Median Modified Rankin Scale Score Research Articles

Modified Park Bench Position for Superior Vermian Arteriovenous Malformations and Dural Fistulas.

Arteriovenous malformations (AVMs) of the superior cerebellar vermis and dural arteriovenous fistulas (dAVFs) draining into tentorial venous structures are uncommon lesions. Various surgical approaches and positions have been used to gain access. We present our experience with 10 superior vermian AVMs and 3 dAVFs with retrograde transverse sinus or torcular drainage, each resected through a supracerebellar infratentorial approach in the park bench position with modification of the neck and head position (vertex tilt-up instead of down). All 13 patients were treated surgically, with 4 receiving adjunctive endovascular embolization. Postoperative digital subtraction angiography confirmed complete resection of lesion in all. One patient experienced superficial wound infection treated by oral antibiotics, and another presented with a cerebrospinal fluid collection due to delayed hydrocephalus requiring insertion of a ventriculoperitoneal shunt. The median modified Rankin Scale score at last follow-up was 1. There were no surgical complications at the time of last follow-up. Our series shows that for superior vermian AVMs or dAVFs with retrograde transverse sinus or torcula venous drainage, the supracerebellar infratentorial approach in a modified vertex tilt-up park bench position is a safe and effective surgical approach.

Autoimmune encephalitis associated with voltage-gated potassium channels-complex and leucine-rich glioma-inactivated 1 antibodies - a national cohort study.

The aim of this study was to describe clinical and paraclinical characteristics of all Danish patients who tested positive for anti-voltage-gated potassium channels (VGKC)-complex, anti-leucine-rich glioma-inactivated 1 (LGI1) and anti-contactin-associated protein-2 antibodies in the serum/cerebrospinal fluid between 2009 and 2013 with follow-up interviews in 2015 and 2016. We evaluated antibody status, symptoms leading to testing, course of disease, suspected diagnosis and time of admission as well as diagnosis and treatment. All magnetic resonance imaging, electroencephalography and 18 F-fluorodeoxyglucose positron emission tomography scans were re-evaluated by experts in the field. A total of 28/192 patients tested positive for VGKC-complex antibodies by radioimmunoassay and indirect immunofluorescence; 17 had antibodies to LGI1 and 6/7 of the available cerebrospinal fluids from these patients were seropositive. These 17 patients all had a clinical phenotype appropriate to LGI1 antibodies. The remaining 11 were LGI1 negative (n = 4) or not tested (n = 7). Of these, two had a phenotype consistent with limbic encephalitis. The remaining phenotypes were Guillain-Barré syndrome, Creutzfeldt-Jakob disease, neuromyotonia and anti-N-methyl-D-aspartate receptor encephalitis. Magnetic resonance imaging abnormalities were demonstrated in 69% of the LGI1-positive patients. Two patients with normal magnetic resonance imaging demonstrated temporal lobe hypermetabolism using 18 F-fluorodeoxyglucose positron emission tomography. Abnormal electroencephalography recordings were found in 86% of the patients. Upon follow-up (median 3.2 years), the median modified Rankin Scale score of anti-LGI1-positive patients was 2 and only two patients reported seizures in the past year. Patients diagnosed with anti-LGI1 autoimmune encephalitis increased significantly from 2009 to 2014, probably due to increased awareness. In contrast to seropositive anti-VGKC-complex patients, all anti-LGI1-positive patients presented with a classical limbic encephalitis. The majority of patients recovered well.

Decannulation and Functional Outcome After Tracheostomy in Patients with Severe Stroke (DECAST): A Prospective Observational Study.

Tracheostomy is performed in ventilated stroke patients affected by persisting severe dysphagia, reduced level of consciousness, or prolonged mechanical ventilation. The study aim was to determine the frequency and predictors of successful decannulation and long-term functional outcome in tracheotomized stroke patients. A prospective single-center observational study recruited ventilated patients with ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage. Follow-up visits were performed at hospital discharge, 3, and 12months. Competing risk analyses were performed to identify predictors of decannulation. We included 53 ventilated stroke patients who had tracheostomy. One year after tracheostomy, 19 patients were decannulated (median [IQR] time to decannulation 74 [58-117] days), 13 patients were permanently cannulated, and 21 patients died without prior removal of the cannula. Independent predictors for decannulation in our cohort were patient age (HR 0.95 [95% CI: 0.92-0.99] per one year increase, p=0.003) and absence of sepsis (HR 4.44 [95% CI: 1.33-14.80], p=0.008). Compared to surviving patients without cannula removal, decannulated patients had an improved functional outcome after one year (median modified Rankin Scale score 4 vs. 5 [p<0.001]; median Barthel index 35 vs. 5 [p<0.001]). Decannulation was achieved in 59.4% of stroke patients surviving the first 12months after tracheostomy and was associated with better functional outcome compared to patients without decannulation. Further prospective studies with larger sample sizes are needed to confirm our results.

