Vertigo

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Vertigo is identified as ‘room spinning around’. It is a type of dizziness. Presyncope, lightheadedness and disequilibrium are other types of dizziness and should be ruled out. The cause of vertigo can be peripheral or central in origin. In peripheral vertigo, dysfunction is in the vestibular system which includes the vestibule (utricle and saccule), semicircular canals, and the vestibular nerve. Central etiologies of vertigo usually originates from the brainstem or cerebellum. Most common causes of vertigo to appear in primary-care are benign paroxysmal positional vertigo, acute vestibular neuronitis, and Ménière’s disease. Best approach to diagnose vertigo etiology is to obtain a complete history paired with a focal examination including assessment of cranial nerves, nystagmus, sensorineural hearing loss (Rinne or Webers test), otoscopic exam of ear canal and tympanic membrane, HINTS (cover/uncover test), Dix-Hallpike maneuver and/or Hennebert’s sign. Acute/severe attacks of vertigo may subside in a day or two after brainstem compensation. Supportive therapy includes bed rest, antihistamine, antiemetic (prochlorperazine, metoclopramide) to relief the symptom. These drugs should not be used for a long period of time as it may delay the compensatory mechanism in the brainstem and result in the prolongation of vertigo symptom.Treating the underlying cause is the definitive treatment of vertigo.

Vertigo is derived from the Latin words vertigin and vertere which means “a whirling or spinning movement,” and “to turn”, respectively.

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 feeling as if they are moving up and down. This usually subsides after a few days.

Disruption in the vestibular system results in vertigo. The region of disruption could be peripheral (labyrinth, vestibular nerve) or central (brainstem, cerebellum). Vestibulo-ocular reflex is responsible for stabilizing gaze during head movement, it is controlled by six neurotransmitters, which are glutamate, acetylcholine, GABA, dopamine, histamine and norepinephrine.

Common causes of vertigo are Ménière’s disease, benign paroxysmal positional vertigo, labyrinthitis, vestibular neuritis. Life-threatening causes include brainstem ischemia/hemorrhage, hypertension crisis, drug overdose, cyanide poisoning.

Vertigo is one of the four type of dizziness, therefore it must be differentiated from other forms of dizziness, presyncope, lightheadedness and disequilibrium.

Among the patient who presents with dizziness in the primary care setting, fifty-four percent have vertigo upon investigation. Benign paroxysmal positional vertigo, acute vestibular neuronitis, and Ménière’s disease account for ninety-three percent of patients diagnosed with true vertigo in a primary care setting.

There are no established risk factors for vertigo, as it is a symptom of an underlying disease. However, vertigo can be prevented in some cases by controlling risk factors for the underlying cause.

There is insufficient evidence to recommend routine screening for vertigo.

There are no established criteria for the diagnosis of vertigo. The best approach to diagnose vertigo etiology is to obtain a complete history paired with a focal examination.

It is important to differentiate between other causes of dizziness before evaluating the cause of vertigo. True vertigo is described as the room spinning around the patient. Once true vertigo is established next step is to identify if the origin of dysfunction is central or peripheral. Detailed investigation of the time course of vertigo and associated signs and symptoms aid in identifying the cause of vertigo.

Physical examination of patients experiencing vertigo should include assessment of cranial nerves, nystagmus, sensorineural hearing loss (Rinne or Webers test), otoscopic exam of the ear canal and tympanic membrane, HINTS (cover/uncover test), Dix-Hallpike maneuver, and/or Hennebert’s sign.

There are no diagnostic laboratory findings associated with vertigo.

There are no ECG findings associated with vertigo. However, an ECG should be ordered to look for cardiac causes of dizziness including bradycardia, orthostatic hypotension resulting in poor circulation, privided true vertigo is not established as the cause od dizziness in the patient

An x-ray of the cervical spine may be helpful in the diagnosis of peripheral vertigo of unknown origin. Findings on an x-ray include, extended cervical spine posture, degenerative changes in the cervical spine can cause peripheral vertigo, and/or uncovertebral arthroses.

There are no echocardiography/ultrasound findings associated with vertigo. However, an echocardiography/ultrasound may be helpful in the diagnosis of underlying etiology of vertigo or to rule out cardiac cause of dizziness if true vertigo is not established. Use of echo-color Doppler ultrasound is helpful to look for plaque in extracranial vessels supplying blood to brain in patients with peripheral vertigo but exact cause still unidentified.

