bluuebunny/crossref_metadata_2025 huggingface dataset:
Crossed hemispheric diaschisis in unilateral cerebellar lesions.
Authors: Rousseaux M , Steinling M
Published: June 2011

We studied 12 patients with unilateral cerebellar hemorrhage to look at its effect on regional cerebral blood flow.

We used single-photon emission computed tomography by continuous inhalation of xenon-133. The blood flow was quantified in the cerebellum and in nine areas of interest on the slice passing through the basal ganglia.

The comparison of the blood flow values of the patients and control subjects showed a significant reduction in the contralateral hemisphere of the patients, predominantly in the frontal region and in the lenticular nucleus of the contralateral hemisphere but also in the anterointernal frontal area of the ipsilateral hemisphere. The analysis of the asymmetry indexes revealed in the same way significant differences between patients and control subjects in the frontal cortex and in the lenticular nucleus.

These results provided concordant evidence suggesting a blood flow reduction in the contralateral hemisphere. This phenomenon of "crossed hemispheric diaschisis" is probably related to the interruption of cerebellocortical tracts.
Partial protection from salt-induced stroke and mortality by high oral calcium in hypertensive rats.
Authors: Peuler J D , Schelper R L
Published: June 2011

Repeated demonstration of an antihypertensive effect of high oral calcium in stroke-prone spontaneously hypertensive rats led us to determine whether it also protects such rats from premature mortality and stroke-related lesions.

Female stroke-prone rats (11-13 per diet) were fed high- and low-calcium (2.0% and 0.4%, respectively) diets with both high and low salt (7.0% and 0.3%, respectively) content from age 4 weeks until spontaneous death. In addition to life span, other variables measured included blood pressures, plasma chemistries, and histological characterization of stroke-related lesions.

Life span was increased from 51 +/- 4 to 68 +/- 1 weeks (p less than 0.05) by high versus low oral calcium in rats fed high-salt diets; it was further increased to greater than or equal to 82 weeks (p less than 0.05) in rats fed low-salt (+/- added calcium) diets. As seen previously, high oral calcium attenuated salt-induced hypertension but did not affect blood pressure in rats fed low-salt diets. High versus low oral calcium exerted contrasting effects (p less than 0.05) on brain lesions (hemorrhages and infarctions) in rats fed high-salt diets, decreasing lesion size (242 +/- 21 versus 712 +/- 276 microns per rat [diameters seen in histological sections]) but increasing lesion number (8.9 +/- 2.4 versus 3.4 +/- 2.2 per rat); it exerted little influence on the few brain lesions that appeared in rats fed low-salt diets.

High oral calcium may protect stroke-prone hypertensive rats from early salt-induced mortality at least partially by decreasing severity (size) of stroke-related lesions, an effect which may relate to decreased blood pressure. However, this protection may be limited by increased number (incidence) of such lesions, an effect which suggests that high oral calcium may increase the number of brain vessels susceptible to stroke-related injury independent of change in blood pressure.
Cerebrovascular responsiveness to hypercapnia in Alzheimer's dementia and vascular dementia of the Binswanger type.
Authors: Kuwabara Y , Ichiya Y , Otsuka M , Masuda K , Ichimiya A , Fujishima M
Published: June 2011

Alzheimer's dementia is thought to be a primary degenerative dementia, whereas vascular dementia of the Binswanger type is an entity of vascular dementia. We evaluated the cerebrovascular responsiveness to hypercapnia to clarify the differences in the cerebral hemodynamics between two groups of patients. The subjects were eight younger control subjects, five age-matched control subjects, five Alzheimer's patients, and five patients with vascular dementia of the Binswanger type.

In the resting state, the regional cerebral blood flow was low in both Alzheimer's dementia and vascular dementia of the Binswanger type. The responsiveness to hypercapnia was preserved in Alzheimer's dementia, whereas it was impaired in vascular dementia of the Binswanger type in the cerebral cortices and in the deep white matter.

These results suggest that small vascular lesions exist in vascular dementia of the Binswanger type but not in Alzheimer's dementia, even though regional cerebral blood flow was thought to decrease by hypometabolism in both types of dementia.
Cheiro-oral syndrome due to lesions in the corona radiata.
Authors: Omae T , Tsuchiya T , Yamaguchi T
Published: June 2011

We describe three patients with cheiro-oral syndrome caused by a small lesion in the corona radiata confirmed by high-resolution magnetic resonance imaging.

Case 1: A 56-year-old hypertensive man who developed hypesthesia and paresthesia in the left perioral area and hand was found to have a small hematoma just lateral to the right internal capsule. Case 2: A 67-year-old man noticed hypesthesia around the left mouth angle and thumb and index finger. Magnetic resonance imaging revealed a lesion in the right corona radiata. Case 3: A 45-year-old hypertensive man developed numbness in his perioral region and left hand that later spread to his shoulder. Magnetic resonance imaging revealed a recent small infarct in the lower lateral aspect of the right corona radiata.

