Patient social cognition remained stable over 3 years, but its correlation with structural damage in the brain changed over time.
New research shows social cognition in patients with multiple sclerosis (MS) correlates with structural damage in the part of the brain associated with emotion.
It is known that MS can lead to cognitive impairment in patients with MS, but research in recent years has shown how MS can also affect social cognition, which is defined as the ability to infer the feelings of others, read facial expressions, and show empathy. Helen M. Genova, PhD, of the Kessler Foundation’s Center for Neuropsychology and Neuroscience Research and Rutgers University, and colleagues, had previously shown that social cognition could be a problem for patients with MS even if they were otherwise classified as “cognitive normal.”
In the new study, Genova and colleagues sought to better understand how social cognition and brain structure changed over time in patients with MS. The team recruited 26 cognitively normal patients with relapsing-remitting multiple sclerosis (RRMS) and gave them a battery of neuropsychological, social cognition, and quality of life assessments at baseline and then 3 years later. From these tests, the investigators calculated social cognition composite (SCcomp) scores for each patient. The volunteers were also given 3T-MRI scans at baseline and at 3 years. In the MRIs, investigators calculated both the volume and cortical lesion volume (CLV) of the patients’ amygdalae.
By the 3-year checkpoint, all 25 patients were still categorized as cognitive normal, and their global social cognition performance remained stable. At baseline, Genova and colleagues found a correlation between amygdala CLV and SCcomp (P = .002). However, 3 years later, amygdala volume had become the more important predictor of SCcomp (P = .0035 vs. P = .043 for CLV).
“We confirmed the longitudinal stability of social cognition deficits in cognitively-normal people with relapsing-remitting MS, mirroring the amygdala structural damage and psychological well-being,” Genova said, in a press release.
As for the apparent shift from amygdala CLV being predictive of SCcomp at baseline but less so at 3 years, Genova and colleagues said that by 3 years, “given that atrophy has been described as a probable pathological consequence of cortical lesions, amygdala atrophy had time to progress and therefore to be found associated with [social cognition] performance, even with the strongest correlation compared to the amygdala lesion burden.”
The investigators found that changes in SCcomp over the 3-year period correlated with changes in emotional state, depression, anxiety, fatigue, and quality of life-social functioning.
“These results confirm that social cognition exerts a key role in MS, affecting individuals' everyday lives,” Genova added. “Our research highlights the need to identify treatments to improve social cognition in this population.”
The investigators noted a number of limitations. Among them, the relatively small sample size and the lack of a control group in the baseline study, which they said would have helped to put behavioral changes in the RRMS group into context.
They said future research should include a more comprehensive MRI examination to find out if other regions of the brain besides the amygdala also contribute to social cognition changes.
Ziccardi S, Pitteri M, Genova HM, Calabrese M. Social Cognition in Multiple Sclerosis: A 3-Year Follow-Up MRI and Behavioral Study. Diagnostics (Basel). 2021;11(3):484. doi:10.3390/diagnostics11030484