Abstract 408: Spontaneous intracerebral hemorrhage in a patient with multiple sclerosis : A case of vascular complication of a demyelinating disorder
Authors: Reichman N. , Vijaywargiya D. , Sah S. , Michael M. 
Published: January 2025

Introduction

Intracerebral hemorrhage [ICH] accounts for only 6.5% to 19.6% of strokes, yet with a 40% to 50% 30‐day mortality rate [twice that of ischemic strokes]. It presents as acute onset focal neurological deficits that localize to the area of hemorrhage. Most common causes of spontaneous ICH include hypertension [HTN] and cerebral amyloid angiopathy [CAA]. Multiple sclerosis [MS] is the most prevalent non‐traumatic disabling demyelinating disease that affects young adults. Most commonly, MS presents with optic neuritis or syndromes involving the brainstem or spinal cord. This case aims to bolster the assertion that demyelinating lesions “set the stage” for ICH through a variety of pathophysiologic mechanisms.

Methods [Case Presentation]

A 40 year old woman with a history of chronic well controlled HTN without medications, hypothyroidism, active tobacco use, not on anticoagulation or antiplatelet agents was hospitalized for progressively worsening blurry vision of her left eye. She underwent MRI brain/orbits +/‐ contrast and lumbar puncture and was diagnosed with MS per McDonald's criteria. She completed a five day course of intravenous methylprednisolone. Six days into her hospital stay, just after completing the steroid course, she developed sudden onset of altered mental status and left sided hemiparesis. Imaging revealed a right frontal intraparenchymal hematoma measuring 3.7 times 5.4 times 4.1 cm with surrounding edema causing effacement of the right lateral ventricle and a 5 mm leftward midline shift. Patient required emergent intubation and decompressive craniectomy. She showed no evidence of elevated blood pressures prior to ICH [systolic blood pressure range 95‐146], hypercoagulability or other autoimmune/rheumatological disorders. Digital subtraction angiography did not reveal any vascular malformations. No clear etiology of ICH could be determined and she was discharged to inpatient rehabilitation unit.

Conclusion

This case represents a rare instance of spontaneous ICH in MS patients, in which the pathophysiologic processes are not yet known. One potential hypothesis is the rupture of ‘cryptic’ AVMs that remain undetected on angiography. These aneurysms are prone to rupture in the setting of active ongoing inflammation from demyelination during MS exacerbations. Another possibility is localized vascular inflammation rendering damage to vessel wall structures. A large retrospective cohort study has also shown that age, smoking and anticoagulant use increase the risk of ICH in MS patients. One paper posits that demyelinating lesions set the stage for focal hemorrhage through various mechanisms, including blood brain barrier breakdown at the location of the demyelinating plaques, as well as increased endothelial fragility, transient thrombocytopenia, close proximity of the lesion to blood vessels, and increased fibrinolytic activity. Though theoretical, this may explain the rare hemorrhagic complications in MS patients. While there have been reports of hemorrhagic lesions in tumefactive MS, our case did not reveal any lesions suggestive of the same. The association between ICH and MS remains unclear, and larger studies are needed to investigate such hemorrhagic complications of MS.