A small lesion in the corona radiata can cause cheiro-oral syndrome, whose pathogenetic mechanism in such patients may be explained by the somatotopical location or by the differing vulnerability of the neuropils in the corona radiata.
Urgent therapy for stroke. Part II. Pilot study of tissue plasminogen activator administered 91-180 minutes from onset.
Authors: Haley E C , Levy D E , Brott T G , Sheppard G L , Wong M C , Kongable G L , Torner J C , Marler J R
Published: June 2011

Renewed interest in thrombolytic therapy as potential treatment for patients with acute ischemic stroke prompted a dose-escalation safety study of tissue plasminogen activator in patients with very early (less than or equal to 90 minutes; see Part I) neurological symptoms. To test whether this stringent entry window might be safely lengthened, a second study was organized to test tissue plasminogen activator in patients with symptoms of 91-180 minutes' duration before treatment.

An open-label, dose-escalation design was chosen. Eligible patients had pretreatment head computerized tomographic scanning and treatment begun 91-180 minutes from stroke onset. End points examined included the incidence of symptomatic and asymptomatic intracranial hemorrhage, other bleeding, and clinical outcome at 2 hours, 24 hours, and 3 months after treatment.

Twenty patients were treated at three hospitals in 13 months. Three doses were tested: 0.6 mg/kg (n = 8), 0.85 mg/kg (n = 6), and 0.95 mg/kg (n = 6). Two patients, one each at the two highest doses, sustained fatal intracerebral hemorrhages. Three patients (15%) improved by greater than or equal to 4 points on the National Institutes of Health Stroke Scale by 24 hours.

These observations suggest that tissue plasminogen activator treatment of acute ischemic stroke 91-180 minutes from onset in doses of greater than or equal to 0.85 mg/kg is attended by a risk of intracerebral hemorrhage approximating 17% (range 3-44%, 95% confidence interval). The rate of early neurological improvement observed in this study was small but does not exclude an improvement over the natural history. Future study with placebo control subjects and stratification by time to treatment is indicated.
Changing pattern of brain hemorrhage during 12 years of computed axial tomography.
Authors: Schuetz H , Dommer T , Boedeker R H , Damian M , Krack P , Dorndorf W
Published: June 2011

We examined whether the pattern of cerebral hemorrhage changed after the introduction of computed tomography.

Using a prospective data base we analyzed the case-fatality ratio, early mortality, and the incidences of hypertension and anticoagulant medication in 488 consecutive cases with supratentorial hemorrhage between 1978 and 1989. Blood pressure at admission of all patients for the years 1978-1979 and 1988-1989 and the Mathew and activities of daily living scores for the years 1978-1979, 1982-1983, and 1988-1989 were assessed retrospectively.

The case-fatality ratio decreased from 49% in the period 1978-1981 to 31% in 1986-1989 (p = 0.006); early mortality (day 1-4) decreased from 28% to 12% (p = 0.0017). The incidence of hypertension decreased from 78% in the period 1978-1981 to 64% in 1986-1989 (p = 0.01). Systolic and diastolic blood pressure at admission sank (p = 0.09). The decrease of the case-fatality ratio correlated best with a less severe initial disturbance of consciousness (p less than 0.01) and with a higher Mathew score (p = 0.038). The activities of daily living score remained unchanged.

The case-fatality ratio and early mortality decreased after the introduction of computed tomography. This was basically due to a decreased incidence of comatose and stuporous patients with severe neurological deficit paralleled by a decrease of mean systolic and diastolic blood pressure values at admission.
Antithrombotic effects of a platelet fibrinogen receptor antagonist in a canine model of carotid artery thrombosis.
Authors: Willette R N , Sauermelch C F , Rycyna R , Sarkar S , Feuerstein G Z , Nichols A J , Ohlstein E H
Published: June 2011

Platelet-fibrin thrombi in the lumen of atherostenotic carotid arteries may underlie transient ischemic attacks and cerebral infarction. For this reason, we investigated the antiplatelet and antithrombotic effects of a novel and potent platelet fibrinogen receptor (glycoprotein IIb/IIIa) antagonist (SK&F 106760).

The effects of 0.1-3.0 mg/kg i.v. SK&F 106760 on platelet aggregation were examined ex vivo in canine platelet-rich plasma (n = 20). In addition, the antithrombotic effects of SK&F 106760 were compared with those of aspirin in an acute canine model of extracranial carotid artery thrombosis with high-grade stenosis. Sham-operated (n = 4), vehicle-treated (n = 6), SK&F 106760-treated (n = 8), aspirin-treated (n = 9), and SK&F 106760+aspirin-treated (n = 5) dogs were examined.

The intravenous administration of SK&F 106760 caused a dose-related inhibition of ex vivo platelet aggregation. In the carotid artery thrombosis model, an occlusive thrombus formed at stenotic sites in the region of the carotid bifurcation. The thrombogenic process caused a progressive reduction in carotid blood flow and reduced the cortical microvascular perfusion and electroencephalographic power. Based on nuclear magnetic resonance spectroscopy, the occlusive events depleted the stores of high-energy phosphates (adenosine triphosphate and phosphocreatine) and increased the lactate concentration in the forelimb somatosensory area of the parietal cortex. In this model, the administration of 1 mg/kg i.v. SK&F 106760 prevented thrombosis of the stenotic carotid artery. Consequently, neurophysiological, cerebral hemodynamic, and metabolic parameters were all improved significantly in the SK&F 106760-treated group. No dog receiving SK&F 106760 reoccluded during the 1-hour posttreatment observation period. In contrast, thrombosis of the carotid artery was associated with neurophysiological deterioration in six of the nine dogs treated with 5 mg/kg i.v. aspirin. Both spontaneous and evoked (increased carotid stenosis) aspirin-resistant thrombosis were abolished by SK&F 106760 treatment.

