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October 1994

Anti—Myelin Basic Protein and Anti—Proteolipid Protein Antibody-Secreting Cells in the Cerebrospinal Fluid of Patients With Acute Optic Neuritis

Author Affiliations

From the Department of Neurology, Golstrup Hospital, University of Copenhagen, Golstrup, Denmark (Drs Sellebjerg and Frederiksen), and the Department of Neurology, Karolinska Institute, Huddinge Hospital, Huddinge, Sweden (Dr Olsson).

Arch Neurol. 1994;51(10):1032-1036. doi:10.1001/archneur.1994.00540220078017

Objective:  To study the intrathecal synthesis of antimyelin basic protein (MBP) and anti-proteolipid protein (PLP) antibodies in patients in the early stages of multiple sclerosis.

Design and Setting:  A study of consecutive patients with acute optic neuritis (ON) who were undergoing lumbar punctures in an ambulatory unit.

Patients:  Eleven patients with acute idiopathic ON and 14 patients with acute ON as a symptom of definite multiple sclerosis (the diagnosis of which was supported by clinical or laboratory findings). Nineteen patients with other neurological diseases (10 with inflammatory diseases) served as controls.

Main Outcome Measures:  Numbers of anti-MBP and anti-PLP antibody-secreting cells in peripheral blood and cerebrospinal fluid samples that were enumerated with an immunospot assay.

Results:  Cerebrospinal fluid cells that secreted anti-MBP or anti-PLP antibodies were detected in 10 of 15 and in 21 of 23 patients with acute ON, while they were detected in nine of 18 and in six of 18 patients with other neurological diseases, respectively. Patients with ON had significantly more anti-PLP-secreting cells than did patients with other neurological diseases (P<.01). No difference was observed for anti—MBPsecreting cells. A significant correlation between the time from onset and the number of anti—PLP-secreting cells was found in patients with idiopathic ON (P<.02).

Conclusions:  These data suggest that anti-PLP antibodies are a more specific finding in demyelinating disease than anti-MBP antibodies. Furthermore, they suggest that anti—PLP antibodies may arise as a consequence of the demyelinating process.

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