Complete ENT (Otorhinolaryngology) question bank — ear, nose, throat, larynx, airway & head-neck — in explanation-first exam-topper style, with 72 diagrams.
12chapters144questions77High-Yield
THE CONCEPT
Vertigo is a false sensation of movement (usually spinning) of oneself or the surroundings, arising from a disorder of the balance (vestibular) system. It is distinct from light-headedness, disequilibrium or presyncope. The central clinical task is to localise it to a peripheral cause (the labyrinth or vestibular nerve) or a central cause (the brainstem or cerebellum), because these differ greatly in cause and urgency.
The vestibular labyrinth
superior SCC
posterior SCC
lateral SCC
utricle &saccule
ampullae
cochlea (hearing)
SCCs sense rotation (angular); otolith organs sense linear acceleration & gravity
The vestibular labyrinth: three semicircular canals, each with an ampulla, sense angular (rotational) acceleration, while the otolith organs (utricle and saccule) sense linear acceleration and gravity; the cochlea handles hearing. All connect to the eighth nerve.
HOW BALANCE WORKS & THE CAUSES
Balance depends on vestibular, visual and proprioceptive inputs integrated in the brainstem and cerebellum; vertigo is a disorder of this system. Peripheral causes (the commonest) include BPPV, Meniere's disease, vestibular neuritis/labyrinthitis, acoustic neuroma, ototoxicity, trauma and perilymph fistula. Central causes include vertebrobasilar ischaemia/stroke, vestibular migraine, multiple sclerosis and cerebellar lesions/tumours.
PERIPHERAL versus CENTRAL
Feature
Peripheral
Central
Severity
Severe, sudden
Often milder
Nystagmus
Horizontal/rotatory, unidirectional, suppressed by fixation
Any direction (vertical=central), may change, not suppressed
Hearing loss/tinnitus
Often present
Usually absent
Other neuro signs
Absent
Present (dysarthria, diplopia, ataxia)
Gait
Can walk (leans)
Cannot walk (severe imbalance)
ASSESSMENT
Assessment includes the history (duration, triggers, associated hearing/neuro symptoms), examination of nystagmus, the Dix-Hallpike test, Romberg and gait, cranial nerves and hearing, and the HINTS examination (Head Impulse, Nystagmus, Test of Skew) to separate peripheral from central, with audiometry and MRI for central or asymmetric features.
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CLINICAL PEARL: Vertigo = an illusion of movement (spinning) from a vestibular disorder. Localise: peripheral (labyrinth/VIII — BPPV, Meniere's, vestibular neuritis, acoustic neuroma; severe, unidirectional horizontal/rotatory nystagmus suppressed by fixation, ± hearing loss, can walk) versus central (brainstem/cerebellum — stroke, migraine, MS; vertical/direction-changing nystagmus not suppressed by fixation, other neuro signs, cannot walk). Use HINTS; MRI for central/asymmetric.
WHY LOCALISING PERIPHERAL VS CENTRAL IS THE KEY TASK
The reason so much emphasis is placed on separating peripheral from central vertigo is that the two carry completely different implications for the patient. A peripheral vertigo — from the labyrinth or vestibular nerve — is usually benign and self-limiting (BPPV, vestibular neuritis) or manageable (Meniere's), and the patient can generally be reassured and treated symptomatically. A central vertigo — from the brainstem or cerebellum — may be a stroke, a demyelinating lesion or a tumour, which can be life-threatening and demands urgent imaging and treatment. Because both can present with acute vertigo, nausea and unsteadiness, the clinician cannot rely on the symptom itself and must use the discriminating signs — the type of nystagmus, the presence of other neurological features, and the ability to walk — to decide which pathway the patient is on. Getting this localisation right is the single most important decision in assessing acute vertigo.
THE VALUE OF THE HINTS EXAMINATION
A modern refinement worth understanding is the HINTS examination (Head Impulse, Nystagmus, Test of Skew), a bedside battery that can be more sensitive than early MRI for detecting a stroke in a patient with acute continuous vertigo. In a peripheral lesion, the head-impulse test is abnormal (a corrective saccade), the nystagmus is unidirectional and horizontal, and there is no vertical skew — a reassuring combination. Paradoxically, a normal head-impulse test, direction-changing nystagmus or a skew deviation in a patient with acute vestibular syndrome points to a central (stroke) cause. The value of HINTS is that it lets a trained examiner distinguish a dangerous central cause from a benign peripheral one at the bedside, guiding who needs urgent imaging — a good example of how careful clinical examination can outperform an initial scan.
THE BOTTOM LINE
The whole assessment of vertigo turns on localising it: a benign peripheral cause (labyrinth/vestibular nerve) is separated from a potentially dangerous central one (brainstem/cerebellum) using the nystagmus pattern, associated neurological signs, gait and the HINTS examination, with MRI reserved for central or atypical cases.
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KEY POINTS / NUMBERS (viva)
Vertigo = illusion of movement (spinning) from a vestibular disorder; distinct from light-headedness/presyncope/disequilibrium.
Peripheral: severe, horizontal/rotatory unidirectional nystagmus suppressed by fixation, ± hearing loss, can walk. Central: vertical/direction-changing nystagmus not suppressed by fixation, other neuro signs, can't walk. Assess with HINTS (head impulse, nystagmus, test of skew); MRI if central/asymmetric.
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KEY POINTS TO REMEMBER
Vertigo = false sensation of movement (spinning) from a vestibular disorder; distinguish from light-headedness/presyncope.
Central causes: vertebrobasilar ischaemia/stroke, vestibular migraine, MS, cerebellar lesions/tumours.
Peripheral: severe, unidirectional horizontal/rotatory nystagmus suppressed by fixation, ± hearing loss, can walk; Central: vertical/direction-changing nystagmus not suppressed, other neuro signs, cannot walk.