These results suggest that antagonism of fibrinogen binding to platelet glycoprotein IIb/IIIa (the final common pathway for aggregation) may represent a new and more effective antithrombotic approach to the treatment of cerebral transient ischemic attacks and infarction associated with extracranial carotid artery disease.
Emphasized selective vulnerability after repeated nonlethal cerebral ischemic insults in rats.
Authors: Inoue T , Kato H , Araki T , Kogure K
Published: June 2011

We examined the density and distribution of brain damage after repeated periods of nonlethal ischemic insult in rats in comparison with damage after single lethal periods of ischemic insult.

Transient cerebral ischemia was induced by four-vessel occlusion for 3, 10, 20, and 30 minutes, and 3-minute periods of ischemia were repeated two, three, or five times at 1-hour intervals, followed by 7 days of survival.

Three minutes of ischemia produced no brain damage, but 10-30 minutes of ischemia produced neuronal damage, depending on the length of ischemia, to the selectively vulnerable forebrain regions such as hippocampal CA1 and CA4 subfields, neocortex, striatum, and ventral thalamus, as well as to the brain stem structures (medial geniculate body, substantia nigra, and inferior colliculus) and cerebellar Purkinje cells. Two 3-minute periods of ischemic insult produced neuronal damage to the hippocampal CA1 subfield. Three and five 3-minute insults produced neuronal damage extensively to the selectively vulnerable forebrain areas. An intense cumulative effect of damage was observed in the ventral thalamus, whereas the substantia nigra and the inferior colliculus were resistant to repeated ischemic insults.

Our data indicate that the density and distribution of neuronal damage after repeated ischemic insults are altered as compared with after single ischemia.
Postprandial triglyceridemia and carotid atherosclerosis in middle-aged subjects.
Authors: Ryu J E , Howard G , Craven T E , Bond M G , Hagaman A P , Crouse J R
Published: June 2011

It has been suggested that a postprandial accumulation of triglyceride-rich lipoproteins promotes the development of atherosclerosis. This study was designed to test the hypothesis that postprandial lipemia is independently associated with intima-media thickening of the extracranial carotid arteries.

Forty-seven middle-aged, moderately hypercholesterolemic individuals were recruited for a 1-day study of the lipemic response to a standard high-fat test meal. The formula was fed at a dose of 65 g fat/m2 body surface area, after a 14-hour fast, and blood was obtained for triglyceride analysis hourly for 8 hours. A baseline lipid profile was obtained. Each subject underwent a carotid ultrasound examination. The extent of alimentary lipemia (peak triglyceride response) was correlated with the carotid artery wall thickness as measured by B-mode ultrasound.

Univariate analyses indicated an inverse correlation between peak triglyceride response and high density lipoprotein cholesterol concentration and a direct correlation with male sex, baseline triglyceride concentration, background fat intake, and waist-to-hip ratio. Of these, the only variable that showed a univariate correlation with B-mode score was peak triglyceride response. Age and cigarette smoking were also correlated with B-mode score in univariate analyses. The correlation coefficient (r = 0.52) between peak triglyceride response to a fat-rich meal and B-mode score was significant (p less than 0.002) and remained so in multivariate analysis. Forward-selection stepwise regression resulted in the inclusion of only peak triglyceride response (p = 0.001) and smoking history (p = 0.005) as important predictors of carotid wall thickness in a linear model.

The association between lipemic response and carotid wall thickness suggests that prolonged exposure of arterial wall cells to triglyceride-rich chylomicron remnants enhances the atherogenic process.
Lifestyle factors and risk of cerebral infarction.
Authors: Ellekjaer E F , Wyller T B , Sverre J M , Holmen J
Published: June 2011

We evaluated the impact of lifestyle factors on the risk of ischemic stroke.

We used a nested case-control design. The cases comprised 163 persons (median age 69 years) admitted to a stroke unit and diagnosed with acute cerebral infarction. All cases had earlier participated in the North Trøndelag Health Survey. The controls comprised 567 participants from the North Trøndelag Health Survey, matched by sex and year of birth.

Raised systolic (p less than 0.001) and diastolic (p = 0.02) blood pressure, antihypertensive treatment (p less than 0.001), previous myocardial infarction (p less than 0.001), prior stroke (p = 0.002), diabetes (p less than 0.001), and former daily smoking (p = 0.02) were identified as significant risk factors by univariate conditional logistic regression. No difference in risk was detected at different levels of alcohol consumption, salt intake, physical activity, or body mass index. Current smokers had virtually the same risk as nonsmokers. No association was found between stroke and the number of cigarettes smoked per day or the number of years of smoking. Multivariate conditional logistic regression identified diabetes (p = 0.002), raised systolic blood pressure (p less than 0.001), and former daily smoking (p = 0.01) as significant and independent risk factors. Previous myocardial infarction (p = 0.07), previous stroke (p = 0.1), and current daily smoking (p = 0.1) were of marginal significance.

The established medical risk factors for stroke are confirmed. With the possible exception of smoking, we have not identified any lifestyle factor with a significant impact on the risk of ischemic stroke.
Brain and tissue distribution of polyethylene glycol-conjugated superoxide dismutase in rats.
Authors: Yoshida K , Burton G F , McKinney J S , Young H , Ellis E F
Published: June 2011

The purpose of this study was to determine the distribution of polyethylene glycol-conjugated superoxide dismutase in the brain, cerebrospinal fluid, and various organs.

