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Relationship between the Oxfordshire Community Stroke Project classification and vascular abnormalities in patients with predominantly intracranial atherosclerosis.

Li H, Wong KS, Kay R.

Division of Neurology, Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, China.


J Neurol Sci. 2003 Mar 15;207(1-2):65-9. Related Articles, Links

Relationship between the Oxfordshire Community Stroke Project classification and vascular abnormalities in patients with predominantly intracranial atherosclerosis.

Li H, Wong KS, Kay R.

Division of Neurology, Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, China.

BACKGROUND: The Oxfordshire Community Stroke Project (OCSP) classification is a stroke classification based on clinical features collected at bedside. Previous studies reported good correlation between vascular abnormalities and OCSP mainly in populations not at risk of intracranial atherosclerosis. There have been limited data on the relationship between intracranial atherosclerosis and the OCSP classification. METHODS: Consecutive Chinese patients admitted to a regional hospital with acute ischemic stroke were studied in Hong Kong. Stroke subtype was classified as total or partial anterior circulation infarct (TACI or PACI), posterior circulation infarct (POCI), or lacunar infarct (LACI), according to the OCSP method. Transcranial Doppler (TCD) was performed whenever possible to evaluate the intracranial arteries as well as the carotid arteries. National Institute of Health Stroke Scale (NIHSS) was used to assess the severity of stroke on admission.

RESULTS: Six hundred and ninety-nine consecutive patients were studied. On admission, 24 patients were classified as TACI (3.4%), 96 PACI (13.7%), 111 POCI (15.9%), and 468 LACI (67.0%). Of the 345 patients who had TCD evidence of intracranial or carotid artery abnormalities, 75% had intracranial involvement only, 5% extracranial involvement only and 20% had both intracranial and extracranial involvement. The frequencies of arterial abnormalities were found in 58% of TACIs, 48% of PACIs, 48% of POCIs and 50% of LACIs. There was no evidence that the frequencies of arterial abnormalities were different between the OCSP groups (P=0.8). Middle cerebral artery velocity was abnormal in 9 TACIs (38%), 32 PACIs (33%), 35 POCIs (32%) and 177 LACIs (38%) (P=0.6). Vertebrobasilar velocities were abnormal in 4 TACIs (17%), 20 PACIs (21%), 29 (26%) and 87 LACIs (19%) (P=0.3). The OCSP subtypes were associated with POCIs the severity of stroke. NIHSS score of > or =9 was found in 83% of TACIs, 18% of PACIs, 9% of POCIs, and 12% of LACIs (P<0.0001).

CONCLUSIONS: OCSP classification is not significantly related to the presence of vascular abnormalities among patients with predominantly intracranial atherosclerosis.


Prevalence of cerebrovascular lesions in Parkinson's disease. A postmortem study.

Jellinger KA.

Institute of Clinical Neurobiology, Kenyongasse 18/7, 1070 Vienna, Austria.

Acta Neuropathol (Berl). 2003 May;105(5):415-9 Abstract quote

Data on the relationship between Parkinson's disease (PD) and stroke have been conflicting, some studies showing a reduced risk of stroke during life, and others indicating an increased risk of stroke-related death.

Consecutive cases (n=617) of autopsy-proven idiopathic PD (Lewy body disease of the brain stem type) and age-matched controls (n=535) were compared using current routine and immunohistochemical methods.

The total frequency of cerebrovascular lesions (lacunes, amyloid angiopathy, white matter lesions, old and recent ischemic infarcts and hemorrhages) in PD (44.0%) was higher than in controls (32.8%), while acute, often fatal ischemic or hemorrhagic strokes were less frequent in parkinsonian patients (1.8% vs 2.6%). Like previous postmortem findings in a smaller cohort, these findings neither indicate a protective effect against stroke nor a greater susceptibility to death from stroke in the populations studied.

Cognitive impairment in PD appears to be largely independent from coexistent vascular pathology except in cases with severe cerebrovascular lesions.






Functional magnetic resonance imaging in stroke recovery.

Cramer SC.

Department of Neurology, University of Washington, 1959 NE Pacific, Room RR650, Box 356465, Seattle, Washington 98195-6465, USA.

