Ana Luisa

Electrical stimulation of the centromedian thalamic nucleus (ESCM) has been used in cases of difficult to control seizures with multifocal onset in frontal and temporal lobes, as well as in cases of seizures with no evidence of focal onset, such as Lennox-Gastaut syndrome. The stimulation program consists of 1 min stimulation on one side, 4 min interval OFF stimulation and 1 min stimulation on the other side, alternating from one side to the other for 24 h, at 60-130 Hz, 2.5-5.0 V, 0.21-0.45 ms. 49 cases have been treated and followed for periods of 6 months to 15 years. Results indicate that ESCM is highly efficient to control generalized tonic clonic seizures (GTC), atypical absences (AA) and tonic seizures (TS) and less efficient to control complex partial seizures (CxP).

We studied the effect of electrical stimulation of centromedian thalamic nuclei (ESCM) on seizure control and paroxysmal EEG activity in 23 patients. We report the effect of chronic ESCM on psychological performance and background EEG activity of patients with various intractable seizure patterns. In each patient, a simple specifically designed neuropsychological scales (one for adults and one for children) was administered at the end of the baseline (BL), ESCM, and poststimulation (Post) periods; and 14 consecutive EEG recordings during these periods were performed to determine the degree of neuropsychological improvement and the temporal course of EEG changes. A significant increase in psychological scores and the number of background EEG waves per 10 s was noted in groups A (generalized tonic-clonic seizures, GTC), C (complex partial seizures, CPS), and D (generalized tonic seizures) and the total group of patients from BL to ESCM and from BL to Post periods. Group B patients showed a substantial increase (partial motor seizures) during the same periods. Improvement on psychological performance correlated better with age and baseline degree of deterioration than with the nature of the particular psychological improvement in any given subtest. The improvement in EEG background rhythm was most noticeable at the end of ESCM and at the beginning of the Post periods. Complete normalization of neuropsychologic scores and EEG rhythms was rare, but improvement was significant for both. Psychological scores increased from BL 14 ± 2 to ESCM 21 ± 2 and Post 23 ± 2 (normal expected 26), and EEG background rhythm increased from BL 42 ± 2 to ESCM 62 ± 2 and Post 54 ± 2 EEG waves/10 s. (normal expected >80).

The following two different modulatory procedures to control intractable epileptic seizures are presented: (1) chronic electrical stimulation of the centromedian-thalamic nucleus (ESCM) for control of generalized tonic-clonic seizures and atypical absences, and (2) subacute hippocampal stimulation (SAHCS) and chronic hippocampal stimulation for control of nonlesional temporal lobe seizures. The ESCM antiepileptic effect seems to be the result of activation of a nonspecific reticulothalamocortical system responsible for generalized electrocortical responses (recruiting, desynchronization, negative direct current shifts, and three spike-wave complexes per second). The success of the ESCM procedure depends on the following predictor factors: case selection (primary and secondary tonic-clonic seizures and atypical absences of the Lennox Gastaut syndrome), ventriculographic and electrophysiologic definition of the optimal stereotactic targets (based on the anterior commissure, posterior commissure, and the vertical line perpendicular to the posterior commissure and electrocortical recruiting responses), periodic electrophysiologic monitoring of the reliability of ESCM in the absence of the patient's subjective sensations and with totally internalized subcutaneous stimulation systems (by recording scalp electrocortical recruiting, desynchronizing, and direct current responses), quantitative evaluation of clinical and EEG improvement, and analysis of the ON and OFF effects, taking into account a long-lasting (possibly plastic) effect of ESCM. SAHCS blocks clinical and EEG signs of temporal lobe epileptogenesis with no additional damage of the stimulated hippocampal tissue. Preliminary results suggest that this antiepileptic effect is, at least in part, the result of a physiologic inhibition of the stimulated hippocampal tissue, because after SAHCS the authors found the following: (1) increased threshold and decreased duration, propagation, and blockage of the clinical signs accompanied with the hippocampal afterdischarge; (2) flattening of the hippocampal-evoked response recovery cycles; (3) single photon emission computed tomographic hypoperfusion; and (4) increased concentration of benzodiazepine receptor binding at the stimulated hippocampal region. Chronic hippocampal stimulation persistently blocked temporal lobe epileptogenesis in one patient under open protocols during 24 months with no apparent additional alterations in recent memory.