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Brain & Heart Neurologic manifestations of IBD

men and women of childbearing potential should stop PML is a particularly severe neurological complication
taking the drug for a period before conceiving. 55 associated with immunosuppressive therapy in IBD, notably
Biologic therapies targeting specific immune pathways with the use of natalizumab. This disorder is caused by the
have transformed the treatment for IBD. TNFα inhibitors reactivation of the John Cunningham virus within the
such as infliximab and adalimumab are associated CNS, leading to progressive and often fatal demyelination.
with serious infections, including tuberculosis, and Patients with compromised immune surveillance face an
opportunistic infections such as histoplasmosis. There is increased risk of PML, which can be a consequence of
also a potential for inducing or exacerbating demyelinating both the underlying IBD and the immunomodulatory
diseases and a slight increase in the risk of malignancy, effects of biological therapies. The management of PML
particularly lymphoma. Natalizumab, used primarily requires vigilant monitoring for early signs of neurological
in CD, carries a risk of PML, a rare but often fatal brain impairment and may necessitate discontinuation of the
58
infection caused by the John Cunningham virus. Mitigating offending agent if PML is suspected.
such risk necessitates strict monitoring and limited usage Taken together, the management of IBD with these
in patients who do not respond to other treatments. 11 medications requires a careful consideration of their
Vedolizumab, an anti-integrin agent, targets gut- potential side effects. Clinicians must balance the benefits
specific lymphocyte trafficking and is associated with of these medications against their risks, tailoring therapy to
fewer systemic infections. However, its side effects include individual patient needs and closely monitoring for adverse
nasopharyngitis, headache, and arthralgia. Its gut-selective effects. This approach is crucial for minimizing complications
action reduces the risk of systemic immunosuppression, and achieving optimal outcomes in the treatment of IBD.
but data on the long-term safety of vedolizumab are still 6. Conclusion
lacking. 57
The neurological manifestations associated with IBD are
Ustekinumab, which targets the p40 subunit of IL-12
and IL-23, is another biologic used in CD treatment. It diverse and complex, with significant implications for
patient management and quality of life. This review article
has a relatively mild side effect profile, with the most highlights the neurological manifestations of IBD, which
common adverse effects being injection site reactions and affect both the CNS and PNS, ranging from common
respiratory infections. However, the long-term impact on
immune function and the potential for serious infections conditions such as peripheral neuropathy to less frequent
but severe complications such as cerebrovascular diseases
remains a concern.
and myopathies.
The administration of anti-TNFα agents such as
The pathophysiology underlying these neurological
infliximab and adalimumab has been implicated in manifestations is multifaceted, involving immune-
the induction or exacerbation of these conditions.
Although TNFα antagonists are effective in controlling mediated mechanisms, vascular abnormalities, nutritional
the inflammatory processes of IBD, they may disrupt deficiencies, and neurotoxic effects of certain medications
used in the treatment of IBD. This complexity underscores
immune homeostasis in the CNS, potentially unmasking the importance of a multidisciplinary approach in treating
or aggravating demyelinating processes. The pathogenic
mechanisms are not entirely understood, but it is IBD patients, involving gastroenterologists, neurologists,
hypothesized that altering TNFα signaling could interfere and other specialists to address a wide range of potential
with neuroprotective pathways or enhance autoimmune neurological complications.
responses against myelin or other CNS components. 57 Furthermore, the management of neurological
Guillain–Barré syndrome and Miller–Fisher manifestations in IBD presents unique challenges. It
syndrome represent acute inflammatory demyelinating requires not only treating the neurological symptoms
polyneuropathies that have also been associated with the themselves but also carefully managing the underlying
use of TNFα inhibitors in IBD patients. These conditions IBD to minimize inflammation and potential triggers
of neurological complications. Adjusting therapeutic
typically manifest with rapid onset of muscle weakness
and are thought to result from a maladaptive immune strategies to avoid exacerbating existing conditions or
response following infection or immunotherapy. The precipitating new ones is crucial, particularly in the use of
link between TNFα blockade and these peripheral medications such as anti-TNFα agents, which may worsen
neuropathies suggests a complex interaction between the or trigger demyelinating disorders.
drug-induced modulation of immune function and the This review highlights the need for increased awareness
PNS’s susceptibility to immune-mediated injury. 30 and a better understanding of the neurological aspects

Volume 2 Issue 4 (2024) 8 doi: 10.36922/bh.3486