Depression in multiple sclerosis: a review

Siegert, Richard J.; Abernethy, David

doi:10.1136/jnnp.2004.054635

Cited by 641 publications

(426 citation statements)

References 90 publications

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“…Patients with and without depression at baseline demonstrated no significant differences in the change in BDI score over 48 months by DMT type. Interestingly, these results are in sharp contrast to those of several previous studies that included published case reports and suggested that IFNβ treatment is associated with an increased incidence of depression in MS patients, 1,[11][12][13] but are in agreement with those of several studies that did not find any relationship between DMT type and depression. [18][19][20] The results of this study also revealed a small, nonsignificant decrease in median BDI scores in both treatment groups over 48 months, suggesting a slight improvement in depressive symptoms while on DMT treatment, which was not dependent on concomitant antidepressant treatment.…”

Section: Discussioncontrasting

confidence: 57%

“…1,2 At any point, it is estimated that 15% to 30% of patients with MS are depressed, and an absence of depression during disease progression and treatment does not exclude the possibility that depression may occur during different stages of disease. 2 The seriousness of depression in MS is illustrated by the fact that more than 40% of depressed patients with MS require pharmacologic intervention for the condition during the course of their disease progression.…”

mentioning

confidence: 99%

“…The manifestation of depression may be related to the natural history of MS, resulting from neuronal damage and/or immune dysfunction, which may induce or propagate depressive symptoms. 1,[5][6][7] Depression can also be a psychological reaction to the lifestyle changes that occur when patients face the reality of living with a chronic disease such as MS. 1,[5][6][7] Finally, depression has been considered as an adverse event, caused by diseasemodifying therapies (DMTs) for MS [8][9][10] ; many prescribers consider the likelihood of a DMT to cause depression when making treatment decisions.…”

mentioning

confidence: 99%

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Relationship Between Disease-Modifying Therapy and Depression in Multiple Sclerosis

Kirzinger¹,

Jones²,

Siegwald³

2013

International Journal of MS Care

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Many prescribers of disease-modifying therapies (DMTs) for multiple sclerosis (MS) believe that interferon beta (IFNβ) is more likely than glatiramer acetate (GA) to increase depression during the course of MS treatment. Therefore, newly diagnosed patients with a history of depression are often placed on GA therapy from the onset of MS treatment. The aim of this study was to examine the relationship between DMT type and depression among patients with relapsing-remitting MS (RRMS). Patients with RRMS who were examined from 2000 to 2007 and who remained on a single course of therapy (either an IFNβ or GA) were included in a retrospective review of medical records. Patients were asked to complete the Beck Depression Inventory (BDI) at treatment initiation and every 6 months thereafter for up to 4 years. Only patients who had completed a BDI within 6 weeks of starting their DMT were included in the analysis. No significant differences in mean change in BDI score were observed from baseline to 48 months between the IFNβ and GA subgroups. Additionally, no significant differences in mean BDI score change were observed between antidepressant-treated and non–antidepressant-treated patients within the IFNβ or GA subgroup. Neither IFNβ nor GA therapy appears to exacerbate depressive symptoms in patients with RRMS who remain on their initial therapy.

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Section: Discussioncontrasting

confidence: 57%

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confidence: 99%

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confidence: 99%

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Relationship Between Disease-Modifying Therapy and Depression in Multiple Sclerosis

Kirzinger¹,

Jones²,

Siegwald³

2013

International Journal of MS Care

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“…Current treatments are often inadequate (Mojtabai, 2009;Wittchen et al, 2011), in large part due to the related issues that each disorder comprises heterogeneous groups of symptoms (DSM-5, 2013) and their aetiopathophysiologies are poorly understood. Furthermore, these disorders often present comorbidly, either with each other or together with other diseases including autoimmune disorders (Bruce, 2008;Siegert and Abernethy, 2004). To help address this situation, specific emotional and cognitive dysfunctions, or research domain criteria (RDoC), have become an important focus in translational psychiatric research, aimed at improved understanding of the aetio-pathophysiology of, and development of novel pharmacotherapies for specific psychopathologies (Cuthbert and Insel, 2013;Insel et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Mouse chronic social stress increases blood and brain kynurenine pathway activity and fear behaviour: Both effects are reversed by inhibition of indoleamine 2,3-dioxygenase

