bluuebunny/crossref_metadata_2025 huggingface dataset:
Asymptomatic bruit, carotid and vertebrobasilar transient ischemic attacks--a clinical and ultrasonic correlation.
Authors: Lo L Y , Ford C S , McKinney W M , Toole J F
Published: June 2011

One hundred patients with asymptomatic carotid bruit or transient ischemic attack (TIA) underwent continuous-wave Doppler (CWD) and real time ultrasound (RTU) testing of their cervical carotid arteries. After ultrasonic studies, 51 patients also underwent bilateral carotid angiography. There was 95% agreement between CWD and angiography for the diagnosis of a significant (greater than 50%) stenosis. The RTU diagnosis of a normal or occluded vessel was correct in 100% of cases. Seven plaques appreciated on RTU may not have been large enough for detection by angiography. In this small series, ulceration confirmed pathologically was more reliably predicted by RTU than by cerebral angiography. Significant ipsilateral carotid plaques occurred more often in patients with amaurosis fugax than in patients with hemispheric TIAs. Ipsilateral plaque ulceration occurred in 50% of symptomatic carotid bruits, but in only 10% of asymptomatic carotid bruits. Plasma concentrations of total cholesterol were significantly higher in TIA patients with carotid stenosis than in controls.
Biological defence mechanism in the pathogenesis of prolonged cerebral vasospasm in the patients with ruptured intracranial aneurysms.
Authors: Sakaki S , Kuwabara H , Ohta S
Published: June 2011

We examined the relationship between the biological protective mechanisms of scavengers and free radicals that are elicited by subarachnoid hemorrhage (SAH) in the pathogenesis of prolonged vasospasm following ruptured intracranial aneurysm. The study included 25 patients treated by early surgery (within 72 hours after SAH). Lipid peroxides concentrations and the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-px) in the cerebrospinal fluid (CSF) were measured. The concentration of lipid peroxides increased significantly more (p less than 0.05) during the first 4 days after SAH in patients with symptomatic vasospasm than in those without. Patients with symptomatic vasospasm had a marked decrease in SOD activity on Days 3 and 4 followed by a gradual decrease, whereas the patients without spasm showed little change (difference between the groups, p less than 0.05). There was a significant difference in catalase activity reversal to SOD activity, but no difference in GSH-px activity. Thus, correlation was close between the increased lipid peroxides concentration and the decrease in SOD activity in CSF (p less than 0.05), suggesting an important mechanism in the pathogenesis of vasospasm.
Neurological deficit and cerebral infarction after temporary middle cerebral artery occlusion in unanesthetized cats.
Authors: Weinstein P R , Anderson G G , Telles D A
Published: June 2011

Forty-four unanesthetized cats underwent temporary middle cerebral artery (MCA) occlusion with an implanted, externally controlled balloon cuff occluder. The occlusion was reversed to allow reperfusion of the MCA after 2 min to 24 hr of ischemia. Fourteen cats had temporary occlusions lasting 2 min to 3 hr; their neurological deficits improved or resolved after reperfusion, and brain sections showed only scattered microscopic areas of necrosis. After a 4-hr occlusion, five of nine cats (55%) recovered completely within 24 hr; two had persistent deficit when sacrificed, 10 days later, and each had a circumscribed infarct. All 18 cats undergoing 5-, 6-, 8-, and 24-hr occlusions sustained permanent neurological deficits. Three 3-hr occlusions at 2-day intervals in three cats resulted in permanent deficits and infarcts that were 25% larger than those after single 8-hr occlusions. Ten cats underwent permanent MCA occlusion; three deteriorated neurologically and died, and the survivors showed no improvement. Infarcts after 5-, 6-, and 8-hr occlusions followed by reperfusion were 66% smaller (p less than 0.05) than those after permanent occlusion; reperfusion after 24 hr of occlusion did not reduce infarct size. Hemorrhagic infarction occurred after two permanent occlusions, but after only one 5-hr temporary occlusion. The results obtained with this method of temporary regional ischemia indicate that restoration of flow after 1-8 hr, but not after 24 hr, of MCA occlusion resulted in less severe neurological deficit and smaller infarcts than did permanent occlusion. The infarct size correlated with the duration of MCA occlusion (p less than 0.05) rather than with the degree of deficit during occlusion.
Cerebral hemorrhagic infarction at autopsy: cardiac embolic cause and the relationship to the cause of death.
Authors: Lodder J , Krijne-Kubat B , Broekman J
Published: June 2011

In 48 patients dying within 15 days following a supra-tentorial cerebral infarct, the presence of hemorrhagic infarction at autopsy was related to a cardiac embolic cause of the infarct, and to the cause of death. Hemorrhagic infarcts were more common among patients dying from brain herniation than among those dying from a non-cerebral cause. Cardiac embolic strokes were more often hemorrhagic at autopsy than strokes without such cause; this could be explained by a significant higher rate of brain herniation and death after embolic stroke. On the other hand infarcts with extended hemorrhages more often tended to have a cardiac than a non-cardiac cause. These data, together with earlier clinical findings suggest that autopsy studies are biased in relating hemorrhagic infarction almost exclusively to a cardiac embolic cause of stroke, although cardiac emboli may produce more extended hemorrhages.
Prediction of function after stroke: a critical review.
Authors: Jongbloed L
Published: June 2011

