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Chapter 62, Laryngeal malignancy, contains some material from Volume 3 Chapters 14: by
Vinidh Paleri, Stuart Winter, Hannah Fox and Nachi Palaniappan, 15: by Yvonne Edels and Peter Clarke, 22: by Mark Sayles, Stephanie L. Koonce, Michael L. Hinni and David G. Grant and 27: by Volkert Wreesman, Jatin Shah and Ian Ganly
Chapter 63, Hypopharynx, contains some material from Volume 3 Chapter 16: by
Prathamesh Pai, Deepa Nair, Sarbani Ghosh Laskar and Kumar Prabhash
Chapter 64, Oropharynx, contains some material from Volume 3 Chapters 13: by Terry
M. Jones with Mererid Evans and 29: by Chris Holsinger, Chafeek Tomeh and Eric M. Genden
Chapter 65, Nasopharyngeal carcinoma, contains some material from Volume 3 Chapter 8:
by Raymond King-Yin Tsang and Dora Lai-Wan Kwong
Chapter 66, Nasal and sinus malignancy, contains some material from Volume 3 Chapter 7:
by Cyrus Kerawala, Peter Clarke and Kate Newbold
Chapter 67, Benign and malignant disease of the oral cavity, contains some material from
Volume 3 Chapters 12: by Tim Martin and Omar A. Ahmed and 42: by Konrad S. Staines and Alexander Crighton
Chapter 68, Management of the unknown primary in head and neck cancer, contains
some material from Volume 3 Chapter 17: by Ricard Simo, Jean-Pierre Jeannon and Maria Teresa Guerrero Urbano
Chapter 69, Metastatic neck disease, contains some material from Volume 3 Chapter 18: by
Vinidh Paleri and James O’Hara
Chapter 70, Prosthetic management of oral and facial defects, contains some material
from Volume 3 Chapter 31: by Chris Butterworth
Chapter 71, Gras and aps in head and neck reconstruction, contains some material from
Volume 3 Chapters 91: by Kenneth Kok and Nicholas White, 92: by Ralph W. Gilbert and John C. Watkinson and 93: by John C. Watkinson and Ralph W. Gilbert
Chapter 72, Radiotherapy and chemotherapy, contains some mater ial from Volume 3 Chapters
19: by Sara Meade and Andrew Hartley and 24: Chemotherapy by Charles G. Kelly
Chapter 73, Immunotherapy in head and neck cancer, contains some material f rom Volume
3 Chapter 30: by Kevin J Herrington and Magnus T. Dillon
Chapter 74, Quality of life, survivorship, and outcomes in head and neck cancer, contains
some material from Volume 3 Chapters 20: by Simon Rogers and Steve omas and 28: by Helen Cocks, Raghav C. Dwivedi and Aoife M. I. Waters
Chapter 76, Benign and malignant conditions of the skin, contains some material from
Volume 3 Chapter 94: by Murtaza Khan and Agustin Martin-Clavijo
Chapter 77, Anatomy and physiology of head and neck endocrine glands, contains some
material from Volume 1 Chapters 53: by Julian A. McGlashan and 55: by Martin O. Weickert
Chapter 78, yroid and parathyroid pathology, contains some material from Volume 1
Chapter 58: by Ram Moorthy, Sonia Kumar and Adrian T. Wareld
Chapter 79, Endocrine imaging, contains some material from Volume 1 Chapter 57: by
Steve Colley and Sabena Fareedi
Chapter 80, Evaluation and investigation of thyroid disease, contains some material from
Volume 1 Chapters 59: by Andrew Coatesworth and Sebastian Wallis, 60: by Anthony P. Weetman and 61: by Christopher M. Jones and Kristien Boelaert
Chapter 81, Benign thyroid disease, contains some material from Volume 1 Chapter 61: by
Christopher M. Jones and Kristien Boelaert
Chapter 82, Management of dierentiated yroid cancer, contains some material from
Volume 1 Chapters 62: by Hisham M. Mehanna, Kristien Boelaert and Neil Sharma, 65: by Iain J. Nixon and Ashok R. Shaha and 66: by Laura Moss
xxx Acknowledgements
Chapter 83, Management of medullary thyroid cancers, contains some material from
Volume 1 Chapter 63: by Barney Harrison
Chapter 84, Management of anaplastic thyroid cancer and lymphoma, contains some
material from Volume 1 Chapter 64: by James D. Brierley and Richard W. Tsang
Chapter 85, yroidectomy, contains some material from Volume 1 Chapters 67: by Ricard