Fuertig

Azzinnari

Bergamini

et al. 2016

Brain, Behavior, and Immunity

118

125

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Psychosocial stress is a major risk factor for mood and anxiety disorders, in which excessive reactivity to aversive events/stimuli is a major psychopathology. In terms of pathophysiology, immuneinflammation is an important candidate, including high blood and brain levels of metabolites belonging to the kynurenine pathway. Animal models are needed to study causality between psychosocial stress, immune-inflammation and hyper-reactivity to aversive stimuli. The present mouse study investigated effects of psychosocial stress as chronic social defeat (CSD) versus control-handling (CON) on: Pavlovian tone-shock fear conditioning, activation of the kynurenine pathway, and efficacy of a specific inhibitor (IDOInh) of the tryptophan-kynurenine catabolizing enzyme indoleamine 2,3-dioxygenase (IDO1), in reversing CSD effects on the kynurenine pathway and fear. CSD led to excessive fear learning and memory, whilst repeated oral escitalopram (antidepressant and anxiolytic) reversed excessive fear memory, indicating predictive validity of the model. CSD led to higher blood levels of TNF-, IFN-, kynurenine (KYN), 3-hydroxykynurenine (3-HK) and kynurenic acid, higher KYN and 3-HK in amygdala and hippocampus. However, CSD was without effect on IDO1 gene or protein expression in spleen, ileum and liver, whilst increasing liver TDO2 gene expression. Nonetheless, oral IDOInh reduced blood and brain levels of KYN and 3-HK in CSD mice to CON levels, and we therefore infer that CSD increases IDO1 activity by increasing its post-translational activation. Furthermore, repeated oral IDOInh reversed excessive fear memory in CSD mice to CON levels. IDOInh reversal of CSD-induced hyper-activity in the kynurenine pathway and fear system contributes significantly to the evidence for a causal pathway between psychosocial stress, immune-inflammation and the excessive fearfulness that is a major psychopathology in stress-related neuropsychiatric disorders. ABSTRACTPsychosocial stress is a major risk factor for mood and anxiety disorders, in which excessive reactivity to aversive events/stimuli is a major psychopathology. In terms of pathophysiology, immune-inflammation is an important candidate, including high blood and brain levels of metabolites belonging to the kynurenine pathway. Animal models are needed to study causality between psychosocial stress, immune-inflammation and hyper-reactivity 3-HK in CSD mice to CON levels, and we therefore infer that CSD increases IDO1 activity by increasing its post-translational activation. Furthermore, repeated oral IDOInh reversed excessive fear memory in CSD mice to CON levels. IDOInh reversal of CSD-induced hyperactivity in the kynurenine pathway and fear system contributes significantly to the evidence for a causal pathway between psychosocial stress, immune-inflammation and the excessive fearfulness that is a major psychopathology in stress-related neuropsychiatric disorders.3

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“…In addition to motor dysfunction, visual and other sensory impairment, patients with the disorder often have neuropsychiatric symptoms such as depressed mood, fatigue, and cognitive impairment. Depression is especially common in this group of patients who have a lifetime risk for major de-pressive disorder as high as 25-50%, 1 and a 12 months' prevalence of up to 25%. 2 Depression in multiple sclerosis has been linked to biological as well as psychological factors and substantially a ects psychosocial function.…”

mentioning

confidence: 99%

An online programme to reduce depression in patients with multiple sclerosis: a randomised controlled trial

Fischer

Schröder

Vettorazzi

et al. 2015

The Lancet Psychiatry

123

131

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Depression in multiple sclerosis: a review

Cited by 641 publications

References 90 publications

Relationship Between Disease-Modifying Therapy and Depression in Multiple Sclerosis

Relationship Between Disease-Modifying Therapy and Depression in Multiple Sclerosis

Mouse chronic social stress increases blood and brain kynurenine pathway activity and fear behaviour: Both effects are reversed by inhibition of indoleamine 2,3-dioxygenase

An online programme to reduce depression in patients with multiple sclerosis: a randomised controlled trial

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