Distribution of iodine-125-labeled polyethylene glycol-conjugated superoxide dismutase was determined in three groups of male Sprague-Dawley rats: a normotensive sham control group (n = 9) and groups given 125I-labeled polyethylene glycol-conjugated superoxide dismutase either 30 minutes before (n = 10) or 30 minutes after (n = 7) norepinephrine-induced hypertensive injury.

In the first 30 minutes after intravenous administration, polyethylene glycol-conjugated superoxide dismutase plasma activity declined to 70% of the initial value and then decreased negligibly between 30 and 90 minutes. Levels of 125I-labeled polyethylene glycol-conjugated superoxide dismutase in normotensive animals were low in the brain and cerebrospinal fluid and highest in kidney. Brain levels of polyethylene glycol-conjugated superoxide dismutase were elevated only in those rats that received it before hypertensive injury; however, cerebrospinal fluid levels were elevated in animals receiving the drug either before or after hypertensive injury.

Our results suggest that the blood-brain barrier becomes more permeable to polyethylene glycol-conjugated superoxide dismutase only during the hypertensive period but that the blood-cerebrospinal fluid barrier sustains more permanent injury. We suggest that the therapeutic effectiveness of polyethylene glycol-conjugated superoxide dismutase in hypertensive brain injury is due to its action in the vascular wall or to its extracellular activity in the cerebrospinal fluid.
Serotonin release into plasma during common carotid artery thrombosis in rats.
Authors: Wester P , Dietrich W D , Prado R , Watson B D , Globus M Y
Published: June 2011

We have tested the hypothesis that platelet-derived serotonin is released into the bloodstream during cerebrovascular thrombosis.

Nonocclusive common carotid artery thrombosis was produced photochemically in 22 anesthetized adult male Wistar rats using the photosensitizing dye rose bengal and irradiation with an argon-pumped dye laser. Plasma serotonin levels were recorded before, during, and after photothrombosis by intra-arterial in vivo microdialysis with the probe placed distal to the site of thrombosis.

During and immediately after the common carotid artery thrombosis, serotonin levels increased significantly to a peak value of 781 nmol/l (p less than 0.001 by analysis of variance), representing a 15-fold increase compared with baseline levels. The increased serotonin levels gradually decreased but remained significantly elevated for 90 minutes. Ultrastructural analysis of the carotid thrombi identified a dense mass of aggregated platelets at various stages of degranulation.

These results are the first to demonstrate directly that serotonin accumulation occurs in plasma during and after the acute phase of common carotid artery thrombosis. Increased plasma serotonin levels may play a major role in the cerebral blood flow and blood-brain barrier abnormalities previously documented in this model of large-vessel thrombotic stroke.
Temporal relation of calcium-calmodulin binding and neuronal damage after global ischemia in rats.
Authors: DeGraba T J , Ostrow P T , Strong R A , Earls R M , Zong Z J , Grotta J C
Published: June 2011

This study explores the temporal relation of the severity of ischemia and calcium-calmodulin binding in vulnerable and resistant brain regions in a commonly used model of global ischemia.

Immunohistochemical assay of free calmodulin unbound to calcium and light microscopic histological damage were measured in rats after 5, 10, or 20 minutes of global ischemia.

After 24 hours of reperfusion, decreased calmodulin staining, representing increased calcium influx and calcium-calmodulin binding, correlated with increasing durations of ischemia across all brain regions. Based on a 4-point scale (4, extensive stain; 0, no staining), calmodulin staining after 5 minutes versus 10 minutes of ischemia was 3.2 versus 1.9, respectively (p less than 0.05) and after 10 minutes versus 20 minutes of ischemia was 1.9 versus 1.0, respectively (p less than 0.01). The CA1 region displayed the greatest sensitivity to ischemia. Similar but less dramatic results were seen after 2 hours of reperfusion. After 72 hours of reperfusion, histological damage closely correlated with calcium-calmodulin binding after variable durations of ischemia. A threshold of 10 minutes of ischemia was required to cause calcium-calmodulin binding and irreversible neuronal damage. Surviving neuronal populations showed recovery of calmodulin staining 7 days after ischemia, representing a return of free calmodulin and normal calcium homeostasis.

These correlations between calcium-calmodulin binding, histological damage, and duration of ischemia support the causal role of calcium influx in global ischemic injury and suggest the need for very rapid intervention after ischemia if calcium-mediated damage is to be prevented.
Increased plasma endothelin-1 in acute ischemic stroke.
Authors: Ziv I , Fleminger G , Djaldetti R , Achiron A , Melamed E , Sokolovsky M
Published: June 2011

Endothelins are a recently discovered group of most powerful vasoconstrictor peptides. Endothelin-1 is produced by endothelial cells, and endothelin-3 is derived from neuronal tissue. Theoretically, endothelin-mediated vasoconstriction may enhance ischemic neuronal damage. This study aimed to measure plasma levels of both endothelins in patients with acute nonhemorrhagic cerebral infarction.

