Opposite changes in dopamine metabolites and met-enkephalin levels in the ventricular CSF of patients subjected to thalamic electrical stimulation.

High-frequency electrical stimulations of thalamic nuclei are currently used for the suppression of parkinsonian or essential tremor and for the relief of some types of intractable pain in man. However, the mechanisms by which such stimulations exert their therapeutic effects are essentially unknown. Attempts were made to provide some insight into these mechanisms by measuring the levels of the dopamine metabolites homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC), the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) and met-enkephalin-like immunoreactivity in ventricular cerebrospinal fluid (CSF) of patients with Parkinson's disease (PD) or multiple sclerosis (MS) after a 30-minute therapeutic electrical stimulation of the ventralis intermedius nucleus of the thalamus. In nonstimulated control patients, the levels of these compounds did not significantly differ in two CSF samples taken 30 minutes apart. In stimulated patients, a decrease in dopamine metabolite levels associated with a relative increase in met-enkephalin-like immunoreactivity were observed in the CSF sample taken after the 30-minute stimulation as compared to the sample taken immediately before the stimulation. In contrast, the levels of 5-HIAA remained unaffected by the stimulation. These data confirmed the existence of negative interactions between dopaminergic and enkephalinergic systems in man similar to those previously demonstrated in rats. In addition, they suggest that alterations in dopaminergic or enkephalinergic neurotransmission might be involved in the therapeutic action of thalamic electrical stimulation in patients with parkinsonian symptoms and other patients.

[Anesthesia for thalamic stimulations: value of flumazenil]. / Anesthésie pour stimulations thalamiques: intérêt du flumazénil.

Five cases are reported of peroperative awakening in order to obtain patient cooperation during stereotaxic procedures. General anaesthesia was induced with 0.25 mg.kg-1 midazolam, 1.5 to 2 micrograms.kg-1 fentanyl, and 0.1 mg.kg-1 vecuronium. Maintenance was obtained with isoflurane, nitrous oxide, and small doses of fentanyl. Isoflurane inhalation was discontinued 30 to 40 min before the time of awakening required by surgery. Once expiratory isoflurane concentration reached a level less than or equal to 0.1%, nitrous oxide administration was stopped, and 0.5 mg flumazenil administered. After surgical checking, on the fully awake patient of the efficiency of thalamic stimulation and the lack of any motor deficit, anaesthesia was deepened again, with either isoflurane or a non benzodiazepine intravenous agent. All five patients recovered rapidly and calmly.