GC221 Vertigo Peripheral And Central
Vertigo is an illusion of rotational movement classified as peripheral when arising from vestibular labyrinth or cranial nerve VIII dysfunction, or central when caused by brainstem or cerebellar pathology.
Vertigo: Peripheral and Central
Lecture Map
A patient says "I'm dizzy." Your single most important job is to figure out what they actually mean — because "dizzy" can mean four completely different things, and only one of them (vertigo) points to the vestibular system. Once you've confirmed true vertigo, the critical next step is distinguishing peripheral (inner ear/vestibular nerve — usually benign) from central (brainstem/cerebellum — potentially life-threatening). This lecture by Dr. Leah Lau (ENT, QMH) walks through the balance mechanism, the four types of dizziness, the key peripheral vs central differentiators, and the major peripheral vestibular disorders with their management. [1]
- Differentiate the four types of dizziness: lightheadedness, pre-syncope, disequilibrium, vertigo
- Understand the balance mechanism and vestibular system anatomy
- Distinguish peripheral from central vertigo using clinical features and nystagmus patterns
- Diagnose and manage BPPV, Ménière's disease, vestibular neuritis, vestibular migraine
- Know when to suspect central causes and escalate
- Understand vestibular rehabilitation principles
"At least 2 sensory inputs should be intact to allow the brain to identify which is the abnormal sensory input and to allow central adaptation" [1]
The brain maintains balance using three sensory inputs:
| Input | Contribution | What It Does |
|---|---|---|
| Vestibular system | ~15% | Detects head position, angular/linear acceleration |
| Vision | ~70% | Dominant input; provides spatial orientation |
| Proprioception (somatosensory) | ~15% | Joint position sense from limbs, especially feet/ankles |
Why does this matter?
- Vision contributes ~70%, so vestibular lesions can often be partially compensated by the visual system — this is the basis for visual fixation suppressing peripheral nystagmus but not central nystagmus.
- If two inputs are lost (e.g., elderly with poor vision AND peripheral neuropathy), the patient has no "tiebreaker" — the brain cannot determine which input is wrong, and central compensation fails → chronic disequilibrium.
- This explains why elderly patients are particularly vulnerable: age-related degeneration hits all three systems simultaneously. [1]
The Vestibular System — Anatomy
Peripheral Vestibular System: Vestibule (saccule and utricle), Semicircular canals, Vestibular nerve [1]
Central Vestibular System: Brainstem, Cerebellum [1]
- Semicircular canals (3 per ear): Detect angular acceleration (rotational head movement). Each canal lies in a different plane (anterior/posterior/lateral). Endolymph moves within them when the head rotates, deflecting hair cells in the ampulla → generating nerve signals.
- Otolith organs (saccule and utricle): Detect linear acceleration and gravity. Contain otoconia (calcium carbonate crystals) embedded in a gelatinous membrane over hair cells. Saccule detects vertical movement; utricle detects horizontal movement.
- Vestibular nerve (CN VIII vestibular division): Transmits signals from the vestibular apparatus to the vestibular nuclei in the brainstem.
What the vestibular-organs figure shows: ampulla with crista / cupula / hair cells, plus utricle–saccule maculae with otoconia — angular sensors (canals) vs linear/gravity sensors (otoliths). [1]
- Vestibular nuclei (in the brainstem at the pontomedullary junction): integrate vestibular input with visual and proprioceptive data
- Cerebellum (especially flocculonodular lobe): calibrates and fine-tunes vestibular reflexes
- Connections to: oculomotor nuclei (for the vestibulo-ocular reflex/VOR), spinal cord (vestibulospinal tract for postural control), cortex (conscious perception of movement)
"Dizzy – A non-specific term, especially true in Chinese. Importance of clarification with history taking. Patients may even use the term 'dizzy' for true LOC or headache." [1]
High Yield: Always Clarify 'Dizzy'
Never accept "dizzy" at face value. In Chinese-speaking populations especially, the term is used for everything from lightheadedness to vertigo to actual syncope to headache. You MUST ask: "Do you feel like the room is spinning? Do you feel like you're going to faint? Do you feel unsteady on your feet?" This is a guaranteed exam discriminator.