CT scan is not the first-line imaging method preferred to determine the underlying cause of central vertigo due to its low sensitivity in identifying ischemic stroke and a negative CT scan cannot completely rule out the central cause of vertigo, it still needs to be further investigated with the help of an MRI.

An MRI is the first-line imaging if the cause of vertigo is suspected to be central in origin. MRI is superior to a CT scan due to its ability to visualize the posterior fossa.

There are no other imaging findings associated with vertigo. However, some underlying cause may benefit from electronystagmography or electroencephalogram. Further imaging should be conducted according to the diagnostic requirements of the etiology behind the symptom of vertigo.

There are no other diagnostic studies associated with vertigo. However, the causes of vertigo should be evaluated further according to its diagnostic protocol.

Acute/severe attacks of vertigo may subside in a day or two after brainstem compensation. Supportive therapy includes bed rest, antihistamine, antiemetic (prochlorperazine, metoclopramide) to relief the symptom. Antihistamine (meclizine,betahistine,dimenhydrinate), antiemetic, anticholinergic (scopolamine) and benzodiazepines (diazepam,lorazepam) are the common medications used to treat vertigo as a symptom. These drugs should not be used for a long period of time as it may delay the compensatory mechanism in the brainstem and result in the prolongation of vertigo symptom. Some patients may be a candidate for vestibular rehabilitation. Treating the underlying cause is the definitive treatment of vertigo.

For the majority of underlying causes of vertigo, the mainstay of treatment is medical therapy. Surgery is usually reserved for patients with either tumor-associated vertigo, cholesteatoma, and/or when it does not respond to multiple medical therapies.

There are no established measures for the primary prevention of vertigo, as it occurs as a symptom of underlying pathology. In some diseases controlling risk factors or triggering, factors can prevent the disease hence preventing the symptoms.

Effective measures for the secondary prevention of vertigo include optimal treatment of the underlying etiology.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Vertigo is derived from the Latin words vertigin and vertere which means “a whirling or spinning movement,” and “to turn”, respectively.

• There is limited information about the historical perspective of vertigo.

• Vertigo is derived from the Latin words vertigin and vertere which means “a whirling or spinning movement,” and “to turn”, respectively.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Vertigo is typically classified into one of two categories depending on the location of the damaged vestibular pathway. These are peripheral or central vertigo. It can also be classified into 3 sub groups based on duration of vertigo. Each category has a distinct set of characteristics and associated findings.

Vertigo may be classified according to location of dysfunction into 2 subtypes and according to time course/duration into 3 subtypes:

Classification of Vertigo[1][2][3]

Based on Location of Dysfunction

Time Course/Duration

Peripheral

Central

Lasting a Day or Longer

Lasting Minutes to Hours

Lasting Seconds

Lesion in inner ear or vestibulocochlear nerve

Lesion in brainstem or cerebellum

Ménière’s disease Benign positional paroxysmal vertigo Acute labyrinthitis Acute vestibular neuronitis Cholesteatoma Otosclerosis Perilymphatic fistula Acoustic Neuroma

Brainstem Stroke Vestibular Migraine Multiple Sclerosis Cerebellar ischemia or hemorrhage Cerebellar tumors Lateral medullary syndrome Chiari malformation

Vestibular neuronitis Vertebrobasilar ischemia with labyrinth infarct Brainstem stroke Inferior cerebellar infarct/bleed

Ménière’s disease Vertebrobasilar transient ischemic attack (TIA) Migraine Headache Perilymph fistula

Benign paroxysmal positional vertigo

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

It is thought that vertigo is the result of a disruption in the vestibular system. It is identified as peripheral vertigo if the lesion is in the labyrinth or vestibular nerve or central vertigo if the area of disruption originates from the brainstem or cerebellum.