A review of 33 studies identifies the factors of prior stroke, older age, urinary and bowel incontinence, and visuo-spatial deficits as adverse prognostic indicators of function. No relationship is shown between sex, hemisphere of stroke, and functional outcome. Functional admission score is a strong predictor of discharge functional status, but its relationship with improvement in function is unclear. Findings regarding the prognostic value of severity of paralysis and onset-admission delay are ambiguous. Comparison among studies is hindered by differences in patient samples, timing of assessments, criteria by which outcome is measured and measuring instrument used. Future studies should measure function at set times post-stroke, use functional scales whose reliability and validity is well established, and be conducted in several treatment centres to ensure that the sample is representative of the population to which the predictor measure is to be applied.
Effects of nimodipine on acute focal cerebral ischemia.
Authors: Barnett G H , Bose B , Little J R , Jones S C , Friel H T
Published: June 2011

Nimodipine is a calcium slow channel blocker with several pharmacologic properties suggesting the potential to favorably modify outcome in focal cerebral ischemia. Thirty adult cats underwent unilateral middle cerebral artery (MCA) occlusion for 4 hours. Seventeen cats were treated with an ipsilateral intracarotid infusion of nimodipine (1 microgram kg-1 min -1) beginning 15 minutes before MCA occlusion and continuing throughout the occlusion period. Eight nimodipine treated cats maintaining MAP greater than 90 mmHg were assigned to a Higher Pressure Nimodipine (HPN) group. The remaining nine treated cats with MAP less than 90 mmHg were assigned to the Lower Pressure Nimodipine (LPN) group. Thirteen cats were untreated, receiving an isovolumetric amount of vehicle through the ipsilateral carotid artery. Local cerebral blood flow (ICBF) was continuously monitored using thermal diffusion probes. The brains, assessed for colloidal carbon perfusion, fluorescein and Evans blue staining, electroencephalographic activity (EEG), and histological changes, revealed no significant differences by any of these methods between the HPN and control animals with the exceptions of: HPN treated cats exhibited a preservation of EEG activity at 15 minutes post-occlusion compared to the untreated cats, and Post-ischemic surface colloidal carbon perfusion was better preserved in the treated cats than in the untreated cats. Mild hypotension, as demonstrated by the LPN group, negated these two positive effects. Prior to MCA occlusion, ICBF was bilaterally significantly increased after nimodipine infusion in the HPN group as compared to vehicle infusion. Intra-arterially infused nimodipine did not reduce infarct size.
Effect of pharmacological doses of 3-0-methyl-D-glucose and 2-deoxy-D-glucose on rat brain glucose and lactate.
Authors: Miller L P , Villeneuve J B , Braun L D , Oldendorf W H
Published: June 2011

The present investigation examined the effects of two glucose analogues, 3-0-methyl-D-glucose (30MG) and 2-deoxy-D-glucose (2DOG) on basal levels of rat brain glucose and lactate. The results showed that pretreatment (iv) with 30MG up to 2 g/kg caused a transient drop in brain glucose levels to 42% of control value within 2.5 min and a drop in lactate levels to 75% of control value by 5 min. 2DOG administration (2 g/kg) affected glucose in a biphasic response with an initial drop to 46% of control value seen by 2.5 min, followed by a progressive increase to 290% of the control value by 40 min. This elevated level of glucose was sustained for approximately 40 min. Lactate levels responded to 2DOG administration by a decrease to 37% of control value within 10 min post-injection and returned to near basal levels by 160 min. A dose response was also examined for both compounds. Behaviorally 30MG had no apparent effects. However, the response to 2DOG was a reduction in voluntary movements, piloerection, irregular clonic jerks, splayed limbs and fits of wild running. These experiments were designed to evaluate the potential of 30MG or 2DOG for attenuating the well documented rise in brain lactate levels following an ischemic insult. Our results suggest that under certain experimental conditions either 30MG or 2DOG could prevent brain lactate rise and might have beneficial effects in minimizing the neuropathological consequences of ischemic damage that could be related to increases in brain lactate.
Selective vulnerability of hippocampus and disturbances of memory storage after mild unilateral ischemia of gerbil brain.
Authors: Bothe H W , Bosma H J , Hofer H , Hossmann K A , Angermeier W F
Published: June 2011

The effect of selective injury of hippocampal neurons on the consolidation of memory traces was studied in gerbils (meriones unguiculatus) after production of mild cerebral ischemia. The right carotid artery was permanently ligated, and animals without gross neurological deficits ("symptom-negative" gerbils) were selected. Eight days and eight weeks after vascular ligation, cell counts of hippocampal neurons were carried out and correlated with regional blood flow and the acquisition of operant behaviour. Eight days after carotid artery occlusion, learning behaviour was significantly impaired although the number of hippocampal neurons had not changed and blood flow had even increased above normal. After eight weeks, learning behaviour and blood flow were normal but now a significant loss of pyramidal neurons was present in the CA1 and CA2 sectors of the hippocampus. Our observations demonstrate that it is possible to detect subtle functional disturbances by appropriate behavioural investigation before manifestation of selective injury of the hippocampus. Recovery of integrative function, despite persistent cellular damage, provides further evidence for central nervous plasticity.
Experimental acute thrombotic stroke in baboons.
Authors: Del Zoppo G J , Copeland B R , Harker L A , Waltz T A , Zyroff J , Hanson S R , Battenberg E
Published: June 2011