The Four Types
| Type | Definition | Key Features | Common Causes |
|---|---|---|---|
| Lightheadedness | Most common; non-specific; never actually falls | Vague "woozy" feeling, no spinning, no near-fainting | Hyperventilation, hypoglycaemia, anaemia, head trauma; psychogenic disorders (depression, anxiety, phobia) |
| Pre-syncope | Sensation of impending faintness or LOC ± generalised weakness | Occurs while rising from lying/sitting; worse in morning | Orthostatic hypotension; autonomic dysfunction (diabetes); cardiovascular (arrhythmias, MI, carotid stenosis); medications (anti-HT, anti-arrhythmics) |
| Disequilibrium | Impaired balance and gait without abnormal head sensation; feeling of unsteadiness, no illusion of movement or sensation of faintness | Walking is the problem, not head sensation | Most common cause: Ageing. Age-related degeneration in semicircular ducts, otolith organs, vestibular nuclei, brainstem pathways, visual acuity, proprioception. Also: peripheral neuropathy, musculoskeletal disorders, gait disorders, Parkinson's disease |
| Vertigo | Hallucination of movement (rotatory or translational); lesion in vestibular system | Spinning or tilting sensation; the environment or the patient appears to move | Peripheral or central vestibular pathology |
Why this classification matters: Each type has a completely different differential diagnosis and workup. A patient with pre-syncope needs cardiac workup (ECG, Holter, orthostatic BP). A patient with vertigo needs vestibular assessment. A patient with disequilibrium needs neurological and falls-risk assessment. Mixing these up wastes time and resources.
This is the single most important table in this lecture for exams:
Peripheral vertigo vs Central vertigo [1]
| Feature | Peripheral Vertigo | Central Vertigo |
|---|---|---|
| Nystagmus direction | Horizontal or torsional, NEVER vertical, unidirectional | Multi-directional, vertical |
| Onset | Acute | Subacute or gradual |
| Visual fixation | Suppressed | Not suppressed |
| Nausea/vomiting | May be severe | Variable |
| Otological symptoms | Common (hearing loss, tinnitus) | Rare |
| Neurological symptoms | Rare | Common |
| Balance | Mild to moderate imbalance | Severe imbalance/ataxia |
| Fatigability | Fatigable | Not fatigable |
| Duration | Temporary, seconds to hours | Persistent, lasts for days |
Why each feature makes physiological sense:
-
Nystagmus direction: Peripheral lesions cause an asymmetric tonic vestibular signal → the brainstem interprets this as head rotation in one direction → compensatory eye drift + fast corrective phase (jerk nystagmus). Since the semicircular canals generate horizontal and torsional signals, peripheral nystagmus is never purely vertical. Vertical nystagmus requires dysfunction of central pathways that process vertical canal input (in the brainstem/cerebellum).
-
Visual fixation: In peripheral disease, the cortex can use visual input to override the abnormal vestibular signal → fixation suppresses nystagmus. In central disease, the problem is in the processing centres themselves → visual fixation cannot compensate.
-
Fatigability: Peripheral nystagmus (especially BPPV) fatigues with repeated testing because the otoconia settle and the neural signal adapts. Central nystagmus reflects ongoing structural pathology and does not fatigue.
-
Otological symptoms: The cochlea and vestibular apparatus are anatomically adjacent in the inner ear, so peripheral vestibular disease often affects hearing. Central structures (brainstem, cerebellum) are anatomically distant from the cochlea.
-
Neurological symptoms in central vertigo: Because the brainstem houses multiple cranial nerve nuclei and long tracts, central vestibular lesions almost always produce additional neurological signs (diplopia, dysarthria, dysphagia, facial numbness, limb weakness/ataxia).
Critical Exam Point
"Most important to rule out central cause of vertigo" [1]. The lecture summary emphasizes this explicitly. Central vertigo can indicate stroke (posterior circulation), tumour, or MS. Missing a cerebellar stroke is catastrophic — it can progress to brainstem herniation. Always look for: vertical nystagmus, non-fatigable nystagmus, neurological deficits, severe ataxia.
