{"paper_id":"041daf13-b4e7-4738-b889-cb36aefa273e","body_text":"1\n2\n3\n4 EEG correlates of auditory rise time processing: A systematic review\n5\n6\n7 Victoria Manasevich1¶*, Daria Kostanian1¶, Anton Rogachev1 and Olga Sysoeva1,2,3\n8\n9\n10\n11\n12\n13 1 Center for Cognitive Sciences, Sirius University of Science and Technology, Sirius, Russia\n14 2 Institute of Higher Nervous Activity and Neurophysiology, RAS, Moscow, Russia\n15 3 Faculty of Biology and Biotechnology, HSE University, Moscow, Russia\n16\n17\n18\n19\n20 * Corresponding author \n21 E-mail: victoria.manasevich@gmail.com (VM)\n22\n23 ¶ These authors contributed equally to this work.\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n1\n24 Abstract\n25 Rise time (RT) is considered to be one of the most significant acoustical characteristics \n26 of auditory speech stimuli. A substantial amount of data has been accumulated on the \n27 neurophysiological mechanisms of RT processing under different conditions and in different \n28 groups of people, but these data have not been systematised. This review focuses on studies \n29 that have investigated electroencephalographic (EEG) markers of RT sensitivity. The present \n30 literature search was conducted according to the PRISMA statement in PubMed, Web of \n31 Science and APA PsychInfo databases. The resultant review comprised 37 studies that \n32 considered diverse aspects of RT processing. The review describes the main stimulation \n33 parameters affecting electrophysiological markers of RT processing reflected in different \n34 components of event-related potentials, brainstem responses and cortical rhythmic activity. The \n35 main finding of this review is that the rise time prolongation leads to a decrease in the amplitude \n36 of the main ERP components and an increase in their latencies. However, the sensitivity of the \n37 EEG markers varied with the earliest components tracking the subtle difference (few tens of \n38 microseconds), while the later components coding the larger one (up to 500 ms). Nevertheless, \n39 the observed effects may vary and depend on some aspects of the experimental paradigm, age \n40 of participants and speech-related problems. Future research may benefit by addressing \n41 understudied clinical groups and ERP components such as P1 and N2, dominated in children.\n42\n43 Introduction\n44 The ability to process the acoustical characteristics of auditory speech stimuli is an \n45 important predictor of speech development. Disturbances in phonological processing may be \n46 one of the factors contributing to the development of different speech disorders – i.e., specific \n47 learning difficulty that impacts reading and spelling [1,2]. One of the most important acoustical \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n2\n48 characteristics of auditory speech stimulus is auditory rise time (or rise time, RT). RT \n49 physically represents the rates at which amplitude or frequency modulations in the speech \n50 signal increase. \n51 The amplitude envelope of a sound describes the variation of its amplitude over time. \n52 In terms of perception, shorter amplitude rise time can create a more abrupt and percussive \n53 sound, while a longer RT can produce a smoother and more gradual onset, often perceived as \n54 softer or more mellow [3]. Very short RTs (<10ms), for example, produce spectral splatter, \n55 which is often perceived as a click. Formant RT refers to the duration it takes for the formant \n56 frequencies to reach their peak amplitudes after the onset of a vowel sound. The RT of formants \n57 can significantly affect speech perception. Formant RT plays a key role in distinguishing \n58 between different speech sounds, especially consonants that differ in the way or place of \n59 articulation. For example, it helps listeners distinguish between pairs of sounds such as /ba/ and \n60 /wa/, where changes in formant frequencies occur at different rates [4] \n61 Psychophysical studies of RT sensitivity provide a framework for assessing the \n62 contribution of phonological processing to speech and language development. The difference \n63 threshold (i.e., the minimal changes in RT at which stimuli are perceived as different) is used \n64 to estimate a measure of RT sensitivity. Individual differences in the ability to discriminate RT \n65 may affect the accuracy of linguistic representations, which may be related to individual \n66 variation in speech performance. Children with dyslexia have demonstrated less sensitivity to \n67 amplitude RT of auditory stimuli than their control group peers [1]. Also, sensitivity to RT in \n68 infancy may act as a predictor of vocabulary development in older age [5].\n69 At the neurophysiological level, sensitivity to RT can be reflected in the event-related \n70 potentials (ERP) components changes. ERP is a commonly used technique for studying brain \n71 responses to stimuli registered with electroencephalogram (EEG). Different ERP components \n72 elicited at specific time intervals reflect stages of neurophysiological processing of the stimulus.\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n3\n73 Both amplitude and formant RTs are crucial for understanding how we perceive sounds \n74 and speech. The scientific community has made efforts to generalize some aspects of existing \n75 knowledge on RT, yet currently, there is no review that encompasses the mechanisms of RT \n76 perception and their reflection in the brain, including both brainstem reactions to short RTs and \n77 later cortical responses. А large amount of data has been accumulated on the \n78 neurophysiological effects of RT in different groups of people using different methods (ERP, \n79 analysis of rhythmic brain activity etc.), but these data are to some degree inconsistent. This \n80 inconsistency and the potential role of neurophysiological processing of RT as a possible \n81 predictor and marker of speech disorders, creates a need to systematize the empirical data \n82 presented in the literature. The aim of this systematic review is to consider evidence of EEG \n83 characteristics as markers of sensitivity to RT changes. To provide the most wide-ranging view \n84 of the available evidence, this review includes studies considering the neurophysiologic \n85 correlates of changes in RT in typically developing children and adults, as well as in groups \n86 with different speech disorders, using various approaches to analyze EEG data.\n87\n88 Methods\n89 This review followed the methodological framework for systematic reviews. To ensure \n90 transparent and complete reporting, we adhered to the PRISMA 2020 guidelines. The PRISMA \n91 2020 checklist has been completed and is available as supplementary material, and the \n92 PRISMA flow diagram (Figure 1) illustrates the study selection process. While a formal review \n93 protocol was not previously registered or published, the search strategy, inclusion criteria, and \n94 data extraction forms were developed a priori and piloted by the research team to minimize \n95 bias.\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n4\n96 Search strategy\n97 We conducted a literature search of the PubMed, Web of Science and APA PsycInfo \n98 databases. The search queries used was “(\"Rise time\"[All Fields] AND (\"evoked \n99 potentials\"[All Fields] OR \"erp\"[All Fields] OR \"evoked response\"[All Fields] OR \"aep\"[All \n100 Fields] OR \"auditory evoked response\"[All Fields] OR \"eeg\"[All Fields] OR \n101 \"electrophysiological\"[All Fields])) AND (\"humans\"[Terms] AND \"english\"[Language]))”. \n102 Identified articles were published prior to January 25, 2024. On February 15, 2026, an updated \n103 search was performed using the same search strategies and databases as the original search. The \n104 search was limited to the period from January 24, 2024, to February 15, 2026, using filters \n105 based on entry date. The updated search did not identify any new studies that met the inclusion \n106 criteria.\n107\n108 Eligibility criteria \n109 Only empirical human studies published in the English language in peer-reviewed \n110 journals were included in the review. Articles were retained if they measured any ERPs or other \n111 EEG data in response to auditory stimuli with varied amplitude/formant RT. Studies were \n112 excluded if they contained only one RT condition with no variation. \n113 All titles and abstracts identified in the search were double blind screened by two \n114 independent experts using SRDR plus platform (https://srdrplus.ahrq.gov) to exclude obviously \n115 irrelevant articles. Any disagreements were resolved through discussion with the involvement \n116 of a third expert. The records that passed the initial screening were evaluated using their full-\n117 text versions. As in abstract screening, two independent decisions were made for each of the \n118 screened items. In case of disagreement, the final decision was made after discussion with the \n119 involvement of a third expert. The remaining articles were included in the review.\n120\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n5\n121 Data extraction \n122 The following data were extracted onto a custom sheet, which included information \n123 about sample (participant groups, sample size, mean age or age range), experimental paradigm \n124 (oddball, block design or other), stimuli information (stimulus type, RT conditions, technical \n125 parameters of presentation), additional assessments used in the study (e.g. reading skills \n126 assessment or additional deviant condition in oddball study) and results (reported as EEG \n127 parameters changes with RT increasing, or observed MMN in response to RT deviants). The \n128 extracted data is provided in Table 1.\n129 The risk of bias of the included studies was assessed according to the OHAT risk of \n130 bias tool [6]. Risk of bias evaluation included 3 sections with several questions inside them: the \n131 selection bias, the detection bias, and the “other sources of bias” sections. A table with the \n132 results of risk of bias evaluation is provided in the supplementary materials section \n133 (Supplementary Material 1).\n134 Results\n135 A total of 281 articles were identified from all of the used databases after duplicates \n136 removal. After abstract and full text screening, 37 articles remained and were included in the \n137 review. A flowchart of this selection process is displayed in Fig 1. Summary details for the \n138 reviewed studies are presented in Table 1. An updated search conducted on February 15, 2026, \n139 identified 13 new records. Titles and abstracts were screened. None of these records met the \n140 inclusion criteria for further review (all 13 records were excluded at the title/abstract screening \n141 stage, either as irrelevant or as not meeting the inclusion criteria). Therefore, the number of \n142 studies included in the review remained unchanged (n=37). The flowchart has been updated \n143 accordingly.\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n6\n144 Table 1. Summary details of included studies. The studies are divided into groups according to the experimental paradigm used, and \n145 organized within each group in ascending order of year.