bluuebunny/crossref_metadata_2025 huggingface dataset:
Blood pressure treatment slows the progression of carotid stenosis in patients with isolated systolic hypertension.
Authors: Sutton-Tyrrell K , Wolfson S K , Kuller L H
Published: June 2011

The Systolic Hypertension in the Elderly Program (SHEP) was a randomized trial testing the efficacy of treating systolic hypertension in older adults. A significant reduction in stroke risk was observed among participants assigned to active treatment. Serial carotid duplex scans were performed on 129 participants at the University of Pittsburgh center, and rates of progression and regression of carotid stenosis were observed.

Changes in blood flow velocity ratios were used to detect progression because they can be reliably measured and their relation to degree of residual lumen is known. Progression required the development of a 40% to 50% diameter stenosis when stenosis was not initially present or, if already present, further reduction in the lumen diameter. Regression required the absence of a 40% to 50% diameter stenosis when stenosis was initially present or a stenosis significantly less severe than that initially seen.

Progression occurred in 22% (28/129) of participants and regression in 16% (8/49). Progression of carotid stenosis occurred more often among participants randomized to placebo as compared with active treatment (31% versus 14%, P = .020). All eight patients exhibiting-regression were randomized to active treatment. In multivariate analysis, participants assigned to placebo had 4.3 times greater odds of progressing than participants assigned to active treatment. Other factors significantly related to progression were higher degree of plaque at baseline, low high-density lipoprotein-3, high lipoprotein(a), and younger age.

Treating systolic hypertension appears to slow progression of carotid stenosis. Similar effects occurring in the intracranial vessels may be one reason for the substantial decrease in stroke among SHEP participants assigned to active treatment.
A comparison of lesions in small intracerebral arteries among Japanese men in Hawaii and Japan.
Authors: Reed D , Jacobs D R , Hayashi T , Konishi M , Nelson J , Iso H , Strong J
Published: June 2011

This report examines the hypothesis that the higher risk of stroke among Japanese men in Japan compared with those in Hawaii is related to pathology in small intracerebral arteries by comparing the prevalence of such lesions in autopsied participants from two cohorts of Japanese men in Japan and Hawaii.

Existing histological sections from the left basal ganglia from 232 men from Japan and 175 men of Japanese ancestry in Hawaii were examined for selected abnormalities in arteries between 100 and 300 microns in diameter by three pathologists. The presence of lacunar infarcts was also noted, and information about cerebral infarcts, cerebral hemorrhages, and atherosclerosis in the circle of Willis was available for the Hawaii group.

Lacunar infarcts and all small intracerebral artery lesions except medial fibrosis were more common at every age in Japan than in Hawaii. By cause of death, all lesions were three or more times more prevalent among men who died of stroke than of noncardiovascular causes in both areas. In the Hawaii group, the small intracerebral artery lesions were significantly associated with autopsy evidence of cerebral and lacunar infarcts, and with atherosclerosis in the large arteries of the circle of Willis. Among a large number of risk factors measured at the baseline examination in Hawaii, only high blood pressure and reported usual Asian diet were significantly associated with one or more measures of small intracerebral artery lesions.

An overview of the accumulated data indicated that small intracerebral artery pathology plays an important role in the high risk of stroke in Japanese men in Japan compared with those in Hawaii. These studies support the idea that hypertension is a necessary factor in the causal pathway, but also indicate that some other factors are involved. Some aspect of an Asian diet continues to be of importance for future research.
What causes false clinical prediction of small deep infarcts?
Authors: Lodder J , Bamford J , Kappelle J , Boiten J
Published: June 2011

Our goal was to identify factors that play a role in false clinical diagnosis of small deep infarcts.

In 350 prospectively registered patients with a first supratentorial ischemic stroke, we clinically differentiated between lacunar and nonlacunar syndromes. Using computed tomography (CT), we distinguished small deep and territorial infarcts and also recorded leukoaraiosis and asymptomatic infarcts. Degree of initial handicap, potential source of cardioembolic stroke, and hypertension were also noted.

