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Patients with subacute spinal cord injury may present electroencephalographic (EEG) features that predate the onset of neuropathic pain and may serve as both markers and predictors of neuropathic pain, in addition to commonly used sensory tests, according to a study published in the Journal of Pain.
There is evidence supporting the notion that extended neuropathic is associated with cortical changes, which are detectable via EEG. The researchers sought to evaluate the sensitivity of brain oscillatory activity for the detection of central nervous system changes that may precede the onset of hyperalgesia and allodynia.
A total of 41 participants were recruited for this clinical trial (ClinicalTrials.gov identifier: NCT02178917), consisting of 10 able-bodied control patients (70.0% men; mean age, 35±7 years) and 31 inpatients with subacute spinal cord injury, all of whom underwent EEG evaluation with 48 electrodes across the scalp.
Participants with spinal cord injury were divided into 3 subgroups: patients with existing neuropathic pain at EEG recording (n=11; 63.6% men; mean age, 45±17 years), patients who developed neuropathic pain after EEG (n=10; 90.0% men; mean age, 47±16 years), and patients without neuropathic pain up to 6 months after EEG recording (n=10; 90.0% men; mean age, 42±13 years). All patients with spinal cord injury completed the Brief Pain Inventory. Quantitative EEG measurements were conducted during spontaneous (relaxed) and induced (motor imagination) states and were categorized by location (lobe) and frequency for theta, alpha, and beta waves.
Among the 20 study participants with spinal cord injury and no neuropathic pain at the time of EEG recording, only 1 (who developed pain later) experienced an unpleasant sensory response when tested for allodynia. In patients presenting with neuropathic pain at time of EEG recording, opening eyes reactivity was reduced across all bands, and in participants who later developed neuropathic pain, this reactivity was decreased in the alpha band and absent in the beta and theta bands. In addition, compared with patients without neuropathic pain up to 6 months, those who had neuropathic pain at or after EEG exhibited lower alpha band power at Brodmann area 7 in the parietal lobe for both the spontaneous and induced states. Last, all 3 spinal cord injury groups showed decreased dominant alpha frequency and reduced beta band power at Brodmann area 7.
Markers and predictors of neuropathic pain included EEG reactivity to eye opening and decreased parietal alpha activity in both the relaxed and motor imagination states.
Study limitations included a lack of EEG recording after development of neuropathic pain, absence of follow-up >6 months, unaccountability of the effects of injury and medication in the neuropathic pain groups, small sample sizes, and a low number of electrodes used in EEG recording.
“This study gives important evidence of early predictors of future, and markers of recently developed [neuropathic pain]. In the future, a machine learning algorithm might be developed to predict the risk of each individual patient developing [neuropathic pain], based on their EEG. This might lead to characterisation of EEG [neuropathic pain] phenotypes and targeted treatments,” concluded the investigators.
Reference
Vuckovic A, Jajrees M, Purcell M, Berry H, Fraser M. Electroencephalographic predictors of neuropathic pain in subacute spinal cord injury [published online May 8, 2018]. J Pain. doi: 10.1016/j.jpain.2018.04.011
