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:
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:
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]
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