Myo-inositol’s Role in Understanding the Pain Perception in Patients with Schizophrenia

Abstract

The molecular explanation for the changes in pain perception in schizophrenia lies in nerve inflammation. The decrease in inositol, mainly localized in glial cells, can support these changes. There are also significant alterations in the viability and functioning of neurons, which are linked to a significant reduction of N-acetyl-aspartate (NAA). Our study demonstrates significantly increased myo-inositol levels in the anterior and posterior cingulate cortex. An increase in the myo-inositol/sum of the creatinine and phosphocreatinine (Cr + PCr) ratio and NAA levels additionally supports the notion of inositol’s beneficial impact on brain metabolism and neuronal integrity, which is particularly relevant to schizophrenia’s neurodegenerative changes. However, varying NAA/Cr + PCr ratios indicate a complex interaction between the brain’s inositol level and energy metabolism or neurochemical balance. These findings highlight inositol’s potential role in modulating neurochemical profiles in schizophrenia. Furthermore, high inositol levels are linked to significant reductions in trauma-related symptoms in schizophrenia, as indicated by the International Trauma Questionnaire and the Child Trauma Questionnaire. Inositol’s potential to mitigate trauma effects, and enhance social functioning and its multifaceted role in schizophrenia, offers a promising avenue for further research into its therapeutic applications.