Peripheral vestibular disorders: BPPV, Meniere's disease, Vestibular neuronitis, Superior canal dehiscence, Labyrinthitis, Perilymph fistula, Syphilis [1]
Additional peripheral causes from the slide listing: Ototoxicity, Trauma (temporal bone fracture/vestibular concussion), Vestibular insufficiency, Vestibular paroxysmia [1]
Vertebrobasilar insufficiency/TIA/Stroke, Tumour, Medication, Multiple sclerosis, Metabolic, Vestibular Migraine, Epilepsy [1]
BPPV — Benign Paroxysmal Positional Vertigo
Most common cause of vertigo [1]
Benign – Self-limiting, 80% spontaneously resolve Paroxysmal – Recurrent Positional – Related to head position (looking up rapidly/rolling over in bed) Vertigo – lasts for seconds to < 1 min [1]
Otoconia dislodged → Otolith deposited in the semicircular canal [1]
How it works from first principles:
- Otoconia are tiny calcium carbonate crystals normally embedded in the gelatinous membrane of the utricle.
- When they dislodge (from head trauma, vestibular damage, or idiopathically), they can migrate into a semicircular canal.
- When the head moves into certain positions, the otoconia move through the canal under gravity, creating abnormal endolymph flow that deflects the cupula → brain perceives rotation → vertigo.
- Once the otoconia settle (seconds), the signal stops → vertigo is brief.
Causes of dislodgement: Idiopathic, Head trauma, Vestibular damage (vestibular neuronitis/labyrinthitis) [1]
Posterior canal 85%, Lateral canal 15%, Superior canal (rare) [1]
Why posterior canal? Because the posterior canal opening is the most gravity-dependent position when lying down. Dislodged otoconia preferentially fall into it.
From senior notes: [2]
- Rotate patient's head ipsilaterally 45° while sitting up (this aligns the posterior semicircular canal with the sagittal plane)
- Quickly move patient to supine position with head 30° below horizontal
- Positive = nystagmus occurs after a delay of a few seconds (latency) → BPPV
- No delay → think central lesion
What the Dix–Hallpike sequence shows: sit → head turned 45° → rapid recline into head-hanging — maximally stimulating the posterior canal; watch for delayed, fatigable torsional–upbeat nystagmus. [1]
The latency occurs because it takes a moment for the otoconia to move through the endolymph. This is a key discriminator from central positional nystagmus (no latency, no fatigue).
Epley Manoeuvre [1]
The Epley manoeuvre is a canalith repositioning procedure. It uses sequential head positions to guide the otoconia out of the posterior semicircular canal back into the utricle, where they can be reabsorbed.
Procedure sequence (example: right posterior canal) [1]:
- Initial positioning — Patient sits upright facing the examiner, grasps the examiner’s forearm for stability, then is moved rapidly supine with the head extended just beyond the table and the affected (right) ear downward.
- Examiner repositioning — Examiner moves to the head of the table and repositions the hands.
- Head rotation — Head is quickly rotated to the opposite side until the affected ear is upward; hold ~30 seconds.
- Side roll — Patient rolls onto the unaffected side while the examiner rotates the head until the nose points toward the floor; hold ~30 seconds.
- Return to sitting — Patient is rapidly returned to sitting. Repeat the whole sequence until no nystagmus can be elicited.
Post-treatment: - Avoid sudden head movement - Sleep in 45 degree prop up position - Avoid sleeping on side of bad ear [1]
HIGH YIELD — Medication is USELESS for BPPV
"Medication is USELESS" [1]. This is a direct slide quote and a common exam trap. Vestibular sedatives (cinnarizine, diazepam) do NOT treat BPPV — they suppress symptoms but don't reposition the otoconia. The Epley manoeuvre is the definitive treatment. Betahistine is for Ménière's, not BPPV.
Ménière's Disease
Idiopathic endolymphatic hydrops [1]
The endolymphatic system (within the membranous labyrinth) normally maintains a careful balance of endolymph production and absorption. In Ménière's disease, there is excess endolymph accumulation (hydrops) → distension of the endolymphatic space → disruption of both cochlear (hearing) and vestibular (balance) function.