To study the effects of antithrombotic therapy in experimental stroke, we have characterized a baboon model of acute cerebrovascular thrombosis. In this model an inflatable silastic balloon cuff has been implanted by transorbital approach around the right middle cerebral artery (MCA), proximal to the take-off of the lenticulostriate arteries (LSA). Inflation of the balloon for 3 hours in six animals produced a stereotypic sustained stroke syndrome characterized by contralateral hemiparesis. An infarction volume of 3.2 +/- 1.5 cm3 in the ipsilateral corpus striatum was documented by computerized tomographic (CT) scanning at 10 days following stroke induction and 3.9 +/- 1.9 cm3 (n = 4) at 14 days by morphometric neuropathologic determinations of brain specimens fixed in situ by pressure-perfusion with 10% buffered formalin. Immediate pressure-perfusion fixation following deflation of the balloon was performed in 16 additional animals given Evans blue dye intravenously prior to the 3 hour MCA balloon occlusion. Light microscopy and transmission electron microscopy consistently confirmed the presence of thrombotic material occluding microcirculatory branches of the right LSA in the region of Evans blue stain, but not those of the contralateral corpus striatum. When autologous 111In-platelets were infused intravenously in four animals from the above group prior to the transient 3 hour occlusion of the right MCA, gamma scintillation camera imaging of each perfused-fixed whole brain demonstrated the presence of a single residual focus of 111In-platelet activity involving only the Evans blue-stained right corpus striatum. Focal right hemispheric activity was equivalent to 0.55 +/- 0.49 ml of whole blood, and the occlusion score derived from histologic examination of the microcirculation of the Evans blue-stained corpus striatum averaged 34.8 +/- 2.8. Similar 111In-platelet imaging and histologic scoring experiments carried out in four animals pretreated with the antithrombotic combination heparin and ticlopidine showed marked reduction of both 111In-platelet activity (0.01 +/- 0.03 ml vs. 0.55 +/- 0.49 ml; p less than 0.01) and thrombotic occlusion of the microcirculation (10.8 +/- 7.4 units vs. 34.8 +/- 2.8 units; p less than 0.01) in the right corpus striatum following 3 hours of MCA occlusion. In separate control experiments 111In-labeled autologous platelets were infused after the 3 hour period of right MCA occlusion and subsequent balloon deflation in two animals; no focus of 111In-platelet activity was demonstrated in fixed whole brain.(ABSTRACT TRUNCATED AT 400 WORDS)
Simultaneous in vivo measurement of lumped constant and rate constants in experimental cerebral ischemia using F-18 FDG.
Authors: Nakai H , Matsuda H , Takara E , Diksic M , Meyer E , Yamamoto Y L
Published: June 2011

Lumped and transfer rate constants in ischemic brain tissue must be measured to estimate accurately cerebral glucose utilization by the deoxyglucose method. We studied the bilateral middle cerebral artery occlusion model in 17 cats, 5 with a 1-hour occlusion, 5 with a 4-hour occlusion, and 7 with a sham operation. The time course of cerebral tissue radioactivity (Ci*(t)) was monitored by external coincidence counting during a programmed infusion of [18F]-2-deoxy-2-fluoro-d-glucose (18F-2-FDG). Arterial plasma concentration (Cp*(t)) of the tracer was kept constant during the first 45 minutes. Rate constants were estimated from Ci*(t) and Cp*(t) by a nonlinear least-squares fitting routine. The lumped constant was estimated from the fit of the ratio of extraction fractions of glucose and 18F-2-FDG by nonweighted, nonlinear least-squares fitting. In the 4-hour-occlusion model, the transfer constant k1* was 23% lower, k3* 39% lower, and the lumped constant 78% higher than in the sham-operated animals. In the 1-hour-occlusion model, k3* was 26% lower than in the sham-operated animals but the lumped constant was not significantly different. The rate of glucose utilization was significantly different in the 4-hour-occlusion model compared to the sham-operated animals (48% decrease, p less than 0.05) but was not significantly different in the 1-hour-occlusion model.
Binding of the hypoxia tracer [3H]misonidazole in cerebral ischemia.
Authors: Hoffman J M , Rasey J S , Spence A M , Shaw D W , Krohn K A
Published: June 2011

Radiolabelled misonidazole, a radiosensitizing drug that binds to viable hypoxic tumor cells, may be useful in identifying hypoxic cells in cerebrovascular disease. Its potential was investigated in the gerbil stroke model. Biodistribution of [3H]misonidazole was measured in normal gerbils and animals that had been subjected to right common carotid artery ligation to produce cerebral ischemia. The uptake of [3H]misonidazole in the right cerebral hemisphere and right/left hemispheral uptake ratios correlated positively with the severity of the stroke when measured 6-9 hours after carotid ligation. Histologic studies in symptomatic ligated animals showed ipsilateral widespread but patchy acute ischemic changes as well as areas that showed no morphological changes. Microscopic autoradiography in these animals showed diffuse heavy labelling only in the ipsilateral hemisphere. This was over areas that had histological damage as well as in adjacent areas that appeared intact. Studies comparing blood flow measured with [14C]iodoantipyrine and [3H]misonidazole retention in gerbils with carotid artery ligations indicated that flow is not a major determinant of retention of this hypoxia tracer. We conclude that a misonidazole congener labelled with a gamma- or positron-emitting isotope may be useful in nuclear imaging of the degree and regional distribution of hypoxic tissue in cerebrovascular disease.
Cerebral amyloid angiopathy presenting as a mass lesion.
Authors: Briceno C E , Resch L , Bernstein M
Published: June 2011

