Anatomy and physiology of speech and hearing

In short

This topic covers the structures and working of the two systems a clinician treats: the speech mechanism (respiration, phonation, resonance, articulation and its neural control) and the auditory mechanism (outer, middle and inner ear, the VIII nerve and the central auditory pathway). It is the single foundation paper of the BASLP course — every later subject (audiology diagnostics, voice disorders, dysarthria, cochlear implants, aural rehabilitation) is applied anatomy and physiology. It is examined in university Semester I–II papers, in AIISH/NISH/AYJNISHD and university PG entrance tests, and in technical rounds for audiologist and speech-language pathologist posts in hospitals, ENT clinics, hearing-aid companies (Phonak, Oticon, Signia, Starkey, Cochlear, MED-EL) and NGO/early-intervention centres. Practice in India is regulated under the Rehabilitation Council of India Act, 1992 (RCI registration is compulsory to practise) and services are delivered under the RPwD Act, 2016, NPPCD and the ADIP scheme.

Explained

Respiratory system: the power supply for speech

• Framework: thoracic cage (12 pairs of ribs, sternum, thoracic vertebrae), lungs, bronchial tree, trachea (16–20 incomplete cartilage rings).
• Muscles of inspiration: diaphragm (chief muscle, nerve supply phrenic nerve, C3–C5), external intercostals; accessory — sternocleidomastoid, scalenes, pectorals.
• Muscles of expiration: passive elastic recoil at rest; internal intercostals, rectus abdominis, transverse and oblique abdominals for forced/speech expiration.
• Quiet breathing vs speech breathing: quiet — inspiration ≈40%, expiration ≈60% of cycle, tidal volume ~500 mL, 12–18 cycles/min. Speech — rapid inspiration (~10%), long controlled expiration (~90%), 8–12 cycles/min, using roughly 20–25% of vital capacity per breath group.
• Lung volumes: TV, IRV, ERV, residual volume (RV, cannot be exhaled); vital capacity VC = TV + IRV + ERV; total lung capacity TLC = VC + RV; functional residual capacity FRC = ERV + RV, the resting expiratory level around which speech breathing is organised.
• Checking action: inspiratory muscles are held active early in an utterance to oppose excess recoil pressure, keeping subglottal pressure steady at about 5–10 cm H₂O.
• Clinical measures: maximum phonation time (MPT, normal adults ~18–25 s), s/z ratio, vital capacity by spirometer.

Phonation: larynx and vocal fold physiology

• Cartilages: unpaired — thyroid, cricoid, epiglottis; paired — arytenoid, corniculate, cuneiform. Joints: cricothyroid (rocking/gliding, pitch change) and cricoarytenoid (rotation/gliding, abduction–adduction).
• Intrinsic muscles (all CN X, recurrent laryngeal nerve, except cricothyroid by external branch of superior laryngeal nerve):
  • Posterior cricoarytenoid (PCA) — the only abductor.
  • Lateral cricoarytenoid, interarytenoid (transverse/oblique) — adductors.
  • Thyroarytenoid/vocalis — shortens and thickens folds, lowers pitch, medial compression.
  • Cricothyroid (CT) — lengthens and tenses folds, raises pitch.
• Extrinsic muscles: suprahyoid (digastric, stylohyoid, mylohyoid, geniohyoid — elevate larynx) and infrahyoid/strap (sternohyoid, sternothyroid, thyrohyoid, omohyoid — depress larynx); they fix laryngeal height.
• Layered structure of the vocal fold (Hirano): epithelium (stratified squamous) → lamina propria superficial layer (Reinke's space, gelatinous — site of oedema and polyps) → intermediate (elastic) and deep (collagenous) layers which together form the vocal ligament → thyroarytenoid muscle. Mechanically this reduces to cover (epithelium + superficial LP) and body (ligament + muscle) — the body–cover theory of pitch and register control.
• Myoelastic–aerodynamic theory (van den Berg): folds are adducted → subglottal pressure builds until it exceeds the closing force → folds are blown apart from below upward → air flows, inter-glottal pressure falls (Bernoulli effect) and elastic recoil pulls the folds back together → pressure rebuilds; the cycle self-sustains. Vibration is passive, not a muscle twitch per cycle.
• Glottal cycle phases: opening, open, closing, closed; the mucosal wave travels upward along the cover. Vertical phase difference (lower margin leads upper) is essential for sustained oscillation.
• Control parameters: F₀ rises with fold tension/length (CT) and with subglottal pressure (~2–5 Hz per cm H₂O); intensity rises with subglottal pressure and longer closed phase. Average F₀: adult male 100–150 Hz, adult female 180–230 Hz, children 250–400 Hz.
• Registers: modal, falsetto (thin, stiff cover, no mucosal wave), glottal fry/pulse.
• Protective and biological functions: airway protection, cough, effort closure (Valsalva), respiration.