Phys Med Rehabil Clin N Am. 2003 Feb;14(1 Suppl):S47-55. Abstract quote

A better understanding of brain reorganization following stroke may have value in predicting outcome defining the targets of restorative therapies, measuring the physiology of recovery, and in serving as a biologic marker in studies targeting stroke recovery.

Measures of brain organization may provide insights as to which patients retain relevant substrate for therapies that target restorative events.

Brain reorganization can be studied with many different methods that often have complementary value. Functional MR imaging provides insights into brain plasticity after stroke and remains a valuable tool in the study of motor recovery after stroke.




Acute infarction limited to the lenticular nucleus: clinical, etiologic, and topographic features.

Russmann H, Vingerhoets F, Ghika J, Maeder P, Bogousslavsky J.

Department of Neurology, Centre Hospitalier Universitaire Vaudois, CH-1011 Lausanne, Switzerland.

Arch Neurol. 2003 Mar;60(3):351-5. Abstract quote

BACKGROUND: Chronic diseases involving the putamen and globus pallidus induce parkinsonism and other movement disorders. Sensory and motor dysfunction from deep middle cerebral artery infarction is usually due to an involvement of the internal capsule. The clinical picture associated with isolated infarction of the lenticular nucleus is less well established.

OBJECTIVE: To analyze clinical features, topographic correlations, and cause of purely lenticular ischemic infarction.

PATIENTS AND METHODS: We reviewed 820 consecutive patients with deep hemispheral infarct included in the Lausanne Stroke Registry between 1986 and 1998 and selected those with isolated lenticular involvement on computed tomography or magnetic resonance imaging.

RESULTS: Thirteen patients had pure lenticular infarction. All had faciobrachiocrural hemisyndrome, while none showed acute or delayed parkinsonism or abnormal movement. Nine patients had a lesion restricted to the putamen. Two of them had ataxic motor hemisyndrome and 7 had sensorimotor hemisyndrome (with ataxia in 4, left hemineglect in 1, and deep pain in the arm and leg in 1). Four patients had a lesion of putamen and globus pallidus externus.Three of them had motor hemisyndrome (with nonfluent aphasia in 2 and ataxia in 1) and 1 had ataxic sensorimotor hemisyndrome. All infarcts were in the territory of the medial perforating branches of the medial cerebral artery. Presumed cause of stroke was small-artery disease in 5, artery-to-artery embolism in 4, cardioembolism in 3 and undetermined in 1.

CONCLUSIONS: Acute lenticular infarction induces mainly hemiparesis but no movement disorder. Associated sensory deficits, aphasia, and hemineglect underline clinically the function of the lenticular nucleus in connection with the prefrontal, temporal, and parietal cortices.


Ischaemic stroke subtypes in children and adults.

Wraige E, Hajat C, Jan W, Pohl KR, Wolfe CD, Ganesan V.

Department of Paediatric Neurology, Newcomen Centre, Guy's Hospital, London, UK.

Dev Med Child Neurol. 2003 Apr;45(4):229-32. Abstract quote

Ischaemic stroke subtypes in children and adults were compared to determine the similarity in aetiologies. Thirty-six children (22 females, 14 males; median age 5 years 7 months, range 6 weeks to 15 years 10 months) and 50 adults (35 males, 15 females; median age 44 years, range 17 years 2 months to 49 years 11 months) who had presented with ischaemic stroke between 1995 and 2000, were categorized using a modified version of the Trial of Org 10172 in Acute Stroke Therapy (TOAST) classification.

Proportions of patients in the subtypes of the TOAST classification system were significantly different in the two groups (chi2 test, p<0.01). The first three subtypes (large artery atherosclerosis, cardioembolic, and small vessel disease) accounted for the majority of adult strokes (27 of 50). In contrast, only three of 36 children were accounted for within these three subtypes. The majority of children (29 of 36) were classified within the 'other determined aetiology' subtype. Aetiology was undetermined in 12 of 50 adults compared with three of 36 children.

Causes of ischaemic stroke in children and adults are distinct. A classification system for ischaemic stroke in children would be useful for collaborative studies.

Arterial strokes in children.

Carvalho KS, Garg BP.

James Whitcomb Riley Hospital for Children, Section of Pediatric Neurology, Indiana University Medical Center, 702 Barnhill Drive, Room #1757, Indianapolis, IN 46202-5200, USA.

