Please provide detailed notes on Auditory Evoked Potentials. ECochG, ABR, MLR, LLR, MMN, ASSR, c-VEMP, o-VEMP, N200, N400, P300, P600 and if i have missed any add them also.

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N400 P600 N200 auditory evoked potentials clinical applications neuroscience

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Auditory Evoked Potentials (AEPs) - Comprehensive Notes

Auditory Evoked Potentials (AEPs) are electrical responses recorded from the scalp or near the ear that reflect neural activity along the auditory pathway following acoustic stimulation. They are also called Electrical Response Audiometry (ERA). AEPs are broadly classified by response latency (the time from stimulus onset to peak response), which determines where along the auditory pathway the generator lies.

Classification by Latency

Category	Latency Range	Tests Included
Short-latency (EALR)	0 - 10 ms	ECochG, ABR
Middle-latency (MLR)	10 - 50 ms	MLR, ASSR (40 Hz)
Long-latency / Slow (LLR/CAEP)	50 - 300 ms	LLR (N1-P2), P1
Cognitive / Event-related (ERPs)	>200 ms	P300, MMN, N200, N400, P600
Vestibular-evoked	Myogenic	c-VEMP, o-VEMP

1. Electrocochleography (ECochG / ECoG)

What it is: Records electrical potentials generated in the cochlea and the most distal (peripheral) portion of the auditory nerve (CN VIII). It is the shortest-latency AEP.

Three components recorded:

Component	Generator	Nature
Cochlear Microphonic (CM)	Outer hair cells (OHCs), organ of Corti	AC voltage; mirrors the acoustic stimulus
Summating Potential (SP)	Inner hair cells (>50%), OHCs, organ of Corti	DC shift; reflects hair cell receptor activity
Compound Action Potential (CAP / AP)	Spiral ganglia, distal CN VIII afferent fibers	Sum of all synchronous auditory nerve fiber discharges

Cochlear Microphonic (CM): The CM is an alternating current voltage primarily from OHCs and the organ of Corti. It exactly echoes the acoustic stimulus at low-to-moderate stimulus levels, which makes it difficult to distinguish from stimulus artifact using noninvasive techniques. Using alternating polarity stimuli causes the CM to cancel out, leaving the SP and AP more visible.

Summating Potential (SP): A DC shift that rides along the CM. The SP:AP ratio is the key clinical measure - a ratio >0.4-0.5 (or SP/AP amplitude ratio >40%) is considered abnormal and suggests endolymphatic hydrops.

Electrode placement:

Tympanic membrane (TM) surface electrode - most common clinical approach today (extratympanic)
Transtympanic (needle through TM onto promontory) - most sensitive but invasive
External auditory canal (EAC) foam electrode

Clinical applications:

Meniere's disease / Endolymphatic hydrops: Enlarged SP:AP ratio is the hallmark. ECochG is considered more reliable than VEMPs in patients who cannot cooperate (elderly, frail, cervical issues).
Superior Semicircular Canal Dehiscence (SSCD): Enhanced SP amplitude and abnormally low thresholds.
Auditory Neuropathy Spectrum Disorder (ANSD): CM present but AP/ABR absent or grossly abnormal - confirms cochlear (hair cell) function is preserved but neural synchrony is disrupted.
Intraoperative monitoring: During acoustic neuroma surgery, ECochG monitors cochlear function; ABR monitors the intracranial portion of CN VIII.
Threshold estimation: Less commonly used than ABR for this purpose.

Key clinical note: "With the advent of tympanic membrane surface electrode recordings, the clinical contributions of ECochG are receiving increased recognition." - Cummings Otolaryngology

2. Auditory Brainstem Response (ABR)

Synonyms: BERA (Brainstem Evoked Response Audiometry), BAER (Brainstem Auditory Evoked Response), BAEP (Brainstem Auditory Evoked Potential)

What it is: A surface-recorded averaged response representing the electrical activity of the distal auditory pathway, from the auditory nerve through the brainstem. Recorded within 10 ms of stimulus onset.

