Autoimmune Cerebellar Ataxia Associated with TNF-Alpha Blocking Therapy in a Patient with Rheumatoid Arthritis: A Case Report and Literature Review
Tomohide Ando1, Nobuaki Yoshikura1, Takayoshi Shimohata1, Akio Kimura1
1neurology, gifu university
Objective:
OBJECTIVE: To elucidate the clinical course of autoimmune cerebellar ataxia following tumor necrosis factor (TNF)-alpha blocking therapy in a patient with rheumatoid arthritis (RA).
Background:
BACKGROUND: TNF-alpha blocking agents are widely used to treat autoimmune diseases, particularly RA, due to their inflammatory pathway-modulating activity.
Design/Methods:
Here, we present a case report detailing the clinical progression and diagnostic findings of a patient who developed isolated cerebellar ataxia post-TNF-alpha blocking therapy with accompanying literature review. Imaging (magnetic resonance imaging, single-photon emission computed tomography, and fluorodeoxyglucose-positron emission tomography) and immunohistochemical analysis using frozen rat brain tissues with cerebrospinal fluid (CSF) to assess the anti-neuronal antibodies were performed.
Results:
A 55-year-old female recently treated with golimumab for RA presented with an 8-month history of progressive gait instability with dysarthria that commenced one month after therapy initiation. Neurological examination revealed scanning speech, right-predominant limb ataxia, and ataxic gait. Brain magnetic resonance imaging demonstrated cerebellar atrophy with a distorted atypical “hot cross bun” sign. Single-photon emission computed tomography imaging and fluorodeoxyglucose-positron emission tomography revealed hypoperfusion and hypometabolism in the right predominant bilateral cerebellum, respectively. CSF analysis revealed an elevated IgG index. Comprehensive testing for antineuronal antibodies yielded negative results. Immunohistochemistry of rat brain tissues with CSF revealed subtle neuropil reactivity in the cerebellar molecular layer. Golimumab cessation and administration of two courses of intravenous methylprednisolone significantly improved the patient clinical symptoms, imaging abnormalities, and IgG index. Additionally, we performed a literature review and identified several reports of cerebellar ataxia in patients with RA but none directly attributable to TNF-alpha blocking therapy.
Conclusions:
This case provided two critical insights. (1) TNF-alpha blocking therapy may induce autoimmune cerebellar ataxia; therefore, patients receiving such treatment should be carefully monitored. (2) Autoimmune cerebellar ataxia secondary to TNF-alpha inhibition responds to corticosteroid therapy and can be possibly reversed with appropriate interventions.
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