The Ear

Fig. 8.119 — Parts of the middle ear: external acoustic meatus → tympanic membrane → ossicles (malleus, incus, stapes) → oval window into the internal ear; pharyngotympanic tube below.

Gray's Anatomy for Students, 4e

Purple = External ear  ·  Teal = Middle ear cavity  ·  Gold = Cochlea/Inner ear  ·  Blue = Semicircular canals

Fig. 8.118 — Tympanic membrane (right ear). A. Diagram showing the four quadrants, handle of malleus and cone of light. B. Otoscopic view.

Gray's Anatomy for Students, 4e

The external ear is a funnel system — the auricle collects sound and channels it through the S-shaped external auditory meatus (EAM) to the tympanic membrane, converting pressure waves into mechanical vibration. The EAM is cartilaginous in its outer third (with hair follicles and ceruminous glands) and bony in its inner two-thirds; its curve must be straightened by pulling the auricle upward and backward in adults — downward and backward in children — before otoscopy can reach the drum. The tympanic membrane has a large taut pars tensa and a small lax pars flaccida (Shrapnell's membrane) above the malleolar folds — cholesteatoma originates at the pars flaccida, while the safe anteroinferior quadrant of the pars tensa is where myringotomy incisions are placed to avoid the ossicles, chorda tympani, and facial nerve. Arnold's nerve (auricular branch of CN X) supplying part of the posterior EAC explains why syringing or otoscopy can trigger a vagal cough reflex or syncope.

The middle ear is a box with six walls, each with its own clinical story: the thin tegmen above separates it from the middle cranial fossa (cholesteatoma erosion here causes meningitis or temporal lobe abscess), the jugular floor overlies the high-riding jugular bulb visible on otoscopy, and the anterior wall contains the auditory tube and the thin bone of the carotid canal. The medial wall is most event-rich — the oval window (sealed by the stapes footplate) transmits vibration into the perilymph, the round window provides a pressure-relief outlet, and the promontory of the basal cochlear turn carries the tympanic plexus of CN IX. Crossing the middle ear unsheathed between the malleus handle and the long process of the incus is the chorda tympani, carrying taste from the anterior two-thirds of the tongue and parasympathetic supply to the submandibular and sublingual glands — naked exposure to any middle ear pathology or surgery. Cholesteatoma — a locally destructive accumulation of desquamating keratin — is the most important disease of this space, eroding ossicles, the facial canal, the tegmen, and the sigmoid sinus plate through collagenase activity.

Fig. 8.123 — Auditory ossicles. A. Malleus. B. Incus. C. Stapes — the chain transmitting vibration from the tympanic membrane to the oval window.

Gray's Anatomy for Students, 4e

The ossicular chain — malleus, incus, stapes — forms a mechanical lever bridging the air-filled middle ear to the fluid-filled inner ear, amplifying sound pressure roughly 22-fold to overcome the impedance mismatch between air and perilymph. The malleus and incus derive from the first pharyngeal arch (Meckel's cartilage), while the stapes comes from the second arch (Reichert's cartilage); the stapes footplate plugging the oval window is the smallest bone in the body. Two intratympanic muscles protect the chain from loud sounds: tensor tympani (innervated by CN V3) dampens malleus movement, and stapedius (innervated by CN VII) stiffens the stapes — loss of stapedius in Bell's palsy unmasks hyperacusis because loud sounds can no longer be attenuated. Otosclerosis illustrates ossicular pathology at its most teachable: abnormal bone deposition fuses the stapes footplate to the oval window, producing progressive conductive hearing loss with a Carhart's notch at 2 kHz on audiometry, corrected surgically by stapedectomy.

