Medicine:N100

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Short description: Evoked potential in the brain

In neuroscience, the N100 or N1 is a large, negative-going evoked potential measured by electroencephalography (its equivalent in magnetoencephalography is the M100); it peaks in adults between 80 and 120 milliseconds after the onset of a stimulus, and is distributed mostly over the fronto-central region of the scalp. It is elicited by any unpredictable stimulus in the absence of task demands. It is often referred to with the following P200 evoked potential as the "N100-P200" or "N1-P2" complex. While most research focuses on auditory stimuli, the N100 also occurs for visual (see visual N1, including an illustration),[1] olfactory,[2] heat,[3] pain,[3] balance,[4] respiration blocking,[5] and somatosensory stimuli.[6]

The auditory N100 is generated by a network of neural populations in the primary and association auditory cortices in the superior temporal gyrus in Heschl's gyrus[7] and planum temporale.[8] It also could be generated in the frontal and motor areas.[9] The area generating it is larger in the right hemisphere than the left.[7]

The N100 is preattentive and involved in perception because its amplitude is strongly dependent upon such things as the rise time of the onset of a sound,[10] its loudness,[11] interstimulus interval with other sounds,[12] and the comparative frequency of a sound as its amplitude increases in proportion to how much a sound differs in frequency from a preceding one.[13] Neuromagnetic research has linked it further to perception by finding that the auditory cortex has a tonotopic organization to N100.[14] However, it also shows a link to a person's arousal[15] and selective attention.[16] N100 is decreased when a person controls the creation of auditory stimuli,[17] such as their own voice.[18]

Types

There are three subtypes of adult auditory N100.[9]

  • N100b or vertex N100, peaking at 100 ms.
  • T-complex N100a, largest at temporal electrodes at 75 ms
  • T-complex N100c, follows N100a and peaks at about 130 ms. The two T-complex N100 evoked potentials are created by auditory association cortices in the superior temporal gyri.

Elicitation

The N100 is often known as the "auditory N100" because it is elicited by perception of auditory stimuli. Specifically, it has been found to be sensitive to things such as the predictability of an auditory stimulus, and special features of speech sounds such as voice onset time.

During sleep

It occurs during both REM and NREM stages of sleep though its time is slightly delayed.[19] During stage 2 NREM it seems responsible for the production of K-complexes.[20] N100 is reduced following total sleep deprivation and this associates with an impaired ability to consolidate memories.[21]

Stimulus repetition

The N100 depends upon unpredictability of stimulus: it is weaker when stimuli are repetitive, and stronger when they are random. When subjects are allowed to control stimuli, using a switch, the N100 may decrease.[17] This effect has been linked to intelligence, as the N100 attenuation for self-controlled stimuli occurs the most strongly (i.e., the N100 shrinks the most) in individuals who are also evaluated as having high intelligence. Indeed, researchers have found that in those with Down syndrome "the amplitude of the self-evoked response actually exceeded that of the machine-evoked potential".[17] Being warned about an upcoming stimulus also reduces its N100.[22]

The amplitude of N100 shows refractoriness upon repetition of a stimulus; in other words, it decreases at first upon repeated presentations of the stimulus, but after a short period of silence it returns to its previous level.[9] Paradoxically, at short repetition the second N100 is enhanced both for sound[23] and somatosensory stimuli.[6]

With paired clicks, the second N100 is reduced due to sensory gating.[24]

Voice onset time

The difference between many consonants is their voice onset time (VOT), the interval between consonant release (onset) and the start of rhythmic vocal cord vibrations in the vowel. The voiced stop consonants /b/, /d/ and /g/ have a short VOT, and unvoiced stop consonants /p/, /t/ and /k/ long VOTs. The N100 plays a role in recognizing the difference and categorizing these sounds: speech stimuli with a short 0 to +30 ms voice onset time evoke a single N100 response but those with a longer (+30 ms and longer) evoked two N100 peaks and these are linked to the consonant release and vocal cord vibration onset.[25][26]

