#ResearchSpeak: depression in MS is associated with focal brain damage

Would you be surprised if I told you that the black dog is associated with structural changes in the brains of pwMS? #ResearchSpeak #MSBlog

The smallish study below shows that depressive symptoms in pwMS is associated with gray matter loss in the left temporal lobe. The implication is that damage in the neuronal pathways that are linked to this particular area of the brain is associated with depression in MS. This is not surprising. Depression, like all symptoms, must have a neuroanatomical and/or neurophysiological correlate; in other words depression must be linked to malfunctioning of the brain. 

We know that the life-time prevalence of depression in pwMS is close to 50%; if this is causally linked to structural changes in the brain then preventing these changes should reduce the incidence and life-time prevalence of depression in MS. I wonder if this is occurring in pwMS who are being effectively treated with disease-modifying therapies?

Depression is part of a complex of hidden symptoms that are seldom discussed with pwMS who are early in the course of their disease. The others are anxiety, fatigue and cognitive impairment. If we made the point that depression, and these other symptoms, are linked to structural damage to the brain caused by MS would that affect decision-making around early-effective treatment? 

Depression has a major affect on quality of life and if we want to treat MS holistically we need to do everything possible to prevent this awful complication of MS and its consequences. Do you agree?    

Stuke et al. Cross-Sectional and Longitudinal Relationships between Depressive Symptoms and Brain Atrophy in MS Patients. Front Hum Neurosci. 2016 Dec 16;10:622.

Introduction: Depressive symptoms are a frequent and distressing phenomenon in Multiple Sclerosis (MS) patients. Cross-sectional research links these symptoms to reduced brain gray matter volumes in parts of the prefrontal and temporal lobe as well as subcortical structures like the hippocampus, nucleus caudatus and globus pallidus. Nevertheless, prospective relationships between regional gray matter volume and the course of depressive symptoms are poorly understood. 

Methods: Forty-four patients with relapsing-remitting or secondary progressive MS participated in a prospective study with two assessments of depressive symptoms and high-resolution MRI with an inter-test-interval of 17 months. Relationships between baseline gray matter volume and baseline depressive symptoms, as well as prospective associations between the development of atrophy and depression were assessed using voxel-based morphometry (VBM). 

Results: Cross-sectional analyses revealed an association between depressive symptoms and gray matter loss in the left temporal lobe. Prospective analysis showed that gray matter losses in the right middle cingulate and middle frontal gyrus at baseline predicted increasing depressive symptoms during follow-up. Increase in depressive symptoms was related to a concomitant increase in atrophy in the left thalamus and right globus pallidus. 

Discussion: Our results fit well into the concept of a disturbed cortico-striatal-pallido-thalamic loop in depression. In this framework, progressive gray matter loss in limbic basal ganglia structures including globus pallidus and thalamus may lead to depression-typical deficits in hedonic motivation, whereas atrophy of the prefrontal cortex may contribute to maladaptive coping strategies, promoting an unfavorable development of depressive symptoms.

7 thoughts on “#ResearchSpeak: depression in MS is associated with focal brain damage”

  1. Personally I've been (sub)depressed for a many years before any other MS symptoms appeared, and treatment with as potent agent as alemz did not helped with this much.Testosterone said to reverse cortical GM atrophy, wonder if this have to do anything with this matter

  2. My GP told me that a change in mental state occurs in everyone diagnosed with a long-term condition. If this is true, are you saying that MS leads to even more change than being dxd with other conditions?

  3. Prof G, I hear your message loud and clear. I followed the highly effective treatment option – glad that I did. Isn't there some real data to convince people? Lemtrada has been used since c. the early 90s. Can't a reasearcher do the following: find 150 peope diagnosed with RRMS in 2006 who have not received any disease modifying treatment. What percentage are now SPMS? What is the average EDSS score? How many have died. The same analysis should be done for one of the interferons, copaxone, Tysabri and Lemtrada. A simple table could set out the information for each of the five scenarios. A new RRMSer could then see what treatment is best for reducing conversion to SPMS, which is best for delivering the lowest EDSS…. The data would also help a patient make a more informed choice about safety – we know that the first generation of DMTs are safe, but they mostly likely have little impact on disability.

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