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5 AN IMITATOR OF GUILLAIN-BARRÉ SYNDROME.
  1. A. Sumrall1,
  2. R. Fredericks1
  1. 1University of Mississippi Medical Center, Jackson, MS.

Abstract

A 26-year-old previously healthy white male presented to the emergency department complaining of a 4-day history of bilateral arm pain that had progressed to weakness 24 hours prior to presentation. His physical examination at admission was unremarkable except for strength of 2/5 in bilateral upper extremities. He was admitted to the hospital and received EMG testing, which revealed a demyelinating-type polyneuropathy. CSF testing revealed an elevated CSF serum IgG index of 0.78. MRI of the brain and cervical spine and screening for heavy metals, porphyria, Lyme disease, West Nile virus, and other suspected etiologies, were unremarkable. It was believed that the patient had Guillain-Barré syndrome (GBS), and he was started on intravenous immunoglobulin (IVIG) at 400 mg/kg daily for 5 days. He showed minimal improvement in his strength and was discharged home. During his workup, the patient had a chest radiograph showing bilateral hilar adenopathy. A CT scan of the chest confirmed that the patient had lymphadenopathy in the peritracheal, hilar, and subcarinal regions. A mediastinoscopy was conducted, successfully removing noncaseating granulomas. Although the patient was diagnosed with sarcoidosis, it was still felt that the patient's weakness was attributable to GBS. Steroid therapy was not initiated for sarcoidosis as it was felt to be potentially harmful in a patient with concomitant GBS. The patient returned to clinic 2 weeks later and complained of worsening muscle weakness and pleuritic chest pain. Examination revealed strength of 2/5 in bilateral upper extremities with muscle atrophy, decreased sensation, and absent reflexes. He was readmitted to the hospital and received another 3 days of IVIG therapy for presumed GBS. A repeat EMG again showed a demyelinating neuropathy, which was consistent with GBS. After the patient failed to improve, the diagnosis was reconsidered. Based on a tentative diagnosis of neurosarcoidosis, therapy with prednisone was initiated at a dose of 1.5 mg/kg daily. After the first dose, he was able to lift his arms above his head with minimal effort. His strength quickly returned to his baseline. He was kept on steroids and discharged home with a tapering regimen. Although only 5% of patients with sarcoidosis will experience neurologic involvement, nearly half of those patients will initially present with neurologic complaints. Although there have been case reports of GBS coexisting with neurosarcoidosis, these patients will respond to IVIG therapy. Our patient appeared to have true neurosarcoidosis as evidenced by his quick response to steroid therapy.

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