Simo, Iain J. Nixon and Ralph P. Tufano, 69: by Neil S. Tolley and 70: by Neeraj Sethi, Josh Lodhia and R. James A. England
Chapter 86, Surgery for metastatic and locally advanced thyroid cancer, contains some
material from Volume 1 Chapter 68: by Joel Anthony Smith and John C. Watkinson
Chapter 87, Investigation of hypercalcemia, contains some material from Volume 1 Chapter
71: by Mo Aye and ozhukat Sathyapalan
Chapter 88, Management of hyperparathyroidism, contains some material from Volume 1
Chapter 73: by Neil J. L. Gittoes and John Ayuk
Chapter 89, Parathyroid surgery, contains some material from Volume 1 Chapters 76: by
R. James A. England and Nick McIvor and 77: by Parameswaran Rajeev and Gregory P. Sad ler
Chapter 90, Medicolegal aspects of thyroid and parathyroid surgery, contains some mate-
rial from Volume 1 Chapter 81 by Barney Harrison
Chapter 91, Evaluation and investigation of pituitary disease, contains some material
from Volume 1 Chapters 82: by Sean Carrie, John Hill and Andrew James and 83: by ozhukat Sathyapalan and Stephen L. Atkin
Chapter 92, Primary pituitary disease, contains some material from Volume 1 Chapter 84:
by Christopher M. Jones and John Ayuk
Chapter 93, Management of pituitary disease, contains some material from Volume 1
Chapters 85: by Mihir R. Patel, Leo F.S. Ditzel Filho, Daniel M., 86: by Andy Levy and
115: by Philip G. Chen and Peter-John Wormald
Chapter 94, e paediatric consultation, contains some material from Volume 2 Chapters 1:
by Raymond W. Clarke, 2: by Raymond W. Clarke and 3: by Julian Gaskin, Raymond W. Clarke and Claire Westrope
Chapter 95, Paediatric anaesthesia, contains some material from Volume 2 Chapter 4: by
Crispin Best
Chapter 96, Hearing testing, contains some material from Volume 2 Chapters 8: by Sally
A.Wood and 9: by Glynis Parker
Chapter 97, Management of the hearing‑impaired child, contains some material from
Volume 1 Chapters 2: by Mohammed-Iqbal Syed, Volume 2 Chapter 10: by Chris H. Raine, Sue Archbold, Tony Sirimanna and Soumit Dasgoupta and 12: by Jonathan P. Harcourt
Chapter 98, Otitis media, contains some material from Volume 2 Chapters 14: by Peter A.
Rea and Natalie Ronan and 15: by William P.L. Hellier
Chapter 99, Embryological developmental disorders, contains some material from Volume
2 Chapters 16: by Iain Bruce and Jaya Nichani, 18: by David M. Wynne and Louisa Ferguson, 19: by Benjamin Robertson, Sujata De, Astrid Webber and Ajay Sinha, 30: by Chris Jephson and 42: by Daniel J. Tweedie and Benjamin E.J. Hartley
Chapter 100, Imbalance, contains some material from Volume 2 Chapter 20: by Louisa
Murdin and Gavin A.J. Morrison
Chapter 101, Nasal obstruction, contains some material from Volume 2 Chapters 23: by
Michelle Wyatt and 26: by Peter J. Robb. Tunde Oremule is also acknowledged for his assistance
Acknowledgements xxxi
Chapter 102, Rhinosinusitis and lacrimal disorders, contains some material from Volume
2 Chapters 24: by Daniel J. Tweedie and 25: by Caroline J. MacEwen and Paul S. White
Chapter 103, Adenotonsillar conditions and obstructive sleep apnoea, contains some
material from Volume 2 Chapters 26: by Peter J. Robb, 27: by Steven Powell and 38: by Yogesh Bajaj and Ian Hore
Chapter 104, Acquired laryngotracheal stenosis, contains some material from Volume 2
Chapters 31: by Michael J. Rutter, Alessandro de Alarcón and Catherine K. Hart and 32:
by Rania Mehanna and Michael Kuo
Chapter 105, Stridor, contains some material from Volume 2 Chapters 28: by Kate Stephenson
and David Albert and 29: by Lesley Cochrane
Chapter 106, Foreign bodies in the ear, nose and throat, contains some material from
Volume 2 Chapter 34: by Adam J. Donne and Katharine Davies
Chapter 107, Childhood malignancies, cysts, and sinuses of the head and neck, contains
some material from Volume 2 Chapters 40: by Fiona McGregor and James Hayden and 41: by Keith G. Trimble and Luke McCadden
Chapter 108, Drooling, aspiration, and oesophageal problems, contains some mate-