\nStimuli\nStudy\nSample\nN (gender)\nMean Age \n(sd)\n[Age range], \nyears\nParadig\nm Stimuli type RT\nParameters of \npresentation\nStatistical \nmethods\nResults (in relation to RT \nincrease)\nTotal risk \nof bias \nscore\nCobb et al. \n(1978)\nN=7 (f:5)\nadults\nABR 1 kHz tones 0.01, 0.5, 1, 2.5, 5 \nms \nBinaurally\n20, 40, 60 dB SPL\nRate 10/s\nMean, SD\n60 dB:\nlat I–VII ↑;\n40 dB:\nlat  I–V ↑; lat VI–VII ↓ \nbetween 10 µs and 0.5 ms \nthan ↑ but ns\n6\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n7\nStapells & \nPicton \n(1981)\nN=11 (f:5)\n[22–30]\nABR\nExp 1–4:  0.5 kHz tones\nExp 5: 0.5, 1, 2, 4 kHz \ntones\nExp 6: +noise                                                                      \nplateau duration: 0.01ms\nFT=RT\nExp 1–4: \n5 ms\nExp 5–6: \n1, 2, 5, 8 ms\nMonaurally (left \near);\n115 dB SPL\nANOVA\namp V ↓\nlat V ↑ 7\nSuzuki & \nHoriuchi \n(1981)\nN=8 (f:8)\n[21–34]\nABR\n2 and 0.5 kHz series of \ntone pips\nFT=RT\n2kHZ: \n0.5, 1, 1.5, 2, 3, 5 \nms\n \n0.5 kHz:\n1, 2, 3, 4, 6, 10 ms  \nBinaurally, \nearphones\n15–50 dB nHL\nRate 13.3/s\nMean, SD\n2kHZ: \namp ns\nlat V ns on 50 dB nHL\nlat V ↓ on 30–40 dB nHL\n0.5kHz:\n amp V ↑\nlat V ↑\n8\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n8\nHecox & \nDeegan \n(1983)\nN=8 (f:8)\nExp 1: N=6\nExp 2: N=4 \n[21–27]\nABR\nNoise bursts;\nDurations 4 and 10 ms\nFT=RT\nExp1: \n0, 1, 2, 5 ms\nExp2: \n0, 2, 5 ms \nMonourally\n50 dB above \npersonal threshold \n(72dB white noise \nSPL)\nRate 31/s\nPairwise \ncomparison, \nregression \nanalysis\namp ns\nlat V ↑ 10\nSalt & \nThornton \n(1984)\n(N=8) ABR\nCondensation and \nrarefaction clicks 0.17–0.58 ms\nMonourally (left \near), 106dB SPL\nRate 9.1/s\nT-test amp depends on polarity\nlat I–VI ↑ \n7\nFolsom & \nAurich \n(1987)\ninfants: N=10,\n[11–13] \nweeks,\nadults: N=10\nABR\nGated noise bursts;\nplateau duration: 20ms\nFT=RT\n0.1, 2.5, 5 ms\nEarphones, 50 dB \nnHL\nRate 16/s\nANOVA\namp V ↓\n lat V ↑\n10\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n9\n[20–30] years\nGerull et \nal. (1987)\n(N=12)\n[25–45]\nABR\nCondensation and \nrarefaction clicks, single-\nslope stimuli\n0.1, 0.3, 1.0, 3.0 \nms\nEarphones, 80–120 \nSPL\nRate 12/s\nT-test\namp  V ↓ \nlat V ↑ 9\nBarth & \nBurkard \n(1993)\nN=10\nadults\nABR\nNoise bursts;\nDurations 5.0, 5.67, 6.66 \nand 8.33 s\n0, 0.5, 1.25, 2.5 \nms\nMonourally\n15 dB, 30 dB, 45 \ndB, 70 dB SPL\nLinear \nregression, \nrmANOVA\namp V ↓\nlat V ↑\n10\nVan \nCampen et \nal. (1996)\nN=40 (f:20)\nM=26, \n[20–30]\nABR\nTone bursts (0.5 and 2 \nkHz) \nDuration 10 ms\nFT=RT\n0.5, 1, 2.5, 5 ms\nMonourally\n103 dB peSPL \n(peak)\n87.5 dB peSPL \n(peak-to-peak)\nRate 6.3/s\nANOVA\nExp1 (RT 0.5 VS 1 ms):\namp onset and offset V  ↓\n(both 0.5 and 2 kHz)\n lat onset and offset V ↑\nExp2 (RT 0.5 VS 5 ms):\namp offset V ↓ for 2 kHz\n10\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n10\n(for 0.5 kHz ns)\n lat offset V ↑\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n11\nKodera et \nal. (1979)\nN=8\n[24-32]\nABR, \nERP \n1 kHz tone bursts; \nduration 43ms;\nFT=RT\n5, 10, 20 ms\nMonourally (right \near) \nheadphones\n 60 dB SPL for 5ms \nRT, for other \nequivalent db SPL\nRate 2/s\norder balanced \nwithin and between \nsubjects\nANOVA\namp ABR↓;\namp ABR-Na↓;\namp Na-Pa↓; \namp Pa-Nb↓;\namp P1-N1↓;\namp N1-P2: ns\nlat ABR↑;\nlat Na↑;\nlat Pa↑;\nlat  P1↑;\nlat  N1↑\nlat P2↑\n7\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n12\nSkinner & \nAntinoro \n(1971)\nN=20 (f:12)\n[18–24]\nERP\nExp1:\n1 kHz tone bursts;\nplateau duration: 10ms\nExp2:\n1 kHz tone burst;\ndurations at 0.01ms RT \ncondition: 0.2, 0.4, 10, \n20, 30, 40, and 50 ms;\ndurations at 5ms RT \ncondition: 1, 5, 10, 20, \nand 40 ms\nExp1: \n0.01, 0.5, 2.5, 5, \n10, 25 ms\nExp2: \n0.01 and 5 ms\nMonourally \n40 dB SPL\nNA\nExp1:\namp Na-Pa and Pa-Nb ↓;\namp P0-Na and Nb-Pb ↓ \nat 25ms RT condition, in \nother condition ns\nExp 2:\namp Na-Pa, \nPa-Nb,P0-Na ↓\n8\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n13\nOnishi and \nDavis \n(1968)\nN=7\nAdults\nERP\nExp1:\n1 kHz tone bursts;\nplateau durations: 0, 3, \n10, 30, 100, and 300 ms;\nFT=RT\nExp2: \n1 kHz tone bursts;\nplateau duration: 2.5 ms;\nFT=RT\nExp1: \n3 or 30 ms\nExp2: \n3, 10, 30, 50, 100, \nand 300 ms\nBinaurally\nEarphones, \nExp1:\nISI: 2500ms\n15–85 dB SPL \n(varied)\nExp2: \nISI: 5000ms\n45–85 dB SPL \n(varied)\nonly mean and \nsd\nExp1: \namp N1-P2 ↓ \nExp2: \namp N1-P2 ↓ (beyond \nabout 30 ms)\nlat N1 ↑\n6\nSkinner & \nJones \n(1968)\nN=40 (f:30)\n[18–24]\nERP\n1 kHz tone bursts; \nplateau duration: 75 ms \n10 μs, 5, 10, 25, \n50 ms\nEarphones, 30, 50, \n70, and 90 dB SPL \n*ISI: 3800ms\n random order\nonly means \ncomparison\namp P1-N2↓\nlat P1 ns\nlat N2 ns\n8\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n14\nElfner et \nal. (1976)\nExp1: \nN=7\n[18–22]\nExp2: N=12\n[19–27]\nERP\nExp1:\n1 kHz sinusoids\ndurations: 5000 ms;\noffset duration: 50 ms\nExp2:\n1 kHz sinusoids\ndurations: 1000, 3000, \nand 5000 ms (random \nbetween participants);\noffset duration: 50 ms\nExp1: \n0, 50, 150, 500, \n1500, 4960 ms\nExp2: \n50, 100, 300, 500, \n700, 1000 ms\nBinaurally\nearphones, 45 dB \nSPL\nExp1:\nISI: 10000 ms\nExp2:\nISI: 10000, 12000, \n14000 ms (random)\nRT conditions \nseparate in different \ntrials, trials order \nrandomized\nExp1: \nNA\nExp2: \nANOVA\nExp1: \namp N1-P2↓ from 50 to \n500, then ns\nExp2: \namp N1-P2 ns \n8\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n15\nZito (1978)\nN=10\nadults\nERP \nTone bursts (0.5, 1, 3 \nkHz);\nplateau duration: 200 ms\n5, 250, 500 ms\n70 dB SPL\nISI: 800 ms \nNA\nlat N1↑\nlat P2↑\n6\nPrasher \n(1980)\nN=15 (f:7)\nAdults\nERP\n1 kHz tone and white-\nnoise burst; \nduration: 500 ms;\nFT=RT\n0.02, 2.5 and 50 \nms\nMonourally (right \near) \nHeadphones, 80 and \n40 dB SPL\nRate 1/2000 ms\n*ISI: 1500 ms\nT-test\n2.5ms →50 ms\namp N1-P2↓ (for tone, but \nnot for noise);\nlat N1 ns;\n20μs →2.5 ms\namp N1P2 ns\n7\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n16\nPutnam & \nRoth \n(1990)\nN=16 (f:8)\nMean Age=22\n [18–30]\nERP\n1 kHz tones:\ndurations: 51, 55, 60 and \n65 ms (correspond to \neach RT condition);\nFT=RT\n3, 15, 30 and 45 \nms\nBinaurally\nHeadphones, 110 \ndBA SPL\nISI: 8400ms\ncontrolled \npermutation order\n2 runs of paradigm\nANOVA\namp N110 ↓ (only 1st run);\namp P190 ↓;\namp P300 ↓;\nSlow wave: ↓;\n10\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n17\nHämäläine\nn et al. \n(2007)\nTD\n N=20 (f:7)\nMean \nAge=9.3(±0.4\n1)\n[8.83–10.5]\nRD \nN=19 (f:10)\nMean \nAge=9.5 \n(±0.33)\n[8.83–10.5]\nERP \npairs of \ntones\nTones pairs \n1st tone composed of \nsinusoids (0.3, 0.6, 0.9, \nand 1.2 kHz)\n2nd tone in 5ms RT of \nsinusoids (0.75, 1.5, 2.25, \n3 kHz);\n in 80ms RT of sinusoids \n(0.5, 1, 1.5, and 2 kHz);\n1st tone duration: 100ms; \n2nd tone duration: \n150ms;\n FT: 5ms; \nWPI: 10 or 130 ms \n1st tone 80 ms;\n 2nd tone 10 or 80 \nms\nBinaurally\nLoudspeakers, 75 ± \n0.5 dB SPL\nISI: 1000-5000 ms\nMANOVA\namp N1: ↓ TD (In 10ms \nWPI)\nRD ns\n9\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n18\nHämäläine\nn et al. \n(2011)\nTD\n N=11 (f:5)\nMean \nAge=24.5 \n(±3.9)\nDyslexia \nN=11 (f:6)\nMean \nAge=26.0 \n(±10.1)\nERP\n0.5 kHz sine tone;\nduration: 200 ms;\nFT: 50 ms\n10, 30, 60, 90, \n120 ms\nBinaurally\nHeadphones, 75 dB \nSPL\nISI:2500–3500 ms\nrandomly with equal \nprobability\nANOVA\namp N1↓ (both groups);\namp P2↓ (both groups);\namp Na ns;\namp Ta ns;\namp Tb↓ (only in\n dyslexia);\nlat N1↑ (both groups);\nlat P2 ns;\nlat Na↑ \n11\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n19\nStefanics \net al. \n(2011)\nTD N=20 \n(f:13)\nMean \nAge=8.6 \n(±0.85) [7.25–\n10.08]\nDyslexia \nN=18 (f:9)\nMean \nAge=9.25 \n(±1.08) [7.42–\n11.41]\nERP\n0.5 kHz sine tone;\nduration: 200 ms; \nFT: 15 ms\nstandard: 15 ms;\n deviant: 90 ms\nBinaurally\nHeadphones, 75 dB \nSPL\nISI: 500 ms\nOddball condition: \n(RT, Intensity and \nDuration deviants) \nBlocked condition: \n(each stimulus type \nin separate blocks)\nANOVA\nOddball condition\namp P1 ↓ (in Dyslexia \ngroup) \nlat P1 ↑\nlat P1 Dyslexia > TD \namp N1c (FT7-FT8)↓\nlat N1c ns\namp N2 ↓\nlat N2 ↑\n-MMN\nBlocked condition\namp P1 ns \nlat P1 ↑ \n12\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n20\namp N1c (FT7-FT8) ↓\namp N1c (FT7-FT8)  \nDyslexia group at  90ms > \nTD at 15ms \nlat N1c ns\namp N2 ↓\nlat N2 ns\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n21\nEaswar et \nal. (2012a)\nN=16 (f: 9)\nMean \nAge=23.9 \n[20.3–29.3]\nERP\nSyllabes (/afil/ and /fi/);\nduration: 150 ms\n21.7 and 79.1 ms\nMonourally (ears \nalternated across \nsubjects)\n60 dB SPL\nRate 0.49/1000 ms\n*ISI: 1853 ms \nconditions assessed \nin separate sessions \nconducted within a \nseven-day period\nrmANOVA\namp N1-P2 ↓\nlat N1 ↑\nlat P2 ↑\n9\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n22\nEaswar et \nal., \n(2012b)\nN=16 (f=9)\nMean \nAge=24.2 \n(±2.1)\nERP\n1 kHz tone bursts\nduration 90 ms\nFT=RT \n7.5 and 20 ms\nMonourally (ears \nalternated across \nsubjects)\n80 dB SPL\nISI:1910 ms\nconditions assessed \nin separate sessions \nconducted within a \nseven-day period\nANOVA\namp N1-P2 ns\nlat N1 ns\nlat P2 ns\n9\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n23\nCarpenter \nand Shahin \n(2013)\nChildren\nN=15 (f:7)\n[4–6.11] \nAdult\nN=12 (f:6)\n[18–25]\nfor analysis 3 \ngroups:\n N=6 [4–5] \n N=6 [6] \nN=15 [18–25] \nERP \n speech tokens\n/ba/ and /wa/, and a /ba/ \nwith a /wa/-like RT;\nduration 300 ms\nNA in text \n/ba/ RT< /wa/RT\nBinaurally\nEarphones, 60–65 \ndB SPL\nISI: 1500–2000 ms\nANOVA\namp N1-P2↓ (in adults and \n6 years old, but not in 4-5 \nyear old children)\n11\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n24\nLyytinen et \nal., (1992)\nN=6\n[18–27]\nOddball,\nERP\n1 kHz tones\nduration 50 ms\nstandard: 24 ms;\n deviant: 2 ms\nBinaurally\nHeadphones, 74 dB \nSPL\nISI: 750 ms\noddball\nMANOVA \nand \nrmANOVA\n+MMN (150-250ms) for \nRT deviant\n+P3, late positive shift \n(250-450ms) for RT deviant\n10\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n25\nHämäläine\nn et al. \n(2008)\nShort WPI \ncondition\nTD \nN=30 (f:14)\n Mean \nAge=9.4 \n(±0.25) [8.5–\n10.0]\nRD\n N=22 (f:13)\n  Mean \nAge=9.4 \n(±0.33) \n[8.8–10.3]\nLong WPI \nOddball \nPairs of 0.5 kHz tones\n1st tone duration: 100 \nms; \n2nd tone duration: 150 \nms; \nFT: 5 ms\nShort WPI condition: 10 \nms;\nLong WPI condition: 255 \nms\nStandard pairs: 1st \ntone 80 ms, 2nd \ntone 130 ms\nDeviant pairs: 1st \ntone 80 ms, 2nd \ntone 10 ms\nBinaurally\nLoudspeakers, 75 \ndB SPL\npairs of tones \noddball\nTemporal \nprincipal \ncomponents \nanalysis \n(PCA); \nMANOVA\nShort WPI condition:\n+MMN (124 ms) for RT \ndeviant;\n-LDN for RT deviant;\namp MMN ↑ in right \nmastoid (both TD and \nRD);\namp LDN ns;\nLong WPI condition\n+MMN (119 ms) for RT \ndeviant;\n+LDN (375–645 ms) for RT \ndeviant;\n10\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n26\ncondition\nTD\n N=25 (f:13) \nMean \nAge=9.4 \n(±0.33)\n[8.5–10.0]\nRD\n N=21 (f:12)\nMean \nAge=9.4 \n(±0.33) [8.8–\n10.3]\nMMN RD> TD at fronto-\ncentral channels;\nLDN TD  > RD at right \nfrontal and central\nchannels and left mastoid \nchannel\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n27\nThomson \net al. \n(2009)\nExp1\n N=12 (f:7)\n Mean \nAge=26 \n[20–42]\nExp2\n N=14 (f:11) \nMean Age=26\n[20–42]\nOddball\n0.5 kHz sine tones;\nduration: 260 ms;\nFT: 50 ms\nExp2\nStandart: 15 or 50 ms IM\nExp1\n 15 and 185 ms\nExp2\n 50 ms, 15 ms \nintensity matched \nto 50 ms (IM) and \n15 ms intensity \nnot matched \n(INM)\nBinaurally\nHeadphones, 75 dB \nSPL\nISI: 240 ms\nExp1 \ncounterbalanced \noddball\nExp2\n oddball\nANOVA\nExp1\namp N1 ↓;\n+MMN (150–250 ms) for \nboth deviants;\nExp2\namp N1 ↓;\nwhen 50 ms standart:\n-MMN for 15 ms IM \ndeviant  \n+MMN (but ns) (175–\n275ms) for 15ms INM \ndeviant\nwhen 15ms IM standart\n11\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n28\n+MMN (175–275ms) for \n50ms deviant\nPlakas, et \nal. (2013)\nControl \nN=13\nTypical \nreaders at risk\nN=15\n Dyslexic at \nrisk\nN=10\nMean \nAge=3,4 \nOddball\n0.5 kHz tone;\nduration: 155 ms;\nFT: 50 ms\nstandart 15 ms;\ndeviant 90 ms\nBinaurally\nSpeakers, 75 dB \nSPL\nISI: 450 ms\noddball\nANOVA\nControl \n+MMR (peak at 346 ms)  \nfor RT deviant\nTypical readers at risk: \n–MMR for RT deviant\nDyslexics at risk\n–MMR  for RT deviant\nMMR in control >\nMMR at risk\nMMR Typical readers at \nrisk =\nMMR Dyslexic at risk\n11\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n29\nMoberly et \nal., (2014)\nN=13 (f=8)\nMean \nAge=25.2\n[19–42]\nOddball\nspeech tokens\n/ba/ and /wa/\nART/ba/–FRT/ba/;\nART/wa/–FRT/wa/;\nART/wa/–FRT/ba/;\nduration: 370ms\nART/ba/ 10 ms, \nART/wa/70 ms;\nFRT/ba/ 30 ms, \nFRT/wa/110 ms\nBinaurally\nFree-field, 70 dB \nSPL\nISI:1000 ms\ncounterbalanced \noddball\nANOVA\n+MMN (150–350 ms) for \nART deviants\n+MMN (150–350 ms) for \nFRT deviants\nMMN for FRT \ndeviant>MMN for ART \ndeviant\n10\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n30\nHakvoort, \net al. \n(2015)\nGroup no FR \nno dyslexia\n N = 15\nMean \nAge=11.96 \n(±0.6)\nFR no \ndyslexia \nN = 24\nMean \nAge=11.9 \n(±0.6)\nFR dyslexia N \n= 15\nOddball\n 523 Hz sine tone\nduration: 400 ms; \nFT: 50 ms\nstandart: 15 ms;\n deviant:  90, 180 \nand 270 ms\n80 dB SPL\nISI: 250 ms\noddball\nANOVA\n+MMN (peak at 260 ms) \n(all groups)\n+LDN (peak at 420 ms) (all \ngroups)\nno difference between \ngroups\n12\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n31\nMean \nAge=11.84 \n(±0.5)\nMoberly et \nal., (2016)\nN=20, \ncochlear \nimplants\n[18–62]\nOddball\nspeech tokens\n/ba/ and /wa/;\nART/ba/–FRT/ba/;\nART/wa/–FRT/wa/;\nART/wa/–FRT/ba/; \nduration: 370 ms\nART/ba/ 10 ms, \nART/wa/ 70 ms;\nFRT/ba/ 30 ms, \nFRT/wa/ 110 ms\nBinaurally\nSpeakers, 68 dB \nSPL\nISI:1000 ms\ncounterbalanced \noddball\nANOVA\n+MMN (150–350 ms) for \nART deviants\n+MMN (150–350 ms) for \nFRT deviants\nMMN (150–350 ms) for \nFRT deviant=MMN (150–\n350 ms) for ART deviant\n11\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n32\nOu and \nLaw \n(2016)\n[+Per+Pro]\n(Good tone \nperception \nand \nproduction)\nN=20\nMean \nAge=22.0(±0.