The general physical exam

Always check the blood pressure lying down and standing — a drop of more than 20 mmHg systolic or 10 mmHg diastolic within three minutes is orthostatic hypotension, a very common cause of "dizziness" in older adults and in patients on blood-pressure or antidepressant medications.

The 2011 consensus statement defines orthostatic hypotension as a ≥20 mmHg systolic or ≥10 mmHg diastolic fall within 3 minutes of standing.1It manifests as presyncope rather than vertigo and is easily mistaken for a peripheral vestibular disorder unless the BP is checked supine and standing.

POTS — a sustained heart-rate rise of ≥30 bpm on standing without orthostatic hypotension — presents with chronic dizziness, fatigue and exercise intolerance and is best identified at the bedside before invasive cardiovascular testing.

In the emergency department, patients presenting with dizziness who have cardiovascular risk factors warrant ECG, continuous monitoring, and a careful cardiac history — atrial fibrillation, bradyarrhythmias, and structural heart disease cause transient cerebral hypoperfusion that mimics vestibular disease.2Examine pulse rhythm, jugular venous pressure and heart sounds; auscultate the carotids for bruits; remember that vertebrobasilar insufficiency can present with positional vertigo on neck extension.

A focused neurological screen catches the central nervous-system causes that masquerade as inner-ear vertigo. Test the cranial nerves (especially the eye movements), look for limb weakness or numbness, watch the gait, and check the cerebellar signs (finger-nose, heel-shin, tandem walk).

Diplopia, dysarthria, dysphagia, hemisensory loss, hemiparesis, pronator drift, or any cerebellar sign in a patient with vertigo should trigger urgent imaging. Cerebellar disease produces limb dysmetria and a wide-based gait; midline (vermal) lesions give predominantly truncal ataxia with relatively preserved limb coordination.3

Distinguish sensory ataxia (impaired proprioception, intact vision compensates) from cerebellar ataxia (unsteady with eyes open OR closed) and from vestibular imbalance (lateralising signs on HIT and Fukuda). Functional gait disorders are inconsistent on repeat assessment and disproportionate to objective findings.

Look in the ears. Effusion, perforation, granulation tissue or cholesteatoma can cause secondary vestibular disturbance. Vertigo provoked by sneezing or tragal pressure is Hennebert's sign, classical of labyrinthine fistula and superior canal dehiscence.

Examine the external auditory canal and tympanic membrane, palpate over the mastoid, and perform tuning-fork tests if hearing is reported as altered. The Tullio phenomenon — vertigo on loud sound — points to a third-window lesion. Always assess the cervical range of motion; cervicogenic dizziness reproduces with neck rotation in a fixed posture and is a not-uncommon contributor to multifactorial imbalance.

Otoscopy guides the urgency: acute otitis media with vertigo and hearing loss suggests labyrinthitis; cholesteatoma with positional vertigo demands imaging for fistula. The vertebral arteries are vulnerable to mechanical compression on head turn or extension; provocation testing is informative but should be cautious in patients with vascular risk factors.

Anaemia, thyroid disease, dehydration and hypoglycaemia are common but under-recognised causes of dizziness. Look for pallor, tachycardia, weight change, goitre, tremor, dry skin, and a recent finger-prick glucose. In an alcoholic or malnourished patient with confusion, ataxia and gaze palsy, give empirical IV thiamine for Wernicke's encephalopathy before any glucose.

Hyperthyroidism produces dizziness through autonomic hypersensitivity and tachyarrhythmia; subclinical thyroid dysfunction is a controversial but worth- considering contributor in older adults.4 Wernicke's classic triad (confusion + ataxia + ophthalmoplegia/nystagmus) appears in a minority at presentation, so treat on any single feature in at-risk patients.5

Capillary glucose at the bedside in any dizzy diabetic patient on sulfonylureas or insulin is essential — silent hypoglycaemia is common and rapidly reversible. Iron-deficiency anaemia, B12 deficiency, and renal failure each contribute to multifactorial unsteadiness, especially in the elderly.

A significant proportion of patients seen in dizziness clinics have anxiety, panic, or persistent postural-perceptual dizziness as a primary cause or as an overlay after an acute vestibular insult. Recognising these contributors early shortens the diagnostic odyssey and points to effective treatment.

PPPD is a chronic functional vestibular disorder — non-spinning dizziness for ≥3 months, worse on upright stance, on motion, and in visually complex environments, often arising after an acute vestibular event.8 It has a recognised neurobiological substrate of altered visuo-vestibular cortical connectivity.9 Anxiety and depression overlap with chronic dizziness in both directions — anxiety can precipitate, perpetuate, and follow vestibular disorders.7,6

Treat PPPD with vestibular rehabilitation, CBT, and selectively with SSRI/SNRI — the combination outperforms any single modality.10 Test for the cognitive deficit of an unrecognised delirium in older patients; brief screens like the Mini-Cog catch what an unhurried examination misses.12 Calling functional dizziness "non-organic" is unhelpful and clinically wrong — the substrate is real.