• Vestibular system is part of the inner ear. It is made of the utricle, the saccule, and three semicircular canals.
• The vestibular system along with the visual pathway prevents blurring of vision duringhead movement. This is called the vestibulo-ocular reflex.
• Disruption of the vestibular system can lead to vertigo and associated signs and symptoms.^[1]

• Disruption in the vestibular system results in vertigo. The region of disruption could be peripheral (labyrinth, vestibular nerve) or central (brainstem, cerebellum).
• Pathophysiology Behind Common Causes of Vertigo:

Pathophysiology of Common Causes of Vertigo[2]
Ménière’s disease	Increased endolymph volume in semicircular canals.
Benign paroxysmal positional vertigo	Dislodged otoliths stimulate vestibular sense organ.
Acute labyrinthitis	Inflammation of labyrinth/ viral or bacterial.
Acute vestibular neuritis	Inflammation of vestibular nerve caused by viral infection.
Cholesteatoma	Cyst/sac of keratin debris in middle ear.
Otosclerosis	Abnormal bone growth in the middle ear.
Perilymphatic fistula	Abnormal connection between the middle ear and inner ear.

• Neurochemistry of Vertigo:
  • 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.^[3]
  • Three neurotransmitters that work peripherally and centrally include:
    • Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate synaptic transmission in all 3 neurons of the vestibulo-ocular reflex system.
    • Acetylcholine appears to function as an excitatory neurotransmitter.
    • GABA is thought to be inhibitory.
  • Three other neurotransmitters work centrally.
    • Dopamine may accelerate vestibular compensation.
    • Norepinephrine regulates the strength of central responses to vestibular stimulation and mediates compensation.
    • Histamine is only present centrally and its role is unclear. Centrally acting antihistamines are noted to regulate the symptoms of motion sickness and acute vertigo.^[4].
  • 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^[5].
  • GABA inhibits central emesis reflexes.
  • Serotonin is involved in central and peripheral control of emesis but has little influence on vertigo and motion sickness.

Vertigo as a symptom has no genetic origin. However, some diseases associated with vertigo can have genetic factors involved:

• Otosclerosis^[6]
• Familial Ménière’s disease
• Familial episodic ataxia
• Vestibular migraine
• Bilateral vestibular hypofunction

Conditions associated with vertigo include:^[7]

• Vestibular neuritis
• HSV oticus
• Meniere disease,
• Labyrinthine concussion
• perilymphatic fistula
• Semicircular canal dehiscence syndrome
• vestibular paroxysmia
• Cogan syndrome
• Vestibular schwannoma
• Otitis media
• Aminoglycoside toxicity
• Recurrent vestibulopathy
• Vestibular migraine
• Epileptic vertigo
• Multiple sclerosis
• brain tumors
• Cerebellar infarction/hemorrhage
• Brainstem ischemia
• chiari malformation
• Parkinson.

There are no gross pathology findings associated with vertigo.

There are no microscopic histopathological characteristic findings associated with vertigo.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Common causes of vertigo may include Ménière’s disease, benign paroxysmal positional vertigo, labyrinthitis, vestibular neuritis. Less common causes of vertigo may include mood disorder, anxiety, and migraine. Life-threatening causes include brainstem ischemia/hemorrhage, hypertension crisis, drug overdose, cyanide poisoning.

• Common causes of vertigo may include:

Peripheral Vertigo Causes[1]
Ménière’s disease	Increased endolymph volume in semicircular canals. Recurrent vertigo, aural fullness, hearing loss and tinnitus
Acoustic neuroma	tinnitus, ear pain, aural fullness, headache, facial weakness.
Benign paroxysmal positional vertigo	Dislodged otoliths stimulate vestibular sense organ. Recurrent vertigo, nausea, vomiting, torsional nystagmus
Acute labyrinthitis	Inflammation of labyrinth/ viral or bacterial. Temporary hearing loss, vertigo, off balance, tinnitus
Acute vestibular neuritis	Inflammation of vestibular nerve caused by viral infection. Vertigo, hearing intact
Herpes Zoster Oticus	Ear pain, facial palsy, hearing loss, tinnitus vertigo herpetic eruptions of the auricle and/or external auditory canal.
Cholesteatoma	Cyst/sac of keratin debris in middle ear. Fullness/pressure in the ear, vertigo, hearing loss, pain
Otosclerosis	Abnormal bone growth in the middle ear. Vertigo, tinnitus and, sensorineural hearing loss
Central Vertigo Causes[2]
Brainstem Stroke	Vertigo, imbalance, double vision, slurred speech, and altered consciousness.
Vestibular Migraine	Mostly unilateral severe throbbing headache, vertigo lasting minutes to hours, sensitivity to motion/light/smell/noise, nausea, vomiting, imbalance.
Multiple Sclerosis	Vertigo may accompany other symptoms like vision problem, fatigue, numbness/tingling, limited mobility, bladder/bowel/speech/swallowing impairment.
Cerebellopontine angle tumors	Meningioma or schwannoma in cerebellopontine angle can cause vertigo due to pressure on vestibular nerve.
Lateral medullary syndrome	Results from ischemia in the lateral part of the brainstem(medulla oblongata). Associated with ataxia, nystagmus, vertigo, dysphagia, dysarthria.
Chiari malformation	Extension of brainstem into spinal canal. Associated with numbness/tingling of hands and feet, dysphagia, vertigo, unsteady gait, hoarseness.
Other Causes
Medication induced	Aminoglycosides, anticonvulsants(phenytoin), anti-depressants(tricyclic antidepressants, monoamine oxidase), antihypertensives, diuretics (furosemide), barbiturates, cocaine, nitroglycerin, salicylates
Psychogenic	Mood, anxiety, or alcohol abuse disorders

