MERCOLEDI' 5 OTTOBRE SALA C ORE 9 - Avenue media

MODALITÀ IN CUI SONNO E PRIVAZIONE DI SONNO MODULANO LA REATTIVITÀ
CORTICALE E I SUOI EFFETTI SULL‟EPILESSIA MIOCLONICA GIOVANILE: UNO
STUDIO COMBINATO EEG – TMS.
A Del Felice a , S Savazzi b , LG Bongiovanni a , A Fiaschi a , P Manganotti a
a Dip . di Scienze neurologiche , neuropsichiatriche, morfologiche e motorie ,
sezione Neurologia , Università di Verona
b Dip . di Scienze neurologiche , neuropsichiatriche, morfologiche e motorie ,
sezione Psicologia , Università di Verona
OBJECTIVE: Simultaneous EEG-TMS permits to investigate cortical reactivity to external
perturbations. TMS evoked potentials (TEPs) are described in normals during sleep (S)
and wake (W) but neither after sleep deprivation (SD) nor in the frame of pathologically
enhanced excitability – i.e. epilepsy. The aim of our study is to identify TEPs and their
modifications during W, SD and S in normals and in juvenile myoclonic epileptics using
EEG-TMS coregistration. MATERIALS AND METHODS: Focal TMS was delivered to the
left primary motor cortex at 110% of motor threshold in 12 controls and 10 epileptics.
Patients mantained therpeutic regimen throughout the study. TMS was delivered randomly
8-15 sec during W, SD and S. At least 150 stimuli were recorded for each condition. EEG
was simultaneously acquired from 32 scalp electrodes with the Brain Vision Recorder
system. RESULTS: TMS induced a reproducible sequence of deflections on EEG. An
amplitude’s statistically significant difference between states was observed for the late
peaks (P100 and N190). In normals, after SD P100 amplitude showed a globally
distributed increase, while N190 slighlty augmented over the posterior ares. In patients,
both after SD and during S, ampiltude enhancement was evident for the P100 and N190
peak over the antero-central derivations. Comparing the two groups, epileptics showed
overall higher amplitude potentials, with P100 more evident over the posterior areas in S2,
and N190 more represented anteriorly in S2 and centrally during SD. DISCUSSION: We
demonstre an overll higher cortical excitability in epileptics. Moreover, the same group
showed an amplitude increase of TEPs over the anterior areas after sleep deprivation and
during rebound sleep.This phenomenon could relate to the disfunction of the
corticothalamic circuit supposed to cause myoclonic epilepsy and the higher susceptibility
to the effects of sleep deprivation of frontal and prefrontal areas. CONCLUSION: sleep
deprivation is an effective enhacer of cortical excitability, expecially in the epileptic,
pathologically hyperexcitable, brain
5