This page compiles our content related to vertigo. For further information on diagnosis and treatment, follow the links below to our full BMJ Best Practice topics on the relevant conditions and symptoms.
Vertigo is the sensation that the environment is spinning around relative to oneself (objective vertigo) or vice versa (subjective vertigo). The term is sometimes used erroneously to mean any form of dizziness. True vertigo is described as a rotary sensation of the patient or surroundings, and is often of vestibular origin. Vertigo may result from diseases of the inner ear or disturbances of the vestibular centres or pathways in the central nervous system (e.g., Meniere's disease, arteriosclerosis of cerebral vessels, brain lesion, head injury, motion sickness, or large and rapid variations in barometric pressure). Depending on the underlying cause/condition, it may be associated with nausea and vomiting, or accompanied by other symptoms and signs (e.g., headaches and visual symptoms). Most causes of vertigo are peripheral and non-life-threatening. However, those few central causes (vascular and neoplastic) are emergencies that should not be overlooked.
Patients may use the term dizziness to describe vertigo, pre-syncope, disequilibrium and lightheadedness (or non-specific dizziness). The most common causes of dizziness in primary care settings are benign paroxysmal positional vertigo (vertigo caused by the presence of a canalith in the vestibular apparatus), Meniere's disease, and acute vestibular neuritis (vestibular neuronitis). These all present with vertigo symptoms.
A peripheral vestibular disorder characterised by sudden-onset, severe attacks of vertigo usually lasting <30 seconds and precipitated by specific head movements (e.g., looking up or bending down, getting up, turning the head, or rolling over to one side in bed). Diagnosis is clinical with other key diagnostic factors including episodic vertigo (repeated attacks over days, weeks, or months), absence of associated neurological or otological symptoms, normal neurological examination, and positive Dix-Hallpike manoeuvre (posterior canal BPPV) or supine lateral head turn (lateral canal BPPV).
Auditory and vestibular disease characterised by an episodic, sudden onset of vertigo; hearing loss and roaring tinnitus; and a sensation of pressure or discomfort in the affected ear. Vertigo lasts minutes to hours and may be associated with nausea and vomiting. Hearing loss is usually worse during acute attacks, especially in early stages of the disease. As the disease progresses, hearing loss increases in severity and may become constant. Risk factors for Meniere’s disease include family history, recent viral infection, and autoimmune disorders.
An inflammatory condition, which affects the labyrinth in the cochlea and vestibular system of the inner ear. Viral labyrinthitis is typically associated with a preceding upper respiratory tract infection. Other aetiological viral agents include varicella zoster virus, cytomegalovirus, mumps, measles, rubella, and HIV. Bacterial labyrinthitis is associated with acute or chronic otitis media, meningitis, and cholesteatoma. Labyrinthitis may also manifest in certain autoimmune conditions (e.g., Cogan's syndrome or Behcet's disease). Patients typically present with severe room-spinning vertigo and associated nausea and vomiting. They may have unilateral hearing loss and tinnitus. Most acute episodes are short-lived and self-limited.
A common cause of vertigo and the most common cause of spontaneous episodic vertigo. It affects approximately 10% of patients with migraine. Symptoms include spontaneous and positional vertigo, head motion vertigo/dizziness and ataxia, all of variable duration, ranging from seconds to days, and independent of migraine associated headache. Photophobia, phonophobia, or aura may be diagnostic symptoms. Management is similar to the recommended treatment of migraine headaches, and includes dietary and lifestyle modifications, and prophylactic therapies (beta blockers, calcium channel blockers, and tricyclic antidepressants).
A common cause of unilateral peripheral vestibular loss, vestibular neuritis (vestibular neuronitis) is an acute peripheral vestibulopathy due to reactivation of a viral infection, most commonly herpes simplex virus. It affects the vestibular ganglion, vestibular nerve, labyrinth, or a combination of these sites.
Typically, occurs as a result of blunt head trauma such as a fall, an assault, or a motor vehicle accident. Presenting symptoms may be of a traumatic perilymphatic fistula or post-traumatic Meniere's disease. Patients may complain of vertigo, disequilibrium, tinnitus, pressure, headache, and diplopia. Other causes are postsurgical (middle-ear surgery, cochlear implantation) and diving. Superior semicircular canal dehiscence should be differentiated from post-traumatic vertigo; it is characterised by episodes of vertigo associated with loud sounds and/or altered middle-ear pressure.
Dizziness is a common presenting feature in cerebrovascular events. Cerebellar stroke (due to infarction or haemorrhage) may present in a similar fashion to peripheral causes of vertigo with sudden intense vertigo, nausea, and vomiting. Nystagmus (bilateral or vertical) may suggest a central cause of the vertigo. Other neurological signs include limb ataxia and impaired gait. Patients with cerebellar stroke usually cannot stand without support, even with the eyes open, whereas a patient with acute vestibular neuritis or labyrinthitis is usually able to do so. Unlike peripheral causes, the head-impulse test is negative (no saccadic adjustment of the eyes on sudden head twisting). Urgent magnetic resonance imaging should be requested in all patients with acute vertigo who have significant risk factors for a cerebellar stroke, such as hypertension, diabetes mellitus, smoking, and cardiovascular disease, since it is possible that central signs on examination may not present.
Intracranial tumours and vestibular schwannomas may present with vertigo, as well as other symptoms such as signs of intracranial pressure (e.g., headache, altered mental status, nausea, and/or vomiting) and gait abnormality. Cranial nerve deficits may also manifest. Neuroimaging with computed tomography/magnetic resonance imaging is essential.
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