One hundred forty-seven patients had a lacunar and 203 a nonlacunar syndrome. Forty-two (12%) had a lesion visualized by CT that was compatible with a recent infarct but was considered inappropriate for the clinical syndrome: nineteen had a nonlacunar syndrome but a small deep infarct, and 23 had a lacunar syndrome but a territorial infarct. Patients with a nonlacunar syndrome but a small deep infarct were more severely disabled (a modified Rankin scale rating of 5) (odds ratio [OR], 4.31; 95% confidence interval [CI], 1.25 to 14.88) and had a cardioembolic source (OR, 4.07; 95% CI, 1.04 to 15.95), leukoaraiosis (OR, 3.79; 95% CI, 1.32 to 10.05), or asymptomatic infarcts visualized by CT (OR, 4.13; 95% CI, 1.45 to 11.71) compared with 124 patients with a correctly diagnosed small deep infarct. Twelve of 19 patients with a nonlacunar syndrome but a small deep infarct had a lesion in the left hemisphere, and 9 of these 12 had "aphasia." Patients with a lacunar syndrome but a territorial infarct more often had a cardioembolic source (OR, 4.02; 95% CI, 1.15 to 14.03) and a pure motor syndrome (OR, 4.52; 95% CI, 1.55 to 13.18) than those with lacunar syndrome but a small deep infarct, although 21 (91%) were in the right hemisphere. Of the first 103 patients with lacunar stroke diagnosed by two of the study neurologists, 5 had an inappropriate lesion compared with 14 of the later 40 diagnosed by colleagues without a specific interest in cerebrovascular diseases (OR, 0.09; 95% CI, 0.03 to 0.26).

(1) Diagnosis of lacunar syndromes should not be influenced by deficit severity or the presence of a potential cardiac source of embolism. (2) Speech disorders should carefully be classified. (3) Routine tests of nondominant higher functions may be inadequate. (4) Doctors interested in cerebrovascular neurology have a lower failure rate in differentiating small deep infarcts from territorial infarcts than those less well-trained or interested in neurology. (5) Among the lacunar syndromes, pure motor syndrome may be the least specific predictor of a small deep infarct.
Pure motor hemiparesis and sensorimotor stroke. Accuracy of very early clinical diagnosis of lacunar strokes.
Authors: Toni D , Del Duca R , Fiorelli M , Sacchetti M L , Bastianello S , Giubilei F , Martinazzo C , Argentino C
Published: June 2011

Clinical differentiation of lacunar from nonlacunar strokes in the very early phase could help to exclude patients with lacunar stroke from pharmacologic trials designed for nonlacunar strokes, namely, those with thrombolytic agents. In a continuous series of acute ischemic stroke patients, we evaluated how accurately a clinical diagnosis of pure motor hemiparesis or sensorimotor stroke formulated in the first hours from onset predicts a lacunar stroke documented by cerebral computed tomography or by autopsy.

We examined 517 patients (299 men, 218 women; mean +/- SD age, 67 +/- 10 years) within 12 hours (mean +/- SD, 6.1 +/- 3.2 hours) of the event. At hospital admission, we observed 151 (29%) patients with pure motor hemiparesis and 68 (13%) patients with sensorimotor stroke.

Computed tomography or autopsy was compatible with a lacunar stroke (ie, detection of a lacune or permanently negative computed tomography) in 170 (33%) patients, of whom 123 (72%) had pure motor hemiparesis and 47 (28%) had sensorimotor stroke. This led to a sensitivity of 72%, a specificity of 72%, a positive predictive value of 56%, and a negative predictive value of 84%. Overall positive predictive value of pure motor hemiparesis was 58% (60% for two areas and 58% for three areas involved), and that of sensorimotor stroke was 51% (87% for two areas and 40% for three areas involved). By separately evaluating the sides of lesions, we found a positive predictive value of 46% for right-side infarcts and of 72% for left-side infarcts. Right-side lesions constituted 51% of lesions in lacunar syndrome patients with lacunar stroke, 76% in those with nonlacunar stroke, 19% in nonlacunar syndrome patients with lacunar stroke, and 31% in those with nonlacunar stroke (P < .0001). During the first days of hospital stay we observed a deterioration of 21% of lacunar syndrome patients with nonlacunar stroke and an improvement of 49% of nonlacunar syndrome patients with lacunar stroke, with appearance and disappearance of symptoms of cortical involvement, respectively. The examination of these patients after the occurrence of these clinical changes would have led to a daily increase of the positive predictive value up to a maximum of 66% at day 7.

