Cranial Nerve Palsies: Sarcoidosis to Systemic Lupus Erythematosus

Cranial palsies are a very rare feature of SLE. Similarly, peripheral sensory-motor axonal neuropathy is very uncommon in SLE. The combination of the two as the presenting symptoms of SLE is a diagnostic challenge particularly in an elderly male patient with a known diagnosis of sarcoidosis. This case serves to highlight the diagnostic considerations in such a patient. The lack of response to standard therapy and the presence of subtle clues like anemia, proteinuria, and mild serositis should prompt the physician to look for alternate diagnoses. The potential association of SLE and sarcoidosis is also discussed. SLE can be present in elderly male patients with cranial and peripheral neuropathy. 1. Introduction Central nervous system (CNS) involvement in systemic lupus erythematosus (SLE) is approximated at 50% and ranges from 14 to 75% [1]. Cranial palsies are an unusual central nervous system manifestation of SLE and account for 0.5–1.0% of neuropsychiatric manifestations [2]. Most frequent cranial neuropathies involve the eighth nerve followed by the oculomotor set (third, fourth, and sixth), and then the fifth and seventh nerves [3]. In sarcoidosis, 10% patients develop CNS involvement with 50–75% of cases having cranial involvement, most commonly the facial nerve [4]. Of anecdotal interest, SLE is the most frequent connective tissue disease associated with sarcoidosis [5] and the two share some underlying pathophysiological mechanisms [6]. We report a case of multiple cranial nerve palsies and subacute progressive, symmetric peripheral neuropathy simulating Guillain-Barre syndrome (GBS) in a patient with sarcoidosis who was eventually diagnosed with SLE. 2. Case Report A 61-year-old African-American male presented to the emergency room with a few days history of double vision, left eyelid droop, and numbness and tingling in both hands and feet. He also endorsed one month history of profound fatigue and a progressive weakness with overhead movements and climbing stairs. Now to the point he was unable to ambulate and a recent fall triggered his visit. He had a history of biopsy proven sarcoidosis in 1970. He was treated with steroids for one year. He had gout, dyspepsia, and mild obstructive pulmonary disease. His medications included an albuterol inhaler, allopurinol, and omeprazole. He reported a weight loss of 30 pounds in the preceding six months. He had a chronic dry cough. Physical examination revealed a thin man with normal vital signs. Pertinent findings on exam were a significant ptosis of the left eye with only 1？mm aperture, an inability to