Plasma levels of endothelin-1 and endothelin-3 were measured by radioimmunoassay in 16 consecutive patients within the first 72 hours after the onset of nonhemorrhagic cerebral infarct, as diagnosed clinically and by computed tomography. There was a marked (fourfold) elevation in plasma endothelin-1 levels in the patients (median, 11.7 pg/ml; 25th and 75th centiles, 5.4 and 13.2 pg/ml) compared with those in a control group of 13 age-matched subjects (median, 2.56 pg/ml; 25th and 75th centiles, 2.4 and 3.0 pg/ml; p less than 0.0001). The first 24 hours after stroke onset were associated with higher endothelin-1 levels, and there was a trend to elevated levels with more severe neurological deficits. In all patients and controls endothelin-3 levels were below 0.5 pg/ml.

Ischemic stroke is associated with acute and marked increases in plasma levels of endothelin-1. This may reflect enhanced production by damaged endothelial cells within the infarcted tissue. Local leakage of endothelin-1 may induce severe and prolonged constriction of collateral vessels and may therefore have a deleterious role in the pathogenesis and final outcome of cerebral infarction.
Spontaneous vertebral artery dissection initially mimicking myocardial infarction.
Authors: Linden D , Steinke W , Schwartz A , Hennerici M
Published: June 2011

Vertebral and carotid artery dissections may present with very different signs and symptoms, making early recognition difficult. However, diagnosis should be established as soon as possible to prevent unnecessary diagnostic investigations and to institute adequate treatment.

A 46-year-old man presented with severe intermittent pain of his left upper arm and general discomfort. During extensive cardiological evaluation for suspected myocardial infarction, a severe brain stem syndrome occurred. Ultrasound Doppler studies detected vertebral artery dissection, which was confirmed by angiography.

The unusual initial presentation of vertebral artery dissection delayed an early diagnosis and adequate treatment. Because noninvasive methods are available today, their applications are recommended in similarly uncharacteristic circumstances.
Coronary artery disease and cardiac events with asymptomatic and symptomatic cerebrovascular disease.
Authors: Love B B , Grover-McKay M , Biller J , Rezai K , McKay C R
Published: June 2011

The purpose of this study was to evaluate the prevalence of coronary artery disease and coronary events during follow-up in patients with asymptomatic carotid stenosis, transient ischemic attacks, or small strokes.

We prospectively studied 60 consecutive patients with thallium-201 scintigraphy followed by coronary arteriography according to an established protocol.

The 201Tl testing was abnormal in seven of 15 patients (47%) with asymptomatic carotid stenosis and in 19 of 44 patients (43%) with transient ischemic attacks or small strokes (p greater than 0.05). In 33 patients with no history of coronary artery disease, 11 (33%) had reversible 201Tl defects. In 26 patients with a history of coronary artery disease, 15 (58%) had reversible and/or fixed defects (p = 0.054 compared with patients with no history). A history of peripheral vascular disease was the only risk factor significantly associated with an abnormal 201Tl test (p = 0.032). Coronary artery stenosis of greater than 50% was identified in one or more vessels in 14 of 15 patients undergoing coronary arteriography. Over a mean follow-up period of 311 days, four patients (7%) developed new onset of angina. There were four coronary events among 14 patients (29%) with both a reversible area on the 201Tl and abnormal coronary arteriography. In comparison, there were only four coronary events among 46 patients (9%) without reversible defects on the 201Tl studies (p = 0.055).

Our study demonstrates that one third of patients with no history of coronary artery disease had an abnormal 201Tl test and that nearly one half of patients with either symptomatic or asymptomatic cerebrovascular disease had abnormal 201Tl tests. Patients with a reversible 201Tl defect and significant stenosis by coronary arteriography were at higher risk for subsequent cardiac events. These findings demonstrate the utility of screening patients with asymptomatic and symptomatic cerebrovascular disease for cardiac disease.
Pure sensory stroke. Clinical-radiological correlates of 21 cases.
Authors: Kim J S
Published: June 2011

Although pure sensory stroke is a relatively common lacunar syndrome, the responsible lesions are often unidentified because of their small size. I reported 21 cases of pure sensory stroke in which the lesions could be identified by head computed tomography and/or magnetic resonance imaging and correlated the clinical findings with the radiological lesions.

Eleven patients had thalamic strokes. Lacunes confined to the posterolateral part of the thalamus were found in nine cases, and hemorrhages of relatively large size were found in two. Five patients showed a loss of all sensory modalities, but six with very small lacunes showed minor or restricted sensory changes. Seven patients with lacunes or hemorrhages in the lenticulocapsular region or corona radiata showed abnormalities of spinothalamic tract sensation. Two patients with a small lacune and a hemorrhage in the pontine tegmentum showed a selective sensory deficit of the medial lemniscal type. One patient with a small cortical infarct showed a cortical sensory loss that was preceded by cortical sensory transient ischemic attacks.

Pure sensory stroke can occur with lesions in various areas of the somatosensory system. Hemisensory deficits of all modalities usually are associated with a relatively large lacune or hemorrhage in the lateral thalamus, whereas tract-specific or restricted sensory changes suggest very small strokes in the sensory pathway from the pons to the parietal cortex.
Short-term prognosis of stroke due to occlusion of internal carotid artery based on transcranial Doppler ultrasonography.
Authors: Hedera P , Traubner P , Bujdáková J
Published: June 2011

The clinical course of stroke due to occlusion of the internal carotid artery is influenced by amount of collateral flow. We measured mean frequency shifts in the middle cerebral artery by transcranial Doppler ultrasonography to determine its prognostic value.