The auditory tube is the middle ear's pressure-equalisation and drainage channel — 35 mm long, running downward, forward, and medially from the middle ear to the nasopharynx, with its lateral third bony and its medial two-thirds fibrocartilaginous and normally collapsed at rest. It opens transiently during swallowing or yawning via tensor veli palatini, levator veli palatini, and salpingopharyngeus, equalising middle ear pressure — which is why chewing relieves the pressure change of aircraft descent. In children, the tube is shorter, more horizontal, and relatively wider, making bacterial ascent from the nasopharynx far easier and explaining why acute otitis media (AOM) is overwhelmingly a paediatric disease. Chronic Eustachian tube dysfunction creates sustained negative middle ear pressure, drawing the pars flaccida inward to form the retraction pocket that becomes an acquired cholesteatoma.

Connects the middle ear to the nasopharynx (~35 mm long). Lateral 1/3 = bony (in temporal bone). Medial 2/3 = fibrocartilaginous (collapsed at rest — opens on swallowing/yawning via tensor veli palatini, levator veli palatini, salpingopharyngeus). Orientation: runs downward, forward, medially from middle ear to nasopharynx (hence why children get more OM — tube more horizontal + shorter).

Fig. 8.129 — Bony labyrinth: cochlea, vestibule and three semicircular canals enclosing the perilymph-filled spaces of the internal ear.

Gray's Anatomy for Students, 4e

The bony labyrinth is a set of fluid-filled cavities carved into the petrous temporal bone, housing the entire apparatus for hearing and balance. The cochlea spirals 2¾ turns around its central modiolus, divided by Reissner's membrane and the basilar membrane into three channels: the perilymph-filled scala vestibuli and scala tympani (communicating at the helicotrema at the apex) flank the endolymph-filled scala media where hair cell transduction occurs. The vestibule contains the utricle and saccule for linear acceleration, while three semicircular canals set at right angles to each other detect angular acceleration in all planes. Critically, the inner ear has only one blood supply — the labyrinthine artery from AICA — with no collateral circulation, so even brief ischaemia irreversibly kills hair cells; this is why sudden sensorineural hearing loss is an audiological emergency, and why AICA infarcts (hearing loss + vertigo) are distinguished from PICA infarcts (Wallenberg syndrome, intact hearing).

Perilymph: similar to CSF (high Na⁺, low K⁺); in bony labyrinth surrounding membranous labyrinth. Endolymph: unique composition (high K⁺, low Na⁺ — like intracellular fluid); produced by stria vascularis; inside membranous labyrinth. The K⁺ gradient is essential for hair cell depolarisation.

Fig. 8.131 — Membranous labyrinth: cochlear duct, utricle, saccule and semicircular ducts (endolymph) housing the organ of Corti, maculae and cristae.

Gray's Anatomy for Students, 4e

The membranous labyrinth sits within the bony labyrinth, bathed in endolymph (high K⁺, low Na⁺ — uniquely intracellular-like, produced by the stria vascularis), and contains all the sensory receptors for hearing and balance. In the cochlea, the organ of Corti rests on the basilar membrane: inner hair cells transmit the signal to CN VIII, while outer hair cells amplify it; the basilar membrane is tonotopically organised — narrow and stiff at the base encodes high frequencies, wide and floppy at the apex encodes low frequencies, which is why aminoglycoside ototoxicity and noise-induced damage cause high-frequency loss first. The otolith organs detect linear acceleration using otoconia (calcium carbonate crystals) that weigh on hair cell stereocilia; when otoconia dislodge from the utricular macula and enter the posterior semicircular canal, they cause BPPV — the most common vestibular disorder, producing brief intense positional vertigo that is both diagnosed and treated by sequential head manoeuvres (Dix-Hallpike for diagnosis; Epley for repositioning the otoconia back into the vestibule).

The vestibulocochlear nerve (CN VIII) exits the inner ear through the internal acoustic meatus alongside CN VII and the labyrinthine artery, traverses the posterior fossa, and enters the brainstem at the cerebellopontine (CP) angle — a compact anatomical space where tumours, vessels, and cranial nerves converge. Two tuning-fork tests at the bedside localise hearing loss: Rinne compares air conduction (AC, fork near EAM) with bone conduction (BC, fork on mastoid) — normally AC > BC; a negative Rinne (BC > AC) means the middle ear is blocked and bone bypasses it to reach the cochlea directly. Weber (fork on the midline) lateralises to the deaf ear in conductive loss and to the better ear in sensorineural loss. The CP angle is the classic site of vestibular schwannoma — a slow-growing Schwann cell tumour of CN VIII's vestibular division presenting with unilateral high-frequency SNHL, tinnitus, and imbalance, confirmed by gadolinium MRI; bilateral tumours signal neurofibromatosis type 2 (NF2, chromosome 22, merlin gene).