\n59)\n[+Per–Pro]\n(Good tone \nperception \nand poor \nproduction)\nN=19\nOddball Cantonese tones /fu/;\nduration 500 ms\n120 and 70 ms \nBinaurally\nEarphones, 85 dB \nSPL\nISI: 800 ms\ncounterbalanced \noddball\nANOVA; \ncluster-based \npermutation \ntests;\nT-tests\n[+Per+Pro]\n+MMN (150–200 ms)  \nwhen 70 ms deviant\n+MMN (150–238 ms) when \n120 ms deviant\n[+Per–Pro]\n+MMN (150–200 ms) when \n70 ms deviant\n–MMN when 120 ms \ndeviant\n10\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n33\nMean \nAge=21.24 \n(±0.84)\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n34\nPeter. et \nal., (2016)\nControl:\nN=17 (f:5) \nDyslexia\nN=17 (f:3)\nMean \nAge=8.9 \n(±1.4) \n[6.0–11.8]\nOddball\nspeech tokens\n/ba/ and /wa/\nstandart: ART/ba/–\nFRT/ba/\nART deviant:\nART/midway/–FRT/ba/\n(partial deviant)\nART/wa/–FRT/ba/\n(full deviant)\nFRT deviant:\nART/ba/–FRT/wa/\n(full deviant)\nART/ba/–FRT/midway/ \n(partial deviant)l \nduration: 320 ms\nART/ba/ 10 ms,\nART/midway/ 40 \nms,\n ART/wa/ 70 ms;\nFRT/ba/ 30 ms,\nFRT/midway/ 70 \nms FRT/wa/ 110 \nms\nBinaurally\nLoudspeakers, 75 \ndB SPL\nISI: 180 ms\n oddball\nIndependent \nT-test, cluster-\nbased \npermutation \ntests\nControl:\n–MMR for both ART \ndeviants\n+MMR (200–300 ms) for \nboth FRT deviants\nDyslexia\n–MMR for both ART \ndeviants\n–MMR for partial FRT \ndeviant\n+MMR (200–300 ms) for \nfull FRT deviant\n12\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n35\nOu and \nLaw \n(2017)\n[+Per+Pro]\n(Good tone \nperception \nand \nproduction)\nN=20\nMean \nAge=22.00 \n(±0.59)\n[+Per–Pro]\n(Good tone \nperception \nand poor \nproduction) \nN=19\nOddball\nCantonese tones /fu/\nduration 500 ms\n120 and 70 ms \nBinaurally\nEarphones, 85 dB \nSPL\nISI: 800 ms\ncounterbalanced \noddball\nANOVA; \ncluster-based \npermutation \ntests\n[+Per+Pro]\n+MMN (150–200 ms) when \n70 ms deviant\n+MMN (150–238 ms) when \n120 ms deviant\n[+Per–Pro]\n+MMN (150–200 ms) when \n70 ms deviant\n–MMN when 120 ms \ndeviant\n[–Per–Pro]\n–MMN for both deviants\n12\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n36\nMean \nAge=21.24 \n(±0.84)\n[–Per–Pro]\n(Poor tone \nperception \nand \nproduction)\nN=19\nMean \nAge=21.20 \n(±2.84)\n amp P2 ↓ (70 ms generate \nmore positive response \nthen 120 ms)\nfor 70 ms: [+Per+Pro]>\n[+Per–Pro]=[–Per–Pro]\nfor 120 ms: no difference \nbetween groups\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n37\nPeter, et al. \n(2018)\n6–8 years \nN=12 (f:6)\nMean \nAge=7.18 \n(±0.29)\n8–10 years \nN=12 (f:7)\nMean \nAge=8.87 \n(±0.44)\n10–12 years \nN=12 (f:7)\nMean \nAge=10.92 \nOddball\nspeech tokens\n/ba/ and /wa/\nstandart: ART/ba/–\nFRT/ba/\nART deviant:\nART/wa/–FRT/ba/\nFRT deviant:\nART/ba/–FRT/wa/\nduration: 320ms\nART/ba/ 10 ms, \nART/wa/ 70 ms;\nFRT/ba/ 30 ms, \nFRT/wa/ 110 ms\nBinaurally\nSpeakers, 75 dB \nSPL\nISI: 180 ms\n oddball\nANOVA; \ncluster-based \npermutation \ntests\n6–8 years \n+MMR (200–400 ms) for \nART deviant\n+MMR (200–400 ms) for \nFRT deviant\n8–10 years\n+MMR (200–400 ms) for \nART deviant\n+MMR (200–400 ms) for \nFRT deviant\n10–12 years\n–MMR  for ART deviant\n+MMR (204–316 ms) for \nFRT deviant\nAdults \n–MMR for ART deviant\n12\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n38\n(±0.54)\nAdults \nN=12 (f:6)\nMean \nAge=31.05 \n(±4.41)\n+MMR (168–248 ms) for \nFRT deviant\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n39\nChoisdealb\nha et al. \n(2022)\nSeven months \nN=74\nMean Age=7 \nmonths, 3 \ndays (±5 \ndays)\nEleven \nmonths N=96\nMean Age=11 \nmonths, 2 \ndays (±5 \ndays)\nOddball\nsine tone or SSN (speech \nshaped noise)\nstandart:15 ms\n10 deviants: 161.1 \n–292.7 ms (step of \n14.6 ms)\nBinaurally\nSpeakers\noddball \nregression \nmodel\n+MMR (300–460 ms)\nMMR↑ with deviant RT↑\nMMR more negative with \nAge↑\nMMR for tones=MMN for \nSSN\n11\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n40\nLe Vere et \nal. (1976)\nM=20.3 \n[19–23]\nRhythmic \nactivity\nTones (125 Hz)\n3.24 ms (fast RT) \nand 7.5s (slow \nRT)\nAuditory speaker \nsystem;\nfree field\nANOVA\nAt slow wave Mean \ncortical desynchronization \n↓\nAt fast wave Mean cortical \ndesynchronization nc\n8\nVan \nHirtum et \nal. (2019)\nDyslexia: \nN=20 (f:10)\n[18–25]\nTypical \nreaders: N=18 \n(f:10)\n[18–25]\nASSR\namplitude-modulated \none-octave white noise \nbands centered 1 kHz. \nNoise bands were 100% \namplitude-modulated\namplitude-\nmodulated at \napproximately 4, \n10, 20 and 40 Hz \n(sinusoidal \nenvelope \nmodulation, 10 \nand 30 ms RT)\nMonourally (right \near) \nEarphones, 85 dB \nSPL\nlinear mixed \nmodels, t-test\n4 Hz: ↑ for RT30 and ↓ for \nRT10\n10 Hz: RT10 and RT30 ↓ \ndyslexia only\n20 Hz: RT30 ↓ dyslexia \nonly\n12\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n41\n20 Hz: higher \nsynchronization of beta \nactivity for RT30 related to \nbetter literacy skills\n40 Hz: ↓ SNR dyslexia \nonly in the right \nhemisphere\n40 Hz: correlation of neural \nbackground activity in the \nright hemisphere with \nliteracy and phonology in \nparticipants with dyslexia\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n42\n146 List of abbreviations for Table 1\n147\n148 ABR – auditory brainstem response \n149 ASSR – auditory steady-state response\n150 ERP – event-related potentials\n151 MMN (xxx ms) – mismatch negativity (latency of the component)\n152 MMR  (xxx ms) – mismatch response (latency of the component)\n153 LDN (xxx ms) – late discriminative negativity (latency of the component)\n154 RT – rise time\n155 FT – fall time\n156 ART – amplitude rise time\n157 FRT – formant rise time\n158 ISI – inter-stimulus interval\n159 WPI – within-pair interval\n160 lat – latency\n161 amp – amplitude\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n43\n162 ns – not significant\n163 I, II, III, IV, V, VI, VII, VIII – number of ABR waves\n164 SPL – sound pressure level\n165 nHL– normalized Hearing Level\n166\n167 TD – typically developing\n168 RD – reading disabilities\n169 FR – family risk (of dyslexia)\n170\n171 + – the presence of the response\n172 – – the absence of the response \n173 ↑ –  response increases with increasing of RT\n174 ↓ –  response decreases with increasing of RT\n175\n176\n177 Converted values are marked with an asterisk\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n44\n178\n179 Fig. 1. A PRISMA flow-chart representing a flow of information through the \n180 different phases of a systematic review. \n181\n182 Seven articles were excluded from the study due to unavailability of full texts. This was \n183 due to the fact that the articles were published a long time ago (1964–1994) and their full texts \n184 were not digitized or not available [7–13]. Thirty-seven included studies were divided into \n185 groups according to EEG responses studied and organized in the Table 1 and in text according \n186 to the latency of the brain responses, from earlier to later evoked potentials. The studies \n187 included in the final review ranged in date from 1968 to 2022 (Fig. 2), with an 11–year gap in \n188 rise time studies (there were no published studies between 1996 and 2007) and current gap \n189 within the last four years. \n190\n191 Fig. 2. Histogram of RT studies paradigms over years.\n192\n193 The main categories into which we classified the studies are: (1) early latency \n194 components (auditory brainstem response N=10, (2) middle latency components (Na, Pa, Nb, \n195 N=2), (3) late latency components (P1, N1, P2, N2, P3, N=14), (4) difference waves studies \n196 (mismatch negativity or mismatch response (MMN and MMR), later positive shift, late \n197 discriminative negativity (LDN) – 13 studies and one study on Auditory Steady-State Response \n198 (ASSR) and one on mean cortical desynchronization both categorized as Others. Some studies \n199 described more than one category of EEG-response and, thus, were reviewed in several \n200 sections. Next we describe the results separately for each category.\n201\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n45\n202 Early latency components (auditory brainstem response, ABR)\n203 Auditory brainstem response (ABR) is an early potential that occurs in response to \n204 auditory stimuli, reflecting neural activity along the auditory pathways from the inner ear to the \n205 brainstem. ABR consists of a series of waves (denoted as I–VII) that appear within the first 10–\n206 15 ms after the sound stimulus onset and reflect early auditory processing steps. As ABR occurs \n207 within such early latencies, the typical RT studied in this paradigm varies from 0.5 till 5 ms. \n208 RT has been studied with ABR for a relatively long time, and no modern studies relevant to the \n209 review were found. The most recent study included in this review dates back to 1996. The final \n210 review included 10 articles investigating brainstem evoked potentials. The overwhelming \n211 majority of studies was conducted on adults, only one of them included 11–13 weeks old infants \n212 as one of the experimental groups. However, no difference in the results was found between \n213 the adult group and the infant group [14].\n214 The results obtained in studies of RT perception using ABR are quite congruent. One of \n215 the main conclusions made by the authors in their articles related to the latency and amplitude \n216 of wave V: its latency increases while the amplitude decreases with the RT increase[14–18]. \n217 This tendency remains with any type of stimuli (noise or tone bursts, tone pips or clicks).\n218 An increase in latency with an increase in stimulus RT is also observed in other early \n219 components of brainstem potentials: from waves I to VII, however, the results depended on \n220 stimuli parameters. For example, at 40 dB SPL and for stimuli with the so-called “fast rise \n221 time” (10 µs), the latency of waves VI–VII first decreases (between 10 µs and 0.5 ms) and then \n222 gradually increases, although this effect was statistically insignificant [19]. In the study of \n223 Hecox & Deegan (1983) an increase in the latency of wave V with an increase in RT was also \n224 found in most experimental conditions, however, no significant changes in amplitude were \n225 found [20]. The study by Suzuki & Horiuchi (1981) was distinguished by its findings of \n226 different tendencies depending on stimuli presented. When utilizing 2–kHz tone pips, a \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n46\n227 decrease in wave V latency with RT increase was observed at certain stimulus intensities (only \n228 30–40 dB nHL). At the same time, a RT change did not significantly affect wave V amplitude. \n229 In contrast, with 0.5–kHz tone pips, an increase in stimulus RT correlated with an increase of \n230 the mean wave V amplitude and concurrently, the mean wave V latency also exhibited a \n231 tendency to increase. However, these results should be treated with caution as they were \n232 obtained on a limited sample (N=8, all females) in specific conditions: during sleep induced by \n233 administration of pentobarbital calcium before the test [21].\n234 One of the articles reported morphologically similar to onset brainstem response offset \n235 brainstem response which occurs by long-duration tone burst (>8 ms) within 8 ms after stimulus \n236 offset [22]. Offset ABR was even more affected by stimulus RT than onset ABR. It was \n237 demonstrated that both offset and onset wave V amplitude increased and both offset and onset \n238 wave V latency decreased (for both 0.5 and 2 kHz stimuli) for 1 ms RT in comparison to 0.5 \n239 ms RT.  