Waveform peaks (I-VII), with I, III, V being the most clinically reliable:

Wave	Generator (Moller & Jannetta)
I	Distal (peripheral) end of CN VIII, cochlear end
II	Proximal CN VIII near brainstem entry (porus acusticus)
III	Cochlear nucleus complex + caudal brainstem (trapezoid body area, superior olivary complex)
IV	Superior olivary complex
V	Lateral lemniscus as it enters the inferior colliculus (NOT the inferior colliculus itself)
VI, VII	Inferior colliculus

Stimuli used:

Clicks: 100 µs rectangular pulses, broadband (emphasize 2000-4000 Hz), presented at constant or alternating polarity. Most common. 1000-3000 sweeps averaged.
Tone bursts/pips: Frequency-specific, used for threshold estimation at 500, 1000, 2000, 4000 Hz.
Chirp stimuli: Compensate for cochlear travel time, giving larger wave V amplitude.

Electrode placement:

Non-inverting (positive): High forehead (Fz) or vertex (Cz)
Inverting (negative): Ipsilateral earlobe / mastoid (emphasizes Wave I)
Contralateral earlobe / mastoid (enhances IV-V separation)
Ground: Mid-forehead (Fpz)

Key parameters:

Absolute latencies: Latency of waves I, III, V
Interpeak intervals (IPIs): I-III (cochlear nerve to brainstem), III-V (lower to upper brainstem), I-V (total brainstem transmission time; normal ~4 ms)
Interaural latency difference (ILD): Wave V latency difference between ears (normal <0.3-0.4 ms)
Amplitude ratio: Wave V:I amplitude ratio (normally ≥1)
Threshold: Lowest intensity at which Wave V is identifiable (correlates with behavioral threshold at 2000-4000 Hz, approximately 10-20 dB above behavioral threshold)

ABR interpretation by hearing loss type:

Type	Pattern
Normal hearing	All latencies and morphology within normal limits
Conductive hearing loss	Prolonged absolute latencies (especially Wave I); IPIs normal; shifted thresholds but normal morphology
Sensory (cochlear) hearing loss	Wave I diminished or absent; delayed absolute latencies; poor morphology; IPIs within normal limits
Neural (retrocochlear) loss	Wave I normal latency; prolonged IPIs (especially I-III or I-V); poor morphology

Subtypes of ABR testing:

Threshold ABR: Estimates hearing threshold - wave V tracked to lowest detectable intensity. Standard for neonatal hearing screening and audiometric estimation in infants/difficult-to-test patients.
Diagnostic (Neurologic) ABR: High stimulus level (80-95 dB nHL). Evaluates for retrocochlear pathology - primarily vestibular schwannoma/acoustic neuroma. Sensitivity >90%, specificity ~80%.
Stacked ABR: Derived-band responses across five frequency bands are time-aligned and summed. Enhances sensitivity for small eighth-nerve tumors that can be missed by click ABR.
Intraoperative monitoring ABR: Real-time monitoring during posterior fossa / CPA surgery to detect acute injury to CN VIII and brainstem.

Clinical applications:

Newborn hearing screening
Threshold estimation (pediatric, difficult-to-test, non-organic hearing loss)
Vestibular schwannoma detection
Auditory Neuropathy Spectrum Disorder (ANSD) diagnosis - ABR absent or grossly abnormal, OAEs present
Multiple sclerosis (prolonged IPIs)
Brainstem lesion localization
Depth of anesthesia/sedation monitoring
Coma prognostication

3. Middle Latency Response (MLR)

Latency range: 10-50 ms post-stimulus

Waveform peaks (named with P = positive, N = negative):

Peak	Approximate Latency	Generator
Po	~10 ms	Post-auricular muscle reflex (myogenic, can contaminate)
Na	~18-21 ms	Possibly thalamus (medial geniculate body)
Pa	~25-35 ms	Primary auditory cortex (measured over temporal lobe); subcortical generators also contribute (measured with midline electrode)
Nb	~40 ms	After Pa
Pb (P1)	~50-60 ms	Secondary auditory cortex; marker of auditory cortical maturation

