bluuebunny/crossref_metadata_2025 huggingface dataset:
Moderate alcohol consumption and stroke. The epidemiologic evidence.
Authors: Camargo C A
Published: June 2011

An extensive search of the English-language literature identified 62 epidemiologic studies that examined the relation between moderate alcohol consumption and risk of stroke. Moderate drinking (less than 60 g ethanol/day) and ischemic stroke have a complex association that might be explained by interaction with race; a J-shaped association has been found in predominantly white populations, while little (if any) association has been found among Japanese. By contrast, moderate drinking increases risk of both intracerebral and subarachnoid hemorrhage in diverse populations. There is insufficient epidemiologic evidence to conclude whether recent alcohol use affects risk of either ischemic or hemorrhagic stroke. These distinctive associations help explain contradictory reports on the relation between moderate alcohol consumption and risk of "stroke." The high prevalence of alcohol use throughout the world suggests opportunities for primary prevention and the importance of continued research in this area.
A prospective study of atrial fibrillation and stroke.
Authors: D'Olhaberriague L , Hernández-Vidal A , Molina L , Soler-Singla L , Marrugat J , Pons S , Moral A , Pou-Serradell A
Published: June 2011

In a prospective study of 72 patients with stroke and atrial fibrillation, we classified strokes as cardioembolic or noncardioembolic based on arterial assessment using Doppler sonography and angiography. We analyzed and cross-tabulated 18 clinical characteristics and found four to be significantly associated with a cardioembolic mechanism: stroke with onset during activity and peak deficit at onset (p less than 0.008), previous infarct in a different vascular territory (p less than 0.01), previous transient ischemic attack in a different vascular territory (p less than 0.01), and transient ischemic attack lasting greater than 1 hour (p less than 0.02). Starting with these four characteristics, we used a step-down procedure to select variables for a logistic regression model. Only previous infarct in a different vascular territory (odds ratio = 7.38) and transient ischemic attack lasting greater than 1 hour (odds ratio = 7.89) were selected by the model. Using M-mode and two-dimensional echocardiography, we compared left atrial size in 46 patients with that in 78 controls who had atrial fibrillation without stroke. Left atrial size in patients and controls with mitral valvulopathy was significantly larger than that in patients and controls without mitral valve disease. There was, however, no difference in left atrial size between patients with nonvalvular atrial fibrillation and cardioembolic stroke and controls or patients with nonvalvular atrial fibrillation and noncardioembolic stroke. We concluded that some clinical characteristics are closely related to cardioembolic stroke and that left atrial enlargement reflects underlying cardiopathy rather than atrial emboli-forming capability.
Fatal strokes in hyperglycemic cats.
Authors: de Courten-Myers G M , Kleinholz M , Wagner K R , Myers R E
Published: June 2011

Hyperglycemia is associated with three- to fourfold larger infarcts than normoglycemia following permanent middle cerebral artery occlusion in cats. We investigated the effects of glycemia on brain outcome when middle cerebral artery blood flow was restored (clip release) after 4 hours of occlusion. Seven of 13 hyperglycemic (22 mM) and one of 12 normoglycemic (6 mM) anesthetized cats developed total middle cerebral artery territory infarcts and hemispheric edema and died of brainstem compression. The remaining six and 11 cats recovered fully and later showed no or only small infarcts. Compared with permanent occlusion, restoration of blood flow after 4 hours reduced infarct volume in all normoglycemic and hyperglycemic cats that survived, but caused a much higher proportion (54% vs. 17%) of hyperglycemic and, for the first time, one normoglycemic cat, to die of infarct extension, hemorrhagic infarct conversion, and total territory edema. Thus, clip release after 4 hours caused some cats to show reduced and others to show augmented tissue damage. Rendering cats hyperglycemic substantially worsened their outcome after reperfusion by increasing their death rate from total territory edema sevenfold. Our results demonstrate that risk/benefit analyses for recanalization efforts in humans should take serum glucose concentrations into account.
Influence of antihypertensive treatment with budralazine on autoregulation of cerebral blood flow in spontaneously hypertensive rats.
Authors: Tanaka S , Tanaka M , Akashi A
Published: June 2011

We studied the effect of chronic antihypertensive treatment with budralazine on the lower blood pressure limit of cerebral blood flow autoregulation using spontaneously hypertensive rats. Cerebral blood flow in the parietal cortex and caudate nucleus was measured to determine the lower limit using the hydrogen clearance method. The lower limit in both cerebral regions was significantly higher in 10 untreated spontaneously hypertensive rats than in 10 Wistar-Kyoto rats. The upward-shifted lower limit was restored to close to normal in the caudate nucleus and was partially restored in the parietal cortex of nine rats by 9 weeks of treatment with the high dose (50-68 mg/kg/day) of budralazine, which kept blood pressure constant at approximately normotension during the treatment period; the lower limit was slightly restored in both cerebral regions of seven rats by 4 weeks of treatment with the high dose. However, 9 weeks of treatment with the low dose (19-27 mg/kg/day) of budralazine, which produced moderate continuous hypotension in nine rats, did not apparently influence the lower limit. Our results suggest that long-term antihypertensive therapy with budralazine reduces the upward-shifted lower blood pressure limit of cerebral blood flow autoregulation toward normal and that the restoration induced by budralazine depends on the degree of blood pressure reduction as well as on the duration of the therapeutic period.
Quantification of regional cerebral blood flow with IMP-SPECT. Reproducibility and clinical relevance of flow values.
Authors: Podreka I , Baumgartner C , Suess E , Müller C , Brücke T , Lang W , Holzner F , Steiner M , Deecke L
Published: June 2011