Neurol Clin. 2002 Nov;20(4):1079-100 Abstract quote

Pediatric stroke has received special attention in the recent literature. It is now recognized as an important cause of mortality and morbidity in pediatric population.

Varied and poorly specific symptomatology as well as overlapping risk factors makes the diagnosis of stroke in childhood challenging. Therapy remains controversial. The use of anticoagulation and thrombolysis in the management of acute stroke in children has not been systematically studied.

In this article, we discuss the natural history, investigation, and treatment of pediatric arterial hemorrhagic and ischemic strokes.











Aspirin and ticlopidine for prevention of recurrent stroke in black patients: a randomized trial.

Gorelick PB, Richardson D, Kelly M, Ruland S, Hung E, Harris Y, Kittner S, Leurgans S.

Center for Stroke Research, Rush Medical College, 1645 W Jackson, Suite 400, Chicago, IL 60612.


JAMA. 2003 Jun 11;289(22):2947-57. Abstract quote

CONTEXT: Blacks are disproportionately affected by stroke, and they are about 2 times more likely than most other individuals in the United States to die of or experience stroke.

OBJECTIVE: To determine the efficacy and safety of aspirin and ticlopidine to prevent recurrent stroke in black patients.Design, Setting, and

PATIENTS: Randomized, double-blind, investigator-initiated, multicenter trial of 1809 black men and women who recently had a noncardioembolic ischemic stroke and who were recruited between December 1992 and October 2001 from 62 academic and community hospitals in the United States and followed up for up to 2 years.

INTERVENTION: A total of 902 patients received 500 mg/d of ticlopidine and 907 received 650 mg/d of aspirin.

MAIN OUTCOME MEASURES: Recurrent stroke, myocardial infarction, or vascular death was the composite primary end point (according to intention-to-treat analysis). The secondary outcome was fatal or nonfatal stroke.

RESULTS: The blinded phase of the study was halted after about 6.5 years when futility analyses revealed a less than 1% probability of ticlopidine being shown superior to aspirin in the prevention of the primary outcome end point. The primary outcome of recurrent stroke, myocardial infarction, or vascular death was reached by 133 (14.7%) of 902 patients assigned to ticlopidine and 112 (12.3%) of 907 patients assigned to aspirin (hazard ratio, 1.22; 95% confidence interval, 0.94-1.57). Kaplan-Meier curves for time to event for the primary outcome did not differ significantly (P =.12 by log-rank test). Kaplan-Meier curves for time to the secondary outcome of fatal or nonfatal stroke approached a statistically significant reduction favoring aspirin over ticlopidine (P =.08 by log-rank test). The frequency of laboratory-determined serious neutropenia was 3.4% for patients receiving ticlopdine vs 2.2% for patients receiving aspirin (P =.12) and 0.3% vs 0.2% for thrombocytopenia, respectively (P =.69). One ticlopidine-treated patient developed thrombocytopenia, which was thought to be a case of possible thrombotic thrombocytopenia purpura, and recovered after therapy with plasmapheresis.

CONCLUSIONS: During a 2-year follow-up, we found no statistically significant difference between ticlopidine and aspirin in the prevention of recurrent stroke, myocardial infarction, or vascular death. However, there was a nonsignificant trend for reduction of fatal or nonfatal stroke among those in the aspirin group. Based on these data and the risk of serious adverse events with ticlopidine, we regard aspirin as a better treatment for aspirin-tolerant black patients with noncardioembolic ischemic stroke.

A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease.

Gum PA, Kottke-Marchant K, Welsh PA, White J, Topol EJ.

Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA.


J Am Coll Cardiol. 2003 Mar 19;41(6):961-5. Abstract quote.

OBJECTIVES: This study was designed to determine if aspirin resistance is associated with clinical events. BACKGROUND: Aspirin resistance, defined by platelet function testing and presumed clinical unresponsiveness to aspirin, has been previously reported by our group and others. However, little information exists linking the laboratory documentation of aspirin resistance and long-term clinical events.

