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Stroke. 2002 Dec;33(12):2794-800.
A population-based study of brain arteriovenous malformation: long-term treatment outcomes.
ApSimon HT, Reef H, Phadke RV, Popovic EA.
Interventional Neuroradiology Unit, Department of Neurology, Royal Perth Hospital, Perth, Western Australia. lisa.kellealth.wa.gov.au
BACKGROUND AND PURPOSE: By undertaking long-term follow-up of a functionally isolated population study group, we sought to achieve a true picture of intrinsic brain arteriovenous malformation (BAVM). We sought to assess the validity of earlier population-based series and to determine the effects of newer treatment methods on the overall morbidity and mortality of BAVM. METHODS: We excluded other intracranial vascular pathologies by defining criteria. By retrospective and prospective study, 240 patients with BAVM were followed for a mean of 10.11 years from first diagnosis. RESULTS: Death rates were as follows: all causes, 12.9%; all BAVM related, 8.75%; BAVM related during conservative management, 24.6%; and BAVM related during active management, 3.9% (P=0.031). Mean diagnosis-to-death interval was 10.6 years. Oxford neurological disability scale grades of 209 survivors (July 2001) were as follows: grades 0 to 2, 74.1%; grade 3, 17.2%; and grades 4 to 5, 9.5%. Death rates were higher for patients who had bled or suffered nonhemorrhagic neurological deficit at original presentation. Incidence of first-ever hemorrhage in untreated patients was as follows: 0 to 9 years, 4.6% (P=0.0035); 30 to 39 years, 21% (P=0.02); and 60 to 69 years, 40.0% (P=0.045). The first bleed was fatal in 4.6%. CONCLUSIONS: We find no evidence of a substantial undiagnosed reservoir of nonsymptomatic BAVM. All BAVM are potentially hazardous. The great majority of BAVM patients become symptomatic during the patient's lifetime, and the majority will bleed. The risk of first hemorrhage is lifelong and rises with age. Compared with earlier population-based series, our low overall patient mortality is predominantly due to higher proportions of active treatment in the 1980s and 1990s.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12468772&dopt=Abstract hemorrhage
Stroke. 2002 Dec;33(12):2950-6.
Simvastatin increases endothelial nitric oxide synthase and ameliorates cerebral vasospasm resulting from subarachnoid hemorrhage.
McGirt MJ, Lynch JR, Parra A, Sheng H, Pearlstein RD, Laskowitz DT, Pelligrino DA, Warner DS.
Multidisciplinary Neuroprotection Laboratories, Duke University Medical Center, Duke University School of Medicine Duke University Medical Center, Durham, NC, USA.
BACKGROUND AND PURPOSE: Endothelial nitric oxide synthase (eNOS) activity is decreased after subarachnoid hemorrhage (SAH). Simvastatin increases eNOS activity. We hypothesized that simvastatin would increase eNOS protein and ameliorate SAH-induced cerebral vasospasm. METHODS: Mice were treated with subcutaneous simvastatin or vehicle for 14 days and then subjected to endovascular perforation of the right anterior cerebral artery or sham surgery. Three days later, neurological deficits were scored (5 to 27; 27=normal), and middle cerebral artery diameter and eNOS protein were measured. The study was repeated, but simvastatin treatment was started after SAH or sham surgery. RESULTS: In SAH mice, simvastatin pretreatment increased middle cerebral artery diameter (SAH-simvastatin=74+/-22 micro m, SAH-vehicle=52+/-18 micro m, P=0.03; sham-simvastatin=102+/-8 micro m, sham-vehicle=105+/-6 micro m). Pretreatment reduced neurological deficits (SAH-simvastatin=25+/-2, SAH-vehicle=20+/-2, P=0.005; sham-simvastatin and sham-vehicle=27+/-0). Simvastatin pretreatment also increased eNOS protein. Simvastatin posttreatment caused a modest increase in middle cerebral artery diameter in SAH mice (SAH-simvastatin=56+/-12 micro m, SAH-vehicle=45+/-4 micro m, P=0.03; sham-simvastatin=92+/-13 micro m, sham-vehicle=99+/-10 micro m) and reduced neurological deficits (SAH-simvastatin=21+/-1, SAH-vehicle=19+/-2, P=0.009). Simvastatin posttreatment did not significantly increase eNOS protein. CONCLUSIONS: Simvastatin treatment before or after SAH attenuated cerebral vasospasm and neurological deficits in mice. The mechanism may be attributable in part to eNOS upregulation.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12468796&dopt=Abstract hemorrhage
Stroke. 2002 Dec;33(12):2999-3005.
Thrombolytic treatment of clot embolism in rat: comparison of intra-arterial and intravenous application of recombinant tissue plasminogen activator.
Niessen F, Hilger T, Hoehn M, Hossmann KA.
Department of Experimental Neurology, Max-Planck Institute for Neurological Research, Cologne, Germany.
