Engorged Medullary Veins in Neurosarcoidosis: A Reflection of Underlying Phlebitis?

G Bathla,N Soni,A.A Capizzano,T Moritani

doi:10.3174/ajnr.a5951

Abstract

We read with interest the recent article describing the engorgement of deep medullary veins (DMV) in patients with neurosarcoidosis (NS).[1][1] The findings of DMV engorgement on susceptibility-weighted imaging have also intrigued us, and we recently published our experience in such cases.[2][2] We

Highlights

We read with interest the recent article describing the engorgement of deep medullary veins (DMV) in patients with neurosarcoidosis (NS).1 The findings of DMV engorgement on susceptibility-weighted imaging have intrigued us, and we recently published our experience in such cases.2 We agree with some of the findings reported in this article, such as occurrence of perivascular enhancement (PVE) in about half of these patients, increased occurrence of microhemorrhages, and a tendency toward worse neurologic outcomes
This issue is further compounded by the absence of any correlation with neural tissue biopsy, conventional angiography studies, or any changes in DMV with time, especially with regard to immunosuppressive therapy, which limits any educated extrapolation or inference of the presented data
This is based on the previously reported postmortem literature, which showed that the venous involvement was most common in the paraventricular region, and our own experience, in which we evaluated 4 patients with engorged DMVs

Summary

Introduction

We read with interest the recent article describing the engorgement of deep medullary veins (DMV) in patients with neurosarcoidosis (NS).1 The findings of DMV engorgement on susceptibility-weighted imaging have intrigued us, and we recently published our experience in such cases.2 We agree with some of the findings reported in this article, such as occurrence of perivascular enhancement (PVE) in about half of these patients, increased occurrence of microhemorrhages, and a tendency toward worse neurologic outcomes. Even though the authors mention that the DMV engorgement is not secondary to downstream venous occlusion, they agree that the pathophysiology of these findings remains unclear. This issue is further compounded by the absence of any correlation with neural tissue biopsy, conventional angiography studies, or any changes in DMV with time, especially with regard to immunosuppressive therapy, which limits any educated extrapolation or inference of the presented data.

Results

Conclusion