rial from Volume 2 Chapters 43: by Haytham Kubba and Katherine Ong, 44: by Ravi evasagayam and 45: by Graham Haddock
Chapter 109, Paediatric tracheostomy and paediatric airway management, contains some
material from Volume 2 Chapters 35: by Mike Saunders and 36: by Pensée Wu, May M.C. Yaneza, Haytham Kubba, W. Andrew Clement and Alan D. Cameron
Chapter 110, Pinnaplasty, contains some material from Volume 1, Chapter 86 by Victoria
Harries and Simon Watts
xxxii Acknowledgements
SECTION
1
THE EAR
1. ANATOMY AND PHYSIOLOGY OF HEARING
Anatomy of Hearing
External Ear
e auricle (pinna) is the outermost projection of the ear with its lateral surface character­ised by prominences and depressions (Figure 1.1a). e body is composed of elastic bro- cartilage and is a continuous plate except for a narrow band between the tragus and anterior crus of the helix where endaural incisions can be made. e auricle functions to collect acoustic energy and direct it into the external auditory canal (EAC), and to create incident angle–dependent modications that help with sound localisation. e EAC is a 2.4-cm-long passage formed from cartilage in the lateral third and bone in the medial two-thirds. It is lined with keratinising squamous epithelium, which facilitates migration of desquamated cells toward the external opening of the canal at a rate of 0.1 mm/day. desquamated cells, cerumen, and sebum forms wax.
Both the pinna and EAC derive their blood supply from branches of the external carotid artery (posterior auricular, supercial temporal artery, and internal maxillary arteries). Venous drainage is into the external jugular vein, maxillary veins, and pterygoid plexus while lymphatic drainage is to the nodes at the mastoid tip, pre-auricular nodes, and upper deep cervical nodes. e EAC receives sensory innervation from the trigeminal, facial and vagus nerves. Innervation of the pinna is shown in Figure 1.2.
1
e mixture of these
Middle Ear
e middle ear consists of the tympanic cavity (TC), Eustachian tube (ET) (see Chapter 8) and the mastoid air cell (MAC) system. e mastoid antrum is an air-lled sinus within the petrous temporal bone that communicates with the middle ear by way of the aditus. e MAC system is largely developed by the age of 6.
Tympanic Cavity (TC)
e TC is bounded by the tympanic membrane (TM) laterally and the osseous labyrinth medially (Figure 1.2a). e TM is divided into the pars tensa and pars accida, which sit, respectively, below and above the malleolar folds at the level of the lateral process of the mal­leus. e TM consists of three layers: an outer epithelial layer, middle brous layer (decient in the pars accida), and an inner mucosal layer. It receives sensory innervation from the auriculotemporal nerve, auricular branch of the vagus nerve (Arnold’s nerve), and the tym­panic branch of the glossopharyngeal nerve (Jacobsen’s nerve).
e Ear 1
Great auricular
nerve (C2,3)
esser occipital
Auriculotemporal
ANATOMY AND PHYSIOLOGY OF HEARING
nerve (V3)
L nerve (C2)
CN VII & X
CN VII & X
(a) (b)
Figure 1.1 (a) Anatomy and (b) innervation of the anterior and posterior surfaces of the pinna.
Great auricular nerve (C2,3)
e TC is divided into the following sections by mucosal folds:
1 Epitympanum: It is also known as attic located above the malleolar folds. A bony
crest known as the cog projects from the tegmen tympani caudally and divides the epitympanum into a larger posterior and smaller anterior space where residual cho­lesteatoma may be le in canal wall up surgery. e anterior and posterior isthmus tympani are gaps in mucosal folds that provide the only route of ventilation for the epitympanic space from the mesotympanum. Prussak’s space is found between the pars accida and the neck of malleus and is an important site for cholesteatoma formation.
2 Mesotympanum: is is the part of the middle ear visible through the external canal
with a microscope. e promontory is a rounded elevation, which occupies most of the medial wall, consisting of the basal turn of the cochlea.