Single-photon emission computed tomography with N-isopropyl[123I]-p-iodoamphetamine (IMP-SPECT) was performed in 14 normal volunteers (seven men and seven women aged 25.1 +/- 5.3 years) and 29 patients with cerebrovascular disease (18 men and 11 women aged 54.1 +/- 13.7 years). The fluid microsphere model was used to estimate cerebral blood flow (CBF). Normal subjects were scanned twice, 1 week apart, to determine the reproducibility of the CBF estimates. Hemispheric blood flow (hCBF) was calculated as the mean of regional cerebral blood flow (rCBF) values in 16 gray matter regions per hemisphere. In normal subjects mean hCBF was 68 ml/100 g/min. The highest rCBF was found in the occipital cortex, followed by the frontal, temporal, and parietal cortexes. CBF values were reproducible (p less than 0.001 except the right thalamic region, where p less than 0.01). Intraindividual variation ranged between 0.3% and 15%. Women exhibited significantly higher (16%, p less than 0.02) CBF than men. Patients were subdivided into groups with reversible (n = 19) and persistent (n = 10) symptoms. Significant hCBF differences between the affected and the contralateral hemispheres were recorded only in the group with reversible symptoms (p less than 0.005), whereas the group with persistent symptoms showed a significant bilateral decrease of hCBF compared with normal subjects and patients with reversible symptoms. Focal CBF was significantly lower in patients with completed stroke than in patients with transient symptoms (p less than 0.001). Our results indicate that IMP-SPECT can be used for the routine estimation of CBF in normal and pathologic states.
Changes of blood flow in the cerebral cortex after subcortical ischemic infarction.
Authors: Højer-Pedersen E , Petersen O F
Published: June 2011

The two-dimensional xenon-133 inhalation method was used to measure cortical blood flow in 16 patients with small subcortical ischemic infarcts and in 10 patients with larger cortical infarcts in the chronic phase of stroke. An abnormal hemispheric asymmetry of blood flow was seen, not only in patients with cortical infarcts, but also in those with subcortical infarcts. In the patients with subcortical infarcts, focal areas of reduced cortical blood flow were seen in the symptomatic hemisphere remote from the tissue destruction, usually including part of the noninfarcted frontoparietal cortex. The cortical dysfunction may have contributed to the clinical manifestations including aphasia, which was present in 14 of the 16 patients with subcortical lesions.
Prostaglandins and vasoactive amines in cerebral vasospasm after aneurysmal subarachnoid hemorrhage.
Authors: Chehrazi B B , Giri S , Joy R M
Published: June 2011

Five consecutively admitted patients with aneurysmal subarachnoid hemorrhage were treated with an indwelling lumbar spinal catheter. Daily samples of cerebrospinal fluid were analyzed for erythrocyte, protein, glucose, dopamine, epinephrine, serotonin, 5-hydroxyindoleacetic acid, tryptophan, histamine, thromboxane, 6-ketoprostaglandin F1 alpha, prostaglandin E, and prostaglandin F2 alpha concentrations. The patients' neurologic grade on admission, hospital course, presence of vasospasm, level of consciousness, computed tomographic and angiographic findings, and outcome were compared with the concentrations of the above substances in the cerebrospinal fluid. All patients had elevated concentrations of serotonin, with the highest levels found early in the hospital course of the patients who developed vasospasm. Tryptophan content increased markedly in association with clinical and angiographic vasospasm. Concentrations of prostaglandin F2 alpha correlated highly with development of and fluctuations in clinical vasospasm, with angiographic findings, with neurologic grade on admission, and with outcome. Our results suggest that prostaglandin F2 alpha may be involved in delayed clinical vasospasm in patients with subarachnoid hemorrhage.
Mechanisms of vascular supersensitivity in hypercholesterolemia.
Authors: McCalden T A , Nath R G
Published: June 2011

We have characterized in vitro, for the first time, the phenomenon of acute interaction between hypercholesterolemia and cerebrovascular function. We then used this model to investigate a number of mechanisms for the interaction. Rabbits fed a diet supplemented with 2% cholesterol developed hypercholesterolemia over 4 weeks with no histologically detectable atherosclerosis. This absence of anatomic change was reflected in normal biophysical elastic responses to graded radial stretch and normal optimum tension for responses to exogenous K+ in the selected arteries. However, basilar arteries removed from cholesterol-fed rabbits showed abolished myogenic responses to radial stretch and decreased median effective doses for added norepinephrine. These potentiated constrictor responses to norepinephrine were significantly correlated with increased plasma cholesterol concentration. A mechanism related to the opening of membrane calcium channels may be responsible for the supersensitivity.
Pure sensory stroke due to a pontine lacune.
Authors: Hommel M , Besson G , Pollak P , Borgel F , Le Bas J F , Perret J
Published: June 2011

A 53-year-old hypertensive man presented with the sudden onset of an isolated lemniscal sensory syndrome of the entire left side of his body. Magnetic resonance images showed a small lacune in the right paramedian pons corresponding to the location of the medial lemniscus.
Caregiver assessment of personal adjustment after stroke in a Veterans Administration Medical Center outpatient cohort.
Authors: Evans R L , Noonan W C , Bishop D S , Hendricks R D
Published: June 2011

