Remo Panaccione, MD, on EIMs of the Nervous System in IBD

Dr Panaccione reviews his presentation at the Advances in IBD annual meeting on extraintestinal manifestations of the nervous system, including peripheral neuropathy, cerebral venous thrombosis, and demylenating disorders, of inflammatory bowel disease.

Remo Panaccione, MD, is a Professor of Medicine and the Director of the Inflammatory Bowel Disease Unit at the University of Calgary in Calgary, Alberta, Canada.

TRANSCRIPT:

Hello, everyone. I'm Remo Panaccione, Professor of Medicine and Director of the IBD Unit at the University of Calgary in Calgary, Canada. I just got back from the Advances in IBD meeting in Orlando, Florida, where I was asked to speak on the neurologic system and inflammatory bowel disease. And I thought I'd bring a couple of those important facts to you here.

So we know that extraintestinal manifestations are common in inflammatory bowel disease, and we usually talk about the ocular or the joints or the skin or the liver, but rarely do we talk about the nervous system and how it's related to inflammatory bowel disease. So we need to remember that this isn't common, but it can present as either an extraintestinal manifestation or a complication of inflammatory bowel disease. And if we think about the more common ones, they tend to be peripheral neuropathy, which I'll touch on, cerebrovascular disease, and demyelinating disorders. And you can get rare immune-mediated disorders like myasthenia gravis, but I won't touch on that.

The first thing that we need to ask ourselves is why these may happen. And there's a variety of reasons from a pathogenic standpoint why these happen. They could be immune-mediated mechanisms such as increased in cytokine profiles or autoantibodies. It could be due to vascular abnormalities because we know that IBD patients have a hypercoagulable state and they're prone to vasculitis. We also know that nutritional deficiencies such as vitamin B12 deficiency or vitamin E deficiency can lead to neuropathy. And then there's multiple side effects of medications such as steroids, metronidazole, or some of our advanced therapies, most notably anti-TNF. When we talk about the most common one, which is peripheral neuropathy, this can present as either a mononeuropathy or a polyneuropathy, and it could be either due to sensory nerve damage, motor nerve damage, or autonomic nerve damage.

In our practice, the important thing is to recognize what the symptoms and signs are of the various peripheral neuropathies, and more importantly is ensure that our patients don't develop nutritional deficiencies that can lead to some of these peripheral neuropathies and specifically ask patients who are on anti-TNF about symptoms of peripheral neuropathy, because this is the drug that's most associated with the development of peripheral neuropathy. The good thing about anti-TNF related peripheral neuropathy is that it's reversible. So when you stop the anti-TNF, the oligodendrocytes tend to lay down myelin and it is reversible.

There's also the cerebrovascular complications. There's an increased risk of stroke, but what I want to bring to your attention is something that we don't always talk about, which is cerebral venous thrombosis or CVT. This tends to happen more so in our inpatients and is associated with a high morbidity and sometimes mortality, tends to happen in children more than adults, ulcerative colitis more than Crohn's disease. And as I said, it can be very subtle in the inpatients where they present with new onset headache that gets progressively worse. Sometimes they can get diplopia or visual impairment. The importance is to recognize this early, get the appropriate imaging, which is an MRI with a venography, and get them anticoagulated.

And then there's those demyelinating disorders. So if you look at epidemiological studies, patients with IBD have a 50% increased risk of developing multiple sclerosis and vice versa. And this comes from both MS and IBD epidemiological studies, probably because they share a common genetic underpinning. And this can present some treatment challenges because we know that there's cases with anti-TNF associated with demyelinating disorders, both peripherally and centrally, and it could be a niche use for some drugs like our S1P modulators in ulcerative colitis. It's important to be aware of this relationship, ask about forme fruste of multiple sclerosis such as optic neuritis and a family history of multiple sclerosis.

Even though this is not evidence-based, in my own personal patients, if they have a family history, I will do central imaging in those patients looking for white matter lesions, because those lesions can occur before MS and it will affect my treatment choice because I will tell them about the association with anti- TNF therapy and you may want to stay away from that therapy. There's other specific drug therapies that we could talk about in complications. We talked about anti-TNF agents. We know that JAK agents increase the risk of major adverse cardiac events in certain populations, including stroke. We know that you can see peripheral neuropathy with metronidazole as well. And then if we think about corticosteroids, because we use a lot of these still in our practice, they can be associated with myopathy, psychosis, increased intracranial pressure as well. So we just need to inform our patients when we're prescribing these therapies as some of the rarer side effects.

So that was just a brief review of what I spoke about at AIBD. Hopefully you can take some of those pearls back to your clinical practice, and I look forward to seeing you at a future meeting. Thank you very much.