Key characteristics:

Most clinically difficult AEP to record
Affected by age, sedation level, and alertness/state
Primarily neurogenic (not myogenic as once thought, though myogenic potentials in the Na-Pa range can contaminate the signal)
The 40-Hz steady-state response falls within the MLR latency range

Clinical applications:

Evaluate auditory pathway above the brainstem (thalamocortical and primary auditory cortex)
Auditory Neuropathy Spectrum Disorder evaluation
Non-organic (functional) hearing loss
Lesion localization at thalamocortical level
Frequency-specific auditory sensitivity estimation at cortical level
Cochlear implant effectiveness assessment
Auditory Processing Disorder (APD) assessment
Binaural hearing and auditory language function research
Depth of anesthesia monitoring (MLR suppressed at deeper levels)
Pb/P1 is an important cortical maturation biomarker - used to monitor auditory development in cochlear implant children

4. Long Latency Response (LLR) / Cortical Auditory Evoked Potential (CAEP)

Synonyms: Cortical Electric Response Audiometry (CER/CERA), Auditory Late Response (ALR), N1-P2 complex

Latency range: 50-300 ms

Waveform peaks:

Peak	Approximate Latency	Generator
P1	~50-80 ms	Secondary auditory cortex; maturation marker in children
N1 (N100)	~90-110 ms	Superior temporal gyrus (primary + secondary auditory cortex); most prominent peak in adults
P2	~150-200 ms	Primary or secondary auditory cortex
N2	~200 ms	Frontal cortex; transitions into MMN/P300 territory

Key characteristics:

N1 is the dominant, most reliable peak in awake adults
Greatly affected by subject state: best recorded when patient is awake and attentive
Significant developmental effect: P1 is the dominant peak in infants/young children; the adult N1-P2 morphology emerges with maturation
P1 cortical AEP biomarker: Used specifically in children to monitor efficacy of hearing aids or cochlear implants and to document auditory deprivation effects
The N1 component has predictive value for awakening from coma

Important developmental note: In cochlear implant recipients, studies show that 96% of early-implanted children have normal latency of the post-implantation cortical AEP (P1) compared with only 5% of late-implanted children, reflecting neural plasticity.

Clinical applications:

Threshold estimation in cooperative adults (CERA)
Auditory Processing Disorder
Hearing aid / cochlear implant benefit verification
Monitoring auditory cortex maturation
Coma prognosis (N1/N100)
Cortical hearing loss assessment

5. Mismatch Negativity (MMN)

Latency: ~100-200 ms post-deviant stimulus (obtained by subtracting ERP to standard from ERP to deviant)

Nature: Endogenous, automatic, pre-attentive response

Paradigm: An "oddball" paradigm in which a repetitive standard stimulus is occasionally and randomly interrupted by a deviant stimulus that differs in pitch, duration, intensity, or other acoustic feature. The subject's attention is deliberately directed away (passive task - reading, watching TV).

Generator: Primarily in the superior temporal plane (supratemporal plane of primary auditory cortex, Heschl's gyrus) and prefrontal cortex.

Key characteristics:

Does NOT require active attention (unlike P300) - reflects automatic auditory change detection
Sensitive to virtually any feature of an acoustic stimulus: frequency, duration, intensity, phonemic contrast, rhythmic patterns
Matures by approximately age 5-6 (definitely by age 11)
Decreases with aging
Decreases with sleepiness; can be recorded during stage 2 sleep and REM
Difficult to obtain in infants and young children
High intrasubject variability
Sensitive to sensorineural hearing loss (low-frequency stimuli most affected)

Clinical applications:

Speech perception and phonemic discrimination assessment
Auditory Processing Disorder
Central auditory organization and cortical plasticity monitoring
Monitoring auditory training effectiveness
Schizophrenia biomarker: MMN amplitude is reduced in schizophrenia; longitudinal reduction correlates with progressive Heschl's gyrus gray matter loss
Dyslexia: reduced MMN to rapid speech transitions
Coma prognosis: MMN and N100 have predictive value for awakening after anoxic injury
Depression, alcoholism, dementia research

Difference from P300: MMN does not require attention; P300 requires active task participation. MMN is mainly acoustic; P300 can be elicited by visual stimuli too.

