35th Congress of ECTRIMS, Stockholm, Sweden, 11 - 13 September 2019, pp.849
ntroduction: Clinical disease activity in multiple sclerosis (MS) may manifest as predominant involvement of spinal cord and optic nerve (MS-SCON). In early stages, a major problem in the diagnosis of MS-SCON is distinction of patients presenting as MS-SCON throughout the disease course from those initially presenting as MS-SCON and developing supratentorial attacks later on. Therefore, identification of biomarkers for diagnosis of MS-SCON may be helpful in a clinical setting.
Objectives: To characterize the neuropsychological features of MS-SCON patients and to find a serum-based biomarker to distinguish the MS-SCON subtype.
Methods: Fourteen patients with MS-SCON, 20 conventional MS (CMS) patients without myelitis and optic neuritis attacks and 21 healthy individuals were recruited. Serum levels of a panel of cytokines and chemokines that were previously associated with spinal cord involvement in MS were measured by multiplex assay or ELISA. A panel of neuropsychological tests (selective reminding test, spatial recall test, paced auditory serial addition test, symbol digit modalities test, controlled oral word association test), Beck depression inventory, 9-hole peg and timed 25-foot walk tests were employed to all participants.
Results: CMS and MS-SCON patients showed similar clinical and disability features. Both CMS and MS-SCON patients displayed reduced IL-8 and CXCL2 and increased TNF-α levels than healthy controls, while IL-10 and CXCL5 levels were identical among all groups. MS-SCON patients had significantly lower TNF-α levels than CMS patients. While both CMS and MS-SCON patients showed worse cognitive, mood status and motor function scores than healthy controls, there were no significant differences among test performances of CMS and MS-SCON patients.
Conclusions: CMS and MS-SCON present with similar clinical, neuropsychological and immunological features. Serum TNF-α levels may serve to distinguish MS-SCON and CMS. Cognitive networks of the central nervous system may be damaged during the disease course of MS, despite the absence of clinical attacks characterized by cerebral or cerebellar symptoms.