Long-term outcomes of refractory neurosarcoidosis treated with infliximab.

Central nervous system localizations of sarcoidosis may be refractory to conventional treatment such as steroids and immunosuppressive drugs. Infliximab, a TNF-α antagonist chimeric antibody, has been shown to be effective for treatment of these localizations. The aim of this study was to evaluate the efficacy and safety, in particular the long-term outcomes, of the use of infliximab for the treatment of neurosarcoidosis. We retrospectively reviewed medical records of patients with neurosarcoidosis who had been treated with infliximab between 2009 and 2015. All patients had histologically proven non-caseating granulomas. Eighteen patients with histologically proven sarcoidosis were included in this study. All had neurological involvement consisting of meningeal (n=16), cerebral (n=10), spinal cord (n=6), and/or optic nerve (n=5) involvement. Sixteen patients had previously received at least one immunosuppressive drug in addition to corticosteroids, including cyclophosphamide in 11 patients. All patients received treatment with infliximab (3-7.5mg/kg) associated with corticosteroids (n=18), low-dose methotrexate (n=15), azathioprine (n=2), or mycophenolate (n=1). Sixteen out of 18 patients improved clinically (initial median modified Rankin scale score of 3, final median score of 1; p<0.0001). At 6months after initiation of infliximab, six patients obtained complete remission (33%), ten attained partial remission (56%), and two had stable disease (11%). The median follow-up time was 20months (range 6-93). Nine patients relapsed during follow-up (50%). Eight patients developed toxic side effects and seven of these side effects were infectious events. Infliximab is an efficacious treatment of refractory neurosarcoidosis. However, relapses frequently occurred during follow-up.

Cerebrovascular events as presenting manifestations of Myeloproliferative Neoplasm

AimTo determine the incidence and main characteristics of cerebrovascular events as the presenting manifestations of myeloproliferative neoplasm (MPN). MethodsThe Hematology in Lyon (HEMILY) registry is a prospective database (763 patients) of all cases of MPN diagnosed since 2005 in the Rhône-Alpes district of France. The MPN cases were divided into four groups: polycythemia vera (PV); essential thrombocythemia (ET); myelofibrosis (MF); and atypical MPN. The ischemic stroke subtype was classified according to TOAST criteria. ResultsA stroke history revealed MPN in 35 (4.3%) patients: 22 (63%) had an ischemic stroke; eight (23%) had a transient ischemic attack; four (11%) had cerebral venous thrombosis; and one (3%) had hemorrhagic stroke. All patients had hemoglobin and/or platelet count abnormalities. In addition, 12 (34%) patients had PV, 21 (60%) had ET, one (3%) had MF and one (3%) had atypical/unclassified MPN. The JAK2 V617F mutation was found in 83% of patients. In 18 (51%) patients, an additional mechanism of stroke was present (atherosclerosis in 10 patients, atrial fibrillation in one patient and dissection in another). The median NIHSS score at entry was 2, and the median modified Rankin Scale score at 3 months was 0. Compared with the general MPN population, stroke–MPN patients presented with significantly higher levels of hemoglobin (P<0.001) and were more frequently positive for the JAK2 V617F mutation (P=0.044). ConclusionStroke revealing MPN is rare. However, careful attention should still be paid to blood counts even in patients with obvious stroke etiologies, as early diagnosis permits prompt treatment and decreases the risk of recurrence, thus limiting morbidity and mortality.

