Yiping Li1, Chadd Funk1, Demi Dawkins1, Dustin Simpson2, John-Paul J Yu3, Melanie Boly4, Azam Ahmed5. 1. Department of Neurological Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA. 2. Department of Radiology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA. 3. Department of Radiology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA; Department of Psychiatry, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA; Department of Biomedical Engineering, College of Engineering, University of Wisconsin-Madison, Madison, Wisconsin, USA; Neuroscience Training Program, Wisconsin Institutes for Medical Research, University of Wisconsin-Madison, Madison, Wisconsin, USA. 4. Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA. 5. Department of Neurological Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA; Department of Radiology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA. Electronic address: azam.ahmed@neurosurgery.wisc.edu.
Abstract
OBJECTIVE: To evaluate the relationship between blood-brain barrier disruption and transient neurologic deficits (TNDs) after neuroendovascular interventions (NEIs) using postcontrast T2/FLAIR (pcFLAIR) imaging. METHODS: This is a prospective study of 41 consecutive patients undergoing flow diversion therapy for unruptured aneurysm treatment. Patients underwent postprocedural magnetic resonance imaging within 24 hours of the procedure, including diffusion-weighted imaging (DWI) and pcFLAIR sequences. Regression analyses were performed to identify risk factors for developing TNDs. RESULTS: In total, 13 patients (31.7%) developed neurologic complications ranging from visual field defects to dense hemiplegia. All deficits were transient, resolving spontaneously within 72 hours. Five of 13 patients (38.5%) with TNDs had presence of lesions on DWI whereas the remaining 8 patients (61.5%) did not. In contrast, all patients who developed TNDs had leptomeningeal enhancement on pcFLAIR imaging, and no patient with normal pcFLAIR imaging developed TNDs. Regression analysis revealed the extent of pcFLAIR enhancement is associated with development of postprocedure neurologic deficits (P < 0.0001). Video electroencephalography monitoring was performed in 4 symptomatic patients manifesting severe deficits. In all instances electroencephalography demonstrated ipsilateral hemispheric slowing and eventual resolution corresponding to ensuing clinical improvement. Only 1 of these 4 patients presented with a lesion on DWI. CONCLUSIONS: This study challenges conventional dogma that TNDs are ischemic in etiology and suggests blood-brain barrier impairment may be a potential alternative mechanism. These findings are applicable to stroke and other reversible neurologic diseases.
OBJECTIVE: To evaluate the relationship between blood-brain barrier disruption and transient neurologic deficits (TNDs) after neuroendovascular interventions (NEIs) using postcontrast T2/FLAIR (pcFLAIR) imaging. METHODS: This is a prospective study of 41 consecutive patients undergoing flow diversion therapy for unruptured aneurysm treatment. Patients underwent postprocedural magnetic resonance imaging within 24 hours of the procedure, including diffusion-weighted imaging (DWI) and pcFLAIR sequences. Regression analyses were performed to identify risk factors for developing TNDs. RESULTS: In total, 13 patients (31.7%) developed neurologic complications ranging from visual field defects to dense hemiplegia. All deficits were transient, resolving spontaneously within 72 hours. Five of 13 patients (38.5%) with TNDs had presence of lesions on DWI whereas the remaining 8 patients (61.5%) did not. In contrast, all patients who developed TNDs had leptomeningeal enhancement on pcFLAIR imaging, and no patient with normal pcFLAIR imaging developed TNDs. Regression analysis revealed the extent of pcFLAIR enhancement is associated with development of postprocedure neurologic deficits (P < 0.0001). Video electroencephalography monitoring was performed in 4 symptomatic patients manifesting severe deficits. In all instances electroencephalography demonstrated ipsilateral hemispheric slowing and eventual resolution corresponding to ensuing clinical improvement. Only 1 of these 4 patients presented with a lesion on DWI. CONCLUSIONS: This study challenges conventional dogma that TNDs are ischemic in etiology and suggests blood-brain barrier impairment may be a potential alternative mechanism. These findings are applicable to stroke and other reversible neurologic diseases.
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