Complex regional pain syndrome (CRPS) is a debilitating chronic pain disorder typically in the upper or lower limbs. Whilst CRPS usually develops from a peripheral event, it is likely maintained by central nervous system changes. Indeed CRPS is reported to be associated with sensorimotor cortex changes, or functional 'reorganisation', as well as deficits such as poor tactile acuity. Whilst the mechanisms underpinning cortical reorganisation in CRPS are unknown, some have hypothesised that it involves disinhibition, i.e. a reduction in gamma-Aminobutyric acid (GABA) activity. In this study we addressed this hypothesis by using edited magnetic resonance spectroscopy (MRS) to determine sensorimotor GABA and glutamate concentrations in 16 humans with CRPS and 30 matched controls and the relationship of these concentrations with tactile acuity. We found that individuals with upper limb CRPS displayed reduced tactile acuity in the painful hand compared with the non-painful hand and pain-free controls. Despite this acuity deficit, CRPS was not associated with altered GABA or glutamate concentrations within the sensorimotor cortex on either the side that represents the affected or unaffected hand. Furthermore, there was no significant relationship between sensorimotor GABA or glutamate concentrations and tactile acuity in CRPS or control subjects. Although our sample was small, these data suggest that CRPS is not associated with altered total sensorimotor GABA or glutamate concentrations. Whilst these results are at odds with the sensorimotor cortex disinhibition hypothesis, it is possible that GABAergic mechanisms other than total GABA concentration may contribute to such disinhibition. Complex regional pain syndrome is a debilitating chronic pain disorder that usually affects the limbs. It is associated with altered sensorimotor cortex function including reorganisation and reduced tactile acuity, which are thought to result from reduced on-going inhibition. However, we found that this pain condition is not associated with reduced on-going sensorimotor inhibition in the form of gamma-Aminobutyric acid concentration, the major inhibitory neurotransmitter in the brain. These findings strongly suggest that changes in sensorimotor function in individuals with complex regional pain syndrome are explained by factors other than neurotransmitter concentration.