• Mood disorder^[3][4]
• Anxiety
• Migraine

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Many disease cause vertigo as a symptom, following diseases must be investigated as a differential diagnosis for vertigo symptom: Vestibular neuritis, HSV oticus, Meniere disease, labyrinrhine concussion, perilymphatic fistula, semicircular canal dehiscence syndrome, vestibular paroxysmia, Cogan syndrome, vestibular schwannoma, otitis media, aminoglycoside toxicity, recurrent vestibulopathy, vestibular migraine, epileptic vertigo, multiple sclerosis, brain tumors, cerebellar infarction/hemorrhage, brain stem ischemia, chiari malformation, and Parkinson.

Many disease cause vertigo as a symptom, following diseases must be investigated as a differential diagnosis for vertigo symptom: Vestibular neuritis, HSV oticus, Meniere disease, labyrinrhine concussion, perilymphatic fistula, semicircular canal dehiscence syndrome, vestibular paroxysmia, Cogan syndrome, vestibular schwannoma, otitis media, aminoglycoside toxicity, recurrent vestibulopathy, vestibular migraine, epileptic vertigo, multiple sclerosis, brain tumors, cerebellar infarction/hemorrhage, brain stem ischemia, chiari malformation, and Parkinson.^[1]

Diseases	Clinical manifestations					Para-clinical findings		Gold standard	Additional findings
	Symptoms				Physical examination
						Lab Findings	Imaging
	Acute onset	Recurrency	Nystagmus	Hearing problems
Peripheral
BPPV [2][3][4]	+	+	+/−	−	+ Dix-Hallpike maneuver	−	−	Dix-Hallpike maneuver	May be associated with nausea, vomiting, and gait instability
Vestibular neuritis [5]	+	+/−	+ /− (unilateral)	−	+ Head thrust test	−	−	History/ Physical exam	May be associated with nausea, vomiting, gait instability and previous upper respiratory infection
HSV oticus [6][7][8][9]	+	+/−	−	+/−	Taste loss in the front two-thirds of the tongue Acute facial nerve paralysis Vesicles in the ear canal, the tongue, and/or hard palate	+ VZV antibody titres	In MRI with gadolinium dye we may have enhancement of the facial nerve and cranial nerve VIII	History/ Physical exam	May be associated with otalgia, dry mouth, and dry eyes
Meniere disease [10][11]	+/−	+	+/−	+ (Progressive)	Sensorineural hearing loss	−	In CT scan we may see small or invisible vestibular aqueduct	History/ Physical exam/ Rulling out other diagnoses	May be associated with nausea, vomiting, and tinnitus
Labyrinthine concussion [12][13]	+	−	−	+	high frequency hearing loss	−	We may see other evidences of head trauma or temporal bone fracture	History/ Physical exam	It happens following blunt head trauma May be associated with dizziness or tinnitus
Perilymphatic fistula [14][15][16]	+/−	+	−	+	Tullio phenomenon	−	CT scan may show fluid around the round window recess	History/ Physical exam/Imaging	Can be a complication of a stapedectomy, head injury, or heavy lifting It may be provoked by sneezing, lifting, straining, coughing, and loud sounds
Semicircular canal dehiscence syndrome [17][18]	+/−	+	−	+ (air-bone gaps on audiometry)	Tullio phenomenon	−	CT scan may show defect in the arcuate eminence of the superior semicircular canal	History/ Physical exam/Imaging	It may be provoked by Valsalva maneuver, coughing, and sneezing
Vestibular paroxysmia [19][20][21]	+	+	+/− (Induced by hyperventilation)	−	Impaired caloric testing	−	We may see evidence of vestibulocochlear nerve compression on MRI	History/ Physical exam/Imaging	It may be provoked by head turn or other action They respond well to treatment with carbamazepine or oxcarbazepine
Cogan syndrome [22][23][24]	−	+	+/−	+	Interstitial keratitis Oscillopsia Absent vestibular function on caloric test Systemic vasculitis (Aortitis)	Increased ESR and cryoglobulins	In CT scan we may see calcification or soft tissue attenuation obliterating the intralabyrinthine fluid spaces	History/ Physical exam	It may cause Ménière-like attacks
