#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?
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.