Peripheral versus central vertigo

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

Vertigo is an illusion of movement, usually spinning or tilting, rather than a diagnosis. Peripheral vestibular structures comprise the labyrinth and vestibular nerve; central pathways include the brainstem and cerebellum. The immediate task is to identify a time-sensitive neurological disorder, then to define a vestibular syndrome sufficiently precisely to choose useful tests. Asking whether the room spins is less informative than establishing when symptoms began, how long each episode lasts and whether the patient becomes symptom-free between attacks.

Separate a trigger from an aggravating factor. Turning over in bed may initiate a ten-second spell in BPPV, whereas moving the head intensifies continuous vertigo from either neuritis or stroke. A person who remains dizzy while perfectly still has a different syndrome from someone who feels normal until lying back. Record onset or last known well, vascular risks, headache, neck injury, hearing change, vomiting, medicines and previous episodes. The absence of common stroke risk factors lowers probability but does not exclude dissection or another central cause.

Key points

Establish whether symptoms are continuous, spontaneously episodic or triggered brief attacks.
Head movement worsens many vestibular disorders; worsening alone does not diagnose BPPV.
Use HINTS only in the appropriate ongoing acute vestibular syndrome and with trained expertise.
A normal head impulse, direction-changing nystagmus or skew is a central warning.
Test hearing because new unilateral loss can accompany a vascular vestibular syndrome.
Choose Hallpike for brief positional attacks, after checking movement safety.
Do not use a reassuring routine head CT to exclude posterior circulation infarction.

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

Peripheral disorders

Displaced otoconia, vestibular nerve inflammation and episodic inner-ear dysfunction can each disturb balance, but produce different temporal patterns that guide further assessment.

Central disorders

Posterior circulation ischaemia, haemorrhage, demyelination and migraine may disturb vestibular processing. Their accompanying features and urgency differ, so central vertigo is not synonymous with stroke.

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

1
Asymmetric vestibular signalling
A sudden mismatch between the two vestibular systems is interpreted as movement despite a stationary head, producing vertigo, eye drift and corrective nystagmus.
2
Vestibulo-ocular reflex
The vestibulo-ocular reflex stabilises the visual target during head movement. Peripheral impairment may produce a corrective saccade, although some central lesions also impair this response.
3
Central integration
Brainstem and cerebellar networks combine vestibular, visual and proprioceptive information. Injury can disturb ocular alignment and posture even when limb strength remains normal.

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

Continuous acute vestibular syndrome

Persistent vertigo, nausea or vomiting, spontaneous nystagmus and gait disturbance suggest an acute vestibular syndrome. Symptoms may fluctuate in intensity without genuinely stopping. Establish whether examination occurs during the active syndrome before interpreting an eye-movement battery.

Features favouring peripheral dysfunction

Unidirectional predominantly horizontal nystagmus, a corrective saccade on head impulse towards the affected side and no skew can support peripheral vestibular loss in a suitable patient. These findings require trained interpretation; an isolated abnormal head impulse is insufficient reassurance.

Central eye and gait findings

Gaze-evoked direction-changing nystagmus, vertical ocular misalignment, an otherwise normal head impulse during acute vestibular syndrome, or inability to sit unsupported should increase concern for central disease. Examine speech, limb power, sensation and coordination rather than relying only on the eyes.

Associated hearing symptoms

Sudden unilateral hearing reduction may reflect cochlear disease, but an acute audiovestibular syndrome can also be vascular. Ask directly and compare ears. Hearing loss does not safely convert an uncertain central presentation into a diagnosis of labyrinthitis.

Different patterns of dizziness

Brief triggered spells suggest BPPV; spontaneous attacks lasting minutes to hours prompt consideration of vestibular migraine or Ménière disease. Light-headedness on standing suggests haemodynamic causes, and loss of consciousness requires a syncope or seizure assessment rather than a purely vestibular label.

Red flags requiring action

New diplopia, dysarthria, limb incoordination, severe truncal instability or unilateral deafness accompanying acute vertigo requires immediate assessment for a central or vascular cause.
A new severe occipital headache or neck pain, particularly after trauma, raises concern for haemorrhage or arterial dissection and needs emergency assessment.

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
Immediate observations and targeted neurological assessmentFirst step
Why
Identify physiological instability and neurological features that change urgency.
Interpretation and limitations
Check vital signs, glucose when appropriate, eye movements, cranial nerves, hearing and safe sitting or walking. Correct hypoglycaemia promptly, but persistent focal findings still require the relevant emergency pathway. Do not repeatedly make a severely unstable patient walk unaided.
02
Expert HINTS examination in ongoing acute vestibular syndrome
Why
Distinguish central from peripheral patterns in the validated clinical setting.
Interpretation and limitations
A trained examiner assesses head impulse, nystagmus and skew in ongoing acute vestibular syndrome with spontaneous nystagmus. Any central component warrants immediate neuroimaging. Do not apply the result to brief resolved spells, a symptom-free patient or an examination made unreliable by sedation.
03
Hallpike manoeuvre for brief positional episodes
Why
Demonstrate a positional nystagmus pattern consistent with canal involvement.
Interpretation and limitations
A trained clinician uses Hallpike when the history describes transient rotational vertigo on head movement. Assess cervical safety first. A characteristic posterior-canal response supports BPPV, while persistent or atypical eye movements require further assessment.
04
Emergency brain and vascular imaging
Why
Investigate suspected posterior circulation stroke or another central lesion.
Interpretation and limitations
The stroke team selects CT, angiography and MRI according to presentation and treatment eligibility. Routine non-contrast CT has limited sensitivity for posterior fossa ischaemia; even early MRI may miss an infarct. Persistent clinical concern requires specialist reassessment despite initially negative imaging.
05
Audiometry and selective cardiovascular testing
Why
Characterise hearing loss or investigate a competing non-vestibular mechanism.
Interpretation and limitations
Formal audiometry quantifies suspected hearing asymmetry without delaying urgent sudden-loss referral. Orthostatic blood pressure or ECG is useful when history suggests postural hypotension or arrhythmia. A broad untargeted blood panel does not establish peripheral vertigo.

