bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transcranial Doppler correlation with angiography in detection of intracranial stenosis.
Authors: Rorick M B , Nichols F T , Adams R J 
Published: June 2011

The purpose of this study was to evaluate the use of velocity criteria applied to transcranial Doppler (TCD) signals in the detection of stenosis of the middle cerebral (MCA), distal vertebral, and basilar arteries.
Sixty-five patients who underwent both cerebral angiography and transcranial Doppler examinations in the workup of acute cerebral ischemia were reviewed. Angiography was performed a mean of 7 +/- 5 days (range, 1 to 28 days) after TCD. Interpretation of the angiogram was performed without input regarding the TCD findings. TCD interpretation was performed according to standard criteria.
When we used a mean velocity (MV) cutoff of > or = 80 cm/s in the MCA as the criterion for stenosis, 10 of 12 stenoses of any degree were detected by TCD, with 11 of 87 false-positives. Nine of 12 MCA stem (M1) stenoses were detected when a cutoff of > or = 90 cm/s was used, with 7 of 87 false-positives. When we used an MV cutoff of > or = 70 cm/s as the criterion for > or = 50% stenosis of the vertebrobasilar system, 5 of 6 stenoses were detected, with 15 of 85 false-positives. The most important confounding factor was the presence of > or = 75% stenosis of the extracranial internal carotid artery, resulting in both false-positive (from collateral flow) and false-negative (decreased volume flow from the proximal stenosis without adequate collateral flow) errors in TCD interpretation. When patients with > or = 75% stenosis of the cervical internal carotid artery were excluded from analysis, a TCD MV cutoff of > or = 80 cm/s identified 9 of 10 M1 lesions with 7 of 61 false-positives, and an MV of > or = 70 cm/s identified 3 of 4 vertebrobasilar lesions causing > or = 50% stenosis with 7 of 56 false-positives.
TCD may be an effective screening test for M1 stenosis when velocity criteria alone are used. TCD may less reliably detect intracranial vertebral and basilar artery stenosis.
Predicting survival for 1 year among different subtypes of stroke. Results from the Perth Community Stroke Study.
Authors: Anderson C S , Jamrozik K D , Broadhurst R J , Stewart-Wynne E G 
Published: June 2011

Few studies have evaluated the factors influencing or predicting long-term survival after stroke in an unselected series of patients in whom the underlying cerebrovascular pathology is clearly defined. Moreover, the relative importance of risk factors for stroke, including sociodemographic and premorbid variables, has not been described in detail.
The study cohort consisted of 492 patients with stroke who were registered with a population-based study of acute cerebrovascular disease undertaken in Perth, Western Australia, during an 18-month period in 1989 and 1990. Objective evidence of the pathological basis of the stroke was obtained in 86% of cases, and all deaths among patients during a follow-up of 1 year were reviewed.
One hundred twenty patients (24%) died within 28 days of the onset of stroke. Among the different subtypes of stroke, the 1-year case fatality (mean, 38%) varied from 6% and 16% for boundary zone infarction and lacunar infarction, respectively, to 42% and 46% for subarachnoid hemorrhage and primary intracerebral hemorrhage, respectively. Using Cox proportional-hazards analysis, a predictive model was developed on 321 patients with acute stroke (test sample). The best model contained five baseline variables that were independent predictors of death within 1 year: coma (relative risk [RR], 3.0; 95% confidence interval [CI], 1.1 to 8.4), urinary incontinence (RR, 3.9; 95% CI, 1.4 to 10.6), cardiac failure (RR, 6.5; 95% CI, 2.8 to 15.1), severe paresis (RR, 4.9; 95% CI, 1.6 to 15.5), and atrial fibrillation (RR, 2.0; 95% CI, 1.1 to 3.5). The sensitivity, specificity, and negative predictive value of this model for predicting death were 90%, 83%, and 95%, respectively. When applied to a second randomly selected validation sample of 171 events, sensitivity was 94%, specificity 62%, and negative predictive value 92%, indicating stability of the model.
Although the case fatality, timing, and cause of death vary considerably among the different pathological subtypes of stroke, simple clinical measures that reflect the severity of the neurological deficit and associated cardiac disease at onset independently predict death by 1 year and may help to direct management.
Course of cerebrovascular reactivity in patients with carotid artery occlusions.
Authors: Widder B , Kleiser B , Krapf H 
Published: June 2011

