Vertigo, dizziness and syncope: neurological approach

• Dizziness is a broad symptom, vertigo is the false sense of movement, and syncope is a brief loss of consciousness from cerebral hypoperfusion. Sort the patient into one of these first, because the pathway and the danger differ.
• Most vertigo is peripheral and benign: benign paroxysmal positional vertigo (BPPV), vestibular neuritis and Ménière disease. Central causes (stroke, haemorrhage, demyelination) are less common but are the ones you must not miss.
• The danger in acute vertigo is not the spinning but a posterior circulation stroke. A normal MRI in the first day can still be falsely negative, so the bedside examination matters more than the scanner.
• Syncope is a separate emergency until cardiac causes are excluded. Orthostatic hypotension, vasovagal syncope and arrhythmia share the same first test: the blood pressure and pulse.
• The key tools in this topic are the Dix-Hallpike manoeuvre, the Epley manoeuvre, the HINTS examination (head impulse, nystagmus, test of skew) and an orthostatic blood pressure set.

By the end of this page you should be able to:

1. Define vertigo, dizziness and syncope in the patient's own words, and sort a complaint into one of the three.
2. Group the causes of vertigo by system and mechanism, and recognise the red flags for central and cardiac disease.
3. Take a focused history and perform the neurological and vascular examination that separates peripheral from central vertigo.
4. Plan investigations in a sensible order, knowing why brain imaging is often misleading in the first day.
5. Perform and interpret the Dix-Hallpike and Epley manoeuvres and explain the evidence behind them.
6. Recognise vestibular neuritis and Ménière disease, and understand why the HINTS examination works.
7. Cross-check orthostatic and cardiac syncope, including the correct way to measure orthostatic blood pressure.
8. Recall the common traps and the evidence-based limits of each treatment.

This page is a neurological approach to three overlapping problems: vertigo, dizziness and syncope. The three words are used loosely by patients and clinicians alike, so the first job is to translate the complaint into one of three buckets. Vertigo is the illusion of movement of the self or the world. Dizziness is a broader word that patients use for light-headedness, presyncope, unsteadiness or vague imbalance. Syncope is a transient, self-limited loss of consciousness caused by inadequate blood flow to the brain, with rapid recovery.

The neurological approach starts with mechanism rather than diagnosis. A patient who feels the room spin and vomits has a vestibular problem. A patient who blacked out while sitting quietly may have an arrhythmia. A patient who only feels faint on standing has a circulatory problem of posture. Grouping causes by mechanism (inner ear, brainstem, blood pressure, heart) prevents the common error of ordering a long list of tests in the hope that one of them is abnormal.

The page follows the order in which a student needs the information: the mechanisms and their causes, the dangerous presentations, the history and examination, the investigations, the algorithm, the treatment, the special situations, the pitfalls, and finally the common individual conditions. It refers to the separate cardiology page for the full assessment of syncope; here the aim is the cross-check that a neurologist or general clinician should do before handing over.

The table groups the common causes by where the problem sits. It is not exhaustive; rare causes (tumour, demyelination, drugs, infection) belong under "central" or "systemic" once the common ones are excluded.

Treat these as emergencies. They are the reason a presentation of "just dizziness" cannot be discharged without thought.

• Sudden onset with a focal neurological deficit such as vertical or rotatory nystagmus, new unsteadiness, or new deafness. If BPPV or postural hypotension do not explain the picture, exclude a posterior circulation stroke immediately.^[2]
• Acute vestibular syndrome (sudden continuous vertigo with nausea or vomiting and gait unsteadiness). If no one skilled in the HINTS test is available, refer immediately along stroke pathways.^[2]
• A normal head impulse test in the presence of nystagmus (one element of a "central" HINTS). Direction-changing nystagmus or skew deviation point the same way.^[2][4]
• Severe truncal ataxia (inability to sit or stand unaided). It can be the only sign of a central lesion, including in patients without nystagmus.^[4]
• Acute unilateral hearing loss with vertigo is a red flag for posterior circulation (especially AICA) stroke, not a simple inner ear problem. Hearing must be tested formally in acute vertigo.^[4]
• Head or neck pain with sudden vertigo suggests arterial dissection and needs urgent vascular imaging.^[4]
• Older patients with vascular risk factors, new atrial fibrillation, exertional symptoms or syncope at rest: think cardiac, not vestibular.
• Persistent vomiting and inability to drink leading to dehydration in an acute vestibular syndrome.

