ELECTRICAL-STIMULATION OF PRECENTRAL CORTICAL AREA IN THE TREATMENT OF CENTRAL PAIN - ELECTROPHYSIOLOGICAL AND PET STUDY

The clinical, electrophysiological and haemodynamic effects of precent ral gyrus stimulation (PGS) as a treatment of refractory post-stroke p ain were studied in 2 patients. The first patient had a right hemibody pain secondary to a left parietal infarct sparing the thalamus, while the second patient had left lower limb pain developed after a right m esencephalic infarct. In both cases, spontaneous pain was associated w ith hyperpathia, allodynia and hypoaesthesia in the painful territory involving both lemniscal and extra-lemniscal sensory modalities in pat ient 1, extra-lemniscal sensory modality only in patient 2. Both patie nts were treated with electrical PGS by means of a 4-pole electrode, t he central sulcus being per-operatively located using the phase-revers al of the N20 wave of somatosensory evoked potentials. No sensory side effect, abnormal movement or epileptic seizure were observed during P GS. The analgesic effects were somatotopically distributed according t o the localization of electrode on motor cortex. A satisfactory long-l asting pain control (60-70% on visual analog scale) as well as attenua tion of nociceptive reflexes were obtained during PGS in the first pat ient. Pain relief was less marked and only transient (2 months) in pat ient 2, in spite of a similar operative procedure. In this patient, in whom PGS eventually evoked painful dysesthesiae, no attenuation of no ciceptive RIII reflex could be evidenced during PGS. Cerebral blood fl ow (CBF) was studied using positron emission tomography (PET) with O-1 5-labeled water. The sites of CBF increase during PGS were the same in both patients, namely the thalamus ipsilateral to PGS, cingulate gyru s, orbito-frontal cortex and brainstem. CBF increase in brainstem stru ctures was greater and lasted longer in patient 1 while patient 2 show ed a greater CBF increase in orbito-frontal and cingular regions. Our results suggest that PGS-induced analgesia is somatotopically mediated and does not require the integrity of somatosensory cortex and lemnis cal system. PGS analgesic efficacy may be mainly related to increased synaptic activity in the thalamus and brainstem while changes in cingu late gyrus and orbito-frontal cortex may be rather related to attentio nal and/or emotional processes. The inhibitory control on pain would i nvolve thalamic and/or brainstem relays on descending pathways down to the spinal cord segments, leading to a depression of nociceptive refl exes. Painful dysesthesiae during stimulation have to be distinguished from other innocuous sensory side effects, since they may compromise PGS efficacy.