Vertigo is when a person feels as if they or the objects around them are moving when they're not. Often it feels like a spinning or swaying movement. This might be associated with nausea, vomiting, sweating, or difficulties walking. It is typically worsened when the head is moved. Vertigo is the most common type of dizziness.
The most common diseases that result in vertigo are benign paroxysmal positional vertigo, Ménière's disease, and labyrinthitis. Less common causes include stroke, brain tumors, brain injury, multiple sclerosis, and migraines. Physiologic vertigo might occur following being exposed to motion for a prolonged period such as when on a ship or simply following spinning with the eyes closed. Other causes might include toxin exposures such as to carbon monoxide, alcohol, or aspirin. Vertigo is a problem in a part of the vestibular system. Other causes of dizziness include presyncope, disequilibrium, and non-specific dizziness.
Benign paroxysmal positional vertigo is more likely in someone who gets repeated episodes of vertigo with movement and are otherwise normal between these episodes. The episodes of vertigo should last less than one minute. The Dix-Hallpike test typically produces a period of rapid eye movements known as nystagmus in this condition. In Ménière's disease there's often ringing in the ears, hearing loss, and the attacks of vertigo last more than twenty minutes. In labyrinthitis the onset of vertigo is sudden and the nystagmus occurs without movement. In this condition vertigo can last for days. More severe causes should additionally be considered. This is especially true if additional problems such as weakness, headache, double vision, or numbness occur.
Dizziness affects approximately 20–40% of people at a few point in time while about 7.5–10% have vertigo. About five percent have vertigo in a given year. It becomes more common with age and affects women two to three times more often than men. Vertigo accounts for about 2–3% of emergency department visits in the developed world.
Vertigo is classified into either peripheral or central depending on the location of the dysfunction of the vestibular pathway, although it can additionally be caused by psychological factors.
Vertigo can additionally be classified into objective, subjective, and pseudovertigo. Objective vertigo describes when the person has the sensation that stationary objects in the environment are moving. Subjective vertigo refers to when the person feels as if they're moving. The third type is known as pseudovertigo, an intensive sensation of rotation inside the person's head. While this classification appears in textbooks, it has little to do with the pathophysiology or treatment of vertigo.
Vertigo that's caused by problems with the inner ear or vestibular system, which is composed of the semicircular canals, the vestibule (utricle and saccule), and the vestibular nerve is called "peripheral", "otologic" or "vestibular" vertigo. The most common cause is benign paroxysmal positional vertigo (BPPV), which accounts for 32 percent of all peripheral vertigo. Other causes include Ménière's disease (12%), superior canal dehiscence syndrome, labyrinthitis, and visual vertigo. Any cause of inflammation such as common cold, influenza, and bacterial infections might cause transient vertigo if it involves the inner ear, as might chemical insults (e.g., aminoglycosides) or physical trauma (e.g., skull fractures). Motion sickness is at times classified as a cause of peripheral vertigo.
People with peripheral vertigo typically present with mild to moderate imbalance, nausea, vomiting, hearing loss, tinnitus, fullness, and pain in the ear. In addition, lesions of the internal auditory canal might be associated with facial weakness on the same side. Due to a rapid compensation process, acute vertigo as a result of a peripheral lesion tends to improve in a short period of time (days to weeks).
Vertigo that arises from injury to the balance centres of the central nervous system (CNS), often from a lesion in the brainstem or cerebellum, is called "central" vertigo and is generally associated with less prominent movement illusion and nausea than vertigo of peripheral origin. Central vertigo might have accompanying neurologic deficits (such as slurred speech and double vision), and pathologic nystagmus (which is pure vertical/torsional). Central pathology can cause disequilibrium which is the sensation of being off balance. The balance disorder associated with central lesions causing vertigo is often so severe that a large number of patients are unable to stand or walk.