A rare clinical presentation of cerebral amyloid angiopathy is reported. Our patient presented with the clinical and radiological signs of a right frontal mass lesion suggesting a brain tumor, and a biopsy provided the diagnosis of cerebral amyloid angiopathy. A brief review of the pathology and clinical features of cerebral amyloid angiopathy is presented.
Does cerebral vasospasm result from denervation supersensitivity?
Authors: Duff T A , Feilbach J A , Scott G
Published: June 2011

This study examined the role of denervation supersensitivity in the development of cerebral vasospasm. Adrenergic denervation of cat basilar artery was accomplished by resection of the superior cervical ganglia or by injection of 6-hydroxydopamine into the cisterna magna. In vivo dose-response characteristics were determined for normal and for denervated arteries, and no significant differences were found between topical applications of serotonin, norepinephrine, epinephrine, fresh blood, or incubated blood. In addition, analysis of cat blood incubated in vitro revealed that the levels of serotonin, norepinephrine, and epinephrine diminished over time, whereas levels of hemoglobin and methemoglobin increased up to Day 14. The results of this study indicate that adrenergic denervation is not the cause of cerebral vasospasm and that, whatever the mechanism, hemoglobin is far more likely to play a role than are the other agents.
The paramedian diencephalic syndrome: a dynamic phenomenon.
Authors: Meissner I , Sapir S , Kokmen E , Stein S D
Published: June 2011

The paramedian diencephalic syndrome is characterized by a clinical triad: hypersomnolent apathy, amnesic syndrome, and impaired vertical gaze. We studied 4 cases with computed tomography evidence of bilateral diencephalic infarctions. Each case began abruptly with hypersomnolent apathy followed by fluctuations from appropriate affect, full orientation, and alertness to labile mood, confabulation, and apathy. Speech varied from hypophonia to normal; handwriting varied from legible script to gross scrawl. Psychological testing revealed poor learning and recall, with low performance scores. In 3 patients the predominant abnormality was in downward gaze.
Blood flow through cerebral collateral vessels one month after middle cerebral artery occlusion.
Authors: Coyle P , Heistad D D
Published: June 2011

Acute occlusion of a middle cerebral artery (MCA) reduces cerebral blood flow in normotensive Wistar-Kyoto rats (WKY) and in stroke-prone spontaneously hypertensive rats (SHRSP). The goal of this study was to determine whether MCA occlusion produces a sustained reduction in cerebral blood flow or whether collateral vessels restore blood flow to normal levels. We measured blood flow through cerebral collateral vessels to the territory of the occluded MCA and to homologous tissue of the other hemisphere in WKY 1 month after occlusion of the MCA. Cerebral blood flow, measured with microspheres, was restored to normal levels under control conditions in the territory of the occluded MCA. During vasodilatation produced by seizures, blood flow and vascular conductance were increased to similar levels in tissue distal to the site of MCA occlusion and in the homologous tissue of the other hemisphere. MCA occlusion did not produce infarction in any of the WKY. In contrast, 1 month after MCA occlusion in SHRSP, a large atrophic infarct was invariably present in the territory of the occluded MCA. The number of collateral vessels to the territory of the MCA do not differ in SHRSP and WKY. Internal diameter and orientation of the anastomotic vessels differ in SHRSP and WKY. We conclude that, after 1 month of MCA occlusion, changes in the collateral vessels supplying the territory of the occluded MCA in WKY were sufficient to restore blood flow to normal under control conditions and to virtually normal levels during vasodilatation.(ABSTRACT TRUNCATED AT 250 WORDS)
Identification and quantitative analysis of hydroxy-eicosatetraenoic acids in rat brains exposed to regional ischemia.
Authors: Usui M , Asano T , Takakura K
Published: June 2011

To clarify possible roles in the pathogenesis of ischemic brain edema, identification and quantitative analysis of hydroxy-eicosatetraenoic acids (HETEs) in rat brains exposed to middle cerebral artery occlusion were carried out using high-performance liquid chromatography. Rat brain sampling was done by in situ freezing 24 and 72 hours after occlusion. Only a small amount of 15-HETE was found in control rat brains. Twenty-four hours after ischemia, 11-HETE appeared, and the amount of 15-HETE tended to increase. Seventy-two hours after ischemia, when brain edema reached its maximum, 5-, 8-, 9-, 11-, 12-, and 15-HETEs were identified, and the amounts of all HETEs except 8- and 12-HETE were significantly increased. The detection of 5-HETE in ischemic rat brain indicates the simultaneous production of leukotrienes in the same brain area. The above results support the view that lipoxygenase products may play significant roles in the formation of ischemic brain edema.
Two-year longitudinal study of post-stroke mood disorders: dynamic changes in correlates of depression at one and two years.
Authors: Parikh R M , Lipsey J R , Robinson R G , Price T R
Published: June 2011