Resonance and articulation

• Vocal tract: from glottis to lips (~17–18 cm in adult males, ~14–15 cm females, ~8–9 cm newborn); includes pharyngeal, oral and nasal cavities. It filters the glottal source — the source–filter relationship.
• Articulators: mobile — tongue (intrinsic: superior/inferior longitudinal, transverse, vertical; extrinsic: genioglossus, hyoglossus, styloglossus, palatoglossus), lips (orbicularis oris, buccinator, risorius, levator/depressor group), mandible, velum, pharynx; immobile — teeth, alveolar ridge, hard palate.
• Velopharyngeal mechanism: levator veli palatini (chief elevator), tensor veli palatini (CN V, Eustachian tube opening), palatoglossus, palatopharyngeus, superior constrictor; Passavant's ridge. Closure is needed for all sounds except nasals /m, n, ŋ/; failure gives hypernasality and nasal emission (cleft palate, submucous cleft, post-adenoidectomy).
• Dentition and occlusion: Angle's Class I/II/III malocclusion, open bite, crossbite — affect sibilants and labiodentals.
• Temporomandibular joint: muscles of mastication — masseter, temporalis, medial and lateral pterygoid (all CN V₃).

Neural control of speech

• Cranial nerves for speech: V trigeminal (mastication, tensor veli palatini, facial sensation); VII facial (facial expression, lip rounding, stapedius, taste anterior tongue); VIII vestibulocochlear (hearing, balance); IX glossopharyngeal (stylopharyngeus, pharyngeal sensation, gag); X vagus — superior laryngeal nerve (external branch → cricothyroid; internal branch → sensation above folds) and recurrent laryngeal nerve (all other intrinsic muscles, sensation below folds); XI accessory (with X to pharynx; shoulder); XII hypoglossal (all tongue muscles except palatoglossus).
• Spinal nerves: phrenic (diaphragm), intercostal and abdominal nerves (respiration for speech).
• Cortex: primary motor cortex (precentral gyrus, large orofacial representation — motor homunculus), Broca's area (BA 44/45, posterior inferior frontal gyrus — speech motor programming), supplementary motor area (initiation), Wernicke's area (BA 22, posterior superior temporal gyrus — comprehension), arcuate fasciculus connecting them (conduction aphasia when lesioned), angular and supramarginal gyri (reading/writing). Language is left-dominant in ~95% right-handers.
• Subcortical: basal ganglia (hypokinetic dysarthria in Parkinson's disease, hyperkinetic in Huntington's), cerebellum (ataxic dysarthria), thalamus.
• Pathways: pyramidal — corticobulbar (to cranial nerve nuclei; mostly bilateral supply, so unilateral UMN lesion spares most muscles except lower face and tongue) and corticospinal; extrapyramidal for tone and posture.
• UMN vs LMN signs: UMN — spasticity, hyperreflexia, no atrophy (spastic dysarthria); LMN — flaccidity, atrophy, fasciculation, hyporeflexia (flaccid dysarthria, e.g. vocal fold paralysis after thyroid surgery injuring the RLN).

