Timing and Predictors of Recanalization After Anticoagulation in Cerebral Venous Thrombosis.

BACKGROUND AND PURPOSE Vessel recanalization after cerebral venous thrombosis (CVT) is associated with favorable outcomes and lower mortality. Several studies examined the timing and predictors of recanalization after CVT with mixed results. We aimed to investigate predictors and timing of recanalization after CVT. METHODS We used data from the multicenter, international AntiCoagulaTION in the Treatment of Cerebral Venous Thrombosis (ACTION-CVT) study of consecutive patients with CVT from January 2015 to December 2020. Our analysis included patients that had undergone repeat venous neuroimaging more than 30 days after initiation of anticoagulation treatment. Prespecified variables were included in univariate and multivariable analyses to identify independent predictors of failure to recanalize. RESULTS Among the 551 patients (mean age, 44.4±16.2 years, 66.2% women) that met inclusion criteria, 486 (88.2%) had complete or partial, and 65 (11.8%) had no recanalization. The median time to first follow-up imaging study was 110 days (interquartile range, 60-187). In multivariable analysis, older age (odds ratio [OR], 1.05; 95% confidence interval [CI], 1.03-1.07), male sex (OR, 0.44; 95% CI, 0.24-0.80), and lack of parenchymal changes on baseline imaging (OR, 0.53; 95% CI, 0.29-0.96) were associated with no recanalization. The majority of improvement in recanalization (71.1%) occurred before 3 months from initial diagnosis. A high percentage of complete recanalization (59.0%) took place within the first 3 months after CVT diagnosis. CONCLUSION Older age, male sex, and lack of parenchymal changes were associated with no recanalization after CVT. The majority recanalization occurred early in the disease course suggesting limited further recanalization with anticoagulation beyond 3 months. Large prospective studies are needed to confirm our findings

High ABCD2 Scores and In-Hospital Interventions following Transient Ischemic Attack

Background and Purpose: Following transient ischemic attack (TIA), there is increased risk for ischemic stroke. The American Heart Association recommends admission of patients with ABCD2 scores ≥3 for observation, rapid performance of diagnostic tests, and potential acute intervention. We aimed to determine if there is a relationship between ABCD2 scores, in-hospital ischemic events, and in-hospital treatments after TIA admission. Methods: We reviewed consecutive patients admitted between 2006 and 2011 following a TIA, defined as transient focal neurological symptoms attributed to a specific vascular distribution and lasting 2 scores. Results: Of 249 patients, 11 patients (4.4%) had recurrent TIAs or strokes during their stay (8 TIAs, 3 strokes). All 11 had ABCD2 scores ≥3, and no neurological events occurred in patients with lower scores (5.1 vs. 0%; p = 0.37). Twelve patients (4.8%) underwent revascularization for large artery stenosis, 16 (6.4%) were started on anticoagulants, and no patient received intravenous or intra-arterial reperfusion therapy. The ABCD2 score was not associated with anticoagulation (p = 0.59) or revascularization (p = 0.20). Conclusions: Higher ABCD2 scores may predict early ischemic events after TIA but do not predict the need for intervention. Outpatient evaluation for those with scores <3 would potentially have delayed revascularization or anticoagulant treatment in nearly one-fifth of ‘low-risk' patients

Periprocedural Risk of Stroke Is Elevated in Patients with End-Stage Renal Disease on Hemodialysis

Objective: To describe the most common clinical factors and stroke etiologies in a case series of patients with end-stage renal disease on hemodialysis (ESRD/HD) with transient ischemic attack (TIA) or ischemic stroke (IS). Background: Prior studies have shown that patients on HD are at an elevated risk of stroke, but these studies have focused on the overall stroke risk. This case series sought to determine the percentage of acute ischemic events that occur during or immediately after HD. Methods: ICD-9 codes were used to identify IS and TIA patients with ESRD/HD admitted to the stroke service from August 22, 2011, to June 21, 2014. Charts were reviewed to determine the age, sex, and race/ethnicity of the cohort. TIA/IS diagnosis was confirmed by a vascular neurologist. Clinical factors were assessed, including: onset during or shortly after HD, defined as occurring within 12 h of HD; the presence of a lesion on diffusion-weighted MRI; hypotension, hyponatremia, or hypoglycemia at symptom onset; the stroke etiology; the presence of focal neurologic deficits; whether the patient was in the window period for intravenous tissue plasminogen activator (IVtPA) upon presentation, and whether the patient received IVtPA. Results: We identified 34 ESRD/HD patients with a diagnosis of TIA/stroke in the specified time period. A majority of patients (70.6%) were African American. Patient age ranged from 32 to 84 years, with a median age of 67 years. Twenty-seven patients (79.4%) had confirmed ischemic infarcts on diffusion-weighted MRI. Seven patients (20.6%) were diagnosed with TIA. In 13 patients (38.2%), symptom onset occurred during or shortly after HD. Of these 13 patients, 8 (61.5%) had symptom onset during HD. Three patients (8.8%) had documented hypotension near the time of symptom onset, and 2 (5.9%) were hyponatremic on presentation to the emergency department. The distribution of stroke etiologies was as follows: 4 (11.8%) watershed distribution, 1 (2.9%) large artery atherosclerosis, 2 (20.6%) small vessel disease, 10 (29.4%) cardioembolic, and 9 (26.5%) cryptogenic. In 28 patients (82.4%), focal neurologic deficits were observed on presentation. Nine patients (26.5%) arrived within the window period for IVtPA, and 4 (11.8%) were eligible and received IVtPA. Conclusions: Of all patients with ESRD on HD admitted to the stroke service over the study period, over one third (38.3%) had the onset of their ischemic event during or shortly after HD, and nearly one quarter (23.5%) had the onset during HD. While clinicians may be tempted to attribute neurologic changes after HD to metabolic etiologies, they should also be aware that HD represents a period of elevated risk for acute ischemia