Vestibular schwannoma [25][26]	−	+	+/−	+	Sensorineural hearing loss + Rinne test Lateralization of Weber test to the normal ear	−	In CT scan we may see erosion, and widening of the internal acoustic meatus Hypointense mass on T1-weighted MRI, and hyperintense mass on T2-weighted MRI	Imaging	Gadolinium-enhanced MRI scan is definitive diagnostic test of acoutic neuroma
Otitis media [27][28]	+	−	−	+/−	Fever Presence of effusion in the middle ear	Increased acute phase reactants	Opacification of the middle ear	History/ Physical exam	Patient may show other signs and symptoms of upper respiratory infection such az cough, nasal discharge, and fever
Aminoglycoside toxicity [29]	+	−	−	+	Oscillopsia	−	−	History/ Physical exam	May be associated with nausea, vomiting, and ataxia It may be irreversible Gentamicin is the most common one
Recurrent vestibulopathy [30][31]	+	−	−	−	−	−	−	History/ Physical exam	The underlying pathophysiology is unknown It may happen infrequently, every one to two years It may be associated with nausea and vomiting It may overlap with vestibular migraine
Central
Vestibular migrain [32][33]	–	+	+/−	+/−	History of migraine headaches	−	They may have white-matter hyperintensities (WMHs) on MRI	ICHD-3 criteria	It may be associated with anxiety and depression
Epileptic vertigo [34]	−	+	+/−	−	They may experience loss of consciousness and motor/sensory problems	−	−	EEG	They response well to anti-seizure drugs
Multiple sclerosis [35][36][37]	−	+	+/−	−	Lhermitte’s sign Spasticity Increased reflexes Internuclear ophthalmoplegia Optic neuritis Gait disturbance	Elevated concentration of CSF oligoclonal bands	Brain atrophy and some contrast enhancing plaques on CT scan Cerebral plaques disseminating in space and time on MRI	History and physical examination Imaging CSF analysis	MS is at least two times more common among women than men The onset of symptoms is mostly between the age of fifteen to forty years, rarely before age fifteen or after age sixty
Brain tumors [38]	+/−	+	+	+	Papilledema Focal neurological deficits	Cerebral spinal fluid (CSF) may show cancerous cells	On CT scan most of the brain tumors appears as a hypodense mass lesions On MRI most of the brain tumors appears as a hypointense or isointense on T1-weighted scans, or hyperintense on T2-weighted MRI.	Imaging Biopsy	Patieny may experience headache, seizures, visual changes and changes in personality, mood and concentration
Cerebellar infarction/hemorrhage	+	−	++/−	−	Limb ataxia Gait disturbance Dysarthria	−	Based on the time interval between stroke and imaging we may have different presentations	Imaging	Posterior inferior cerebellar artery is the most common artery that causes vertigo
Brain stem ischemia	+	−	+/−	−	Contralateral body weakness Visual field deficits Oculomotor abnormalities Bulbar findings	−	Based on the time interval between stroke and imaging we may have different presentations For more information click here	Imaging	It may be associated with subclavian steal syndrome
Chiari malformation [39][40]	−	+	+	−	Tachycardia Pupillary dilatation Impaired gag reflex Impaired coordination	−	In CT scan we may see hydrocephalus, herniated cerebellar tonsils, and a flattened spinal cord In MRI we may see cerebellar tonsillar herniation, wedge shaped tonsils, syringohydromyelia, small posterior fossa, obstructive hydrocephalus, and brainstem anomalies	Imaging	Patient may experience ringing in the ears
Parkinson [41][42][43]	−	+	−	−	Hypomimia Cogwheel rigidity Resting tremor Gait problems Bradykinesia	−	On brain CT scan, Parkinson disease is characterized by cortical and subcortical atrophy MRI findings in Parkinson disease are reduction in T2 relaxation time and reduced iron content in putamen and GPe	History and physical examination	Patients may present with slowness of movement (bradykinesia), shaking hands while they are at rest (resting tremor) and muscle stiffness (rigidity).