Outer and middle ear: conduction and impedance matching

• Pinna/auricle: elastic cartilage with helix, antihelix, concha, tragus; collects sound, aids localisation (spectral cues) and gives ~5 dB concha resonance near 5 kHz.
• External auditory canal (EAC): ~25 mm long, S-shaped; outer third cartilaginous with hair, ceruminous and sebaceous glands; inner two-thirds bony. Acts as a closed quarter-wave resonator (~2,500–3,000 Hz, ~10–15 dB gain). Equivalent ear canal volume on tympanometry ≈0.6–2.0 cm³ (adults), 0.3–0.9 cm³ (children).
• Tympanic membrane (TM): ~55–90 mm² total, effective vibrating area ~55 mm²; three layers (outer epithelial, middle fibrous, inner mucosal); pars tensa with annulus and umbo, pars flaccida (Shrapnell's membrane); cone of light.
• Ossicles: malleus (head, neck, manubrium), incus, stapes (head, crura, footplate ~3.2 mm² in the oval window). Suspended by ligaments; the chain converts air pressure to fluid motion.
• Impedance matching (needed because air impedance ≪ cochlear fluid impedance; direct air-to-fluid transfer loses ~30 dB):
  1. Area ratio TM/footplate ≈ 17:1 — the main factor.
  2. Ossicular lever ratio (manubrium : long process of incus) ≈ 1.3:1.
  3. Curved-membrane (catenary/buckling) effect of the TM, ~2 dB.
  4. Combined gain ≈ 25–30 dB, greatest at 500–4,000 Hz.
• Middle ear muscles: tensor tympani (CN V₃, tenses TM) and stapedius (CN VII) — the acoustic (stapedial) reflex stiffens the chain at high levels (~70–100 dB HL), giving low-frequency protection; absent reflex is a key diagnostic sign.
• Eustachian tube: ~36 mm in adults, directed down-forward-medially; equalises pressure, drains and ventilates. In infants it is shorter, wider and nearly horizontal — hence frequent otitis media.
• Mastoid air cells and the facial nerve run in close relation — surgical landmarks.

Inner ear: cochlea, transduction and the cochlear amplifier

• Bony labyrinth: cochlea (2½–2¾ turns, ~35 mm basilar membrane length), vestibule, three semicircular canals; filled with perilymph (Na⁺-rich, like extracellular fluid). Membranous labyrinth contains endolymph (K⁺-rich, ~150 mM).
• Three scalae: scala vestibuli and scala tympani (perilymph, joined at the helicotrema) and scala media/cochlear duct (endolymph), bounded by Reissner's membrane above and the basilar membrane below. Stria vascularis maintains the endocochlear potential of about +80 mV — the battery for transduction.
• Organ of Corti: on the basilar membrane — one row of inner hair cells (~3,000–3,500, the true sensory receptors, flask-shaped) and three rows of outer hair cells (~12,000, cylindrical), pillar/rod cells of Corti with the tunnel of Corti, Deiters', Hensen's and Claudius cells, tectorial membrane overlying the stereocilia.
• Transduction steps: stapes pushes the oval window → pressure wave in perilymph → travelling wave on the basilar membrane → shearing between the tectorial and basilar membranes bends the stereocilia → tip links open mechanoelectrical transduction channels → K⁺ enters down the +80 mV gradient, cell depolarises → Ca²⁺ influx → glutamate released at the ribbon synapse → spikes in the VIII nerve; round window moves to relieve pressure.
• Travelling wave theory (von Békésy): the basilar membrane is narrow and stiff at the base (high frequencies, up to 20 kHz) and wide and lax at the apex (low frequencies, down to 20 Hz) — tonotopic/place coding, preserved all the way to the cortex.
• Coding of frequency: place coding for high frequencies; temporal (phase-locking/volley) coding for low frequencies up to roughly 4–5 kHz; both combine in mid frequencies.
• Cochlear amplifier: OHCs change length via the motor protein prestin (electromotility), adding ~40–50 dB of gain and sharp frequency tuning; they are the source of otoacoustic emissions (TEOAE, DPOAE) used in newborn hearing screening. OHC loss → raised thresholds, poor tuning, loudness recruitment, absent OAEs.
• Innervation: ~30,000–35,000 afferents; type I (myelinated, ~95%) to IHCs with little convergence; type II (unmyelinated) to OHCs. Efferent olivocochlear bundle — medial fibres to OHCs (reduce gain, improve signal-in-noise), lateral to IHC afferents.
• Cochlear potentials: endocochlear (resting, +80 mV), cochlear microphonic (OHC, mirrors the stimulus), summating potential, compound action potential — recorded in electrocochleography.
• Blood supply: labyrinthine (internal auditory) artery from the basilar/AICA — no collateral supply, hence sudden sensorineural hearing loss on occlusion.
• Vestibular part: three semicircular canals with cristae ampullares and cupulae (angular acceleration), utricle and saccule with maculae, otoconia and otolithic membrane (linear acceleration and gravity); drives the vestibulo-ocular reflex, tested by caloric, VNG/VHIT and VEMP.