The hydrops causes intermittent ruptures of the membranous labyrinth → potassium-rich endolymph mixes with sodium-rich perilymph → depolarization block of vestibular and cochlear neurons → acute vertigo attack + hearing loss + tinnitus.
Triad – Vertigo, hearing loss, tinnitus, aural fullness [1]
(The slide says "triad" but lists four symptoms — examiners may accept either "triad" of vertigo/hearing loss/tinnitus, or the full tetrad including aural fullness)
Vertigo episodes 20 mins to 24 hours Fluctuating aural symptoms Progressive hearing loss [1]
Definitive Ménière disease — all of:
- A. ≥2 spontaneous episodes of vertigo, each lasting 20 minutes to 12 hours
- B. Audiometrically documented low- to medium-frequency SNHL in one ear (defines the affected ear), on ≥1 occasion before, during, or after a vertigo episode
- C. Fluctuating aural symptoms in the affected ear — hearing change, tinnitus, and fullness
- D. Not better accounted for by another vestibular diagnosis
Probable Ménière disease — all of:
- A. ≥2 episodes of vertigo or dizziness, each lasting 20 minutes to 24 hours
- B. Fluctuating aural symptoms in the affected ear — hearing change, tinnitus, or fullness
- C. Not better accounted for by another vestibular diagnosis
No serological or genetic marker is used for diagnosis. Clinical “tetrad” framing still helps; the criteria above are what the slide uses for definitive vs probable labelling.
Incidence 0.1%; F:M 3:2; Family history 20%; Young ( < 65 years old) [1]
Management
Vestibular sedatives – Cinnarizine, diazepam Antiemetic – Maxolon (metoclopramide), Stemetil (prochlorperazine), Ondansetron Intratympanic steroid [1]
Low salt diet Diuretics Meniett Device Betahistine Intratympanic gentamicin injection [1]
Why these work:
- Low salt diet + diuretics: Reduce endolymph volume (hydrops is essentially fluid overload in the endolymphatic space)
- Betahistine: H1 agonist/H3 antagonist → improves microcirculation of the inner ear and reduces endolymph pressure
- Intratympanic gentamicin: Gentamicin is selectively vestibulotoxic (more toxic to vestibular hair cells than cochlear) → chemical ablation of the overactive vestibular apparatus → eliminates vertigo but risks hearing loss
- Meniett device: Delivers low-pressure pulses through a tympanostomy tube to the middle ear → thought to promote endolymph drainage
Endolymphatic sac decompression Labyrinthectomy Vestibular neurectomy [1]
Vestibular Neuritis
Acute unilateral peripheral vestibular failure [1]
Most common in patients 40-60 years old Severe vertigo lasting for days Subsequent imbalance for weeks to months No hearing loss Nausea and vomiting Commonly after URI Pathophysiology: Inflammation of vestibular nerve, likely viral origin [1]
Why no hearing loss? The vestibular nerve and cochlear nerve, while both part of CN VIII, travel in separate bundles. Vestibular neuritis selectively inflames the vestibular division, sparing the cochlear division. If hearing IS affected, the condition is called labyrinthitis (inflammation involves the labyrinth including the cochlea).
| Feature | BPPV | Ménière's | Vestibular Neuritis |
|---|---|---|---|
| Duration of vertigo | Seconds ( < 1 min) | 20 min – 24 hours | Days |
| Positional trigger | Yes (head position) | No (spontaneous) | No (spontaneous, but worse with head movement) |
| Hearing loss | No | Yes (fluctuating → progressive) | No |
| Tinnitus | No | Yes | No |
| Aural fullness | No | Yes | No |
| Preceding URI | Uncommon | Uncommon | Common |
| Nystagmus | On Dix-Hallpike only | During attacks | Persistent for days |
Vestibular sedatives Early mobilization Vestibular rehabilitation Surgery is not indicated Antiviral has no effect [1]
Natural course: Symptomatic resolution by 3 months [1]
Why early mobilization? Vestibular compensation depends on the brain recalibrating to the new asymmetric vestibular input. Bed rest delays this adaptation. The sooner the patient moves, the faster the brain "learns" to compensate.