In the block where only two RTs (0.5 vs 5 ms) varied with a constant fall time, the \n240 difference were detected only for the offset ABR: offset ABR latency increased for both types \n241 of stimuli (0.5 and 2 kHz) and offset ABR amplitude decreased for 2 kHz stimuli with longer \n242 RT  [22]. \n243 Stimulus polarity is a physical characteristic of a stimulus that might influence the RT \n244 effect. Stimulus polarity refers to the initial deflection of the transducer diaphragm in relation \n245 to the tympanic membrane during stimulus presentation: a rarefaction stimulus causes the \n246 earphone diaphragm to move outward initially, resulting in an outward movement of the \n247 tympanic membrane, while a condensation polarity stimulus leads to an inward movement of \n248 the diaphragm and consequently an inward movement of the tympanic membrane [23]. Most \n249 ABR studies included in the current review used alternating stimulus polarity (rarefaction and \n250 condensation), thereby cancelling out the polarity-specific effect. Additionally, some \n251 investigations within the ABR-field have explicitly considered stimulus polarity as one of the \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n47\n252 influential acoustic parameters, alongside other stimulus characteristics. Amplitude values of \n253 main ABR components in study of Salt & Thornton depended on polarity of stimuli presented: \n254 direction of amplitude changes was different in rarefaction vs condensation stimuli. In \n255 particular, I, II, III, VI amplitudes in response to rarefaction stimuli tended to be lower with RT \n256 increase and vice versa on condensation stimuli. Amplitude of peak V, on the contrary, arose \n257 with RT in response to rarefaction stimuli and lowered with RT in response to condensation \n258 [24]. However, no statistical testing was applied. Besides, the other study which used clicks of \n259 different polarity as stimuli [16] showed the same direction of amplitude changes in both \n260 stimuli types. However, the latencies in all RT conditions were longer for condensation slope \n261 stimuli, and amplitudes were contrariwise higher for rarefaction stimuli [16]. In the case of \n262 short stimuli with a RT of 170-580 µs, there is a linear tendency towards an increase in the \n263 latency of the main components (waves I–VI) with an increase in RT for stimuli of both \n264 polarities [24]. \n265\n266 Middle latency components\n267 Middle latency components are considered to be driven by the primary auditory cortex \n268 with a substantial contribution of thalamic-cortical pathways and elicited from 10 to 80 ms after \n269 stimulus onset [25]. In this group of components, several successive peaks are distinguished \n270 (P0, Na, Pa, Nb, Pb). Two studies[26,27] demonstrate the modulation of middle latency \n271 components of evoked potentials by RT duration in a group of neurotypical adults. Tone bursts \n272 were used as stimuli. In both of these studies short RT durations were used (up to 25 ms). In \n273 [27], peak-to-peak amplitude of Na–Pa, Pa–Nb components decreased with RT increased \n274 across all conditions, while peak-to-peak amplitude of P0–Na and Nb–Pb components \n275 decreased only in the longest RT condition (25 ms). Notably, no statistical analyses were used \n276 in this study, so the presented results should be considered with caution. In a later study by \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n48\n277 Kodera et al. (1979) [26], the decrease in Na–Pa, Pa–Nb peak-to-peak amplitudes with RT \n278 increased was verified statistically. This article also showed a delay in the Na and Pa \n279 components latencies with RTs prolongation.\n280 P1\n281 The P1 component is a positive peak in the auditory ERP, occurring approximately 50–\n282 100 ms post-stimulus in adults (>100 ms in children), and originating primarily in the primary \n283 and secondary auditory cortex. In neurophysiological research, P1 is optimally recorded from \n284 central midline electrodes, particularly Cz referenced to mastoids or earlobes, and serves as a \n285 biomarker for auditory cortical development and central auditory pathway integrity [28]. P1 \n286 has rarely been an object of interest in RT studies as it is not very prominent in adults: one \n287 study in children and one in adults. Stefanics and colleagues [29] examined P1 modulation by \n288 RT duration in dyslexia and typically reading children (aged 8–10 years) in longitudinal study \n289 that includes oddball and block conditions. Decrease in P1 amplitude with RT increase was \n290 observed only in the group of participants with dyslexia, but not in the control group, where P1 \n291 amplitudes were equivalent across RT conditions. This effect was specific only for oddball \n292 conditions; no significant effects were observed for P1 amplitude in the blocked condition. \n293 Authors attribute this difference to greater responsiveness of the P1 component in oddball \n294 condition, which was related to different probability of occurrence of the stimuli. Both groups \n295 demonstrate prolongation in P1 latency with RT increasing in all conditions. The same \n296 prolongation was observed in Kodera et al. (1979b) [26]. In this study P1 was considered as \n297 part of P1–N1 peak-to-peak amplitude, which demonstrates significant decrease with RT \n298 prolongation. In Skinner and Jones (1968) [30] work no significant effects for P1 latency were \n299 observed.\n300\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n49\n301 N1\n302 The N1 (or N100) is a prominent negative-going component of the auditory ERP \n303 waveform that follows P1 and typically peaks approximately 80–120 milliseconds after \n304 stimulus onset. It is primarily generated in the auditory cortex, including areas within the \n305 superior temporal gyrus (such as Heschl's gyrus and the planum temporale). In EEG recordings, \n306 the N1 component typically exhibits maximal amplitude over fronto-central scalp locations and \n307 is therefore commonly observed and analyzed at midline fronto-central electrodes such as Fz, \n308 FCz, and Cz [31]. \n309 Of all the articles included in the review, thirteen examined the effects of RT on the N1 \n310 component. According to reviewed studies, reduction in N1 amplitude with RT prolongation is \n311 a common pattern for neurotypical adults. In [32] N1 amplitude linearly decreases across RT \n312 prolongation from 3 to 45 ms, but only in the first of two runs of the paradigm. Thomson and \n313 colleagues (2009) [33] shows that N1 amplitude also decreases in longer RT condition, such as \n314 50 and 185 ms. These results are confirmed in the additional part of that study, where stimuli \n315 with different RT were equalized in intensity. Similar reduction of N1 amplitude in longer RT \n316 conditions were obtained for groups of typically reading adults [34] and children [35]. In one \n317 of the studies[26], N1 was assessed as P1–N1 peak-to-peak amplitude, which also demonstrates \n318 significant decrease with RT prolongation from 5 to 20 ms.\n319 Three studies reported significant enhancement of N1 latency with RT \n320 increase[26,34,36]. A similar result was shown in earlier papers [37,38], but was not confirmed \n321 by statistical analysis. In the study by Eswar and colleagues[39], the difference in N1 latency \n322 between RT conditions was not significant, which probably related to minor differences \n323 between RT conditions used in this work (7.5 vs 20 ms). However, even larger contrast (such \n324 as 2.5 vs 50 ms) was also insignificant for 1000 Hz tone burst and white noise burst [40].\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n50\n325  Two studies examined N1 modulation by RT in a group with speech impairment. In \n326 Hämäläinen et al., (2007) [35] in a pair of stimuli with a short within-pair interval, the amplitude \n327 decreases at a longer RT condition (80 ms), but only in typically developing (TD) children. In \n328 the group of children with reading disabilities, the N1 amplitude was equal across RT \n329 conditions. It is important to note that stimuli differed not only in RT but also in frequency and \n330 statistical comparison of different RT conditions was not performed. The more recent work of \n331 this group [34] with stimuli of the equal frequencies showed decrease in N1 amplitude and \n332 prolongation of its latency with RT increase in both typical reading and dyslexic adults groups.\n333\n334 P2\n335 The P2 component is a positive deflection in ERP that follows the N1 component and \n336 occurs approximately 150–200 ms post-stimulus. It is generated in the auditory association \n337 cortex and surrounding areas and thus, is typically recorded from central and frontocentral \n338 electrode sites (Cz, FCz) and suggests to reflect higher-order sound processing, auditory feature \n339 integration, and early attentional mechanisms [31].\n340 Nine of the papers included in the review consider RT effects associated with the P2 \n341 component. Most works estimated P2 effects as related N1–P2 peak-to-peak amplitudes. N1–\n342 P2 peak-to-peak amplitude was considered in seven studies[17,36,37,39–42]. N1–P2 amplitude \n343 tends to decrease with prolongation of the RT. In Onishi & Davis work [37] RT changes did \n344 not affect the N1–P2 amplitude when RTs were less than 30 ms. Decrease in N1–P2 amplitude \n345 was observed only as RT is increased beyond about 30 ms, but no statistical analysis was \n346 performed. In Kodera et al. (1979) [26] no significant difference was shown for N1–P2, but RT \n347 durations used in this study were quite short (5–20 ms), which probably not enough for N1–P2 \n348 modulation. A similar result appears in a more recent study[39], where no difference was found \n349 between 7.5 and 20 ms RT conditions for 1000 Hz tone burst. [40] observed significant \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n51\n350 decreases in P2 for 50 ms RT condition compared to 2.5 ms RT condition for 1000 Hz tone \n351 burst, but not for white-noise burst. In the study by Elfner et al. [42], decrease in N1–P2 \n352 amplitude was shown for prolongation RT from 50 ms to 150 ms and 500 ms, although \n353 continued prolongation from 500 to 1500 and 4960 ms of the RT duration did not produce a \n354 change in N1–P2 amplitude. However, further statistical analysis in the Experiment 2 of this \n355 study showed that the observed RTs prolongation effects are only at the level of tendency and \n356 are not statistically significant. Two studies[36,41] used more natural types of stimuli, such as \n357 speech tokens. N1–P2 amplitude decreased in longer RT (such as 79.1 ms in Easwar et al.; in \n358 Carpenter & Shanin exact RT not reported) in both studies. However,  the effect observed in \n359 adults and 6-years old children, was not present in early childhood (4–5 years) [41]. \n360 Two studies [32,34] considered P2 as an absolute baseline-to-peak value, not as a peak-\n361 to-peak amplitude. Putnam & Roth [32] showed linear decrease of P2 amplitude (considered \n362 as P190 component) with RT prolongation that included RT ranged from 3 to 45 ms. This result \n363 was confirmed in the study by Hämäläinen and colleagues (2011) [34] both for control and \n364 dyslexic adults groups with RT used from 10 to 120 ms. \n365 As in case of N1, P2 latency demonstrated delay with RT prolongation[26,36]. At first, \n366 this effect was described in [38] as shifting of slow V potential (N1–P2 peak-to-peak \n367 component), but was not statistically validated. Later it was confirmed statistically[17,36]. \n368 Nonetheless, in some papers, the differences in P2 latency between different RT conditions \n369 were not significant[34,39].\n370\n371 T–complex\n372 Two of the studies included in the review examined RT effects not only in the central \n373 but also in the temporal channels. Näätänen & Picton [43] define a projection of the P1-N1-P2 \n374 components to the temporal region as T-complex. The T-complex includes three peaks: N1a \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n52\n375 (or Na) (75–95 ms), N1b (or Ta) (100–115 ms), and N1c (or Tb) (130–170 ms). In the study of  \n376 Hämäläinen et al. (2011) that included neurotypical adults and adults with dyslexia, Na and Tа \n377 amplitude did not change between RT conditions in both groups, while amplitude of Tb \n378 decreased with RT prolongation in a group of adults with dyslexia, but not in the control group \n379 of neurotypical adults. There was also prolongation in Na component latency in both groups. \n380 In a group of children (7–10 years) Stefanics and colleagues [29] also showed decrease of N1c \n381 (at FT7–FT8 sites) amplitude with long (90 ms) RT in oddball condition, but in the block \n382 condition RT effects were observed only in dyslexic group. No RT effects on N1c latency were \n383 observed.\n384\n385 N2\n386 The N2 component is a negative deflection in the auditory ERP that follows the P2 \n387 component and occurs approximately 200–250 ms post-stimulus onset. It originates primarily \n388 from frontal cortical regions including the anterior cingulate cortex, which is typically recorded \n389 at frontocentral electrode sites (Fz, FCz) [44]. Only one study [29] considered N2 as a target \n390 for the RT effects in children from 7 to 11 years. Similar to the other components, N2 \n391 demonstrated decrease in amplitude and prolongation of latency with the RT increase. One \n392 more study by Skinner & Jones [30] considered N2 as part of the P1-N2 complex, where the \n393 difference between P1 and N2 components was taken as the amplitude of the auditory evoked \n394 response. It was shown that P1-N2 decreases with RT increase. N2 latency did not show RT \n395 effects, but statistical analyses were not performed. Even though the effects of RT on the N2 \n396 component were not considered in other works, we can assume decrease in amplitude and \n397 latency delay when the RT is prolonged by looking at the figures[34,36].\n398  \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n53\n399 P3\n400 The P3 (or P300) component is a prominent positive wave occurring approximately \n401 250–500 ms following auditory stimulus presentation, generated by distributed neural networks \n402 involving frontal, temporal and parietal cortical regions. P3 is reliably recorded at midline \n403 electrodes (Fz, Cz, Pz) with maximum amplitude typically at Pz [45]. One study [32] \n404 considered the RT effects for late positive component (P300). Amplitude of P300 (at Pz \n405 electrodes) significantly decreased with RT prolongation from 3 to 45 ms, however the RT \n406 prolongation was also accompanied with changes of the total duration of stimuli that can also \n407 influence the observed change [32].