Central auditory pathway and its clinical markers

• Route: cochlea → VIII nerve (cochlear division) → cochlear nucleus (dorsal/ventral, medulla) → superior olivary complex (first site of binaural interaction — MSO for interaural time differences, LSO for level differences) → lateral lemniscus (nucleus of LL) → inferior colliculus (midbrain) → medial geniculate body (thalamus) → primary auditory cortex, Heschl's gyrus in the superior temporal gyrus (BA 41/42).
• Crossings at the trapezoid body, commissure of Probst and commissure of the inferior colliculus mean each ear is represented bilaterally — so a unilateral central lesion rarely causes deafness, but impairs localisation and speech-in-noise.
• ABR generators (commonly taught): wave I — distal VIII nerve; II — proximal VIII nerve/cochlear nucleus; III — cochlear nucleus/trapezoid body; IV — superior olivary complex; V — lateral lemniscus/inferior colliculus. Waves I, III and V and the I–V interval are read clinically.
• Hearing loss types from site of lesion: conductive (outer/middle ear — air–bone gap, normal bone conduction), sensorineural (cochlea or VIII nerve — no gap, both reduced), mixed, central/retrocochlear (normal audiogram possible, abnormal ABR, poor speech scores).

Indian regulation, standards and service framework

• Rehabilitation Council of India Act, 1992: BASLP is an RCI-recognised programme; audiologists and SLPs must hold RCI registration (CRR number) and renew it with continuing rehabilitation education to practise legally.
• Rights of Persons with Disabilities Act, 2016: recognises 21 disabilities including hearing impairment (deaf and hard of hearing) and speech and language disability; 40% impairment = benchmark disability for reservation and concessions; disability certification follows the Gazette guidelines notified in 2018, which grade hearing disability from pure-tone average (with speech discrimination considered) — exact percentage tables are periodically amended, so the notified version in force should be consulted.
• Programmes and schemes: National Programme for Prevention and Control of Deafness (NPPCD, from 2006); ADIP scheme for hearing aids with ALIMCO as the main supplier; district early-intervention and newborn screening under RBSK; cochlear implant support under ADIP and several state schemes.
• Institutions: AIISH Mysuru, AYJNISHD Mumbai, NISH Thiruvananthapuram, SVNIRTAR Cuttack, NIEPMD Chennai; professional body — Indian Speech and Hearing Association (ISHA).
• Equipment and calibration: audiometers, transducers and tympanometers are calibrated to the ISO 389 series (reference equivalent threshold SPLs) and IEC 60645 series, which BIS adopts as Indian Standards; sound-treated rooms follow ANSI/ISO permissible ambient noise limits. Quote the specific IS number only from the current BIS catalogue, as several older numbers have been revised or withdrawn.
• Noise and hearing conservation: occupational noise exposure in India is conventionally limited to 90 dB(A) for 8 hours with a 5 dB exchange rate (internationally 85 dB(A) is now common); the governing framework is now the Occupational Safety, Health and Working Conditions Code, 2020 and its rules, in force from 21 November 2025, which replaced the Factories Act, 1948. Community noise limits are set by the Noise Pollution (Regulation and Control) Rules, 2000 — for example 55 dB(A) day and 45 dB(A) night in residential zones.

