Central versus peripheral vertigo

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Vertigo is an illusion of movement generated by imbalance in vestibular inputs; dizziness can also reflect presyncope, disequilibrium, medication, anxiety and multisensory impairment. Symptom quality alone performs poorly. The timing-and-triggers approach first asks whether the syndrome is continuous, spontaneous episodic or triggered episodic, then applies the correct examination. This prevents performing positional tests on an unstable stroke syndrome or HINTS on brief resolved attacks.

Peripheral vestibular lesions affect labyrinth or eighth nerve; central lesions affect brainstem, cerebellum and networks that integrate vision and balance. Peripheral nystagmus in an acute unilateral vestibulopathy is generally horizontal-torsional and unidirectional, increasing when looking toward the fast phase. Central nystagmus may be vertical, pure torsional or change direction with gaze, but no single description is infallible and medication or poor fixation can alter appearance.

The bedside head impulse tests the vestibulo-ocular reflex. A corrective saccade after a rapid, small-amplitude head turn supports peripheral hypofunction on that side; a normal impulse in acute continuous vertigo can be central. Technique is difficult, bilateral vestibulopathy changes interpretation and an abnormal impulse can rarely occur in stroke. HINTS can outperform early MRI in expert hands but performs badly when applied to the wrong patient or by an untrained examiner.

Imaging strategy follows syndrome. Non-contrast CT is insensitive to small posterior-fossa infarction and should not be used as a reassuring rule-out. Acute focal or central signs prompt the stroke pathway with vascular imaging and MRI as selected by specialists. Typical BPPV is a clinical diagnosis and does not need routine imaging, but atypical positional nystagmus, hearing or neurological progression and failure of correct manoeuvres should trigger review.

Key points

Ask what the patient means by dizziness, then classify timing and triggers: a single continuous acute vestibular syndrome, recurrent spontaneous attacks, brief triggered episodes or chronic disequilibrium generate different differentials.
Movement can worsen almost any vertigo; a true trigger initiates an otherwise absent brief episode. Do not diagnose benign positional vertigo merely because a continuously dizzy patient feels worse turning the head.
Acute vestibular syndrome comprises continuous vertigo or dizziness lasting days, spontaneous nystagmus, nausea or vomiting, head-motion intolerance and gait instability. Important causes include vestibular neuritis and posterior-circulation stroke.
HINTS is not a general dizziness screen. Use it only in a currently symptomatic acute vestibular syndrome with spontaneous nystagmus, and only when the examiner has specific training and can act on the result.
A central HINTS pattern includes normal head impulse, direction-changing gaze-evoked nystagmus or skew; HINTS-plus adds new unilateral hearing loss because anterior inferior cerebellar artery stroke can affect the labyrinth.
Severe truncal ataxia, inability to sit unaided, vertical nystagmus, focal cranial or limb signs, new headache or neck pain and high vascular risk lower the threshold for stroke imaging and specialist review.
Posterior-canal BPPV produces brief episodes triggered by position change with a characteristic delayed, transient upbeat torsional nystagmus on Dix–Hallpike; the Epley manoeuvre treats the affected canal when safe.
A negative or atypical Dix–Hallpike does not exclude horizontal-canal BPPV; persistent downbeat, non-fatiguing or non-canal nystagmus raises central positional disease.
Vestibular neuritis causes prolonged peripheral vestibular symptoms without new hearing loss or focal neurology; hearing loss shifts the differential toward labyrinthitis, Ménière disease or an AICA vascular syndrome.
Ménière disease produces recurrent spontaneous vertigo with fluctuating unilateral hearing, tinnitus or aural pressure; diagnosis requires audiovestibular assessment and exclusion of mimics.
Vestibular migraine can occur with or without simultaneous headache, but a first severe episode or focal signs still requires vascular and structural assessment rather than diagnosis by migraine history alone.
Vestibular suppressants and antiemetics are short-term aids in severe acute peripheral disease; prolonged use can delay central compensation. Early safe mobilisation and vestibular rehabilitation support recovery after dangerous causes are excluded.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Peripheral vestibular disorders

Benign positional vertigo, vestibular neuritis, labyrinthitis and Ménière disease disturb labyrinthine or eighth-nerve input, with timing, triggers, hearing and eye findings separating syndromes.

Central neurological disease

Posterior-circulation stroke, demyelination, tumour and cerebellar degeneration affect brainstem or cerebellar vestibular networks and may add severe truncal or focal neurological signs.

Migraine and medicine effects

Vestibular migraine can cause spontaneous or positional vertigo with or without headache, while sedatives, anticonvulsants and alcohol can impair multisensory balance.

Non-vestibular dizziness

Arrhythmia, orthostatic hypotension, hypoglycaemia, anxiety and multisensory gait impairment may be described as dizziness despite lacking a primary vestibular mechanism.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Asymmetric vestibular signalling
Unequal resting activity between paired labyrinths or their central pathways creates a false signal of head movement despite physical stillness.
2
Vestibulo-ocular mismatch
The brain drives compensatory eye movements in response to the false signal, producing nystagmus, oscillopsia and visual-motion intolerance.
3
Postural and autonomic response
Conflicting vestibular, visual and proprioceptive information destabilises stance and activates nausea, vomiting and sympathetic symptoms until compensation or the lesion resolves.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Posterior-circulation strokeRed flag

Abrupt continuous vertigo with severe truncal ataxia, focal cranial or limb signs, central nystagmus, skew, new hearing loss or headache or neck pain supports urgent brainstem-cerebellar vascular assessment.

