be threshold rather than linear. A narrow transition zone, during which ischemic intracellular pH decreased precipitously with increasing brain lactate, was observed between 17 and 22 mumol/g; below 17 mumol/g, intracellular pH remained stable at 6.8-6.9, whereas above 22 mumol/g, intracellular pH decreased maximally to about 6.2. The marked decrease in intracellular pH that occurs when brain lactate surpasses 17 mumol/g suggests that this sudden drop in intracellular pH may account for the "lactate threshold" for increased cerebral ischemic damage.
Calcium-calmodulin binding in ischemic rat neurons after calcium channel blocker therapy.
Authors: Grotta J C , Picone C M , Earls R , Strong R , Yao L , Dedman J R
Published: June 2011

Calcium channel blockers such as nicardipine improve outcome after global cerebral ischemia and may attenuate ischemic neuronal injury by preventing calcium influx and binding to calmodulin. We followed the temporal and regional sequence of neuronal calcium-calmodulin binding in normal rats (n = 6), untreated ischemic rats (n = 15), and ischemic rats treated with 0.05 mg/kg/hr s.c. nicardipine (n = 13). After 30 minutes of four-vessel occlusion, 40-microns brain sections were incubated in an anti-calmodulin antibody specific for calmodulin not bound to calcium and brain protein. Light-microscopic sections were examined immediately after ischemia and after 2 and 24 hours of reperfusion. Extensive staining of unbound calmodulin was seen in all hippocampal regions and in the cortex in normal rats. In untreated ischemic control rats, staining was lost, indicating calcium-calmodulin binding immediately after ischemia in all regions. However, after 24 hours, staining returned to normal in the cortex and dentate, and minimal staining returned in CA1 and CA3. Nicardipine-treated animals had significantly less calcium-calmodulin binding in CA1 and in the dentate after 2 hours of reperfusion. This study demonstrates that in clinically relevant doses nicardipine has a limited effect on calcium-calmodulin binding in selectively vulnerable regions after severe ischemia.
Magnetic resonance imaging of medial medullary infarction.
Authors: Sawada H , Seriu N , Udaka F , Kameyama M
Published: June 2011

Medial medullary infarction is characterized by ipsilateral hypoglossal nerve palsy, contralateral hemiparesis sparing the face, and contralateral disturbance of deep sensation. Although it is possible to make a clinical diagnosis in typical patients, diagnosis is difficult if hypoglossal nerve palsy is absent. We describe a patient with medial medullary infarction without hypoglossal nerve palsy. The patient suffered from left hemiplegia and homolateral disturbance of deep sensation. Magnetic resonance imaging revealed the site of the lesion to be in the medial portion of the upper medulla oblongata. The result of somatosensory evoked potential testing was compatible with disturbance of the medullary medial lemniscus. In a review of the literature, we examined the relation between clinical features and lesion location in 16 patients with medial medullary infarction and compared these to the present patient. Motor paresis was present in every patient, while disturbance of deep sensation was recorded in nine of 13 patients and hypoglossal nerve palsy in six of 14 patients. In atypical patients with medial medullary infarction (such as the present patient), magnetic resonance imaging is necessary to detect the lesion and to make a clinical diagnosis.
Cognitive changes in patients with multiple cerebral infarcts.
Authors: Babikian V L , Wolfe N , Linn R , Knoefel J E , Albert M L
Published: June 2011

Consensus has not been achieved regarding the impact of multiple cerebral infarcts on neurobehavioral status. To evaluate cognitive function in patients with multiple cerebral infarcts, we administered a comprehensive neuropsychological test battery to 23 consecutive male patients with clinical and brain computed tomographic findings consistent with at least two separate areas of cerebral infarction. Based on brain computed tomographic findings, patients were classified as having either mixed (n = 12) or lacunar (n = 11) infarcts. Results of these two groups were compared with those of 11 age-, sex-, and education-matched controls with no clinical or brain computed tomographic evidence of cerebrovascular disease. The mixed group had significantly lower mean scores than the controls for every cognitive domain tested. The lacune group showed cognitive impairment on most neuropsychological measures but did not differ from the controls in the attention domain. Although some degree of cognitive impairment was detected by the neuropsychological test battery in virtually every patient, only seven of 23 (30%) had Mini-Mental State Examination scores indicating dementia (less than 24). We conclude that virtually every patient with multiple cerebral infarcts has some degree of cognitive impairment but that only a minority can be classified as demented if the Mini-Mental State Examination is used as the primary defining examination.
Prospective comparison of a cohort with asymptomatic carotid bruit and a population-based cohort without carotid bruit.
Authors: Wiebers D O , Whisnant J P , Sandok B A , O'Fallon W M
Published: June 2011