We evaluated 80 stroke patients to examine the contributions of caregiver anxiety, self-care ability, age, time since onset, marital and residential status, and need for health care services on personal adjustment as reported by caregivers. Mean age of the patients was 65.4 years, and the average time from stroke onset to evaluation was 415 days. Multiple regression analyses indicated that a significant amount of variance in patient adjustment was accounted for by caregiver anxiety (R2 = 0.28, p less than 0.05) and patient self-care ability (R2 = 0.13, p less than 0.05). Compared with community norms, stroke patients were reported to be more depressed, confused, and anxious and they demonstrated fewer household management skills. Stroke patients were not different from a normative sample on measures of interpersonal involvement or social activity. Caregivers had high levels of anxiety compared with norms. Our results may aid in developing methods for identifying stroke patients and caregivers at risk for suboptimal adjustment.
Contributions from the upper cervical dorsal roots and trigeminal ganglia to the feline circle of Willis.
Authors: Saito K , Moskowitz M A
Published: June 2011

To further define the sensory projections to the circle of Willis, we measured concentrations of immunoreactive substance P in pial arteries of cats following either bilateral removal of the C1-3 dorsal root ganglia (six cats) or bilateral removal of the trigeminal ganglia (three cats). Removal of the dorsal root ganglia decreased concentrations of the tachykinin substance P in the vertebral artery and the basilar artery and its branches by 72% and 50-66%, respectively. Bilateral removal of the trigeminal ganglia decreased substance P concentrations in all forebrain vessels including the rostral basilar artery, although only concentrations in the anterior cerebral artery were significantly lower than those in unilaterally lesioned cats (p less than 0.01). Hence, the vertebrobasilar artery and its tributaries are invested by substance P-containing fibers originating from the upper cervical dorsal root ganglia, and the anterior cerebral artery is innervated by both trigeminal ganglia. If a similar anatomy exists in humans, our data provide an explanation for the occipital localization of headaches arising from the vertebrobasilar arteries and for bilateral headaches following stimulation of the anterior cerebral artery.
Repeated cranial computed tomographic and magnetic resonance imaging scans in two cases of eclampsia.
Authors: Fredriksson K , Lindvall O , Ingemarsson I , Astedt B , Cronqvist S , Holtås S
Published: June 2011

In two cases of eclampsia with consumptive thrombocytopenia, the maximum increase in blood pressure and the lowest platelet count coincided with the maximum degree of neurologic and neuroradiologic abnormality. Computed tomograms showed decreased attenuation, and T2-weighted magnetic resonance images showed increased signal intensity focally in the cerebral cortex and the deep gray and white matter. Blood pressure, platelet count, clinical status, and roentgenograms normalized completely in both cases. Severe arterial hypertension and disseminated transitory microvascular occlusions presumably caused multiple small foci of brain edema that resolved without remaining detectable ischemic brain damage.
Hemostatic markers in acute stroke.
Authors: Feinberg W M , Bruck D C , Ring M E , Corrigan J J
Published: June 2011

To assess the time course of thrombosis and fibrinolysis after acute stroke, we measured concentrations of fibrinopeptide A (FpA), B-beta 1-42 peptide (B-beta 1-42), B-beta 15-42 peptide (B-beta 15-42), and crosslinked D-dimer (XDP) in 31 patients at varying times following acute ischemic stroke and in 13 neurologically stable patients with chronic strokes. FpA levels were markedly elevated during the first week after stroke and declined slowly during the first month. Mean FpA levels were not significantly elevated in chronic stroke patients. Mean XDP levels were slightly elevated during the first week and increased during the next 2 weeks after stroke. B-beta 1-42 and B-beta 15-42 levels were not elevated at any time following acute stroke. Our data suggest that fibrin formation greatly exceeds endogenous fibrinolysis during the acute phase of ischemic stroke. Endogenous fibrinolysis develops slowly following stroke. Prolonged elevation of FpA concentration suggests that thrombin activity and fibrin formation continue for up to 4 weeks in some patients with ischemic stroke.
Effect of thromboxane synthase inhibition on eicosanoid levels and blood flow in ischemic rat brain.
Authors: Pettigrew L C , Grotta J C , Rhoades H M , Wu K K
Published: June 2011

Reperfusion of ischemic brain is associated with production of thromboxane A2 (TXA2), a proaggregatory vasoconstrictor. We used an animal model of transient forebrain ischemia to study the effects of 1-benzylimidazole (1-BI), a selective inhibitor of thromboxane synthase, upon cerebral eicosanoid levels and cerebral blood flow. Male Wistar rats were subjected to 30 minutes of four-vessel occlusion. The mean +/- SEM brain level of TXB2, the stable metabolite of TXA2, determined after 60 minutes of reperfusion was 101 +/- 20 pg/mg brain protein in five ischemic control rats. Infusion of 10 micrograms/g 1-BI reduced mean +/- SEM cerebral TXB2 concentration to 11 +/- 3 pg/mg brain protein in five rats (p less than or equal to 0.002). Mean +/- SEM hemispheric cerebral blood flow measured in four ischemic control rats after 60 minutes of reperfusion was 42 +/- 9 ml/100 g brain/min compared with 104 +/- 13 ml/100 g brain/min in three 1-BI-treated rats (p less than or equal to 0.001). Mean +/- SEM hippocampal blood flow in four ischemic control rats after 60 minutes of reperfusion was 51 +/- 14 ml/100 g brain/min compared with 125 +/- 25 ml/100 g brain/min in three 1-BI-treated rats (p less than or equal to 0.04). We conclude that selective inhibition of thromboxane synthase may alleviate ischemic brain damage by reducing cerebral TXA2 concentrations and elevating cerebral blood flow.
Positive platelet scintigram of a vertebral aneurysm presenting thromboembolic transient ischemic attacks.
Authors: Maruyama M , Asai T , Kuriyama Y , Sawada T , Ogata J , Nishimura T , Omae T
Published: June 2011