Patients with proven extracranial occlusion of the internal carotid artery and ipsilateral hemispheral stroke were enrolled in our study. We performed transcranial Doppler ultrasonography on 31 patients within 48 hours after the stroke onset and followed up 25 patients in 28 days. At the same time, neurological examination with quantification of neurological deficit was done. We correlated values of flow frequency shifts on the side of stroke with degree of neurological deficit at the onset and at 28 days as well as the degree of clinical improvement and the value of frequency shifts.

We found a negative correlation between blood flow frequency shifts in the middle cerebral artery and degree of neurological deficit at the onset (Spearman rank correlation coefficient, -0.567; p less than 0.001). We also found a positive correlation between the change of the neurological deficit during follow-up and frequency shifts at the onset (Spearman rank coefficient, 0.548; p less than 0.05).

Diminished blood flow velocity (mean frequency shift) in the area of stroke is a negative prognostic factor for the degree of neurological deficit at the onset and a negative prognostic factor for possible improvement. Knowledge of hemodynamic conditions in the stroke area may help to improve therapeutic decisions.
Changes in extracellular glutamate concentration produced in the rat striatum by repeated ischemia.
Authors: Ueda Y , Obrenovitch T P , Lok S Y , Sarna G S , Symon L
Published: June 2011

Evidence suggesting that ischemia-induced neuronal damage may be linked to an extracellular overflow of glutamate has accumulated, and previous studies have shown that repetitive ischemic insults may have a cumulative effect. The purpose of this study was to investigate changes in the extracellular glutamate concentration produced by repeated brief ischemic episodes of varied severity.

Four consecutive 3- or 5-minute periods of bilateral hemispheric ischemia were produced in rats, each ischemic period followed by 27 minutes of reperfusion. Extracellular glutamate in the striatum was monitored using microdialysis, and the electroencephalogram and extracellular direct current potential were recorded in the same tissue site to assess the severity of ischemia.

The results suggest that the kinetics of the increase in the extracellular glutamate concentration produced by a brief ischemic episode are similar, irrespective of whether it is a single insult or part of a repeated sequence. In all cases, the extracellular glutamate concentration increased throughout ischemia and returned to its preischemic level early during reperfusion. The pattern of changes in the ischemia-induced glutamate overflow during repetitive insults varied with the severity of ischemia, in common with the pattern of changes in the direct current potential, supporting the concept that ionic changes associated with anoxic depolarization are a major determinant of ischemia-induced glutamate overflow.

There may be no cumulative effect of brief repeated episodes of ischemia on the extracellular glutamate concentration, even though repeated 5-minute ischemic episodes apparently caused progressive deterioration of ionic homeostasis in some cases.
Time course of cerebral blood flow and histological outcome after focal cerebral ischemia in rats.
Authors: Hakim A M , Hogan M J , Carpenter S
Published: June 2011

The relation between time-dependent changes in cerebral blood flow and the appearance of infarction after focal cerebral ischemia is still a matter for debate. The aim of this study was to measure perfusion after simultaneous occlusions of the left middle cerebral artery and ipsilateral common carotid artery in rats and correlate it with the timing and distribution of histological changes.

We studied histological and cerebral blood flow changes 5 minutes and 4, 24, and 48 hours after the onset of focal ischemia. Blood flow was determined autoradiographically using [14C]iodoantipyrine. A coronal template subdivided into regions of interest was applied to the autoradiographs and the histological data.

In some regions of the nonoccluded hemisphere, cerebral blood flow 5 minutes after occlusion fell below 50% of normal. Many ischemic structures showed stable blood flow for 48 hours after occlusion, confirming that in this model reperfusion is minimal. Infarction occurred eventually in all areas in which blood flow at 5 minutes fell below 10% of that in control rats, but infarction appeared earlier in regions in which blood flow at 5 minutes was below 5% of that in control rats. When blood flow at 5 minutes rose above 12% of that in control rats, the occurrence of infarction became unpredictable.

Despite the general dependence of infarction on perfusion levels, blood flow was not a reliable indicator of those regions committed to infarction.
Prevention of postischemic canine neurological injury through potentiation of brain energy metabolism by acetyl-L-carnitine.
Authors: Rosenthal R E , Williams R , Bogaert Y E , Getson P R , Fiskum G
Published: June 2011

Mechanisms of ischemia/reperfusion brain injury include altered patterns of energy metabolism that may be amenable to pharmacological manipulation. The purpose of this study was to test the effectiveness of postischemic acetyl-L-carnitine administration on potentiation of metabolic recovery and prevention of neurological morbidity in a clinically relevant model of complete, global cerebral ischemia and reperfusion.

Neurological deficit scoring as well as spectrophotometric and fluorescent assays of frontal cortex lactate and pyruvate levels were used in a canine model employing 10 minutes of cardiac arrest followed by restoration of spontaneous circulation for 2 or 24 hours.

Dogs treated with acetyl-L-carnitine exhibited significantly lower neurological deficit scores (p = 0.0037) and more normal cerebral cortex lactate/pyruvate ratios than did vehicle-treated control animals.

