[Cortico-subcortical electrophysiological study during the effects of benzodiazepines in patients with panic disorders].

INTRODUCTION

Tribute to Robert Heath, M.D. a pioneer in human implanted corticosubcortical microelectrodes.

OBJECTIVES

We evaluate retrospective electroencephalography (EEG), local evoked potentials (LEP) and extracellular unitary activity (EUA) of patients with diagnosis of panic disorder in association of simple partial seizures. These patients had presences or absence of agoraphobia. They received treatment with clonazepam or diazepam.

PATIENTS AND

METHODS

Ten patients with implanted corticosubcortical were divided in two groups. The five patients of group A were treated with clonazepam and the five patients of group B with diazepam.

RESULTS

Panic attacks showed EEG thetha activity, increased amplitude of the negative phase of LEP, and an increase in the frequency of EUA in cortico-subcortical organizations. This changes occurred in all organizations with exception of the inhibitory reticular substance. Panic disorder produced abundance of repetitive epileptiform discharges that could precipitate convulsive crisis. Both benzodiazepines were efficacious although results with clonazepam were observed earlier: at 7 to 14 days. Benzodiazepines increased corticosubcortical EEG beta activity, decreased amplitude of negative phase of LEP, and diminution in the frequency of EUA. This changes occurred with exception on the inhibitory reticular system. We postulate: a) That panic disorder hyperexcitability at the cortico-subcortical neuronal level may be the result of gabergic dysfunction, or alteration in neuroinhibitory mechanism through GABAA receptors, and through GABAB neuromodulator receptors, and b) That there is a direct correlation between GABA inhibitory basic mechanism and electroencephalographic beta activity.

CONCLUSIONS

Panic disorder produces neuronal hyperexcitability by gabergic dysfunction both benzodiazepines were efficacious in treatment.