Effect of fentanyl and naloxone on a thalamic induced painful response in intractable epileptic patients.

Acute high-frequency (60/s) high-intensity (2,100-2,300 microA) stimulation of the mesial, caudal and inferior portion of the centromedian thalamic region within or close to the parafascicular nucleus produced a sharp, intense, cramp-like painful response localized to the face and shoulder (medial stimulation) or arm and hand (lateral stimulation) contralateral to the stimulation site in 4 intractable epileptic patients in whom depth electrodes had been implanted as a part of a neuroaugmentive procedure for seizure control. This thalamic induced painful response was always accompanied by objective clinical signs (facial gesticulation and contraction of the corresponding muscles) during thalamic stimulation and significant increments in EEG, EKG and respiratory frequencies and EMG muscular tonus from 10 s before to 10 s after thalamic stimulation. Opioid agonists (fentanyl 5.0 microg/kg) and antagonists (naloxone 3.5 microg/kg) were administered to induce and regulate a state of neuroleptanalgesia used for the subcutaneous internalization of the chronic stimulation systems. Under these conditions, we observed that fentanyl greatly attenuated and naloxone increased the intensity of the painful response, as well as the EEG, somatic and vegetative parameters evaluating such a painful response. Differences were significant when one compares the changes in response to electrical stimulation in EEG, EKG, respiration and EMG after the administration of fentanyl (decrease p = 0.001) and naloxone (increase p = 0.01) compared to those obtained after the administration of saline or no drugs during baseline recordings. These data suggest that this thalamic induced painful response is mediated by inhibition or activation of the morphine receptors of the thalamic cells primarily related to the pain process.