Key points

• Speech subsystems – respiration (power), phonation (source), resonance (filter), articulation (shaping), with neural control over all four.
• Diaphragm – chief inspiratory muscle, phrenic nerve C3–C5; abdominals drive forced expiration for loud speech.
• Subglottal pressure – ~5–10 cm H₂O for conversational speech; raising it raises both intensity and (slightly) F₀.
• PCA – the only vocal fold abductor; its bilateral paralysis causes airway obstruction, not just dysphonia.
• Cricothyroid – pitch-raising muscle, supplied by the external branch of the superior laryngeal nerve (not the RLN).
• Reinke's space – superficial lamina propria; oedema here (smoking, abuse) alters the mucosal wave and lowers pitch.
• Myoelastic–aerodynamic theory – vibration results from aerodynamic force plus tissue elasticity and the Bernoulli effect, not per-cycle muscle contraction.
• Velopharyngeal closure – levator veli palatini is the chief elevator; incompetence gives hypernasality and nasal air escape.
• Cranial nerves of speech – V, VII, IX, X, XI, XII; vagus (RLN) supplies all intrinsic laryngeal muscles except cricothyroid.
• Broca (BA 44/45) vs Wernicke (BA 22) – motor programming vs comprehension; arcuate fasciculus links them.
• Impedance matching – area ratio ≈17:1, lever ratio ≈1.3:1, curved-membrane effect ≈2 dB; total ~25–30 dB gain.
• Eustachian tube in infants – short, wide, horizontal; explains the high incidence of otitis media in children.
• Endocochlear potential – about +80 mV from the stria vascularis; it powers hair-cell transduction.
• IHC vs OHC – ~3,500 IHCs are the sensory receptors (95% of afferents); ~12,000 OHCs are the amplifier, source of OAEs.
• Tonotopy – base stiff and narrow (high frequency), apex wide and lax (low frequency); maintained up to the auditory cortex.
• Prestin – OHC motor protein giving electromotility and ~40–50 dB of cochlear gain with sharp tuning.
• Superior olivary complex – first binaural centre (MSO: timing; LSO: level differences) — the basis of localisation.
• ABR wave V – the most robust wave, generated around the lateral lemniscus/inferior colliculus; used for threshold estimation in infants.

Formulas and examples

Example 1 — Middle ear transformer gain. Effective TM area 55 mm², stapes footplate 3.2 mm², ossicular lever ratio 1.3.

• Area ratio = 55 / 3.2 = 17.19.
• Total pressure ratio = 17.19 × 1.3 = 22.34.
• Gain = 20 log₁₀(22.34) = 20 × 1.3493 = 27.0 dB. Adding ~2 dB for the curved-membrane effect gives ≈29 dB — matching the ~30 dB loss expected from a direct air-to-fluid interface, which is why a destroyed ossicular chain can give a 50–60 dB conductive loss.

Example 2 — Audiogram interpretation. Right ear air conduction 40, 45, 55 dB HL at 500, 1,000, 2,000 Hz; bone conduction 10, 10, 10 dB HL.