A good history is more useful than any test. Ask these questions and you will usually know whether the patient needs a stroke pathway or an Epley manoeuvre.

• "Describe it without using the word dizziness." Ask whether the room spins, whether they feel faint, or whether they are unsteady. This separates vertigo from presyncope and ataxia, three different systems.^[4]
• Onset and course. Seconds to minutes for BPPV; sudden continuous for hours to days for vestibular neuritis or stroke; episodic minutes to hours for Ménière disease or vestibular migraine; sudden seconds for TIA.
• Triggers. Rolling over in bed, looking up, bending down point to BPPV. Standing up points to orthostatic hypotension. Exercise points to cardiac disease. Stress, pain or prolonged standing point to vasovagal syncope. Stress or sleep loss can aggravate Ménière disease.
• Auditory symptoms. Hearing loss, tinnitus or aural fullness in one ear are decisive in Ménière disease, but new unilateral hearing loss in acute vertigo is a red flag for stroke until shown otherwise.^[4]
• Associated neurological symptoms. Diplopia, dysarthria, dysphagia, numbness, weakness, clumsiness or new gait disturbance move the diagnosis to the brainstem or cerebellum.^[4]
• Headache and migraine features. Photophobia, phonophobia, visual aura and a history of recurrent headache support vestibular migraine. Episodes lasting 5 minutes to 72 hours fit this pattern.^[2]
• Vascular risk and family history. Hypertension, diabetes, smoking, atrial fibrillation, prior stroke, cardiac disease, and sudden death in a relative at a young age all increase the probability of stroke or cardiogenic syncope.
• Medication review. Antihypertensives, diuretics, vasodilators and dopaminergic drugs can reproduce or worsen orthostatic and drug-related syncope and dizziness.
• Syncope details. For every faint, document the posture, activity, prodrome, colour, breathing, recovery time and eyewitness description; and ask for an ECG in any patient with syncope or cardiac risk.
• Alcohol, drugs and sleep. These modify the presentation and often explain "dizziness" in otherwise well people.

Examine to decide peripheral versus central, then for the cause. A short, well-chosen examination is worth more than a long unfocused one.

• General and vital signs. Pulse, blood pressure, temperature, oxygen saturation. Look for anaemia, fever, dehydration. Take an accurate orthostatic set in every patient with dizziness on standing (see below).
• Gait and stance. Watch the patient stand and walk. Severe difficulty sitting or standing unaided is a key marker of a central lesion.^[4]
• A complete neurological examination. Cranial nerves (especially eye movements and hearing), motor and sensory testing, coordination, and plantar responses. Look specifically for ocular motor abnormalities: smooth pursuit, saccades, gaze holding, cover tests and skew.
• Eye movement examination. In an acute vestibular syndrome, observe the nystagmus: direction, plane, conjugacy and whether it changes with gaze. Perform head impulse testing (the "H" of HINTS), nystagmus assessment (the "N"), and test of skew (the "T").^[4]
• Dix-Hallpike manoeuvre. In transient rotational vertigo on head movement, offer a Hallpike test if a trained clinician is available. A trained operator is needed; if none is available, refer according to local pathways.^[2]
• Ear examination. Inspect the canals and tympanic membranes; note discharge, perforation or cholesteatoma. Formal hearing testing (audiometry) is required whenever hearing loss is suspected.

Investigate in the order the patient's safety demands, not in alphabetical order.

