Vertigo

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Overview
Vertigo (from the Latin vertigin-, vertigo, "dizziness," originally "a whirling or spinning movement," from vertere "to turn" ) is a specific type of dizziness, a major symptom of a balance disorder. It is the sensation of spinning or swaying while the body is actually stationary with respect to the surroundings.

The effects of vertigo may be slight. It can cause nausea and vomiting and, in severe cases, it may give rise to difficulties with standing and walking.

Definition

 * Illusion of movement caused by acute asymmetry in the vestibular system
 * Cardinal symptom of vestibular dysfunction
 * May be associated with nausea, vomiting, postural instability

Causes
Vertigo is usually associated with a problem in the inner ear balance mechanisms (vestibular system), in the syndrome and Meniere's disease.

Vertigo-like symptoms may also appear as paraneoplastic syndrome (PNS) in the form of opsoclonus myoclonus syndrome, a multi-faceted neurological disorder associated with many forms of incipient cancer lesions or viruses.

Vertigo is typically classified into one of two categories depending on the location of the damaged vestibular pathway. These are peripheral or central vertigo. Each category has a distinct set of characteristics and associated findings.

Vertigo can also occur after long flights or boat journeys where the mind gets used to turbulence, resulting in a person's feeling as if he is moving up and down. This usually subsides after a few days.

Vertigo can also occur when exposed to high levels of sound pressure rattling the inner ear in which throwing off ones balance and others.

Neurochemistry
The neurochemistry of vertigo includes 6 primary neurotransmitters that have been identified between the 3-neuron arc that drives the vestibulo-ocular reflex (VOR). Many others play more minor roles.

Three neurotransmitters that work peripherally and centrally include glutamate, acetylcholine, and GABA.

Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate synaptic transmission in all 3 neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. GABA is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connections between the cerebellar Purkinje cells and the lateral vestibular nucleus, and the vertical VOR.

Three other neurotransmitters work centrally. Dopamine may 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. It is known that centrally acting antihistamines modulate the symptoms of motion sickness.

The neurochemistry of emesis overlaps with the neurochemistry of motion sickness and vertigo. Acetylcholine, histamine, and dopamine are excitatory neurotransmitters, working centrally on the control of emesis. GABA inhibits central emesis reflexes. Serotonin is involved in central and peripheral control of emesis but has little influence on vertigo and motion sickness.

History and Symptoms

 * Time course
 * Most helpful in determining etiology (see above)
 * Brainstem symptoms
 * Diplopia
 * Facial numbness
 * Weakness
 * Hemiparesis
 * Dysphagia
 * Aural fullness with deafness, tinnitus
 * Suggestive of inner ear lesion (Meniere’s, labyrinthitis)
 * History of head trauma or barotrauma and symptoms triggered by straining/sneezing/coughing (perilymphatic fistula)
 * Atherosclerotic risk factors or history coronary artery disease/peripheral vascular disease (CAD/PVD)
 * Increases likelihood vertebrobasilar insufficiency
 * Recurrent episodes with remissions
 * Pattern suggestive of multiple sclerosis (MS), especially if other associated symptoms
 * Prior history of migraines

Physical Examination

 * Vestibular exam
 * Nystagmus
 * Peripheral lesions:
 * Horizontal +/- torsional component, never vertical
 * Fast phase toward the normal ear
 * Never reverses direction
 * Suppressed by visual fixation
 * (Prevent fixation via Frenzel lenses -> increased nystagmus)
 * Central lesions
 * Can be in any direction
 * May reverse direction when patient looks in direction of slow phase
 * Not suppressed by visual fixation
 * Provocative maneuvers
 * Dix-Hallpike (Baranay):	Patient sitting on exam table
 * Lies down with head extending over table edge, 45° to one side
 * Position change can occur slowly; should be held for > 30 sec
 * Repeat with head turned 45° to opposite side, then without turning head
 * Peripheral lesion:
 * 2-20 sec latency before onset of nystagmus
 * Duration of nystagmus < 1 minute
 * Fatigues with repetition of maneuver
 * One type nystagmus (upbeat and torsional)
 * Severe vertigo (spinning toward normal ear)
 * Central lesion:	no latency before onset of nystagmus
 * Duration of nystagmus > 1 minute
 * No fatiguability
 * Direction may change with head position
 * Less severe, if any, vertigo
 * Neurologic exam
 * Cranial nerves
 * Motor/sensory deficits,
 * Deep tendon reflexes (DTRs)
 * Cerebellar signs?
 * Central lesion
 * Romberg
 * Unilateral peripheral lesion -> patient leans/falls to side of lesion, but able to walk
 * Acute cerebellar lesion -> patient unable to walk without falling; variable direction of fall
 * Hearing
 * Test gross hearing with whisper/finger tap
 * If asymmetric hearing loss:
 * Rinne test to confirm sensorineural (vs. conductive) loss
 * Air>bone conduction with sensorineural loss
 * Tympanum membrani (TM) exam to rule out acute or chronic otitis media as etiology
 * Speech discrimination to assess cochlear or retrocochlear
 * Identification of < 20% of 10 2-syllable words whispered into affected ear suggests retrocochlear lesion (acoustic neuroma)
 * Identification of > 70% of words = cochlear disease
 * Identification of 20-70% = indeterminate (audiology)
 * Audiometry referral to confirm hearing loss

