Specific alteration of somatosensory cortical excitability in complex regional pain syndrome (CRPS type I): a paired-pulse SEP study

Introduction: The pathophysiology of the complex regional pain syndrome (CRPS) is widely unknown. CNS involvement is suggested by the symptoms. Bilateral disinhibition in the motor cortex of CRPS patients has recently been found using paired-pulse motor evoked potentials. Several plastic changes have also been described for the somatosensory system (e.g. Pleger et al., 2005). Thus, for the first time, we investigated if bilateral excitability changes can also be found in the somatosensory system of CRPS patients.

Material and Methods: The data of 21 patients with unilateral CRPS type I (aged 52±10.9 years) involving the hand was analysed. Patients with upper limb pain of other non-neuropathic genesis (N=11; aged 46.2±11.7 years) were measured as a control group. Twenty-one healthy subjects (aged 51.3±10.9 years; dominant hand) were included as extra controls. Cortical somatosensory excitability was assessed by recording paired-pulse somatosensory evoked potentials (pp-SEP). Bilateral median nerve stimulation was performed using a block electrode placed on the wrist. The paired-pulse protocol consisted of paired electrical stimulation with an interstimulus interval of 30ms (pulse duration 0.2ms, repetitive rate of the paired stimuli 3Hz). Pp-SEP were recorded over the contralateral somatosensory cortex at the CP3 or CP4 position, respectively (reference=FZ). A total number of 800 stimulus related epochs were recorded and stored for offline averaging and analysis. Additionally, single-pulse SEP of both hands were recorded using the same setup as for the paired-pulse SEP. Linear superposition effects between the first and second paired-pulse stimuli were factored out by subtracting the single-pulse SEP from the paired-pulse SEP. Paired-pulse inhibition was expressed as a ratio (A2s/A1) of the peak-to-peak amplitudes of the second N20-P25 response of the paired-pulse stimulation after linear subtraction (A2s) and the first response of the paired-pulse stimulation before linear subtraction (A1).

Results: We found bilaterally increased amplitude-ratios (A2s/A1), compared with control patients as well as healthy subjects (T-test: affected hand CRPS/control patients, p=0.045; unaffected hand CRPS/control patients, p=0.014; affected hand CRPS patient/healthy subject, p=0.027; unaffected hand CRPS patient/healthy subject, p=0.021). The bilaterally increased amplitude-ratios in CRPS-patients indicate a decreased somatosensory cortical inhibition. No difference was found between control patients and healthy subjects.

Conclusion: In spite of unilateral symptoms, we found cortical disinhibition in both hemispheres in CRPS patients. This phenomenon corresponds to recent findings in the motor cortex (Schwenkreis et al., 2003). The bilateral disinhibition in sensory-motor networks seems to be specific for CRPS patients, since we could not find it in control patients with non-neuropathic pain syndromes.

The results of the present study point up central nervous involvement in the pathogenesis of CRPS, which should be considered in the development of new therapeutic approaches.

This study was funded by the DGUV (FR 115) research support.