Q&A 58: TNF-alpha inhibitors and MS

Q1: Does the fact that no Gd-enhancement mean a lesion is inactive? Q2: Is there a difference between RIS and MS? Q3: Do TNF inhibitors cause MS?

Case study 

“I have recently begun treatment with ocrelizumab (Ocrevus) for Radiologically Isolated Syndrome (RIS). I do not exhibit any classic MS symptoms, but I do experience occasional pain in my left eye. My latest MRI showed inflammation in the left optic nerve, although it did not enhance after administering gadolinium, suggesting it may not be active. My initial brain MRI done in January this year revealed over 20 non-enhancing lesions and one enhancing lesion, and a subsequent MRI 7 months later showed two new lesions but no enhancing ones. This leaves me somewhat confused about whether my condition should be classified as MS or merely RIS.

Additionally, I was hoping to hear your thoughts on previous exposure to adalimumab (Humira) and how this may be linked to my RIS/MS development. Two years ago, I dealt with excruciating lower back pain that resembled sciatica but was not visible on MRIs. After seeing a rheumatologist who diagnosed me with spondyloarthritis, I reluctantly started treatment with Humira, receiving three injections over 6 weeks. However, subsequent evaluations ruled out this diagnosis, and I was advised to wear a back brace and pursue physical therapy, which has since then significantly alleviated my pain.

I've done some research and found reports associating exposure to TNF inhibitors such as adalimumab (Humira) with increased risk for inflammatory CNS events. While I understand this is not a definitive correlation, I am curious if you believe adalimumab (Humira) contributed to my MS or RIS development.”

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Prof G’s answer

I have broken your case down into three main questions.

Q1: Does the fact that no Gd-enhancement mean a lesion is inactive?

Q2: Is there a difference between RIS and MS? 

Q3: Do TNF inhibitors cause MS?