Patients with internal carotid artery occlusions and highly impaired cerebrovascular reactivity have been identified as having an increased risk of stroke. It is still unclear, however, whether cerebral hemodynamics may be restored in the course of time by the development of collaterals.
During a 5-year period we assessed cerebrovascular reactivity in 452 carotid occlusions by transcranial Doppler CO2 testing. Ninety-eight patients could be reinvestigated at least once after 2 to 58 months (mean follow-up time, 26 months).
On admission, patients with recent transient ischemic attack or stroke (< or = 3 months) as well as patients with contralateral carotid stenoses of 80% diameter reduction or greater and occlusions revealed a significantly higher incidence of impaired CO2 reactivity (P < .0001 and P < .01, respectively). During follow-up, 64% of the patients with no or minor contralateral carotid stenoses, but only 22% of the patients with bilateral carotid occlusions, showed a spontaneous improvement in cerebrovascular reactivity (P < .001), mainly during the first few months. In six of eight patients cerebral hemodynamics on the occluded side improved after endarterectomy of a contralateral high-grade carotid stenosis. Five of the patients who did not undergo surgery developed a stroke during follow-up, with three of them occurring in patients with permanently exhausted cerebrovascular reactivity.
In the majority of patients with carotid occlusions an initially impaired cerebrovascular reactivity improves spontaneously with time. This could influence therapeutic decisions: During the first few months antihypertensive treatment may be avoided in such cases until a reestablished reactivity can be demonstrated. If cerebral hemodynamics remain depleted, extracranial-intracranial bypass surgery or endarterectomy of an asymptomatic contralateral high-grade carotid stenosis could be helpful.
Electroencephalography improves the prediction of functional outcome in the acute stage of cerebral ischemia.
Authors: Cillessen J P , van Huffelen A C , Kappelle L J , Algra A , van Gijn J 
Published: June 2011

We studied the value of clinical and electroencephalographic assessment in patients with acute first-ever supratentorial ischemia in predicting functional outcome after 1 year.
In 55 consecutive patients admitted after a median interval of less than 24 hours, the degree of handicap was dichotomized as moderate (Rankin grade 1, 2, or 3) or severe (Rankin grade 4 or 5). Clinical deficits were categorized according to signs of a lacunar or a cortical syndrome. Without knowledge of clinical data, electroencephalograms (EEGs) were classified according to findings predicting good or poor prognosis. The outcome after 1 year was assessed as good (Rankin grade 3 or less) or poor (Rankin grade 4 or 5 or death from stroke) and was correlated to clinical data and to EEG findings in the acute stage.
Thirty patients with a moderate handicap on admission all had a good outcome (predictive value [PV] of the initial handicap, 1.00; 95% confidence interval [CI], 0.88 to 1.00). Of the 25 patients with severe handicap on admission a poor outcome occurred in 13 (PV, 0.52; 95% CI, 0.31 to 0.72). If these patients with severe handicap at baseline were subdivided according to clinical features, a lacunar syndrome predicted good outcome in 4 of 5 patients (PV, 0.80; 95% CI, 0.28 to 1.00), but a cortical syndrome predicted poor outcome in only 12 of 20 patients (PV, 0.60; 95% CI, 0.36 to 0.81). Of the 20 patients with severe handicap and a cortical syndrome at baseline, an EEG with features predicting a good prognosis correctly predicted good outcome in 6 of 7 patients (PV, 0.86; 95% CI, 0.42 to 1.00). An EEG with features predicting poor prognosis correctly predicted poor outcome in 11 of 13 patients (PV, 0.85; 95% CI, 0.55 to 0.98).
Electroencephalography improves the prediction of functional outcome in patients with a severe neurological deficit in the acute stage of cerebral ischemia. This may have implications for the design of future intervention trials in acute stroke.
Effect of plasma fibrinogen concentration on the inhibition of platelet aggregation after ticlopidine compared with aspirin.
Authors: Tohgi H , Takahashi H , Kashiwaya M , Watanabe K 
Published: June 2011