Top-down influences

Traditionally, 50 to 150 ms evoked potentials were considered too short to be influenced by top-down influences from the prefrontal cortex. However, it is now known that sensory input is processed by the occipital cortex by 56 ms and this is communicated to the dorsolateral frontal cortex where it arrives by 80 ms.[27] Research also finds that the modulation effects upon N100 are affected by prefrontal cortex lesions.[28] These higher-level areas create the attentive, repetition, and arousal modulations upon the sensory area processing reflected in N100.[29]

Another top-down influence upon N100 has been suggested to be efference copies from a person's intended movements so that the stimulation that results from them are not processed.[30] A person's own voice produces a reduced N100[18] as does the effect of a self-initiated compared to externally created perturbation upon balance.[31]

Development in children

The N100 is a slow-developing evoked potential. From one to four years of age, a positive evoked potential, P100, is the predominant peak.[32] Older children start to develop a negative evoked potential at 200 ms that dominates evoked potentials until adolescence;[33] this potential is identical to the adult N100 in scalp topography and elicitation, but with a much later onset. The magnetic M100 (measured by MEG rather than EEG) is, likewise, less robust in children than in adults.[34] An adult-like N100-P200 complex only develops after 10 years of age.[35]

The various types of N100 mature at different times. Their maturation also varies with the side of the brain: N100a in the left hemisphere is mature before three years of age but this does not happen in the right hemisphere until seven or eight years of age.[33]

Clinical use

The N100 may be used to test for abnormalities in the auditory system where verbal or behavioral responses cannot be used,[36] such with individuals in coma; in such cases, it can help predict the probability of recovery.[37][38] Another application is in assessing the optimal level of sedation in intensive critical care.[39]

High density mapping of the location of the generators of M100 is being researched as a means of presurgical neuromapping needed for neurosurgery.[40]

Many cognitive or other mental impairments are associated with changes in the N100 response, including the following:

  • There is some evidence that the N100 is affected in those with dyslexia and specific language impairment.[41]
  • The sensory gating effect upon N100 with paired clicks is reduced in those with schizophrenia.[24]
  • In individuals with tinnitus, those with smaller N100 are less distressed than those with larger amplitudes.[42]
  • Migraine is associated with an increase rather than decrease in N100 amplitude with repetition of the high-intensity stimulation.[43]
  • Headache sufferers also have more reactive N100 to somatosensory input than nonsufferers[44]

The N100 is 10 to 20% larger than normal when the auditory stimulus is synchronized with the diastolic phase of the cardiac blood pressure pulse.[45]

Relationship to mismatch negativity

The Mismatch negativity (MMN) is an evoked potential that occurs at roughly the same time as N100 in response to rare auditory events. It differs from the N100 in that:

  • They are generated in different locations.[46]
  • The MMN occurs too late to be an N100.[47]
  • The MMN, unlike N100, may be elicited by stimulus omissions (i.e., not hearing a stimulus when you expect to hear one).[48]

Though this suggests that they are separate processes, arguments have been made that this is not necessarily so and that they are created by the "relative activation of multiple cortical areas contributing to both of these 'components'".[49]

History

Pauline A. Davis at Harvard University first recorded the wave peak now identified with N100.[50] The present use of the N1 to describe this peak originates in 1966[51] and N100 later in the mid 1970s.[52] The origin of the wave for a long time was unknown and only linked to the auditory cortex in 1970.[9][53]

Due to magnetoencephalography, research is increasingly done upon M100, the magnetic counterpart of the electroencephalographic N100. Unlike electrical fields which face the high resistance of the skull and generate secondary or volume currents, magnetic fields which are orthogonal to them have a homogeneous permeability through the skull. This enables the location of sources generating fields that are tangent to the head surface with an accuracy of a few millimeters.[54] New techniques, such as event-related beam-forming with magnetoencephalography, allow sufficiently accurate location of M100 sources to be clinically useful for preparing surgery upon the brain.[40]

