Affiliation:
1. Leeds Teaching Hospitals Trust
2. Siemens Healthcare Ltd
3. University of Manchester
4. University of Leeds
5. Manchester University NHS Foundation Trust
6. Wrightington, Wigan and Leigh NHS Foundation Trust
Abstract
Abstract
GABA (γ-aminobutyric acid) is the major inhibitory neurotransmitter in the brain. In response to injury within the central nervous system, GABA promotes cortical plasticity and represents a potential pharmacological target to improve functional recovery. However, it is unclear how GABA changes in the brain after traumatic brachial plexus injuries (tBPI). Therefore, neurometabolite concentrations were serially quantified in 7 males with acute tBPI, up to 19 months post-injury, using magnetic resonance spectroscopy (MRS). We acquired J-difference editing MRS using a MAGNETOM Prisma 3T (Siemens Healthcare, Erlangen, Germany). Data were analysed in jMRUI blind to clinical information to quantify GABA, GABA, creatine (Cr) and N-acetylaspartate (NAA) concentrations. Interhemispheric means were compared using linear methods. Confidence intervals (CI) were generated to the 95% level. Within weeks of injury, the hemisphere representing the injured upper limb had a significantly lower GABA:NAA ratio (mean difference 0.23 [CI 0.06–0.40]) and GABA:Cr ratio (mean difference 0.75 [CI 0.24–1.25]) than the uninjured side, which equalised 12 months post-injury. After BPI, there are interhemispheric differences in GABA concentrations within the sensory and motor cortex. Pharmacological modulation of these metabolites may enhance cortical plasticity, prolong the available time for reconstructive surgery and ultimately, improve function.
Publisher
Research Square Platform LLC