Summary:Purpose: To assess the effectiveness of slow repetitive transcranial magnetic stimulation (rTMS) as an adjunctive treatment for drug-resistant epilepsy.Methods: Forty-three patients with drug-resistant epilepsy from eight Italian Centers underwent a randomized, doubleblind, sham-controlled, crossover study on the clinical and EEG effects of slow rTMS. The stimulus frequency was 0.3 Hz. One thousand stimuli per day were given at the resting motor threshold intensity for 5 consecutive days, with a round coil at the vertex.Results: "Active" rTMS was no better than placebo for seizure reduction. However, it decreased interictal EEG epileptiform abnormalities significantly (p < 0.05) in one-third of the patients, which supports a detectable biologic effect. No correlation linked the rTMS effects on seizure frequency to syndrome or anatomic classification, seizure type, EEG changes, or resting motor threshold (an index of motor cortex excitability).Conclusions: Although the antiepileptic action was not significant (p > 0.05), the individual EEG reactivity to "active" rTMS may be encouraging for the development of more-powerful, noninvasive neuromodulatory strategies.

Eclampsia is a rare condition peculiar to pregnant and puerperal women, characterized by clinical pre‐eclampsia (hypertension, proteinuria, edema) and generalized seizures. Three cases of eclamptic encephalopathy are reported: CT and MRI demonstrated transient abnormalities in the cortical and subcortical regions of the posterior areas of the brain ‐ namely, parietooccipital lobes ‐ associated with occasional involvement of basal ganglia and/or brainstem. Pathogenesis is still unclear. Strict similarity with the pathological findings characterizing hypertensive encephalopathy suggests that a focal impairment in cerebral autoregulation may be the cause of vasodilation and fluid extravasation leading to hydrostatic edema; selective involvement of posterior areas could be explained by their lesser degree of adrenergic innervation supporting circulatory autoregulation mechanisms.

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