6. Auditory Steady-State Response (ASSR)

Synonyms: Auditory Steady-State Evoked Potential (ASSEP), 40-Hz response (at 40/s modulation rate), Amplitude-Modulating Following Response (AMFR), Envelope Following Response (EFR), Frequency-Following Response (FFR)

What it is: An evoked neural potential that follows the envelope of a continuously modulated stimulus. Unlike the ABR (which uses transient stimuli), ASSR uses a continuous steady-state tonal stimulus that is amplitude-modulated (AM) or both amplitude- and frequency-modulated (AM+FM) at a specific rate.

Principle: A pure tone carrier frequency (CF: 500, 1000, 2000, 4000 Hz) is modulated at a specific rate. The neural response follows the modulation envelope, producing brain electrical activity at the modulation frequency. For example, a 1000 Hz tone modulated at 90 Hz/sec produces an ASSR measurable at 90 Hz in the EEG spectrum.

Modulation rates and generators:

~80-100 Hz: Brainstem generators; not affected by sleep/sedation - preferred in infants and sleeping patients
~40 Hz: Cortical generators (primary auditory cortex); affected by sleep and sedation - better in awake cooperative adults

Detection: Automated statistical analysis (phase coherence, F-test in the frequency domain) rather than visual peak identification - making it fully objective.

Advantages over ABR:

Frequency-specific at 500, 1000, 2000, and 4000 Hz simultaneously
Can estimate severe-to-profound hearing losses (ABR cannot reliably estimate thresholds beyond ~90 dB nHL)
Automated analysis - objective for both examiner and subject
Multiple frequencies tested simultaneously, reducing test time
Better for fitting hearing aids in difficult-to-test populations

Disadvantages:

Requires quiet patient state (sleep or sedation for 80 Hz; sedation impairs 40 Hz)
Possible artifactual responses
Limited anatomical site information
Problematic with bone conduction (masking required)
Questionable results near normal threshold levels - may overestimate actual thresholds
Cannot distinguish profound hearing loss from auditory neuropathy
Normative data still limited for some populations

Clinical applications:

Threshold estimation in infants (combined with tone-burst ABR)
Severe/profound hearing loss assessment
Pre-fitting assessment for hearing aids and cochlear implant candidacy
Difficult-to-test populations

7. Cervical Vestibular Evoked Myogenic Potential (c-VEMP)

What it is: A myogenic (muscle) response, not a neural potential per se - but evoked by sound and mediated through the vestibular system. It is an inhibitory response recorded from the tonically contracted sternocleidomastoid muscle (SCM).

Anatomical pathway (vestibulo-collic reflex): Acoustic stimulus → Saccular macula (responds to high-intensity sound) → Afferent inferior vestibular nerve → Brainstem vestibular nuclei → Medial vestibulospinal tract (uncrossed) → Motoneurons of ipsilateral SCM

Waveform: Early positive-negative complex

P13 (P1): Positive peak ~13 ms - first peak; amplitude-based analysis is key
N23 (N1): Negative peak ~23 ms

Recording requirements:

Patient must maintain tonic SCM contraction (turning head away from stimulus, or elevating head while supine) - because c-VEMP is a brief inhibition of tonic EMG activity
EMG feedback (visual or auditory) helps maintain consistent contraction level
Amplitude is normalized to the background EMG level
Stimuli: Clicks or tone bursts at 500-1000 Hz, high intensity (85-95 dB nHL normally needed)

Key parameters:

Threshold, amplitude, asymmetry ratio (normal 0-40%)
Latency (P13, N23)

Clinical applications and pathological findings:

Condition	c-VEMP Finding
Meniere's disease	Absent, reduced, or enhanced amplitude; more prominent during attacks
Superior Canal Dehiscence (SCD)	Abnormally low threshold (<65 dB nHL); enhanced amplitude; presence of response despite air-bone gap
Vestibular neuritis	Absent or reduced amplitude; may recover over 6 months-2 years
Acoustic neuroma / Vestibular schwannoma	Absent or reduced (inferior vestibular nerve involvement)
Multiple sclerosis / Brainstem stroke	Absent or delayed latencies
Conductive hearing loss	Can obliterate response (intact middle ear required)
Sensorineural hearing loss	Little or no effect on c-VEMP
Bilateral vestibular loss	Absent bilaterally
Otosclerosis	Expected absent (abnormal middle ear)
Migraine	Absent, reduced, delayed, usually unilateral
Benign paroxysmal positional vertigo (BPPV)	Usually normal

Advantage of c-VEMP over VEMP: Does not require active patient cooperation in the same way - useful in elderly, frail, or patients with cervical disease (though some cooperation still needed). ECochG is considered more objective because it requires no active patient participation at all.

Post-surgical c-VEMP: After superior vestibular nerve schwannoma resection - c-VEMP should be present bilaterally if inferior vestibular nerve is intact (useful confirmation).

8. Ocular Vestibular Evoked Myogenic Potential (o-VEMP)

What it is: A myogenic response recorded from the extraocular muscles (inferior oblique/inferior rectus), evoked by sound or vibration. Reflects the vestibulo-ocular reflex.

Anatomical pathway (contested, current evidence): Acoustic stimulus → Utricular macula (primarily) → Superior vestibular nerve → Brainstem → Medial longitudinal fasciculus (crossed pathway) → Contralateral extraocular muscles (inferior oblique)

Key distinction from c-VEMP: o-VEMP is generated by a crossed pathway (contralateral to stimulated ear), while c-VEMP is ipsilateral (uncrossed). o-VEMP primarily tests the utricle and superior vestibular nerve; c-VEMP tests the saccule and inferior vestibular nerve.

Recording: Surface electrodes below the eyes; patient must direct gaze upward (elevate eyes ~20-30°) to pre-activate the inferior oblique muscle.

Waveform: N10-P16 complex (N1 approximately 10 ms, P1 approximately 16 ms)

Clinical applications:

Only test currently available that specifically tests utricular function
Superior canal dehiscence: Enhanced o-VEMP responses
Vestibular schwannoma: If arising from superior vestibular nerve - absent contralateral o-VEMP is expected post-resection
Meniere's disease
Vestibular neuritis
Multiple sclerosis

Pattern interpretation (combined c-VEMP + o-VEMP + calorics):

Normal calorics + Normal c-VEMP + Abnormal o-VEMP = Utricular impairment
Abnormal c-VEMP + Normal calorics + Normal o-VEMP = Saccular impairment
This battery allows superior vs. inferior vestibular nerve differentiation

9. P300 (P3)

Classification: Event-Related Potential (ERP), Endogenous, Long-latency, Cognitive

Latency: ~300 ms (range 250-500 ms; increases with age)

Paradigm - "Oddball paradigm": A series of frequent standard stimuli is randomly interrupted by infrequent target (deviant) stimuli. The subject must actively attend and respond to (count, button-press) the rare target. The P300 reflects the brain's response to detecting the rare, expected target.

Two subcomponents:

P3a (Novelty P3): ~250-280 ms; frontally maximal; generated by novel, unexpected stimuli regardless of task relevance; reflects involuntary attention switching
P3b (Task P3): ~300-400 ms; parietally maximal; the classical P300 reflecting active target detection, working memory update, and cognitive processing

Generator: Distributed network - auditory regions of the hippocampus (medial temporal lobe), frontal cortex, parietal cortex. Multiple generators contribute.