“Awake” clipping of cerebral aneurysms: report of initial series

OBJECTIVE Risk of ischemia during aneurysm surgery is significantly related to temporary clipping time and final clipping that might incorporate a perforator. In this study, the authors attempted to assess the potential added benefit to patient outcomes of "awake" neurological testing when compared with standard neurophysiological testing performed under general anesthesia. The procedure is performed after the induction of conscious sedation, and for the neurological testing, the patient is fully awake. METHODS The authors conducted an institutional review board-approved prospective study of clipping unruptured intracranial aneurysms (UIAs) in 30 consecutive adult patients who underwent awake clipping. The end points were the incidence of stroke/cerebrovascular accident (CVA), death, discharge to a long-term facility, length of stay, and 30-day modified Rankin Scale score. All clinical and neurophysiological intraoperative monitoring data were recorded. RESULTS The median patient age was 52 years (range 27-63 years); 19 (63%) female and 11 (37%) male patients were included. Twenty-seven (90%) aneurysms were anterior, and 3 (10%) were posterior circulation aneurysms. Five (17%) had been coiled previously, 3 (10%) had been clipped previously, 2 (7%) were partially calcified, and 2 (7%) were fusiform aneurysms. Three patients developed synchronous clinical neurological and neurophysiological changes during temporary clipping with consequent removal of the temporary clip and reversal of those clinical and neurophysiological changes. Three patients developed asynchronous clinical neurological and neurophysiological changes. These 3 patients developed hemiparesis without changes in neurophysiological monitoring results. One patient developed linked clinical neurological and neurophysiological changes during final clipping that were not reversed by reapplication of the clip, and the patient had a CVA. Four patients with internal carotid artery ophthalmic segment aneurysms underwent visual testing with final clipping, and 1 of these patients required repositioning of the clip. Three patients who required permanent occlusion of a vessel as part of their aneurysm treatment underwent a 10-minute intraoperative clinical respective-vessel test occlusion. The median length of stay was 3 days (range 1-5 days). The median modified Rankin Scale score was 1 (range 0-3). All of the patients were discharged to home from the hospital except for 1 who developed a CVA and was discharged to a rehabilitation facility. There were no deaths in this series. CONCLUSIONS The 3 patients who developed neurological deterioration without a concomitant neurophysiological finding during temporary clipping revealed a potential advantage of awake aneurysm surgery (i.e., in decreasing the risk of ischemic injury).

Analysis of clinical features and influencing factors of rebleeding after bypass surgery in patients with hemorrhagic moyamoya disease

Objective To analyze the rebleeding features and possible influencing factors after bypass in patients with hemorrhagic moyamoya disease. Methods From May 2005 to May 2010, 89 patients with hemorrhagic moyamoya disease operated with bypass surgery in the Fifth Affiliated Hospital of Zhengzhou University were followed up. The end point event was rebleeding. The clinical features in patients with rebleeding were analyzed. Cox regression model was used to analyze the possible influencing factors of rebleeding. Results They were followed up for 71.3±10.2 months. In 89 patients, 33(37.1%)had rebleeding. The median age of rebleeding was 48 years old, and the peak age of bleeding was 40-50 years old, accounting for 39.4%(13/33). The median time from having nervous system symptoms to the first bleeding was 13.5(4-21)months. The interval time from the first to the second bleeding was 11.5(7-24)months. There was significant difference(P=0.001). The median modified Rankin scale(mRS)score of the first bleeding was 2(0-5), the second bleeding score was 3(1-5). There was significant difference(P=0.002). Multivariate Cox regression analysis showed that in addition to age(RR, 1.288, 95% CI 0.991-1.672, P=0.058), intracranial collateral vessel formation(RR, 1.271, 95% CI 1.009-3.184), the mRS of the first bleeding was >2(RR, 4.173, 95% CI 1.891-7.544), the time from complete evacuation of intracranial hematoma to bypass >1 month(RR, 2.991, 95% CI 2.670-5.978), anterior choroidal artery dilatation(RR, 3.316, 95% CI 1.135-8.741), posterior communicating artery dilatation(RR, 2.971, 95% CI 1.653-4.465), combined aneurysm(RR, 3.059, 95% CI 1.973-5.065), combined hypertension(RR, 5.587, 95% CI 2.345-10.218)were the independent risk factors for affecting rebleeding(all P<0.05). Conclusions The proportion of rebleeding in patients with hemorrhagic moyamoya disease is higher after bypass. The time of rebleeding is shorter, and the conditions become aggravated. The possible risk factors for rebleeding should be prevented and treated as early as possible. Key words: Cerebral bottom abnormal vascular network disease; Disease attributes; Risk factors; Regression analysis; Rebleeding

Early-onset bilateral cerebral arteriopathies: Cohort study of phenotype and disease course.