Elevated levels of plasma fibrinogen are a risk factor for cerebral infarction. Because fibrinogen plays a central role in platelet aggregation and binding of fibrinogen to platelets is inhibited by ticlopidine, we studied the effect of the plasma fibrinogen concentration on the antiaggregatory action of ticlopidine compared with that of aspirin.
We determined platelet aggregability before and after administration of ticlopidine (200 mg/d) or aspirin (81 mg/d) in 61 stroke patients and correlated the changes with the plasma fibrinogen concentration.
In patients receiving ticlopidine, the platelet aggregability induced by 1, 5, and 10 mumol/L adenosine diphosphate significantly decreased compared with aggregability before medication (P < .05), and the reductions had significant negative correlations with the plasma fibrinogen concentration (P < .05). In patients receiving aspirin, the platelet aggregability induced by 2 micrograms/mL collagen and 5 and 10 mumol/L adenosine diphosphate decreased compared with aggregability before medication (P < .005), but the reductions had no significant correlation with the plasma fibrinogen concentration.
The relative antiaggregatory effect of ticlopidine is significantly decreased with higher plasma fibrinogen concentrations. This may explain, at least in part, the individual variation in the response to ticlopidine.
(S)-emopamil reduces brain edema from collagenase-induced hemorrhage in rats.
Authors: Rosenberg G A , Navratil M J 
Published: June 2011

Calcium channel blockers reduce edema due to cerebral ischemia, but little is known about their usefulness in hemorrhage. Therefore, we studied the effect of the calcium channel blocker (S)-emopamil in collagenase-induced hemorrhage.
Adult rats had hemorrhagic necrosis induced by the intracerebral injection of 0.4 U of bacterial collagenase. Six groups of rats were given either 10 or 20 mg/kg (S)-emopamil at different times after induction of the lesion. Brain water and electrolyte levels in these rats were measured 24 hours after collagenase injection. Also, lesion volume in other rats was measured either 4 or 24 hours after formation of the lesion with the drug given at 1 hour or both 1 and 5 hours, respectively.
Administration of 20 mg/kg (S)-emopamil 1 hour after lesion induction significantly decreased water and electrolyte content in both posterior regions (P < .05). This beneficial effect was lost when a second 20-mg/kg dose was given at 5 hours. A single 20-mg/kg injection at 1 hour had no effect on lesion volume at 4 hours. Two doses significantly increased volume at 24 hours (P < .05).
Early administration of (S)-emopamil is beneficial in hemorrhagic lesions, but a subsequent delayed injection may be deleterious. Knowledge of the time of hemorrhage will be important in use of these agents in treating hemorrhage.
Responses of cerebral arterioles to kainate.
Authors: Faraci F M , Breese K R , Heistad D D 
Published: June 2011

Neurons release nitric oxide in response to glutamate. Glutamate acts via activation of different receptor subtypes, including N-methyl-D-aspartate and kainate receptors. This study examined the hypothesis that kainate produces dilatation of cerebral arterioles that is dependent on the formation of nitric oxide.
Diameters of cerebral arterioles were measured by means of a closed cranial window in anesthetized rabbits. Kainate, quisqualate, acetylcholine, and NG-nitro-L-arginine (L-NNA, an inhibitor of nitric oxide synthase) were applied locally in the cranial window. We also examined whether kainate elicited direct vascular effects by the use of isolated cerebral arteries in vitro.
Under control conditions, topical kainate (100 mumol/L) increased the diameter of arterioles by 20 +/- 5% (mean +/- SE), 27 +/- 7%, and 31 +/- 7% at 3, 5, and 9 minutes of application, respectively. After topical application of L-NNA (300 mumol/L), kainate dilated cerebral arterioles by 8 +/- 4%, 9 +/- 5%, and 8 +/- 6% at 3, 5, and 9 minutes, respectively (P < .05 versus the control response). In contrast, quisqualate (100 and 300 mumol/L) did not alter the diameter of cerebral arterioles. In rings of the middle cerebral artery studied in vitro, kainate had no effect on vascular tone, which suggests that cerebral vessels lack receptors for kainate. Thus, cerebral vasodilator effects of kainate do not appear to be due to the direct effect of the excitatory amino acid on cerebral vessels.
These findings suggest that kainate produces dilatation of cerebral arterioles in vivo that is mediated by release of nitric oxide from an extravascular source.
Incidence of transcranial Doppler-detected cerebral microemboli in patients referred for echocardiography.
Authors: Tong D C , Bolger A , Albers G W 
Published: June 2011