Exam Trap: Antivirals
Despite the likely viral aetiology, antivirals have no proven benefit in vestibular neuritis [1]. This is commonly tested. Short courses of corticosteroids (not covered explicitly in this slide set but common in clinical practice) may be given early, though evidence is mixed.
Vestibular Migraine
Most common in young females [1]
At least 5 episodes, lasting 5 min – 72 hr Current or previous history of migraine ± aura One or more migraine features with > 50% of vertigo episodes: - Headache (unilateral/pulsating) - Photophobia/phonophobia - Visual aura [1]
Why this matters: Vestibular migraine is classified as central in the lecture's cause list [1], but it's a functional/neurochemical disorder rather than a structural lesion. The migrainous process affects central vestibular processing areas. It's important because it's common (especially in young women), recurrent, and often misdiagnosed as Ménière's disease.
| Feature | Ménière's | Vestibular Migraine |
|---|---|---|
| Hearing loss | Yes (progressive SNHL) | No/minimal |
| Tinnitus/aural fullness | Yes | Possible but not prominent |
| Episode duration | 20 min – 24 hours | 5 min – 72 hours |
| Migraine features | Not required | Required (headache, photophobia, aura) |
| History of migraine | Not required | Required |
Triptans Tricyclic anti-depressants Beta-blockers [1]
These are standard migraine treatments — triptans for acute attacks, TCAs and beta-blockers for prophylaxis.
| Condition | Key Features |
|---|---|
| Labyrinthitis | Similar to vestibular neuritis BUT with hearing loss (inflammation involves labyrinth including cochlea). Often post-viral or bacterial. |
| Superior Canal Dehiscence | Bony defect over superior semicircular canal → vertigo/oscillopsia triggered by loud sounds (Tullio phenomenon) or pressure changes (Hennebert sign) |
| Perilymph Fistula | Abnormal communication between perilymphatic space and middle ear → vertigo triggered by straining, coughing, or pressure changes. Often post-trauma or post-surgery. |
| Ototoxicity | Aminoglycosides (esp. gentamicin), cisplatin, loop diuretics → bilateral vestibular hypofunction + hearing loss. Progressive, dose-related. |
| Trauma | Temporal bone fracture/vestibular concussion → sudden vertigo + possible hearing loss |
| Vestibular paroxysmia | Neurovascular compression of CN VIII (similar concept to trigeminal neuralgia but for vestibular nerve) → brief attacks of vertigo, responds to carbamazepine |
| Syphilis | Can cause labyrinthitis, endolymphatic hydrops (otosyphilis). Consider in unexplained SNHL + vertigo. |
Central Causes — The Dangerous Differentials
Vertebrobasilar insufficiency/TIA/Stroke, Tumour, Medication, Multiple sclerosis, Metabolic, Vestibular Migraine, Epilepsy [1]
- The vertebrobasilar arterial system supplies the brainstem, cerebellum, and inner ear
- Cerebellar stroke can present as isolated vertigo in 10-20% of cases — mimicking peripheral vestibular disease
- Red flags for central cause: vertical nystagmus, direction-changing nystagmus, severe truncal ataxia (unable to sit unsupported), other neurological signs
The HINTS test (Head Impulse, Nystagmus, Test of Skew) helps distinguish peripheral from central causes of acute vestibular syndrome:
- Head Impulse Test: Normal (no corrective saccade) → worrying for central cause. Abnormal (catch-up saccade) → peripheral
- Nystagmus type: Unidirectional → peripheral. Direction-changing → central
- Test of Skew: Positive (vertical misalignment) → central
Tailored, step-wise program to enhance your vestibular compensation Improving symptoms, postural stability and gaze stability Return to normal activities Four main phases: 1. Clinical diagnosis 2. Patient counselling & explanation 3. Formulate rehab plan & exercises 4. Follow up & monitor [1]
Why it works: The brain has remarkable plasticity for recalibrating vestibular function. Through repetitive exercises (gaze stabilization, balance training, habituation exercises), the central vestibular system learns to rely more heavily on the remaining intact inputs and to suppress the abnormal signals.