As part of a prospective study of 103 stroke patients, we have analyzed the relation between depression and associated variables at 3 months, 6 months, 1 year, and 2 years after stroke. At all intervals up to and including 1 year poststroke, patients with left hemisphere strokes showed a strong relation between severity of depression and distance of the lesion on computed tomography scan from the frontal pole. At 2 years poststroke, this relation was no longer significant. The correlation between depression and impairment in activities of daily living peaked at 6 months and thereafter fell but remained significant at 1 and 2 years poststroke. The correlation between depression and cognitive impairment and between depression and social functioning fluctuated--with most correlations at 1 and 2 years follow-up nonsignificant. Although the conclusions that can be drawn from this study are limited by the fact that less than half of the original patients were followed up at each time, these declining correlations between depression and associated variables at 1 and 2 years follow-up may reflect the natural course of major depression which spontaneously remits between 1 and 2 years after stroke. The persisting significant association of impairment in activities of daily living with depression may reflect the effect of severe depression in sustaining and possibly retarding recovery from physical impairment.
Cerebellar infarction: natural history, prognosis, and pathology.
Authors: Macdonell R A , Kalnins R M , Donnan G A
Published: June 2011

Using clinical and computed tomography (CT) criteria, an analysis of 2,000 consecutive stroke unit patients from 1977 to 1984 revealed 30 patients with cerebellar infarction. The case fatality rate was 23%, higher than for any other location of brain infarction studied over the same period. Death was most often due to concomitant brainstem infarction. Obstructive hydrocephalus occurred in 4 patients (13%), and in 2 cases diagnosis, facilitated by urgent CT scanning, allowed early surgical intervention that was life saving. Patients who survived the acute phase were followed for an average of 21 months, and over that time 22% sustained further brainstem infarction, representing a 13% stroke rate per year. Over the latter 3 years of the clinical study, an autopsy survey revealed 11 cases of cerebellar infarction that had been clinically unrecognized. None of these died as a direct result of their infarction. Mechanisms of infarction inferred from autopsy included in situ thrombosis, embolism, watershed, and lacunar infarction, with in situ thrombosis being the most common. We conclude that the case fatality rate of cerebellar infarction is greater than of any other form of brain infarction, but it may be reduced by prompt recognition of those patients who will benefit from surgical decompression. In survivors, a high risk of subsequent hindbrain stroke exists. More attention needs to be paid to this entity in terms of early diagnosis and prevention of subsequent stroke.
Intracellular acidosis during and after cerebral ischemia: in vivo nuclear magnetic resonance study of hyperglycemia in cats.
Authors: Chopp M , Frinak S , Walton D R , Smith M B , Welch K M
Published: June 2011

In vivo 31P nuclear magnetic resonance spectroscopy was used to monitor the time course of intracellular pH in cat cerebral cortex subjected to global cerebral ischemia under control and hyperglycemic pretreatment conditions. Transient (16 minutes) global cerebral ischemia was induced in 14 cats using an inflatable cervical cuff combined with systemic arterial hypotension. Six cats were pretreated with infusion of 1.5 g/kg glucose prior to ischemia. Relative concentrations of high-energy phosphate metabolites and intracellular pH were continuously monitored before, during, and for 2 hours after cerebral reperfusion. During ischemia, intracellular pH fell to the same level and followed a similar time course in both groups. However, during initial reperfusion in the hyperglycemic group, there was a severe further decline (p less than 0.003) in intracellular pH. We suggest that the increased neurologic deficit and mortality found in hyperglycemic animals subjected to cerebral ischemia may be attributed to this transient severe tissue acidosis.
Variations in middle cerebral artery blood flow investigated with noninvasive transcranial blood velocity measurements.
Authors: Lindegaard K F , Lundar T , Wiberg J , Sjøberg D , Aaslid R , Nornes H
Published: June 2011

Observations on blood velocity in the middle cerebral artery using transcranial Doppler ultrasound and on the ipsilateral internal carotid artery flow volume were obtained during periods of transient, rapid blood flow variations in 7 patients. Five patients were investigated after carotid endarterectomy. A further 2 patients having staged carotid endarterectomy and open heart surgery were investigated during nonpulsatile cardiopulmonary bypass. The patient selection permitted the assumption that middle cerebral artery flow remained proportional to internal carotid artery flow. The integrated time-mean values from consecutive 5-second periods were computed. The arithmetic mean internal carotid artery flow varied from 167 to 399 ml/min in individual patients, with individual ranges between +/- 15% and +/- 35% of the mean flow. The mean middle cerebral artery blood velocity varied from 32 to 78 cm/sec. The relation between flow volume and blood velocity was nearly linear under these conditions. Normalization of the data as percent of the individual arithmetic means permitted a composite analysis of data from all patients. Linear regression of normalized blood velocity (V') on normalized flow volume (Q') showed V' = 1.05 Q' - 5.08 (r2 = 0.898).
Occurrence of stroke in a nonhuman primate model of cerebrovascular disease.
Authors: Prusty S , Kemper T , Moss M B , Hollander W
Published: June 2011

A relation between hypertension, atherosclerosis, and stroke is well documented in humans. We report a similar relation in two hypertensive cynomolgus monkeys with severe cerebral atherosclerosis. In our primate model hypertension is induced by surgical coarctation of the aorta. These monkeys, when fed an atherogenic diet, develop severe cerebrovascular atherosclerosis. In this setting two monkeys developed spontaneous cerebral hemispheric strokes that occurred during treatment of hypertension. Since the strokes were topographically related to severe atherosclerotic narrowing of cerebral arteries and occurred without evidence of either thrombosis or embolization, they are presumed to be related to disturbances of blood flow. In both humans and animals cerebral perfusion is autoregulated to a constant flow over a wide range of mean arterial blood pressures. In hypertension both the upper and lower limits of autoregulation are increased. With treatment of hypertension readaptation to more normal levels is reported to be inconsistent and slow to develop. It is therefore postulated that the strokes in these two monkeys were due to hypoperfusion as a result of the combination of pharmacologic reduction in blood pressure and severe occlusive atherosclerosis.
The relation of retinal artery occlusion and carotid artery stenosis.
Authors: Merchut M P , Gupta S R , Naheedy M H
Published: June 2011