3 Hypotympanum: is lies below the level of the inferior part of tympanic sulcus.
e oor is made up of the bony covering of the jugular bulb, which can be dehis­cent and should be kept in mind when raising the inferior portion of the tympa­nomeatal ap.
4 Retrotympanum: is is an area posterior to mesotympanum. e round window
niche is separated from the promontory by two bony ridges arising from the prom­ontory known as the ponticulus and subiculum (Figure 1.2b). e sinus tympani is a posterior extension of the mesotympanum and lies deep to the facial nerve and pyramid, making it dicult to access during surgery. e facial recess is a groove, which lies between the pyramid, facial nerve medially. and annulus of the TM laterally.
5 Protympanum: is is anterior to the promontory and contiguous with the tympanic
portion of the ET. It’s contents include the following:
(i) Ossicular chain: e malleus, incus, and stapes connect the TM to the oval
wi ndow.
(ii) Muscles: e tensor tympani is supplied by the mandibular nerve. It arises from
a bony canal lying above the ET, passes backward into processus cochleariformis, and turns at a right angle to insert into the malleus handle. e stapedius is sup­plied by the facial nerve, arises from the pyramidal eminence, and inserts onto the stapes superstructure.
(iii) Nerves: e chorda tympani is a branch of the facial nerve. It runs across the
medial surface of the TM between the mucosal and brous layers and passes
2 e Ear
ANATOMY AND PHYSIOLOGY OF HEARING
Figure 1.2 Relationships of the middle ear as shown in a schematic drawing (a) and endoscopic
image (b).
medial to the malleus handle above the tensor tympani tendon. It leaves the TC through the petrotympanic ssure. e tympanic plexus is formed by Jacobsen’s nerve and caroticotympanic nerves on the promontory, providing sensory and parasympathetic branches to the middle ear.
(iv) Mucosa: e middle ear consists of ciliated mucus-secreting respiratory mucosa.
e mucociliary pathways coalesce at the tympanic orice of the ET.
e Ear 3
ANATOMY AND PHYSIOLOGY OF HEARING
Reissner’s
membrane
Scala
membrane
membrane
tympani
Table 1.1 Pattern of structures within the otic capsule
Membranous duct suspended in perilymph and
Bony covering
Cochlea Cochlea duct Inner hair cell on basilar membrane Vestibule Utricle and saccule Hair cell in macula Semicircular canal Semicircular duct Hair cells in crista ampulla
lled with endolymph
Sensory hair receptor cells with a dominant kinocilia
Inner Ear
e inner ear delivers sensory information relating to hearing via the cochlea and balance via the vestibular system. It is formed of
1 Dense bony covering (also called the otic capsule or bony labyrinth), 2 Membranous ducts, and 3 Sensory organs within these ducts (Table 1.1).
e space between the bony and membranous labyrinth is lled with perilymph. is contains high sodium and low potassium ion content (similar to extracellular uid) and communicates variably with cerebrospinal uid via the cochlear aqueduct. e uid within the membranous labyrinth is known as endolymph and contains high potassium and low sodium ion content (similar to intracellular uid).
Cochlea
e cochlea is formed of three parallel scalae (vestibula, media, and tympani) coiled in a spiral around a central modiolus in two and a half turns (Figure 1.3).
Both the scala vestibuli (SV) and scala ty mpani (ST) are lled with peri lymph, whereas the cen­tral scala media (SM) is lled with endolymph. Within the SM is the sensory epithelium of the cochlea, called the organ of Corti. is is a strip of cells coiled in a spiral, resting on the basi­lar membrane (BM), and overlain by the gelatinous tectorial membrane. Ion transportation within the cochlea is mediated by the stria vascularis, which forms the lateral wall of the SM.
Stria
vascularis
Cochlea
duct
Organ
of corti
Spiral
ligament
Basilar
Figure 1.3 Cross section of the cochlea.