1. Bedside evidence first. In acute vertigo the history and examination come before any technology. The HINTS examination, gait assessment and Dix-Hallpike separate peripheral from central better than a first-day scan in many patients.^[2][4]
2. Orthostatic blood pressure. In dizziness or syncope on standing: measure after at least 5 minutes seated, then within 3 minutes of standing, taking the lower of two standing values. A systolic fall of 20 mmHg or more, or a diastolic fall of 10 mmHg or more, supports orthostatic hypotension.^[5]
3. ECG. In every patient with syncope, and in any dizzy patient with cardiac risk. A normal ECG is necessary but does not exclude cardiac syncope.
4. Brain imaging when the presentation demands it. Non-contrast CT has very low sensitivity for stroke in the first day, roughly 16 percent in the first 24 hours after onset, and is of little use for acute ischaemic posterior fossa stroke. Diffusion-weighted MRI misses up to 20 percent of acute posterior circulation strokes if performed less than 24 hours from onset.^[4] Do not let a normal early scan overrule a concerning bedside examination; repeat or escalate when doubt remains.
5. Vascular imaging. CT or MR angiography of the extracranial and intracranial vessels in suspected posterior circulation stroke or dissection, even when parenchymal imaging is normal.^[4]
6. Vestibular function tests. Video or bedside head impulse testing and caloric irrigation support vestibular neuritis or quantify peripheral loss. A working approximation is a vHIT gain (vestibulo-ocular reflex gain measured by video head impulse testing) under 0.7, or a caloric side difference above 25 percent, as pathological. There is no universal cut-off; laboratories should use their own standards.^[3] NICE and vascular considerations take precedence over vestibular testing in the acute setting.
7. Audiometry. Whenever hearing is involved, to document asymmetry and to pick up AICA strokes and Ménière disease.
8. Blood tests. Not routine. Use glucose, a full blood count, electrolytes and renal function to answer a specific clinical question (hypoglycaemia, anaemia, drug toxicity, autonomic failure with diabetes or renal disease).
9. Vestibular testing is not needed for BPPV. If a patient meets diagnostic criteria for BPPV and has no inconsistent features, imaging and vestibular testing are not recommended.^[1]
10. Cardiology tests when the picture is cardiac. Echocardiography, prolonged rhythm monitoring and specialist syncope assessment belong to the cardiology pathway for patients with red-flag features.

Management follows the diagnosis, but the first steps are shared.

• Stabilise first. In acute vertigo keep the patient safe, give fluids, treat nausea with an antiemetic if needed, and offer fall precautions. Avoid sedating patients for long periods.
• Stroke pathway. When central features exist, treat as suspected acute stroke or TIA: swallow screen, vascular risk assessment, vascular imaging, and secondary prevention (antiplatelet therapy, lipid lowering and blood pressure control in suspected posterior circulation cerebrovascular disease) while awaiting definitive diagnosis.^[4]
• BPPV. Posterior canal BPPV should be treated, or the patient referred to someone who can treat it, with a canalith repositioning procedure. A strong recommendation argues against post-procedural postural restrictions after such a procedure.^[1] Observation with follow-up, and vestibular rehabilitation, are options.^[1] The supine roll test assesses lateral canal BPPV when the history fits but the Dix-Hallpike shows horizontal or no nystagmus.^[1] Vestibular suppressant drugs such as antihistamines or benzodiazepines should not be used routinely.^[1] Unstable cervical spine disease prevents a canalith repositioning procedure, and the patient should be referred instead.^[2]
• Vestibular neuritis. The main treatment is vestibular rehabilitation physiotherapy; many patients recover over days without it. Patients with high visual dependence or high anxiety may need earlier targeted rehabilitation.^[4] There is limited evidence that corticosteroids give meaningful benefit, and they are not routinely used in the UK.^[4] Antiemetics are for short-term symptom control only.
• Ménière disease. Cochrane reviews find that the evidence for systemic drugs such as betahistine, diuretics, antivirals or corticosteroids versus placebo or no treatment is very uncertain, with few randomised trials and low or very low certainty evidence.^[6] Any drug-based plan should be shared with the patient as low certainty, and non-pharmacological advice should come from the specialist services that manage hearing and balance. Diuretic-based or other drug-based regimens are clinician choices supported by preference, not by strong trial evidence.
• Orthostatic hypotension. Address volume status, review and reduce offending medications, advise on rising slowly, adequate salt and fluid intake where appropriate, and physical counter-manoeuvres (leg crossing, squatting). For neurogenic cases consider compression garments and specialist referral. Treat the underlying cause (Parkinson disease, diabetes, renal disease) rather than the numbers alone.
• Cardiac syncope. Once suspected, hand over to cardiology for risk stratification, monitoring, imaging and treatment of the underlying rhythm or structural disease. Do not delay while waiting for a normal neurological opinion.
• Vasovagal syncope. Education, trigger avoidance, physical counter-pressure manoeuvres, adequate hydration, and, in recurrent or severe cases, specialist management. When the pattern is clear, do not over-investigate.^[2]
• When to refer. Refer urgently for any red flag, for all suspected central disease, for Ménière disease or vestibular migraine that affects hearing or daily life, and for refractory BPPV.