Assess: history + nystagmus + Dix-Hallpike + gait + cranial nerves + hearing + HINTS; MRI for central/asymmetric features.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
Meniere's disease is an idiopathic inner-ear disorder characterised by episodic vertigo, fluctuating sensorineural hearing loss, tinnitus and aural fullness, caused by endolymphatic hydrops — an over-accumulation and distension of endolymph in the membranous labyrinth.
Endolymphatic hydrops (Meniere's)
Normal
scala vestibuli
scala media (endolymph)
scala tympani
Hydrops
distended endolymph
Over-accumulation of endolymph distends the membranous labyrinth (Reissner's membrane bulges)
Endolymphatic hydrops — the basis of Meniere's disease: an over-accumulation of endolymph distends the membranous labyrinth (the scala media), bulging Reissner's membrane, and the resulting episodic dysfunction produces the vertigo, fluctuating hearing loss, tinnitus and fullness.
PATHOPHYSIOLOGY & THE TETRAD
Endolymphatic hydrops — an increased volume/pressure of endolymph (from impaired absorption or excess production) — distends the membranous labyrinth, and episodic dysfunction/rupture produces the symptoms. The classic tetrad is:
Episodic vertigo — spontaneous, rotatory, lasting 20 minutes to several hours, with nausea/vomiting.
Fluctuating sensorineural hearing loss — low-frequency initially, fluctuating then progressive.
Tinnitus — a low-pitched 'roaring'.
Aural fullness/pressure.
It is usually unilateral, with episodic attacks; between attacks the ear may be normal early on, but hearing progressively worsens.
DIAGNOSIS & MANAGEMENT
Diagnosis is clinical (≥2 spontaneous vertigo episodes ≥20 minutes + documented low-frequency SNHL + tinnitus/fullness), with PTA (low-frequency SNHL), MRI to exclude an acoustic neuroma, and reduced caloric responses. The acute attack is treated with vestibular sedatives (prochlorperazine, antihistamines), antiemetics and bed rest. Long-term prophylaxis is a low-salt diet, avoidance of caffeine/alcohol/stress, betahistine and diuretics; refractory disease may need intratympanic steroids/gentamicin, endolymphatic sac decompression, vestibular nerve section or labyrinthectomy, plus a hearing aid and vestibular rehabilitation.
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CLINICAL PEARL: Meniere's disease = endolymphatic hydrops → a tetrad of episodic vertigo (minutes–hours), fluctuating low-frequency SNHL, roaring tinnitus and aural fullness; usually unilateral. Acute: vestibular sedatives/antiemetics. Prophylaxis: low-salt diet, betahistine, diuretics, avoid caffeine/alcohol. Refractory: intratympanic gentamicin/steroid, sac surgery, labyrinthectomy. Exclude an acoustic neuroma (MRI).
WHY THE SYMPTOMS COME IN A CLUSTER
Understanding endolymphatic hydrops explains why Meniere's produces its particular cluster of symptoms. Because the excess endolymph distends the whole membranous labyrinth — which contains both the balance organs and the cochlea — the disease affects hearing and balance together. The distension and episodic dysfunction of the vestibular part cause the episodic vertigo; the effect on the cochlea causes the fluctuating (initially low-frequency) hearing loss and the roaring tinnitus; and the raised pressure itself is felt as aural fullness. This is why the diagnosis rests on the combination of these features rather than any one of them, and why the hearing loss characteristically fluctuates with the attacks early on — the pressure rises and falls — before becoming progressively permanent as repeated episodes damage the delicate structures.
THE STEPWISE MANAGEMENT LADDER
It is helpful to see Meniere's management as a ladder that escalates only as needed, since most patients are controlled at the lower rungs. The first steps are conservative — a low-salt diet, avoidance of caffeine, alcohol and stress, and betahistine/diuretics — aimed at reducing the endolymph load, and these control the majority. Acute attacks are covered with vestibular sedatives and antiemetics. Only when disabling attacks continue despite this does one climb to intratympanic steroids, then intratympanic gentamicin (a 'chemical labyrinthectomy' that sacrifices vestibular function to stop the vertigo), and finally destructive surgery (labyrinthectomy or vestibular nerve section) reserved for intractable cases, with hearing preservation weighed at each step. This graded approach — conservative first, destructive last — reflects the principle of using the least harmful effective treatment.
A NOTE ON EXCLUDING AN ACOUSTIC NEUROMA
An important part of diagnosing Meniere's is that it remains, to a large extent, a diagnosis of exclusion, and the key condition to rule out is an acoustic neuroma. Because a vestibular schwannoma can also cause unilateral hearing loss, tinnitus and imbalance, an MRI with gadolinium is performed to exclude a tumour before settling on Meniere's, particularly when the features are atypical or strictly one-sided. This safeguard ensures that a treatable, potentially dangerous tumour is not mislabelled as benign Meniere's disease and simply managed with diet and betahistine — a reminder that any unexplained unilateral inner-ear syndrome deserves imaging.
THE BOTTOM LINE
Meniere's disease is endolymphatic hydrops producing episodic vertigo with fluctuating hearing loss, tinnitus and fullness, managed up a ladder from salt restriction and betahistine to intratympanic and destructive procedures, having first excluded an acoustic neuroma.
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KEY POINTS / NUMBERS (viva)
Meniere's = endolymphatic hydrops (distended endolymph in membranous labyrinth); usually unilateral.
SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
Benign paroxysmal positional vertigo (BPPV) is the commonest cause of vertigo: brief episodes of vertigo triggered by changes in head position, caused by displaced otoconia (calcium-carbonate crystals) in a semicircular canal — usually the posterior canal.
BPPV — canalithiasis (posterior SCC)
cupula
otoconia
(crystals)
head-hanging(Dix-Hallpike)
Free crystals move the endolymph on head movement → cupula deflection → brief positional vertigo
BPPV (canalithiasis): otoconia (calcium-carbonate crystals) dislodged from the utricle fall into the (usually posterior) semicircular canal; a change in head position (as in the Dix-Hallpike test) makes them move the endolymph and deflect the cupula, causing a brief burst of vertigo.