This study is a prospective analysis of the predictive value of diffuse and localized carotid bruit. Patients with asymptomatic carotid bruits are compared with a population-based age- and sex-matched control group known not to have carotid bruit, in regard to subsequent transient ischemic attack, stroke, and death. Each person was followed until death or for 5 years. Among the 566 patients with asymptomatic carotid bruit, the annual stroke rate given survival was 1.5%/yr or 7.5% at 5 years by actuarial analysis. The annual stroke rate given survival for the 428 patients in the population-based cohort was 0.5%/yr or 2.4% at 5 years. Patients with localized carotid bruit were not significantly different from those with diffuse carotid bruits in regard to subsequent cerebral ischemic events (p = 0.11). These data indicate that patients with asymptomatic diffuse or localized carotid bruit are approximately three times more likely to have ischemic stroke than an age- and sex-matched population sample known not to have carotid bruit.
Hypercarbia depresses cerebral oxygen consumption during cardiopulmonary bypass.
Authors: Prough D S , Rogers A T , Stump D A , Mills S A , Gravlee G P , Taylor C
Published: June 2011

No human studies have systematically examined the relations among PaCO2, cerebral blood flow, and the cerebral metabolic rate for oxygen during hypothermic cardiopulmonary bypass. We varied PaCO2 during hypothermic (26-28 degrees C) cardiopulmonary bypass and estimated the cerebral metabolic rate for oxygen by multiplying cerebral blood flow (measured using xenon-133 clearance) by the cerebral arteriovenous difference in oxygen contents. Patients were randomly assigned to either of two methods of managing PaCO2 (uncorrected for body temperature). In group 1 (PACO2 32-48 mm Hg, n = 13) the mean +/- SD cerebral metabolic rate for oxygen was 0.40 +/- 0.11 ml O2 X 100 g-1 X min-1 at a mean +/- SD PaCO2 of 36 +/- 2.0 mm Hg and 0.40 +/- 0.14 ml O2 X 100 g-1 X min-1 at a mean +/- SD PaCO2 of 45 +/- 2 mm Hg. and 49-72 mm Hg, n = 12) the mean +/- SD cerebral metabolic rate for oxygen was 0.31 +/- 0.09 ml O2 X 100 g-1 X min-1 at a mean +/- SD PaCO2 of 55 +/- 3 mm Hg and 0.21 +/- 0.07 ml O2 X 100 g-1 X min-1 at a mean +/- SD PaCO2 of 68 +/- 2 mm Hg. Group 2 values differed significantly from those in Group 1 (p less than 0.05). In both groups, cerebral blood flow increased as PaCO2 increased. During cardiopulmonary bypass, increasing PaCO2 increases cerebral blood flow and decreases the cerebral metabolic rate for oxygen.
Mannitol therapy in perinatal hypoxic-ischemic brain damage in rats.
Authors: Mujsce D J , Towfighi J , Stern D , Vannucci R C
Published: June 2011