A number of conditions that involve the central nervous system might lead to vertigo including: lesions caused by infarctions or hemorrhage, tumors present in the cerebellopontine angle such as a vestibular schwannoma or cerebellar tumors, epilepsy, cervical spine disorders such as cervical spondylosis, degenerative ataxia disorders, migraine headaches, lateral medullary syndrome, Chiari malformation, multiple sclerosis, parkinsonism, as well as cerebral dysfunction. Central vertigo might not improve or might do so more slowly than vertigo caused by disturbance to peripheral structures.
Signs and symptoms
Vertigo is a sensation of spinning while stationary. It is commonly associated with nausea or vomiting, unsteadiness (postural instability), falls, changes to a person's thoughts, and difficulties in walking. Recurrent episodes in those with vertigo are common and frequently impair the quality of life. Blurred vision, difficulty in speaking, a lowered level of consciousness, and hearing loss might additionally occur. The signs and symptoms of vertigo can present as a persistent (insidious) onset or an episodic (sudden) onset.
Persistent onset vertigo is characterised by symptoms lasting for longer than one day and is caused by degenerative changes that affect balance as people age. Naturally, the nerve conduction slows with ageing and a decreased vibratory sensation is common. Additionally, there's a degeneration of the ampulla and otolith organs with an increase in age. Persistent onset is commonly paired with central vertigo signs and systems.
The characteristics of an episodic onset vertigo is indicated by symptoms lasting for a smaller, more memorable amount of time, typically lasting for only seconds to minutes. Typically, episodic vertigo is correlated with peripheral symptoms and can be the result of but not limited to diabetic neuropathy or autoimmune disease.
Motion sickness is one of the most prominent symptoms of vertigo and develops most often in persons with inner ear problems. The feeling of dizziness and lightheadedness is often accompanied by nystagmus (an involuntary movement of the eye characterised by a smooth pursuit eye movement followed by a rapid saccade in the opposite direction of the smooth pursuit eye movement). During a single episode of vertigo, this action will occur repeatedly. Symptoms can fade while sitting still with the eyes closed.
Tests for vertigo often attempt to elicit nystagmus and to distinguish vertigo from additional causes of dizziness such as presyncope, hyperventilation syndrome, disequilibrium, or psychiatric causes of lightheadedness. Tests of vestibular system (balance) function include: electronystagmography (ENG), Dix-Hallpike maneuver, rotation tests, head-thrust test, caloric reflex test, and computerized dynamic posturography (CDP). The HINTS test, which is a combination of three physical exam tests that might be performed by physicians at the bedside has been deemed helpful in differentiating between central and peripheral causes of vertigo. The HINTS test involves: the horizontal head impulse test, observation of nystagmus on primary gaze, and the test of skew. CT scans or MRIs are at times used by physicians when diagnosing vertigo.
Tests of auditory system (hearing) function include pure tone audiometry, speech audiometry, acoustic reflex, electrocochleography (ECoG), otoacoustic emissions(OAE), and the auditory brainstem response test.
A number of specific conditions can cause vertigo. In the elderly, however, the condition is often multifactorial.
Benign paroxysmal positional vertigo
Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder and occurs when loose calcium carbonate debris has broken off of the otoconial membrane and enters a semicircular canal thereby creating the sensation of motion. Patients with BPPV might experience brief periods of vertigo, usually under a minute, which occur with change in position. This is the most common aetiology of vertigo. It occurs in 0.6% of the population yearly with ten percent having an attack throughout their lifetime. It is believed to be due to a mechanical malfunction of the inner ear. BPPV might be diagnosed with the Dix-Hallpike test and can be effectively treated with repositioning movements such as the Epley maneuver.
Ménière's disease is a vestibular disorder of unknown origin, but is thought to be caused by an increase in the amount of endolymphatic fluid present in the inner ear (endolymphatic hydrops). Notwithstanding this idea hasn't been directly confirmed with histopathologic studies but electrophysiologic studies have been suggestive of this mechanism. Ménière's disease frequently presents with recurrent, spontaneous attacks of severe vertigo in combination with ringing in the ears (tinnitus), a feeling of pressure or fullness in the ear (aural fullness), severe nausea or vomiting, imbalance, and hearing loss. As the disease worsens, hearing loss will progress.