PATHOPHYSIOLOGY & CAUSES
Otoconia dislodge from the utricular macula and enter a semicircular canal (usually the posterior canal, the most dependent) — 'canalithiasis'. On head movement the crystals move the endolymph, abnormally deflecting the cupula and producing a brief burst of vertigo (in 'cupulolithiasis' the crystals stick to the cupula). Causes are idiopathic (commonest), head trauma, post-vestibular-neuritis, ageing and prolonged bed rest.
CLINICAL FEATURES
Brief (seconds, <1 minute) episodes of rotatory vertigo triggered by a change in head position (rolling in bed, looking up, bending).
No hearing loss, tinnitus or aural fullness (which distinguishes it from Meniere's).
Nausea; recurrent episodes.
DIAGNOSIS & MANAGEMENT
The diagnostic test is the Dix-Hallpike manoeuvre — positive when it reproduces vertigo with a characteristic torsional/up-beating nystagmus that appears after a short latency, is transient (<1 minute) and fatigues on repetition. Treatment is particle repositioning — the Epley manoeuvre for the posterior canal (very effective) — with reassurance (it is benign and often self-limiting) and vestibular rehabilitation (Brandt-Daroff exercises). Long-term vestibular sedatives are avoided (they hinder compensation).
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CLINICAL PEARL: BPPV = the commonest vertigo: brief (seconds) positional rotatory vertigo from displaced otoconia in the (usually posterior) semicircular canal (canalithiasis), with no hearing loss/tinnitus. Diagnose with the Dix-Hallpike test (latency, fatigable, torsional up-beating nystagmus). Treat with the Epley repositioning manoeuvre (very effective) and Brandt-Daroff exercises; avoid long-term vestibular sedatives.
WHY THE CRYSTALS CAUSE POSITIONAL VERTIGO
The mechanism of BPPV elegantly explains its characteristic features. Normally the semicircular canals sense rotation only, via endolymph movement deflecting the cupula, and gravity has no direct effect on them. In BPPV, heavy calcium-carbonate crystals (otoconia), which have fallen from the utricle into a canal, make that canal abnormally sensitive to gravity: when the head moves into a certain position, the crystals tumble under gravity, dragging the endolymph and deflecting the cupula, which the brain interprets as a sudden spin. This is why the vertigo is positional (provoked by specific head movements), brief (the crystals soon settle), and shows a latency and fatigability (the crystals take a moment to move and disperse on repetition). Understanding that displaced crystals turn a rotation-sensor into a gravity-sensor makes the whole clinical picture — and the logic of repositioning treatment — immediately clear.
WHY REPOSITIONING WORKS AND SEDATIVES DO NOT
A key therapeutic principle in BPPV is that the correct treatment is mechanical, not pharmacological. Since the problem is simply crystals sitting in the wrong place, the solution is to move them back to where they belong — which is exactly what the Epley (canalith-repositioning) manoeuvre does, using a sequence of head positions to guide the otoconia out of the canal and back into the utricle, where they no longer cause symptoms. This is why a single, correctly-performed manoeuvre can cure the condition immediately, whereas vestibular sedatives merely blunt the sensation without addressing the cause, and prolonged use actually delays the brain's natural compensation. Recognising BPPV as a mechanical problem with a mechanical cure — rather than reaching for drugs — is one of the most satisfying and important lessons in the management of vertigo.
THE BOTTOM LINE
BPPV is the common, benign, positional vertigo of displaced canal crystals, diagnosed by the Dix-Hallpike test and cured mechanically by the Epley repositioning manoeuvre rather than by drugs.
A NOTE ON DISTINGUISHING IT FROM OTHER VERTIGOS
A useful clinical skill is recognising how BPPV differs from the other common vertigos, since the distinction guides management. Unlike Meniere's disease, BPPV has no hearing loss, tinnitus or aural fullness, and unlike vestibular neuritis, its vertigo is brief and strictly positional rather than a constant spinning lasting days. The very short duration (seconds), the clear provocation by specific head movements, and the absence of cochlear symptoms together point firmly to BPPV, allowing the clinician to proceed confidently to a Dix-Hallpike test and, if positive, an Epley manoeuvre — rather than embarking on the imaging or medical treatment appropriate to those other conditions. This ability to separate BPPV from its mimics at the bedside is what makes such a common and treatable cause of vertigo so satisfying to manage.
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KEY POINTS / NUMBERS (viva)
BPPV = commonest cause of vertigo; brief (secs, <1 min) positional rotatory vertigo from displaced otoconia in the (usually posterior) SCC — canalithiasis (cupulolithiasis if stuck on cupula).
Triggered by head-position change (rolling in bed, looking up, bending); NO hearing loss/tinnitus/fullness; causes idiopathic (commonest), trauma, post-neuritis, ageing.
Avoid long-term vestibular sedatives (they hinder central compensation).
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Vestibular neuritis and labyrinthitis are acute peripheral vestibular disorders, usually post-viral. Vestibular neuritis is inflammation of the vestibular nerve → acute vertigo without hearing loss, whereas labyrinthitis is inflammation of the whole labyrinth (vestibular + cochlear) → acute vertigo with hearing loss and tinnitus.
AETIOLOGY & FEATURES
Both are usually viral/post-viral (following a URI); labyrinthitis may be bacterial (suppurative — from otitis media/meningitis) or serous.
Vestibular neuritis: sudden, severe rotatory vertigo lasting days, with nausea/vomiting and unsteadiness, horizontal nystagmus (fast phase to the healthy side), and no hearing loss/tinnitus; worse on head movement.
Labyrinthitis: the same features plus sensorineural hearing loss and tinnitus.
