Defective interhemispheric inhibition in drug-treated focal epilepsies.

Background: Focal epilepsies (FEs) arise from a lateralized network, while in generalized epilepsies (GEs) there is a bilateral involvement from the outset. Intuitively, the corpus callosum is the anatomical substrate for interhemispheric spread.

Objective: We used transcranial magnetic stimulation (TMS) to explore whether there are any physiological differences in the corpus callosum of drug-treated patients with FE and those with genetic GE (GGE), compared to healthy subjects (HS).

Overactive visuomotor connections underlie the photoparoxysmal response. A TMS study.

Objective: The photoparoxysmal response (PPR) involves rapid spread of epileptic activity from visual to parietal and frontal areas. We used a transcranial magnetic stimulation (TMS) technique to assess the physiologic connections between primary visual (V1) and motor (M1) areas in patients with idiopathic generalized epilepsy (IGE). We hypothesized that in PPR-positive patients, M1 would respond excessively to inputs from V1.

Abnormal motor cortex plasticity in juvenile myoclonic epilepsy.

Purpose: Abnormal cortical plasticity has been hypothesized to play a crucial role in the pathogenesis of juvenile myoclonic epilepsy (JME). To study the motor cortical plasticity we used paired associative stimulation (PAS). When a repetitive electrical stimulus to the median nerve is paired with a transcranial magnetic stimulus (TMS) pulse over the controlateral motor cortex with at an interstimulus interval (ISI) of 21.

Impaired visual inhibition in migraine with aura.

Objective: The pathophysiology of migraine with or without aura (MA, MO) is still a matter of debate. We thus studied patients with MA and MO by means of paired-pulse flash-visual evoked potentials (paired F-VEPs). This technique, recently revived, analyses the overall excitability of visual system as detected from the cortical occipital signal.

Interictal ghrelin levels in adult patients with epilepsy.

Purpose: In vitro or in animal models of epilepsy, ghrelin showed a clear anticonvulsant action, whose mechanisms are somewhat obscure. In humans however, a controversial relation exists between ghrelin and epilepsy. Yet most studies investigated just total ghrelin levels, without a proper distinction between acylated (AG) or unacylated ghrelin (UAG).