Case Presentation: We present the case of a 39-year-old woman with Crohn’s disease who recently began adalimumab (Humira) and subsequently developed four days of progressive blurry vision, weakness, and paresthesia in all extremities. Extensive infectious and neurologic workups were unrevealing. Positron emission tomography/computed tomography (PET/CT) performed to assess for systemic sarcoidosis was nondiagnostic, while magnetic resonance imaging (MRI) of the brain demonstrated diffuse pial enhancement over the brainstem and multiple cranial nerves, findings most consistent with adalimumab-induced neurosarcoidosis, though multiple sclerosis could not be excluded. The patient declined intracranial biopsy and opted for medical therapy. She required two courses of high-dose corticosteroids and plasma exchange before gradual improvement. Adalimumab was discontinued. Follow-up MRI demonstrated resolution of enhancement without new lesions, and her symptoms continued to improve.
Discussion: Sarcoidosis is a multisystem granulomatous disorder characterized by noncaseating granulomas in the absence of an identifiable cause. It most often affects the lungs and lymph nodes of middle-aged adults and is diagnosed by (1) compatible clinical and radiologic findings, (2) histologic confirmation, and (3) exclusion of alternative etiologies. Neurologic involvement occurs in 3–10% of cases and may cause significant morbidity if unrecognized. Although tumor necrosis factor-alpha (TNF-α) inhibitors such as adalimumab are established treatments for refractory sarcoidosis, paradoxical induction of sarcoid-like reactions has been reported. More than 90% of neurosarcoidosis cases are associated with systemic disease; thus, isolated central nervous system involvement, as in this patient, complicates diagnosis. Given the invasiveness and uncertain yield of neural biopsy, histologic confirmation was deferred. High-dose corticosteroids remain the first-line therapy, while plasma exchange or additional immunosuppressants may be considered for persistent or refractory symptoms. This case highlights the diagnostic and therapeutic challenges of new neurologic deficits in patients receiving biologic therapy. Hospitalists often serve as the first clinicians to recognize paradoxical inflammatory syndromes such as TNF-alpha–inhibitor–induced neurosarcoidosis. Prompt multidisciplinary coordination, drug discontinuation, and corticosteroid therapy were key to the patient’s recovery. Awareness of these rare reactions can improve diagnostic accuracy, expedite treatment, and support coordinated care transitions for complex autoimmune patients.
Conclusions: Sarcoidosis remains a diagnosis of exclusion requiring integration of clinical, radiologic, and pathologic evidence. Although TNF-alpha inhibitors effectively treat sarcoidosis, they may paradoxically trigger granulomatous inflammation, including isolated neurosarcoidosis. This case emphasizes the importance of recognizing TNF-alpha–inhibitor–induced neurologic disease early to prevent irreversible deficits.