\n408\n409 Difference waves (MMN, MMR, Late positive shift, LDN) \n410 Many studies investigating RT processing have employed the oddball paradigm, where \n411 deviant stimuli with different RTs are embedded within streams of standard stimuli with fixed \n412 RTs [33,46–48]. These deviant stimuli typically elicit a mismatch negativity (MMN) or \n413 mismatch response (MMR). MMN is obtained as a difference between ERP in response to \n414 standard (frequent) stimuli and ERP in response to deviant (rare) stimuli. Sometimes, especially \n415 in children, the response to a different stimulus may appear as a more late positive component \n416 on a difference wave, which is known as a Mismatch response (MMR). Mismatch Response \n417 (MMR) refers to the corresponding response in infants and young children, which can be \n418 positive (pMMR) or negative (nMMR) in polarity, with a broader scalp distribution and more \n419 variable latency than adult MMN, reflecting the developing auditory system [49]. Twelve of \n420 the reviewed papers examined sensitivity to RT changes using this paradigm, with the MMN \n421 component serving as the primary measure of distinguishability between standard and deviant \n422 stimuli. Two studies considered also late discriminative negativity (LDN), a later (from 400 ms \n423 post-stimulus) component at the difference wave evoked by a deviant stimulus and also \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n54\n424 suggested to be localized in associative areas of the auditory cortex. Although originally LDN \n425 was called the late MMN [50,51], included studies considered it as a separate component to \n426 highlight the difference in time of occurrence and to separate the RT effects.\n427 The first study reported MMN (in time window 150–250 ms) elicited by RT deviants \n428 in neurotypical adults, used short RT durations (24 ms in standard and 2 ms in deviant) [52], \n429 also late positive shift in differenсе waves (at time window at 280–500 ms) was described in \n430 this work. Later study of neurotypical adults [33] used two RT durations (15 and 185 ms). Each \n431 type of stimulus was used as standards and as deviants in different blocks. Both types of deviant \n432 elicited MMN response (in time window 150–250 ms) in frontal and temporal areas. In the \n433 second part of this study, four types of stimuli were used: one with long RT (50 ms), two with \n434 RT 15 ms (one of them was intensity matched to stimulus with 50 ms RT, and other was not), \n435 and one with short RT stimuli that was equivalent in intensity to long RT stimulus (intensity \n436 matched deviant). This contrast was introduced to separate the influences of intensity and RT \n437 effects, as changing RT inevitably influences intensity especially with long RT. When 50 ms \n438 RT stimuli were used as standard intensity-not-matched deviant with shorter RT elicited a \n439 MMN response at time window 175–275 ms (but not significant), while intensity-matched \n440 deviant did not elicit any MMN at all. However, in the exchanged condition where intensity-\n441 matched 15 ms RT stimuli were used as standards and 50 ms RT stimuli were used as deviants, \n442 a mismatch response was observed in the time window of 175–275 ms even for intensity-\n443 matched condition. According to these results, authors suggested that MMN is sensitive to the \n444 “content” of the change (RT) but not purely to the amount of stimulus energy (intensity). \n445 Meanwhile the context effect, i.e. the observation of  prominent MMN only for conditions with \n446 longer RT for the deviant than the standard, was left unexplained.\n447 Controversial results were obtained concerning the MMN to RT deviant as neuromarker \n448 for reading problems. The first study [53] considered MMN in response to deviants with short \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n55\n449 RTs (10 vs 130 ms RT in standard stimuli) in typical reading children and children with reading \n450 disabilities (RD) (8–10 years). The study included two conditions with different intervals \n451 between stimuli in the presented pair. The authors chose a varying Within-Pair Interval (WPI) \n452 design to investigate if children with reading problems exhibit deficits in rapid auditory \n453 processing, expecting larger differences with short WPIs, and also to determine if they process \n454 rise times differently at an early stage, regardless of the WPI length. This approach allowed \n455 them to examine how both rapid presentation rates and rise time variations influence early \n456 neural responses in children with and without reading difficulties. Each trial presented a pair of \n457 tones under two timing conditions: a short gap condition with 10 ms between tones (within-\n458 pair interval, WPI) and a longer gap condition with 255 ms between tones. The experimental \n459 design included 80% standard pairs (where both tones had expected properties) and 20% \n460 deviant pairs. In deviant pairs, the second tone differed either in RT (10% of trials, 10 ms \n461 instead of 130 ms) or in pitch (10% of trials, 750 Hz instead of 500 Hz). The first tone remained \n462 consistent across all pairs (100 ms duration, 80 ms rise time, 300 Hz frequency), while the \n463 second tone in standard pairs had 150 ms duration, 130 ms RT, and 500 Hz frequency. All tone \n464 pairs were separated by a consistent 610 ms interval (ISI), regardless of condition.While in the \n465 longer interval condition (255 ms), MMN response (at latency 119 ms from the deviancy onset) \n466 was larger than in the shorter interval (10 ms) in both groups, children with RD demonstrated \n467 a larger MMN than typically developing (TD) children only in this longer interval condition. \n468 This study also considered LDN. In conditions with a short (10 ms) interval after the previous \n469 stimulus, LDN was not presented. In long within-pair intervals (255 ms) conditions, an LDN \n470 response was observed at 375–645 ms. In this condition, the control group showed larger LDN \n471 than children with RD. \n472 A traditional non-paired oddball design was employed by Plakas et al. (2013) [47] in their study \n473 of younger children (3 years old). A negative mismatch response at 346 ms for longer RT \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n56\n474 deviants (90 vs 15 ms RT in standard stimuli) was observed in the control group but not in \n475 people with dyslexia and typical reading, but with familial risk groups. The study by Hakvoort \n476 and colleagues (Hakvoort et al., 2015) involves similar groups of children, but the age of the \n477 participants was older (11 years). MMN and LDN, responses peaking around 260 ms and 420 \n478 ms respectively to RT deviants with longer RT (90, 180 or 270 vs 15 ms RT in standard stimuli) \n479 were observed for all groups (typically developing children, children with dyslexia, and \n480 children with familial risk of dyslexia) and did not differ between groups. The influence of \n481 different RT durations of deviant stimuli was not considered in this study. The interstimulus \n482 interval in this study was close to the long within-pair intervals condition in the Hämäläinen et \n483 al. (2008) study (250 ms). These findings suggest that the presence and magnitude of the LDN \n484 component may depend on the timing between stimuli and vary across populations with reading \n485 difficulties.\n486 A number of studies have used speech stimuli [4,54–56]. In these studies, the amplitude \n487 RT (ART) changes are usually contrasted with the formant RT (FRT) changes. Syllables /ba/ \n488 and /wa/ are commonly used stimuli in this type of study. Syllable /ba/ has a short ART (10 \n489 ms) and FRT (30 ms), /wa/ has more prolonged ART (70 ms) and FRT (110 ms). The third \n490 synthetic token usually used in this approach combines a /ba/-like FRT (30 ms) with a /wa/-\n491 like ART (70 ms). The Moberly et al. study [4] found that while neurotypical adults show MMN \n492 response between 150–350 ms for changes in both ART and FRT deviants, the MMN is \n493 significantly larger and more consistently observed across individuals for FRT deviants. In a \n494 further study of this research group [54], similar experimental paradigms were used for adults \n495 with cochlear implant sample. MMN response was observed for ART and FRT deviants and \n496 did not differ between contrasts. Peter et al. [55] implicated FRT and ART oddball paradigm \n497 to typically developing children and those with dyslexia (mean age=8.9 years). This study \n498 inclined additional tokens with partial ART (40 ms) and FRT (70 ms) durations as ART and \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n57\n499 FRT deviants. ART deviants did not elicit any mismatch response in either groups. Both partial \n500 and full FRT deviants produce mismatch effects at time window 200–300 ms in the control \n501 group. In the group of people with dyslexia, mismatch response was elicited only by full FRT \n502 deviant. The developmental track of sensitivity was considered in a follow-up study by this \n503 research group [56], including three age groups of children (6–8, 8–10, 10–12 years) and adults. \n504 Сhildren younger than 10 years showed positive mismatch response between 200 and 400 ms \n505 to both ART and FRT conditions. 10–12-year-old children and adults were sensitive only to \n506 FRT deviants.\n507 Two papers [57,58] examined the MMN response to the Cantonese syllables with \n508 different RTs (/fu/ with RT 120 and 70 ms). In [57] deviant with 70 ms RT elicited more \n509 positive mismatch responses (in time windows 150-200 ms after 70 ms RT and 150–238 ms \n510 after 120 ms RT) than 120 ms RT deviant. A group of participants with good production and \n511 good perception of Cantonese tones showed mismatch responses in both types of \n512 counterbalanced contrasts, while a group with good perception but poor production of tones \n513 demonstrated mismatch response only when stimulus with a shorter RT (70 ms) was used as a \n514 deviant. In the following paper [58] additional group with poor speech production and poor \n515 speech perception was also included in the analysis. In this group no significant mismatch \n516 responses were observed for both contrasts (120 ms and 70 ms deviants). The amplitude of ERP \n517 to stimulus with 70 ms RT at the time window 50–150 ms (P2) was more positive in good \n518 production – good perception group than in good perception – poor production group and in \n519 poor production – poor perception group. No significant difference between poor production – \n520 good perception group and poor production – poor perception group was shown. MMN to 120 \n521 RT deviants did not show any significant difference between groups. \n522 Choisdealbha and colleagues [48] provide a longitudinal study of RT perception \n523 involving 7 month infants that was followed four months later. Sine tones and speech shaped \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n58\n524 noise were used as stimuli and RT of standard stimuli was 15 ms and RT of deviants ranging \n525 from 161.1 ms to 292.7 ms, in steps of 14.6 ms. It was shown that larger differences in standard \n526 and deviant RT produce more positive mismatch response (at time window 300–460 ms). At \n527 the same time amplitude of mismatch response becomes more negative in older infants. \n528 Stimulus type did not influence the response. The proportion of infants exhibiting MMN or \n529 MMR to deviants with different RT was broadly similar across all of the used oddball stimuli.\n530\n531 ASSR\n532 The study by Van Hirtum and colleagues considered auditory steady-state response \n533 (ASSR, an electrophysiological response expressed in neural tuning to the frequency of an \n534 auditory stimulus) to RT changes in typical readers and adults with dyslexia [59]. As a stimuli, \n535 they used white noise with amplitude modulation at 4, 10, 20, and 40 Hz, with two RT \n536 conditions: 10 ms and 30 ms , without affecting the amplitude modulation rate. A sinusoidal \n537 envelope modulation was carried out as a baseline condition. As a measure of ASSR strength, \n538 the authors considered signal-to-noise (SNR) ratio of ASSR response to an auditory stimulus. \n539 ASSR responses were considered in the same EEG frequency ranges as the stimuli.