To study the efficacy of mannitol in reducing cerebral edema and improving the ultimate neuropathologic outcome in perinatal cerebral hypoxia-ischemia, 67 7-day postnatal rats were subjected to unilateral common carotid artery ligation followed by exposure to 8% oxygen at 37 degrees C for 3 hours. Twenty-seven rat pups received a subcutaneous injection of 0.1 ml mannitol in a dosage of 4 mg/kg body wt immediately following cerebral hypoxia-ischemia and every 12 hours thereafter for a total of four doses. Control animals received either no therapy (n = 16) or an equivalent volume of normal saline (n = 24). Mannitol injections in six rat pups not subjected to hypoxia-ischemia produced no mortality but significantly increased serum osmolality from 287 to 361 mos/l (p less than 0.01). Preliminary studies indicated that substantial mortality occurred when greater doses of mannitol were administered to rats. After 48 hours of recovery from hypoxia-ischemia, the animals were killed and their brains were examined for either tissue water content (33 rat pups) or the presence of neuropathologic alterations (34 rat pups). Mannitol significantly reduced (p less than 0.001) brain water content, as a reflection of cerebral edema, in both the ipsilateral (88.5% compared with 90.6% in controls) and the contralateral (85.0% compared with 87.2% in controls) cerebral hemispheres. Mannitol therapy did not ameliorate the incidence, distribution, or severity of tissue injury in the cerebral cortex, subcortical white matter, hippocampus, striatum, or thalamus of the ipsilateral cerebral hemisphere compared with the controls. Thus, while mannitol substantially reduces the extent of cerebral edema following hypoxia-ischemia, no beneficial affect on ultimate brain damage occurs.(ABSTRACT TRUNCATED AT 250 WORDS)
Color-coded Doppler imaging of normal vertebral arteries.
Authors: Trattnig S , Hübsch P , Schuster H , Pölzleitner D
Published: June 2011

Using color-coded Doppler sonography, we studied the vertebral arteries of 42 persons without history or physical signs of vertebrobasilar disease. The intertransverse portion of the vertebral artery was visualized in all persons on both sides. Its origin was visualized in 37 persons (88.1%) on the right side and in 28 (66.7%) on the left; the atlas loop was visualized in 32 persons (76.2%) on the right side and in 36 (85.7%) on the left. Four vertebral arteries were hypoplastic. Peak systolic blood velocity ranged from 19 to 98 (mean 56) cm/sec and peak diastolic blood velocity ranged from 6 to 30 (mean 17) cm/sec. Resistive indices ranged from 0.62 to 0.75 (mean 0.69). Thus, color-coded Doppler sonography seems to be a promising noninvasive method for the evaluation of hemodynamics in the extracranial portion of the vertebral arteries.
Effect of capsular infarct size on clinical presentation of stroke.
Authors: Sohn Y H , Lee B I , Sunwoo I N , Kim K W , Suh J H
Published: June 2011

We reviewed the medical records and cranial computed tomograms of 74 patients with acute capsular infarcts to investigate the correlation between infarct size and clinical symptoms. Average infarct size varied significantly by clinical syndrome; patients with sensorimotor stroke had the largest infarcts, patients with pure motor hemiparesis had middle-sized infarcts, and patients with ataxic hemiparesis or the dysarthria-clumsy hand syndrome had the smallest infarcts. Although it has been proposed that the type of lacunar syndrome is determined entirely by the infarct location, our results suggest that infarct size is another important factor influencing the clinical presentation of lacunar syndromes.
Large-dose infusions of heparinoid ORG 10172 in ischemic stroke.
Authors: Massey E W , Biller J , Davis J N , Adams H P , Marler J R , Goldstein L B , Alberts M , Bruno A
Published: June 2011

We evaluated the safety and possible efficacy of large doses of the heparinoid ORG 10172 in 57 patients with acute or progressing ischemic stroke. Patients received a loading bolus of the drug followed by a maintenance intravenous infusion for 7 days. The plasma level of ORG 10172 was monitored by the degree of inhibition of coagulation factor Xa. In general, the drug was well tolerated and few hemorrhagic complications occurred. Two patients with large cardioembolic hemispheric strokes had intracranial hemorrhagic complications. Most patients improved during treatment. By 3 months after the stroke, 37 patients (65%) had a favorable outcome (minimal or no residual disability). This study suggests that high-dose intravenous infusions of ORG 10172 can be safely given to patients with acute ischemic stroke.
Noninvasive assessment of cerebral collateral blood supply through the ophthalmic artery.
Authors: Schneider P A , Rossman M E , Bernstein E F , Ringelstein E B , Otis S M
Published: June 2011