We describe a patient with transient ischemic attacks secondary to a giant aneurysm who showed increased activity on platelet scintigrams at the origin of the left vertebral artery. This is assumed to be the first report of a presumed embolizing aneurysm with positive activity of labeled platelets. Platelet scintigraphy is useful for diagnosing transient ischemic attacks as being secondary to an aneurysm and was proved to provide direct evidence of a thromboembolic source in vivo.
Effect of indomethacin and a free radical scavenger on cerebral blood flow and edema after cerebral artery occlusion in cats.
Authors: Johshita H , Asano T , Hanamura T , Takakura K
Published: June 2011

Using the middle cerebral artery occlusion model in cats, we evaluated the possible role of the cyclooxygenase pathway in alterations of local cerebral blood flow and the development of cortical edema following prolonged ischemia or recirculation. We divided 57 cats into three groups, and each cat received saline (control), indomethacin, or the free radical scavenger ONO-3144. Each group was subdivided into prolonged ischemia (4 hours of occlusion: PI) and recirculation (2 hours of occlusion followed by 2 hours of recirculation: RC) subgroups. We compared local cerebral blood flow and cortical specific gravity between the PI and RC subgroups of the control and drug-treated groups. In the PI subgroup, indomethacin did not influence the time course of local cerebral blood flow but significantly worsened the decrease in cortical specific gravity. On the other hand, indomethacin significantly improved postischemic hypoperfusion and ameliorated the decrease in cortical specific gravity in the RC subgroup. The effects of ONO-3144 were similar to those of indomethacin, except that ONO-3144 did not affect cortical specific gravity in the PI subgroup. Indomethacin inhibits cyclooxygenase activity, whereas ONO-3144 scavenges the oxygen-centered radical released in the conversion of prostaglandin G2 to prostaglandin H2. Thus, prostaglandins do not seem to play a major role in the occurrence of brain edema due to prolonged regional ischemia. By contrast, oxygen-centered radicals released from the cyclooxygenase pathway appear to be at least partially responsible for the occurrence of recirculation-induced edema and postischemic hypoperfusion.
Blood cell rheology in acute cerebral infarction.
Authors: Mercuri M , Ciuffetti G , Robinson M , Toole J
Published: June 2011

Recently it has been hypothesized that leukocyte rheology could be a relevant variable of the microcirculation during cerebral ischemia. However, relatively few studies have been carried out on the rheologic behavior of leukocytes in vascular diseases. This study aimed at quantifying the filterability through Nuclepore filters (mean pore diameter 5 microns) of both leukocyte subpopulations and red blood cells in patients with acute stroke compared with age-matched healthy controls. Leukocytes were separated by density into polymorphonuclear and mononuclear cells. Filterability of the red blood cells and polymorphonuclear and mononuclear subpopulations in buffer was measured using a constant-flow and low-positive pressure system. We used one-way analysis of variance, signed rank sum, and simple and multiple regression tests for statistical analysis. Twenty consecutive male patients with acute ischemic infarction were compared with 20 age-matched healthy subjects. Mononuclear cell filterability was impaired in acute stroke (7.26 +/- 2.00) compared with the controls (5.55 +/- 1.23) (p less than 0.01). Polymorphonuclear cell filterability was less, but still significantly (p less than 0.05), impaired in acute infarction (5.75 +/- 0.87 vs. 4.19 +/- 0.43). The results show that leukocyte and, especially, mononuclear cell filterability is impaired in acute infarction, while no differences exist in red blood cell filterability.
Risk factors for stroke and other embolic events in patients with nonrheumatic atrial fibrillation.
Authors: Flegel K M , Hanley J
Published: June 2011

Factors associated with stroke and other cardiac embolic events in subjects with nonrheumatic atrial fibrillation were examined in a retrospective study of 91 patients from a teaching hospital clinic. There were 28 first strokes during 355 person-years of follow-up (7.9 per 100 person-years). Patients who had experienced one or more previous events were approximately 2.3 times more likely to have a subsequent event (hazard ratio 2.3, 95% confidence interval 1.5-3.4) than patients who had experienced no events. A univariate analysis of factors associated with a first stroke of any cause or other embolic event showed that age of greater than 75 years (hazard ratio 2.5) and systolic blood pressure of greater than 160 mm Hg (hazard ratio 6.4) were significant factors. After adjusting for the effect of age and systolic blood pressure, previous events still carried an increased risk for subsequent events. Subject with nonrheumatic atrial fibrillation who have had one or more embolic events are at high risk of further emboli. They require special consideration when treatment is being planned.
Doppler ophthalmic blood pressure measurement in the hemodynamic evaluation of occlusive carotid artery disease.
Authors: Strauss A L , Rieger H , Roth F J , Schoop W
Published: June 2011