To describe characteristics of young children with arterial ischemic stroke (AIS) and bilateral cerebral arteriopathies. Retrospective review of clinical features, course, and outcome. Neuroimaging was analyzed for infarct pattern, cerebrovascular diagnosis (anatomic/Childhood Arterial Ischemic Stroke Standardized Classification and Diagnostic Evaluation [CASCADE] criteria), and disease progression. In the 31 children (median age, 18 months), presentations included acute hemiparesis (n=23) and focal seizures (n=12). Seven had systemic arterial disease; 13 had cardiac abnormalities. Twenty had recurrent AIS or transient ischemic attack (after median of 3 months); 16 had >1 recurrence. Median modified Rankin Scale score was 3, with motor impairments in 20, cognitive impairments in 11, and seizures in 7. At presentation, 17 had old and acute infarcts. Twenty-five had high signal in white matter. A total of 13/23 reimaged patients accrued further infarcts over a median of 39 months. Arteriopathy involved the carotid circulation bilaterally in all; 6 had posterior circulation and 11 had extracranial involvement. Arteriopathy distribution was symmetric in 24/31. CASCADE categories were 3A in 19, 3B in 5, 3C in 5, and 7 in 2. After a median of 35 months, 14 had had progression of arteriopathy. Patients categorized as CASCADE 3A (moyamoya) had significantly shorter time to recurrence than other groups. Young children with bilateral cerebral arteriopathies (particularly meeting criteria for CASCADE 3A) have a malignant course, with frequent recurrent events, progressive disease, and poor outcomes. Current classifications are limited in characterizing disease in many cases. Symmetric involvement suggests these arteriopathies may be developmentally determined, while systemic involvement suggests potential genetic etiology.

Quality of Life after Young Ischemic Stroke of Mild Severity Is Mainly Influenced by Psychological Factors

Long-term prognosis in terms of quality of life (QoL) in young stroke patients is of importance because they usually have a long life expectancy and extensive daily life demands. We aimed at determining which medical and psychological factors influence the QoL in young stroke patients (<50 years), after long-term follow-up. Young ischemic stroke patients admitted to the St. Elisabeth Hospital and the TweeSteden Hospital, Tilburg, the Netherlands, between 2000 and 2010 were included. One hundred seventy patients and 61 controls filled out the following questionnaires: (1) the Hospital Anxiety and Depression Scale, (2) the Fatigue Assessment Scale, and (3) the shortened World Health Organization Quality of Life scale. Using linear multiple regression analysis, we assessed the factors influencing QoL. QoL did not differ significantly between patients (median modified Rankin Scale score at follow-up, 0) and controls after a mean follow-up of 4.5 (standard deviation, 2.8) years. The presence of excessive fatigue was associated with lower scores on all domains of the QoL (P ≤ .003), but not for general health domain (P = .010). Similarly, depression was associated with worse QoL on the physical (P = .004) and psychological (P = .001) domains and anxiety with lower scores on the psychological (P < .001) QoL domain. No relationship was found between stroke-specific factors and QoL. Fatigue and to a lesser extent depression and anxiety affect the QoL in young adults after ischemic stroke of mild severity. Therefore, young stroke patients should be informed about, screened, and, if possible, treated for fatigue, depression, and anxiety.

Impairments and comorbidities of polyneuropathy revealed by population-based analyses.

To quantify polyneuropathy impairments and comorbidities utilizing the Rochester Epidemiology Project (2010 census = 148,201). ICD-9-CM coding identified polyneuropathy cases (2006-2010) and their 5:1 age- and sex-matched controls. Mortality and impairments were evaluated while identifying and adjusting for Charlson Index comorbidities. Overall prevalence of polyneuropathy was 1.66%, and markedly rose to 6.6% in persons older than 60 years. Cases (n = 2,892) had more comorbidities than controls (n = 14,435) with higher median Charlson Index (6 vs 3, p < 0.001). Diabetes with end-organ disease represented the largest increased comorbidity in cases compared with controls (46.8% vs 6.5%). Diabetic polyneuropathy was the most common specific subtype (38.2%). Miscoded idiopathic cases and false-negative controls also commonly had diabetic polyneuropathy. Median modified Rankin Scale score was considerably higher for cases than controls (4 vs 1, p < 0.001). Multiple comorbidities were found associated with polyneuropathy after adjusting for diabetes co-occurrence, including pulmonary disease, dementia, and others. Polyneuropathy was an independent contributor to multiple functional impairments including difficulty walking (odds ratio [OR] = 1.9), climbing stairs (OR = 2.0), using an assistive device (OR = 2.0), fall tendency (OR = 2.4), work disability (OR = 4.2), lower limb amputations (OR = 3.9), and opioid use (OR = 2.7). Prevalent cases had a younger median age at death than controls (80 vs 86 years, p < 0.001), and incident cases had a 6-month shorter survival. Polyneuropathies have notable neurologic impairments beyond their identified multiple comorbidities. Life expectancy is shortened. Diabetic polyneuropathy is underidentified. The quantified extent of the disease burden and refined comorbidity associations emphasize that greater research efforts and health care initiatives are needed.

