A Longitudinal Study on Attenuated Structural Covariance in Patients With Somatic Symptom Disorder, 2022, Park et al

Objective: This study was performed to investigate altered regional gray matter volume (rGMV) and structural covariance related to somatic symptom disorder (SSD) and longitudinal changes after treatment. Additionally, this study examined the relationships of structural alteration with its phenotypic subtypes.

Methods: Forty-three unmedicated patients with SSD and thirty normal controls completed psychological questionnaires and neurocognitive tests, as well as brain magnetic resonance imaging. Voxel-based morphometry and structural covariances were compared between groups and between subgroups within the SSD group. After 6 months of treatment, SSD patients were followed up for assessments.

Results: Patients with SSD exhibited attenuated structural covariances in the pallidal-cerebellar circuit (FDR < 0.05–0.1), as well as regions in the default mode and sensorimotor network (FDR < 0.2), compared to normal controls. The cerebellar rGMVs were negatively correlated with the severity of somatic symptoms. In subgroup analyses, patients with somatic pain showed denser structural covariances between the bilateral superior temporal pole and left angular gyrus, the left middle temporal pole and left angular gyrus, and the left amygdala and right inferior orbitofrontal gyrus, while patients with headache and dizziness had greater structural covariance between the right inferior temporal gyrus and right cerebellum (FDR < 0.1–0.2). After 6 months of treatment, patients showed improved symptoms, however there was no significant structural alteration.

Conclusion: The findings suggest that attenuated structural covariance may link to dysfunctional brain network and vulnerability to SSD; they also suggested that specific brain regions and networks may contribute to different subtypes of SSD.

Open access, https://www.frontiersin.org/articles/10.3389/fpsyt.2022.817527/full

 

Doesn’t this raise the possibility that what we are seeing is a neurological condition. Further I assume the ‘improved symptoms’ are self reported and as such there is the possibility that there was no objective change, with the failure to identify any changes in brain function rather being confirmation that the positive subjective effects only indicate a response bias.

[added - if the symptom improvement did turn out to be an objective phenomenon, there is also the possibility that their patient group did have a neurological condition that was unaffected by their intervention, but the experimental context offered opportunity for them to compensate behaviourally for an impaired neurology, that is a functional improvement in the symptoms of a biomedical condition.]

 

If they don't state sensitivity or specificity of the associations then it cannot be considered a biomarker.

Nonetheless, if it was a hypothetical biomarker, it suggests the reported improvements on the questionnaires at the 6 month followup are biased/in error.