Neuroinflammation Drives Anxiety and Depression in Relapsing-Remitting Multiple Sclerosis  

Oleh:

Rossi, Silvia ; Motta, Caterina ; Studer, Valeria ; Polidoro, Serena ; Perugini, Jacopo ; Macchiarulo, Giulia ; Giovannetti, Ambra Mara ; Pareja-Gutierrez, Lorena ; Calo, Andrea ; Colonna, Isabella ; Furlan, Roberto ; Martino, Gianvito ; Centonze, Diego

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Neurology (Official Journal of The American Academy of Neurology) vol. 89 no. 13 (Sep. 2017), page 1338-1347.
Topik: Multiple Sclerosis; MS
Fulltext: N11 v89 n13 p1338 kelik2017.pdf (625.51KB)

Ketersediaan

Perpustakaan FK Nomor Panggil: N11.K Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

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-a 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.

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