Intracranial pressure monitoring following decompressive hemicraniectomy for malignant cerebral infarction

Randomized controlled trials have demonstrated the efficacy of decompressive craniectomy in substantially decreasing mortality and improving functional outcome in middle cerebral artery infarction. The role of intracranial pressure (ICP) monitoring following decompressive craniectomy for stroke has not been well studied. We present a retrospective review of our experience with postoperative ICP monitoring in 12 stroke patients who underwent decompressive craniectomy. All elevations of ICP above a 20mmHg threshold were noted. ICP was recorded for 1417 hours during which 68 ICP elevations were seen. Nine out of 12 patients had events of raised ICP, including eight with more than three elevations. A total of 81 interventions were employed to treat elevated ICP; 71 were effective in reducing ICP below the 20mmHg threshold. The most frequent intervention was cerebrospinal fluid drainage via an external ventricular drain, which was effective in 85.4% of cases. Eleven out of 12 patients survived (92%) and attained a median modified Rankin Scale score of 4 (interquartile range 4–5) at a mean 15month follow-up. In our experience, elevated ICP may commonly occur following decompressive craniectomy for stroke. Monitoring ICP influenced postoperative management and standard measures for reducing ICP were usually effective in the current series.

Glycine receptor antibodies in PERM and related syndromes: characteristics, clinical features and outcomes.

The clinical associations of glycine receptor antibodies have not yet been described fully. We identified prospectively 52 antibody-positive patients and collated their clinical features, investigations and immunotherapy responses. Serum glycine receptor antibody endpoint titres ranged from 1:20 to 1:60 000. In 11 paired samples, serum levels were higher than (n = 10) or equal to (n = 1) cerebrospinal fluid levels; there was intrathecal synthesis of glycine receptor antibodies in each of the six pairs available for detailed study. Four patients also had high glutamic acid decarboxylase antibodies (>1000 U/ml), and one had high voltage-gated potassium channel-complex antibody (2442 pM). Seven patients with very low titres (<1:50) and unknown or alternative diagnoses were excluded from further study. Three of the remaining 45 patients had newly-identified thymomas and one had a lymphoma. Thirty-three patients were classified as progressive encephalomyelitis with rigidity and myoclonus, and two as stiff person syndrome; five had a limbic encephalitis or epileptic encephalopathy, two had brainstem features mainly, two had demyelinating optic neuropathies and one had an unclear diagnosis. Four patients (9%) died during the acute disease, but most showed marked improvement with immunotherapies. At most recent follow-up, (2-7 years, median 3 years, since first antibody detection), the median modified Rankin scale scores (excluding the four deaths) decreased from 5 at maximal severity to 1 (P < 0.0001), but relapses have occurred in five patients and a proportion are on reducing steroids or other maintenance immunotherapies as well as symptomatic treatments. The glycine receptor antibodies activated complement on glycine receptor-transfected human embryonic kidney cells at room temperature, and caused internalization and lysosomal degradation of the glycine receptors at 37°C. Immunoglobulin G antibodies bound to rodent spinal cord and brainstem co-localizing with monoclonal antibodies to glycine receptor-α1. Ten glycine receptor antibody positive samples were also identified in a retrospective cohort of 56 patients with stiff person syndrome and related syndromes. Glycine receptor antibodies are strongly associated with spinal and brainstem disorders, and the majority of patients have progressive encephalomyelitis with rigidity and myoclonus. The antibodies demonstrate in vitro evidence of pathogenicity and the patients respond well to immunotherapies, contrasting with earlier studies of this syndrome, which indicated a poor prognosis. The presence of glycine receptor antibodies should help to identify a disease that responds to immunotherapies, but these treatments may need to be sustained, relapses can occur and maintenance immunosuppression may be required.

