Background and Purpose-Independently assessed data on frequency, severity, and determinants of neurological deficits after endovascular treatment of brain arteriovenous malformations (AVMs) are scarce. Methods-From the prospective Columbia AVM Study Project, 233 consecutive patients with brain AVM receiving Ն1 endovascular treatments were analyzed. Neurological impairment was assessed by a neurologist using the Rankin Scale before and after completed endovascular therapy. Multivariate logistic regression models were used to identify demographic, clinical, and morphological predictors of treatment-related neurological deficits. The analysis included the components used in the Spetzler-Martin risk score for AVM surgery (AVM size, venous drainage pattern, and eloquence of AVM location). Results-The 233 patients were treated with 545 endovascular procedures. Mean follow-up time was 9.6 months (SD, 18.1 months). Two hundred patients (86%) experienced no change in neurological status after treatment, and 33 patients (14%) showed treatment-related neurological deficits. Of the latter, 5 (2%) had persistent disabling deficits (Rankin score Ͼ2), and 2 (1%) died. Increasing patient age [odds ratio (OR), 1.04; 95% confidence interval (CI), 1.01 to 1.08], number of embolizations (OR, 1.41; 95% CI, 1.16 to 1.70), and absence of a pretreatment neurological deficit (OR, 4.55; 95% CI, 1.03 to 20.0) were associated with new neurological deficits. None of the morphological AVM characteristics tested predicted treatment complications. Conclusions-From independent neurological assessment and prospective data collection, our findings suggest a low rate of disabling treatment complications in this center for endovascular brain AVM treatment. Risk predictors for endovascular treatment differ from those for AVM surgery.

Background and Purpose-Compliance with pharmacological therapy is essential for the efficiency of secondary prevention of ischemic stroke. Few data exist regarding patient compliance with antithrombotic and risk factor treatment outside of controlled clinical trials. The aim of the present study was to assess the rate of and predictors for compliance with secondary stroke prevention 1 year after cerebral ischemia and to identify reasons for noncompliance. Methods-Patients with a diagnosis of ischemic stroke or TIA and antithrombotic discharge medication were prospectively recruited. At 1 year, the proportion of patients compliant with antithrombotic treatment and with medication for risk factors (eg, hypertension, diabetes, hyperlipidemia) was evaluated through structured telephone interviews. In addition, the reasons for nontreatment with antithrombotic and risk factor medication were determined. Independent predictors for compliance were analyzed by logistic regression analyses. Results-Of 588 consecutive patients admitted to our stroke unit, 470 had a discharge diagnosis of cerebral ischemia (TIA 26.2%, cerebral infarct 73.8%) and recommendations for antithrombotic therapy. At 1 year, 63 patients (13.4%) had died and 21 (4.5%) were lost to follow-up, thus, 386 could finally be evaluated. Of the patients, 87.6% were still on antithrombotic medication, and 70.2% were treated with the same agent prescribed on discharge. Of the patients with hypertension, diabetes, and hyperlipidemia, 90.8%, 84.9%, and 70.2% were still treated for their respective risk factors. Logistic regression analyses revealed age (OR 1.03, 95% CI 1.00 to 1.06), stroke severity on admission (OR 1.09, 95% CI 1.00 to 1.20), and cardioembolic cause (OR 4.13, 95% CI 1.23 to 13.83) as independent predictors of compliance. Conclusions-Compliance with secondary prevention in patients with ischemic stroke is rather good in the setting of our study. Higher age, a more severe neurological deficit on admission, and cardioembolic stroke cause are associated with better long-term compliance. Knowledge of these determinants may help to further improve the quality of stroke prevention.

Background and Purpose-We sought to define determinants of neurological deficit after surgery for brain arteriovenous malformation (AVM). Methods-One hundred twenty-four prospective patients (48% women, mean age 33 years) underwent microsurgical brain AVM resection. Patients were examined by 3 study neurologists immediately before surgery, postoperatively in-hospital, by in-person long-term follow-up, and with a structured telephone follow-up. . At long-term follow-up (mean follow-up time 12 months), 47 patients (38%) revealed surgery-related neurological deficits (6% disabling; 32% nondisabling). The rate of neurological complications increased by Spetzler-Martin grade. Female gender, AVM size, and deep venous drainage were significantly associated with neurological deficits at in-hospital and long-term evaluation. For patient age and AVM location, no significant association was found. Conclusions-The findings suggest that female gender, AVM size, and AVM drainage into the deep venous system may be determinants of neurological deficit after microsurgical AVM resection.

Correlation of albumin quotient with body mass index and related variables may be mediated by spinal CSF resorption, which should be impaired in overweight patients with elevated venous pressure. Negative correlation of albumin quotient with iodine resorption from spinal CSF supports this assumption. Correlation of albumin quotient with narrowing of lumbosacral canal should be due to slowed spinal CSF flow which does increase protein concentration. Tested variables explain part of variation of CSF protein concentration. Other variables like blood-CSF barrier permeability and pulsatile spinal CSF flow should have additional influence.

Background and Purpose: Infarct patterns on brain imaging contribute to the etiologic classification of ischemic stroke. However, the association of specific subtypes of infarcts and etiologic mechanisms is often weak, and acute lesions are frequently missed on initial computed tomography (CT). Diffusion-weighted imaging (DWI) is superior in visualizing acute ischemic lesions as compared to CT and conventional magnetic resonance imaging (MRI). In our prospective study, we addressed the question whether a distinct pattern of infarction on DWI is associated with infarct etiology and clinical outcome. Methods: Sixty-two patients with clinical signs of acute ischemic stroke and negative acute CT upon admission underwent DWI within 10 days after the ictus. Neurological status was documented using the NIH stroke scale. A scattered lesion pattern was defined by at least 2 separate hyperintense DWI lesions within the territory of one of the major cerebral arteries. Ischemic lesions were defined as acute if the region was demarcated strongly hyperintense in all DW images, and if the apparent diffusion coefficient was below normal. Results: In 32 patients, DWI revealed a scattered lesion pattern, while in 30 patients a single acute lesion was detected. In patients with scattered lesions, potential arterial or cardiac embolic sources were detected in 26 patients (81.3%), as compared to 5 patients (16.6%) in the group with single lesions (χ² test, p < 0.0001). The neurological status of patients with scattered lesions improved significantly more than among patients with single lesions (Mann-Whitney test, p < 0.0003). Conclusion: A scattered lesion pattern on DWI in patients with acute brain infarction and negative initial CT scan is associated with an embolic etiology and may indicate a favorable clinical outcome.

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QAlb and QIgG of intra-individual sequential portions correlated highly with each other (median r = 0.95), suggesting lumbar CSF flow as the main thecal determinant of lumbar QAlb and QIgG variation. In addition, QIgG, relative to QAlb, was significantly lower in study patients compared with a reference patient sample (P = 0.002), implying an alteration of the blood-CSF barrier permeability as a minor determinant of QAlb and QIgG variation in study patients.

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