The acute phase is severe (days), then gradually improves over weeks by central compensation.
EXAMINATION & DIAGNOSIS
Examination shows spontaneous horizontal nystagmus (fast phase to the healthy ear), a positive head-impulse test toward the affected side, and a tendency to fall to the affected side, with no central signs. Diagnosis is clinical with a peripheral HINTS pattern; audiometry confirms the SNHL of labyrinthitis, and MRI is done for atypical/central features (to exclude a stroke, especially in the elderly/those with vascular risk).
MANAGEMENT
WHY THE ACUTE VERTIGO SETTLES OVER TIME
A feature that reassures both patient and clinician in vestibular neuritis is that, although the acute vertigo is severe and disabling for days, it steadily improves over the following weeks even though the vestibular nerve may remain damaged — and understanding why explains the whole approach to treatment. The recovery is due to central compensation: the brain gradually learns to rebalance the now-asymmetric signals from the two labyrinths, recalibrating so that the mismatch no longer produces vertigo. This is why the emphasis is on getting the patient moving and into vestibular-rehabilitation exercises as early as possible — movement drives the compensation — and why prolonged bed rest and long-term vestibular sedatives are counterproductive, since they suppress the very signals the brain needs in order to adapt. The natural history of good recovery through compensation is the reason the condition is generally benign despite its dramatic acute presentation.
THE IMPORTANT MIMIC TO EXCLUDE
The crucial safety point in acute vestibular syndrome is that a cerebellar or brainstem stroke can mimic vestibular neuritis, and missing it can be fatal. Both present with acute, continuous, severe vertigo, nausea, vomiting and unsteadiness, so the clinician must actively look for the features that distinguish them. Findings that should raise concern for a central cause include a normal head-impulse test, direction-changing or vertical nystagmus, a skew deviation, an inability to stand or walk at all, and any other neurological signs — in contrast to the reassuring peripheral pattern of vestibular neuritis. In an older patient with vascular risk factors, this distinction is especially important, and any atypical or worrying features warrant urgent MRI to exclude a stroke rather than a diagnosis of benign neuritis. Never assuming that acute vertigo is 'just labyrinthitis' is a key clinical discipline.
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DANGER / REMEMBER: Acute treatment is vestibular sedatives (prochlorperazine, antihistamines) and antiemetics — short-term only (long-term use hinders compensation) — with hydration. Corticosteroids may improve recovery in vestibular neuritis, and antibiotics are given for a bacterial (suppurative) labyrinthitis. The key to recovery is vestibular rehabilitation exercises (to promote central compensation).
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CLINICAL PEARL: Vestibular neuritis = acute (viral) vestibular-nerve inflammation → severe rotatory vertigo for days, nausea, horizontal nystagmus (to the healthy side), a positive head-impulse test, and NO hearing loss. Labyrinthitis = the same plus SNHL/tinnitus (the whole labyrinth). It shows a peripheral HINTS pattern. Treat with short-term vestibular sedatives/antiemetics and steroids, then vestibular rehabilitation; exclude a central cause (stroke) if atypical.
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KEY POINTS / NUMBERS (viva)
Vestibular neuritis = acute (viral) inflammation of the vestibular nerve → vertigo WITHOUT hearing loss; labyrinthitis = whole labyrinth → vertigo WITH SNHL + tinnitus (may be bacterial/suppurative).
Sudden severe rotatory vertigo for DAYS, nausea/vomiting; spontaneous horizontal nystagmus (fast phase to healthy ear), positive head-impulse test (to affected side), falls to affected side; then improves over weeks (compensation).
Vestibular rehabilitation exercises are key to recovery (central compensation).
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
An acoustic neuroma (vestibular schwannoma) is a benign, slow-growing tumour arising from the Schwann cells of the vestibular division of the eighth nerve, in the internal auditory canal/cerebellopontine (CP) angle. It is the commonest CP-angle tumour (and, despite the name, it is not a tumour of the cochlear nerve).
Acoustic neuroma (CP angle)
brainstem /cerebellum
internal auditory canal
tumour
(VIII n.)
VII (facial)
V (trigeminal)
grows into CP angle
Benign vestibular-nerve schwannoma → unilateral SNHL + tinnitus → enlarges to press V, VII, cerebellum
Acoustic neuroma (vestibular schwannoma): a benign tumour of the vestibular nerve grows in the internal auditory canal and cerebellopontine angle, first causing unilateral hearing loss and tinnitus, and later pressing on the trigeminal (V) and facial (VII) nerves and the cerebellum.
ORIGIN & ASSOCIATION
It arises from the Schwann cells of the vestibular nerve (usually the superior vestibular) at the internal auditory meatus and grows into the CP angle. It is bilateral in neurofibromatosis type 2 (NF2).
CLINICAL FEATURES
The features are progressive and unilateral:
Unilateral progressive sensorineural hearing loss (the commonest, with disproportionately poor speech discrimination — a retrocochlear pattern) and unilateral tinnitus.
Imbalance/unsteadiness rather than acute vertigo (slow growth allows compensation).
As it enlarges (a CP-angle syndrome): trigeminal (V) involvement (facial numbness, reduced corneal reflex), facial (VII) weakness (late — VII is resistant), cerebellar signs (ataxia) and raised intracranial pressure (large tumours).
INVESTIGATION & MANAGEMENT
Investigation is with audiometry (unilateral SNHL with poor discrimination), BERA (delayed waves) and MRI with gadolinium (the gold standard — an enhancing IAM/CP-angle mass), with reduced/absent calorics on the affected side. Management depends on size, age and hearing: observation with serial MRI (small tumours/elderly), stereotactic radiosurgery (gamma knife — small-to-medium), or surgical excision (large/growing/young — translabyrinthine/retrosigmoid/middle-fossa), with risk to the facial nerve and hearing.