• Older adults. Orthostatic hypotension, multifactorial dizziness and falls dominate. Autonomic function declines, drugs accumulate and a posture change is enough to cause syncope. Take a lying and standing set and review medication before ordering brain scans.^[5]
• Diabetes. Autonomic neuropathy can produce neurogenic orthostatic hypotension; new cranial or peripheral signs with acute vertigo must exclude stroke, not just glucose.
• Parkinson disease and neurodegenerative disease. Neurogenic orthostatic hypotension is common and can mimic vertigo. Treatment of the blood pressure can worsen standing tolerance and vice versa.
• Pregnancy. Avoid unnecessary ionising imaging; use MRI when needed, and be cautious with medications. Refer if red flags arise.
• Children. The causes of episodic vertigo differ and deserve a paediatric approach; red flags are the same. This page covers adults, the target of the NICE guideline quoted here.
• Low-resource settings. A trained clinician with a blood pressure cuff, a head impulse test at the bedside, and a safe space to perform Dix-Hallpike is better than an early brain scan. Posterior circulation stroke is missed most often where imaging is scarce, so clinical pathways and referral agreements matter more than machines.

• Calling a HINTS result "positive" or "negative". HINTS is always abnormal in the sense that nystagmus is present. Describe the three findings (head impulse, nystagmus direction and skew) instead of using "positive".^[4]
• A normal early MRI does not exclude stroke. Up to 20 percent of acute posterior circulation strokes are missed within 24 hours; clinical judgement overrides imaging early on.^[4]
• Treating BPPV with vestibular suppressants. Antihistamines and benzodiazepines do not fix the canal problem and delay compensation. They should not be used routinely.^[1]
• Assuming all positional dizziness is BPPV. Central positional nystagmus and brainstem or cerebellar lesions can look positional, and a Dix-Hallpike can be used to detect central nystagmus as well.^[4]
• The bedside head impulse test has low sensitivity and specificity. Video or quantitative testing is more reliable, and a normal vHIT with a clinical suspicion does not settle the diagnosis.^[3]
• Calling complex partial seizures "vertigo". Recurrent fixed-pattern dizziness with altered consciousness needs an epileptic assessment, not more vestibular testing.^[2]
• Labelling syncope as a seizure. Tongue biting and incontinence can occur in vasovagal syncope; a cardiac work-up is essential in the middle-aged and older patient.

BPPV is the commonest cause of vertigo in primary care and in specialist clinics. It is a disorder of the inner ear in which otoconia (crystals) have moved from the otolith organs into a semicircular canal. Head movement then stimulates that canal and produces a brief, intense sensation of spinning. The guideline that defines this approach is the 2017 update of the American Academy of Otolaryngology-Head and Neck Surgery Foundation clinical practice guideline for benign paroxysmal positional vertigo (an update of the 2008 guideline).^[1]

Diagnosis. Posterior semicircular canal BPPV is diagnosed when vertigo associated with torsional, upbeating nystagmus is provoked by the Dix-Hallpike manoeuvre. The manoeuvre is performed by bringing the patient from an upright to a supine position with the head turned 45 degrees to one side and the neck extended 20 degrees, with the affected ear down.^[1] A trained operator is needed. If no one with that training is available, referral proceeds down local pathways.^[2]

Assessment of the lateral canal. If the patient has a history compatible with BPPV and the Dix-Hallpike shows horizontal or no nystagmus, a supine roll test should be performed (or the patient referred to someone who can perform it) to assess for lateral semicircular canal BPPV.^[1]

Treatment. Posterior canal BPPV should be treated, or the patient referred to a clinician who can treat it, with a canalith repositioning procedure. The Epley manoeuvre is the commonest example. A strong recommendation argues against post-procedural postural restrictions after such a procedure.^[1] Observation with follow-up, and vestibular rehabilitation, are options.^[1]

What not to do. Radiographic imaging is not recommended for a patient who meets diagnostic criteria for BPPV in the absence of additional signs or symptoms inconsistent with BPPV that warrant imaging. Vestibular testing is likewise not recommended for such a patient. Vestibular suppressant medications such as antihistamines and benzodiazepines should not be used routinely.^[1] BPPV is common after head injury or labyrinthitis, which is a useful memory.^[2]

Vestibular neuritis (acute unilateral vestibulopathy) is one of the three most common causes of acute vertigo and is a frequent reason for an acute vestibular syndrome that is not a stroke. The diagnostic criteria below are those of the Committee for the Classification of Vestibular Disorders of the Bárány Society, published in 2022, which treats "acute unilateral vestibulopathy" as the preferred neutral term and "vestibular neuritis" as an acceptable synonym.^{[3] [4]}

Definition. Acute unilateral vestibulopathy is an acute vestibular syndrome caused by acute unilateral loss of peripheral vestibular function without evidence for acute central or acute audiological symptoms or signs.^[3]

Diagnostic criteria (definite, current). All of the following must be met.