Transcranial Doppler can detect cerebral microemboli. These emboli may be a risk factor for embolic stroke. We studied the prevalence of microemboli in patients referred for echocardiography.
Forty-two patients were evaluated. Patients were studied with continuous monitoring over one middle cerebral artery for 30 minutes, and the number of microemboli was recorded. Patients were divided into three groups, those with prosthetic heart valves (group A, n = 15), atrial fibrillation (group B, n = 14), and no major cardiac risk factor (group C, n = 14).
Seventeen percent (7 of 42) of all patients had microemboli. In group A, 5 of 15 (33%) had microemboli. In group B, 2 of 13 (15%) patients had microemboli. Twenty-five percent (7 of 28) of patients in groups A and B combined (A+B) had microemboli. No patients (0 of 14) in group C had microemboli. Groups A and A+B had significantly more emboli than group C (P < .05). Prosthetic heart valve patients with emboli more commonly had a history of prior stroke than valve patients without emboli (3 of 5 versus 2 of 10). The number of emboli seen per 30-minute monitoring session was greater in patients with a prior history of stroke than in patients without (10 microemboli versus 3).
Microemboli can be found in a significant percentage of selected patients referred for echocardiography. The prevalence of microembolism is greater in patients with a known high risk of embolization (eg, prosthetic valves) and less in patients with a lower risk of embolization (eg, atrial fibrillation). These microemboli may be associated with an increased prevalence of previous stroke in patients with prosthetic valves.
Gastrointestinal bleeding in stroke.
Authors: Wijdicks E F , Fulgham J R , Batts K P 
Published: June 2011

Patients with ischemic or hemorrhagic stroke are at risk for systemic complications. The reasons why gastrointestinal bleeding occurs after stroke are unknown and have intuitively been attributed to stress ulcers. No study to date has addressed causes of gastrointestinal hemorrhage in stroke.
Between 1976 and 1994, 17 patients identified from the Mayo Clinic medical record system as having gastrointestinal hemorrhage and ischemic stroke (n = 14) or intracerebral hemorrhage (n = 3) were reviewed for presentation, associated causes, and outcome. Results of the endoscopic procedures were compiled, and available gastric biopsies were reviewed.
In 17 patients with gastrointestinal bleeding after stroke, sudden hematemesis, a decrease in hemoglobin level, or orthostatic hypotension was found as a presenting feature. One patient presented with massive hematemesis, exsanguination, and cardiac arrest. Endoscopic findings were available in 14 patients and included gastroesophageal erosions, hemorrhagic gastritis, and gastric ulcer. In one patient, an adenocarcinoma of the gastric cardia was found. Putative pathogenetic agents were found in 16 of 17 patients and included a long history of nonsteroidal anti-inflammatory drugs (n = 6), acetylsalicylic acid (n = 3), grossly prolonged anticoagulation (n = 4), Helicobacter pylori (n = 2), and corticosteroids (n = 1).
Gastrointestinal bleeding after stroke is rarely severe and may not contribute significantly to mortality. Medication-induced gastrointestinal hemorrhage may be underappreciated in this setting.
Pontine infarction extending to the basal surface.
Authors: Toyoda K , Saku Y , Ibayashi S , Sadoshima S , Ogasawara T , Fujishima M 
Published: June 2011

Etiology and symptomatology in pontine infarction extending to the basal surface are supposed to be different from those in deep pontine infarction of the lacunar type. The aim of this study was to compare the infarct size and location, vascular lesions, risk factors, and neurological deficits in three different types of acute pontine infarction.
We studied isolated pontine infarction extending to the basal surface on brain imaging (group 1, n = 30), deep pontine infarction without extension to the basal surface (group 2, n = 23), and pontine infarction with simultaneous extrapontine infarct in the posterior circulatory system (group 3, n = 20). Clinical features, angiographic findings, and risk factors such as emboligenic heart disease, hypertension, and hypercholesterolemia were compared among the groups.
The infarct area was 2.5 times greater in group 1 than in group 2. On angiogram, atherosclerotic stenosis of the basilar trunk was observed in 50% of the patients studied in group 1, in 0% in group 2, and in 78% in group 3. Emboligenic heart diseases were observed in 23%, 0%, and 30% in groups 1, 2, and 3, respectively. However, hypertension (60% to 65%), diabetes mellitus (35% to 45%), and hypercholesterolemia (13% to 17%) were equally distributed among the three groups. Classic lacunar syndromes were seen in 14 patients (47%) in group 1, in 20 patients (87%) in group 2, but in none of the patients in group 3. Patients belonging to group 1 showed a higher incidence of hemiparesis involving the face (37%), sensorimotor stroke (20%), and hemiparesis with confusion (17%) than those in group 2 (22%, 0%, and 4%, respectively) or in group 3 (0%, 5%, and 0%, respectively).
Pontine infarction in group 1 may have several different causes, such as cardioembolism, artery-to-artery embolism, or atherosclerosis of the basilar artery affecting pontine branches. Severe neurological symptoms often result that differ from those seen in the deep pontine lacunar infarction in group 2.
Effect of gamma-aminobutyric acid modulation on neuronal ischemia in rabbits.
Authors: Madden K P 
Published: June 2011