\n540 The study explored auditory processing differences between individuals with and \n541 without dyslexia, focusing on their ability to discriminate RTs and perceive speech in noise. \n542 Behavioral results revealed that individuals with dyslexia performed similarly to typical readers \n543 in discriminating RT and intensity changes and in speech in noise perception. EEG showed \n544 distinct neural responses to varying RTs based on the presence of dyslexia. Specifically, \n545 participants with dyslexia showed reduced 10 Hz SNRs in 10 and 30 ms RT conditions, lower \n546 20 Hz SNRs for 30 ms RT envelopes, and smaller 40 Hz SNRs for all RTs in the right \n547 hemisphere compared to typical readers. No effects were found for 4 Hz SNR. Interestingly, a \n548 30% larger relative increase in RT processing was observed for typical readers in the right \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n59\n549 hemisphere compared to participants with dyslexia. Increased neural background activity at 40 \n550 Hz in the right hemisphere in participants with dyslexia also correlated with poor literacy and \n551 phonological skills. In contrast, increased neural background activity of beta activity at 20 Hz \n552 was significantly related to better literacy skills. The findings suggest that dyslexia is associated \n553 with distinct alterations in neural processing of auditory RTs and increased neural background \n554 activity, impacting speech perception and literacy skills. These results are considered within \n555 the context of impaired phonological processing in participants with dyslexia, which is \n556 manifested in a decrease in SNR by a short RT for stimuli with frequencies of 10 Hz and 20 \n557 Hz. The authors also attribute the decrease in SNR in the 40 Hz range to a decrease in \n558 phonological processing and the formation of atypical phonological representations. The lack \n559 of an effect for 4 Hz is discussed in the context of theta rhythm, which is associated with neural \n560 tracking of syllable rhythm, which may not be impaired in participants with dyslexia, unlike \n561 phonological processing.\n562\n563 Rhythmic activity\n564 The study by Le Vere and colleagues considered a mean cortical desynchronization \n565 during sleep in relation to different rise times perception [60]. As stimuli, a random noise \n566 centered at 125 Hz with two rise time conditions (fast, approximately 3.24 ms, and slow, 7.5 \n567 s), were used in the experiment. This study found that both fast-rise and slow-rise auditory \n568 stimuli could induce arousal during sleep. However, the effectiveness of the stimulus's rise time \n569 depended on the sleep stage. During non-REM fast-wave sleep, both stimulus types were \n570 equally effective. In contrast, during slow-wave sleep, a fast-rise stimulus produced \n571 significantly more arousal than a slow-rise stimulus, despite the slow-rise stimulus having a \n572 greater total energy and duration. This highlights the importance of rapid onset, rather than \n573 overall energy, in capturing attention and causing arousal during deeper stages of sleep.\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n60\n574 Discussion\n575 In the current review, we present the main studies focused on the electrophysiological \n576 correlates of RT perception. As can be seen from the given above outcomes, the field under \n577 consideration is quite broad and includes a large number of both older classical and modern \n578 studies. The main outcomes of the reviewed studies generally are consistent with each other \n579 and generalize to the overall framework: The prolongation of the RT leads to a decrease in the \n580 amplitude of the main ERP components and an increase in their latencies. Nevertheless, the \n581 observed effects may vary and depend on some aspects of the experimental paradigm, that is \n582 considered below.\n583\n584 Stimulation characteristics influencing RT effect\n585 The effect of RT might be influenced by the other stimulation parameters. Below we \n586 discuss some of them, such as stimulus presentation rate and stimulus intensity effects on \n587 neurophysiological encoding of RT, and suggest optimal stimulation parameters for \n588 experimental design. In the following block we also discuss how the stimulus type affects RT \n589 decoding as RT might be more crucial for speech sounds. We conclude this section by \n590 presenting differential sensitivity to RT changes at different stages of auditory processing.\n591\n592 Inter-stimulus interval (ISI)\n593 The ISI is an important parameter, especially for ERP studies, due to its effect on the \n594 amplitude of the components [61,62]. Different inter-stimulus intervals significantly influence \n595 the main ERP components, with component amplitudes generally increasing as the interval \n596 lengthens. Moreover, this modulation by stimulus presentation rate varies across developmental \n597 stages, reflecting ongoing maturation of neural processing [63]. The reviewed studies used \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n61\n598 quite variable durations of ISI: from 22 to 457 ms for ABR studies (most often reported as \n599 presentation rate); from 500 ms [29] to 14 s [42] for middle and late latency studies; from 10 \n600 ms [64] to 1 s [4,54] for MMN/MMR studies. Among ABR and middle and late latency studies \n601 included in the review, none compared conditions with different ISI. One MMN study [64] \n602 considered the effect of the duration of the interval between stimuli in a pair, which was equal \n603 to 10 or 250 ms (design was described in more detail earlier in section 3.9). When the within-\n604 pair interval was extremely short (10 ms) RT deviants elicited small MMN and did not elicit \n605 any LDN, while in condition with longer interval after previous stimulus both of these \n606 components were observed. Another study of this group [35] meanwhile demonstrated the RT \n607 effect in a similar short interval: typically developing children showed larger N1 responses to \n608 the short RT than to the long RT (10 vs 80 ms). However, in this study, stimuli with different \n609 RTs had different frequencies, so the observed results may be related to pitch changes, even \n610 authors do not discuss that it could have affected the final outcome. At short intervals after the \n611 previous stimulus, masking of the rise time effects may be due to the overlap between the \n612 response to the stimulus onset and the response to the previous stimulus offset, or due to \n613 insufficient time period for recovery of specific neuronal populations after stimulus-specific \n614 adaptation. \n615 In summary of the included studies, we can conclude that an interval of 250 ms is \n616 sufficient to detect effects associated with the oddball paradigm (MMN, LDN) [64,65], and an \n617 interval of 500 ms is sufficient to observe effects on middle and late latency \n618 components[26,29], as at shorter intervals the effect may be masked due to the stimulus-specific \n619 adaptation. In ABR studies, the interstimulus interval varied from 22 to 457 ms and did not \n620 affect the either amplitude or latency of the component.\n621\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n62\n622 Stimulus type\n623 Studies included in the review used different types of stimuli that can be divided into \n624 three main groups: noise bursts (white nose or speech shaped nose), sine tones and speech \n625 tokens. Different types of stimuli were compared in the same sample only in two of the \n626 reviewed studies [40,48]. In Prasher (1980) study RT effects on N1-P2 amplitude were \n627 observed only for tone stimuli, but not for white noise. At the same time, prolongation in N1 \n628 latency with RT increasing was observed for both types of stimuli. The author explains this by \n629 noting that white noise's spectral content remains unchanged with varying RT, whereas for tone \n630 stimuli shorter RT (e.g., 2.5 ms) can introduce high-frequency transients due to the abrupt onset, \n631 making the stimulus sound sharper or harsher. When longer RT were used and tone stimuli \n632 were contrasted with speech-shaped noise in the sample of infants, no difference between \n633 conditions were observed [48].\n634 A general consideration of the other studies shows that the neurophysiological effects \n635 of RT have been successfully detected both in the case of tones and speech stimuli. Some \n636 particular discrepancies like in Easwar’s and colleagues’ works[36,39], where significant \n637 decrease in N1-P2 amplitude with RT prolongation was observed for syllables but not for 1000 \n638 Hz tone burst, are rather due to other stimulation parameters (too tiny difference in RT \n639 conditions for the tones). The acceptability of all possible stimulus types for the investigation \n640 of RT sensitivity is also supported by a recent longitudinal behavioral study [66]. It was shown \n641 that RT sensitivity thresholds measured with different stimulus types are significantly \n642 correlated with each other.\n643 The findings from various studies investigating neural responses to speech sound \n644 characteristics suggest that formant RT processing often yields particularly distinct or robust \n645 effects in neurotypical populations when compared to other groups. For instance, research of \n646 Moberly et al., 2014 has indicated that while MMN responses can be elicited by both amplitude \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n63\n647 and formant RT (ART and FRT) deviants, the brain's response to formant RT changes is \n648 sometimes significantly stronger and more consistently observed across individuals. This \n649 pattern of heightened FRT sensitivity in neurotypical group appears to differ from observations \n650 in adults with cochlear implants [54], where such a specific enhancement for FRT processing \n651 in MMN responses was not evident. Studies involving children also highlight differences based \n652 on neurotypical development: typically developing children have been shown to exhibit \n653 mismatch responses to a broader range of FRT deviants (including both partial and full \n654 changes) compared to children with dyslexia, who may only demonstrate responses to more \n655 substantial FRT alterations, implying a more finely tuned FRT processing mechanism in their \n656 neurotypical peers [55]. Furthermore, developmental research points to an increasing \n657 specialization for FRT in neurotypical individuals. While younger children (e.i., those under 10 \n658 years old) might respond to changes in both ART and FRTs, older neurotypical children (e.i., \n659 10–12 years old) and adults tend to show sensitivity primarily to FRT deviants, suggesting a \n660 maturation of this specific auditory processing capability [56]. Although not all investigations \n661 into RT processing have found group-based differences for every neural component studied, \n662 the collective evidence from MMN/MMR studies using specific FRT manipulations, supports \n663 the notion that FRT serves as a salient acoustic cue for which neurotypical auditory systems \n664 demonstrate more specialized processing.\n665\n666 Intensity of stimulation\n667 The RT changes accompany the total changes of the stimulus energy, such as intensity \n668 and also significantly influences perceived loudness of a sound. This effect is associated with \n669 the reduction of the plateau duration (period at which the stimulus has maximal intensity) if RT \n670 is increased. Therefore, stimuli with the same duration but different RTs will have different \n671 cumulative intensity and can be perceived as stimuli of different loudness. In order to \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n64\n672 distinguish RT and intensity effects, Thomson and colleagues (2008) used two types of deviant \n673 stimuli: deviant with a shorter RT (15 ms) than in standard stimulus (50 ms) and deviant with \n674 the same short RT but matched with the standard stimulus in intensity. When intensity of RT \n675 deviant was matched, no significant mismatch response was found, while traditionally used RT \n676 deviant, that is unmatched in intensity, produced some MMN (but it was not significant). \n677 However, in the opposite condition, when the standard and deviant stimuli were switched, \n678 matched in intensity deviant with longer than standard RT (50 ms) elicited MMN. Thus, MMN \n679 is sensitive to the RT per se, but dependent on the context. In ERP study by Kodera and \n680 colleagues (1979), stimuli with different RT were matched in intensities. Despite this, the \n681 authors obtained significant RT effects for latency and amplitude of ABR and main middle and \n682 late latency components (except N1-P2 peak-to-peak amplitude). The absence of an effect for \n683 the N1-P2 component is quite unusual, as most studies have associated this component with \n684 the RT effects. This effect may be related to the fact that when intensity is equated, the main \n685 effects of RT are related to the signal detection time. When stimuli are equalized in intensity, \n686 the point at which stimuli with different rise times begin to be perceived as equivalent occurs \n687 earlier. In this case, such difference in stimulus detection time could be less critical for effects \n688 on later components, especially when the difference between the RT conditions is small (15 ms \n689 in Kodera work). In relation to ABR, due to the even smaller difference in the durations of the \n690 RTs studied, this problem is relevant only in the sense that some RT+intensity combinations \n691 are below the response elicitation threshold and, accordingly, cannot be compared.