Properties (15)
Id 95a5e9b3-7239-46ce-aee1-837b78b53743
Year 2025
Abstract
Cssclasses
- purpleRed
Aliases
- Multichannel auditory cortical responses in misophonia
- (Karupaiah et al., 2025)
Import Date 04-21-2026
Template Version Notes •corrected error in rendering the linked PDF in metadata section • added the tag “noted” to the definition of comments to ignore ( like with the “in another note” tag. this is so that when making notes on chapters of a textbook, i can still export things for manual addition to the obsidian note without having to keep track of what has already been added ). Also moved the version notes to the yaml section • this version added the bookmarks section to auto collect all bookmarks. it also dropped the template auto fill of the initial source field because we never got it working and just overwrote it manually anyway. this version also added logic to handle “in another note” tag. annotations marked with this are completely ignored. used when i have information covered in a bigger note, but still want to highlight that part in text for visual clarity (so as to avoid duplicates of the same information) • running the import more then once will overwrite the file, so do not import again if you have made changes in obsidian that are not in the zotero article.
Dv Authors Kamalakannan Karupaiah, Rakesh Trinesh, Ajith Kumar Uppunda, Prashanth Prabhu,
Dv Initial Source Misophonia MOC
Dv Status #status/reviewed
Dv Limitations • All-female sample limits generalizability. • No formal diagnostic criteria for misophonia; group assignment based solely on questionnaire cutoffs. • Non-trigger stimulus (/da/) precludes conclusions about trigger-specific vs. generalized auditory differences. • Small sample (n = 15 per group). • No severity subgroup analysis (all misophonia participants fell in mild–moderate range). • Cannot determine whether electrophysiological differences are predisposing or acquired.
Dv Future Directions • Replicate with trigger-specific stimuli (chewing, swallowing, lip-smacking) to test generalizability of N1 findings. • Longitudinal and interventional studies examining whether ALLR markers change with treatment. • Studies across misophonia severity levels. • Source localization and functional connectivity analyses to map cortical/subcortical networks. • Evaluate clinical utility of multichannel ALLR for diagnosis and treatment monitoring.
Dv Relevance • looked at differences in auditory late latency responses (ALLR) resposnes using 32 channel EEG , focusing on P2-N1-P2 peaks in Misophonics vs controls using a voiced consonant as a stimulus • findings showed earlier and reduced N1 amplitudes in the Misophonia group • results conflict with schroderDiminishedN1Auditory2014\(Schröder et al., 2014) who didn’t find any differences in N1 latency, though this may be due to methods differences • also found the Misophonia group to show a centro-parietal activation topography compared to the control groups fronto-central • proposes reduced N1 amplitude as a possible biomarker for Misophonia
Zotero Note Link Generated true
Checked For Zettle Notes true
•
Multichannel auditory cortical responses in misophonia: A neurophysiological investigation
Status:: #status/reviewed
Metadata
- Item Type: #journalArticle
- Authors:: Kamalakannan Karupaiah, Rakesh Trinesh, Ajith Kumar Uppunda, Prashanth Prabhu,
- Date Added: January 25, 2026
- URL: https://linkinghub.elsevier.com/retrieve/pii/S037859552500276X
- DOI: 10.1016/j.heares.2025.109458
- Cite Key: karupaiahMultichannelAuditoryCortical2025
- Tags: #Misophonia, #EEG, #ALLR, #auditory-long-latency-resposne, #cortical-auditory-processing
- PDF Attachments
Abstract
