Abstracts

RATIONALE: TGB is a specific inhibitor of GABA recapture and is effective as add-on therapy in refractory partial epilepsy. Several cases of nonconvulsive status have been described, reversible after stopping TGB. Question remains open about the etiology of such status: non convulsive status, toxic encephalopathy or both. We described the EEG clinical evolution of 5 patients with acute and intermittent confusional status in 3 of them.
METHODS: 5 partial epilepsy patients (4F, 22-38 years old) have been treated according to a slow up-titration of TGB (5mg/day/week) as monotherapy in 1 case and add-on therapy in the others (2 CBZ, 2 VPA, 2TPM, 1 LTG). All patients have simple and complex partial seizures, 3 secondary to mesio-temporal sclerosis (1 right), 1 to holoprosencephaly and 1 to cortico-temporal trauma. Comedication remained unchanged during the titration and the treatment. of TGB.
RESULTS: 5 partial epilepsy patients presented confusional status in 3 cases. At the beginning of the treatment, there was no problem. However after the dose of 30 to 60 mg/day (0.6 to 0.75 mg/kg/day), they presented a progressive and chronic confusion in 2 cases while acute, intermittent and relapsing in the 3 other cases. There was no concomittant sudden seizure control. The confusion started relatively abruptly 1 to 2 hours after TGB intake and disappeared spontaneously after 2 to 3 hours. This happened twice or thrice a day, more severely at the end of the day. When the patient was confused, for all of them, EEG was characterised by a high amplitude delta wave EEG without (true) spikes. TGB was then progressively downtitrated and all symptoms disappeared under the dose of 30 to 40 mg/day while for another patient the situation (clinical and EEG) was dramatically improved by BZD injection.
For these patients, TGB was further continued with lower doses (20 to 30 mg/day) without specific problems.
CONCLUSIONS: We presented 5 patients developping confusion when TGB was progressively increased. In the litterature, such cases are presented as nonconvulsive status. However, some of these cases could be related to a toxic encephalopathy as previously described with VPA i.e. In this case, the use of BZD is rarely helpful. Probably, confusion related to TGB treatment is secondary to several mechanisms including non convulsive status and/or toxic encephalopathy. These mechanisms are important to be known, because therapeutic approach could be quite different.