See also


References

  1. ↑ Warnke, A.; Remschmidt, H.; Hennighausen, K. (1994). "Verbal information processing in dyslexia--data from a follow-up experiment of neuro-psychological aspects and EEG". Acta Paedopsychiatrica 56 (3): 203–208. PMID 7521558. 
  2. ↑ Pause, B. M.; Sojka, B.; Krauel, K.; Ferstl, R. (1996). "The nature of the late positive complex within the olfactory event-related potential (OERP)". Psychophysiology 33 (4): 376–384. doi:10.1111/j.1469-8986.1996.tb01062.x. PMID 8753937. 
  3. ↑ 3.0 3.1 Greffrath, W.; Baumgärtner, U.; Treede, R. D. (2007). "Peripheral and central components of habituation of heat pain perception and evoked potentials in humans". Pain 132 (3): 301–311. doi:10.1016/j.pain.2007.04.026. PMID 17533117. 
  4. ↑ Quant, S.; Maki, B. E.; McIlroy, W. E. (2005). "The association between later cortical potentials and later phases of postural reactions evoked by perturbations to upright stance". Neuroscience Letters 381 (3): 269–274. doi:10.1016/j.neulet.2005.02.015. PMID 15896482. 
  5. ↑ Chan, P. -Y. S.; Davenport, P. W. (2008). "Respiratory-related evoked potential measures of respiratory sensory gating". Journal of Applied Physiology 105 (4): 1106–1113. doi:10.1152/japplphysiol.90722.2008. PMID 18719232. 
  6. ↑ 6.0 6.1 Wang, A. L.; Mouraux, A.; Liang, M.; Iannetti, G. D. (2008). Lauwereyns, Jan. ed. "The Enhancement of the N1 Wave Elicited by Sensory Stimuli Presented at Very Short Inter-Stimulus Intervals is a General Feature across Sensory Systems". PLOS ONE 3 (12): e3929. doi:10.1371/journal.pone.0003929. PMID 19081790. Bibcode: 2008PLoSO...3.3929W. 
  7. ↑ 7.0 7.1 Zouridakis, G.; Simos, P. G.; Papanicolaou, A. C. (1998). "Multiple bilaterally asymmetric cortical sources account for the auditory N1m component". Brain Topography 10 (3): 183–189. doi:10.1023/A:1022246825461. PMID 9562539. 
  8. ↑ Godey, B.; Schwartz, D.; De Graaf, J. B.; Chauvel, P.; Liégeois-Chauvel, C. (2001). "Neuromagnetic source localization of auditory evoked fields and intracerebral evoked potentials: A comparison of data in the same patients". Clinical Neurophysiology 112 (10): 1850–1859. doi:10.1016/s1388-2457(01)00636-8. PMID 11595143. https://hal.archives-ouvertes.fr/hal-01454201/file/ClinNeuroPhysiol2001.pdf. 
  9. ↑ 9.0 9.1 9.2 9.3 Näätänen, R.; Picton, T. (1987). "The N1 wave of the human electric and magnetic response to sound: A review and an analysis of the component structure". Psychophysiology 24 (4): 375–425. doi:10.1111/j.1469-8986.1987.tb00311.x. PMID 3615753. 
  10. ↑ Spreng, M. (1980). "Influence of impulsive and fluctuating noise upon physiological excitations and short-time readaptation". Scandinavian Audiology. Supplementum (Suppl 12): 299–306. PMID 6939101. 
  11. ↑ Keidel, W. D.; Spreng, M. (1965). "Neurophysiological Evidence for the Stevens Power Function in Man". The Journal of the Acoustical Society of America 38 (2): 191–195. doi:10.1121/1.1909629. PMID 14341718. Bibcode: 1965ASAJ...38..191K. 
  12. ↑ Davis, H.; Mast, T.; Yoshie, N.; Zerlin, S. (1966). "The slow response of the human cortex to auditory stimuli: Recovery process". Electroencephalography and Clinical Neurophysiology 21 (2): 105–113. doi:10.1016/0013-4694(66)90118-0. PMID 4162003. 
  13. ↑ Butler, R. A. (1968). "Effect of changes in stimulus frequency and intensity on habituation of the human vertex potential". The Journal of the Acoustical Society of America 44 (4): 945–950. doi:10.1121/1.1911233. PMID 5683660. Bibcode: 1968ASAJ...44..945B. 