1. Differentiate the types of dizziness 2. Detailed history taking and physical examination 3. Most important to rule out central cause of vertigo 4. Manage according to diagnosis 5. BPPV is common but not all dizziness worsened by motion is BPPV [1]
Not All Motion-Worsened Dizziness = BPPV
This is explicitly stated in the lecture summary. Many types of vertigo (and even non-vestibular dizziness) worsen with head movement. The hallmark of BPPV is brief (seconds), positional (specific head positions like looking up or rolling over), fatigable episodes with positive Dix-Hallpike. Vestibular neuritis also worsens with movement but lasts days and is not positional.
Clinical Approach — History, Examination, Investigations
- Clarify "dizzy": Spinning? Near-faint? Unsteady? Lightheaded?
- Duration of episodes: Seconds (BPPV) → minutes to hours (Ménière's) → days (vestibular neuritis) → variable (vestibular migraine)
- Triggers: Positional (BPPV), spontaneous (Ménière's, vestibular neuritis), loud sounds/pressure (superior canal dehiscence)
- Associated symptoms:
- Otological: hearing loss, tinnitus, aural fullness → Ménière's
- Neurological: diplopia, dysarthria, dysphagia, weakness, numbness → central cause
- Migraine features: headache, photophobia, visual aura → vestibular migraine
- Preceding URI → vestibular neuritis
- Medications: ototoxic drugs, anti-hypertensives (pre-syncope), sedatives
- Past medical history: head trauma, cardiovascular risk factors, migraine history, autoimmune disease
- Vital signs: orthostatic BP (pre-syncope workup)
- Otoscopy: middle ear pathology, cholesteatoma, perforation
- Nystagmus assessment: direction, suppressibility with fixation, fatigability
- Dix-Hallpike manoeuvre: for BPPV
- Cranial nerve examination: especially CN V, VII, VIII, IX-XII
- Cerebellar signs: finger-nose test, heel-shin test, dysdiadochokinesis, truncal ataxia, gait
- Romberg test: positive suggests proprioceptive or vestibular deficit (central compensation removed when eyes closed)
- Hearing tests: Weber and Rinne (bedside); audiometry
| Investigation | When/Why |
|---|---|
| Pure tone audiometry | Ménière's (low-frequency SNHL), acoustic neuroma, labyrinthitis |
| CT brain | Acute setting to rule out haemorrhage |
| MRI brain (+ IAM) | Suspected central cause, acoustic neuroma, MS |
| ECG | Pre-syncope workup |
| Blood tests (FBC, glucose, TFTs) | Anaemia, hypoglycaemia, metabolic causes |
| Caloric testing | Assess unilateral vestibular hypofunction (canal paresis) |
| Videonystagmography (VNG) | Objective nystagmus documentation |
Integration with Related Material
"Clarify meaning of 'dizziness'; Central vs peripheral; Red flags; Most common diagnosis of true vertigo is 'vertigo NYD'; Acute vertigo: viral labyrinthitis, BPV, Eustachian tube dysfunction, Meniere's disease"
This reinforces that in primary care, many patients with vertigo end up with a diagnosis of "vertigo not yet diagnosed" — underscoring the importance of systematic history taking.
Posterior circulation stroke presenting as isolated vertigo is a critical differential. The 2020 SAQ (Question 4) tested exactly this — a patient with sudden vertigo + cerebellar signs → think cerebellar infarction.
Multiple sclerosis can cause central vertigo. Demyelinating plaques in the brainstem or cerebellar peduncles disrupt central vestibular pathways. Vertigo may be the presenting symptom of MS in young patients.
Vestibular dysfunction is listed as an intrinsic risk factor for falls in the elderly. Disequilibrium from age-related vestibular degeneration is a major contributor to falls risk.