Pure motor hemiparesis and sensorimotor stroke diagnosed within 12 hours of the event are poorly predictive of lacunar strokes. Hence, the very early identification of these syndromes cannot be used for patient selection in therapeutic trials.
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.
Equivalence of measurements of carotid stenosis. A comparison of three methods on 1001 angiograms. European Carotid Surgery Trialists' Collaborative Group.
Authors: Rothwell P M , Gibson R J , Slattery J , Sellar R J , Warlow C P
Published: June 2011

There is confusion about how carotid stenosis should be measured on angiograms. If the results of research based on different methods of measurement of stenosis are to be discussed and the results of clinical trials properly applied to routine clinical practice, measurements made by the different methods must be formally compared.

The method of measurement of stenosis used in the European Carotid Surgery Trial (ECST), that used in the North American Symptomatic Carotid Endarterectomy Trial (NASCET), and a method based on measurement of the common carotid (CC) artery lumen diameter were compared. Carotid stenosis was measured by two observers, working independently and using the three different methods of measurement, on the angiographic view of the symptomatic carotid stenosis that showed the most severe disease in 1001 patients from the ECST.

The results of using the ECST and CC methods differed from those of using the NASCET method in the classification of stenoses as mild (0% to 29%), moderate (30% to 69%), or severe (70% to 99%) in 51% of measurements. The ECST and CC methods indicated that twice as many stenoses were severe as did the NASCET method, and classified less than a third of the number of stenoses as mild. The results of the ECST and CC methods differed from each other in 15% of measurements. The relations between measurements made by each method to those made by the others were approximately linear, so a simple equation could be derived to convert measurements made by one method to measurements made by the others.

There were major and clinically important disparities between measurements of stenosis made using different methods of measurement on the same angiograms. However, it is possible to convert measurements made by one method to those of another using a simple arithmetic equation.
Association of occurrence of aneurysmal bleeding with meteorologic variations in the north of France.
Authors: Lejeune J P , Vinchon M , Amouyel P , Escartin T , Escartin D , Christiaens J L
Published: June 2011

Previous reports have established that the incidence of stroke may be influenced by meteorologic variations. However, no significant correlation was clearly demonstrated concerning aneurysmal bleeding.

From January 1, 1989, to December 31, 1991, 238 patients with angiographically confirmed diagnoses of subarachnoid hemorrhage were registered in the North of France region. For each day, the weather variables were provided by the national meteorologic office (Meteo France). We compared the meteorologic variables of days when subarachnoid hemorrhage occurred with the variables of days without subarachnoid hemorrhage in a multivariate model.

We observed a seasonal pattern in the occurrence of subarachnoid hemorrhage, with a low frequency of rupture in June and July and maximum frequency in April and September (P < .05). The days of occurrence were associated with short duration of sunshine (P < .00006), low minimal level of hygrometry (P < .0002), low maximal temperature (P < .005), and low atmospheric pressure the day before the event (P < .05).

Aneurysmal bleeding was significantly associated with weather variables. Cold-induced hypertension may explain these fluctuations in the occurrence of aneurysmal bleeding.
Does age affect benefits of stroke unit rehabilitation?
Authors: Kalra L
Published: June 2011

The influence of age on benefits of stroke unit rehabilitation is largely unknown.

A prospective controlled study was undertaken in 245 stroke survivors randomized to a stroke unit or to general wards 2 weeks after stroke. Patients were divided into older (75 years and over) and younger (under 75 years) age groups, and their characteristics, prognosis, duration, and type of therapy input and outcome were compared in different settings.

Younger (n = 101) and older (n = 144) stroke patients were comparable for neurological and functional deficits and were distributed equally between the stroke unit and general wards. The duration of therapy input was similar in younger patients in either setting. Older patients received more occupational therapy in both settings (10.7 +/- 2.4 versus 7.9 +/- 04.1) and more physiotherapy (18.4 +/- 9.6 versus 15.2 +/- 7.8) on general wards. Younger patients on the stroke unit showed better outcome compared with those on general wards (discharge home, 83% versus 60%; median Barthel score, 17 versus 13; median length of hospital stay, 27 versus 56 days) and with older patients on the stroke unit (discharge home, 83% versus 65%; median Barthel score, 17 versus 14). Outcome in older stroke patients was similar in both settings except for a shorter median length of hospital stay on the stroke unit (36 versus 84 days). Outcome in younger patients managed on general wards was worse than that in older patients with similar prognostic expectations (discharge home, 41% versus 61%; median Barthel score, 11 versus 13).