In 102 patients with angiographically proven occlusive carotid artery disease of 60-100% diameter reduction, Doppler ophthalmic artery pressure and blood flow direction were recorded by the recently developed ophthalmomanometry-Doppler technique. Among these 102 patients, 50 presented with complete carotid artery occlusions and 52 with carotid artery diameter stenoses of greater than or equal to 60%. Mean +/- SD Doppler ophthalmic artery pressure was 69 +/- 15 mm Hg ipsilateral to the occlusion and 86 +/- 18 mm Hg ipsilateral to a stenosis of the carotid artery (p less than 0.001). The mean +/- SD Doppler ophthalmic pressure index (ratio of the ophthalmic artery to systemic blood pressure) was lower ipsilateral to the occlusion (0.46 +/- 0.08) than ipsilateral to a carotid artery stenosis (0.54 +/- 0.08; p less than 0.001); in both, the index was clearly diminished compared with normal values (0.68 +/- 0.04; p less than 0.001). It is concluded that the intracranial hemodynamic consequences in the patients with occlusion are on average more profound than in the patients with stenosis. In carotid artery occlusions, the mean +/- SD ipsilateral ophthalmic pressure index was 0.46 +/- 0.06 for antegrade and 0.46 +/- 0.09 for retrograde ophthalmic artery blood flow. In carotid artery stenoses, the mean +/- SD ipsilateral ophthalmic pressure index was 0.55 +/- 0.07 for antegrade and 0.48 +/- 0.06 for retrograde ophthalmic artery blood flow (p less than 0.01). These results indicate that in carotid stenoses the collateral capacity of the ophthalmic artery is insufficient compared with intracranial collaterals, while in carotid occlusions the blood flow direction in the ophthalmic artery does not predict intracranial hemodynamic compensation.
Nimodipine does not improve neurologic outcome after 14 minutes of cardiac arrest in cats.
Authors: Tateishi A , Fleischer J E , Drummond J C , Scheller M S , Zornow M H , Grafe M R , Shapiro H M
Published: June 2011

We tested the effects of nimodipine upon neurologic outcome in 31 cats subjected to 14 minutes of cardiac arrest followed by resuscitation. With the dose schedule used, nimodipine had no effect upon neurologic outcome or upon the percentage of ischemic neurons in frontal, hippocampal, occipital, or cerebellar brain sections. The electroencephalographic recovery pattern did not correlate with neurologic or pathologic findings.
The TOPOSCOUT expert system for stroke localization.
Authors: Spitzer K , Thie A , Caplan L R , Kunze K
Published: June 2011

Clinically, strokes are localized by the findings on neurologic examination. TOPOSCOUT is an expert system designed to diagnose the anatomic location and the corresponding vascular territory of strokes based on the clinical signs and symptoms. The inference engine of TOPOSCOUT uses a backtracking algorithm and a rule-based data base that includes associations of neurologic signs with vascular and anatomic areas. TOPOSCOUT is capable of detecting typical stroke patterns, for example, "top-of-the-basilar" or Wallenberg's syndromes. The accuracy of TOPOSCOUT's diagnoses has been tested for conformity with the final diagnoses of 129 patients in the Hamburg Stroke Data Bank, and a high level of agreement was found for hemispheric lesions. The program runs on microcomputers with MS-DOS and is intended as a practical aid for physicians not fully familiar with topologic stroke diagnosis and as an interactive teaching device.
Endothelium-dependent relaxation of human basilar arteries.
Authors: Kanamaru K , Waga S , Fujimoto K , Itoh H , Kubo Y
Published: June 2011

We studied the effects of acetylcholine and calcium ionophore A23187 on human basilar artery rings. Among 11 arteries, both agents produced significant relaxations in five, A23187 but not acetylcholine caused a response in six, and neither agent was effective in four. After rubbing off the endothelium, the relaxations induced by both agents were significantly attenuated. Indomethacin (a cyclooxygenase inhibitor) and AA861 (a specific inhibitor of 5-lipoxygenase) did not but SKF525A (an inhibitor of cytochrome P450-dependent monooxygenase) did significantly inhibit the acetylcholine-induced relaxation in human basilar arteries. On the other hand, AA861 inhibited while neither indomethacin nor SKF525A had any effect on the A23187-induced relaxation. Our results suggest that different mechanisms may be involved in acetylcholine and A23187-induced relaxations in human basilar arteries.
Neuronal network disturbance after focal ischemia in rats.
Authors: Kataoka K , Hayakawa T , Yamada K , Mushiroi T , Kuroda R , Mogami H
Published: June 2011

We studied functional disturbances following left middle cerebral artery occlusion in rats. Neuronal function was evaluated by [14C]2-deoxyglucose autoradiography 1 day after occlusion. We analyzed the mechanisms of change in glucose utilization outside the infarct using Fink-Heimer silver impregnation, axonal transport of wheat germ agglutinin-conjugated-horseradish peroxidase, and succinate dehydrogenase histochemistry. One day after occlusion, glucose utilization was remarkably reduced in the areas surrounding the infarct. There were many silver grains indicating degeneration of the synaptic terminals in the cortical areas surrounding the infarct and the ipsilateral cingulate cortex. Moreover, in the left thalamus where the left middle cerebral artery supplied no blood, glucose utilization significantly decreased compared with sham-operated rats. In the left thalamus, massive silver staining of degenerated synaptic terminals and decreases in succinate dehydrogenase activity were observed 4 and 5 days after occlusion. The absence of succinate dehydrogenase staining may reflect early changes in retrograde degeneration of thalamic neurons after ischemic injury of the thalamocortical pathway. Terminal degeneration even affected areas remote from the infarct: there were silver grains in the contralateral hemisphere transcallosally connected to the infarct and in the ipsilateral substantia nigra. Axonal transport study showed disruption of the corticospinal tract by subcortical ischemia; the transcallosal pathways in the cortex surrounding the infarct were preserved. The relation between neural function and the neuronal network in the area surrounding the focal cerebral infarct is discussed with regard to ischemic penumbra and diaschisis.
Protective effect of N-methyl-D-aspartate antagonists after focal cerebral ischemia in rabbits.
Authors: Steinberg G K , Saleh J , Kunis D , DeLaPaz R , Zarnegar S R
Published: June 2011