We retrospectively studied 46 patients with symptomatic retinal artery occlusion and assessed the pattern and extent of carotid artery disease ipsilateral to the retinal artery occlusion. Ipsilateral internal carotid artery atherosclerotic lesions were virtually limited to the cervical arterial segment; 50% of such lesions were plaques or stenoses of less than or equal to 60%, whereas 15% of the angiograms were normal. No clinical features were significantly associated with a flow-limiting carotid stenosis of greater than 60%. Contrary to previous reports, the type of retinal artery occlusion, whether branch or central artery occlusion, was not predictive of severe underlying carotid stenosis or occlusion. Likely mechanisms of retinal artery occlusion include in situ thrombosis and emboli from carotid, and possibly cardiac, sources. Extension of thrombus from an occluded carotid artery into the ophthalmic artery did not appear to be a mechanism of retinal artery occlusion.
Cognition and cerebral blood flow fluctuate together in multi-infarct dementia.
Authors: Meyer J S , Rogers R L , Judd B W , Mortel K F , Sims P
Published: June 2011

Longitudinal measurements of cognitive ability measured by serial testing using the Cognitive Capacity Screening Examination (CCSE) were correlated with cerebral blood flow (CBF) throughout (mean +/- SD) 19.9 +/- 12.6 months among 57 patients with multi-infarct dementia, 17 with dementia of the Alzheimer's type, 10 with both, and among 32 age-matched elderly normal controls. Longitudinal CCSE and CBF measurements among controls yielded stable normative values. Reduced mean CCSE scores correlated directly with CBF reductions in patients with multi-infarct dementia (p less than 0.0005) and dementia of the Alzheimer's type (p less than 0.028). Patients with multi-infarct dementia had CCSE scores with retest variability exceeding those of controls (p less than 0.001) and of patients with dementia of the Alzheimer's type (p less than 0.003). CCSE scores and CBF changed together 78.6% (p less than 0.001) of the time in patients with multi-infarct dementia compared with 66.2% of the time (p less than 0.01) in those with both, 62.9% of the time (p less than 0.05) in those with dementia of the Alzheimer's type, and 47.7% of the time (NS) in controls. Further analyses indicated that changes in CCSE scores and CBF were predominantly progressive declines in patients with dementia of the Alzheimer's type, whereas the changes were more bidirectional (both increases and decreases) in patients with multi-infarct dementia; these differences were also significant. Results support the diagnostic usefulness of the Hachinski ischemic scale and confirm that both cognition and CBF fluctuate together among patients with multi-infarct dementia, whereas patients with dementia of the Alzheimer's type exhibit a more stable course, with progressive declines in cognition and CBF.
Amaurosis fugax in a Danish community: a prospective study.
Authors: Andersen C U , Marquardsen J , Mikkelsen B , Nehen J H , Pedersen K K , Vesterlund T
Published: June 2011

A prospective study of amaurosis fugax was carried out in a Danish community (population 481,000); case ascertainment was based on the collaboration of practicing ophthalmologists and general practitioners. Over a 3-year period we registered 131 cases; the annual incidence of "first amaurosis fugax episodes coming to medical attention" was 8.6 and 6.2 per 100,000 population for men and women, respectively. On the basis of a comparison of the age-incidence curves for cerebral and retinal ischemic attacks, the "true" incidence of amaurosis fugax is estimated to be approximately 14/100,000/yr, or 25-30% of the reported incidence of transient ischemic attacks. Clinical and/or radiologic signs of a carotid lesion on the appropriate side were present in 56% of the patients, and an additional 27% had symptoms or signs of other organic cardiovascular disorders. Forty-three (68%) of the 63 patients who underwent arteriography had an atheromatous lesion apparently amenable to carotid endarterectomy. In spite of the case-finding procedures employed in the study, cases of amaurosis fugax suitable for carotid surgery were thus ascertained at a rate of only 3/100,000/yr. This suggests that surgical treatment of patients with retinal ischemic attacks is of minor importance as a preventive measure against stroke in the community.
Transesophageal two-dimensional echocardiography in young patients with cerebral ischemic events.
Authors: Zenker G , Erbel R , Krämer G , Mohr-Kahaly S , Drexler M , Harnoncourt K , Meyer J
Published: June 2011

