Neuroimaging of Excitatory and Inhibitory Neurotransmitters in Patients With Chronic Pelvic Pain (CPP) – UROP Spring Symposium 2024

Neuroimaging of Excitatory and Inhibitory Neurotransmitters in Patients With Chronic Pelvic Pain (CPP)

Vasiliki Amourgianos

Pronouns: she/her/hers

Research Mentor(s): Chelsea Kaplan
Research Mentor School/College/Department: Chronic Pain and Fatigue Research Center, Department of Anesthesiology / Medicine
Program:
Authors: Vasiliki Amourgianos, Eric Ichesco, Chelsea Kaplan
Session: Session 1: 9:00 am – 9:50 am
Poster: 70

Abstract

Chronic Pelvic Pain (CPP) affects nearly 15-20% of women. This persistent pain diminishes patients’ overall quality of life, affecting their social, professional, sexual and psychological well-being, even after CPP diagnosis and hysterectomy treatment. There is evidence that CPP, like other chronic pain conditions, is derived from complex nervous system interactions where peripheral and central sensitization amplify pain perception. Specifically, changes in glutamate and gamma-amino-butyric acid (GABA), the brain’s major excitatory and inhibitory neurotransmitters, concentrations in pain processing regions of the brain have been found in many chronic pain conditions. Proton magnetic resonance spectroscopy (1H-MRS) is a noninvasive MRI technique that measures the concentration of metabolites, specifically Glx (glutamate and glutamine) and GABA. In this study, we used 1H-MRS to measure right anterior (aIC) and posterior insula (pIC) concentrations of Glx and GABA and correlated those concentrations with patient reported measures of clinical pain. 76 CPP patients undergoing hysterectomy were enrolled in this study. Participants underwent a magnetic resonance imaging (MRI) scan session prior to treatment which included PRESS (Glx) and MEGA PRESS (GABA) scans within both the aIC and pIC using parameters previously described. Patients also completed behavioral questionnaires that recorded clinical pain measures. Raw 1H-MRS data from each single voxel sequence underwent manual post-processing using dedicated 1H-MRS software (LCModel for Glx and Gannet for GABA). Values for Glx were calculated as concentrations corrected for cerebrospinal fluid and ratios to total creatine within the voxel and concentrations for GABA were calculated as concentrations corrected for cerebrospinal fluid. Clinical pain was reported using the Brief Pain Inventory (BPI), which asks patients to evaluate their current pain intensity (and in the last 24-hours) on a 1-10 scale. Linear correlations between brain metabolites and reported clinical pain were performed in SPSS version XX. Results and conclusions TBD.

Biomedical Sciences, Interdisciplinary, Natural/Life Sciences

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