Key characteristics:

Endogenous - depends on subject's attention, cognitive state, task demands
Amplitude decreases and latency increases with age (latency increases ~1-2 ms per year after age 25)
Latency reflects the speed of cognitive processing (information evaluation time)
Can be elicited by auditory, visual, or somatosensory stimuli
Robust and stable within individuals across sessions

Clinical applications:

Cognitive aging and age-related decline in central processing
Alzheimer's disease and dementia (prolonged latency, reduced amplitude)
Schizophrenia (reduced amplitude, especially P3b)
ADHD
Coma assessment and prognosis
Brain-Computer Interface (BCI) applications
Intraoperative depth of anesthesia monitoring
Sleep research

10. N200 (N2)

Classification: ERP, late endogenous component

Latency: ~200-350 ms

What it reflects: Target detection, cognitive conflict, and stimulus discrimination. The N200 is often seen as a transition between the automatic MMN/N1 response and the later cognitive P300 response.

Subcomponents:

N2a: Overlaps with MMN; related to automatic mismatch detection (pre-attentive)
N2b: Attention-dependent; peaks ~200-300 ms; reflects conscious discrimination and target identification - often precedes P300
N2c: Related to stimulus categorization

Relationship to P300: N2 and P300 often occur as an N2-P3 complex in oddball tasks. The N2 reflects the detection/discrimination process, while P300 reflects the subsequent cognitive updating.

Clinical relevance:

Language processing disorders
Attention disorders (ADHD)
Age-related cognitive decline
Schizophrenia

11. N400

Classification: ERP, late cognitive component

Latency: ~400 ms

Discovery: First described by Marta Kutas and Steven Hillyard (1980) during reading of semantically incongruous sentence endings.

What it reflects: Semantic processing - specifically, the brain's response to semantic incongruity or the difficulty of integrating a word/concept into the current semantic context. It occurs whenever a word or meaningful stimulus is semantically unexpected or unusual in context.

Examples:

"He spread the warm bread with socks" - elicits large N400 (semantic violation)
"He spread the warm bread with butter" - small or absent N400 (semantically congruent)

Generator: Broadly distributed; temporal-parietal regions (superior temporal sulcus), hippocampus, left frontal regions

Key characteristics:

Amplitude is inversely correlated with semantic fit (larger N400 = less expected word)
Sensitive to context, word frequency, and prior probability
Present for words in sentences, pictures, faces, and even non-linguistic stimuli if learned associations exist

Clinical and research applications:

Language comprehension disorders (aphasia)
Autism Spectrum Disorder (atypical social semantic processing)
Schizophrenia (abnormal semantic processing)
Alzheimer's disease
Assessment of awareness in disorders of consciousness / coma
Language development in children
Second-language acquisition research

12. P600 (Syntactic Positive Shift, SPS)

Classification: ERP, late cognitive component

Latency: ~500-800 ms (peak ~600 ms)

What it reflects: Syntactic processing - specifically, the brain's response to grammatical/syntactic violations or ambiguities in language. It reflects the processes of syntactic reanalysis and repair when the brain detects an ungrammatical sentence structure.

Examples:

"The cat that the dog chased runned away" - grammatical violation (runned vs. ran) elicits P600
Syntactically complex but correct sentences can also elicit P600 (reflecting increased processing load)

Generator: Left perisylvian language regions, parieto-occipital regions

Key characteristics:

Complementary to N400: N400 = semantic violation; P600 = syntactic violation
Can follow a preceding ELAN (Early Left Anterior Negativity) which occurs ~100-200 ms and reflects initial syntactic structure building
Increased P600 amplitude with degree of syntactic complexity or degree of violation
Present across modalities (auditory, visual, sign language)

Clinical and research applications:

Language processing disorders
Agrammatic aphasia
Specific Language Impairment (SLI)
Schizophrenia (syntactic processing abnormalities)
Language acquisition research

Additional AEPs Not Listed (But Clinically/Scientifically Relevant)

13. Acoustic Change Complex (ACC)

A cortical response elicited by a change in an ongoing acoustic stimulus (rather than at stimulus onset). Tests the auditory system's ability to detect within-stimulus changes - relevant for speech perception assessment and hearing aid/cochlear implant benefit monitoring.