Using transesophageal echocardiography, cardiac structures can be imaged with high resolution. The aim of our study was to evaluate whether transesophageal echocardiography is superior in detecting mitral valve prolapse and other cardiac abnormalities compared with transthoracic echocardiography in an age-matched control group and in young patients with cerebral ischemic events (patient group). Forty patients with cerebral ischemic events (mean age 35.2 years) and 29 controls (mean age 30.4 years) were examined using both methods. Transthoracic and transesophageal echocardiography showed a significantly higher incidence of mitral valve prolapse in the patient group compared with the control group (p less than 0.001). By means of transesophageal echocardiography, it was possible to measure highly significant bulging in both the anterior and the posterior mitral leaflet in the patient group compared with the control group (p less than 0.001), and the thickness of the mitral leaflets was significantly higher in the patient group. In 9 of 20 (45%) patients with normal transthoracic echocardiograms, transesophageal echocardiography showed pathologic findings. We found transesophageal echocardiography to be a sensitive method for detecting mitral valve prolapse as well as valve changes and other cardiac abnormalities not detectable by conventional echocardiography. Our study underlines the role of mitral valve prolapse in young stroke patients as a relevant risk factor and emphasizes the importance of changed mitral valve morphology.
Strong attenuation of ischemic and postischemic brain edema in rats by a novel free radical scavenger.
Authors: Abe K , Yuki S , Kogure K
Published: June 2011

Regional changes in the amount of free fatty acids, polyphosphoinositides, and water content in the cerebral cortex were examined using a middle cerebral artery occlusion model of rats. The amount of various free fatty acids increased as polyphosphoinositides decreased during 3 and 6 hours of ischemia in the occluded middle cerebral artery territory. After 3 hours of reperfusion following 3 hours of ischemia, free fatty acids partially recovered while polyphosphoinositides did not. Water content increased significantly after 3 and 6 hours of ischemia, and a further increase was found after 3 hours of reperfusion following 3 hours of ischemia. The change of polyenoic fatty acids in this occluded middle cerebral artery territory was much smaller than that in the case of decapitation ischemia, although the amounts of polyphosphoinositides and monoenoic and saturated fatty acids showed almost identical changes in both cases, probably because polyenoic fatty acids may be washed out and/or peroxidatively consumed in the middle cerebral artery occlusion model due to its residual blood flow. Changes in the area surrounding the occluded middle cerebral artery territory were similar to the above results, although less dramatic. However, there was no change in free fatty acids, polyphosphoinositides, and water content in the contralateral cortex. A novel free radical scavenger (MCI-186), which prevents both nonenzymatic peroxidation and lipoxygenase activity in vitro, markedly attenuated the ischemic and postischemic brain swelling. These results suggest that free radical mechanisms may be involved in ischemic and postischemic brain edema.
Autoregulatory capacity and the effect of isovolemic hemodilution on local cerebral blood flow.
Authors: von Kummer R , Scharf J , Back T , Reich H , Machens H G , Wildemann B
Published: June 2011

The effect of isovolemic hemodilution with dextran 40 on local cerebral blood flow was measured in eight cats by means of the hydrogen clearance technique. Under normotension the decrease of hematocrit from 35% to 25% causes a sudden increase of up to 30% in local cerebral blood flow. After lowering the mean arterial blood pressure from 140 to 80 mm Hg, hemodilution did not alter cerebral blood flow significantly. From this observation it is concluded that the increase of cerebral blood flow following hemodilution is caused by compensatory vasodilatation and not by reduction of blood viscosity. This could imply that hemodilution cannot improve blood flow in areas of impaired autoregulation.
Sleep apnea as a feature of bulbar stroke.
Authors: Askenasy J J , Goldhammer I
Published: June 2011

Medullary disorders can be associated with a sleep apnea syndrome. The present patient developed a sleep apnea syndrome with approximately 25 episodes of apnea or hypopnea during each hour of sleep following a lateral medullary infarction. The presence of predisposing factors and involvement of respiratory centers in the area of the medullary lesion may determine the appearance of sleep apnea with brainstem infarction. Investigation of breathing during sleep may be helpful in such cases.
Triple-tracer autoradiography demonstrates effects of hyperglycemia on cerebral blood flow, pH, and glucose utilization in cerebral ischemia of rats.
Authors: Nakai H , Yamamoto Y L , Diksic M , Worsley K J , Takara E
Published: June 2011

Triple-tracer autoradiography was used to measure topographic changes in local cerebral blood flow, cerebral tissue pH, and local cerebral glucose utilization in hyperglycemic and normoglycemic rats, all of which had undergone occlusion of the middle cerebral artery. More severe and extensive reduction of all three variables was observed in the hyperglycemic than in the normoglycemic rats. In seven normoglycemic rats, significant reduction in local cerebral blood flow (p less than 0.025) was observed in the ischemic but not in the contralateral nonischemic side at the lateral portion of the caudate nucleus and the neocortex. Tissue pH was significantly lower (p less than 0.025) only at the lateral portion of the caudate nucleus in the ischemic side. No significant differences in local cerebral glucose utilization were observed when the two hemispheres were compared. In the ischemic hemisphere of five hyperglycemic rats, the caudate nucleus and the neocortex exhibited significant reduction (p less than 0.025) in local cerebral blood flow, tissue pH, and local cerebral glucose utilization. Even in the nonischemic hemisphere of the hyperglycemic rats, local cerebral blood flow in the caudate nucleus and the neocortex was significantly reduced (p less than 0.025) compared with the normoglycemic rats. No significant change in tissue pH or local cerebral glucose utilization was observed throughout the nonischemic hemisphere of the hyperglycemic compared with the normoglycemic rats. Tissue pH was systematically lower in the hyperglycemic than in the normoglycemic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
A prospective study of cerebral artery atherosclerosis.
Authors: Reed D M , Resch J A , Hayashi T , MacLean C , Yano K
Published: June 2011