Younger stroke patients benefited more by stroke unit rehabilitation compared with older patients, not only because of their age but also because of differences in the multidisciplinary input available for elderly patients outside the stroke unit.
Serial assessment of acute stroke using the NIH Stroke Scale.
Authors: Wityk R J , Pessin M S , Kaplan R F , Caplan L R
Published: June 2011

The National Institutes of Health (NIH) Stroke Scale has been used in clinical trials to assess neurological outcome after investigational therapy for acute stroke. We used the NIH Stroke Scale to study the degree and time course of recovery in patients with acute stroke who were treated with conventional therapy.

We serially assessed 50 patients with ischemic stroke who presented within 24 hours of onset of symptoms. Patients were grouped by stroke subtype. Major neurological improvement was defined as a decrease in the stroke score by 4 points or more.

The mean NIH stroke score for all patients improved significantly by 7 to 10 days and at last follow-up (average, 44 days). Major neurological improvement was seen in 5 of 41 patients (12%; 95% confidence interval [CI], 2% to 22%) by 24 hours, 11 of 40 patients (28%; 95% CI, 14% to 41%) by 48 hours, and 19 of 37 patients (51%; 95% CI, 35% to 67%) by follow-up. The subgroup of patients with middle cerebral artery territory embolism showed a similar pattern of improvement; in contrast, patients with lacunar infarcts did not show significant change in scores during the study period. The score on admission did not correlate with the degree of subsequent improvement or deterioration.

A significant percentage of patients with acute ischemic stroke treated with conventional therapy show early improvement as assessed by the NIH Stroke Scale. The degree and time course of recovery may be influenced by stroke type.
Feeding dependence and nutritional status after acute stroke.
Authors: Unosson M , Ek A C , Bjurulf P , von Schenck H , Larsson J
Published: June 2011

We assessed the nutritional status of patients with acute stroke and evaluated it in relation to the patients' dependence on assistance with feeding.

Fifty patients aged 70 years or older, admitted from their homes, were included. Weight index, triceps skinfold thickness, arm muscle circumference, serum proteins, delayed hypersensitivity, body composition measured by bioelectric impedance, and functional condition were determined on admission and 2 and 9 weeks after admission. Food and fluid consumption were also recorded.

On admission, four patients were regarded as protein-energy malnourished. Those who required assistance with feeding after admission (n = 18, 36%) had lower serum albumin (P < .05), lower body cell mass (P < .01), and were more anergic than the independent patients (P < .01) on admission. The mean food consumption was 72% of the food served without significant difference between dependent and independent patients. Nine weeks after the onset of stroke symptoms, the patients who were dependent on assisted feeding showed a decrease in body cell mass. The loss of body cell mass was related to their activity and feeding dependence.

Low serum albumin and anergy commonly occur in elderly patients with acute stroke, and they occur more prevalently among those with a severely impaired functional condition. During the recovery period, the patients use body fat to compensate for energy needs, and immobility leads to loss of body cell mass.
Comparison of magnetic resonance volume flow rates, angiography, and carotid Dopplers. Preliminary results.
Authors: Levine R L , Turski P A , Holmes K A , Grist T M
Published: June 2011

We compared the results of conventional angiography, carotid Doppler, and magnetic resonance angiography volume flow rates to determine the clinical utility of volume flow rate assessment of blood flow to the anterior circulation in patients with carotid occlusive disease.

From 11 symptomatic patients, a total of 22 extracranial carotid arteries were studied with all three techniques. The studies were independently read, and regression analysis was used to compare the measurements.

Carotid Doppler measurements of the distal extracranial carotid arteries were proportional to the inverse of the extracranial carotid volume flow rate (r = .53, R2 = 29%, P < .01), volume flow rates were proportional to the inverse of measured percent stenosis on angiography (r = .84, R2 = 71%, P < .01), and Dopplers were proportional to angiography (r = .94, R2 = 90%, P < .01). Symptomatic Doppler systolic velocity was significantly higher (P < .002), symptomatic measured stenosis was significantly higher (P < .002), and symptomatic volume flow rate was significantly lower (P < .01) than their respective asymptomatic-side values. These preliminary observations, however, may well change once a large data set, especially one in which more patients with high-grade carotid stenosis are included, is studied.

