ELSEVIER Thalamus & Related Systems 1 (2002) 387-398 Thalamus & Related Systems www.elsevier.com/locate/tharel Centromedian nucleus stimulation for epilepsy Clinical, electroencephalographic, and behavioral observations Francisco Velasco*, Marcos Velasco, Fiacro Jimenez, Ana Luisa Velasco, Beatriz Rojas, Martha Luisa Perez Unit for Stereotactic and Functional Neurosurgery, Hospital General de Mexico and Unit for Medical Research in Neurophysiology, National Medical Center, Creston 116, Jardines Del Pedregal, IMSS Mexico D.F. 01900, Mexico Accepted 31 January 2002 Abstract A series of 49 cases with difficult to control seizures and non-candidates for ablation of the epileptic focus has been treated with electrical stimulation of the centromedian thalamic nuclei (ESCM). Selected cases were: (1) epilepsia partialis continua (EPC) (n = 5); (2) partial complex seizures (n = 16); (3) bilateral frontal parasagittal seizures (n = 6); (4) Lennox-Gastaut syndrome (n = 22). All patients had four contact electrodes placed bilaterally through frontal parasagittal burr holes and guided by ventriculograms. Plotting of electrodes on sagittal and frontal sections of the Schaltenbrand and Bailey's atlas permitted to determine their location. Electrodes were left externalized for periods of weeks to months to carry out the following tests. (1) Recordings of spontaneous seizures occurring during wakefulness and sleep. (2) Electrophysiological confirmation of their position by means of recruiting responses and desynchronization induced by low and high frequency stimulation. (3) Effects of high frequency stimulation on interictal and ictal activities. Electrodes were internalized and connected to a subcutaneous pulse generator programmed for alternating right and left ESCM 1 min ON and 4 min OFF at 60-130 Hz, 0.21-0.45 ms, 3-5 V forward and backward for 24 h per day. Repeated EEG recordings and a calendar of seizures were used for follow-up from 1 to 9 years. CM paroxysmal discharges followed the initiation of seizures in cortical areas, occurred simultaneously with spike wave (SKW) complexes in cortical areas in Lennox-Gastaut syndrome and preceded the initiation of cortical SKW and clinical seizures in typical absences. Low frequency stimulation (6-8 cps) induced recruiting responses that were associated with those electrodes that produced best seizure control. Good to excellent results were obtained in cases of EPC and Lennox-Gastaut syndrome and on generalized tonic clonic convulsions (GTCs) and atypical absences (AA) with tonic or clonic components. Consequently, we came to the conclusions that the CM participates in the propagation of most seizure types and also in the genesis of some of them and that ESCM is a safe and useful alternative for the treatment of some of the most difficult cases of uncontrollable seizures. © 2002 Elsevier Science Ltd. All rights reserved. Keywords: Electrical stimulation; Physiopathology of seizures; Neuromodulation; Sleep and epilepsy; Recruiting responses 1. Introduction The participation of intralaminar and midline thalamic nu- clei (that corresponds to the so-called non-specific thalamic system (Jasper, 1960; Monnier et al., 1960; Mehler, 1966; Jasper, 1969; Scheibel and Scheibel, 1967; McLachlan et al., 1984a,b) in the genesis and propagation of epileptic attacks was proposed on the basis of clinical observations long-ago (Penfield and Jasper, 1954). Experimental studies demon- strated that while high frequency stimulation of this sys- tem induced cortical EEG desynchronization (Moruzzi and * Corresponding author. Tel.: +52-55-5606-0393; fax: +52-55-5606-0393. E-mail address: fvelazco@netservice.com.mx (F. Velasco). Mogoun, 1949; Miller and Farandelli, 1990) low frequency (3-8 Hz) induced cortical synchronization (Dempsey and Morison, 1942b,c; Hess, 1954; Akimoto et al., 1956; Pollen et al., 1963; Skinner and Lindsley, 1973) and these studies may reproduce the clinical and EEG events of typical ab- sence attacks (Hunter and Jasper, 1949; Pollen et al., 1963). Other experiments extended the participation of anatomical structures involved in the onset of epileptic seizures fur- ther down to the brain stem structures anatomically linked with the non-specific thalamic system (for a review see Velasco and Velasco, 1990). Although the controversy on the anatomical initiation of the epileptic attacks remains and there are strong arguments favoring a cortical origin (Gloor et al., 1977; Quesney et al., 1977; Gloor, 1979; Harabaugh and Wilson, 1982) versus a subcortical origin (Miller et al., 1472-9288/02/$ - see front matter © 2002 Elsevier Science Ltd. All rights reserved. PII: S1472-9288(02)0001 1-0