  14. ↑ Pantev, C.; Hoke, M.; Lehnertz, K.; Lütkenhöner, B.; Anogianakis, G.; Wittkowski, W. (1988). "Tonotopic organization of the human auditory cortex revealed by transient auditory evoked magnetic fields". Electroencephalography and Clinical Neurophysiology 69 (2): 160–170. doi:10.1016/0013-4694(88)90211-8. PMID 2446835. 
  15. ↑ Nash, A. J.; Williams, C. S. (1982). "Effects of preparatory set and task demands on auditory event-related potentials". Biological Psychology 15 (1–2): 15–31. doi:10.1016/0301-0511(82)90028-x. PMID 7138998. 
  16. ↑ Hillyard, S. A.; Hink, R. F.; Schwent, V. L.; Picton, T. W. (1973). "Electrical signs of selective attention in the human brain". Science 182 (4108): 177–180. doi:10.1126/science.182.4108.177. PMID 4730062. Bibcode: 1973Sci...182..177H. 
  17. ↑ 17.0 17.1 17.2 Schafer, E. W.; Marcus, M. M. (1973). "Self-stimulation alters human sensory brain responses". Science 181 (4095): 175–177. doi:10.1126/science.181.4095.175. PMID 4711735. Bibcode: 1973Sci...181..175S. 
  18. ↑ 18.0 18.1 Curio, G.; Neuloh, G.; Numminen, J.; Jousmäki, V.; Hari, R. (2000). "Speaking modifies voice-evoked activity in the human auditory cortex". Human Brain Mapping 9 (4): 183–191. doi:10.1002/(SICI)1097-0193(200004)9:4<183::AID-HBM1>3.0.CO;2-Z. PMID 10770228. 
  19. ↑ Nordby, H.; Hugdahl, K.; Stickgold, R.; Bronnick, K. S.; Hobson, J. A. (1996). "Event-related potentials (ERPs) to deviant auditory stimuli during sleep and waking". NeuroReport 7 (5): 1082–1086. doi:10.1097/00001756-199604100-00026. PMID 8804056. 
  20. ↑ Niiyama, Y.; Satoh, N.; Kutsuzawa, O.; Hishikawa, Y. (1996). "Electrophysiological evidence suggesting that sensory stimuli of unknown origin induce spontaneous K-complexes". Electroencephalography and Clinical Neurophysiology 98 (5): 394–400. doi:10.1016/0013-4694(96)95103-2. PMID 8647042. 
  21. ↑ Mograss, M. A.; Guillem, F.; Brazzini-Poisson, V.; Godbout, R. (2009). "The effects of total sleep deprivation on recognition memory processes: A study of event-related potential". Neurobiology of Learning and Memory 91 (4): 343–352. doi:10.1016/j.nlm.2009.01.008. PMID 19340944. 
  22. ↑ Schafer, E. W.; Amochaev, A.; Russell, M. J. (1981). "Knowledge of stimulus timing attenuates human evoked cortical potentials". Electroencephalography and Clinical Neurophysiology 52 (1): 9–17. doi:10.1016/0013-4694(81)90183-8. PMID 6166459. 
  23. ↑ Budd, T. W.; Michie, P. T. (1994). "Facilitation of the N1 peak of the auditory ERP at short stimulus intervals". NeuroReport 5 (18): 2513–2516. doi:10.1097/00001756-199412000-00027. PMID 7696592. 
  24. ↑ 24.0 24.1 Hanlon, F. M.; Miller, G. A.; Thoma, R. J.; Irwin, J.; Jones, A.; Moses, S. N.; Huang, M.; Weisend, M. P. et al. (2005). "Distinct M50 and M100 auditory gating deficits in schizophrenia". Psychophysiology 42 (4): 417–427. doi:10.1111/j.1469-8986.2005.00299.x. PMID 16008770. 
  25. ↑ Steinschneider, M.; Volkov, I. O.; Fishman, Y. I.; Oya, H.; Arezzo, J. C.; Howard III, M. A. (2004). "Intracortical Responses in Human and Monkey Primary Auditory Cortex Support a Temporal Processing Mechanism for Encoding of the Voice Onset Time Phonetic Parameter". Cerebral Cortex 15 (2): 170–186. doi:10.1093/cercor/bhh120. PMID 15238437. 
