Introduction

In 1909, Baglioni and Magnini observed that local strychninization of the motor cortex produced myoclonus in the dog. Later, Amantea (1921) demonstrated that such myoclonus was not only intensified by cutaneous stimulation of the area corresponding to the strychninized cortex, but also induced secondary generalized convulsions: he had discovered experimental reflex epilepsy. This work was extended by Clementi (1929), who described visual, acoustic, olfactory and gustative reflex epilepsy in the dog by locally increasing the excitability of individual sensory cortices while stimulating the corresponding sensory receptors (see Moruzzi, 1950). It was also extended by Terzian and Terzuolo (1951), who showed that reflex epilepsy is accompanied by an EEG afterdischarge. Although mentioned for the first time in the human by Gowers (1885) and called for a certain period of time ‘Brown–Sequard's epilepsy’ (see Pagniez et al., 1933), it was not until the 1920s that acquired reflex epilepsy in humans was fully described to be the result of a local pathological increased excitability of the cortex (see Penfield & Jasper, 1954). In these focal epilepsies of animals and humans, the seizure is obtained by the coincidence of an hyperexcitable sensory cortex and the arrival to this cortex of an adequate input from the homologous sensory modality.

In addition, in animals and humans having ‘no detectable’ lesion, transitory increased neuronal excitability leading to reflex epilepsy can be acquired subsequent to a metabolic or toxic disorder or under the influence of subliminal doses of known convulsant drugs.

In some susceptible individuals of a particular species there is no need for cortical strychninization or injection of convulsant drugs to obtain reflex seizures.