We studied the efficacy of postischemic, systemic treatment with the N-methyl-D-aspartate (NMDA) receptor antagonists dextromethorphan and dextrorphan in a rabbit model of transient focal cerebral ischemia. Twenty-two rabbits underwent 1-hour occlusion of the left internal carotid and anterior cerebral arteries followed by 4.5 hours of reperfusion before sacrifice. One hour after the onset of ischemia, immediately after removing the arterial clips, the rabbits were blindly assigned to treatment with dextromethorphan (20 mg/kg i.v. loading dose followed by 10 mg/kg/hr maintenance infusion, n = 7), dextrorphan (15 mg/kg i.v. loading dose followed by 15 mg/kg/hr maintenance infusion, n = 7), or an equivalent volume of normal saline alone (n = 8). The maintenance infusion of drugs or saline was continued for the duration of the experiment. The formalin-fixed brains were analyzed with magnetic resonance imaging using coronal T2-weighted images, and ischemic neuronal damage was assessed on standard coronal hematoxylin-and- eosin-stained sections. The area of neocortical ischemic neuronal damage was significantly reduced in the groups treated with dextromethorphan (4.2%, p less than 0.01) and dextrorphan (6.1%, p less than 0.01) compared with the controls (36.2%). Magnetic resonance imaging demonstrated significantly smaller areas of cortical edema in the groups treated with dextromethorphan (14.6%, p less than 0.01) and dextrorphan (8.0%, p less than 0.01) compared with the controls (32.9%). These clinically tested antitussives with NMDA-antagonist properties may have therapeutic value in the treatment of human cerebrovascular disease.
Slowly progressive ischemic stroke as first manifestation of essential thrombocythemia.
Authors: Benassi G , Ricci P , Calbucci F , Cacciatore F M , D'Alessandro R
Published: June 2011

We report a case of essential thrombocythemia, the only clinical manifestation of which consisted of neurologic symptoms, including anomic aphasia, tactile and painful hypesthesia in the right hand, headache, and Gerstmann syndrome, with a relatively benign and slowly progressive clinical course. Neuroradiologic examination disclosed a large ischemic area in the left temporoparietal region. Cerebral angiography revealed an occlusion of the cortical branches of the left middle cerebral artery with total sparing of the carotid vessel. These findings are discussed in relation to the possible pathogenetic mechanisms of the vascular occlusion due to abnormal platelet function in essential thrombocythemia.
Magnetic resonance and clinical cerebrovascular disease. An update.
Authors: Ramadan N M , Deveshwar R , Levine S R
Published: June 2011

MRI is becoming the imaging modality of choice in patients with ischemic cerebrovascular disease although CT is still the test of choice to exclude acute hemorrhagic stroke. We have briefly reviewed characteristic features of ischemic and hemorrhagic cerebrovascular disease as well as vascular anomalies as seen on MRI. In time MRS should provide useful noninvasive metabolic data to complement the anatomical data in patients with cerebrovascular disease.
Hyperbaric oxygen increases survival following carotid ligation in gerbils.
Authors: Reitan J A , Kien N D , Thorup S , Corkill G
Published: June 2011

We studied the effects of graded exposure to hyperbaric (1,875 mm Hg) oxygen therapy in an acute stroke model prepared by unilateral carotid artery interruption in gerbils. Pentobarbital alone, superoxide dismutase alone, two periods of hyperbaric oxygen alone, and each agent combined with hyperbaric oxygen were administered to investigate possible mechanisms of protection from cerebral ischemia. Survival rates and neurologic deficit scores over 5 days in all treated groups were compared with those in a control group. Survival rates in the groups subjected to 2 (63.9 +/- 4.0%) and 4 hours (70.1 +/- 5.2%) of hyperbaric oxygen alone were significantly higher than in the control group (53.6 +/- 4.2%). The group treated with pentobarbital alone also demonstrated increased survival (69.8 +/- 7.0%), but the combination of therapeutic regimens offered no apparent additive protection. By 5 days there were no differences in the neurologic deficit scores of the survivors in the groups. The toxic pulmonary effects of hyperbaric oxygen were assessed in a pilot LD50 study. The pressure used caused no mortality during 4 hours of exposure, and the calculated LD50 was 7.26 hours. This investigation demonstrates that graded doses of hyperbaric oxygen given after the insult increase survival in a gerbil model of stroke.
Magnetic resonance imaging of flow dynamics in the circle of Willis.
Authors: Edelman R R , Mattle H P , O'Reilly G V , Wentz K U , Liu C , Zhao B
Published: June 2011

Magnetic resonance angiography was applied to the study of blood flow dynamics in the circle of Willis in nine patients with cerebrovascular disease and two normal volunteers. In conjunction with two-dimensional or three-dimensional gradient-echo acquisitions, selective presaturation of individual vessels was used to determine the direction of blood flow and the origin of the vascular supply. Presaturation causes signal loss within the territory supplied by the presaturated artery, without affecting vessels not crossing the presaturation slab. The results were correlated with those from transcranial Doppler sonography and conventional angiography. Magnetic resonance angiography was able to demonstrate the direction of blood flow, the presence or absence of collateral blood flow, and the blood supply to the pericallosal arteries, as well as the presence of a fetal posterior circulation. Magnetic resonance angiography is a noninvasive means for imaging the blood supply of the major intracranial arteries.
Predictors of stroke outcome using objective measurement scales.
Authors: Loewen S C , Anderson B A
Published: June 2011