  26. ↑ Steinschneider, M.; Volkov, I. O.; Noh, M. D.; Garell, P. C.; Howard III, M. A. (1999). "Temporal encoding of the voice onset time phonetic parameter by field potentials recorded directly from human auditory cortex". Journal of Neurophysiology 82 (5): 2346–2357. doi:10.1152/jn.1999.82.5.2346. PMID 10561410. 
  27. ↑ Foxe, J.; Simpson, G. (2002). "Flow of activation from V1 to frontal cortex in humans". Experimental Brain Research 142 (1): 139–150. doi:10.1007/s00221-001-0906-7. PMID 11797091. 
  28. ↑ Blenner, J. L.; Yingling, C. D. (1994). "Effects of prefrontal cortex lesions on visual evoked potential augmenting/reducing". The International Journal of Neuroscience 78 (3–4): 145–156. doi:10.3109/00207459408986053. PMID 7883451. 
  29. ↑ Coull, J. T. (1998). "Neural correlates of attention and arousal: Insights from electrophysiology, functional neuroimaging and psychopharmacology". Progress in Neurobiology 55 (4): 343–361. doi:10.1016/S0301-0082(98)00011-2. PMID 9654384.  PDF
  30. ↑ Kudo, N.; Nakagome, K.; Kasai, K.; Araki, T.; Fukuda, M.; Kato, N.; Iwanami, A. (2004). "Effects of corollary discharge on event-related potentials during selective attention task in healthy men and women". Neuroscience Research 48 (1): 59–64. doi:10.1016/j.neures.2003.09.008. PMID 14687881. 
  31. ↑ Mochizuki, G.; Sibley, K. M.; Cheung, H. J.; McIlroy, W. E. (2009). "Cortical activity prior to predictable postural instability: Is there a difference between self-initiated and externally-initiated perturbations?". Brain Research 1279: 29–36. doi:10.1016/j.brainres.2009.04.050. PMID 19422812. 
  32. ↑ Kushnerenko, E.; Ceponiene, R.; Balan, P.; Fellman, V.; Huotilaine, M.; Näätäne, R. (2002). "Maturation of the auditory event-related potentials during the first year of life". NeuroReport 13 (1): 47–51. doi:10.1097/00001756-200201210-00014. PMID 11924892. 
  33. ↑ 33.0 33.1 Pang, E. W.; Taylor, M. J. (2000). "Tracking the development of the N1 from age 3 to adulthood: An examination of speech and non-speech stimuli". Clinical Neurophysiology 111 (3): 388–397. doi:10.1016/S1388-2457(99)00259-X. PMID 10699397. 
  34. ↑ Paetau, R.; Ahonen, A.; Salonen, O.; Sams, M. (1995). "Auditory evoked magnetic fields to tones and pseudowords in healthy children and adults". Journal of Clinical Neurophysiology 12 (2): 177–185. doi:10.1097/00004691-199503000-00008. PMID 7797632. 
  35. ↑ Shibasaki, H.; Miyazaki, M. (1992). "Event-related potential studies in infants and children". Journal of Clinical Neurophysiology 9 (3): 408–418. doi:10.1097/00004691-199207010-00007. PMID 1517407. 
  36. ↑ Hyde, M. (1997). "The N1 response and its applications". Audiology and Neuro-Otology 2 (5): 281–307. doi:10.1159/000259253. PMID 9390837. 
  37. ↑ Fischer, C.; Morlet, D.; Giard, M. (2000). "Mismatch negativity and N100 in comatose patients". Audiology and Neuro-Otology 5 (3–4): 192–197. doi:10.1159/000013880. PMID 10859413. 
  38. ↑ Fischer, C.; Luauté, J.; Adeleine, P.; Morlet, D. (2004). "Predictive value of sensory and cognitive evoked potentials for awakening from coma". Neurology 63 (4): 669–673. doi:10.1212/01.wnl.0000134670.10384.e2. PMID 15326240. 
  39. ↑ Yppärilä, H.; Nunes, S.; Korhonen, I.; Partanen, J.; Ruokonen, E. (2004). "The effect of interruption to propofol sedation on auditory event-related potentials and electroencephalogram in intensive care patients". Critical Care 8 (6): R483–R490. doi:10.1186/cc2984. PMID 15566595. 
