social and physical anhedonia and lower ratings on empathy thancontrol mothers. The ERP analysis also revealed differences inresponse to affective stimuli related to neutral stimuli in bothtypes of mother. Neglectful mothers had a more unspecific brainresponse to the different valence of affective stimuli, and the anhe-donia was a crucial variable modulating this lack of specificity.Differences found in anhedonia and in brain processing of affec-tive stimuli extend previous findings about other personality char-acteristics and psychophysiological variables that havedistinguished between neglectful and control mothers. A betterunderstanding of both the psychological and the electrophysiolog-ical style of response to affective stimuli in neglected mothers willhelp to better understand their disrupted parenting behavior.

doi:10.1016/j.clinph.2008.04.274

259. Application of the magnetoencephalography to study the

auditory mismatch response in neonates—J.C. Hernandez,M. Sosa, W.J. Lutter, R.T. Wakai (Mexico)

Magnetoencephalography (MEG) is a powerful neuroimagingtechnique that detects the brain’s magnetic field generated by neu-ronal electric currents. This work purposes to employ MEG inorder to study auditory discrimination during the first monthsof life. The subjects were 5 neonates, born at conceptional age(CA) 35–39 weeks. During each session, several 28-min MEGrecordings were acquired in the presence of auditory stimulation.The stimuli consisted of 0.1 sec 1000 Hz tones (standard tones)and occasional 0.1 sec 1050 Hz tones (deviant tones), presentedpseudo randomly in a 7:1 ratio. The MEG signals and stimulustrigger were digitalized continuously at 520.8 Hz and digitally fil-tered using a 0.5–20 Hz passband. The classic Mismatch Negativ-ity ‘‘MMN” commonly found in adults is not present innewborns. However, an extra component in the deviant responsewas observed at longer latencies (400–600 ms). Furthermore, thelatency of this extra component decreased with CA. Our findingssuggest that adult-like MMN is not present in newborns. It is pos-sible that this reflects the immaturity of the brain at this age. Onthe other hand, the presence of the late component in the deviantresponse implies that newborns are nonetheless able to discrimi-nate the standard and deviant tones. MEG is a valuable toolfor the study of brain activity during early infancy.

doi:10.1016/j.clinph.2008.04.275

260. Positive vs. Negative reinforcement in neurofeedback

applied to learning disabled children—T. Fernandez, F.

Garcıa, R.A. Prado Alcala, E. Santiago, A. Fernandez

Bouzas, T. Harmony, L. Dıaz Comas, H. Belmont (Mexico)

This study purposes to compare the Neurofeedback (NFB)using positive reinforcement vs. NFB using negative reinforce-ment. NFB is an operant conditioning procedure, whereby anindividual can learn to modify the electrical activity of his orher own brain. LD children have an EEG slower than normalchildren of the same age. Sixteen LD children with abnormallyhigher theta/alpha ratio were assigned to any of two groups: toone (NFB+) a positive reward was given when the value of

theta/alpha ratio was reduced, to the other (NFB�) a punishmentwas given when the value increased. Each subject obtained thepositive or negative reward (a tone of 500 Hz), depending onthe group. NFB training consisted of 30 sessions of 30 min eachone. In both groups there was an improvement of the IQ, intellec-tual maturity, attention, academic achievement and self-esteem.In addition, in NFB- group there was significant improvementin the understanding of reading and reasoning. In both groupsthere were changes in the EEG compatible with EEG maturation,with greater changes in NFB- group. NFB given with either posi-tive or negative reinforcement is useful for the treatment of LDchildren. However, NFB applied with negative reward induces agreater and quicker improvement in behavior and EEG thanNFB applied with positive reward.

doi:10.1016/j.clinph.2008.04.276

261. Sleep disorder: A possible cause of attention deficit in

school children with Chiari malformation type II—P.S.A.

Henriques Filho, R. Pratesi (Brazil)

Attention deficit may be related to sleep disorders in Chiarimalformation type II (CM II). The aim of the current study isidentify sleep disorders, and their specific contribution in atten-tion deficit. Methods: Among 103 patients with CM I and II, wereselected 24 patients with CMII and 24 without CMII. DSM IVcriteria and a neuropsychological analysis were applied in all.All patients underwent full night polysomnography. StatisticalAnalysis: Analysis of variance, Pearson correlations and Fisherexact test were applied. 14 CM II patients presented sleep apneasyndrome, RBD and PLMS; six patients without CMII presentedsleep apnea syndrome. Among these patients, 12 (six with CMIIand six without CMII) presented attention deficit related to thesleep disorders. Sleep disorders may impair cognitive functions,as attention, and contribute to poor quality of learning either inpatients with CM II.

doi:10.1016/j.clinph.2008.04.277

262. Cortical mechanisms involved in inhibition of automatic

consumption behaviour in high craving smokers—M.A.

Munoz, M.I. ViedmadelJesus, L. Anllo-Vento, A.G. Lopez,

J. Vila (Spain)

The term craving refers to ‘‘the motivation to use a psychoac-tive substance which previously has been consumed”. The theoriesof craving contemplate the compulsive consumption of the sub-stance as one of its main characteristics. On the other hand, theN200 potential has been related with the mechanisms which inhi-bit automatic behaviours. The goal of the present study was toexamine the modulation of N200 when deprived smokers (highcraving) and non deprived smokers (low craving) have the expec-tative to smoke. Participants executed an implicit learning tasktwice, the first time being abstinent, and the second time after hav-ing smoked. During the learning task, correct responses were fol-lowed by an asterisk indicating that they could win points(probabilities 60%) to stop the experiment and smoke, whereasincorrect responses were followed by a number sign indicating

Society Proceedings / Clinical Neurophysiology 119 (2008) e99–e164 e163