Postischemic administration of acetyl-L-carnitine potentiates normalization of brain energy metabolites and substantially improves neurological outcome in a clinically relevant model of global cerebral ischemia and reperfusion.
Increases in cerebral blood flow in rat hippocampus after medial septal injection of naloxone.
Authors: Nishimura J , Endo Y , Kimura F
Published: June 2011

In a previous study, we occasionally found that the rat given naloxone in the preoptic region develops behavioral seizures. In view of knowledge that the forebrain including the medial septal nucleus provides cholinergic projections to the hippocampal formation, the present study examined the effects of naloxone injected into the medial septal nucleus on the local blood flow in the hippocampus.

A polyurethane-coated platinum electrode with a 1-mm bare tip for measurement of blood flow and a guide cannula made of stainless steel tube for naloxone injection were implanted chronically into the brain. The cerebral blood flow was measured by the hydrogen clearance method in freely moving rats.

The injection of 50 micrograms naloxone caused a significant increase in hippocampal blood flow, with its peak at 20 minutes. Twenty micrograms naloxone caused a similar increase, but 10 micrograms caused only a slight increase that peaked at 30 minutes, suggesting a dose-response of naloxone effect. Hippocampal blood flow was not changed after the injection of saline into the medial septal nucleus and after the injection of naloxone into the caudate nucleus.

Taken together with previous findings, the results suggest that endogenous opioids exert a decreasing effect on the local blood flow in the hippocampus, probably mediated by the magnocellular cholinergic neurons projecting to the hippocampus.
Effect of oral nimodipine on platelet function.
Authors: Feinberg W M , Bruck D C
Published: June 2011

Nimodipine, a calcium antagonist, has been reported to have beneficial effects in acute ischemic infarction. Some calcium channel antagonists have antiplatelet effects. We investigated the effect of oral nimodipine on platelet function in healthy volunteers.

Twelve healthy volunteers (6 men and 6 women, mean age 32.9 +/- 5.6 years) took 30 mg nimodipine every 6 hours for 24 hours, followed by a week with no medication, followed by 60 mg every 6 hours for 24 hours. Ex vivo platelet function was measured at baseline, 1 hour after the first dose at each dosage strength, and 1 hour after the last dose at each dosage. Platelet studies included aggregation and adenosine triphosphate release in response to collagen, epinephrine, and adenosine diphosphate; maximal rate of primary aggregation; threshold adenosine diphosphate concentration for second-phase aggregation; and thromboxane B2 release at threshold aggregation. The bleeding time was measured at baseline and after the last 60-mg dose of nimodipine.

No change in any platelet function study was seen with 30 mg nimodipine every 6 hours. Platelet function studies were also unchanged after 60 mg every 6 hours, except for a slight decrease in aggregation and adenosine triphosphate release in response to suprathreshold (10 microM) adenosine diphosphate (p = 0.001, Student's paired t test). There was no significant change in bleeding times.

Oral nimodipine has minimal antiplatelet activity in young, healthy subjects.
Flow-induced relaxation of the rabbit middle cerebral artery is composed of both endothelium-dependent and -independent components.
Authors: Gaw A J , Bevan J A
Published: June 2011

The flow-induced relaxation of a branch of the rabbit middle cerebral artery was examined to determine if an endothelial-independent as well as -dependent component occurs in pial as well as systemic small arteries and the possible role of products of the cyclooxygenase and the L-arginine nitric oxide synthase pathways.

Intraluminal flow was achieved by the infusion of a tissue bath solution into isometrically mounted rabbit pial arteries in a resistance artery myograph through a small pipette.

Intraluminal flow caused relaxation of the artery segment precontracted with 10 microM histamine. Treatment of endothelium-intact vessels with the nitric oxide synthase inhibitors NG-nitro-L-arginine (L-NNA) (100 microM) or NG-nitro-L-arginine methyl ester (L-NAME) (0.3 mM) significantly reduced the relaxation at flow rates of 5-30 microliters/min. This effect was partially reversed by 1 mM L-arginine. These inhibitors had no effect on the flow-induced relaxation of endothelium-denuded vessels. L-NNA did not influence the relaxation to 1 and 3 microM papaverine. Exposure to 10 microM aspirin, 10 microM indomethacin, or 300 nM tetrodotoxin had no effect on the flow-induced relaxation of either endothelium-intact or -denuded vessels (n = 6). Flow-induced relaxation was attenuated, but not abolished, by removal of the cerebrovascular endothelium. This reduction was not statistically significant.

These results show that intraluminal flow caused relaxation of a branch of the rabbit middle cerebral artery, in part through a mechanism sensitive to inhibitors of nitric oxide synthase, most likely the generation of nitric oxide from the vascular endothelium. The major component of the relaxant response is independent of the endothelium and of nitric oxide synthesis through an L-NNA- or L-NAME-sensitive mechanism. The relaxation does not involve cyclooxygenase products nor neurogenic mediators. These results suggest that pial arteries, like those of the rabbit ear, exhibit a novel mechanism for the flow-induced relaxation of agonist-induced tone that is intrinsic to the tissues of the vascular wall subjacent to the endothelium.
Ischemic stroke due to deficiency of coagulation inhibitors. Report of 10 young adults.
Authors: Martinez H R , Rangel-Guerra R A , Marfil L J
Published: June 2011

Deficiencies in coagulant inhibitors protein C, protein S, and antithrombin III increase the risk of venous thrombosis. We describe 10 young adults with cerebral arterial thrombosis due to deficiencies in these factors.

