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Emergency and Acute Medicine: Vertigo
Vertigo is a specific type of dizziness characterized by the false sensation of movement—typically spinning—either of the patient or the surrounding environment. It accounts for a significant proportion of emergency department visits and can arise from dysfunction in any of the three systems responsible for balance: the visual, proprioceptive, and vestibular systems. Clinically, vertigo must be distinguished from other nonspecific dizziness symptoms such as lightheadedness or presyncope, as it more often reflects an underlying neurologic or vestibular disorder.
Vertigo is broadly classified into peripheral and central causes. Peripheral vertigo, which originates from the inner ear or vestibular nerve, tends to produce severe, episodic symptoms lasting seconds to minutes, often triggered by head movement. It is commonly associated with horizontal or torsional nystagmus that fatigues and improves with visual fixation. Common causes include Benign Paroxysmal Positional Vertigo, the most frequent etiology due to displaced otoliths in semicircular canals; Vestibular Neuritis, which presents as continuous vertigo without hearing loss; and Ménière Disease, characterized by episodic vertigo, hearing loss, and tinnitus. In contrast, central vertigo arises from pathology in the brainstem or cerebellum, such as Vertebrobasilar Insufficiency, stroke, multiple sclerosis, or tumors. Central causes often present with milder but continuous vertigo, non-fatigable or vertical nystagmus, and associated neurologic deficits.
The history is crucial in distinguishing etiologies. Sudden, brief episodes triggered by head movement strongly suggest BPPV, whereas continuous vertigo lasting days suggests vestibular neuritis. Recurrent episodes with auditory symptoms point toward Ménière disease. Red flags for central causes include neurologic symptoms such as diplopia, dysarthria, limb weakness, ataxia, or severe imbalance out of proportion to vertigo. Stroke risk factors, including older age and vascular disease, further increase suspicion for a central cause.
Physical examination focuses on eye movements and neurologic assessment. Evaluation of nystagmus provides key diagnostic clues: unidirectional horizontal nystagmus suggests peripheral vertigo, whereas vertical, bidirectional, or non-fatigable nystagmus suggests central pathology. The head impulse test helps identify vestibular dysfunction, while skew deviation testing can indicate central lesions. The Dix–Hallpike maneuver is used to diagnose posterior canal BPPV, and the supine roll test assesses lateral canal involvement. A full neurologic exam is essential to identify subtle deficits suggestive of central causes.
Management depends on the underlying etiology. Peripheral vertigo is typically treated symptomatically with antihistamines (e.g., meclizine), benzodiazepines, and antiemetics. Repositioning maneuvers such as the Epley or Semont maneuvers are highly effective for BPPV. In contrast, central vertigo requires urgent evaluation and management of the underlying cause, such as stroke or hemorrhage, often involving neuroimaging and specialist consultation. Admission is indicated for serious causes like cerebellar infarction, vertebrobasilar insufficiency, or intractable symptoms preventing ambulation or oral intake.
A key clinical pearl is that vertigo can be the sole presenting symptom of a posterior circulation stroke. Therefore, clinicians must maintain a high index of suspicion, especially when vertigo is accompanied by neurologic signs or occurs in patients with vascular risk factors.
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