CN VIII (vestibulocochlear nerve) = cochlear division (hearing) + vestibular division (balance). Exits inner ear via internal acoustic meatus (IAM) — in petrous temporal bone — alongside CN VII. Passes into posterior cranial fossa → enters brainstem at pontomedullary junction at the cerebellopontine (CP) angle. The CP angle also contains the anterior inferior cerebellar artery (AICA).

Vestibular disorders produce nystagmus — involuntary rhythmic eye movements with a slow vestibular-driven phase and a fast corrective phase — and the character of the nystagmus separates peripheral from central causes: peripheral nystagmus has a latency before onset, is suppressed by fixation, and fatigues on repeated testing; central nystagmus is immediate, not suppressed by fixation, and may be purely vertical or direction-changing. Ménière's disease demonstrates endolymphatic hydrops clinically as a characteristic tetrad: episodic vertigo (minutes to hours), fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness — the low-frequency involvement is the key that separates it from noise- or age-related loss. Vestibular neuritis causes sudden severe prolonged vertigo without hearing loss (differentiating it from labyrinthitis, which does cause SNHL), with a positive head impulse test (HIT) indicating ipsilateral peripheral vestibular hypofunction. The caloric test (COWS: Cold Opposite, Warm Same — the fast phase direction) directly tests each horizontal semicircular canal's excitability; canal paresis >25% asymmetry is the most sensitive caloric indicator of vestibular schwannoma.

The facial nerve (CN VII) travels a longer intratemporal course than any other cranial nerve, passing through four named segments — meatal, labyrinthine, tympanic (horizontal), mastoid (vertical) — before exiting at the stylomastoid foramen. The labyrinthine segment, only 2–4 mm long and 0.68 mm wide, is the narrowest point and most vulnerable to ischaemic compression in Bell's palsy, which represents HSV-1 reactivation in the geniculate ganglion. Each segment gives off key branches that allow topographic localisation of any lesion: the greater superficial petrosal nerve (tear production via the lacrimal gland) at the geniculate ganglion, the nerve to stapedius at the tympanic segment, and the chorda tympani (taste + submandibular/sublingual parasympathetics) 6 mm above the stylomastoid foramen. The clinical rule: loss of lacrimation → lesion proximal to the geniculate; hyperacusis without taste loss → tympanic segment; isolated taste loss → between chorda tympani takeoff and stylomastoid foramen.

14.9.1 — Intratemporal Segments of CN VII

Fig. 8.133 — A. Facial nerve in the temporal bone (labyrinthine, tympanic and mastoid segments; geniculate ganglion). B. Chorda tympani branching within the temporal bone.

Gray's Anatomy for Students, 4e

Segment	Course	Key Features
Meatal	Brainstem → internal acoustic meatus (with CN VIII + labyrinthine artery)	No branches; runs in the IAM superior to CN VIII. Meningioma/acoustic neuroma can compress here
Labyrinthine	IAM fundus → geniculate ganglion (genu = bend). Between cochlea + anterior semicircular canal	Shortest (2–4 mm) + narrowest (0.68 mm) segment → most vulnerable to ischaemic compression in Bell's palsy. Geniculate ganglion (cell bodies of taste fibres) gives off: greater superficial petrosal nerve (GSP N — parasympathetics to lacrimal gland via pterygopalatine ganglion; runs under temporal lobe dura; damaged in petrous ridge fractures → dry eye)
Tympanic (horizontal)	Geniculate → 2nd genu. Runs horizontally above oval window + below lateral semicircular canal; forms medial wall of middle ear (visible as bulge = facial nerve prominence)	The dehiscence (congenital absence of bony covering) in 57% of cases → vulnerable to otitis media, cholesteatoma. Gives nerve to stapedius just before 2nd genu
Mastoid (vertical)	2nd genu → stylomastoid foramen (exits skull). Runs vertically through mastoid bone	Gives chorda tympani (6 mm above stylomastoid foramen) → crosses middle ear (taste anterior 2/3 tongue + parasympathetics to submandibular + sublingual glands). At stylomastoid foramen gives posterior auricular nerve + nerve to digastric posterior belly + nerve to stylohyoid. Then enters parotid

