ABSTRACT
The aim of the present study is to evaluate the composite role of k index in the initial assessment of Multiple Sclerosis (MS) patients and to select useful cut-offs exportable in clinical practice. We analysed CSF/serum samples of 140 patients and followed-up the CIS/MS subgroup for 7 years. Our results suggest κ index as a quantitative diagnostic and prognostic biomarker in MS, significantly associated to baseline lesion load and to successive clinical course. We propose k index ≥106 as a prognostic cut-off to select patients at major risk of relapse, potentially influencing initial therapeutic decisions.
Subject(s)
Immunoglobulin kappa-Chains , Multiple Sclerosis , Humans , Multiple Sclerosis/diagnosis , Prognosis , BiomarkersABSTRACT
OBJECTIVE: To explore the inflammatory processes in the pathogenesis of psychiatric symptoms and the prognostic value of psychiatric comorbidities in multiple sclerosis (MS). METHODS: Four hundred five patients with relapsing-remitting (RR) MS underwent psychiatric evaluation by means of Beck Depression Inventory II (BDI-II) and State/Trait Anxiety Inventory (STAI-Y). The inflammatory activity level was assessed by MRI. In a subset of 111 treatment-naive patients, CSF levels of proinflammatory cytokines were determined. Correlation and regression analyses were performed to determine associations between variables. RESULTS: Relapsing patients demonstrated greater values of STAI-state and BDI-II compared with remitting patients but comparable trait-anxiety scores. There were no significant differences in psychometric parameters between relapsing and asymptomatic MRI-active patients, highlighting the effect of subclinical inflammation on mood disturbances. A significant reduction of STAI-state and BDI-II scores was recorded, along with the subsiding of neuroinflammation. Interleukin-2 CSF levels were found to correlate with STAI-state, while tumor necrosis factor-α and interleukin-1ß correlated with BDI-II. Because emotional disorders were associated with subclinical inflammation, variations of the psychometric profile were able to detect subclinical reactivation earlier. In line with this, high STAI-state values considerably predicted the possibility of disease reactivation. CONCLUSIONS: Mood alterations are induced by intrathecal inflammation, even though not clinically apparent, and are able to predict inflammatory reactivations in RRMS. Inflammation is therefore a biological event, not less important than the traditional psychosocial factors, involved in mood disorders.
Subject(s)
Anxiety/immunology , Depression/immunology , Multiple Sclerosis, Relapsing-Remitting/immunology , Multiple Sclerosis, Relapsing-Remitting/psychology , Adult , Anti-Inflammatory Agents/therapeutic use , Anxiety/complications , Anxiety/diagnostic imaging , Anxiety/drug therapy , Brain/diagnostic imaging , Brain/immunology , Comorbidity , Depression/complications , Depression/diagnostic imaging , Depression/drug therapy , Disability Evaluation , Female , Follow-Up Studies , Humans , Interleukin-1beta/cerebrospinal fluid , Interleukin-2/cerebrospinal fluid , Linear Models , Logistic Models , Magnetic Resonance Imaging , Male , Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging , Multiple Sclerosis, Relapsing-Remitting/drug therapy , Multivariate Analysis , Psychiatric Status Rating Scales , Tumor Necrosis Factor-alpha/cerebrospinal fluidABSTRACT
BACKGROUND: Sympathovagal imbalance has been associated with poor prognosis in chronic diseases, but there is conflicting evidence in multiple sclerosis. OBJECTIVES: The objective of this study was to investigate the autonomic nervous system dysfunction correlation with inflammation and progression in multiple sclerosis. METHODS: Heart rate variability was analysed in 120 multiple sclerosis patients and 60 healthy controls during supine rest and head-up tilt test; the normalised units of low frequency and high frequency power were considered to assess sympathetic and vagal components, respectively. Correlation analyses with clinical and radiological markers of disease activity and progression were performed. RESULTS: Sympathetic dysfunction was closely related to the progression of disability in multiple sclerosis: progressive patients showed altered heart rate variability with respect to healthy controls and relapsing-remitting patients, with higher rest low frequency power and lacking the expected low frequency power increase during the head-up tilt test. In relapsing-remitting patients, disease activity, even subclinical, was associated with lower rest low frequency power, whereas stable relapsing-remitting patients did not differ from healthy controls. Less sympathetic reactivity and higher low frequency power at rest were associated with incomplete recovery from relapse. CONCLUSIONS: Autonomic balance appears to be intimately linked with both the inflammatory activity of multiple sclerosis, which is featured by an overall hypoactivity of the sympathetic nervous system, and its compensatory plastic processes, which appear inefficient in case of worsening and progressive multiple sclerosis.
