Vertigo and Dizziness: Peripheral or Central? A Diagnostic Approach

When a patient complains of "dizziness", the first task is to categorise the symptom. Vertigo is the perception that the environment or the person is spinning — rotational in character, usually of vestibular origin. Pre-syncope, near-fainting and light-headedness are typically cardiovascular or orthostatic in origin.

Disequilibrium is loss of balance during movement or upright stance; seen in multi-sensory neuropathy, proprioceptive loss, cerebellar disorders or peripheral vestibular hypofunction. Persistent Postural-Perceptual Dizziness (PPPD) is a chronic, continuous "floating" sensation with a strong anxiety component.

This distinction matters: rotational vertigo points to ENT, pre-syncope to cardiology or internal medicine, disequilibrium often to neurology or a multidisciplinary team. A patient who can describe the symptom accurately accelerates diagnosis. We expand on the clinical framework in our otology and hearing centre.

Benign Paroxysmal Positional Vertigo (BPPV) arises when otoconia (calcium-carbonate crystals) detach from the utricle and fall into the semicircular canals. The posterior canal is most often involved. Position change — rolling in bed, head extension, bending forward — triggers vertigo.

Clinical picture: brief, intense rotational vertigo lasting 10-60 seconds. The patient describes onset with movement, resolution with stillness. Nausea is common; vomiting less so. Hearing is normal, no ear fullness.

Diagnosis is the Dix-Hallpike manoeuvre. From seated, the head is rotated 45° toward the side to be tested, then the patient is rapidly laid supine with head extended 30°. Posterior-canal BPPV shows a 5-10-second latency upbeat-torsional (geotropic) nystagmus plus vertigo. The "roll test" tests the horizontal canal.

Treatment is the Epley manoeuvre — a series of positions to relocate the crystals back into the utricle. One session gives 70-80% success; two sessions over 90%. Surgery is rarely needed. Recurrence is possible (30% over 3 years).

Meniere disease is characterised by endolymphatic hydrops (increased pressure of inner-ear fluids). Diagnosis rests on a classical tetrad: episodic vertigo (20 minutes to 12 hours), fluctuating sensorineural hearing loss (particularly low-frequency), tinnitus and aural fullness.

Attacks usually come without warning; the patient must lie down; nausea and vomiting are severe. Between attacks the patient may be asymptomatic, or a permanent hearing reduction may have set in. As the disease progresses hearing loss becomes permanent and attacks may cluster.

Diagnosis is clinical; the AAO-HNS criteria are used. Audiometry at each visit (confirms the fluctuating pattern). MRI is requested to evaluate the inner ear and cerebellopontine angle (to exclude vestibular schwannoma). Low-sodium diet (<1.5 g/day), diuretic (hydrochlorothiazide + amiloride) and betahistine form the medical basis.

In refractory disease, options include intratympanic steroid, intratympanic gentamicin ablation, or endolymphatic-sac surgery. Total vestibular ablation (labyrinthectomy) is reserved for those whose hearing is already severely lost.

Vestibular neuritis is a sustained vertigo from presumed viral inflammation of the vestibular nerve. Onset is typically explosive over hours to days. Severe rotational vertigo for 1-3 days, gradual improvement over 1-2 weeks. Hearing is preserved (differs from labyrinthitis).

Labyrinthitis is the same process but extends into the cochlea — hearing loss and tinnitus accompany vertigo. Bacterial labyrinthitis (spread from middle-ear infection) is an emergency; viral labyrinthitis is supported symptomatically.

Treatment: vestibular suppressants (meclizine, dimenhydrinate, promethazine) and antiemetics in the first 24-48 hours. Steroids (methylprednisolone) given in the first week can shorten and soften the attack. Vestibular rehabilitation should start early — long-course suppressants delay central compensation and are kept under 3 days. For the related clinical reference, see vertigo page.

Vestibular migraine has a population prevalence over 1% and is often mistaken for Meniere. Diagnostic criteria: recurrent vestibular symptoms (5 minutes to 72 hours), lifetime migraine history, and migraine features (pulsating headache, photophobia / phonophobia, visual aura) in ≥50% of attacks.

The clinical distinction from Meniere matters. In vestibular migraine, hearing loss is not typical; tinnitus and fullness are less prominent. Headache need not be present during every attack. Triggers: stress, sleep disruption, hormonal cycle, certain foods (cheese, chocolate, wine), bright light.

Treatment is two-pronged. Acute attack: triptan, antiemetic, NSAID. Prophylaxis: beta-blocker (propranolol), topiramate, amitriptyline, flunarizine, magnesium, riboflavin. Lifestyle modification (regular sleep, trigger avoidance) helps most patients meaningfully.

MRI for every dizzy patient is unnecessary. Indications: sudden hearing loss with vertigo, unilateral progressive hearing loss with tinnitus (suspecting vestibular schwannoma), associated neurological signs (positive HINTS, dysarthria, ataxia, cranial nerve involvement), atypical nystagmus (vertical, direction-changing), new vertigo over age 50, vascular risk factors.

If stroke is suspected (high-risk profile, abnormal HINTS, focal sign), order diffusion-weighted MRI urgently. CT within 24-48 hours is inadequate for stroke diagnosis — especially in the posterior fossa. Posterior circulation stroke accounts for 3-5% of acute vertigo and missing it has serious consequences.

Vestibular schwannoma: unilateral asymmetric sensorineural hearing loss or unilateral tinnitus mandates a gadolinium-enhanced internal-auditory-canal / cerebellopontine-angle MRI. Early detection enables small-tumour observation or gamma-knife options.

After a peripheral vestibular insult, the central nervous system develops new balance strategies — central compensation. Vestibular rehabilitation, delivered by a trained physiotherapist with gaze-stabilisation and balance-adaptation exercises, accelerates this process.

Classic protocols (Cawthorne-Cooksey, gaze-stabilisation exercises) run 2-3 times daily for 10-15 minutes over 6-12 weeks. Exercise can transiently increase dizziness — this is expected, persistence is needed. Avoidance strategies (bed rest, head splinting) delay compensation.

Vestibular rehabilitation works in BPPV (after Epley), unilateral vestibular hypofunction (after neuritis), bilateral vestibular hypofunction (after ototoxicity), chronic disequilibrium and PPPD. In vestibular migraine and Meniere benefit is more limited but useful for between-attack stability. Related reading: our patient testimonials.