METHODS: We prospectively enrolled 326 stable cardiovascular patients from 1997 to 1999 on aspirin (325 mg/day for > or =7 days) and no other antiplatelet agents. We tested for aspirin sensitivity by optical platelet aggregation using adenosine diphosphate (ADP) and arachidonic acid (AA). The primary outcome was the composite of death, myocardial infarction (MI), or cerebrovascular accident (CVA). Mean follow-up was 679 +/- 185 days. Aspirin resistance was defined as a mean aggregation of > or =70% with 10 microM ADP and > or =20% with 0.5 mg/ml AA.

RESULTS: Of the patients studied, 17 (5.2%) were aspirin resistant and 309 (94.8%) were not aspirin resistant. During follow-up, aspirin resistance was associated with an increased risk of death, MI, or CVA compared with patients who were aspirin sensitive (24% vs. 10%, hazard ratio [HR] 3.12, 95% confidence interval [CI] 1.10 to 8.90, p = 0.03). Stratified multivariate analyses identified platelet count, age, heart failure, and aspirin resistance to be independently associated with major adverse long-term outcomes (HR for aspirin resistance 4.14, 95% CI 1.42 to 12.06, p = 0.009).

CONCLUSIONS: This study demonstrates the natural history of aspirin resistance in a stable population, documenting a greater than threefold increase in the risk of major adverse events associated with aspirin resistance.


Neuroprotective effect of granulocyte colony-stimulating factor after focal cerebral ischemia.

Schabitz WR, Kollmar R, Schwaninger M, Juettler E, Bardutzky J, Scholzke MN, Sommer C, Schwab S.

Department of Neurology, University of Heidelberg, Heidelberg, Germany.


Stroke. 2003 Mar;34(3):745-51 Abstract quote

BACKGROUND AND PURPOSE: The potential neuroprotective effect of the granulocyte colony-stimulating factor (G-CSF) after glutamate-induced excitotoxicity in cell culture and after focal cerebral ischemia in rats was studied. We hypothesized the existence of the G-CSF receptor (G-CSFR) as a main G-CSF effector on neurons, and immunohistochemistry, immunoblotting, and polymerase chain reaction were performed. The G-CSFR-mediated action was studied by activation of signal transducer(s) and activator(s) of transcription-3 (STAT3) in the periphery of the infarction.

METHODS: Neuroprotection of various G-CSF concentrations on glutamate-induced excitotoxicity was studied in cell culture. In vivo, ischemia was induced by use of a suture occlusion model of the middle cerebral artery (90-minute occlusion) in the rat. Thirty minutes after the induction of ischemia, the animals (n=12 per group) received G-CSF at 60 microg/kg body wt IV for 90 minutes or vehicle (saline). Infarct volume was calculated on the basis of 2,3,5-triphenyltetrazolium chloride staining 24 hours after ischemia. Expression of the G-CSFR was studied by immunohistochemistry and verified by reverse transcription-polymerase chain reaction and immunoblotting. Expression of STAT3 was determined by immunohistochemistry.

RESULTS: In cell culture, G-CSF exhibited a significant neuroprotective effect after glutamate-induced excitotoxicity (P<0.05). A G-CSF concentration of 10 ng/mL was maximally effective, resulting in a nearly complete protection. In vivo, G-CSF reduced infarct volume to 47% (132.0+/-112.7 mm3 versus 278.9+/-91.6 mm3 [P<0.05] in the control group). Immunohistochemistry, Western blotting, and reverse transcription-polymerase chain reaction revealed the existence of G-CSFRs in neurons and glial cells. Animals treated with G-CSF significantly upregulated STAT3 in the periphery of the infarction compared with control animals (P<0.05).

CONCLUSIONS: G-CSF achieved a significant neuroprotective effect in cell culture and after intravenous administration after stroke. Increased STAT3 expression in the penumbra of G-CSF-treated rats suggests mediation by G-CSFR.

Ximelagatran vs warfarin for stroke prevention in patients with nonvalvular atrial fibrillation: a randomized trial.

Albers GW, Diener HC, Frison L, Grind M, Nevinson M, Partridge S, Halperin JL, Horrow J, Olsson SB, Petersen P, Vahanian A; SPORTIF Executive Steering Committee for the SPORTIF V Investigators.

Stanford Stroke Center, Palo Alto, Calif, USA.

JAMA. 2005 Feb 9;293(6):690-8. Abstract quote

CONTEXT: In patients with nonvalvular atrial fibrillation, warfarin prevents ischemic stroke, but dose adjustment, coagulation monitoring, and bleeding limit its use.