• AC PTA = (40 + 45 + 55)/3 = 140/3 = 46.7 dB HL (moderate loss).
• BC PTA = 30/3 = 10 dB HL → ABG = 36.7 dB.
• Large gap with near-normal bone conduction ⇒ conductive loss (e.g. otosclerosis or ossicular discontinuity); tympanometry and reflexes localise the lesion. Being below the 40 dB range in the better ear matters for RPwD benchmark certification.

Example 3 — Laryngeal airway resistance. Subglottal pressure 8 cm H₂O, mean phonatory airflow 150 mL/s.

• U = 150 mL/s = 0.15 L/s.
• R = 8 / 0.15 = 53.3 cm H₂O/(L/s) — within the normal adult band (~35–55); a hyperfunctional voice shows much higher values, and vocal fold paralysis much lower with high airflow.
• In SI: 8 cm H₂O × 98.07 = 785 Pa.

Example 4 — Fundamental frequency from fold properties. Vibrating length 1.0 cm, longitudinal stress 10 kPa, ρ = 1,040 kg/m³.

• √(σ/ρ) = √(10,000 / 1,040) = √9.615 = 3.101 m/s.
• F₀ = 3.101 / (2 × 0.01) = 155 Hz — a typical adult male modal pitch. Quadrupling stress to 40 kPa gives √38.46 = 6.202 → F₀ = 310 Hz, i.e. F₀ scales with the square root of tension, which is why cricothyroid contraction raises pitch steeply.

Example 5 — Cochlear place and vocal tract resonance.

• Greenwood at x = 0.5 (mid-cochlea): 10^{2.1 × 0.5} = 10^1.05 = 11.22; (11.22 − 0.88) = 10.34; F = 165.4 × 10.34 ≈ 1,710 Hz. At x = 0.9: 10^1.89 = 77.6; (77.6 − 0.88) = 76.8; F ≈ 12,700 Hz — the basal end codes high frequencies, so a basal electrode array in a cochlear implant is mapped to high-frequency channels.
• Vocal tract, L = 17.5 cm, c = 350 m/s: F₁ = 350/(4 × 0.175) = 500 Hz, F₂ = 3 × 500 = 1,500 Hz, F₃ = 2,500 Hz — the neutral-vowel pattern; a child's 9 cm tract gives F₁ = 350/0.36 ≈ 972 Hz, which is why child formants are much higher.

Where it is used

• Hospital audiology and ENT departments (AIIMS, PGIMER, CMC Vellore, Apollo, Fortis, district hospitals under NPPCD): audiogram interpretation, tympanometry, ABR/OAE, pre- and post-operative evaluation for tympanoplasty, stapedotomy and cochlear implantation.
• Newborn and school hearing screening: OAE/AABR protocols under RBSK and state programmes depend on cochlear and brainstem physiology for pass/refer logic.
• Hearing-aid and implant industry: audiologist and clinical-trainer roles with Phonak, Oticon, Signia, Starkey, Widex, ReSound, Cochlear, MED-EL, Advanced Bionics and retail chains; ear-mould and real-ear measurement work uses ear-canal acoustics directly.
• Speech-language pathology practice: voice therapy (laryngeal muscle function), dysarthria and dysphagia management after stroke or head injury, cleft palate teams, laryngectomy rehabilitation, early intervention for children with hearing loss.
• Industrial and occupational hearing conservation: audiometric surveillance and noise control in factories, mining, railways, defence and aviation under the OSH&WC Code, 2020 framework and the Noise Pollution Rules, 2000.
• Academics, research and certification: RCI-recognised BASLP/MASLP teaching, disability certification boards, medico-legal assessment of hearing loss and voice disability, forensic and speech-technology work on the source–filter model.