MRI and CT

 * MRI/MRA:
 * If history/physical examination suggests central cause of vertigo
 * If unable to distinguish central vs. peripheral etiology in patient with risk factors for cerebrovascular accident (CVA)
 * Sensitivity/specificity of MRA > 95% for posterior circulation lesion
 * CT less optimal for imaging cerebellum
 * MRI of internal auditory canal/cerebellopontine angle
 * If acoustic neuroma suspected
 * Incidence of acoustic neuroma in patients with vertigo and no hearing loss: 1/9000
 * Incidence of acoustic neuroma in patients with dizziness and asymmetric hearing loss: 1/600

Other Diagnostic Studies

 * Audiometry:
 * More sensitive detection of hearing loss at specific frequencies
 * Better test for speech discrimination (disproportionately affected in retrocochlear disease)
 * Most useful for distinguishing cochlear vs. retrocochlear causes of peripheral lesion
 * Detects sensorineural hearing loss in almost all cases acoustic neuroma

Differential Diagnosis
 Distinguish cause of vertigo based on: 
 * Time course
 * Duration
 * Recurrence

 Alternative anatomic classification: central vs. peripheral 
 * Lasting a day or longer
 * Vestibular neuronitis
 * Onset over hours, peaks in first day, improves within days
 * May recur episodically for weeks to months
 * Vertebrobasilar ischemia with labyrinth infarct
 * Abrupt onset, improves within 1 week
 * Symptomss resolve within weeks to months
 * Brain-stem stroke: usually other symptoms vertebrobasilar ischemia
 * Inferior cerebellar infarct/bleed: similar symptoms/time course to vestibular neuritis
 * Multiple sclerosis: vestibular symptoms evolve over hours to days
 * Lasting minutes to hours
 * Meniere’s disease: episodic/recurrent
 * Vertebrobasilar transient ischemic attack (TIA): typically lasts < 30 minutes, may recur
 * Migraine Headache: episodic/recurrent
 * Perilymph fistula: episodic; precipitated by exertional straining or change in air pressure
 * Lasting seconds
 * Benign paroxysmal positional vertigo (BPPV): usually lasts < 1 minute
 * Central (20%):
 * Caused by damage to vestibular structures in brainstem or cerebellum
 * Associated with other brainstem deficits
 * Vertigo and nystagmus can be bidirectional or vertical
 * Vertebrobasilar insufficiency:
 * Accounts for ½ of central causes
 * Brainstem or cerebellar territory (anterior inferior cerebellar artery (AICA), posterior inferior cerebellar artery (PICA)) -> transient ischemic attack (TIA) or cerebrovascular accident (CVA)
 * Associated diplopia, dysarthria, dysphagia, hemiparesis, etc.
 * Cerebellar infarct may present with isolated vertigo
 * Can have pontine lacunes, labyrinthine infarcts
 * Multiple sclerosis:	associated brainstem symptoms may be subtle (facial numbness)
 * Vertiginous symptoms may be sudden, transient, recurrent or persistent
 * Migraine:	vertigo precedes headache and may last afterward
 * Atypical form of migraine with aura -> may respond to migraine therapy
 * Drugs
 * Sedatives, anticonvulsants may cause central vertigo in high/excess doses
 * Anticonvulsants in prescription doses may cause nystagmus (phenytoin, carbamazepine)
 * Peripheral (80%):
 * Caused by damage to vestibular labyrinth, vestibular nerve
 * Associated tinnitus, hearing loss if auditory component of CN VIII affected
 * Vertigo and nystagmus are unidirectional, and not vertical
 * BPPV
 * Accounts for more than ½ of cases peripheral vestibular dysfunction
 * Common in the elderly (patients usually > 60)
 * Episodes of sudden onset, short duration -> condition often remits in 6 months
 * Mechanism = stimulation of labyrinth by debris in posterior semicircular canal
 * Vestibular neuronitis
 * Accounts for ¼ of cases peripheral vestibular dysfunction
 * Isolated vertigo due to viral infection involving labyrinth (after URI)
 * Acute labyrinthitis
 * Viral involvement of cochlea and labyrinth after upper respiratory infection (URI)
 * Vertigo associated with tinnitus and hearing loss
 * symtpoms resolve completely within 3-6 weeks
 * Meniere’s disease
 * Idiopathic endolymphatic hydrops -> damage to hair cells
 * Tinnitus, ear pressure and hearing loss associated with vertigo
 * Paroxysmal episodes lasting minutes to hours
 * Frequency of episodes waxes and wanes over time
 * Hearing loss can become permanent
 * Acoustic neuroma
 * Benign tumor, but can cause brainstem compression if unprescribed
 * Retrocochlear hearing loss, tinnitus, vague dizziness
 * Very gradual symptom onset with progressive asymmetric hearing loss
 * Vertigo not prominent because gradual time course allows central nervous system adaptation
 * Ototoxins:	hearing impairment usually >> vestibular symptoms
 * Gentamicin, streptamicin most injurious to vestibular portion of CN VIII