Atherosclerosis in the circle of Willis and its major branches was studied prospectively in 198 men in the Honolulu Heart Program who were free of cardiovascular disease at the entry examination. The level of atherosclerosis was greater in the large arteries of the circle of Willis than in the small arteries, and autopsy-verified cerebral infarction was strongly associated with increasing severity of atherosclerosis in both. Analyses of the association of atherosclerosis scores with biologic and lifestyle characteristics measured at entry into the study indicated that atherosclerosis in the large arteries was consistently related to age, diastolic blood pressure, serum cholesterol, and height (inversely). Weak trends of association were also found with increasing serum glucose concentration, increasing cigarette use, and decreasing alcohol intake. Atherosclerosis scores in the small arteries were associated with diastolic blood pressure and serum triglyceride concentration. Analysis of dietary intake indicated that atherosclerosis scores were higher for men who reported low intakes of fat and animal protein and high intakes of vegetable protein and total carbohydrates. These patterns were consistent with similar findings on the incidence of clinical stroke in this cohort. Age-adjusted and -specific atherosclerosis scores from both the large and small arteries declined significantly during the period 1965-1983.
Cerebral infarction due to moyamoya disease in young adults.
Authors: Bruno A , Adams H P , Biller J , Rezai K , Cornell S , Aschenbrener C A
Published: June 2011

Moyamoya disease was diagnosed as the cause of cerebral infarction in eight young adults (seven women, one man), aged 17-40 (mean 33) years. All had angiographic abnormalities characteristic of moyamoya disease. Single-photon emission tomography showed bilateral carotid circulation hypoperfusion and posterior circulation hyperemia in all seven patients with regional cerebral blood flow studies. All seven women had used oral contraceptives before cerebral infarction. Four patients were treated medically; one died of a second cerebral infarction 9 months after diagnosis. Four patients underwent superficial temporal-to-middle cerebral artery anastomosis; they did well. Moyamoya disease should be included in the differential diagnosis of cerebral infarction as well as intracranial hemorrhage in young adults, particularly women. A possible relation between moyamoya disease and oral contraceptive use deserves investigation.
Results of the seven-year prospective study of stroke patients.
Authors: Scmidt E V , Smirnov V E , Ryabova V S
Published: June 2011

Using the registry method, 1,538 stroke patients were detected in one district of Moscow between January 1, 1972, and December 31, 1974. Of the 965 patients who survived the acute stage of stroke (the first 3 weeks after onset), 941 (505 women and 436 men) were followed for the next 7 years. We analyzed incidence and types of recurrent strokes. During this 7-year follow-up, we recorded 32.1% of the patients as having recurrent strokes, most of which developed in the first 3 years and especially during the first year after the index stroke. The majority of recurrent strokes were of the same type as the index stroke and were localized in the same area of the brain. The cumulative mortality rates for the initial 1,538 patients were 37.3% dead by 3 weeks, 63.6% dead by 3 years, 72.1% dead by 5 years, and 76.5% dead by 7 years. In the first 3 months (excluding the first 3 weeks), most patients who died died of pulmonary thromboembolism. The mortality rate from recurrent strokes and pneumonia was higher than that from cardiovascular mortality. Transient ischemic attacks occurred in 49.5% of all patients and myocardial infarction in 16.4%. Functional prognosis was determined mainly by age, motor function, and concomitant diseases. After 1 year, 68.2% of the surviving patients were fully independent, while 81% of those surviving 7 years had reached this level. A significant number of patients were capable of returning to their previous work.
Noninvasive assessment of CO2-induced cerebral vasomotor response in normal individuals and patients with internal carotid artery occlusions.
Authors: Ringelstein E B , Sievers C , Ecker S , Schneider P A , Otis S M
Published: June 2011

To evaluate the CO2-induced vasomotor reactivity of the cerebral vasculature, relative changes of blood flow velocity within the middle cerebral artery were measured by transcranial Doppler ultrasonography during normocapnia and various degrees of hypercapnia and hypocapnia. We studied 40 normal individuals and 40 patients with unilateral and 15 patients with bilateral internal carotid artery occlusions. When blood flow velocity changes as percent of normocapnic values were plotted against end-tidal CO2 volume percent, a biasymptotic curve (a tangent-hyperbolic function) gave the best fit of the scattergram. The distance between the upper and lower asymptotes was defined as cerebral vasomotor reactivity. In the normal individuals, mean +/- SD vasomotor reactivity was 85.63 +/- 15.96%. In patients with internal carotid artery occlusions, vasomotor reactivity was significantly lower than normal on both the occluded (mean 45.2%, median 50.4%; p less than 0.0001) and the nonoccluded (mean +/- SD 67.7 + 13.3%, p less than 0.01) sides in the unilateral group and on both sides (mean +/- SD 36.6 +/- 15.9% and 44.9 +/- 24.6%, p less than 0.0001) in the bilateral group. The difference between vasomotor reactivity for symptomatic and asymptomatic unilateral occlusions was also highly significant (mean 37.6% and 62.9%, p less than 0.006). Vasomotor reactivity was also significantly lower in patients with low-flow infarctions on computed tomography than in patients with normal scans (mean +/- SD 36.7 +/- 25% and 60.2 +/- 16.9%, p less than 0.008). A striking association of low-flow infarctions, ischemic ophthalmopathy, and hypostatic transient ischemic attacks was found with vasomotor reactivities of less than 34% or even paradoxical reactions.(ABSTRACT TRUNCATED AT 250 WORDS)