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

Postural hypotension

Symptoms follow standing and reflect reduced cerebral perfusion rather than canal stimulation. Medication review and appropriately measured postural blood pressure help establish the mechanism.

Vestibular migraine

Episodes accompanied by migraine history or sensory sensitivity can mimic inner-ear disease. Duration and associated headache features are more informative than dizziness severity alone.

Cardiac presyncope

Palpitations, exertional symptoms or impending loss of consciousness suggest circulatory compromise. ECG and cardiovascular assessment may be more useful than positional vestibular manoeuvres.

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

01EmergencyPossible posterior circulation eventFirst stepNew continuous vertigo accompanies central signs or remains diagnostically unsafe.

1Record onset, activate the stroke pathway and arrange emergency transfer; do not wait for routine outpatient ENT review.
2Provide monitored supportive care, assess hydration and swallowing safety, and communicate any anticoagulant use or recent neck trauma.
3If trained HINTS expertise is unavailable and BPPV or postural hypotension does not explain acute vestibular syndrome, refer immediately under NICE NG127.
4EscalationEscalate continuing concern after apparently reassuring imaging; neither temporary symptomatic improvement nor an antiemetic response proves a peripheral cause.

02PositionalBrief attacks provoked by positionShort stereotyped spells occur with specific head positions and settle between attacks.

1Confirm that position triggers a discrete episode, and look for neurological or auditory features suggesting an additional diagnosis.
2Arrange trained Hallpike testing and, when BPPV is established and movement is safe, a canalith repositioning manoeuvre.
3Explain recurrence and arrange reassessment when positional symptoms persist, change character or resist correctly selected treatment.

03PeripheralSupported acute vestibular hypofunctionAppropriate assessment supports a peripheral disorder without remaining central warning signs.

1Treat disabling nausea briefly, support fluid intake and confirm that the person can mobilise safely with available assistance.
2Give a specific return plan for hearing change, new neurological symptoms, worsening headache or failure to improve.
3Introduce tolerable activity as the acute phase settles and consider vestibular rehabilitation for persistent functional imbalance.

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

Missed posterior circulation stroke

Delayed recognition can postpone reperfusion assessment and monitoring for neurological deterioration. Small initial deficits do not predict a harmless subsequent course.

Falls and injury

Impaired postural control, vomiting-related dehydration and sedating medicines can combine to make transfers unsafe, particularly in older adults living without immediate help.

Persistent activity restriction

Fear of provoking dizziness can lead to prolonged immobility and deconditioning. Once dangerous causes are excluded, graded recovery should address both balance and confidence.

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

Repeat neurological and hearing assessment when symptoms evolve; an earlier peripheral impression should not prevent recognition of a new central sign.
Before discharge, confirm tolerable oral intake, a safe route to the toilet, appropriate assistance and understanding of the return instructions.
Review medicines that can worsen balance through sedation, hypotension or vestibular toxicity; consider their timing without assuming they explain every new symptom.
Assess persisting disability after the acute illness, including falls, visual blurring on head movement, anxiety and reduced ability to work or travel.

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

The HINTS selection problem

The test answers a narrow question in an active syndrome. Its published performance cannot be transferred automatically to untrained use or to everyone with dizziness. Recording the three individual findings is more useful than documenting an unexplained positive or negative result.

Forehead and face examination

Brainstem disease can affect a facial nerve nucleus or fascicle and produce complete ipsilateral facial weakness. A peripheral-looking facial pattern therefore needs interpretation alongside eye movements, hearing, limb findings and gait.

Migraine and vascular overlap

Recurrent attacks with migraine features can support vestibular migraine, but a first abrupt atypical attack merits its own assessment. A familiar diagnostic label should not absorb new persistent symptoms or neurological deficits.

Communicating uncertainty safely

Describe the syndrome and remaining concern in a referral: for example, continuous vertigo with inability to stand and no trained HINTS assessment. This conveys the reason for urgent review more clearly than a provisional label of labyrinthitis.

11Common pitfallsFrequent interpretation and management errors.

01
Calling all motion-sensitive vertigo BPPV confuses aggravation with a true positional trigger and may delay stroke assessment.
02
Using HINTS after symptoms have resolved or without spontaneous nystagmus can generate misleading reassurance from an unsuitable examination.
03
Treating sudden hearing loss as proof of benign labyrinthitis overlooks both sudden sensorineural loss and vascular audiovestibular disease.
04
Discharging someone because vomiting stopped ignores the diagnostic uncertainty and practical danger of persistent severe gait instability.