We assessed the potential of 2-MHz pulsed-wave transorbital Doppler ultrasonography to delineate the role of the ophthalmic artery as a source of collateral cerebral blood supply by comparing oculopneumoplethysmography, transorbital Doppler ultrasonography, periorbital continuous-wave Doppler ultrasonography, and transcranial Doppler ultrasonography in 25 patients with unilateral internal carotid artery occlusion and five controls with 10 normal internal carotid arteries. Systolic ophthalmic artery blood velocity was reduced ipsilateral to an internal carotid artery occlusion (38.2 +/- 10.2 cm/sec) compared with the contralateral and control velocities (46.0 +/- 10.3 and 47.5 +/- 6.8 cm/sec, respectively; p less than 0.05). Ophthalmic systolic pressure measured by oculopneumoplethysmography was 94.7 +/- 13.2 mm Hg ipsilateral to an internal carotid artery occlusion compared with 108.4 +/- 15.3 mm Hg on the contralateral side (p less than 0.01). Transorbital and periorbital Doppler ultrasonography detected reversed ophthalmic artery blood flow ipsilateral to an internal carotid artery occlusion in 44.0% and 40.0% of the patients, respectively. Systolic middle cerebral artery blood velocity was 55.2 +/- 22.3 cm/sec ipsilateral to an internal carotid artery occlusion compared with 79.4 +/- 23.5 cm/sec on the contralateral side (p less than 0.05) and 101.2 +/- 18.9 cm/sec in the controls (p less than 0.05). Reversed ophthalmic artery blood flow was associated with a low middle cerebral artery blood velocity and lack of major intracerebral collaterals. Transorbital Doppler ultrasonography permits noninvasive evaluation of the ophthalmic artery.(ABSTRACT TRUNCATED AT 250 WORDS)
Cerebral infarction in patients with nephrotic syndrome.
Authors: Marsh E E , Biller J , Adams H P , Kaplan J M
Published: June 2011

We describe two adult patients who presented with acute cerebral infarction and were found to have a hypercoagulable state due to nephrotic syndrome. One patient had a deficiency of free protein-S. The other patient had a pulmonary embolus 4 months after the stroke. Our cases demonstrate that the hypercoagulable state associated with nephrotic syndrome can be associated with cerebral arterial thrombosis and infarction in adults. Examination of the urine remains an important part of the evaluation of patients with recent stroke. The presence of severe proteinuria and a low serum albumin content should prompt consideration of a hypercoagulable state. Our experience suggests that anticoagulant drugs may be required to reduce the risk of new thrombotic events.
Systemic vascular changes in spontaneous occlusion of the circle of Willis.
Authors: Ikeda E
Published: June 2011

We examined the presence of systemic etiologic factors causing vascular changes in so-called "spontaneous occlusion of the circle of Willis" (cerebrovascular moyamoya disease) to determine whether extracranial, as well as intracranial, vessels are involved in this disease.

Histopathologic examination and morphometric analysis of the extracranial vessels were performed in 13 patients with this disease.

The histopathologic findings of the extracranial vessels were as follows: 1) advanced intimal fibrous thickening similar to that of the intracranial vessels; and 2) characteristic intimal fibrous nodular thickening, which may indicate organization of mural thrombi, at the proximal portions of the pulmonary arteries in three of 13 patients. Morphometric analysis revealed significant intimal thickening of the pulmonary arteries (p less than 0.05), renal arteries (p less than 0.05), and pancreatic arteries (p less than 0.01) in patients with this disease as compared with age- and sex-matched control patients.

On the basis of these findings, it is highly likely that this disease has systemic etiologic factors, as well as focal etiologic factors, that work to create vascular change in both the intracranial and extracranial vessels.
Clinical significance of new coagulation and fibrinolytic markers in ischemic stroke patients.
Authors: Ono N , Koyama T , Suehiro A , Oku K , Fujikake K , Kakishita E
Published: June 2011

We investigated plasma levels of D-dimer products of crosslinked fibrin degradation products, thrombin-antithrombin III complex, and plasmin-alpha 2-antiplasmin complex for detecting coagulation system activation in ischemic stroke patients to determine the possible effect of age on these marker levels.