Labyrinthitis presents with severe vertigo with associated nausea, vomiting, and generalised imbalance and is believed to be caused by a viral infection of the inner ear though several theories have been put forward and the aetiology remains uncertain. Individuals with vestibular neuritis don't typically have auditory symptoms but might experience a sensation of aural fullness or tinnitus. Persisting balance problems might remain in thirty percent of people affected.
Vestibular migraine is the association of vertigo and migraines and is one of the most common causes of recurrent, spontaneous episodes of vertigo. The aetiology of vestibular migraines is currently unclear; however, one hypothesised cause is that the stimulation of the trigeminal nerve leads to nystagmus in individuals suffering from migraines. Other suggested causes of vestibular migraines include the following: unilateral neuronal instability of the vestibular nerve, idiopathic asymmetric activation of the vestibular nuclei in the brainstem, and vasospasm of the blood vessels supplying the labyrinth or central vestibular pathways resulting in ischemia to these structures. Vestibular migraines are estimated to affect 1-3% of the general population and might affect ten percent of migraine patients. Additionally, vestibular migraines tend to occur more often in women and rarely affect individuals after the sixth decade of life.
A stroke (either ischemic or hemorrhagic) involving the posterior fossa is a cause of central vertigo. Risk factors for a stroke as a cause of vertigo include increasing age and known vascular risk factors. Presentation might more often involve headache or neck pain, additionally, those who have had multiple episodes of dizziness in the months leading up to presentation are suggestive of stroke with prodromal TIAs. The HINTS exam as well as imaging studies of the brain (CT, CT angiogram, and/or MRI) are helpful in diagnosis of posterior fossa stroke.
The neurochemistry of vertigo includes six primary neurotransmitters that have been identified between the three-neuron arc that drives the vestibulo-ocular reflex (VOR). Glutamate maintains the resting discharge of the central vestibular neurons, and might modulate synaptic transmission in all three neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. Gamma-Aminobutyric acid (GABA) is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connexions between the cerebellar Purkinje cells, and the lateral vestibular nucleus, and the vertical VOR.
Three additional neurotransmitters work centrally. Dopamine might accelerate vestibular compensation. Norepinephrine modulates the intensity of central reactions to vestibular stimulation and facilitates compensation. Histamine is present only centrally, but its role is unclear. Dopamine, histamine, serotonin, and acetylcholine are neurotransmitters thought to produce vomiting. It is known that centrally acting antihistamines modulate the symptoms of acute symptomatic vertigo.
Definitive treatment depends on the underlying cause of vertigo. Ménière's disease patients have a variety of treatment options to consider when receiving treatment for vertigo and tinnitus including: a low-salt diet and intratympanic injections of the antibiotic gentamicin or surgical measures such as a shunt or ablation of the labyrinth in refractory cases. Common drug treatment options for vertigo might include the following:
- Anticholinergics such as hyoscine hydrobromide (scopolamine)
- Anticonvulsants such as topiramate or valproic acid for vestibular migraines
- Antihistamines such as betahistine, dimenhydrinate, or meclizine, which might have antiemetic properties
- Beta blockers such as metoprolol for vestibular migraine
- Corticosteroids such as methylprednisolone for inflammatory conditions such as vestibular neuritis or dexamethasone as a second-line agent for Ménière's disease
In the Alfred Hitchcock film Vertigo, the hero, played by James Stewart, has to resign from the police force after an incident which causes him to develop both acrophobia and vertigo. Early on in the film he faints while climbing a stepladder. There are numerous references throughout the film to fear of heights and falling, The dolly zoom camera effect, additionally called the "vertigo effect", was first used in this film.