\n692 RT discrimination thresholds are influenced by the overall stimulus intensity [67]. \n693 While many studies in the literature, particularly those focusing on language development or \n694 clinical applications, control for intensity by presenting sounds at comfortable listening levels, \n695 the general psychophysical principles suggest an intensity dependence. It is generally \n696 understood that at very low sound levels, the auditory system has fewer activation, leading to \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n65\n697 poorer discrimination. As intensity increases, more auditory nerve fibers are recruited, \n698 providing a more robust and detailed representation of the sound's temporal envelope, which \n699 can lead to improved RT discrimination. This complex interaction between intensity and \n700 temporal processing is crucial for understanding how we perceive sounds in various real-world \n701 environments. So, it is important to consider whether intensity is an essential characteristic for \n702 detecting RT effects on the ERP. Some classical auditory perception studies have investigated \n703 the effects of RT at different intensities. Onishi and Davis (1968) have found that the \n704 prolongations in N1 latency and decrease in N1-P2 peak-to-peak amplitude with RT increase \n705 were observed in all intensity levels (45, 65, and 85 dB), notable that latency increase was \n706 particularly marked at the lowest (45 dB) intensity level. However, in the second part of their \n707 study, an intensity condition of 15 was used, at this condition response was above noise level \n708 for only one participant for the rise time of 3 ms, and only for two participants for rise time of \n709 30 ms. Nevertheless, the authors report that the amplitude of N1P2 was systematically lower at \n710 3 ms RT than at 30 ms RT, at all intensity levels. No interaction between RT and intensity \n711 effects was found in the Skinner and Jones study [30]. However, it should be noted that no \n712 statistical analyses were performed in the two given studies. In Prasher study (1980) the \n713 observed RT effects did not differ between intensity conditions (80 and 40 dB SPL). Overall, \n714 no clear association between the observed RT effects and intensity was reported in the included \n715 in the review studies. Thus, modulation of amplitude and latency by the RT duration can be \n716 detected even at low intensities (15–45 dB SPL), especially if the difference between the RT \n717 durations is large enough [27,30,37,42].\n718 Thus, the findings of this systematic review suggest that variations in intensity across \n719 different RT conditions did not influence the neurophysiological discrimination, but could \n720 potentially confound the interpretation of results. However, there is no effective way to separate \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n66\n721 the effect of RT and cumulative intensity as inevitable matching of cumulative intensity of \n722 stimuli with different RT lead to their difference in maximal intensity. \n723\n724 Differential sensitivity to the rise time duration changes across stages of \n725 auditory processing \n726 The reviewed studies cover a very wide difference in RT from microseconds to \n727 hundreds of milliseconds, all of them indexing some aspects of the natural environment. Fast \n728 abrupt changes activate the alerting system and also important for consonant discrimination, \n729 RT between 15 to 100 ms are crucial for vowel perception, while RT changes in slowed rate \n730 represent the background auditory scene analysis, emotional component of speech and prosody \n731 [68–70].\n732 A summary of differences in RT durations for different ERPs can be seen on Figure 3. \n733 In most ABR-studies RT differences varied from tens of microseconds (the smallest value 90 \n734 µs or 0.09 ms in Salt & Thornton study) to 7 ms, while in some studies this difference reached \n735 15 ms. Noteworthy, for each contrast the significant changes in ABR latencies were found. \n736 Middle latency components were studied only in two studies with the RT range from 0.49 ms \n737 to 24.99 ms and the components modulation were demonstrated for all used contrasts. The \n738 range of RT differences, which showed significant results for late latency (components was \n739 from 4.99 ms to 500 ms, in most cases considered as N1P2 peak-to-peak amplitude). The \n740 optimal RT ranges also differed within late latency components being smaller for N1, and larger \n741 for P2 (>30 ms). RT differences less than 4.99 ms (namely 2.49 ms in Prasher study, 1980) and \n742 more than 500 ms (in Elfner study, 1976) showed no significant changes in amplitude or \n743 latency.\n744 In most recent studies on the RT perception, a RT of 15 ms is usually used as the \n745 minimum value [29,33,47,48,65]. This concerns those evoked potentials that arise in the \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n67\n746 cerebral cortex as opposed to those that are associated with activity, for example, in the \n747 brainstem, namely, the ABRs, which are produced on the earlier stages of auditory processing \n748 and are not accessible for behavioral discrimination. In auditory discrimination tasks, 15 ms is \n749 widely utilized as a standard reference point which is compared to a longer RT. This \n750 standardization allows for consistent experimental protocols and comparable results across \n751 studies. According to research on auditory processing and phonological development, this \n752 parameter provides an optimal baseline for discrimination tasks. In RT discrimination tasks, \n753 researchers typically present target sounds gradually logarithmically ranging from 15 ms (the \n754 standard) to longer durations. This methodological approach has been validated through \n755 multiple studies, which explore relationships between RT sensitivity and reading development \n756 [29,48,71]. Research has also demonstrated that 15 ms RT effectively balances the need to \n757 avoid spectral splatter while maintaining temporal precision in auditory stimuli. This technical \n758 consideration is crucial for creating clean experimental stimuli without introducing \n759 confounding variables [72]. The 15 ms RT parameter aligns with critical amplitude RTs in the \n760 speech envelope that significantly impact speech intelligibility. This connection to natural \n761 speech processing makes it particularly relevant for studying both typical and atypical language \n762 development, as demonstrated in research on auditory temporal processing and phonological \n763 awareness [73].\n764\n765 Fig. 3 Differences in rise time durations (in ms) in studies observed.\n766\n767 Thus, the optimal time window for detecting RT effects varies depending on the level \n768 of processing. For brainstem structures, the response of which is detected by ABRs, it is very \n769 short. For subcortical structures it is longer, and for cortical structures (late potentials) it is the \n770 longest and in most works is not less than 15 ms. While ABRs are remarkably sensitive to RT \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n68\n771 differences as tens of microseconds, reflecting their role in processing the immediate onset of \n772 sound, subcortical structures demonstrate a longer optimal window. This extended window is \n773 evidenced by studies on middle latency components, which showed modulations across a range \n774 of RT differences from 0.49 ms to 24.99 ms. This suggests that subcortical processing integrates \n775 auditory information over a slightly more prolonged period than the brainstem, allowing for the \n776 detection of RT effects that unfold over hundreds of microseconds to several milliseconds. \n777 Further extending this temporal integration, cortical structures, responsible for late potentials, \n778 exhibit the longest optimal window for RT effects. In the majority of research, this window is \n779 not less than 15 ms. This is because late cortical components are involved in higher-level \n780 processing, where the brain is analyzing more complex features of the sound stimulus. \n781 Consequently, to observe significant effects, a more substantial difference in the RT between \n782 conditions – typically exceeding 15 ms – is required for the distinctions to be sufficiently \n783 pronounced to modulate cortical responses. This extended temporal requirement reflects the \n784 cortical areas' role in integrating information over longer durations for perceptual \n785 discrimination, language processing, and cognitive functions, where the precise, rapid onset \n786 information critical for brainstem responses has already been processed and is being interpreted \n787 within a broader temporal context.\n788\n789 Developmental changes in electrophysiological markers of rise time \n790 perception\n791 The main ERP components undergo significant developmental changes across the \n792 lifespan, reflecting the maturation of the auditory processing system. Already the earliest, \n793 subcortical auditory responses like ABR demonstrate significant age-related changes, with \n794 research showing progressive increases in peak latencies of waves I, III, and V through \n795 ontogenesis [74]. A systematic search, however, found only one RT study in children that \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n69\n796 examined ABR: the results for infants in this study were no different from those for adults [14].  \n797 No RT studies for children concerning middle latency potentials were found. \n798 Late latency components like N1 demonstrate prolonged development. In early \n799 childhood, auditory evoked potentials are dominated by the P1 and N2 components, while the \n800 N1 and P2 components response becomes more prominent with maturation at about 10-12 years \n801 of age. Also latency of such components decreased with age. The MMN component, which \n802 reflects automatic auditory change detection,  develops from positive to negative through \n803 childhood. MMN has been directly linked to auditory discrimination abilities that evolve \n804 throughout the lifespan [75]. These developmental changes in ERPs considered in relation to \n805 RT perception have important implications for understanding both typical auditory \n806 development and disorders characterized by impaired rise time processing.\n807 Studies of neurotypical adults demonstrated that the main effects of RT are observed on \n808 N1 and P2 components. However, in young children these components are not yet fully \n809 developed [76], which suggests that the typical pattern of ERP components modulation by the \n810 rise time duration may change with age. Only three studies included in the review examined \n811 the RT effects of main ERP components in children [29,35,41]. Two of them considered RT \n812 effects on N1–P2 peak-to-peak amplitude in children samples [35,41]. In the study by Carpenter \n813 & Shanin (2013) [41] decreasing N1-P2 amplitude was observed only after 6 years, while 4–5 \n814 years old children did not demonstrate any RT effects, which may be related to the poor \n815 development of this component in this age group. In Hämäläinen (2007) [35] study, typically \n816 reading children (aged 8.8–10.5 years) demonstrate N1 decrease with RT prolongation. The \n817 third of the included studies concerning RT in children [29] showed that in children the RT \n818 related effects can be transferred to adjacent components (P1 and N2), which probably absorb \n819 some functions from not fully developed N1 and P2 components. Thus, in children (aged 7–11 \n820 years), P1 demonstrates a latency delay with RT increasing. It was also shown that at these ages \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n70\n821 RT effects are observed for the N2 component, which demonstrates a decrease in amplitude \n822 and prolongation of latency with RT increasing.