Abstract 092: Vasospasm as a Consequence of IVIg Usage for GBS.

Introduction The relationship between Intravenous Immunoglobulin (IVIg) and cerebrovascular vasospasm is poorly and incompletely understood. Some case reports have identified IVIg as potential therapy for vasospasm, while others have implicated it as a causative agent in primarily coronary artery va...

Full description

Saved in:
Bibliographic Details
Main Author: Connor D Welsh
Format: Article
Language:English
Published: Wiley 2023-11-01
Series:Stroke: Vascular and Interventional Neurology
Online Access:https://www.ahajournals.org/doi/10.1161/SVIN.03.suppl_2.092
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849309539219800064
author Connor D Welsh
author_facet Connor D Welsh
author_sort Connor D Welsh
collection DOAJ
description Introduction The relationship between Intravenous Immunoglobulin (IVIg) and cerebrovascular vasospasm is poorly and incompletely understood. Some case reports have identified IVIg as potential therapy for vasospasm, while others have implicated it as a causative agent in primarily coronary artery vasospasm and the development of atypical angina. This case illustrates a situation in which a patient with Guillain‐Barre Syndrome (GBS) was started on IVIg and developed subsequent vasospasm with cerebral infarcts requiring intra‐arterial therapy. Methods Case Report Results Our patient is a 62 year old female with a history of cervicothoracic subdural hematoma status postevacuation with left leg weakness, hypertension, known right ICA aneurysm, and chronic left ICA occlusion who presented as a transfer from an outside facility where she initially presented with progressive back pain, lower extremity weakness, areflexia and dysautonomia. MRI brain initially demonstrated posterior‐predominant T2 hyperintensities affecting subcortial white tracts suggestive of PRES. Lumbar puncture demonstrated cytoalbuminologic dissociation supporting a superimposed GBS. IVIg was initiated, however the patient's mentation and examination declined. Repeat MRI demonstrates bilateral, posterior‐predominant acute multifocal ischemic infarcts. Vessel imaging demonstrated vasospasm of the basilar and bilateral anterior Circle of Willis. Oral Verapamil was initiated. Digital Subtraction Angiography confirmed these findings; intra‐arterial verapamil was utilized with significant improvement in the patient's examination. Conclusion IVIg has only a weak association with coronary artery vasospasm, however is heavily implicated in the onset of this patient's diffuse vasospastic ischemic disease. Prompt identification and aggressive initiation of treatment is essential in minimizing the burden of ischemic stroke and optimizing outcomes for these complex patients.
format Article
id doaj-art-bc88ef6c3bd7479693565c3e5e2f5085
institution Kabale University
issn 2694-5746
language English
publishDate 2023-11-01
publisher Wiley
record_format Article
series Stroke: Vascular and Interventional Neurology
spelling doaj-art-bc88ef6c3bd7479693565c3e5e2f50852025-08-20T03:54:07ZengWileyStroke: Vascular and Interventional Neurology2694-57462023-11-013S210.1161/SVIN.03.suppl_2.092Abstract 092: Vasospasm as a Consequence of IVIg Usage for GBS.Connor D Welsh0Barrow Neurological Institute Arizona United StatesIntroduction The relationship between Intravenous Immunoglobulin (IVIg) and cerebrovascular vasospasm is poorly and incompletely understood. Some case reports have identified IVIg as potential therapy for vasospasm, while others have implicated it as a causative agent in primarily coronary artery vasospasm and the development of atypical angina. This case illustrates a situation in which a patient with Guillain‐Barre Syndrome (GBS) was started on IVIg and developed subsequent vasospasm with cerebral infarcts requiring intra‐arterial therapy. Methods Case Report Results Our patient is a 62 year old female with a history of cervicothoracic subdural hematoma status postevacuation with left leg weakness, hypertension, known right ICA aneurysm, and chronic left ICA occlusion who presented as a transfer from an outside facility where she initially presented with progressive back pain, lower extremity weakness, areflexia and dysautonomia. MRI brain initially demonstrated posterior‐predominant T2 hyperintensities affecting subcortial white tracts suggestive of PRES. Lumbar puncture demonstrated cytoalbuminologic dissociation supporting a superimposed GBS. IVIg was initiated, however the patient's mentation and examination declined. Repeat MRI demonstrates bilateral, posterior‐predominant acute multifocal ischemic infarcts. Vessel imaging demonstrated vasospasm of the basilar and bilateral anterior Circle of Willis. Oral Verapamil was initiated. Digital Subtraction Angiography confirmed these findings; intra‐arterial verapamil was utilized with significant improvement in the patient's examination. Conclusion IVIg has only a weak association with coronary artery vasospasm, however is heavily implicated in the onset of this patient's diffuse vasospastic ischemic disease. Prompt identification and aggressive initiation of treatment is essential in minimizing the burden of ischemic stroke and optimizing outcomes for these complex patients.https://www.ahajournals.org/doi/10.1161/SVIN.03.suppl_2.092
spellingShingle Connor D Welsh
Abstract 092: Vasospasm as a Consequence of IVIg Usage for GBS.
Stroke: Vascular and Interventional Neurology
title Abstract 092: Vasospasm as a Consequence of IVIg Usage for GBS.
title_full Abstract 092: Vasospasm as a Consequence of IVIg Usage for GBS.
title_fullStr Abstract 092: Vasospasm as a Consequence of IVIg Usage for GBS.
title_full_unstemmed Abstract 092: Vasospasm as a Consequence of IVIg Usage for GBS.
title_short Abstract 092: Vasospasm as a Consequence of IVIg Usage for GBS.
title_sort abstract 092 vasospasm as a consequence of ivig usage for gbs
url https://www.ahajournals.org/doi/10.1161/SVIN.03.suppl_2.092
work_keys_str_mv AT connordwelsh abstract092vasospasmasaconsequenceofivigusageforgbs