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CLINICAL PEARL: Acoustic neuroma (vestibular schwannoma) = a benign Schwann-cell tumour of the vestibular nerve at the IAM/CP angle (the commonest CP-angle tumour; bilateral in NF2). It gives unilateral progressive SNHL with poor speech discrimination + tinnitus + imbalance, and, as it enlarges, V (facial numbness/loss of corneal reflex), VII (late) and cerebellar signs. Diagnose with MRI + gadolinium (gold standard) and BERA. Manage by observation (small/elderly), radiosurgery, or surgical excision.
WHY IT PRESENTS SO INSIDIOUSLY
A characteristic and important feature of an acoustic neuroma is that, despite arising on the balance (vestibular) nerve, it rarely causes dramatic vertigo — and understanding why explains its insidious presentation. Because the tumour grows extremely slowly, the brain compensates for the gradually failing vestibular input as it goes, so instead of acute spinning the patient feels only vague, progressive unsteadiness. Meanwhile the tumour compresses the adjacent cochlear nerve fibres, producing the slowly progressive unilateral hearing loss and tinnitus that are usually the first symptoms. This is why the classic presentation is a gradual, one-sided hearing loss with poor speech discrimination rather than balance failure, and why any unexplained asymmetric sensorineural hearing loss or unilateral tinnitus must be taken seriously and imaged — the slow, silent growth means the diagnosis is easily missed until the tumour is large.
WHY MRI AND EARLY DIAGNOSIS MATTER
The emphasis on MRI with gadolinium as the gold standard reflects both how easily the tumour hides and why finding it early matters so much. A small intracanalicular schwannoma can be invisible on CT and asymptomatic apart from subtle hearing asymmetry, yet clearly shown as an enhancing mass on MRI. Detecting it while small is important because management is far easier and safer then — small tumours can be watched or treated with radiosurgery, often preserving hearing and the facial nerve — whereas a large tumour that has filled the CP angle threatens the trigeminal and facial nerves, the cerebellum and, ultimately, the brainstem, making surgery riskier and cure less certain. This is why the threshold for imaging an unexplained unilateral sensorineural hearing loss or tinnitus is deliberately low: catching the tumour early transforms the outlook.
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KEY POINTS / NUMBERS (viva)
Acoustic neuroma = benign schwannoma of the VESTIBULAR nerve (Schwann cells, usually superior vestibular) at the IAM/CP angle; commonest CP-angle tumour; bilateral in NF2.
Unilateral progressive SNHL with POOR speech discrimination (retrocochlear) + unilateral tinnitus + imbalance; enlarging → V (facial numbness, absent corneal reflex), VII (late — resistant), cerebellar ataxia, raised ICP.
Ix: audiometry (unilateral SNHL, poor discrimination), BERA (wave delay), MRI + gadolinium (gold standard), reduced calorics. Rx: observation (small/elderly, serial MRI), stereotactic radiosurgery (gamma knife), surgical excision (translabyrinthine/retrosigmoid/middle fossa) — risk to VII & hearing.
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KEY POINTS TO REMEMBER
Acoustic neuroma (vestibular schwannoma) = benign Schwann-cell tumour of the vestibular nerve at the IAM/CP angle; commonest CP-angle tumour; bilateral in NF2.
Rx: observation (small/elderly), stereotactic radiosurgery, or surgical excision (risk to facial nerve & hearing).
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
Nystagmus is an involuntary, rhythmic oscillation of the eyes. Jerk nystagmus has a slow drift and a fast corrective phase (and is named by the direction of the fast phase), whereas pendular nystagmus has equal phases; vestibular nystagmus is of the jerk type.
PERIPHERAL versus CENTRAL
Peripheral (vestibular) nystagmus: horizontal or horizonto-rotatory, unidirectional (fast phase away from the lesion), suppressed by visual fixation, fatigable, and accompanied by vertigo.
Central nystagmus: any direction (vertical nystagmus is central), may be bidirectional/direction-changing, is NOT suppressed by fixation (may worsen), has less vertigo and is accompanied by other neurological signs.
SIGNIFICANCE
Assessing the direction, the effect of fixation and any associated signs helps localise the lesion. Vertical, direction-changing, non-fatiguable or fixation-non-suppressed nystagmus points to a central (concerning) cause.
A NOTE ON WHY FIXATION MATTERS
The single most useful bedside feature in interpreting nystagmus is the effect of visual fixation, and understanding it repays study. A peripheral vestibular nystagmus is generated by an imbalance in the labyrinths, and the brain's visual-fixation mechanism can partly override it — so asking the patient to fix on a target suppresses (reduces) the nystagmus. A central nystagmus, arising from the very brainstem/cerebellar circuits that would normally suppress it, is NOT damped by fixation and may even worsen. This is why examining nystagmus both with and without fixation (using Frenzel glasses or a blank field to remove fixation) is so informative: suppression with fixation reassures toward a peripheral cause, while persistence or worsening points to a central one — a simple observation that helps localise the lesion.
THE BOTTOM LINE
Nystagmus is analysed for direction and its response to fixation: a horizontal, unidirectional, fixation-suppressed pattern is peripheral, whereas vertical, direction-changing or fixation-resistant nystagmus is central and concerning.
A further practical point is that eliciting nystagmus reliably often requires removing fixation — using Frenzel glasses or asking the patient to look in a blank field — because a peripheral nystagmus that the patient suppresses when staring at the examiner may only become apparent once fixation is taken away, so its absence on casual inspection does not exclude a peripheral lesion.
In practice, a systematic description of any nystagmus — its direction, whether it is horizontal, rotatory or vertical, whether it changes with gaze direction, and whether fixation suppresses it — is one of the most valuable pieces of information the examiner can gather in a dizzy patient, often pointing to the site of the lesion before any investigation is done.
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KEY POINTS TO REMEMBER
Nystagmus = involuntary rhythmic eye oscillation; jerk (slow drift + fast phase, named by fast phase) vs pendular; vestibular is jerk type.
