Cerebrospinal fluid evaluation in patients with progressive motor impairment due to critical central nervous system demyelinating lesions

Background Elevated intrathecal immunoglobulin G (IgG; oligoclonal bands (OCBs)) or IgG in people with progressive motor impairment due to critical demyelinating lesions are of uncertain significance. Objective Compare clinical/radiological features of people with critical demyelinating lesion-induced progressive motor impairment with/without elevated intrathecal IgG synthesis. Methods A total of 133 people with progressive motor impairment attributable to critical demyelinating lesions (corticospinal tract location, consistent with the progressive motor deficit) were compared regarding clinical and radiological presentation with and without >= 2 unique cerebrospinal fluid (CSF) OCB and/or IgG index >= 0.85. Results Ninety-eight (74%) had CSF-elevated OCB and/or IgG index, higher with increased magnetic resonance imaging-lesion burden. No differences were found with/without CSF abnormalities in sex (46 of 98 female (47%) vs. 22 of 35 (63%), p = 0.11), onset-age (median 49 vs. 50 years, p = 0.5), progression from onset (62 of 98 (63%) vs. 25 of 35 (71%)), progression post-relapse (36 of 98 (37%) vs. 10 of 35 (29%), p = 0.4), and duration between demyelinating disease onset and CSF examination (30 (0-359) vs. 48 (0-323) months p = 0.7). Critical lesions were radiologically similar, most commonly cervical spine located (72 of 98 (74%) vs. 19 of 35 (54%), p = 0.18) both with/without CSF abnormalities. Conclusions People with critical demyelinating lesion-induced progressive motor impairment typically have elevated intrathecal IgG (OCB and/or IgG) and similar clinical and radiological presentation regardless of CSF findings, therefore representing valid presentations of progressive demyelinating disease.

Automated summary

People with critical demyelinating lesion-induced progressive motor impairment typically have elevated levels of intrathecal IgG synthesis. Their clinical and radiological presentation is similar regardless of abnormal cerebrospinal fluid findings, indicating that this is a valid manifestation of progressive demyelinating disease.