4 e Ear
vestibuli
Tectorial
Cochlear duct
Cochlear nerve
Scala
ANATOMY AND PHYSIOLOGY OF HEARING
Bill’s Bar Superior vestibular
Opening of
It contains the Na+/K+-ATPase, which maintains the high endolymphatic K+ concentration and the +80-mV electrical potential of the cochlea endolymph, relative to the perilymph.
e cochlea’s blood supply is the spiral modiolar artery, which is a branch from an end artery called the vestibulocochlear artery (VCA) from the anteroinferior cerebellar artery.
e organ of Corti contains the cylindrical-shaped outer hair cells (OHCs) and goblet-shaped inner hair cells (IHCs). ere are four times more OHCs, which form three rows, compared with one row of IHCs. e IHCs form the primary receptor cell, innervated by the majority of cochlear aerent nerves. e OHCs play more of an eerent and modulating role. ey respond to BM motion to amplify signal and improve frequency selectivity reaching the IHCs.
e hair cells have rows of motile microvilli-like structures called stereocilia, which increase in height in one particular direction (see Chapter 2 for further details of hair cell microanatomy).
e spiral ganglion is the collection of cell bodies from two types of aerent nerve bres, namely:
Type 1 neurons (myelinated): ey innervate IHCs, have large diameters, and consti-
tute 95% of the nerve bre population. One type 1 bre innervates one IHC, but one IHC may synapse with several nerve bres. Type 2 neurons (unmyelinated): ey innervate OHCs and are smaller than type 1
neurons. One type 2 bre innervates many OHCs.
e aerent auditory pathway involves spiral ganglion central axons projecting via the cochlear nerve, into the cochlear nucleus of the brainstem. From here auditory information is conveyed bilaterally to the superior olivary nuclei (SON) in the pons, and then to the lateral lemniscus and inferior colliculus of the midbrain, medial geniculate nucleus of the thalamus, and the primary auditory cortex in the Sylvian ssure of the temporal lobe (Brodmann area 41, Heschl’s gyrus, also known as the transverse temporal gyrus). Functional magnetic resonance imaging (MRI) studies indicate the presence of two broad cortical processing pathways: an anterior ‘what sound’ pathway and a posterior ‘where is it coming from’ pathway.
Connections from the SON to the facial nuclei mediate the stapedius reex, which occurs in response to loud sounds (70–90 dB above threshold).
e eerent auditory pathway arises from projections from both the lateral olive and the medial olivary complex, which synapse mostly with type 1 and 2 spiral ganglion cells, respectively, and thus connect to both the IHCs and the OHCs. e eerent bres are carried by the inferior vestibular nerve and meet at the anastomosis of Oort through the saccular branch of the nerve to join up with the cochlear nerve, forming the vestibulocochlear nerve. e cochlear nerve traverses the internal auditory canal (IAC), which is roughly 1 cm in length and its contents are shown in Figure 1.4.
facial canal
Figure 1.4 Contents of the internal auditory canal (IAC). A, anterior, P, posterior; S, superior; I inferior.
Cochlear
fossa
fossa
Falciform crest
Inferior vestibular fossa
Foramen singulare
e Ear 5
ANATOMY AND PHYSIOLOGY OF HEARING
Table 1.2 Derivatives of rst and second branchial arch
Cartilage Nerve Artery Muscle
First branchial arch derivatives
Meckel’s cartilage
Malleus Incus ‘Mandible’ Anterior malleolar ligament Sphenomandibular ligament
Second arch derivatives
Reichert’s cartilage
Stapes superstructure Styloid process Lesser cornu of hyoid Stylohyoid ligament
Mandibular branch
of trigeminal nerve
Facial nerve Stapedial Stapedius
Tensor tympani
Eighty percent of these eerent bres synapse directly with OHCs, with the remainder ter­minating on aerent nerve bres. e ratio of eerent to aerent bres in the OHC is 1:2, whereas those in the IHCs is 1:7. is suggests eerent function is mainly to biologically amplify sound, modulate signals (protective damping of loud sounds), and frequency selec­tivity, via the OHCs. e medial system innervates both ears while the lateral system supplies only the ipsilateral cochlea. Both project to the dierent parts of the ventral cochlear nucleus.
Embryology of the Ear
e pinna develops from hillocks (swellings) on the rst and second pharyngeal arches. Abnormalities of the pinna may therefore be associated with abnormalities of other rst and sec­ond arch derivatives. e EAC develops from the ectoderm of the rst branchial groove (cle) while the ET and middle ear are derived from the second branchial pouch. e ossicular chain and middle ear muscles are derived from the rst and second branchial arches (Table 1.2).
e inner ear develops independently of the middle and external ears. e otic capsule (contain­ing the cochlea, vestibule, and three semicircular canals) develops from the mesoderm, whereas the membranous labyrinth develops from an ectodermal thickening (otic placode) on the side of the head between days 22 and 35 and is fully formed by 25 weeks of gestation to an adult state.