| Background/Purpose | Background- • Misophonia defined by intense emotional/physiological responses to specific auditory triggers; neurophysiological basis remains unclear. • fMRI studies show heightened activation in amygdala, anterior insula, auditory cortex, and ACC in misophonia. • Prior EEG work (Schröder et al., 2014) reported reduced N1 amplitude using pure tones; proposed as neurophysiological biomarker. • MMN reductions also documented, suggesting altered pre-attentive processing (Schröder et al., 2013; Patro et al., 2025). • Aryal & Prabhu (2023) found earlier P1/N1 latencies and reduced P1-N1 amplitudes using tone burst stimuli. • Multichannel EEG provides spatial distribution of neural generators with high temporal resolution, enabling topographic analysis not available in single-channel paradigms. • Prior CAEP studies did not characterize scalp-wide spatiotemporal distribution; no multichannel ALLR study in misophonia existed. Purpose- • Investigate multichannel ALLR (P1-N1-P2) in individuals with and without misophonia using a non-trigger speech stimulus. • Compare peak latencies and amplitudes at midline sites (Fz, Cz, Pz). • Characterize scalp-wide spatiotemporal distribution differences between groups. • Identify potential electrophysiological markers for diagnosis and treatment monitoring. |
| Participants/samples | • N = 30 female participants; ages 18–30. • Misophonia group: n = 15; MisoQuest ≥61, RAMISO-S ≥11 (mild–moderate severity range). • Control group: n = 15; MisoQuest ≤16, RAMISO-S 0–10 (subclinical). • All-female sample; not a priori restriction, outcome of recruitment. • Exclusion: tinnitus, hyperacusis, phonophobia, hearing loss, otological disorders, ototoxic medication, noise exposure. • Normal peripheral hearing confirmed via PTA, tympanometry, DPOAEs. |
| Measures | • MisoQuest (presence of misophonia) • RAMISO-S (severity of misophonia) • Tinnitus Handicap Inventory, Modified Khalfa Hyperacusis Questionnaire, DSTS-S (exclusion screening) • 32-channel EEG (Quik-Cap Neo Net, Grael amplifier; Compumedics); 10–20 system; referenced to right mastoid • ALLR peak latency and amplitude at Fz, Cz, Pz for P1, N1, P2 • Scalp topography via cluster-based permutation testing (BESA Statistics v2.1) |
| Procedures | • Passive listening paradigm; participants watched silent closed-captioned video to maintain alertness. • Stimulus: voiced alveolar stop /da/, 130 ms duration, 80 dB SPL, ISI 2000 ms; 200 sweeps. • Stimulus confirmed not to overlap with any participant's personal misophonic triggers. • EEG: 0.1–100 Hz online bandpass, 1024 Hz sampling; offline processed in BESA (0.1 HP, 30 Hz LP). • Artifact rejection: ocular correction via BESA algorithm; epoch threshold ±100 µV; spherical spline interpolation for ≤2 bad channels. • Waveform analysis: M1-M2 average reference; spatiotemporal analysis: average reference. • Epochs: −100 to 500 ms; peak identification automated then manually verified by two experts. • Statistics: independent samples t-tests (two-tailed); Bonferroni-Holm correction for amplitude comparisons; Shapiro-Wilk normality confirmed. |
| Results | • Misophonia group showed earlier latencies across all P1-N1-P2 peaks at all three electrode sites (Fz, Cz, Pz); large effect sizes throughout. • N1 amplitude was significantly reduced in the misophonia group at all three electrode sites; P1 and P2 amplitudes did not differ significantly between groups. • Scalp topography differed significantly between groups in a ~198–254 ms window, primarily over Fz, FPz, Cz, CPz. • At N1 peak: misophonia group showed centro-parietal distribution; controls showed fronto-central distribution. • At P2 peak: misophonia group showed frontal distribution; controls showed central distribution. • Butterfly plots confirmed earlier latency and reduced N1 amplitude in misophonia grand average waveforms. |
| Discussion/Limits | Conclusion- • The authors conclude that earlier P1-N1-P2 latencies indicate faster neural transmission or heightened neuronal excitability at generators of the P1-N1-P2 complex (superior temporal gyrus, primary auditory cortex, subcortical regions). • The findings indicate earlier latencies may reflect overactive auditory-limbic pathways consistent with anterior insula hyperactivity documented in neuroimaging studies. • The authors conclude it remains equally plausible that accelerated processing is a consequence of misophonia rather than a predisposing cause, consistent with neuroplastic changes from repeated emotional reactivity. • The data support reduced N1 amplitude as a candidate neurophysiological biomarker of misophonia, replicating Schröder et al. (2014) with a speech stimulus. • The findings indicate altered spatial distribution of auditory cortical responses (centro-parietal vs. fronto-central), suggesting atypical spatial organization of auditory processing. • The authors conclude the observed patterns may reflect auditory-limbic dysregulation consistent with anterior insula and emotion-network hyperactivity. • The findings indicate that using non-trigger stimuli reveals fundamental cortical processing differences independent of emotional reactivity. |