\n823 Age-specific phenomenon was also observed for studies carried out in the oddball \n824 paradigm. Generally, the latency of the difference-wave mismatched response decreases with \n825 age. Decreasing in MMN latency in older children is a common fact associated with age-related \n826 reduction in latency of ERP components [77]. This is also typical for the mismatch response \n827 evoked by a deviant stimulus with a different RT, which can be seen in studies, included in this \n828 review. Six of the oddball studies included in this review also examined children. In particular, \n829 in studies including adult participants, MMN to RT changes was observed in a time window \n830 from 150 to 350 ms [4,52,54,57,58]. In children, this time window can be shifted and is \n831 considered as a mismatch response [47,56,56,65]. At 11 years the peak of mismatch response \n832 appears at 256 ms [65], while at age of 3 years – at 346 ms [47]. In infants, the response time \n833 window is shifted even more: from 300 ms to 460 ms [48]. Also, age could affect MMN \n834 amplitude, which tends to be larger in children than in adults [77,78]. From the works presented \n835 in the review we can also observe the change of configuration of the mismatch response on \n836 difference wave, which becomes more negative in older participants. The beginnings of these \n837 changes can already be observed in infants, but the response remains positive (Choisdealbha et \n838 al., 2022). At around 10 years, the positive MMR is replaced by a negative response, known as \n839 MMN [56]. \n840 Behavioral studies have established that discriminatory sensitivity to acoustic RT \n841 changes throughout ontogenesis [71]. In particular, six-year-old children have significantly \n842 lower RT thresholds (83.6 ms for sine tones, 150.26 ms for noise, 61.06 ms for speech token) \n843 than four-year-olds (205.37 ms for sine tones, 257.69 ms for noise, 105.91 ms for speech token). \n844 However, the neurophysiological underpinnings of this developmental trajectory remain \n845 insufficiently characterized, largely due to a scarcity of research focused specifically on \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n71\n846 pediatric populations. The existing literature provides glimpses into these developmental shifts. \n847 For example, Peter et al. (2018) studied speech tokens and demonstrated a clear age-dependent \n848 pattern where children younger than 10 showed a positive mismatch response to both ART and  \n849 FRT deviants, whereas children aged 10-12 and adults exhibited sensitivity primarily to FRT \n850 changes. This suggests a maturational process that refines neural specialization for speech \n851 sounds. Consequently, while it is clear that neural sensitivity to RT evolves with age, a \n852 comprehensive map of how specific neurophysiological markers for different types of RT \n853 develop in children is still needed. \n854 Thus, it is important to take into account that the main target components of ERPs \n855 showing RT effects quite significantly varies with age. Thus, the ERP configuration in each \n856 age group has to be considered in order to more accurately interpret the RT effects and to be \n857 able to compare the results of different studies. \n858\n859 Rise time perception and speech disorders\n860 Eight of included studies were focused on the neurophysiological specifics of RT \n861 processing in speech disorders (particularly dyslexia). Four of them consider MMN or MMR \n862 measured in oddball paradigm as possible neuromarker of RT processing in speech impediment \n863 groups [47,55,64,65], three works consider late latency ERP components (such as P1, N1, P2 \n864 and N2 [29,34,35] and one work was focused on ASSR [59]. The observed results were very \n865 controversial. Several studies indicated that some patterns of ERP modulation by RT that were \n866 observed in the typically-developing group were not present in groups with reading disabilities \n867 [35,47,55]. In contrast, other studies have shown that RT-related changes that were not \n868 characteristic of the typically-developing group are observed in reading disorders [29,34,64]. \n869 Alternatively, there may be no differences between groups at all [65]. \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n72\n870 Research into the RT processing of individuals with dyslexia, particularly concerning \n871 the MMN and other ERP components in response to changes in stimulus RT, has yielded varied \n872 results. One key finding from Hämäläinen and colleagues (2008) indicated a larger MMN to \n873 RT changes in children with reading difficulties when preceding stimuli were sufficiently \n874 separated. However, this observation was tempered by the suggestion that an elevated N1 \n875 component in dyslexia [79] might contribute to this effect through overlap. In subsequent work, \n876 Hämäläinen et al. (2011) noted that individuals with dyslexia exhibited less negative amplitudes \n877 of the T-complex with prolonged RTs, which they attributed to an enlarged Tb component, \n878 potentially enabling better detection of RT effects despite other processing differences. Other \n879 studies also explored this area, with Stefanics (2011) reporting the increased P1 latency and \n880 bigger fronto-temporal N1c amplitude (for 90 ms RT in dyslexia group vs 15 ms RT in TD \n881 group) for RT changes in children with dyslexia as compared to neurotypical controls.\n882 Despite these findings, the Peter (2016) study introduced a nuanced perspective, \n883 suggesting that the perception of formant RT differences might be a more informative marker \n884 for dyslexia than amplitude RT differences. This raises questions about the overall utility of the \n885 MMN response to amplitude RT deviants as a definitive indicator of dyslexia. Further insights \n886 come from Plakas (2013), whose study on three-year-old children revealed a critical distinction: \n887 MMR in response to a 90 ms RT tone within a stream of 15 ms RT tones was exclusively \n888 observed in typically-developing children without a familial risk of dyslexia. Children with a \n889 familial risk, regardless of a dyslexia diagnosis, did not exhibit this response. This result points \n890 towards a genetic predisposition to dyslexia, rather than merely reflecting the diagnosis itself, \n891 and suggests that these early childhood MMR differences might signify a general susceptibility \n892 to phonological challenges that could be mitigated by the development of other language skills \n893 in older age. Collectively, these studies underscore the complex and multifaceted nature of \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n73\n894 auditory processing deficits in dyslexia, highlighting the need for continued research to refine \n895 our understanding and identify robust diagnostic markers.\n896\n897 Directions for further research\n898 As previously mentioned, there are certain areas in RT research where the findings are \n899 largely consistent, such as decrease in amplitude and increase in latency for the main \n900 components of ABRs and ERPs. Conversely, the existing results do not permit us to draw clear \n901 conclusions about the mechanisms underlying RT effects, particularly in studies related to \n902 MMN, LDN, and research involving individuals with dyslexia. It is worth noting that many of \n903 the studies yielding consistent results were conducted quite some time ago, which suggests that \n904 new methodological approaches and more advanced technology could potentially reinterpret \n905 these findings. This is particularly relevant for ABR-studies. Due to methodological limitations, \n906 including outdated technology, small sample sizes, and manual measurements, existing ABR \n907 rise time studies, the most recent of which dates back to 1996 with a significant portion \n908 conducted in the 1970s-1980s, may be biased, highlighting the need for replication with modern \n909 equipment, larger samples, and design-appropriate statistics. Another clear gap in knowledge \n910 that is evident at Fig.2, is the absence of research on the main ERP components after 2014, with \n911 the field dominated by an oddball paradigm. While oddball paradigm allows assessing the \n912 neurophysiological response to the sound differences, it has several drawbacks, such as \n913 increased duration of stimulation, low signal to noise ratio, ambiguity of results interpretation \n914 and so on [49,80]. Thus, the recent neurophysiological studies on RT can be largely \n915 supplemented by the analysis of main ERP components in response to repetitive stimulation.\n916 In this review, we aimed to observe all RT electrophysiological human studies. \n917 However, studies in the children population, especially for basic ERP components, such as P1, \n918 N1, P2 and N2 are lacking, while investigation of the developmental trajectory for the rise time \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n74\n919 neurophysiological sensitivity is crucial for linking it with speech perception ability. A similar \n920 gap is seen for the studies in the clinical group, only participants with speech and reading \n921 difficulties were found to be included in the review. At the same time, impaired ability to \n922 process phonological features of auditory stimuli is observed not only in patients with other \n923 speech and language disorders, but also in patients with developmental disorders, primarily \n924 with ASD [81]. In particular, it was reported about an auditory temporal-envelope resolution \n925 deficit in this population [82], which might cause the delay of phonological categories \n926 development in children with ASD [83]. Temporal resolution of the auditory cortex is often \n927 assessed using amplitude modulated stimuli [84], and such a characteristic as RT can be also \n928 differently processed in people with ASD. Thus, investigation of RT neurophysiological \n929 discrimination in people with ASD seems like a logical continuation of such research in clinical \n930 groups.\n931\n932 Limitations\n933 Several limitations of this review should be acknowledged. First, our search strategy \n934 was restricted to publications in English and to major electronic databases, which may have \n935 introduced language and publication biases, potentially omitting relevant studies published \n936 elsewhere. \n937 Second, there was substantial methodological and conceptual heterogeneity across \n938 studies in some sections. This heterogeneity precluded a quantitative meta-analysis and \n939 necessitated a narrative synthesis, which is more susceptible to subjective interpretation. To \n940 enhance objectivity, we used a pre-defined framework for synthesis and independent \n941 assessment by two reviewers.\n942 Third, the methodological quality of the primary studies was sometimes suboptimal, \n943 with frequent unclear or high risk of bias, as assessed by the OHAT tool. Consequently, the \n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n75\n944 overall confidence in the body of evidence for outcomes in some sections, as per our OHAT-\n945 based assessment, was not high enough. This fundamentally qualifies the strength of our \n946 conclusions, which should be viewed as hypothesis-generating rather than definitive.\n947 Finally, despite our comprehensive search, the possibility of unpublished null results \n948 (publication bias) remains a concern that could skew the presented narrative towards an \n949 overestimation of reported effects.\n950\n951 Author contributions\n952 V.M.: Conceptualization, Full-text screening, Analysis, Writing – original draft, \n953 Writing – review and editing, Visualization.  D.K.: Conceptualization, Abstract screening, Full-\n954 text screening, Analysis, Writing – original draft, Writing – review and editing. A.R.: Abstract \n955 screening, Full-text screening, Writing – original draft, Writing – review and editing. O.S.: \n956 Conceptualization, Writing – review and editing, Supervision\n957\n958 Funding sources\n959 Supported by the Ministry of Science and Higher Education of the Russian Federation, \n960 (Agreement 075-10-2025-017 from 27.02.2025)\n961\n962 Declaration of competing interest\n963 The authors, who are all academic researchers, declare that they have no affiliations \n964 with or involvement in any organization or entity with any financial or non-financial interest in \n965 the subject matter or materials discussed in this systematic review.\n966\n967\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n76\n968 References\n969 1. Goswami U. 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It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint \n\n.CC-BY 4.0 International licensemade available under a \n(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is \nThe copyright holder for this preprintthis version posted March 9, 2026. ; https://doi.org/10.64898/2026.03.06.710012doi: bioRxiv preprint","source_license":"CC-BY-4.0","license_restricted":false}