Exam Intelligence
| Trap | Correct Reasoning |
|---|---|
| Giving betahistine for BPPV | Betahistine is for Ménière's. BPPV treatment = Epley manoeuvre. Medication is USELESS for BPPV. |
| Calling vertical nystagmus "peripheral" | Peripheral nystagmus is NEVER vertical — this is a central red flag |
| Diagnosing Ménière's when no hearing loss | Ménière's requires the triad/tetrad. Vertigo without hearing loss/tinnitus → think vestibular neuritis or BPPV |
| Prescribing antivirals for vestibular neuritis | Antiviral has no effect despite likely viral aetiology |
| Assuming all positionally-worsened vertigo = BPPV | "BPPV is common but not all dizziness worsened by motion is BPPV" — lecture summary explicitly warns against this |
| Missing cerebellar stroke | Vertigo + severe ataxia + non-fatigable nystagmus + neurological signs → central cause → urgent imaging |
| Confusing labyrinthitis with vestibular neuritis | Both are post-viral, but labyrinthitis = vertigo + hearing loss; vestibular neuritis = vertigo WITHOUT hearing loss |
| Feature | BPPV | Ménière's | Vestibular Neuritis | Vestibular Migraine | Central |
|---|---|---|---|---|---|
| Duration | Seconds | Hours | Days | Minutes to hours | Days+ |
| Hearing loss | No | Yes | No | No | Rare |
| Positional | Yes | No | No | Variable | Variable |
| Neuro signs | No | No | No | ± | Yes |
| Nystagmus | On Dix-Hallpike | During attack | Persistent | Variable | Multi-directional/vertical |
| Treatment | Epley | Betahistine/low salt | Vestibular rehab | Triptans/prophylaxis | Treat cause |
From CFB (FM02): "Most common diagnosis of true vertigo is 'vertigo NYD'" [3] — this is worth knowing for the exam as it reinforces that many patients with vertigo do not receive a definitive diagnosis on first presentation.
High Yield Summary
- Always clarify "dizzy" → four types: lightheadedness, pre-syncope, disequilibrium, vertigo.**
- Vertigo = hallucination of movement → lesion in vestibular system.**
- Peripheral vs Central: Peripheral = horizontal/torsional nystagmus, fatigable, suppressed by fixation, otological symptoms, NO neurological signs. Central = vertical/multidirectional nystagmus, non-fatigable, NOT suppressed by fixation, neurological signs, severe ataxia.**
- BPPV: Most common cause of vertigo. Seconds, positional, Dix-Hallpike positive. Treat with Epley manoeuvre. MEDICATION IS USELESS.**
- Ménière's: Endolymphatic hydrops. Vertigo (hours) + hearing loss + tinnitus + aural fullness. Low salt diet, betahistine, diuretics, intratympanic gentamicin. Surgery if medical therapy fails.**
- Vestibular neuritis: Post-URI, vertigo lasting DAYS, NO hearing loss. Vestibular sedatives + early mobilization + rehab. Antivirals do NOT work. Resolves by 3 months.**
- Vestibular migraine: Young females, 5+ episodes, migraine features with > 50% of vertigo episodes. Triptans, TCAs, beta-blockers.**
- MOST IMPORTANT: Rule out central cause. Cerebellar stroke can mimic peripheral vertigo. Look for vertical nystagmus, non-fatigable nystagmus, neurological signs, severe ataxia.**
- Not all motion-worsened dizziness = BPPV.**
Active Recall - Vertigo Peripheral and Central
[1] Lecture slides: GC 221. Vertigo Peripheral and central.pdf [2] Senior notes: Ryan Ho Fundamentals.pdf (p.98, CN VIII section); Ryan Ho Neurology.pdf (p.20) [3] Lecture slides: CFB (FM02) Introduction to common problems - Differentiating the normal from the abnormal.pdf (p.35) [4] Lecture slides: GC 082. Severe headache_headache and neuralgia; neuro-imaging I.pdf [5] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf [6] Lecture slides: GC 225. Neuroimmunological disorders of the central nervous system.pdf [7] AOS material: AOS - Geriatrics.pdf (p.10)
GC220 Upper Airway Obstruction And Tracheostomy
Upper airway obstruction is a partial or complete blockage of the airway above the tracheal bifurcation that may necessitate tracheostomy—a surgical opening in the anterior tracheal wall—to establish a secure airway and maintain ventilation.
GC222 I Want To Donate My Organs
A UK General Medical Council guidance topic addressing the principles and processes by which individuals can express their wish to donate organs after death, including consent, registration, and the roles of healthcare professionals in facilitating organ donation.