Treatment

 * Central disorders
 * Treat underlying disease
 * Vertebrobasilar ischemia
 * Vertigo usually resolves on its own
 * Risk factor modification to decrease recurrence
 * +/- Revascularization or anticoagulation
 * Migraine: adequate treatment of headache improves vertigo in 90%
 * Multiple sclerosis (MS): Therapy for MS alleviates vertiginous symptoms as well
 * Drugs: discontinue offending agents
 * Peripheral disorders
 * General management
 * Physical therapy
 * Beneficial in patients with permanent peripheral vestibular dysfunction
 * Unknown benefit in patients with central disorders
 * Vestibular rehabilitation
 * Activity enables CNS adaptation to loss of vestibular input
 * Visual compensation during head motion
 * Balance shown to improve in randomized controlled trials of vestibular exercises
 * Unclear if long-term benefits or if decreased fall risk
 * Avoidance of inactivity
 * Avoid deconditioning and loss of postural reflexes

Acute Pharmacotherapies

 * Peripheral disorders
 * Specific management
 * BPPV
 * Epley maneuver --> in a randomized controlled trial, symptoms resolved in 50% vs. 19% sham therapy by mean 10 days
 * Meclizine (12.5-50 mg every 6 hours as often as necessary) or promethazine (25 mg every 6 hours as often as necessary) for severe symptoms
 * Meniere’s disease: low-salt diet and diuretics to reduce endolymph production


 * Peripheral disorders
 * General management
 * Pharmacologic therapy
 * For acute episodes: Avoid long-term therapy if symptoms last > few days (will reduce CNS adaptation)
 * Anticholinergics
 * Scopolamine: Side effect urinary retention, dry mouth
 * Antihistamines
 * Meclizine, dimenhydrinate, diphenhydramine (anti-Ach effects)
 * Meclizine is drug of choice in pregnancy. Side effect: sedation
 * Phenothiazines
 * prochlorperazine, promethazine (anti-Ach effects): More sedating, but also have antiemetic effects. Risk: extrapyramidal side effect (second-line)
 * Benzodiazepines
 * Diazepam, lorazepam, clonazepam (GABA-ergic effects): For patients with contraindications to anti-Ach prescription (benign prostatic hypertrophy)

Surgery and Device Based Therapy

 * Perilymphatic fistula
 * Bed rest, head elevation, avoidance of straining
 * Surgical patch if no resolution after several weeks
 * Acoustic neuroma: surgical therapy

Additional Resources
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