Neuroinflammation drives anxiety and depression in relapsing-remitting multiple sclerosis

S Rossi, V Studer, C Motta, S Polidoro, J Perugini, G Macchiarulo, AM Giovannetti, L Pareja-Gutierrez, A Calò, I Colonna, R Furlan, G Martino, D Centonze

Research output: Contribution to journalArticle

Abstract

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-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. 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. © 2017 American Academy of Neurology.
Original languageEnglish
Pages (from-to)1338-1347
Number of pages10
JournalNeurology
Volume89
Issue number13
DOIs
Publication statusPublished - 2017

Fingerprint

Relapsing-Remitting Multiple Sclerosis
Anxiety
Depression
Equipment and Supplies
Inflammation
Psychiatry
Psychometrics
Mood Disorders
Interleukin-1
Multiple Sclerosis
Interleukin-2
Comorbidity
Tumor Necrosis Factor-alpha
Regression Analysis
Drive
Cytokines
Psychology

Cite this

Neuroinflammation drives anxiety and depression in relapsing-remitting multiple sclerosis. / 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.

In: Neurology, Vol. 89, No. 13, 2017, p. 1338-1347.

Research output: Contribution to journalArticle

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 2017, 'Neuroinflammation drives anxiety and depression in relapsing-remitting multiple sclerosis', Neurology, vol. 89, no. 13, pp. 1338-1347. https://doi.org/10.1212/WNL.0000000000004411
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. In: Neurology. 2017 ; Vol. 89, No. 13. pp. 1338-1347.
@article{6ffc862c056f4d758725edc77d0f22af,
title = "Neuroinflammation drives anxiety and depression in relapsing-remitting multiple sclerosis",
abstract = "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-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. 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. {\circledC} 2017 American Academy of Neurology.",
author = "S Rossi and V Studer and C Motta and S Polidoro and J Perugini and G Macchiarulo and AM Giovannetti and L Pareja-Gutierrez and A Cal{\`o} and I Colonna and R Furlan and G Martino and D Centonze",
year = "2017",
doi = "10.1212/WNL.0000000000004411",
language = "English",
volume = "89",
pages = "1338--1347",
journal = "Neurology",
issn = "0028-3878",
publisher = "Lippincott Williams and Wilkins",
number = "13",

}

TY - JOUR

T1 - Neuroinflammation drives anxiety and depression in relapsing-remitting multiple sclerosis

AU - Rossi, S

AU - Studer, V

AU - Motta, C

AU - Polidoro, S

AU - Perugini, J

AU - Macchiarulo, G

AU - Giovannetti, AM

AU - Pareja-Gutierrez, L

AU - Calò, A

AU - Colonna, I

AU - Furlan, R

AU - Martino, G

AU - Centonze, D

PY - 2017

Y1 - 2017

N2 - 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-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. 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. © 2017 American Academy of Neurology.

AB - 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-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. 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. © 2017 American Academy of Neurology.

U2 - 10.1212/WNL.0000000000004411

DO - 10.1212/WNL.0000000000004411

M3 - Article

VL - 89

SP - 1338

EP - 1347

JO - Neurology

JF - Neurology

SN - 0028-3878

IS - 13

ER -