Venous sinus stenting: a therapeutic alternative for refractory idiopathic intracranial hypertension

Idiopathic intracranial hypertension (IIH) is a disease of elevated intracranial pressure (ICP) characterized by optic disc edema, visual loss and positional headache (1). Treatment strategies to prevent catastrophic visual loss include carbonic anhydrase inhibition and weight loss but selected patients require surgical intervention including cerebrospinal fluid diversion or optic nerve sheath fenestration. Transverse venous sinus stenosis is a potential pathophysiological mechanism leading transverse venous sinus stenting to be proposed as an alternative procedure to reduce ICP and thereby arrest disease progression (2, 3)

Yield of Diagnostic Imaging in Atraumatic Convexity Subarachnoid Hemorrhage

INTRODUCTION: Atraumatic convexity subarachnoid hemorrhage is a subtype of spontaneous subarachnoid hemorrhage that often presents a diagnostic challenge. Common etiologies include cerebral amyloid angiopathy, vasculopathies, and coagulopathy; however, aneurysm is rare. Given the broad differential of causes of convexity subarachnoid hemorrhage, we assessed the diagnostic yield of common tests and propose a testing strategy. METHODS: We performed a single-center retrospective study on consecutive patients with atraumatic convexity subarachnoid hemorrhage over a 2-year period. We obtained and reviewed each patient\u27s imaging and characterized the frequency with which each test ultimately diagnosed the cause. Additionally, we discuss clinical features of patients with convexity subarachnoid hemorrhage with respect to the mechanism of hemorrhage. RESULTS: We identified 70 patients over the study period (mean (SD) age 64.70 (16.9) years, 35.7% men), of whom 58 patients (82%) had a brain MRI, 57 (81%) had non-invasive vessel imaging, and 27 (38.5%) underwent catheter-based angiography. Diagnoses were made using only non-invasive imaging modalities in 40 patients (57%), while catheter-based angiography confirmed the diagnosis in nine patients (13%). Further clinical history and laboratory testing yielded a diagnosis in an additional 17 patients (24%), while the cause remained unknown in four patients (6%). CONCLUSION: The etiology of convexity subarachnoid hemorrhage may be diagnosed in most cases via non-invasive imaging and a thorough clinical history. However, catheter angiography should be strongly considered when non-invasive imaging fails to reveal the diagnosis or to better characterize a vascular malformation. Larger prospective studies are needed to validate this algorithm

Mild Luminal Stenosis of Parent Artery and Neurologic Deterioration After Acute Lacunar Stroke

Background Early neurologic deterioration (END) occurs in a quarter of acute lacunar infarcts, but the underlying pathophysiological features are poorly understood. We sought to determine the association between luminal stenosis (50%) in the parent vessel and no cardioembolic source. We defined END as any neurologic deterioration referable to the acute lacunar stroke and not related to a medical or noncerebrovascular neurological complication. We used univariate and logistic regression analyses to determine associations between luminal stenosis (<50%) and the odds of END. Furthermore, we attempted to validate findings using the Columbia University Medical Center stroke registry and perform a meta‐analysis combining the derivation and validation groups because of the expected small samples and event rates. Results The New York University Langone Health and Brown University sample included 205 patients, of whom 41 (20%) had END. In adjusted models, we found no definite association between luminal stenosis (<50%) and END (adjusted odds ratio [OR], 1.74; 95% CI, 0.73–4.14). From Columbia University Medical Center, 361 total patients were included, of whom 59 (16%) had END. In adjusted models, we found an association between luminal stenosis (<50%) and END (adjusted OR, 2.28; 95% CI, 1.15–4.50). Meta‐analysis of both cohorts found luminal stenosis (<50%) associated with END (relative risk, 1.69; 95% CI, 1.17–2.43). Conclusions In this multicenter study, luminal stenosis (<50%) may be associated with END following an acute lacunar infarct. Larger studies using vessel wall imaging are needed to validate our findings