• Acute or subacute onset of sustained spinning or non-spinning vertigo of moderate to severe intensity, with symptoms lasting at least 24 hours. ^[3]
• Spontaneous peripheral vestibular nystagmus with a trajectory appropriate to the semicircular canal afferents involved, generally horizontal-torsional, direction-fixed and enhanced by removal of visual fixation.
• Unambiguous evidence of reduced vestibulo-ocular reflex function on the side opposite the direction of the fast phase.
• No acute central neurological, otological or audiological symptoms.
• No acute central neurological signs, in particular no pronounced skew deviation and no gaze-evoked nystagmus, and no acute audiological signs.
• Not better accounted for by another disorder.^[3]

If the syndrome fully recovers before 24 hours, the diagnosis is unlikely and other causes should be considered.^[3]

Onset and symptoms. Unambiguous evidence of reduced function can come from quantitative video head impulse testing or caloric irrigation; a working approximation is a vHIT gain under 0.7, or a side difference above 0.3, or a caloric side difference above 25 percent. The committee strongly recommends vHIT because it discriminates peripheral from central lesions in the emergency department, and notes the low sensitivity and specificity of the bedside head impulse test.^[3] Up to a quarter of patients may have a vertigo or dizziness episode lasting several hours in the two days before the sustained vertigo begins.^[3]

Clinical features of vestibular neuritis. It presents with acute spinning vertigo, oscillopsia, imbalance, nausea or vomiting, and no auditory or broader neurological symptoms. The key ocular findings are unidirectional horizontal nystagmus (often with a minor torsional component) beating away from the affected ear, a positive head impulse test towards the lesioned side, and gait unsteadiness that is moderate rather than the severe truncal instability of some cerebellar strokes.^[4] The presence of both unidirectional nystagmus and a corresponding abnormal head impulse test constitutes the minimum for the diagnosis. Any bidirectional, vertical or purely torsional nystagmus, or abnormalities of smooth pursuit, saccades or ocular alignment, should prompt a central work-up.^[4]

HINTS is only useful in trained hands. Bedside tests applied inconsistently report conflicting accuracy, so describe the individual findings rather than calling a result "positive" or "negative".^[4]

Treatment. Vestibular rehabilitation physiotherapy is the main treatment, and many patients recover over days without it. Patients with high visual dependence or high anxiety may need earlier rehabilitation. Evidence that corticosteroids give a meaningful benefit is limited, and they are not routinely used in the UK.^[4]

Ménière disease is an idiopathic disorder of the inner ear defined by recurrent episodes of vertigo associated with hearing loss and tinnitus.^[6] The Bárány Society, with the Japan Society for Equilibrium Research, EAONO, the AAO-HNS and the Korean Balance Society, published the consensus diagnostic criteria in 2015.

Clinical picture. Recurrent spontaneous attacks of vertigo with fluctuating hearing loss, tinnitus and aural fullness, confined to one ear in most patients, with recovery between episodes. The two conditions it most often has to be distinguished from are vestibular migraine and BPPV. Vestibular migraine is suggested by episodes of dizziness lasting 5 minutes to 72 hours with a history of recurrent headache.^[2]

Evidence and treatment. A Cochrane review of systemic pharmacological interventions for Ménière disease included 10 randomised trials with 848 participants and evaluated betahistine, diuretics, antivirals and corticosteroids against placebo or no treatment. The evidence was of low or very low certainty throughout, with few trials meeting selection criteria and no meta-analysis possible for the main outcomes. The reviewers' conclusion is that the evidence for systemic pharmacological interventions is very uncertain.^[6] Clinically that means: treat the patient, explain the uncertainty honestly, and prefer an otology or audiovestibular service that can manage hearing and offer endolymphatic or intratympanic options under a clear framework. No licence for any single drug as first-line can be claimed from this evidence base.

Inner-ear imaging and hearing. Audiometry documents the fluctuating, usually low-frequency, hearing loss. Formal hearing assessment and referral are appropriate when attacks are frequent or affect quality of life, in line with hearing pathways.