Sixty patients younger than 45 years were hospitalized because of acute ischemic stroke diagnosed through computed tomography or magnetic resonance imaging. Cerebral angiography was performed in 54 cases. Hematologic and coagulation profiles, autoantibody screen, syphilis serology, and lupus anticoagulant were analyzed in all patients. Among the total cases, Holter monitoring was performed in 13 patients, echocardiography in 20, and cerebrospinal fluid studies for cysticercosis and tuberculosis in two. The quantitative analysis of protein C, protein S (by Laurell rocket immunoelectrophoresis), and antithrombin III (by radial immunodiffusion) was performed on admission and 3 months after stroke in all patients and in relatives of six patients.

In 10 cases (17%) the stroke was attributed to deficiency of coagulation inhibitors: three men had protein C deficiency, two women had protein S deficiency, and five had antithrombin III deficiency (three men and two women). The cerebral infarction involved the carotid territory in these 10 patients. None had previous thromboembolic disease. Eight patients showed a complete recovery. An acquired disorder was presumed in one protein S-deficient and in two antithrombin III-deficient patients; the remainder were considered heterozygous.

The cerebral vasculature may be primarily involved in the deficiency of these natural anticoagulants. Young adults seem to be the most often affected. A knowledge of these new clotting defects will enable the clinician to improve the prevention and treatment of this devastating neurological disease.
Decline in autopsies for deaths attributed to cerebrovascular disease.
Authors: Lanska D J
Published: June 2011

United States national autopsy rates have declined in recent years. In the present study, changes in autopsy rates for deaths due to stroke are examined and compared with changes in autopsy rates for all deaths.

National Center for Health Statistics data on United States national autopsy rates were examined for the years 1955, 1958, and 1972-1988.

Since at least 1955, nonstroke deaths were more than twice as likely to be autopsied as deaths due to cerebrovascular disease. The annual autopsy frequency for all deaths, for deaths due to stroke, and for deaths due to each stroke subtype declined precipitously after 1972. Since 1982, less than 5 percent of deaths attributed to stroke have been documented by autopsy. Information obtained at autopsy was frequently ignored in the determination of cause of death on the death certificate.

Careful consideration of the value of autopsy for education, research, and quality assurance is urgently needed. Unless the present problems in obtaining, processing, disseminating, and using autopsy data are adequately addressed, the autopsy rate will continue to decline.
Regional cerebral blood flow in chronic stroke patients.
Authors: Rodriguez G , Nobili F , De Carli F , Francione S , Marenco S , Celestino M A , Hassan K , Rosadini G
Published: June 2011

The aim of this study was to investigate regional cerebral blood flow parameters during the postacute phase of unilateral ischemic stroke and to correlate them with clinical data.

Regional cerebral blood flow was measured in 187 patients in the stabilized phase of stroke by the xenon-133 inhalation method with 32 extracranial detectors. Thirty-eight patients were reexamined after a mean +/- SD time of 32 +/- 21.4 months.

The overall detection of hypoperfusion was 92.0%, with asymmetries as the most sensitive index, especially for patients with a lesser degree of neurological disability. Neurological disability score was strongly associated with regional cerebral blood flow in the affected hemisphere (p < 0.0001) and with asymmetries (p < 0.0001). The presence of carotid obstruction further decreased the regional cerebral blood flow in the affected hemisphere and significantly increased asymmetry (p < 0.0001). Subjects who had no hypoperfusion at absolute values analysis were more frequently free of carotid disease and had less severe disability than those who had bilateral or unilateral regional absolute cerebral blood flow reduction. In 38 patients without new cerebrovascular events, a significant (p = 0.005) reduction of hemispheric regional cerebral blood flow asymmetries was found on a follow-up examination.

These data confirm the value of regional cerebral blood flow asymmetries in stroke detection and point out that important clinical information is also contained in absolute values analysis.
Thrombolytic therapy in acute ischemic stroke. A Danish pilot study.
Authors: Overgaard K , Sperling B , Boysen G , Pedersen H , Gam J , Ellemann K , Karle A , Arlien-Søborg P , Olsen T S , Videbaek C
Published: June 2011

In a feasibility and safety study of thrombolytic therapy in acute ischemic stroke, we explored the usefulness of measurements of regional cerebral blood flow.

Twenty-three patients with acute ischemic stroke were treated with 100 mg recombinant tissue plasminogen activator infused intravenously over 1 hour. Thrombolytic therapy was initiated 78 to 355 minutes after onset of symptoms.

Angiography 16 to 24 hours after treatment in 17 patients showed patient intracranial arteries in 12, partial occlusion of the middle cerebral artery in 3, and total occlusion of the middle cerebral artery in 2. rCBF with 99mTc-hexamethylpropyleneamine oxime intravenously was measured 5 minutes before and within 24 hours after thrombolytic therapy in 12 patients. 10 of the 12 patients showed brain tissue reperfusion and 2, with angiographically documented middle cerebral artery occlusion, showed no reperfusion, thus documenting a relationship between reperfusion measured by regional cerebral blood flow and angiographic patency (P = .015). Three patients died. Patients who were reperfused within 24 hours (documented by repeated regional cerebral blood flow measurements) showed greater clinical improvement on the Scandinavian Stroke Scale the sooner their thrombolytic therapy was started and the more severe their neurological deficits.

Acute cerebral ischemia can be documented by rCBF measurements without delay of thrombolytic therapy, and repeated rCBF measurements can reveal whether cerebral reperfusion has occurred. In our study, early reperfusion was associated with clinical improvement.