14. P50 (Sensory Gating / Pb)

Latency: ~50 ms (same as Pb in MLR)
Reflects sensory gating - the brain's suppression of repeated stimuli (paired-click paradigm: S1-S2). Normal: S2 P50 < 50% of S1 P50.
Reduced gating (high S2/S1 ratio) is a marker in schizophrenia and other psychiatric conditions.
Also a maturation marker in cochlear implant children.

15. N100 (N1) - Standalone Significance

As a standalone ERP, the N1 (100 ms) has been studied as a predictor of awakening from coma after anoxic brain injury (alongside MMN).

16. Contingent Negative Variation (CNV)

Latency: Slow negative shift ~800 ms
Reflects expectancy and motor preparation between a warning and an imperative stimulus
Used in cognitive neuroscience and psychiatric research

17. 40-Hz Steady-State Response

A special case of ASSR using ~40 Hz modulation rate. Primarily a cortical response. High amplitude, frequency-specific. Used for hearing threshold estimation in awake adults and depth of anesthesia monitoring. More susceptible to sleep and sedation than the 80 Hz ASSR.

18. Frequency-Following Response (FFR) / Subcortical Auditory Evoked Potential

Reflects phase-locked neural activity in the auditory brainstem (inferior colliculus) to the fine structure of continuous periodic sounds, especially speech sounds
Used to study auditory-to-cognitive linkages, noise-induced hearing changes, and language/music experience effects on neural encoding

Quick Reference: Summary Table

Test	Latency	Generator	Stimulus	Requires Attention?	Key Clinical Use
ECochG	0-5 ms	Cochlea, distal CN VIII	Click/tone burst	No	Meniere's disease, SSCD, ANSD
ABR	1-10 ms	CN VIII to lateral lemniscus	Click/tone burst	No	Hearing threshold, schwannoma, ANSD, IOM
MLR	10-50 ms	Thalamus, primary auditory cortex	Click/tone burst	No (light sedation OK)	APD, thalamocortical lesions, cochlear implant
LLR (N1-P2)	50-300 ms	Primary/secondary auditory cortex	Any	Awake preferred	CERA, hearing aid benefit, cortical maturation
ASSR	80-100 Hz SS	Brainstem (80 Hz) / Cortex (40 Hz)	AM/FM pure tones	No (sleep OK for 80 Hz)	Frequency-specific thresholds, profound loss
c-VEMP	13-23 ms	Saccule, inferior vestibular nerve, SCM	Click/tone burst	Requires SCM contraction	Meniere's, SCD, vestibular neuritis
o-VEMP	10-16 ms	Utricle, superior vestibular nerve	Click/tone burst	Requires eye elevation	Utricular disorders, SCD, CN VIII tumor
MMN	100-200 ms	Superior temporal + prefrontal cortex	Oddball (passive)	No	Speech discrimination, APD, schizophrenia
P300	250-500 ms	Hippocampus, frontal-parietal	Oddball (active)	Yes - active task	Cognitive aging, dementia, schizophrenia
N200	200-350 ms	Frontal-temporal cortex	Oddball	Yes	Discrimination, ADHD, cognition
N400	~400 ms	Temporal-parietal	Language/semantic	Yes	Semantic processing, aphasia, dementia
P600	500-800 ms	Perisylvian language	Language/syntactic	Yes	Syntactic processing, aphasia, SLI

Sources

Cummings Otolaryngology Head and Neck Surgery - Chapters 130, 134, 166
K.J. Lee's Essential Otolaryngology - Chapter 15: Electrical Response Audiometry
Scott-Brown's Otorhinolaryngology Head & Neck Surgery - Vols. 1 & 2
Shambaugh Surgery of the Ear - Auditory Evoked Potentials
Kaplan & Sadock's Comprehensive Textbook of Psychiatry - EEG, ERPs, Mismatch Negativity
Plum and Posner's Diagnosis and Treatment of Stupor and Coma - Electrophysiological Testing
Bradley and Daroff's Neurology in Clinical Practice - Evoked Potentials
University of Cape Town AEP Underlying Principles resource

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