Peripheral: horizontal/horizonto-rotatory, unidirectional (fast phase away from lesion), suppressed by fixation, fatigable, with vertigo.
Central: any direction (vertical = central), may change direction, NOT suppressed by fixation, less vertigo, other neuro signs.
Vertical/direction-changing/non-fatiguable/fixation-non-suppressed nystagmus → central (concerning) cause.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
The caloric test assesses vestibular (horizontal semicircular canal) function, testing each labyrinth separately, by irrigating the ear canal with warm (44°C) and cold (30°C) water (the Fitzgerald-Hallpike test). The temperature sets up convection currents in the horizontal-canal endolymph, generating nystagmus.
INTERPRETATION
The direction follows the mnemonic COWS — Cold Opposite, Warm Same (cold water drives the fast phase to the opposite side, warm to the same side). A canal paresis (reduced/absent response) indicates a peripheral lesion of that labyrinth/nerve (e.g. vestibular neuritis, Meniere's, acoustic neuroma), and a directional preponderance may be seen. It is used to lateralise and quantify vestibular hypofunction, and in a comatose patient an absent response indicates brainstem dysfunction. It is now often replaced by the video head-impulse test and videonystagmography.
A NOTE ON ITS UNIQUE ADVANTAGE
The special value of the caloric test is that it is the one investigation able to assess each labyrinth entirely separately. Most vestibular tests stimulate both ears together or rely on head movement, but by irrigating one ear canal at a time, the caloric test isolates and measures the function of that single horizontal canal, allowing a reduced or absent response ('canal paresis') to be attributed confidently to that side. This makes it particularly useful for lateralising a unilateral vestibular lesion — for example confirming reduced function on the side of an acoustic neuroma or a burnt-out Meniere's ear. Although newer, quicker tests such as the video head-impulse test have largely replaced it in routine practice, the caloric test's ability to test one labyrinth in isolation keeps it valuable in selected cases.
THE BOTTOM LINE
The caloric test uniquely assesses each labyrinth separately by warm/cold irrigation (COWS), detecting a canal paresis that lateralises a peripheral vestibular lesion.
A further consideration is that the caloric test can be uncomfortable and provoke marked nausea and vertigo, and is contraindicated in the presence of a perforated eardrum with water irrigation (air calorics may be used instead), which — together with the availability of quicker, better-tolerated tests — has reduced its routine use while leaving it valuable for specific lateralising questions.
In practice, the caloric test is reserved for situations where lateralising or quantifying a vestibular deficit will change management — for example before destructive treatment for Meniere's or in the work-up of an asymmetric loss — rather than being used routinely in every dizzy patient, most of whom are better assessed by history, positional testing and the video head-impulse test.
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KEY POINTS TO REMEMBER
Caloric test = tests horizontal-canal (vestibular) function of each ear separately by warm (44°C)/cold (30°C) water irrigation (Fitzgerald-Hallpike).
Convection currents in the horizontal-canal endolymph generate nystagmus; COWS — Cold Opposite, Warm Same.
Canal paresis (reduced/absent response) = peripheral lesion of that labyrinth/nerve (vestibular neuritis, Meniere's, acoustic neuroma); directional preponderance.
Lateralises/quantifies vestibular hypofunction; absent response in coma = brainstem dysfunction; now often replaced by vHIT/VNG.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
The Dix-Hallpike test is the diagnostic manoeuvre for posterior-canal BPPV, and the Epley manoeuvre is the therapeutic (canalith-repositioning) manoeuvre.
Epley manoeuvre (posterior-canal BPPV)1. sit, head 45°to affected side2. lie back,head hanging3. turn head 90°to other side4. roll body +head, then sit upEach position held ~30 s → gravity moves the crystals out of the canal back into the utricleThe Epley (canalith-repositioning) manoeuvre for posterior-canal BPPV: a sequence of timed head and body positions that uses gravity to move the displaced crystals out of the semicircular canal and back into the utricle, where they no longer cause vertigo.
DIX-HALLPIKE TEST
The patient sits with the head turned 45° to the test side, then is laid rapidly supine with the head extended ~30° over the edge (head-hanging), and observed. A positive test is a torsional/up-beating nystagmus that appears after a short latency, is transient (<1 minute) and fatigues on repetition — confirming BPPV of the dependent (test) ear.
EPLEY MANOEUVRE
The Epley manoeuvre is a sequence of head and body positions that moves the displaced otoconia out of the posterior canal back into the utricle, resolving the BPPV. It is very effective and may be repeated (the Semont manoeuvre is an alternative, and a BBQ roll is used for lateral-canal BPPV).
A NOTE ON WHY THEY GO TOGETHER
It is worth appreciating that the Dix-Hallpike and Epley manoeuvres form a neat diagnose-then-treat pair for the same condition. The Dix-Hallpike deliberately provokes the vertigo by moving the affected ear into the dependent position, both confirming the diagnosis and identifying which ear and canal is involved; the Epley then uses that same knowledge to reposition the crystals out of that specific canal. Because they are performed in the same setting and rely on the same understanding of canal anatomy, a patient can often be diagnosed and cured in a single visit — the manoeuvre that reproduced their vertigo flowing straight into the one that relieves it. This makes BPPV one of the most rewarding conditions to manage, and the two manoeuvres are best learned and remembered as a linked sequence.
THE BOTTOM LINE
The Dix-Hallpike diagnoses posterior-canal BPPV and the Epley treats it, forming a diagnose-then-treat pair that can cure the condition in a single visit.
A practical caution is that these manoeuvres involve rapid head movements and extension, so they are performed carefully (or modified) in patients with neck problems, vertebrobasilar insufficiency or limited mobility, and the patient is warned that the Dix-Hallpike will briefly reproduce their vertigo — preparation that improves cooperation and the reliability of the test.
