An Underperforming Basketball Player

1Hofstra North Shore-LIJ School of Medicine, Long Island Jewish Medical Center, New Hyde Park, NY
2 Hofstra North Shore-LIJ School of Medicine, Manhasset, NY

Meeting: Hospital Medicine 2015, March 29-April 1, National Harbor, Md.

Abstract number: 650


Case Presentation: A 37 year old African-American man presented with numbness in the hands and weakness of both the upper and lower extremities for a month’s duration. Patient stated that the proximal muscle weakness has worsened in the past week with diffuse myalgia. Of note, patient experienced an erythematous papular rash on his upper and lower extremities, which resolved prior to his presentation. Rash was not painful nor pruritic. He was in his normal state of health until 1 month ago. He was very athletic: an active basketball player that became easily tired and found difficulty standing. 
He appeared comfortable upon assessment. Vital signs were stable. Physical exam revealed no cranial nerve deficits. However, there was the following: Decreased strength (4/5) in both upper and lower extremities. Decreased light touch sensation is noted in bilateral fingers and toes. Deep tendon reflexes were intact and symmetrical. There was no visible muscle atrophy, nor palpable muscle tenderness. Patient had difficulty walking secondary to weakness. Gait appeared to be normal. No rash was visualized on screen exam. CBC and BMP were unremarkable. Plain films of the thoracic and lumbar spines were reported as unremarkable. Upon further investigation, MRI of the spine revealed diffuse abnormal increased T2 signal and expansion involving the spinal cord from the C1-T2 levels with nodular areas of postcontrast enhancement involve the spinal cord. Mild spinal cord compression was present from the C3-C4 through C6-C7 levels secondary to disc bulges, disc herniations, and facet degenerative changes. Extensive mediastinal lymphadenopathy was noted in the right paratracheal, subcarinal, and bilateral hilar regions. Lumbar puncture was performed with elevated protein level on 71 mg/dl. Further serologies as notable for an elevated ACE level of 158 u/L. Patient underwent EBUS for lymph node biopsy. Lymph node biopsy suggested granulomtaous lymphadenitis. These findings in concurrence with patient’s symptoms and history denote that he developed neurosarcoidosis. Patient was on Decadron IV as an inpatient regimen and discharged with Prednisone PO upon improvement of symptoms. 

Discussion: Given the gravity of patient’s symptoms, there was a concern for acute phenomenon and initial differential was vast. In this patient’s case urgent diagnostic workup was necessary: spinal fluid assessment and MRI was esssential. In his case: neurosarcoidosis was found. Of note, definite diagnosis was of neurosarcoidosis is via nervous system biopsy. About 50% of neurosarcoidosis patients present with neurologic deficits at times of first diagnosis. Treatment consists of corticosteroids and immunomodulators. Resection is rarely indicated. Radiation therapy is indicated for refractory disease and should be considered if patients fail corticosteroid therapy and trials of at least two alternative agents.

Conclusions: Sarcoidosis can affect persons from various ethnicities: In the US sarcoid is more common in people of African decent. Sarcoidosis commonly affects young adults of both sexes: It occurs most commonly in adults from 20 to 40 years of age. There is also report of second peak of sarcoid over the age of 50. 30% of patients present with extrapulmonary sarcoid. Furthermore neurologic complications occur in ~5%-10% of sarcoid cases. Therefore, it is wise to keep in mind young patients with neurologic deficts should have neurosarcoidosis in the differential.

To cite this abstract:

Wang Y, Pershad V. An Underperforming Basketball Player. Abstract published at Hospital Medicine 2015, March 29-April 1, National Harbor, Md. Abstract 650. Journal of Hospital Medicine. 2015; 10 (suppl 2). Accessed May 27, 2019.

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