MMN

MMN - What does it mean?

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Mismatch negativity (MMN) is elicited by any discriminable change in any repetitive aspect of auditory input. It is elicited irrespective of the subject or patient’s attention or behavioural task which implicates the occurrence of an automatic comparison between the current input and the representation, or the memory trace, of the preceding auditory events. This change-detection process occurs unconsciously in the auditory cortices (generating the auditory-cortex subcomponent of the MMN). However, it activates, with a very short time delay, frontal-cortex mechanisms (generating the frontal subcomponent of the MMN) controlling the direction of attention, which leads to attention switch to, and conscious perception of, sound change [1]. Thus, the MMN is also involved in initiating a cerebral warning mechanism which is of great biological significance.

While the basic mechanism of the MMN is simple, with appropriate experimental manipulations, it is a versatile tool for investigating various aspects of auditory perception and attention. Here are some examples on the applicability of the MMN for neuroscience studies:

  • The effects of the auditory experience can be investigated with MMN. For instance, the sensitivity of the auditory system is enhanced for familiar sounds, such as to native-language speech sounds [2,3].
  • The neural determinants of musical expertise and musicality can be determined with MMN recordings [4-8].
  • The development of native-language speech sound representations can be followed-up since the infancy [9]. MMNs for sound changes can be recorded as early as in the fetal stage [10].
  • Our auditory system is continuously modelling and making predictions on the auditory scene. Violations of the auditory regularities elicit an MMN even when the individual cannot consciously detect such violations [11,12].
  • The awakening from a coma can be predicted with the MMN [13,14].
  • The MMN reflects plastic changes caused by learning prior to birth [15]
  • The MMN reflects plastic changes in the auditory cortex of the blind but does not reflect the cross-modal reorganization. This type of reorganization is evident in the processes following the MMN, such as the N2b [16].
  • The MMN reflects plastic neural changes caused by the intervention of audiovisual processes in dyslexic children [17].

Traditionally, the MMN has been recorded with an oddball paradigm, which typically includes a repetitive standard stimulus (e.g., a 1000 Hz tone, p. 0.9) occasionally replaced by a deviant stimulus (e.g., 1100 Hz, p. 0.1). This approach is very time consuming, always having the trade-off of MMN signal quality and the amount of information obtained (the number of different deviant types for which the MMN is recorded). Especially for investigating patient groups and young children, this approach is not optimal since the recording times should be kept minimal. At the same time, the EEG trial loss may be high due to, e.g., movements. To overcome these problems, Näätänen et al., [18] developed a new multi-feature MMN paradigm, called initially “Optimum-1”, with which MMN for five different types of deviant sounds can be recorded in the same time as for one deviant type in the oddball paradigm described above. The deviants included in such multi-feature sequence are alternating with the standard stimulus, and each deviant stimulus should differ from the rest of the stimuli in one feature only. The rationale of this paradigm is that besides serving as a deviant, each deviant stimulus type also strengthens the memory trace for the features it shares with the rest of the stimuli, thereby acting as a “standard”. For example, if only the frequency of a sound changes, this sound still strengthens the memory traces for sound duration, intensity, and location.

References:

  1. Näätänen, Beh. Brain Sciences, 1990 https://doi.org/10.1017/S0140525X00078407
  2. Näätänen et al., Nature, 1997; https://doi.org/10.1038/385432a0
  3. Winkler et al., Psychophysiology, 1999 https://doi.org/10.1111/1469-8986.3650638
  4. Tervaniemi et al., Neurosci Lett. 1997; https://doi.org/10.1016/S0304-3940(97)00217-6
  5. Tervaniemi et al., Learn Mem. 2001; https://doi.org/10.1101/lm.39501
  6. Tervaniemi et al., NeuroReport 2006; https://doi.org/10.1097/01.wnr.0000230510.55596.8b
  7. van Zuijen et al., Brain Res. 20042005; https://doi.org/10.1016/j.cogbrainres.2004.10.007
  8. Brattico et al., Brain Res., 2006 https://doi.org/10.1016/j.brainres.2006.08.023
  9. Cheour-Luhtanen et al., Nature Neurosci., 1998 https://doi.org/10.1016/S1388-2457(99)00191-1
  10. Huotilainen et al., NeuroReport, 2005 https://journals.lww.com/neuroreport/Fulltext/2005/01190/Short_term_memory_functions_of_the_human_fetus.19.aspx
  11. Näätänen et al., TINS, 2001; https://doi.org/10.1016/S0166-2236(00)01790-2
  12. van Zuijen et al., J. Cogn. Neurosci., 2006 https://doi.org/10.1162/jocn.2006.18.8.1292
  13. Kane et al., The Lancet, 1993; https://doi.org/10.1016/0140-6736(93)90453-N
  14. Fischer et al., Crit. Care Med., 2006; https://doi.org/10.1097/01.CCM.0000215823.36344.99
  15. Partanen et al., Proc. Natl. Acad. Sci., USA, 2013 https://doi.org/10.1073/pnas.1302159110
  16. Kujala et al., TINS, 2000 https://doi.org/10.1016/S0166-2236(99)01504-0
  17. Kujala et al., Proc. Natl. Acad. Sci., 2001; https://doi.org/10.1073/pnas.181589198
  18. Näätänen et al., (Clin. Neurophysiol., 2004)  https://doi.org/10.1016/j.clinph.2003.04.001