the potential for treatment of such patients with these two drugswhich merits further multicenter investigation.

doi:10.1016/j.jns.2013.07.2038

Abstract — WCN 2013No: 281Topic: 36 — Other TopicLimbic encephalitis in a child with an atypical presentation

A.A. Mahmoud. Pediatric Neurology Department, KFMC,Riyadh, Saudi Arabia

Background: Limbic encephalitis (LE) is a rare disorder that generallyhas a subacute onset evolving over days to weeks. Patients presentwitha variable combination of memory loss, seizures, and psychiatricdisturbance, and it is not rare for patients to be initially misdiagnosed.Patient: We report a previously healthy twelve-year-old boy whodeveloped hisfirst episode of seizures at eight years of age. He had a totalof eight prolonged focal seizure episodes, and each episodewas followedby a month of behavioral changes and short term memory loss. Therewas no family history of seizures or other neurological disorders, and hehad an otherwise unremarkable neonatal and past medical history.Results: Magnetic resonance imaging during each episode of seizuresshowed alternating unilateral brain hemispheric involvement consistentwith LE that was followed by resolution for a total of six times. Despite anegative laboratory evaluation for a large panel of paraneoplasticantibodies, the clinical scenario and exclusion of other possible disordersmade recurrent LE the most likely diagnosis.Conclusion: Limbic encephalitis is a rare disorder diagnosed primarilyon clinical criteria and often associated with the presence of aparaneoplastic antibody. However, the lack of a positive paraneopalsticantibody in a patientwith a triad of seizure, behavioral changes and shortmemory loss dose not exclude the diagnosis. The unique presentation ina seronegative patient like ours may indicate a previously unrecognizedantibody. To the best of our knowledge, such a case has never beenreported.

doi:10.1016/j.jns.2013.07.2039

Abstract — WCN 2013No: 46Topic: 36 — Other TopicHomeostatic plasticity and human visual system

T. Boccia,b, N. Francinic, M. Caleod, S. Tognazzie, L. Maffeid, S. Rossib,A. Priorif, F. Sartuccia,d. aDepartment of Neuroscience, Unit of Neurology,Pisa University Medical School, Pisa, Italy; bDepartment of Neuroscience,Neurology and Clinical Neurophysiology Section, Azienda OspedalieraUniversitaria Senese, Siena, Italy; cDepartment of Neuroscience, Universityof Pisa, Italy; dCNR Neuroscience Institute, Pisa University Medical School,Pisa, Italy; eDepartment of Neuroscience, Cisanello Neurology Unit, PisaUniversityMedical School, Pisa, Italy; fDepartment of Neurological Sciences,University of Milan, Fondazione IRCCS Ospedale Maggiore Policlinico,Milan, Italy

Background and objective: The ability of cortical networks to regulateneuronal activity within a useful dynamic range, called homeostaticplasticity, has received growing attention. The threshold and direction ofexcitability changes primed by low- and high-frequency rTMS in theprimary motor cortex (M1) can be reverted by a preceding session oftDCS.Whether there is a similarmechanism in human visual pathways isa matter of debate.Materials and methods: In 15 healthy subjects we evaluated changesin visual evoked potential (VEP) amplitude at two different contrasts

(K90% and K20%) by applying anodal or cathodal tDCS (20′, 1.5 mÅ) tooccipital cortex, followed by low- or high-frequency rTMS (0.5 for 20′and 5 Hz for 60″, respectively).Results: Anodal tDCS improved the amplitude of VEPs and this effectwas reverted by applying high-frequency rTMS (two-way ANOVA,p b 0.001). Concurrently, cathodal tDCS led to a decrease in VEPamplitude, which is reverted in its turn by a subsequent applicationof 0.5 Hz rTMS (two-way ANOVA p b 0.01). There are no significantchanges in RMT values over time (p N 0.5), confirming the spatialselectivity of our protocol.Conclusion: Our data show that preconditioning excitability with tDCSover the V1 can modulate the direction of plasticity induced bysubsequent application of 1 or 5 Hz rTMS. This pattern was observedfor both N1 and P1 components; since they appear to be generated instriate and extrastriate cortex, respectively, these findings indicate thathomeostatic mechanisms could operate in both primary and higher-order visual areas.

doi:10.1016/j.jns.2013.07.2040

Abstract - WCN 2013No: 53Topic: 36 - Other TopicTongue's motor evoked potentials in the differentialdiagnosis between amyotrophic and primarylateral sclerosis: A preliminary report

T. Boccia,b, L. Briscesea, E. Giorlia,b, S. Tognazzic, M. Naracic, F. Sartuccia,c,d.aDepartment of Neuroscience, Unit of Neurology, Pisa University MedicalSchool, Pisa, Italy; bDepartment of Neuroscience, Neurology and ClinicalNeurophysiology Section, Siena University Medical School, Siena, Italy;cDepartment of Neuroscience, Cisanello Neurology Unit, Pisa UniversityMedical School, Italy; dCNR Neuroscience Institute, Pisa, Italy

Introduction: Primary lateral sclerosis (PLS) is a neurodegenerativedisorder due to a selective loss of precentral pyramidal neurons. Ourpurpose was to evaluate preferential impairment of pyramidal tractto bulbar muscles in patients with PLS and identify a reliableelectrophysiological method to help clinicians in the differentialdiagnosis from amyotrophic lateral sclerosis (ALS).Materials and methods: We recorded motor evoked potentials(MEPs) from tongues and anterior tibialis muscles in six patientswith PLS and compared the results, in terms of central motorconduction time (CMCT), amplitude and duration of contralateralsilent period (cSP), with those obtained both from age-matchedhealthy volunteers and patients affected by ALS.Results: For lower limbs, CMCT resulted significantly increased inPLS and ALS compared with healthy subjects (p b 0.01); we did notdisclose differences between ALS and PLS groups (p = 0.417). Fortongue's recordings, CMCT, absolute amplitude of MEPs and cSP weresignificantly altered in PLS patients towards both ALS patients(p b 0.05) and healthy volunteers (p b 0.01).Discussion: We showed that tongue's MEPs are selectively impairedin PLS compared with other motorneuron diseases. Our resultsstrengthen the hypothesis of a proximal axonal degeneration as apathological marker of PLS, probably reflecting a greater loss ofcorticomotoneuronal connections rather than in ALS patients. Thatcould be confirmed by the shortening of cSP in cranial nerves, sincefor bulbar muscles the spinal contribution for the generation of cSP isruled out.Tongue's MEPs could represent an interesting electrodiagnostic test,potentially useful for the early diagnosis of PLS.

doi:10.1016/j.jns.2013.07.2041

Abstracts / Journal of the Neurological Sciences 333 (2013) e579–e628e584