Abstracts / Clinical Neurophysiology 127 (2016) e18–e132
Methods: Eleven patients with idiopathic generalized epilepsy and photosensitivity were compared to 11 healthy subjects. We measured the resting motor threshold of the left hand motor area and the phosphene threshold. The paradigm consisted in a conditioning stimulus (CS) delivered over the phosphene hotspot of the visual cortex and followed at random interstimulus intervals (15–40 ms) by a test stimulus over the left motor cortex to evoke a motor evoked potential (MEP) of 1 mV from right FDI. The conditioned-MEP was expressed as a percentage of the unconditioned-MEP amplitude. Results: In healthy subjects the CS over the visual cortex produced significant inhibitory changes on the corticospinal excitability with a time course between 18 and 40 ms. Patients with IGE and photosensitivity showed a failure of the physiological inhibition. Conclusions: In photosensitive patients the alteration of the normal visuo-motor functional connectivity could be responsible for the origin/propagation of the PPR from the hyper-excitable visual cortex to the motor cortex. doi:10.1016/j.clinph.2015.11.282
ID 253 – Good functional outcome after prolonged postanoxic coma and myoclonic status epilepsy—S. Yagüe a, N. Mas b, M. Martínez-Corral b, A. Aceituno b, N. Ailouti a, M. Vicente a, R. Belvis b, X. Salas-Puig b,c (a Neurophysiology, Hospital Universitario Quirón-Dexeus, Barcelona, Spain, b Neurology, Hospital Universitario Quirón-Dexeus, Barcelona, Spain, c Neurology, Hospital Universitario Vall d’Hebron, Barcelona, Spain) Objective: Present the possibility of a reasonable neurological recovery in early onset myoclonic status epilepsy (MSE) and prolonged postanoxic coma (PC). Methods: A 43-year-old woman suffered a severe respiratory failure due to an anaphylactic reaction during anaesthetic induction before surgery. She required an urgent tracheostomy and remained in PC with reactive pupils and corneal reflexes, but with no withdrawal reaction to painful stimuli. Over the next hour she showed diffuse myoclonic jerks refractory to different antiepileptic drugs, midazolam and propofol. The EEG pattern revealed diffuse epileptiform discharges suggestive of MSE. Therapeutic hypothermia was induced, as was a barbituric coma using tiopental. Results: PC and MSE persisted after suppression of the barbituric coma. The MRI was normal and repeated EEG confirmed MSE with stimulus-induced discharges. Cortical somatosensory evoked potentials (CSEP) were preserved and a second barbituric coma was induced. 48 days later the patient regained consciousness and was able to interact, being discharged on day 90. Conclusions: Even in the event of an unfavourable initial prognosis, preserved brainstem reflexes, CSEP and EEG reactivity indicate the requirement for an intensive treatment of postanoxic status epilepsy. Key message: Despite early onset of MSE and prolonged PC a global evaluation is necessary before establishing an accurate prognosis. doi:10.1016/j.clinph.2015.11.283
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ID 258 – Defective motor cortex plasticity in juvenile myoclonic epilepsy—C. Pizzamiglio, G. Strigaro, L. Falletta, E. Matino, G. Tondo, C. Varrasi, R. Cantello (Department of Translational Medicine, Section of Neurology, University of Piemonte Orientale ‘‘A. Avogadro”, Novara, Italy) Objective: 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 25 ms, a long-term potentiation (LTP)-like synaptic plasticity is induced in the corticospinal system. Aim of this study was to investigate the motor cortex LTP-like synaptic plasticity by means of PAS in patients with JME. Methods: Twelve adult patients with JME were compared with 13 healthy subjects of similar age and sex. PAS consisted of 180 electrical stimuli of the right median nerve paired with a single TMS over the hotspot of right APB at ISI of 25 ms (PAS25). We measured motor evoked potentials (MEPs) before and after each intervention for up to 30 min. Results: In healthy subjects the PAS25 protocol was followed by a significant increase of MEP amplitude. On the contrary, in patients with JME, the MEP amplitude did not change. Conclusions: Defective motor cortex plasticity may be involved in the pathogenesis of JME. doi:10.1016/j.clinph.2015.11.284
ID 294 – Clinical and electroencephalographic features of patients with symptomatic epilepsy—H. Ertasßog˘lu Toydemir, D. Bozkurt, F. Azman, B. Yurtsever, H. Örnek, V. Yayla (Bakırköy Dr. Sadi Konuk Training and Research Hospital, Neurology Department, Turkey) Objective: We aimed to evaluate the clinical and electroencephalographic features of symptomatic epilepsy (SE) patients. Method: A retrospective analysis was performed to 143 patients with SE attending to our epilepsy department between 2011 and 2014. Results: Mean age of 60F:83M patients was 32.2 ± 14.2 years. Neurological examination was unremarkable in 57.1% of the patients. The most common etiologic factor was trauma (41%). The seizure types were GTCS (52.4%), complex PS (47.6%), secondary GS (26.6%) and simple PS (23.8%). More than one seizure type was detected in 46% of them. EEG revealed pathologic patterns in 61.5% patients: Focal epileptogenic focus (56%), focal slowing (41%), generalized slowing (23%), generalized epileptogenic activity (15%) and nonspecific paroxysmal activity (10%). More than one type of pathologic EEG pattern was observed in 19% of the patients. Abnormalities on CT/MRI were detected in 74.8% of the patients. Conclusion: Although clinical and electroencephalographic findings of SE patients vary according to the underlying etiological factors, more than one type of seizure or pathological EEG pattern may be detected in the same patient. The management of SEs could be more complex than it seems.