We set out to determine if rehabilitation variables predicted the motor and functional outcomes of stroke patients. Using the Modified Motor Assessment Scale (motor status) and the Barthel Index (functional status), we tested 50 stroke patients less than or equal to 3 days, 1 week, and 1 month after their stroke and at discharge from the hospital. Both measures are reliable and valid. We used the Spearman correlation coefficient (r) and stepwise regression analysis to analyze the data. Balanced sitting and bladder control scores at 1 week correlated significantly with motor score at discharge (r = 0.83), Barthel Index score at discharge (r = 0.82), and walking score at discharge (r = 0.80). The combined arm score at 1 month correlated significantly with the combined arm score at discharge (r = 0.94). Regression equations using the scores at 1 month produced the highest r2 values (range 0.76-0.95) in predicting the Barthel Index, motor, walking, and arm recovery scores at discharge. The correlation coefficients and the regression equations have uses in both research and clinical settings. We suggest that these objective predictors of recovery be used as adjuncts in prioritizing and directing the rehabilitation management of patients with stroke.
Risk factors for white matter changes detected by magnetic resonance imaging in the elderly.
Authors: Sullivan P , Pary R , Telang F , Rifai A H , Zubenko G S
Published: June 2011

We found increased age (p = 0.001) and history or evidence of stroke (p = 0.016) to be significant independent multivariate predictors of the presence and severity of leukoencephalopathy on magnetic resonance imaging brain scans in a mixed population of 35 elderly psychiatric patients and 25 neurologically healthy elderly volunteers. These results suggest that subcortical ischemia, as well as age-related changes that may not be vascular in origin, contribute to the emergence of periventricular and other deep white matter hyperintensities that are commonly seen on the magnetic resonance imaging brain scans of older adults.
Cerebral blood flow in experimental ischemia assessed by 19F magnetic resonance spectroscopy in cats.
Authors: Brunetti A , Nagashima G , Bizzi A , DesPres D J , Alger J R
Published: June 2011

We evaluated a 19F magnetic resonance spectroscopic technique that detects Freon-23 washout as a means of measuring cerebral blood flow in halothane-anesthetized adult cats during and after transient cerebral ischemia produced by vascular occlusion. The experiments were performed to test the ability of this recently developed method to detect postischemic flow deficits. Results were consistent with postischemic hypoperfusion. The method also proved valuable for measuring small residual flow during vascular occlusion. Our experiments indicate that this method provides simple, rapid, and repeatable flow measurements that can augment magnetic resonance examinations of cerebral metabolic parameters in the study of ischemia.
Beneficial effect of 1,3-butanediol on cerebral energy metabolism and edema following brain embolization in rats.
Authors: Gueldry S , Marie C , Rochette L , Bralet J
Published: June 2011

We assessed the effect of 1,3-butanediol on cerebral energy metabolism and edema after inducing multifocal brain infarcts in 108 rats by the intracarotid injection of 50-microns carbonized microspheres. An ethanol dimer that induces systemic ketosis, 25 mmol/kg i.p. butanediol was injected every 3 hours to produce a sustained increase in the plasma level of beta-hydroxybutyrate. Treatment significantly attenuated ischemia-induced metabolic changes by increasing the concentrations of phosphocreatine, adenosine triphosphate, and glycogen and by reducing the concentrations of pyruvate and lactate. Lactate concentration 2, 6, and 12 hours after embolization decreased by 13%, 44%, and 46%, respectively. Brain water content increased from 78.63% in six unembolized rats to 80.93% in 12 saline-treated and 79.57% in seven butanediol-treated rats 12 hours after embolization. (p less than 0.05). The decrease in water content was associated with significant decreases in the concentrations of sodium and chloride. The antiedema effect of butanediol could not be explained by an osmotic mechanism since equimolar doses of urea or ethanol were ineffective. Our results support the hypothesis that the beneficial effect of butanediol is mediated through cerebral utilization of ketone bodies arising from butanediol metabolism, reducing the rate of glycolysis and the deleterious accumulation of lactic acid during ischemia.
Cerebral venous thrombosis due to heparin-induced thrombocytopenia.
Authors: Kyritsis A P , Williams E C , Schutta H S
Published: June 2011

A patient with polycythemia vera who was treated with heparin for superficial septic thrombophlebitis developed heparin-induced thrombocytopenia and cerebral venous thrombosis with superior sagittal sinus occlusion 11 days after the institution of heparin therapy. We suggest that the severe thrombotic response to the heparin-induced platelet disorder in this patient occurred because the polycythemia vera and the purulent infection enhanced the thrombophilia caused by heparin-induced thrombocytopenia. This condition can be avoided in most instances if heparin is used for no longer than 5 days.
High ethanol consumption as risk factor for intracerebral hemorrhage in young and middle-aged people.
Authors: Monforte R , Estruch R , Graus F , Nicolas J M , Urbano-Marquez A
Published: June 2011

