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Brain & Heart Neurologic manifestations of IBD

2. Pathophysiology 2.3. Nutritional deficiencies

The pathogenesis of neurologic disorders associated with Malabsorption, common in IBD, can lead to deficiencies
IBD has not been fully delineated, but several mechanisms of essential vitamins such as B12, Vitamin E, and folate,
are known to potentially influence their pathogenesis. which are crucial for nerve function and integrity.
The most common mechanisms include immunologic Deficiencies in these nutrients can cause or exacerbate
abnormalities prothrombotic states, malabsorption and conditions such as peripheral neuropathy and cognitive
nutritional deficiencies, metabolic agents, iatrogenic impairments. 14
complications of medical and surgical treatment of IBD, as
well as the brain-gut axis interactions (Figure 1). 12 2.4. Side effects of medications
The treatment of IBD often involves the use of medications
2.1. Immune-mediated mechanisms that can have neurological side effects. For example,
Many neurological complications in IBD are believed to metronidazole, commonly used to treat IBD, can cause
be immune-mediated. This includes the production of peripheral neuropathy. Similarly, corticosteroids and
autoantibodies, cytokine-mediated inflammation, and immunosuppressants can increase susceptibility to
immune complex deposition. These mechanisms can lead to infections, including those affecting the CNS. Anti-TNFα
conditions such as peripheral neuropathy, MG, and MS. The therapy, while effective for managing IBD, is contraindicated
inflammatory milieu in IBD, characterized by elevated levels in patients with demyelinating diseases such as MS due to
of TNFα, interleukin (IL)-6, and other pro-inflammatory the risk of exacerbating neurological symptoms. 11
cytokines, can disrupt normal immune function and
promote autoimmunity that targets neural tissues. 13 3. Neurological manifestations
2.2. Vascular abnormalities 3.1. Peripheral neuropathy

Patients with IBD are at an increased risk of thromboembolic Peripheral neuropathy is one of the most common
events, including stroke, particularly during disease flares. neurological involvements in both CD and UC and
This risk is compounded by the hypercoagulable state occurs at a higher incidence in individuals with IBD
3
associated with chronic inflammation, which can lead to compared to the general population. Several types of
abnormalities in coagulation pathways and endothelial polyneuropathy have been identified in IBD patients,
dysfunction. In addition, vasculitis, although extremely involving demyelination or axonal damage, including
rare in IBD, can contribute to neurological symptoms by autonomic neuropathy, sensory polyneuropathy, acute
affecting blood vessels in the CNS and PNS. 2 and chronic inflammatory demyelinating polyneuropathy
(CIDP), mononeuropathy, multifocal neuropathy, cranial
neuropathy, and plexopathy. The frequency of these
14
conditions remains undetermined, ranging between 0.25%
and 35.7% across various studies. A study conducted in
15
Greece observed neurological abnormalities in two out of
45 IBD patients; one with a history of acute motor sensory
polyneuropathy complicated by UC and another with mild
incidental carpal tunnel syndrome. 15
The underlying pathophysiology of neuropathy in IBD
patients remains unclear, potentially due to immunological
anomalies, drug exposure, or nutritional deficiencies.
Nemati et al. reported a clinical response in a CD patient
16
treated with intravenous immunoglobulin at a dose of
2 g/kg administered twice daily, which aligns with the
immune-based theory. Notably, two pathogenic hallmarks
of IBD – intestinal dysbiosis and loss of mucosal integrity –
in the GI tract have also been implicated in the neuropathy. 17
Studies on microbial-induced neurological disorders
in IBD remain relatively limited. Didesch et al.
18
Figure 1. Pathophysiology of neurological manifestations of inflammatory reported that a 71-year-old with Clostridioides difficile
bowel disease. (Image credit: Ashita Rukmini Vuthaluru) infection developed acute demyelinating sensorimotor

Volume 2 Issue 4 (2024) 3 doi: 10.36922/bh.3486