| Limitations:: | • All-female sample limits generalizability. • No formal diagnostic criteria for misophonia; group assignment based solely on questionnaire cutoffs. • Non-trigger stimulus (/da/) precludes conclusions about trigger-specific vs. generalized auditory differences. • Small sample (n = 15 per group). • No severity subgroup analysis (all misophonia participants fell in mild–moderate range). • Cannot determine whether electrophysiological differences are predisposing or acquired. |
| Future Directions:: | • Replicate with trigger-specific stimuli (chewing, swallowing, lip-smacking) to test generalizability of N1 findings. • Longitudinal and interventional studies examining whether ALLR markers change with treatment. • Studies across misophonia severity levels. • Source localization and functional connectivity analyses to map cortical/subcortical networks. • Evaluate clinical utility of multichannel ALLR for diagnosis and treatment monitoring. |
| Relevance:: | • looked at differences in auditory late latency responses (ALLR) resposnes using 32 channel EEG , focusing on P2-N1-P2 peaks in Misophonics vs controls using a voiced consonant as a stimulus • findings showed earlier and reduced N1 amplitudes in the Misophonia group • results conflict with (Schröder et al., 2014) who didn’t find any differences in N1 latency, though this may be due to methods differences • also found the Misophonia group to show a centro-parietal activation topography compared to the control groups fronto-central • proposes reduced N1 amplitude as a possible biomarker for Misophonia |
Notes
key terms and concepts
Auditory Late Latency Response (ALLR) – cortical auditory evoked potential comprising P1-N1-P2 peaks reflecting early cortical auditory processing and attentional mechanisms; recorded ~50–250 ms post-stimulus onset.
N1 component – prominent negative peak within ALLR associated with attention allocation to auditory stimuli; proposed neurophysiological biomarker of misophonia.
Scalp topography – spatial distribution of electrical potentials across the scalp reflecting underlying neural generator patterns; analyzed via cluster-based permutation testing.
Sensory gating – neural inhibitory mechanism reducing cortical responses to redundant or irrelevant stimuli; impairment implicated in misophonic hyperreactivity.
Cluster-based permutation testing – nonparametric statistical method controlling family-wise error rate across electrode-time comparisons; 2000 permutations used.
MisoQuest – 14-item self-report questionnaire for presence of misophonia; scores ≥61 indicate misophonia.
RAMISO-S – Revised Amsterdam Misophonia Scale; quantifies misophonia severity (0–10 subclinical; 11–20 mild; 21–30 moderate; 31–40 severe).
my engagement notes
my questions
my comments
Bookmarks
reading notes
contextual statement
In a 2025 study, Karupaiah et al. investigated multichannel auditory late latency responses (ALLR) in misophonia by comparing P1-N1-P2 peak latencies, amplitudes, and scalp topographies between 15 misophonic and 15 control adult females using a 32-channel EEG passive listening paradigm with a non-trigger speech stimulus (/da/).
summary statement
In a 2025 study, Karupaiah et al. examined auditory cortical processing in misophonia by recording multichannel ALLR to a non-trigger speech syllable in matched misophonia and control groups. They found that individuals with misophonia showed earlier latencies across all P1-N1-P2 peaks, selectively reduced N1 amplitudes, and distinct centro-parietal (vs. fronto-central) scalp topographies compared to controls. From this they concluded that misophonia involves generalized alterations in early auditory cortical processing and spatial generator organization, with reduced N1 amplitude proposed as a candidate neurophysiological biomarker, though whether these differences are predisposing or acquired remains unresolved.
Zettelkasten
contrasting findings from Schroder 2014
Idea of observed processing differences being a result of rather then cause of Misophonia
topographical and spatiotemporal differences in Misophonia