Bypass surgery for complex middle cerebral artery aneurysms: impact of the exact location in the MCA tree

The object of this study was to describe the authors' institutional experience in the treatment of complex middle cerebral artery (MCA) aneurysms necessitating bypass and vessel sacrifice. Cases in which patients with MCA aneurysms were treated with a combination of bypass and parent artery sacrifice were reviewed retrospectively. The authors identified 24 patients (mean age 46 years) who were treated with bypass and parent artery sacrifice. The aneurysms were located in the M1 segment in 7 patients, MCA bifurcation in 8, and more distally in 9. The mean aneurysm diameter was 30 mm (range 7-60 mm, median 26 mm). There were 8 saccular and 16 fusiform aneurysms. Twenty-one extracranial-intracranial and 4 intracranial-intracranial bypasses were performed. Partial or total trapping (only) of the parent artery was performed in 17 cases, trapping with resection of aneurysm in 3, and aneurysm clipping with sacrifice of an M2 branch in 4. The mean follow-up period was 27 months. The aneurysm obliteration rate was 100%. No recanalization of the aneurysms was detected during follow-up. There was 1 perioperative death (4% mortality rate) and 6 cerebrovascular accidents, causing permanent morbidity in 5 patients. The median modified Rankin Scale score of patients with an M1 aneurysm increased from 0 preoperatively to 2 at latest follow-up, while the score was unchanged in other patients. Most of the permanent deficits were associated with M1 aneurysms. Twenty-one patients (88%) had good outcome as defined by a Glasgow Outcome Scale score of 4 or 5. Bypass in combination with parent vessel occlusion is a useful technique with acceptable frequencies of morbidity and mortality for complex MCA aneurysms when conventional surgical or endovascular techniques are not feasible. The location of the aneurysm should be considered when planning the type of bypass and the site of vessel occlusion. Flow alteration by partial trapping may be preferable to total trapping for the M1 aneurysms.

Worse stroke outcome in atrial fibrillation is explained by more severe hypoperfusion, infarct growth, and hemorrhagic transformation.

Atrial fibrillation is associated with greater baseline neurological impairment and worse outcomes following ischemic stroke. Previous studies suggest that greater volumes of more severe baseline hypoperfusion in patients with history of atrial fibrillation may explain this association. We further investigated this association by comparing patients with and without atrial fibrillation on initial examination following stroke using pooled multimodal magnetic resonance imaging and clinical data from the Echoplanar Imaging Thrombolytic Evaluation Trial and the Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution studies. Echoplanar Imaging Thrombolytic Evaluation Trial was a trial of 101 ischemic stroke patients randomized to intravenous tissue plasminogen activator or placebo, and Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution was a prospective cohort of 74 ischemic stroke patients treated with intravenous tissue plasminogen activator at three to six hours following symptom onset. Patients underwent multimodal magnetic resonance imaging before treatment, at three to five days and three-months after stroke in Echoplanar Imaging Thrombolytic Evaluation Trial; before treatment, three to six hours after treatment and one-month after stroke in Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution. Patients were assessed with the National Institutes of Health Stroke Scale and the modified Rankin scale before treatment and at three-months after stroke. Patients were categorized into definite atrial fibrillation (present on initial examination), probable atrial fibrillation (history but no atrial fibrillation on initial examination), and no atrial fibrillation. Perfusion data were reprocessed with automated magnetic resonance imaging analysis software (RAPID, Stanford University, Stanford, CA, USA). Hypoperfusion volumes were defined using time to maximum delays in two-second increments from >4 to >8 s. Hemorrhagic transformation was classified according to the European Cooperative Acute Stroke Studies criteria. Of the 175 patients, 28 had definite atrial fibrillation, 30 probable atrial fibrillation, 111 no atrial fibrillation, and six were excluded due to insufficient imaging data. At baseline, patients with definite atrial fibrillation had more severe hypoperfusion (median time to maximum >8 s, volume 48 vs. 29 ml, P = 0.02) compared with patients with no atrial fibrillation. At outcome, patients with definite atrial fibrillation had greater infarct growth (median volume 47 vs. 8 ml, P = 0.001), larger infarcts (median volume 75 vs. 23 ml, P = 0.001), more frequent parenchymal hematoma grade hemorrhagic transformation (30% vs. 10%, P = 0.03), worse functional outcomes (median modified Rankin scale score 4 vs. 3, P = 0.03), and higher mortality (36% vs. 16%, P = 0·.3) compared with patients with no atrial fibrillation. Definite atrial fibrillation was independently associated with increased parenchymal hematoma (odds ratio = 6.05, 95% confidence interval 1.60-22.83) but not poor functional outcome (modified Rankin scale 3-6, odds ratio = 0.99, 95% confidence interval 0.35-2.80) or mortality (odds ratio = 2.54, 95% confidence interval 0.86-7.49) three-months following stroke, after adjusting for other baseline imbalances. Atrial fibrillation is associated with greater volumes of more severe baseline hypoperfusion, leading to higher infarct growth, more frequent severe hemorrhagic transformation and worse stroke outcomes.