In practice, once a clinician is confident with these two linked manoeuvres, a large proportion of patients presenting with positional vertigo can be diagnosed and treated at the first consultation without any investigation, which is why competence in performing and interpreting the Dix-Hallpike and delivering the Epley is regarded as an essential, high-yield skill.
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KEY POINTS TO REMEMBER
Dix-Hallpike = diagnostic test for posterior-canal BPPV: sit, head 45° to test side, lay rapidly supine head-hanging, observe.
Positive: torsional/up-beating nystagmus with latency, transient (<1 min), fatigable — confirms BPPV of the dependent ear.
Epley = therapeutic canalith-repositioning manoeuvre (sequence of head/body positions) that moves otoconia back to the utricle.
Very effective, repeatable; Semont is an alternative; BBQ roll for lateral-canal BPPV.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Motion sickness is a syndrome of nausea, vomiting, pallor, sweating and malaise provoked by real or apparent motion, due to a sensory conflict/mismatch between the vestibular, visual and proprioceptive inputs — for example, reading in a moving car (the eyes signal 'still' while the vestibule signals 'moving').
SUSCEPTIBILITY & FEATURES
It is common in car, sea and air travel, and in susceptible individuals (children aged 2–12, women, and migraineurs). It is self-limiting once the motion stops.
PREVENTION & MANAGEMENT
Behavioural measures help: look at the horizon, sit in the front seat, avoid reading, get fresh air, semi-recline, and eat small light meals. Medications include antihistamines (cinnarizine, promethazine, dimenhydrinate) and hyoscine (scopolamine — an anticholinergic, available as a patch), and habituation (repeated exposure) leads to adaptation.
A NOTE ON WHY SENSORY CONFLICT IS THE KEY
The concept of sensory conflict is the key to understanding, preventing and treating motion sickness. The syndrome arises when the balance system receives contradictory information — typically the vestibular system detecting motion while the eyes report a stationary scene (or vice versa) — and the brain, unable to reconcile the mismatch, triggers the autonomic response of nausea and vomiting. This explains why reading in a moving vehicle is so provocative (eyes fixed on a still page, vestibule sensing motion) and why looking at the horizon helps (it restores agreement between vision and balance). It also explains why habituation works — with repeated exposure the brain learns that the conflicting signals are not dangerous and stops reacting — and why treatments target the vestibular/autonomic pathways. Grasping the sensory-conflict basis makes the practical advice logical rather than arbitrary.
THE BOTTOM LINE
Motion sickness is a sensory-conflict phenomenon between vestibular, visual and proprioceptive inputs, prevented by aligning these cues and treated with antihistamines/hyoscine and habituation.
It is also worth noting that susceptibility varies widely and tends to lessen with age and repeated exposure, which is why seasoned travellers and sailors often 'get their sea legs', and why gradual, repeated exposure (habituation) is used deliberately to build tolerance in those who must travel frequently despite being prone to the condition.
In practice, most people manage motion sickness with simple behavioural measures and, where needed, a single dose of an antihistamine or a hyoscine patch taken before travel, reserving stronger measures for those with severe, predictable symptoms such as sailors or frequent flyers who cannot avoid the provoking motion.
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KEY POINTS TO REMEMBER
Motion sickness = nausea/vomiting/pallor/sweating from real or apparent motion, due to sensory conflict (vestibular vs visual vs proprioceptive).
Common in car/sea/air travel; susceptible — children 2–12, women, migraineurs; self-limiting when motion stops.
Behavioural: look at the horizon, front seat, avoid reading, fresh air, semi-recline, small light meals.
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Balance (equilibrium) is maintained by the integration of three sensory inputs — vestibular (the labyrinth), visual and proprioceptive — in the brainstem and cerebellum, producing reflex eye (vestibulo-ocular reflex) and postural (vestibulospinal) adjustments.
THE VESTIBULAR APPARATUS
The vestibular apparatus has two parts: the three semicircular canals, which detect angular (rotational) acceleration via the cupula in each ampulla, and the otolith organs (utricle and saccule), which detect linear acceleration and gravity via otoconia on the macula. Hair cells transduce movement into nerve signals → the vestibular nerve → the vestibular nuclei → the eyes (the VOR stabilises gaze), the spinal cord (posture) and the cerebellum.
VERTIGO & COMPENSATION
Vertigo results when these inputs mismatch or a lesion occurs. After a unilateral vestibular loss, central compensation allows recovery — the basis of vestibular rehabilitation.
A NOTE ON WHY THREE INPUTS ARE NEEDED
The design of the balance system — relying on three overlapping sensory inputs rather than one — is worth appreciating because it explains both its robustness and its failure modes. Having vestibular, visual and proprioceptive information all reporting on the body's position and movement gives redundancy: if one input is lost or unreliable, the others can often compensate, which is why a person with a vestibular deficit may cope well in good light on firm ground but struggle in the dark or on soft, uneven surfaces where visual and proprioceptive cues are also reduced. It also explains vertigo as a mismatch phenomenon — trouble arises not only when an input fails but when the inputs disagree. This integrated, redundant design underlies both the resilience of normal balance and the rationale for vestibular rehabilitation, which trains the brain to make better use of the remaining inputs.
THE BOTTOM LINE
Balance depends on the integration of vestibular, visual and proprioceptive inputs, with the semicircular canals sensing rotation and the otolith organs sensing linear acceleration and gravity.
A further point is that this three-input design is also the basis of clinical balance testing: manoeuvres such as the Romberg test deliberately remove visual input (eyes closed) to reveal whether a patient is over-reliant on vision to compensate for a vestibular or proprioceptive deficit, translating the physiology directly into a simple bedside assessment.
In practice, understanding this integrated system explains why balance problems in the elderly are so often multifactorial — combining reduced vestibular function, failing vision, peripheral neuropathy and weakness — and why addressing several of these inputs together, rather than any one alone, gives the best improvement in stability and falls prevention.
