Medizinische Universität Graz - Research portal

Logo MUG Resarch Portal

Selected Publication:

SHR Neuro Cancer Cardio Lipid Metab Microb

Rossi, S; Studer, V; Motta, C; Polidoro, S; Perugini, J; Macchiarulo, G; Giovannetti, AM; Pareja-Gutierrez, L; Calò, A; Colonna, I; Furlan, R; Martino, G; Centonze, D.
Neuroinflammation drives anxiety and depression in relapsing-remitting multiple sclerosis.
Neurology. 2017; 89(13): 1338-1347. Doi: 10.1212/WNL.0000000000004411
Web of Science PubMed FullText FullText_MUG

 

Co-authors Med Uni Graz
Colonna Isabella
Altmetrics:

Dimensions Citations:

Plum Analytics:

Scite (citation analytics):

Abstract:
To explore the inflammatory processes in the pathogenesis of psychiatric symptoms and the prognostic value of psychiatric comorbidities in multiple sclerosis (MS). 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. 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-1β 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. 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. © 2017 American Academy of Neurology.
Find related publications in this database (using NLM MeSH Indexing)
Adult -
Anti-Inflammatory Agents - therapeutic use
Anxiety - complications
Anxiety - diagnostic imaging
Anxiety - drug therapy
Anxiety - immunology
Brain - diagnostic imaging
Brain - immunology
Comorbidity -
Depression - complications
Depression - diagnostic imaging
Depression - drug therapy
Depression - immunology
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
Multiple Sclerosis, Relapsing-Remitting - immunology
Multiple Sclerosis, Relapsing-Remitting - psychology
Multivariate Analysis -
Psychiatric Status Rating Scales -
Tumor Necrosis Factor-alpha - cerebrospinal fluid

© Med Uni GrazImprint