Vestibular neuritisRed flag

Acute continuous vertigo over days with nausea, unidirectional horizontal-torsional nystagmus and impaired head impulse, but no new hearing loss or focal neurology, supports unilateral peripheral vestibular failure after stroke assessment.

Posterior-canal BPPV

Recurrent seconds-long vertigo triggered by lying back, rolling or looking up with a delayed transient upbeat torsional response on the provoking Dix–Hallpike supports posterior-canal canalithiasis.

Ménière-type syndrome

Spontaneous attacks lasting tens of minutes to hours with fluctuating unilateral sensorineural hearing loss, tinnitus or aural fullness suggests Ménière disease and needs audiological and ENT confirmation.

Vestibular migraine

Recurrent vestibular episodes with migraine history and migrainous light, sound, visual or headache features can support vestibular migraine after attack duration and alternative ear, vascular and neurological causes are assessed.

Central positional nystagmusRed flag

Immediate persistent downbeat, pure vertical or direction-incongruent nystagmus, minimal fatigability, prominent gait ataxia or other focal signs during positional testing points away from typical canal BPPV.

Presyncope rather than vertigoRed flag

Light-headedness, visual dimming and weakness after standing with orthostatic pressure fall, bleeding, arrhythmia or vasovagal prodrome suggests global perfusion disturbance rather than a primary vestibular lesion.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Full neurological, ocular-motor and gait examinationFirst step
Why
Identify central signs and establish whether the patient can sit, stand and walk safely.
Interpretation and limitations
Test gaze, nystagmus, skew, cranial nerves, limbs, sensation, coordination and truncal stability. Inability to walk is not dismissed as nausea and may be the dominant posterior-stroke sign.
02
HINTS-plus by a trained clinician
Why
Differentiate central from peripheral causes within the narrowly defined acute vestibular syndrome and screen new hearing asymmetry.
Interpretation and limitations
Do not apply to resolved, intermittent or purely positional symptoms or without spontaneous nystagmus. Any central component or unreliable examination triggers stroke assessment rather than averaging results.
03
Dix–Hallpike and supine roll testing
Why
Diagnose posterior or horizontal canal BPPV by reproducing the characteristic vertigo and nystagmus.
Interpretation and limitations
Note latency, direction, duration and fatigability. Modify or avoid manoeuvres with unstable cervical disease, severe vascular risk, recent surgery or inability to tolerate positioning.
04
Audiometry and otological examination
Why
Confirm sensorineural hearing asymmetry and distinguish Ménière, labyrinthine, sudden-hearing-loss and cerebellopontine-angle syndromes.
Interpretation and limitations
Bedside finger rub and tuning forks are screens. Sudden sensorineural loss is urgent; in acute vestibular syndrome it can be a vascular central warning as well as ear disease.
05
CT angiography and MRI brain
Why
Assess posterior-circulation occlusion, dissection, haemorrhage and small brainstem or cerebellar infarction when central disease is possible.
Interpretation and limitations
Non-contrast CT alone has limited posterior-fossa sensitivity. Early diffusion MRI can also be negative, so coherent persistent central signs warrant specialist review and sometimes repeat imaging.
06
ECG, orthostatic observations and targeted blood tests
Why
Identify arrhythmia, orthostatic hypotension, anaemia, glucose or electrolyte disturbance in non-vestibular dizziness and mixed falls.
Interpretation and limitations
Select from timing and triggers rather than ordering a generic dizziness panel. A patient can have BPPV plus orthostatic hypotension, so reproduced physiology should be documented separately.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Presyncope

Dim vision, sweating and near-collapse on standing with a measured pressure or rhythm disturbance favour cerebral hypoperfusion rather than an illusion of movement.

Cerebellar ataxia

Persistent limb dysmetria, dysarthria and broad-based gait without a dominant motion illusion suggest cerebellar disease, although cerebellar stroke often presents with vertigo.

Vestibular migraine

Recurrent episodes with migraine history, sensory sensitivity or aura support vestibular migraine, but a first severe or focal episode still requires vascular assessment.

Functional persistent dizziness

Chronic visually induced swaying and motion sensitivity with positive functional features may follow an acute vestibular event; structural and cardiovascular causes should be assessed proportionately.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Acute continuous vertigoProtect the posterior circulationFirst stepVertigo or dizziness is continuous for hours to days with spontaneous nystagmus, vomiting, motion intolerance or gait unsteadiness.

1Perform ABCDE and glucose, establish last known well, headache and neck pain, vascular risk and hearing change and examine eye movements, skew, cranial nerves, limbs, sensation, coordination and sitting or walking ability.
2If trained and the syndrome is appropriate, perform HINTS-plus; any central feature, severe truncal ataxia, new hearing loss or unreliable examination prompts immediate stroke-team and vascular-imaging assessment.
3After stroke is reasonably excluded, use only short symptomatic medication if needed, encourage safe mobilisation and arrange vestibular rehabilitation and review of persistent or changing signs.