BACKGROUND AND PURPOSE: We sought to test the hypothesis that intra-arterial recombinant tissue plasminogen activator (rtPA) treatment of thromboembolic stroke is more efficient than intravenous application. METHODS: Rats were embolized by intracarotid injection of autologous fibrin-rich blood clots. One hour later rtPA (10 mg/kg) was infused either intravenously (n=8) or intra-arterially (n=8). Control rats (n=8) received intra-arterial infusion of saline. Treatment was monitored by MR perfusion-weighted imaging and apparent diffusion coefficient (ADC) imaging, and outcome was evaluated by comparing incidence of hemorrhages and lesion volumes of ATP and pH. RESULTS: Clot embolism led to a decline of perfusion-weighted imaging signal intensity in the middle cerebral artery territory to <40% of control. Both intra-arterial and intravenous treatment significantly improved blood flow in cerebral cortex but not in caudate putamen. In untreated animals, ATP and pH lesion volumes were 510.3+/-94.5 and 438.6+/-39.2 mm(3) at 7 hours after clot embolism, respectively. Both intravenous and intra-arterial rtPA treatment produced hemorrhagic complications but reduced ATP lesion size to 296.2+/-136.1 and 370.3+/-103.7 mm(3) and reduced pH lesion size to 263.3+/-114.6 and 303.3+/-103.0 mm(3), respectively (P<0.05 for untreated versus treated rats; no difference between intravenous and intra-arterial treatment). ADC imaging revealed that lesion reduction was due to inhibition of infarct growth but not to reversal of primary injury. CONCLUSIONS: This study documents reduction of injury by rtPA treatment but does not reveal a difference between intra-arterial and intravenous application. Our data do not support an advantage of intra-arterial thrombolysis.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12468803&dopt=Abstract hemorrhage
Stroke. 2002 Dec;33(12):3012-8.
Delayed argatroban treatment reduces edema in a rat model of intracerebral hemorrhage.
Kitaoka T, Hua Y, Xi G, Hoff JT, Keep RF.
Department of Neurosurgery, University of Michigan, Ann Arbor, USA.
BACKGROUND AND PURPOSE: Studies indicate that thrombin plays an important role in intracerebral hemorrhage (ICH)-induced edema formation. Although thrombin is produced as the blood clots, it may be bound to fibrin and only gradually released from the clot. The time window for administration of a thrombin inhibitor to reduce ICH-induced edema is unknown. Whether this time window extends beyond the period when a thrombin inhibitor might exacerbate rebleeding is also unknown. METHODS: This study examines (1) whether argatroban, an inhibitor of both free and fibrin-bound thrombin, can reduce edema formation after intracerebral infusion of 100 micro L of blood in the rat; (2) the therapeutic time window for argatroban; and (3) whether argatroban promotes rebleeding in a model in which ICH was induced by intracerebral injection of collagenase. RESULTS: Intracerebral infusion of blood caused a marked increase in perihematomal water content. Intracerebral injection of argatroban 3 hours after ICH caused a significant reduction in edema measured at 48 hours (80.9+/-1.0% versus 82.6+/-0.8%; P<0.01). The systemic administration of high-dose argatroban (0.9 mg/h) starting 6 hours after ICH also significantly reduced edema (80.3+/-1.1% versus 82.0+/-1.3% in vehicle controls; P<0.05). There was no protection when the onset of argatroban administration was delayed to 24 hours after ICH or if a lower dose of argatroban (0.3 mg/h) was used. Argatroban did not increase collagenase-induced hematoma volume when given into the clot after 3 hours or given systemically at 6 hours. CONCLUSIONS: Our data suggest that argatroban may be an effective therapy for ICH-induced edema.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12468805&dopt=Abstract hemorrhage
Neurosurgery. 2003 Feb;52(2):296-307; discussion 307-8.
Analysis of factors predictive of success or complications in arteriovenous malformation radiosurgery.
Friedman WA, Bova FJ, Bollampally S, Bradshaw P.
Department of Neurosurgery, University of Florida, Gainesville, Florida 32610, USA. friedmaeurosurgery.ufl.edu
OBJECTIVE: This study was undertaken to determine which factors were statistically predictive of radiological and clinical outcomes in the radiosurgical treatment of arteriovenous malformations (AVMs). METHODS: The computerized dosimetric and clinical data for 269 patients were reviewed. The AVM nidus was hand-contoured on successive enhanced computed tomographic slices through the nidus, to allow detailed determinations of nidus volume, target miss, normal brain tissue treated, dose conformality, and dose gradient. In addition, a number of patient and treatment factors, including Spetzler-Martin grade, presenting symptoms, dose, number of isocenters, radiological outcome, and clinical outcome, were subjected to multivariate analysis. RESULTS: Two hundred twenty-five patients were treated with radiosurgery for the first time, and 44 patients underwent radiosurgical retreatment. One hundred forty-three patients had AVMs located in or near "eloquent" brain areas and 126 patients did not. Seventy patients demonstrated preoperative neurological findings related to the AVM and 199 did not. Twenty-six patients had previously undergone endovascular treatment and 10 patients had previously undergone surgical treatment of their AVMs. Of the 269 patients studied, 228 experienced no complication, 10 (3.7%) experienced a transient radiation-induced complication, 3 (1%) experienced a permanent radiation-induced complication, and 28 (10%) experienced posttreatment hemorrhage. CONCLUSION: None of the analyzed factors was predictive of hemorrhage after radiosurgery in this study. The 12-Gy volume was predictive of permanent radiation-induced complications. Eloquent AVM location and 12-Gy volume were correlated with the occurrence of transient radiation-induced complications. Better conformality was correlated with a reduced incidence of transient complications. Lower Spetzler-Martin grades, higher doses, and steeper dose gradients were correlated with radiological success.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12535357&dopt=Abstract hemorrhage
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