Interview questions

• Q: Why does the middle ear need an impedance-matching mechanism? A: Air has far lower acoustic impedance than cochlear fluid, so direct transfer would lose about 30 dB; the TM-to-footplate area ratio, ossicular lever and curved-membrane effect recover roughly 25–30 dB.
• Q: Which of the three impedance-matching factors contributes most? A: The area ratio of the effective tympanic membrane (~55 mm²) to the stapes footplate (~3.2 mm²), about 17:1, giving ~25 dB of the total gain.
• Q: Name the only abductor of the vocal folds and its nerve supply. A: The posterior cricoarytenoid, supplied by the recurrent laryngeal nerve, a branch of the vagus.
• Q: State the myoelastic–aerodynamic theory in one line. A: Vocal folds oscillate passively because subglottal air pressure blows the adducted folds apart while tissue elasticity and the Bernoulli-driven negative pressure close them again, repeating self-sustainingly.
• Q: What is the endocochlear potential and why does it matter? A: A standing +80 mV in the endolymph maintained by the stria vascularis; it supplies the driving force for K⁺ entry into hair cells, so damage to the stria raises thresholds even with intact hair cells.
• Q: Which hair cells generate otoacoustic emissions, and what does that let you test? A: Outer hair cells, through prestin-based electromotility; absent OAEs with a normal middle ear indicate cochlear outer hair cell dysfunction, which is the basis of newborn screening.
• Q: How are low and high frequencies coded in the cochlea? A: High frequencies by place (stiff narrow base), low frequencies mainly by temporal phase locking up to about 4–5 kHz, with both operating in the mid frequencies.
• Q: Why is the acoustic reflex a useful diagnostic test? A: Its arc runs cochlea → VIII nerve → cochlear nucleus → superior olivary complex → CN VII → stapedius bilaterally, so the pattern of present/absent ipsi- and contralateral reflexes localises middle ear, cochlear, VIII nerve, brainstem or facial nerve lesions.
• Q: A patient is hoarse after thyroid surgery but can still raise pitch. Which nerve is affected? A: The recurrent laryngeal nerve on the operated side; the cricothyroid is spared because it is supplied by the external branch of the superior laryngeal nerve.
• Q: Why does a unilateral lesion of the auditory cortex not cause deafness in one ear? A: Because the pathway decussates extensively from the cochlear nucleus upward, each ear is represented bilaterally; such lesions impair localisation and speech-in-noise rather than thresholds.
• Q: Why do infants get middle ear infections more often than adults? A: Their Eustachian tube is shorter, wider and more horizontal, so nasopharyngeal secretions reflux easily and ventilation is poorer.
• Q: Which registration is legally required to practise as an audiologist or SLP in India? A: Registration with the Rehabilitation Council of India under the RCI Act, 1992, renewed through continuing rehabilitation education.

Common mistakes

• Treating vocal fold vibration as a muscle contraction per cycle instead of a passive aerodynamic–elastic oscillation.
• Attributing all intrinsic laryngeal muscles to the recurrent laryngeal nerve and forgetting the cricothyroid's superior laryngeal supply.
• Using total tympanic membrane area (~85 mm²) instead of the effective vibrating area (~55 mm²) in area-ratio calculations, and forgetting to multiply by the lever ratio before converting to dB.
• Swapping the cochlear tonotopic ends — writing that the apex codes high frequencies; and confusing basilar membrane width (wider at apex) with cochlear duct diameter (wider at base).
• Calling outer hair cells the main sensory receptors; they are the amplifier, while inner hair cells carry ~95% of afferent information.
• Averaging four frequencies or including 4,000 Hz in the standard three-frequency PTA, and reading an air–bone gap without masking, giving a false conductive picture.
• Mixing units in aerodynamic measures — mL/s with L/s, or cm H₂O with Pa (1 cm H₂O ≈ 98.07 Pa) — in resistance calculations.

Related topics

Speech and hearing science: acoustics, phonetics and psychoacoustics · Linguistics basics · Developmental psychology · Audiological diagnostics and tympanometry · Hearing aids and cochlear implants · Voice, fluency and motor speech disorders