  40. ↑ 40.0 40.1 Cheyne, D.; Bostan, A. C.; Gaetz, W.; Pang, E. W. (2007). "Event-related beamforming: A robust method for presurgical functional mapping using MEG". Clinical Neurophysiology 118 (8): 1691–1704. doi:10.1016/j.clinph.2007.05.064. PMID 17587643. 
  41. ↑ Shaul S. (2007). Evoked response potentials (ERPs) in the study of dyslexia: A review. pp. 51–91. In (Breznitz Z. Editor) Brain Research in Language. Springer ISBN:978-0-387-74979-2
  42. ↑ Delb, W.; Strauss, D. J.; Low, Y. F.; Seidler, H.; Rheinschmitt, A.; Wobrock, T.; d’Amelio, R. (2008). "Alterations in Event Related Potentials (ERP) Associated with Tinnitus Distress and Attention". Applied Psychophysiology and Biofeedback 33 (4): 211–221. doi:10.1007/s10484-008-9065-y. PMID 18836827. 
  43. ↑ Wang, W.; Timsit-Berthier, M.; Schoenen, J. (1996). "Intensity dependence of auditory evoked potentials is pronounced in migraine: An indication of cortical potentiation and low serotonergic neurotransmission?". Neurology 46 (5): 1404–1409. doi:10.1212/wnl.46.5.1404. PMID 8628490. 
  44. ↑ Marlowe, N. (1995). "Somatosensory evoked potentials and headache: A further examination of the central theory". Journal of Psychosomatic Research 39 (2): 119–131. doi:10.1016/0022-3999(94)00072-d. PMID 7595870. 
  45. ↑ Sandman, C. A.; O'Halloran, J. P.; Isenhart, R. (1984). "Is there an evoked vascular response?". Science 224 (4655): 1355–1357. doi:10.1126/science.6729458. PMID 6729458. Bibcode: 1984Sci...224.1355S. http://www.escholarship.org/uc/item/1889h4km. 
  46. ↑ Alho, K. (1995). "Cerebral generators of mismatch negativity (MMN) and its magnetic counterpart (MMNm) elicited by sound changes". Ear and Hearing 16 (1): 38–51. doi:10.1097/00003446-199502000-00004. PMID 7774768. 
  47. ↑ Näätänen, R.; Alho, K. (1995). "Mismatch negativity—a unique measure of sensory processing in audition". The International Journal of Neuroscience 80 (1–4): 317–337. doi:10.3109/00207459508986107. PMID 7775056. 
  48. ↑ Yabe, H.; Tervaniemi, M.; Sinkkonen, J.; Huotilainen, M.; Ilmoniemi, R. J.; Näätänen, R. (1998). "Temporal window of integration of auditory information in the human brain". Psychophysiology 35 (5): 615–619. doi:10.1017/s0048577298000183. PMID 9715105. 
  49. ↑ May, P. J.; Tiitinen, H. (2004). "The MMN is a derivative of the auditory N100 response". Neurology & Clinical Neurophysiology 2004: 20. PMID 16012601. 
  50. ↑ Davis PA. (1939). Effects of acoustic stimuli on the waking human brain. J Neurophysiol 2: 494–499 abstract
  51. ↑ Davis, H; Zerlin, S (1966). "Acoustic relations of the human vertex potential". The Journal of the Acoustical Society of America 39 (1): 109–16. doi:10.1121/1.1909858. PMID 5904525. Bibcode: 1966ASAJ...39..109D. 
  52. ↑ Donchin, E.; Tueting, P.; Ritter, W.; Kutas, M.; Heffley, E. (1975). "On the independence of the CNV and the P300 components of the human averaged evoked potential". Electroencephalography and Clinical Neurophysiology 38 (5): 449–461. doi:10.1016/0013-4694(75)90187-x. PMID 50170. 
  53. ↑ Vaughan Jr, H. G.; Ritter, W. (1970). "The sources of auditory evoked responses recorded from the human scalp". Electroencephalography and Clinical Neurophysiology 28 (4): 360–367. doi:10.1016/0013-4694(70)90228-2. PMID 4191187. 
  54. ↑ Hämäläinen M, Hari R, Ilmoniemi RJ, Knuutila J. (1993). Magnetoencephalography-theory, instrumentation, and applications to noninvasive studies of the working human brain. Reviews of modern Physics. 65: 413–497. OCLC 197237696



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