◆ CN VII Branches in Temporal Bone — Mnemonic: "Got Students Never Cramming Correctly"

Greater superficial petrosal nerve (geniculate ganglion) → Stapedius nerve (tympanic segment, just before 2nd genu) → Chorda tympani (mastoid segment, 6 mm above stylomastoid foramen) → at stylomastoid foramen: posterior auricular nerve + digastric (post) + stylohyoid. Then in parotid → Temporal, Zygomatic, Buccal, Marginal mandibular, Cervical (To Zanzibar By Motor Car).

All hearing loss is either conductive (failure to conduct sound to the cochlea through the external or middle ear) or sensorineural (failure of the cochlea, CN VIII, or central pathways). The audiogram distinguishes them cleanly: conductive loss shows an air-bone gap (bone conduction normal, air conduction raised), while sensorineural loss raises both equally. The same information comes from bedside tests — a negative Rinne (BC > AC) and Weber lateralising to the deaf ear both signal conductive pathology, while a positive Rinne with Weber to the better ear signals sensorineural. Tympanometry adds middle ear mechanics: type B (flat) means fluid or perforation, type As (shallow) means a stiffened ossicular chain (otosclerosis), and type Ad (deep/hypercompliant) means ossicular discontinuity. Ototoxic drugs complete the picture — aminoglycosides damage the cochlear base first (high-frequency SNHL), their pattern shifting apically with continued exposure; cisplatin causes irreversible SNHL requiring pre- and intra-treatment monitoring audiometry.

Mastoiditis develops when acute otitis media spreads beyond the tympanic cavity into the mastoid antrum and air cells, typically within 2–3 weeks of inadequately treated AOM; coalescent mastoiditis — breakdown of bony septa into a single pus-filled cavity — requires CT to confirm and cortical mastoidectomy to treat. The pathognomonic clinical picture is a pinna displaced anteroinferiorly by post-auricular swelling and tenderness, but the real danger lies in which direction the infection spreads. Lateral cortex erosion creates a subperiosteal abscess (most common extracranial complication); medial mastoid tip erosion tracks pus under the sternocleidomastoid as a Bezold's abscess, which can descend to the mediastinum. Intracranially, meningitis is most common, but sigmoid sinus thrombosis (picket-fence fever + papilloedema), brain abscess, and Gradenigo's syndrome (petrositis — CN VI palsy + deep facial pain + otorrhoea, from petrous apex involvement) are the high-stakes complications that distinguish a thorough examination answer from a superficial one.

Malignant otitis externa is not a cancer — the name reflects its aggressive behaviour, a Pseudomonas aeruginosa osteomyelitis of the temporal bone and skull base spreading from the external auditory canal via fissures of Santorini (congenital fibrous gaps between EAC cartilage plates) through the parotid to the stylomastoid foramen and beyond. It occurs almost exclusively in elderly diabetics or the immunocompromised — glucose-rich EAC secretions nourish Pseudomonas, and impaired neutrophil function permits unchecked spread. The pathognomonic sign is granulation tissue at the bony-cartilaginous junction of the EAC floor, combined with disproportionately severe nocturnal otalgia; cranial nerve involvement worsens the prognosis stage by stage (CN VII at the stylomastoid foramen → IX/X/XI at the jugular foramen → XII → VI with intracranial extension). Treatment is ciprofloxacin for 6–8 weeks, with duration guided by Gallium-67 scintigraphy — not CT, which remains abnormal long after cure because bone remodels slowly — alongside strict glycaemic control.