We examined the prevalence of high ethanol intake, hypertension, and other risk factors for intracerebral hemorrhage in a case-control study of 24 young and middle-aged patients with intracerebral hemorrhage. We recorded ethanol consumption, history of hypertension, liver disease, cigarette smoking, and mild or severe coagulation disorder in each case of intracerebral hemorrhage and in 48 control patients matched by sex and age. In univariate matched analyses, the frequencies of high ethanol intake (p = 0.009), hypertension (p = 0.05), and coagulation disorder (p = 0.05) were higher in the cases than in the controls. After controlling for possible confounding factors, we found that high ethanol intake and hypertension were the only independent risk factors for intracerebral hemorrhage (p = 0.02 and p = 0.05, respectively). The hemorrhagic lesion found in cases with a high ethanol intake tended to be located in the cerebral lobes (p = 0.01), contrasting with the typical basal ganglia location of hypertensive hematomas (p = 0.009). We conclude that chronic, high ethanol intake should be considered as an important risk factor for lobar hematomas in young and middle-aged people.
Protective effects of a monosialoganglioside derivative following transitory forebrain ischemia in rats.
Authors: Seren M S , Rubini R , Lazzaro A , Zanoni R , Fiori M G , Leon A
Published: June 2011

We evaluated the effects of treatment with the inner ester derivative of the monosialoganglioside GM1 on cortical electroencephalographic activity and hippocampal CA1 morphology after transitory, near-complete cerebral ischemia in rats. Ischemia was induced by the four-vessel occlusion method, and we studied only the 58 rats that showed flattening of the cortical electroencephalogram for the entire 30 minutes of occlusion. The ganglioside (n = 30) or saline (n = 28) was administered intravenously immediately after release of the carotid clips and then intramuscularly for 21 days of observation. Cortical electroencephalographic activity was monitored throughout the experiment. After 21 days of recirculation we assessed hippocampal CA1 damage by light microscopy. The results indicate that treatment with the ganglioside reduces postischemic secondary damage to the cortical circuitry (as indicated by significantly higher cortical electroencephalographic activity late after reperfusion) and limits neuronal loss in the CA1 region. Our results lend support to the possible therapeutic use of ganglioside in human pathologic conditions associated with cerebrovascular insufficiencies.
Progressing cerebral infarction in relation to plasma glucose in gerbils.
Authors: Vázquez-Cruz J , Martí-Vilalta J L , Ferrer I , Pérez-Gallofré A , Folch J
Published: June 2011

We studied neurologic morbidity and its evolution during hyperglycemia induced immediately after permanent unilateral common carotid artery ligation in Mongolian gerbils. A total of 60 animals were divided into five groups: one experiencing severe hyperglycemia for 1 hour after the onset of ischemia (brief hyperglycemia group, n = 13), a normoglycemic control group for the brief hyperglycemia group (n = 12), a group with severe hyperglycemia for 4 hours after the onset of ischemia (prolonged hyperglycemia group, n = 11), a normoglycemic control group for the prolonged hyperglycemia group (n = 13), and a hyperosmolar normoglycemic control group for the prolonged hyperglycemia group (n = 11). Neurologic morbidity and mortality were higher in the two hyperglycemic groups than in the three normoglycemic control groups. The neurologic deficit progressed according to the duration of severe hyperglycemia. In the three normoglycemic control groups neurologic status stabilized 120 minutes after the onset of ischemia, in the brief hyperglycemia group stabilization occurred at 210 minutes, and in the prolonged hyperglycemia group neurologic deficit progressed for approximately 360 minutes, coinciding with the death of all but one gerbil, in which the neurologic deficit remained stable until death 23 hours after ischemia. We suggest that hyperglycemia is another cause of progressing cerebral infarction.
The syndrome of bilateral hemispheric border zone ischemia.
Authors: Sloan M A , Haley E C
Published: June 2011

Symptoms compatible with vertebrobasilar ischemia have been reported in patients with unilateral or bilateral carotid occlusive disease. Intracranial steal phenomena have been proposed to explain the symptoms. In a review of 54 patients with angiographically documented severe bilateral carotid stenosis (less than or equal to 2 mm residual lumen) or occlusion, eight had symptoms suggesting vertebrobasilar insufficiency. Five patients were identified retrospectively, and the other three were evaluated prospectively. Symptoms included various combinations of hemodynamically mediated, transient bilateral motor, sensory, or visual impairment. Dysarthria, dysphagia, and diplopia were generally absent. Each patient also described additional symptoms compatible with transient hemispheric or retinal ischemia. The anatomic regions subserving the bilateral vertebrobasilar-like symptoms could be correlated with angiographically estimated arterial border zones in both hemispheres and may thus represent bilateral hemispheric border zone ischemia rather than brain stem ischemia. An intracranial steal need not be invoked.
Elastic skeleton of intracranial cerebral aneurysms in rats.
Authors: Yamazoe N , Hashimoto N , Kikuchi H , Hazama F
Published: June 2011

In an attempt to clarify the developmental mechanism of cerebral aneurysms, we studied the elastic skeleton of experimentally induced cerebral aneurysms in rats under scanning electron microscopy after hot formic acid extraction followed by freeze-drying. We produced cerebral aneurysms in 19 rats by unilaterally ligating the common carotid artery, inducing renal hypertension, and feeding beta-aminopropionitrile fumarate. The first noted change was the loss of folds protruding from the internal elastic lamina. Morphologic changes of the internal elastic lamina, considered to be primarily responsible for aneurysmal formation, occurred after the loss or disintegration of the elastic skeleton of first the intima, then the media. In large aneurysms with thick domes, we found proliferation of elastic lamellae that may reduce the risk of rupture. It seems probable that the complex elastic skeleton of the arterial wall may account for the mechanical properties of the artery and that growth of an aneurysm occurs due to disintegration of the elastic skeleton and not simply to rupture of the internal elastic lamina. We believe that such changes in the elastic skeleton are a property of the functional state of the cells that produce elastin.