Abstracts

EVIDENCE OF IMPAIRED AUDITORY INFORMATION PROCESSING IN CHILDREN WITH INTRACTABLE EPILEPSY: MEG STUDY

Abstract number : 2.046
Submission category : 3. Clinical Neurophysiology
Year : 2009
Submission ID : 9763
Source : www.aesnet.org
Presentation date : 12/4/2009 12:00:00 AM
Published date : Aug 26, 2009, 08:12 AM

Authors :
Milena Korostenskaja, M. Pardos, T. Kujala, P. Horn, H. Fujiwara, D. Brown, P. Alku, Y. Wang, D. Rose, J. Xiang, A. Byars, T. Degrauw, R. Naatanen and K. Lee

Rationale: Studies of auditory information processing as far as epilepsy patients are concerned are of particular importance. These patients have structural and metabolic abnormalities of areas involved in auditory processing. There is evidence that impaired detection of auditory physical stimulus features leads to consequent cognitive delay. Event-related potentials (ERPs) and event-related fields (ERFs) provide the information about the neural substrates of auditory memory processing. In fact, N1 response, which indexes the transient encoding of physical stimulus features, was delayed in adults with focal epilepsy associated with spikes at the primary auditory cortex 1 and in children with Landau-Kleffner syndrome 2. Furthermore, later stages of auditory information processing such as sensory memory formation were shown to be abnormal as reflected in delayed latency of mismatch negativity component (MMN) 3 or absence of MMN response 4 in children with benign rolandic epilepsy. In this magnetoencephalography (MEG) study for the first time we investigated the changes of auditory information processing by registering magnetic MMN response (MMNm) with multi-feature paradigm in a group of children with intractable epilepsy. Methods: We used multi-feature sound MMN paradigm 5 to study nine children with intractable epilepsy and nine age- and gender- matched healthy controls (M/F 4/6, Mean/SD 12.4±2.2 yr.). Latencies and amplitudes of magnetic N1, P2, and MMN fields were measured. Results: In patients both N1m and MMNm (to change in sound duration, frequency and intensity) amplitudes were significantly decreased (Fig. 1). This could be interpreted as a lack of neuronal resources, participating in detection of physical stimuli and in auditory sensory memory formation. Current results are in line with previous studies demonstrating impaired auditory sensory memory mechanism in drug-resistant epilepsy 6. Moreover, we observed a clear difference in MMNm responses recorded from healthy hemisphere and from hemisphere with epileptogenic zone (Fig. 2). Our results support the view of differences in information processing between healthy and epileptogenic neural substrates 1. Finally, we found a strong significant correlation between subject’s ERF components and results of neuropsychological testing: a correlation between ERF component P2m and Boston Naming Test (BNT), and between P2m, and MMNm components and Pegboard Test. Conclusions: Auditory information processing is impaired in patients with drug-resistant epilepsy, beginning with encoding of physical stimulus features (reflected in N1m ) and continuing with sensory memory formation (reflected in MMNm) abnormalities. The impairment in auditory information processing is associated with the location of epileptogenic zone (healthy vs. one with epileptogenic focus) and with patient’s cognitive performance (reflected in BNT and Pegboard Test scores). References 1 Kubota et al 2007 2 Seri et al 1998 3 Boatman et al 2008 4 Liasis et al 2006 5 Naatanen et al 2004 6 Borghetti et al 2007
Neurophysiology