P2-44 Burden of stroke and its related disabilities in a rural community of Bangladesh

IntroductionDemographic changes and increased exposure to stroke risk factors are expected to give rise to high stroke burden in countries like Bangladesh. However data on stroke prevalence and its related...

The Importance of Size

We hypothesize that in acute middle cerebral artery stroke, thrombus lengths measured in thin-slice nonenhanced CT images define a limit beyond which systemic thrombolysis will fail to recanalize occluded arteries. In 138 patients who presented with acute middle cerebral artery stroke and who were treated with intravenous thrombolysis (IVT), we measured lengths of thrombotic clots depicted as arterial hyperdensities in admission nonenhanced CT images with 2.5-mm slice width. Vascular recanalization was investigated after thrombolysis and recanalization results were related to thrombus lengths by logistic regression. In 62 patients, IVT resulted in recanalization; among these patients, no thrombus length exceeded 8 mm. The median modified Rankin scale score at hospital discharge was 2. In the remaining 76 patients, thrombus lengths mostly exceeded 8 mm and IVT failed in recanalization. These patients were discharged with a median modified Rankin scale score of 5. This study shows that in acute middle cerebral artery stroke, IVT has nearly no potential to recanalize occluded vessels if thrombus length exceeds 8 mm.

Recanalisation of cerebral venous thrombosis

Objective: To investigate recanalisation in the first 12 months after cerebral venous thrombosis. Methods: 33 consecutive patients presenting with cerebral venous thrombosis were enrolled in the study. Diagnosis was made...

Aptiganel Hydrochloride in Acute Ischemic Stroke

Tissue plasminogen activator is the only thrombolytic agent approved in the United States for treatment of acute ischemic stroke, and has limitations. Aptiganel hydrochloride is a novel and selective ligand for the ion-channel site of the N-methyl-D-aspartate receptor-channel complex and a promising neuroprotective agent in animal models of focal brain ischemia. To determine whether aptiganel improves the clinical outcome for acute ischemic stroke patients. Nested phase 2/phase 3 randomized controlled trial conducted between July 1996 and September 1997. One hundred fifty-six medical centers in the United States, Canada, Australia, South Africa, England, and Scotland. A total of 628 patients with hemispheric ischemic stroke (50.3% male; mean age, 71.5 years). Patients were randomly assigned within 6 hours of stroke to receive 1 of 3 treatment regimens: high-dose aptiganel (5-mg bolus followed by 0.75 mg/h for 12 hours; n = 214); low-dose aptiganel (3-mg bolus followed by 0.5 mg/h for 12 hours; n = 200); or placebo (n = 214). The primary efficacy end point was the Modified Rankin Scale score at 90 days after stroke onset. Secondary end points included mortality and change in National Institutes of Health (NIH) Stroke Scale score at 7 days after stroke. The trial was suspended by the sponsor and the independent data and safety monitoring board because of both a lack of efficacy and a potential imbalance in mortality. There was no improvement in outcome for either aptiganel (low-dose or high-dose) group compared with the placebo group at 90 days (median Modified Rankin Scale score for all 3 treatment groups = 3; P =.31). At 7 days, placebo-treated patients exhibited slightly greater neurological improvement on the NIH Stroke Scale than high-dose aptiganel patients (mean improvement for placebo group, -0.8 points vs for high-dose aptiganel, 0.9 points; P =.04). The mortality rate at 120 days in patients treated with high-dose aptiganel was higher than that in patients who received placebo (26.3% vs 19.2%; P =.06). Mortality in the low-dose aptiganel group was 22.5% (P =.39 vs placebo). Aptiganel was not efficacious in patients with acute ischemic stroke at either of the tested doses, and m ay be harmful. The larger proportion of patients with favorable outcomes and lower mortality rate in the placebo group suggest that glutamate blockade with aptiganel may have detrimental effects in an undifferentiated population of stroke patients.