The central causes include posterior circulation stroke and TIA (PICA, AICA and SCA territory infarction), cerebellar and brainstem haemorrhage, demyelination, tumour, infection and drug toxicity. In posterior circulation stroke with dizziness, misdiagnosis is common: up to 35 percent of such strokes presenting with dizziness are initially missed, and acute vertigo accounts for roughly 4 percent of emergency department visits in the United States and Europe.^[4]

Pathophysiology and territory. PICA territory strokes produce vertigo and truncal ataxia and may lack the classic cerebellar signs, because PICA supplies the posterior inferior cerebellum (including the nodulus, uvula and flocculus) and the ipsilateral pontomedullary vestibular nucleus. AICA strokes more often include acute unilateral hearing loss. SCA strokes are more typically "cerebellar" with limb ataxia and dysarthria. Head or neck pain with sudden vertigo should prompt evaluation for vertebral dissection.^[4]

HINTS. The HINTS examination (Head Impulse, Nystagmus, Test of Skew) is a bedside test used to differentiate peripheral from central causes of acute vertigo.^[4] "HINTS plus" adds an assessment of hearing and increases sensitivity for stroke involving the labyrinthine artery supply, because sudden unilateral hearing loss with acute vertigo is a red flag.^[4] HINTS is only applicable when nystagmus is present; in its absence, use the rest of the neurological examination. A negative HINTS test (that is, a benign pattern) makes stroke very unlikely, while indications of stroke are a normal head impulse, direction-changing nystagmus or skew deviation.^[2][4]

Imaging limits. Computed tomography has very low sensitivity for stroke in the first 24 hours, roughly 16 percent, especially in the posterior fossa. Diffusion-weighted MRI misses up to 20 percent of acute posterior circulation strokes if performed less than 24 hours from onset.^[4] Clinical assessment therefore outranks a normal early scan.

Evidence on gait. Severe difficulty standing is a key feature of central vestibular disorder, present in 55 percent of patients with AVS of central cause, and is often under-recognised. Up to 15 percent of patients with acute truncal ataxia may lack nystagmus yet have central causes such as cerebellar or thalamic stroke.^[4]

Auditory clues. In a cohort of 71 patients presenting to the emergency department with vertigo or dizziness, only seven reported any auditory symptoms; subsequent audiometry found asymmetrical sensorineural hearing loss in 11, six of whom were later diagnosed with acute vascular events initially overlooked.^[4]

This section is the neurological part of the syncope assessment. The full pathway, risk scores and management belong to the cardiology topic; here the aim is the checks a neurologist or general clinician must not skip.

Define orthostatic hypotension. Orthostatic hypotension is defined as a fall in systolic blood pressure of 20 mmHg or more, or a diastolic fall of 10 mmHg or more, within 3 minutes of standing. The definition used here is reproduced in modern reviews.^[5]

How to measure it properly. Seat the patient for at least 5 minutes and measure twice, taking the average. Then stand them, measure twice within 3 minutes, and take the lower value. Use an adequate cuff, a thermoneutral room and avoid post-prandial testing. A drop in systolic pressure of 20 mmHg or more within 3 minutes of standing from sitting is taken as orthostatic hypotension.^[5]

Sort orthostatic hypotension into neurogenic and non-neurogenic. Non-neurogenic causes (volume depletion, drugs, prolonged bed rest, cardiac deconditioning) are more common than neurogenic ones. Neurogenic hypotension arises from structural lesions of autonomic pathways found in Parkinson disease, diabetes mellitus and chronic kidney disease, among others. The neurogenic form may be accompanied by a failure of the pulse to rise on standing, which is a useful clue.^[5]

Cardiac red flags. Any syncope that is exertional, occurs while lying flat, or is accompanied by palpitations or chest discomfort, any patient with known cardiac disease, an abnormal ECG, or a family history of sudden death at a young age needs cardiology. Syncope in the elderly with vascular risk factors should be assumed cardiac until excluded. The cardiology page covers risk stratification.