ABBREVIATIONS

VZV= Varicella zoster virus, MRI= Magnetic resonance imaging, ESR= Erythrocyte sedimentation rate, EEG= Electroencephalogram, CSF= Cerebrospinal fluid, GPe= Globus pallidus externa, ICHD= International Classification of Headache Disorders

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Among the patient who presents with dizziness in the primary care setting, fifty-four percent have vertigo upon investigation. Benign paroxysmal positional vertigo, acute vestibular neuronitis, or Ménière’s disease account for ninety-three percent of patients diagnosed with true vertigo in primary care setting. Eighty-percent of patients noticed that vertigo impacted their employment status and increased the need for medical attention. Annual incidence of vertigo is 1.4%. With age prevalence increases. One-year prevalence of vertigo is 5%. Women are two to three times more susceptible than men.

• Annual incidence of vertigo is 1.4%.^[1]
• Among the patient who presents with dizziness in the primary care setting, fifty-four percent have vertigo upon investigation.^[2]
• Benign paroxysmal positional vertigo, acute vestibular neuronitis, or Ménière’s disease account for ninety-three percent of patients diagnosed with true vertigo in primary care setting.^[3]
• Eighty-percent of patients noticed that vertigo impacted their employment status and increased the need for medical attention.

• One-year prevalence of vertigo is 5%.^[1]

• With age prevalence increases.

• Women are two to three times more susceptible than men.^[4]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Common risk factors in the development of vertigo include: Immunosuppression can provoke Herpes zoster oticus, upper respiratory viral illness can lead to acute vestibular neuritis, drug-induced vertigo: Dose reduction or discontinuation of the medication in patients presenting with vertigo may decrease the future incidence, head injury can trigger epileptic vertigo, changes in head position can provoke vertigo in acute labyrinthitis, benign positional paroxysmal vertigo, cerebellopontine angle tumor, multiple sclerosis, perilymphatic fistula, perilymphatic fistula can be triggered by loud noises, changes in ear pressure, excessive straining, head trauma.

• Common risk factors in the development of vertigo include:^[1][2][3]
  • Immunosuppression can provoke Herpes zoster oticus.
  • Upper respiratory viral illness can lead to acute vestibular neuritis.
  • Drug-induced vertigo: Dose reduction or discontinuation of the medication in patients presenting with vertigo may decrease the future incidence.
  • Head injury can trigger epileptic vertigo.
  • Changes in head position can provoke vertigo in acute labyrinthitis, benign positional paroxysmal vertigo, cerebellopontine angle tumor, multiple sclerosis, perilymphatic fistula.
  • Perilymphatic fistula can be triggered by loud noises, changes in ear pressure, excessive straining, head trauma.

• Less common risk factors in the development of vertigo include:
  • Recognized triggers including altered sleep patterns, chocolate, red wine, ripened/aged cheese, can provoke vestibular migraine.
  • Increased stress can cause psychological vertigo.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

There is insufficient evidence to recommend routine screening for vertigo.

There is insufficient evidence to recommend routine screening for vertigo.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

If left untreated vertigo can affect quality of life and could a symptom of a more serious underlying cause. Common complications include mood instability, falls. Prognosis depends upon the etiology.

• If left untreated persistent or permanent vertigo can lead to depression, falls, dependency, decreased physical activity, social and work limitations.^[1]
• It can be detrimental if the symptom is not evaluated for an underlying cause as some causes of vertigo can be fatal: brainstem stroke, cerebellopontine angle tumor, hypertensive crisis, drug overdose, cerebellar hemorrhage.

• Complications include:
  • Anxiety
  • Depression
  • Difficulty performing daily tasks
  • Diminished quality of life
  • Impaired balance and coordination
  • Falls

• Prognosis of vertigo depends upon treating the underlying cause. However, vertigo due to a tumor has a poor prognosis compared to other causes of vertigo.

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