OBJECTIVE: To compare the efficacy of the oral direct thrombin inhibitor ximelagatran with warfarin for prevention of stroke and systemic embolism.

DESIGN, SETTING, AND PARTICIPANTS: Double-blind, randomized, multicenter trial (2000-2001) conducted at 409 North American sites, involving 3922 patients with nonvalvular atrial fibrillation and additional stroke risk factors.

INTERVENTIONS: Adjusted-dose warfarin (aiming for an international normalized ratio [INR] 2.0 to 3.0) or fixed-dose oral ximelagatran, 36 mg twice daily.

MAIN OUTCOME MEASURES: The primary end point was all strokes (ischemic or hemorrhagic) and systemic embolic events. The primary analysis was based on demonstrating noninferiority within an absolute margin of 2.0% per year according to the intention-to-treat model. RESULTS: During 6405 patient-years (mean 20 months) of follow-up, 88 patients experienced primary events. The mean (SD) INR with warfarin (2.4 [0.8]) was within target during 68% of the treatment period. The primary event rate with ximelagatran was 1.6% per year and with warfarin was 1.2% per year (absolute difference, 0.45% per year; 95% confidence interval, -0.13% to 1.03% per year; P<.001 for the predefined noninferiority hypothesis). When all-cause mortality was included in addition to stroke and systemic embolic events, the rate difference was 0.10% per year (95% confidence interval, -0.97% to 1.2% per year; P = .86). There was no difference between treatment groups in rates of major bleeding, but total bleeding (major and minor) was lower with ximelagatran (37% vs 47% per year; 95% confidence interval for the difference, -14% to -6.0% per year; P<.001). Serum alanine aminotransferase levels rose to greater than 3 times the upper limit of normal in 6.0% of patients treated with ximelagatran, usually within 6 months and typically declined whether or not treatment continued; however, one case of documented fatal liver disease and one other suggestive case occurred.

CONCLUSIONS: The results establish the efficacy of fixed-dose oral ximelagatran without coagulation monitoring compared with well-controlled warfarin for prevention of thromboembolism in patients with atrial fibrillation requiring chronic anticoagulant therapy, but the potential for hepatotoxicity requires further investigation.
Costs and effectiveness of ximelagatran for stroke prophylaxis in chronic atrial fibrillation.

O'Brien CL, Gage BF.

Washington University School of Medicine, St Louis, Mo 63110, USA.

JAMA. 2005 Feb 9;293(6):699-706. Abstract quote  

CONTEXT: Recent trials have found that ximelagatran and warfarin are equally effective in stroke prevention for patients with atrial fibrillation. Because ximelagatran can be taken in a fixed, oral dose without international normalized ratio monitoring and may have a lower risk of hemorrhage, it might improve quality-adjusted survival compared with dose-adjusted warfarin.

OBJECTIVE: To compare quality-adjusted survival and cost among 3 alternative therapies for patients with chronic atrial fibrillation: ximelagatran, warfarin, and aspirin.

DESIGN: Semi-Markov decision model.

PATIENTS: Hypothetical cohort of 70-year-old patients with chronic atrial fibrillation, varying risk of stroke, and no contraindications to anticoagulation therapy.

MAIN OUTCOME MEASURES: Quality-adjusted life-years (QALYs) and costs in US dollars.

RESULTS: For patients with atrial fibrillation but no additional risk factors for stroke, both ximelagatran and warfarin cost more than 50,000 dollars per QALY compared with aspirin. For patients with additional stroke risk factors and low hemorrhage risk, ximelagatran modestly increased quality-adjusted survival (0.12 QALY) at a substantial cost (116,000 dollars per QALY) compared with warfarin. For ximelagatran to cost less than 50,000 dollars per QALY it would have to cost less than 1100 dollars per year or be prescribed to patients who have an elevated risk of intracranial hemorrhage (>1.0% per year of warfarin) or a low quality of life with warfarin therapy.

CONCLUSION: Assuming equal effectiveness in stroke prevention and decreased hemorrhage risk, ximelagatran is not likely to be cost-effective in patients with atrial fibrillation unless they have a high risk of intracranial hemorrhage or a low quality of life with warfarin.

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