Physiology of the Hearing
e human ear has a huge dynamic range and is able to hear frequencies of 2–20 kHz and inten­sities up to 120 dB. e ears are most sensitive to frequencies between 2 and 5kHz.
e pinna reects sound from various directions into the EAC. e acoustic signal then trav­els down the EAC where it undergoes a resonance boost between 2.5 and 3.5 kHz in adults.
e middle ear acts as an ecient transformer to conduct acoustic energy from the low­impedance high-velocity TM, to the high-impedance, low-velocity uid-lled cochlea. e impedance dierence is mainly matched by the ratio of the surface area of the TM to the stapes footplate (approximately 18:1, or about 25 dB). A much smaller part is played by the lever action of the ossicles. e stapedius muscle plays a role in reex contraction and stiening of the ossic­ular chain to protect the cochlea’s sensory epithelium from high-amplitude sounds (see below). In humans, the role of the tensor tympani is unknown, but it does not normally contract in response to sound. Aside from air conduction, the cochlea can also be directly stimulated by vibration of the bony skull (through the bone of the EAC, ossicles or cochlea). e middle ear has a resonant frequency around 1–3 kHz. If this resonance is reduced by a mechanical problem in the ossicular chain (e.g. xation), the ossicular component of bone conduction is aected and results in a drop in the bone-conduction threshold. is classically appears at 2 kHz as Carhart’s notch in the bone-conduction threshold in otosclerosis; however, Carhart’s eect may be present between 1 and 4 kHz in any pathology aecting the ossicles.
6 e Ear
ANATOMY AND PHYSIOLOGY OF BALANCE
Once sound is delivered into the cochlea through the stapes-oval window interface, a cochlear traveling wave is generated that traverses the BM. e arrangement of organ of Corti and basilar and tectorial membranes across the length of the cochlea gives rise to a ‘tonotopic’ relationship due to the variations in stiness, thickness, and mass along these structures from base to apex. High-frequency sounds are best represented at the basal end and low frequencies at the apex. e movement of the BM creates relative motion between the tectorial mem­brane and the stereocilia of the IHCs. is allows ion channels to open and depolarise the cell, resulting in synaptic release of glutamate and ring of aerent nerve bres.
Aerent nerve bres on OHCs form a feedback loop with eerent bres, which result in a change in the shape of OHCs and active modication of BM motion. is results in signal amplication at low intensity levels, improving hearing sensitivity and also improves spectral resolution. e OHCs are responsible for otoacoustic emissions and the cochlear microphonic potential.
Information on timing, frequency, and intensity of sound is encoded by the rate, number, location, and timing of auditory nerves ring. For sound localisation, encoding of interaural time dierences (for low-frequency sounds) and interaural level dierences (high-frequency sounds) in the auditory pathway are important.
KEY POINTS
The external and middle ear develops from the rst and second branchial arches,
whereas the inner ear arises independently from an ectodermal thickening.
The middle ear provides critical modications and matches the change of impedance
of sound as it moves between differing mediums, mainly by the ratio of the surface area of the TM to the stapes footplate (18:1).
The BM within the cochlear is tonotopic, with high-frequency sounds producing
displacement toward the base of the cochlea and low-frequency sounds toward the apex. These are inuenced by active mechanisms of the OHC and the passive arrangement of the BM.
Sound from the auditory nerve is propagated to the cochlear nucleus, SON, inferior
colliculus, medial geniculate nucleus, and nally the auditory cortex.
Further Reading
1. Pickles JO. An Introduction to the Physiology of Hearing. 4th ed. Boston, MA: Brill;
2013.
2. Ahveninen J, Kopčo N, Jääskeläinen IP. Psychophysics and neuronal bases of sound localization in humans. Hear Res. 2014;307:86–97. doi:10.1016/j.heares.013.07.008.
2. ANATOMY AND PHYSIOLOGY OF BALANCE
Introduction
e role of the vestibular system is to maintain visual xation and posture by (1) detecting changes in head motion, position, and spatial orientation and (2) stabilising eye, head, and body position.
e vestibular system is housed in the labyrinth of each ear. e main components of the vestibular system are three semicircular canals and two otolith organs (utricle and
e Ear 7