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KEY POINTS TO REMEMBER
Balance = integration of vestibular + visual + proprioceptive inputs in the brainstem/cerebellum → VOR (eye) + vestibulospinal (postural) reflexes.
Semicircular canals (3): detect angular/rotational acceleration (cupula in ampulla); otolith organs (utricle/saccule): detect linear acceleration & gravity (otoconia on macula).
Vertigo occurs with input mismatch or a lesion; central compensation allows recovery after unilateral loss (basis of vestibular rehab).
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Vestibular rehabilitation is a programme of exercises to promote central compensation and recovery after vestibular disorders, especially unilateral hypofunction (vestibular neuritis, post-labyrinthectomy) and chronic imbalance.
PRINCIPLE & COMPONENTS
The principle is that the brain adapts to and compensates for a vestibular deficit through repeated exposure and exercise (habituation, adaptation and substitution). Components include gaze-stabilisation (VOR) exercises, balance and gait training, habituation exercises (Cawthorne-Cooksey) and, for BPPV, Brandt-Daroff exercises.
KEY PRINCIPLE
It encourages movement rather than prolonged rest or sedatives (which delay compensation), and it improves balance and reduces dizziness. It is a key treatment for chronic vestibular dysfunction, and vestibular sedatives should be used only short-term.
A NOTE ON WHY MOVEMENT BEATS REST
The central, slightly counter-intuitive principle of vestibular rehabilitation is that movement, not rest, is the route to recovery. It is natural for a patient made dizzy by movement to avoid it and to rely on vestibular sedatives, but this is exactly the wrong approach: central compensation — the brain's recalibration to the altered vestibular signals — is driven by exposure to movement, and is delayed or prevented by prolonged rest and by sedative drugs that suppress the signals the brain needs. Vestibular rehabilitation therefore deliberately exposes the patient to the movements and situations that provoke symptoms, in a graded way, so that the brain habituates and adapts. This is why the modern management of chronic vestibular dysfunction emphasises early, active exercise and the sparing, short-term use of sedatives, rather than the older instinct simply to rest and medicate.
THE BOTTOM LINE
Vestibular rehabilitation uses graded movement, not rest, to drive the central compensation that restores balance after vestibular loss, which is why sedatives are kept short-term.
It is also worth appreciating that vestibular rehabilitation is tailored to the specific problem — canalith-repositioning for BPPV, gaze-stabilisation and balance work for a stable unilateral deficit, and broader conditioning for chronic dizziness — and that its success depends heavily on the patient persevering with the exercises, since compensation is an active, practice-driven process.
In practice, vestibular rehabilitation is increasingly delivered by trained physiotherapists as a structured programme, and its effectiveness across BPPV, unilateral vestibular loss and chronic dizziness has made it a cornerstone of modern balance care, complementing rather than being replaced by medication.
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KEY POINTS TO REMEMBER
Vestibular rehabilitation = exercises promoting central compensation/recovery after vestibular disorders (esp unilateral hypofunction, chronic imbalance).
Principle: the brain adapts/compensates via repeated exposure (habituation, adaptation, substitution).
Encourages movement (not prolonged rest/sedatives, which delay compensation); vestibular sedatives only short-term.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
A perilymph fistula is an abnormal communication between the perilymph-filled inner ear and the middle ear — usually at the oval or round window — allowing a perilymph leak, which causes episodic vertigo and fluctuating/progressive sensorineural hearing loss.
CAUSES & FEATURES
Causes include barotrauma (flying/diving/straining), head or ear trauma, stapes surgery, cholesteatoma erosion and sudden pressure changes. The features are vertigo/imbalance and hearing loss provoked by pressure changes (straining, Valsalva, or loud sound — the Tullio phenomenon), with a positive fistula test (pressure on the tragus or pneumatic otoscopy provoking vertigo/nystagmus).
DIAGNOSIS & MANAGEMENT
Diagnosis is clinical (with the fistula test), and exploratory tympanotomy is definitive (visualising the leak). Management is conservative first (bed rest, head elevation, avoiding straining — many heal), with surgical repair (grafting the window) if it persists.
A NOTE ON THE DIAGNOSTIC DIFFICULTY
A recognised challenge with perilymph fistula is that it can be genuinely difficult to diagnose with certainty, because its symptoms — episodic vertigo with fluctuating hearing loss — overlap with those of Meniere's disease and other inner-ear disorders, and no single test is definitive. The history of a precipitating event (barotrauma, straining, trauma or recent stapes surgery) and the provocation of symptoms by pressure or loud sound (the Tullio phenomenon) are important clues, and the fistula test may support the diagnosis, but the leak itself is often only confirmed at exploratory tympanotomy. This diagnostic uncertainty is why management usually starts conservatively — many fistulae seal spontaneously with rest and avoidance of straining — with surgery reserved for persistent or clearly-documented cases, balancing the wish to confirm and repair the leak against the invasiveness of exploration.
THE BOTTOM LINE
A perilymph fistula is a leak at the oval/round window causing pressure-provoked vertigo and hearing loss, diagnosed largely clinically and managed conservatively first, with surgical repair if it persists.
A final practical point is that, because a perilymph fistula can closely mimic other inner-ear disorders and often seals with conservative measures, clinicians generally avoid rushing to surgery, instead advising rest and avoidance of straining and pressure changes first, and reserving exploratory tympanotomy and window repair for symptoms that persist or a diagnosis that must be confirmed.
In practice, the possibility of a perilymph fistula should be kept in mind in any patient who develops vertigo and hearing loss after barotrauma, straining or ear surgery, since recognising the precipitating event is often the crucial step that separates it from the many other causes of an inner-ear syndrome.
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KEY POINTS TO REMEMBER
Perilymph fistula = abnormal communication (usually oval/round window) leaking perilymph from the inner to the middle ear.