02Brief positional attacksConfirm the canal and repositionEpisodes last seconds and are consistently initiated by rolling, lying back, getting up or looking vertically, with no ongoing focal neurology.

1Check neurological red flags and cervical or vascular safety, then perform Dix–Hallpike on each appropriate side while observing the direction, latency and duration of nystagmus.
2For a typical positive posterior-canal response, perform an Epley or locally recommended canalith-repositioning manoeuvre and explain short-term recurrence of symptoms and fall precautions.
3Use supine roll testing or specialist vestibular referral for suspected horizontal-canal disease, and image or refer atypical persistent, downbeat or treatment-resistant positional findings.

03Recurrent spontaneous vertigoUse hearing and migraine phenotypeDiscrete attacks recur without a consistent positional trigger and the patient is largely well between episodes.

1Document attack duration, unilateral hearing, tinnitus, fullness, migraine features, triggers, vascular symptoms, loss of consciousness and medicines and examine hearing and neurology between and during attacks when possible.
2Arrange audiology and ENT review for fluctuating hearing, migraine or neurology review for the appropriate phenotype and cardiac assessment when the history suggests presyncope or arrhythmia.
3EscalationProvide attack, driving and fall safety advice and escalate first, prolonged or changing episodes with focal signs rather than assuming a prior migraine or Ménière label explains them.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Moves free otoconia from the symptomatic semicircular canal toward the vestibule and often resolves brief positional vertigo without medication.

Canalith-repositioning manoeuvre for posterior-canal BPPV

A trained clinician performs one Epley sequence for the affected posterior canal and repeats or reviews according to symptom and nystagmus response, local competence and patient tolerance.

Confirm a typical canal pattern and assess cervical, vascular, retinal, mobility and vomiting risks; stop for neurological symptoms and do not use a generic manoeuvre for atypical central nystagmus.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Falls and injury

Severe postural instability, especially with visual loss, neuropathy or sedating treatment, increases fractures, head injury and fear-driven restriction of activity.

Missed posterior-circulation stroke

Misclassifying central eye signs or inability to stand as peripheral disease delays reperfusion and recognition of cerebellar swelling or basilar occlusion.

Dehydration and medicine harm

Persistent vomiting causes volume and electrolyte loss, while prolonged vestibular suppressants can cause sedation, falls and delayed central compensation.

Chronic imbalance and participation loss

Incomplete vestibular compensation can leave motion sensitivity, oscillopsia and reduced driving, work or social participation, benefiting from targeted rehabilitation.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat neurological, hearing and gait assessment if continuous vertigo evolves, because a peripheral-looking first examination may become a clear central syndrome.
Document nystagmus direction in primary and eccentric gaze, head-impulse side, skew and exact assistance needed to stand rather than writing only 'HINTS negative'.
After repositioning, review resolution and recurrence and repeat canal-specific testing before applying multiple unsupervised manoeuvres.
Limit vestibular suppressants to the shortest appropriate period and reassess sedation, falls and delayed mobilisation in older or frail patients.
Track audiometry and attack duration in suspected Ménière disease and urgently reassess sudden or progressive unilateral hearing change.
Give emergency advice for new diplopia, dysarthria, weakness, numbness, inability to sit, severe headache, neck pain or persistent vomiting.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Worse with movement is non-specific

Patients with neuritis, migraine and stroke often avoid head movement because it amplifies symptoms. BPPV requires a brief attack initiated by a particular positional transition.

FAST misses posterior signs

A cerebellar or brainstem stroke can preserve facial movement and arm power while causing disabling gait ataxia, nystagmus, dysphagia or hearing loss.

HINTS is a three-part decision

One apparently peripheral component cannot outweigh skew, direction-changing nystagmus or a normal impulse. Any central sign makes the overall bedside result central.

CT cannot reassure alone

Posterior-fossa bone artefact and small infarcts reduce non-contrast CT sensitivity. Imaging and follow-up are driven by the syndrome, vascular study and MRI where appropriate.

Hearing can be vascular

The internal auditory artery often arises from AICA. New unilateral hearing loss with acute vestibular syndrome may therefore accompany posterior-circulation ischaemia.

BPPV can recur

Successful repositioning treats the current canal episode but does not confer immunity. Teach patients how to seek reassessment and distinguish a future atypical continuous syndrome.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing BPPV because head movement worsens continuous vertigo.
02
Using HINTS in brief positional dizziness, resolved symptoms or without spontaneous nystagmus.
03
Calling HINTS peripheral when any one component is central or technically unreliable.
04
Excluding posterior stroke from a normal non-contrast CT or negative FAST screen.
05
Ignoring new hearing loss in acute vestibular syndrome.
06
Performing an Epley manoeuvre without assessing cervical and vascular safety or nystagmus pattern.
07
Continuing vestibular suppressants for weeks and delaying compensation and rehabilitation.