Vasovagal syncope. A reflex arc with vagal cardiac inhibition and vasodilatation, often triggered by emotion, pain, prolonged standing or heat, with a prodrome of warmth, nausea, sweating and tunnel vision and rapid recovery. Brief jerking and incontinence can occur and do not prove seizure. Clear-cut vasovagal syncope in a young person does not need referral. Fixed-pattern dizziness with alteration of consciousness, or any atypical feature, should be assessed for epilepsy.^[2]

Why this cross-check matters neurologically. Pure autonomic failure, multiple system atrophy, Parkinson disease and diabetic autonomic neuropathy all present with syncope before other features. Orthostatic blood pressure measurement is therefore part of the neurological examination in older dizzy patients. A lying and standing set costs nothing and finds what brain imaging does not.

• AAO-HNS Foundation clinical practice guideline: Benign Paroxysmal Positional Vertigo (Update), 2017 (Bhattacharyya N, et al.; update of the 2008 guideline): the source of the Dix-Hallpike technique, posterior canal diagnosis, Epley/canalith repositioning, supine roll test, no post-procedural restrictions, the imaging and vestibular testing recommendations, and the advice against routine vestibular suppressants.^[1]
• NICE guideline NG127, Suspected neurological conditions: recognition and referral (published 2019, last updated 2 October 2023): sudden onset dizziness and focal deficit, acute vestibular syndrome and HINTS, referral for stroke, Hallpike and Epley with cervical spine caution, vestibular migraine, epilepsy assessment and the vasovagal blackout advice.^[2]
• Bárány Society diagnostic criteria for Acute Unilateral Vestibulopathy / vestibular neuritis, 2022 (Strupp M, et al.): the neutral AUVP terminology and the diagnostic criteria, vHIT expectations and treatment notes.^[3]
• Bárány Society international diagnostic criteria for Ménière disease (2015), with the Japan Society for Equilibrium Research, EAONO, the AAO-HNS and the Korean Balance Society: named for the disorder's definition and natural history.
• Kaski (2026), "Acute vertigo: stroke or not?" review in Current Opinion in Neurology: acute vertigo presentation, HINTS plus, central mimics, imaging sensitivity and treatment notes.^[4]
• Getu et al (2021) for the orthostatic blood pressure definition and measurement.^[5]
• Webster et al (2023) Cochrane review for the evidence behind systemic drug treatment in Ménière disease.^[6]

No claim in this page exceeds what those sources support.

• Sort the complaint first: vertigo, dizziness or syncope, because the dangers and pathways differ.
• Most vertigo is peripheral and benign; the one not to miss is posterior circulation stroke.
• In acute vestibular syndrome a normal early MRI does not exclude stroke; the bedside examination, including HINTS plus, is decisive.
• HINTS is applicable only when nystagmus is present, and the findings should be described, not called "positive" or "negative".
• BPPV is diagnosed by the Dix-Hallpike manoeuvre with the head turned 45 degrees and the neck extended 20 degrees, and is treated by a canalith repositioning (Epley) procedure without post-procedural restrictions. Vestibular suppressants such as antihistamines or benzodiazepines are not routine.^[1]
• Unstable cervical spine disease is a contraindication to a canalith repositioning procedure; refer instead.
• Vestibular neuritis is an acute vestibular syndrome lasting at least 24 hours without auditory or central signs, with unidirectional horizontal-torsional nystagmus and a positive head impulse towards the affected side.
• Video head impulse testing is preferred to the bedside test, which has low sensitivity and specificity. A working approximation of abnormal is a vHIT gain under 0.7.
• Ménière disease is recurrent vertigo with fluctuating unilateral hearing loss, tinnitus and aural fullness. Evidence for systemic drug treatment is very uncertain.
• Orthostatic hypotension is a systolic fall of 20 mmHg or more, or a diastolic fall of 10 mmHg or more, within 3 minutes of standing, measured properly after 5 minutes seated.
• Cardiac syncope is an emergency until excluded; exertional, recumbent and familial features are red flags.
• Clear-cut vasovagal syncope in a young person does not need referral; fixed-pattern dizziness with altered consciousness needs an epileptic assessment.
• Severe truncal ataxia, skew deviation, direction-changing nystagmus or a normal head impulse in the presence of nystagmus means central disease until proven otherwise.

• Syncope (cardiology): full risk stratification, monitoring and treatment.
• Stroke and transient ischaemic attack in older adults: vascular investigation and secondary prevention.
• Vertigo and equilibrium: clinical examination and vestibular rehabilitation.
• Pharmacology of antiemetics and vestibular suppressants.
• Parkinson disease, diabetes mellitus and autonomic failure as causes of orthostatic syncope.