We measured plasma levels of these three markers in 54 acute ischemic stroke patients within 5 days of stroke onset, in 44 chronic ischemic stroke patients over 3 months from onset, and in 50 age-matched healthy subjects. We divided the stroke patients into two subgroups, those with visible occlusion and those with nonvisible occlusion having obstruction of the major cerebral artery.

The plasma levels of these three markers were significantly (p less than 0.01) higher in the stroke patients than in controls. Significant differences did not exist at any level between the patients and controls in the younger-aged subjects (less than or equal to 64 years of age), but did exist in the older-aged subjects (greater than or equal to 75 years of age). An age-related increase of the marker levels was noted between stroke patients and controls. No significant difference in the three markers was found among any of the stroke patients.

Increased levels of these markers in stroke patients seem to be related mostly to age.
14,15-Epoxyeicosatrienoic acid inhibits platelet aggregation in mouse cerebral arterioles.
Authors: Heizer M L , McKinney J S , Ellis E F
Published: June 2011

Epoxygenase metabolites of arachidonic acid are produced by several tissues and have been shown to inhibit in vitro platelet aggregation. The purpose of the present investigation was to determine whether 14,15- or 8,9-epoxyeicosatrienoic acid, epoxygenase derivatives of arachidonic acid, affect the speed of platelet aggregation in in vivo mouse cerebral arterioles.

We performed a craniectomy in 116 anesthetized male mice and observed the pial arterioles by microscopy. We induced in situ platelet aggregation using a mercury light and intravascularly injected fluorescein dye.

Indomethacin (0.5 mg/kg i.p.), a known cyclooxygenase inhibitor, and 14,15-epoxyeicosatrienoic acid (0.3 mg/kg i.v.) increased the time necessary for the light plus dye to induce the first arterial platelet aggregate by 35% and 26%, respectively, whereas 8,9-epoxyeicosatrienoic acid (0.3 mg/kg i.v.) had no effect. Analysis of mouse serum by radioimmunoassay showed that the degree of inhibition of platelet aggregation by indomethacin and epoxyeicosatrienoic acids correlated with the degree of inhibition of thromboxane production.

We conclude that 14,15-epoxyeicosatrienoic acid is a potent inhibitor of in vivo platelet aggregation but cannot conclusively confirm that its effect on aggregation occurs via its reduction of platelet thromboxane A2. Because epoxyeicosatrienoic acids are produced by several tissues, including brain and vascular tissue, they may be important in vivo modulators of platelet aggregation and hemostasis.
Endothelium-independent contractions to NG-monomethyl-L-arginine in canine basilar artery.
Authors: Katusić Z S
Published: June 2011

NG-substituted analogues of L-arginine are potent and selective inhibitors of nitric oxide synthase(s). The present study was designed to determine the effects of these analogues on the vascular smooth muscle of isolated canine basilar arteries.

Basilar artery rings without endothelium were suspended for isometric tension recording in Krebs-Ringer bicarbonate solution bubbled with 94% O2-6% CO2 (temperature = 37 degrees C, pH = 7.4). A radioimmunoassay technique was used to determine the levels of guanosine 3',5'-cyclic monophosphate (cyclic GMP).

NG-Monomethyl-L-arginine (L-NMMA) caused concentration-dependent contractions, whereas the D-enantiomer and NG-nitro-L-arginine did not. Contractions to L-NMMA were reduced in the presence of L-arginine but not in the presence of D-arginine. Superoxide anions generated by xanthine plus xanthine oxidase in the presence of catalase abolished contractions to L-NMMA but did not affect contractions to the prostaglandin H2/thromboxane A2 agonist U46619. Zaprinast, a selective cyclic GMP phosphodiesterase inhibitor, caused concentration-dependent relaxations. L-NMMA selectively inhibited these relaxations. The inhibitory effect of L-NMMA was reversed in the presence of L-arginine. L-NMMA selectively reduced the basal production of cyclic GMP.

These studies suggest that in cerebral arteries, contractions of smooth muscle cells to L-NMMA are mediated by inhibition of nitric oxide synthase with a resultant decrease in the basal production of nitric oxide.