In complex regional pain syndrome (CRPS), sensory deficits and/or hyperalgesia often extend beyond the affected limb to encompass other sites on the ipsilateral side of the body. The aim of this study was to determine whether hyperalgesia in the ipsilateral forehead reflects disinhibition and/or sensitization of trigeminal afferent or second-order neurons on the CRPS-affected side.
To investigate this, blink reflexes to supraorbital electrical stimuli (a 2▒mA triple pulse delivered via a concentric electrode) were recorded bilaterally in 30 CRPS patients and 20 controls of similar age and sex distribution. In addition, the effect of acoustic startle stimuli on pain and blink reflexes to supraorbital electrical stimuli was explored.
Supraorbital electrical stimulation was more painful on the affected than unaffected side in patients (P<0.05), and was more painful on both sides in patients than controls (P <0.001). In addition, electrical stimulation of the ipsilateral forehead increased loudness and auditory discomfort to acoustic startle stimuli (P <0.05). However, blink reflexes were similar on both sides in patients, and smaller in amplitude and of longer latency in patients than controls (P <0.05).
These findings suggest that trigeminal sensory nerve input activates sensitized and/or disinhibited nociceptive circuits in the thalamus or higher cortical centres in CRPS. This not only evokes ipsilateral supraorbital hyperalgesia but also compromises auditory perception. Hence, crosstalk between auditory and nociceptive signals at sites of convergence within the central nervous system may generate hyperacusis in CRPS.