Antagonists of excitatory neurotransmitters are effective in limiting ischemic damage to the brain and spinal cord, but use in clinical stroke may be limited by side effects. Agonists of inhibitory neurotransmitters, such as gamma-aminobutyric acid (GABA), may provide similar neuroprotection with less severe side effects. This study examines the effect of an agonist and antagonist of the GABA-A receptor on neuronal ischemic damage.
Either muscimol (a GABA-A agonist) or bicuculline (a GABA-A antagonist) was administered intravenously to groups of rabbits exposed to reversible spinal cord ischemia induced by temporary occlusion of the infrarenal aorta. The duration of occlusion for individual animals was varied, providing a range of ischemia for each experimental group. The group P50 represents the duration (in minutes) associated with 50% probability of resultant permanent paraplegia. Neuroprotection was demonstrated if a drug prolonged the P50 compared with the control group.
The P50 of the control group was 26.3 +/- 2.0 minutes. Treatment with intravenous muscimol at 5 mg/kg significantly prolonged the P50 (32.4 +/- 1.3; P = .01). Treatment with intravenous bicuculline at 0.1 mg/kg significantly shortened the P50 (20.6 +/- 1.5; P = .03). The physiological and apparent behavioral effects of the drugs at these doses did not appear substantial.
Pharmacological manipulation of the GABA-A receptor may offer another avenue of therapy for central nervous system ischemia, possibly with less severe associated physiological side effects than other effective drugs.
Writing tremor after discrete cortical infarction.
Authors: Kim J S , Lee M C 
Published: June 2011

Hand tremor is a rare manifestation of stroke, and writing tremor has not been reported to be produced by stroke. We describe a patient who developed a unilateral hand tremor mimicking primary writing tremor after discrete cerebral cortical infarction.
A 67-year-old man developed mild right hemiparesis. Brain magnetic resonance imaging showed a discrete cortical infarct in the left frontal area. After recovery of motor power, the patient showed significant right hand tremor exclusively during writing or similar motor activities including tooth brushing or shaving. The tremor was temporarily alleviated by clonazepam but persisted until 7 months of follow-up. Medical history suggested that the patient had mild essential tremor, but he did not experience tremor on writing before the onset of stroke.
This observation suggests that unilateral hand tremor mimicking primary writing tremor may be produced by cortical infarction. It remains unclear whether the patient's previous essential tremor played an additional role in the development of this symptom.
Carotid angioplasty. Detection of embolic signals during and after the procedure.
Authors: Markus H S , Clifton A , Buckenham T , Brown M M 
Published: June 2011

Carotid angioplasty may offer an effective treatment for carotid stenosis, but there has been concern about the incidence and clinical consequences of distal embolization. Transcranial Doppler monitoring in carotid endarterectomy has demonstrated embolic signals during this procedure. We used this technique in patients undergoing carotid angioplasty.
Transcranial Doppler ultrasound was used to monitor for embolic signals in the ipsilateral middle cerebral artery before and during 10 technically successful carotid angioplasties and at various standardized times in the following month.
In the month before angioplasty asymptomatic embolic signals were detected in 3 of 10 patients. During angioplasty multiple embolic signals were detected immediately after balloon inflation in 9 of 10 subjects. A minor ipsilateral cerebral ischemic event occurred in 1 of these 9, but the other 8 were asymptomatic. Embolic signals were common immediately after the procedure and intra-arterial femoral catheter removal (8 of 10 subjects) but thereafter became less frequent and were present in 1 of 5 at 4 hours, 2 of 10 at 48 hours, 1 of 6 at 7 days, and 1 of 10 at 1 month.
Embolization at the time of carotid angioplasty is very common but usually asymptomatic; monitoring by means of Doppler ultrasound will allow the effectiveness of measures to reduce this embolization to be studied. Late embolization occurs in a minority of patients and may account for the small but significant risk of delayed stroke. Doppler monitoring may allow identification of patients at risk and assessment of the effectiveness of prophylactic therapy.