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Brain & Heart Neurologic manifestations of IBD

to the commonality of non-specific white matter changes on 5.3. Related medications
MRIs and other demyelinating disorders linked to biological IBD can be treated with various medications. Most of
treatments. The correlation between MS and IBD has been them have been reported to result in various neurological
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long suspected and supported by genetic studies, which manifestations as summarized in Table 1.
have identified multiple genetic links between MS and
CD through common single nucleotide polymorphisms. Corticosteroids such as prednisone are frequently
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These diseases share similar demographics, clinical employed in the acute management of IBD due to their
manifestations, and geographical distributions, yet the potent anti-inflammatory effects. However, their side
exact pathophysiological links remain elusive. There is also effects are numerous and can be severe, particularly
evidence suggesting a shared immunologic origin based on with long-term use. These include osteoporosis, adrenal
the clustering of chronic inflammatory diseases. Moreover, suppression, hyperglycemia, increased susceptibility to
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the recent hypothesis posits a role of the microbiome in MS infection, and psychiatric disturbances such as mood
pathogenesis, indicated by elevated antibody responses to swings and psychosis. Corticosteroids can also increase the
GI antigens in MS patients, suggesting a potential overlap in risk of cataracts, skin thinning, and easy bruising. The risk
pathogenic mechanisms or co-occurrence. 54 of infection is particularly concerning, as corticosteroids
Furthermore, there may be a reciprocal relationship can mask the symptoms of severe infections, potentially
between IBD and MS. Recent research suggests that the leading to delayed diagnosis and management. 35
microbiome may play a significant role in the development Immunosuppressants, including azathioprine and
of MS. Studies indicate that MS patients exhibit a higher methotrexate, play a crucial role in maintaining remission
frequency of antibody responses to GI antigens than in IBD. Azathioprine can lead to leukopenia, hepatotoxicity,
healthy individuals. However, whether this heightened and an increased risk of lymphoma. It may also cause
immune reaction, targeting substances such as gliadin, nausea, vomiting, and pancreatitis in some patients.
tissue transglutaminase, intrinsic factor, parietal cells, Methotrexate, known for its efficacy in reducing the need
and Saccharomyces cerevisiae, stems from a common for steroids, carries risks of hepatotoxicity, pulmonary
pathogenic origin or merely coincidental coexistence toxicity, and myelosuppression. Since it is teratogenic, both
remains to be clarified. Further research is necessary to
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determine if these increased antibody levels correlate with Table 1. Complications of therapeutic agents for IBD
changes in the gut microbiota and related T-cell responses.
The prevalence of GI among patients with these antibodies Medication Side effects
may also signal dysfunction within the digestive system. Mesalamine Peripheral neuropathy, Guillain–Barré
Research by Banati et al. has demonstrated the presence of syndrome, headache, dizziness, confusion, and
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GI antibodies in MS patients, suggesting that the immune seizures
system, while typically benign, becomes aggressively auto- Steroids Myopathy, tremor, insomnia, psychosis, and
reactive under pathological conditions. This shift is often posterior reversible encephalopathy syndrome
linked to environmental factors, particularly microbial Metronidazole Headache, dizziness and vertigo, ataxia,
infections. Berer et al. have shown that even in the absence irritability, insomnia, confusion, seizures,
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of pathogens, the normal gut flora can activate myelin- posterior reversible encephalopathy syndrome,
tremors, and peripheral neuropathy (sensory and
specific CD4+ T cells, potentially triggering relapses in ataxic or autonomic)
experimental autoimmune encephalomyelitis. Sulfasalazine Encephalopathy and peripheral neuropathy
Managing MS in patients with IBD is complex, requiring Anti-TNFα agents Ischemic stroke, posterior reversible
meticulous drug selection. Both conditions respond to (infliximab, encephalopathy syndrome, vasculitis, TNFα-
steroids, but the rising number of patients developing adalimumab, and induced lupus with vasculitis, demyelinating
certolizumab)
diseases, optic neuritis, acute disseminated
steroid dependence necessitates careful escalation of encephalomyelitis, multiple sclerosis-like
treatment. TNFα inhibitors are typically ineffective in polyneuropathy, Guillan–Barre syndrome, and
MS and may exacerbate IBD, whereas interferons can progressive multifocal leukoencephalopathy
worsen IBD symptoms. Conversely, natalizumab has Anti-α4 integrin Progressive multifocal leukoencephalopathy
proven effective for both conditions, though its use is (natalizumab)
limited in IBD patients due to the risk of developing Cyclosporine A Peripheral and central neuropathy
leukoencephalopathy. Thus, treatment must be customized Tofacitinib Reversible multifocal CNS demyelination
for each individual, with careful monitoring of adverse Abbreviations: CNS: Central nervous system; IBD: Inflammatory bowel
effects to prevent complications. 56 disease.

Volume 2 Issue 4 (2024) 7 doi: 10.36922/bh.3486