Assessment of carotid volume flow rates by magnetic resonance angiography quantifies flow reduction secondary to atherosclerotic occlusive disease. The easily obtained flow data add both documentation of arterial flow characteristics related to internal carotid stenosis and information regarding the adequacy of collateral pathways.
Delayed protection by MK-801 and tetrodotoxin in a rat organotypic hippocampal culture model of ischemia.
Authors: Vornov J J , Tasker R C , Coyle J T
Published: June 2011

The hippocampus demonstrates a regional pattern of vulnerability to ischemic injury that depends on its characteristic differentiation and intrinsic connections. We now describe a model of ischemic injury using organotypic hippocampal culture, which preserves the anatomic differentiation of the hippocampus in long-term tissue culture.

Ischemic conditions were modeled by metabolic inhibition. Cultures were briefly exposed to potassium cyanide to block oxidative phosphorylation and 2-deoxyglucose to block glycolysis. The fluorescent dye propidium iodide was used to observe membrane damage in living cultures during recovery.

2-Deoxyglucose/potassium cyanide incubation resulted in dose-dependent, regionally selective neuronal injury in CA1 and the dentate hilus, which began slowly after 2 to 6 hours of recovery. Subsequent histological examination of cultures after 1 to 7 days of recovery demonstrated neuronal pyknosis that was correlated with the early, direct observation of membrane damage with propidium. Both propidium staining and histological degeneration were prevented by the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 when administered 30 minutes after the end of the exposure to 2-deoxyglucose and potassium cyanide. Tetrodotoxin, which blocks voltage-dependent sodium channels, had protective effects that were greatest during the period of 2-deoxyglucose and potassium cyanide incubation but also produced protection against the mildest conditions of metabolic inhibition when administered after 30 minutes of recovery.

This in vitro model reproduced elements of the time course, regional vulnerability, and pharmacologic sensitivities of in vivo ischemic hippocampal injury. Inhibition of metabolism in organotypic culture provides a rapid, easily controlled injury and reproduces the in vitro pattern of hippocampal regional vulnerability to ischemia. It is the first in vitro model of ischemia to exhibit complete protection by delayed administration of an NMDA receptor antagonist during recovery from a brief insult. The protective effects of tetrodotoxin suggest that an early period of sodium entry into cells during and after ATP depletion may be responsible for the more prolonged period of toxic NMDA receptor activation.
Calcium/calmodulin-dependent protein kinase II activity in focal ischemia with reperfusion in rats.
Authors: Hanson S K , Grotta J C , Waxham M N , Aronowski J , Ostrow P
Published: June 2011

Evidence linking changes in calcium/calmodulin-dependent protein kinase II activity with ischemic cell death has been reported in animal models of global ischemia. The purpose of this study was to delineate the course of these changes after focal ischemia and to clarify the relation of changes in activity of calcium/calmodulin-dependent protein kinase II to the process of ischemic cell death.

Change in calcium/calmodulin-dependent protein kinase II activity was evaluated in a rat model of focal ischemia after 5 minutes, 30 minutes, and 1 hour of tandem middle cerebral artery and common carotid artery occlusion both with and without reperfusion.

Calcium/calmodulin-dependent protein kinase II activity was significantly decreased after all three durations of ischemia followed by immediate decapitation compared with sham-operated animals, in both ischemic core and border-zone regions (P < .05 for all groups). Depression of activity occurred in a regionally graded fashion, with the most severe decrease in infarct core and progressively smaller decreases in samples moving out from the center, corresponding to the severity of histological injury later detected in infarct core and border-zone regions. There were only minor differences between the three durations of ischemia in the degree of enzyme depression noted in the more peripheral regions, indicating that the initial decrease in calcium/calmodulin-dependent protein kinase II activity is an early, sensitive marker for an ischemic insult. After reperfusion, the differences between the 5-minute group and longer periods of ischemia widened because of an increase toward baseline in the 5-minute group and a trend toward further decrease in the 30- and 60-minute groups.

The extreme sensitivity of calcium/calmodulin-dependent protein kinase II to focal ischemia and the parallel temporal and regional changes in its activity to those of more delayed cell injury point to a potential role for this enzyme in the process of excitotoxic injury.