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{{Vertigo}}
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==Overview==
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.


==Classification==
==Classification==
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====Lasting Seconds====
====Lasting Seconds====
* Benign paroxysmal positional vertigo (BPPV):  usually lasts < 1 minute
* Benign paroxysmal positional vertigo (BPPV):  usually lasts < 1 minute
===Alternative Anatomic ClassificationCentral vs. Peripheral===
 
===Classification Based Upon Location of Dysfunction===
===Central vs. Peripheral===
====Central (20%):====
====Central (20%):====
Vertigo that arises from injury to the balance centers of the [[central nervous system]] (CNS), often from a lesion in the [[brainstem]] or [[cerebellum]] and is generally associated with less prominent movement illusion and [[nausea]] than vertigo of peripheral origin.<ref name="Dieterich (2007)">{{cite journal|last=Dieterich|first=Marianne|title=Central vestibular disorders|journal=Journal of Neurology|year=2007|volume=254|pages=559–568|doi=10.1007/s00415-006-0340-7|url=http://www.springerlink.com/content/x62437220t306gr6/}}</ref>  Central vertigo has accompanying [[neurological deficit|neurologic deficits]] (such as [[slurred speech]] and [[diplopia|double vision]]), and [[pathologic nystagmus]] (which is pure vertical/torsional).<ref name="Karatas (2008)" /><ref name="Dieterich (2007)" /> Central pathology can cause [[Equilibrioception|disequilibrium]] which is the sensation of being off-balance. The [[balance disorder]] associated with central lesions causing vertigo are often so severe that many patients are unable to stand or walk.<ref name="Karatas (2008)" />
A number of conditions that involve the [[central nervous system]] may lead to vertigo including:  lesions caused by [[infarction]]s or [[hemorrhagic stroke|hemorrhage]], [[brain tumor|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|migraine headaches]], [[lateral medullary syndrome]], [[Chiari malformation]],[[multiple sclerosis]], [[parkinsonism]], as well as cerebral dysfunction.<ref name="Karatas (2008)" /> Central vertigo may not improve or may do so more slowly than vertigo caused by disturbance to peripheral structures.<ref name="Karatas (2008)" />
* Caused by damage to vestibular structures in brainstem or cerebellum
* Caused by damage to vestibular structures in brainstem or cerebellum
* Associated with other brainstem deficits
* Associated with other brainstem deficits
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# Sedatives, anticonvulsants may cause central vertigo in high/excess doses
# Sedatives, anticonvulsants may cause central vertigo in high/excess doses
# Anticonvulsants in prescription doses may cause nystagmus (phenytoin, carbamazepine)
# Anticonvulsants in prescription doses may cause nystagmus (phenytoin, carbamazepine)
====Peripheral (80%):====
====Peripheral (80%):====
Vertigo caused by problems with the [[inner ear]] or [[vestibular system]], which is composed of the [[semicircular canal]]s, the [[vestibule of the ear|vestibule]] ([[utricle (ear)|utricle]] and [[saccule]]), and the [[vestibular nerve]] is called "peripheral", "otologic" or "vestibular" vertigo.<ref name="Karatas (2008)">{{cite journal|last=Karatas|first=M|title=Central Vertigo and Dizziness|journal=The Neurologist|year=2008|volume=14|issue=6|pages=355–364|pmid=19008741|doi=10.1097/NRL.0b013e31817533a3|url=http://www.ncbi.nlm.nih.gov/pubmed/19008741}}</ref> The most common cause is benign paroxysmal positional vertigo ([[BPPV]]), which accounts for 32% of all peripheral vertigo.<ref name="Karatas (2008)" /> Other causes include [[Ménière's disease]] (12%), [[superior canal dehiscence syndrome]], [[labyrinthitis]] and visual vertigo.<ref name="Karatas (2008)" /><ref>{{cite journal|title=Visual vertigo: symptom assessment, spatial orientation and postural control|journal=Brain|volume=124|issue=8|pages=1646&ndash;1656|year=2001|url=http://brain.oxfordjournals.org/cgi/content/full/124/8/1646|doi=10.1093/brain/124.8.1646|last1=Guerraz|first1=M.|pmid=11459755}}</ref>  Any cause of inflammation such as [[common cold]], [[influenza]], and bacterial infections may cause transient vertigo if it involves the inner ear, as may chemical insults (e.g., [[aminoglycoside]]s)<ref name="aminoglycoside">{{cite journal|last1=Xie|first1=J|last2=Talaska|first2=AE|last3=Schacht|first3=J|title=New developments in aminoglycoside therapy and ototoxicity.|journal=Hearing research |year=2011|volume=281|issue=1-2|pages=28–37|pmid=21640178|doi=10.1016/j.heares.2011.05.008|pmc=3169717}}</ref> or physical trauma (e.g., skull fractures).  [[Motion sickness]] is sometimes classified as a cause of peripheral vertigo.
Patients with peripheral vertigo typically present with mild to moderate [[balance disorder|imbalance]], [[nausea]], [[vomiting]], [[deafness|hearing loss]], [[tinnitus]], fullness, and pain in the ear.<ref name="Karatas (2008)" /> In addition, lesions of the internal auditory canal may be associated with ipsilateral facial weakness.<ref name="Karatas (2008)" /> 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).<ref name="Karatas (2008)" />
* Caused by damage to vestibular labyrinth, vestibular nerve
* Caused by damage to vestibular labyrinth, vestibular nerve
* Associated tinnitus, hearing loss if auditory component of CN VIII affected
* Associated tinnitus, hearing loss if auditory component of CN VIII affected
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# Viral involvement of cochlea and labyrinth after upper respiratory infection (URI)
# Viral involvement of cochlea and labyrinth after upper respiratory infection (URI)
# Vertigo associated with tinnitus and hearing loss
# Vertigo associated with tinnitus and hearing loss
# symtpoms resolve completely within 3-6 weeks
# Symtpoms resolve completely within 3-6 weeks
* Meniere’s disease
* Meniere’s disease
# Idiopathic endolymphatic hydrops -> damage to hair cells
# Idiopathic endolymphatic hydrops -> damage to hair cells
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* Ototoxins: hearing impairment usually >> vestibular symptoms
* Ototoxins: hearing impairment usually >> vestibular symptoms
# Gentamicin, streptamicin most injurious to vestibular portion of CN VIII
# Gentamicin, streptamicin most injurious to vestibular portion of CN VIII
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
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[[Category:Signs and symptoms]]
[[Category:Signs and symptoms]]
[[Category:Primary care]]
[[Category:Primary care]]
[[Category:Needs overview]]


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Revision as of 14:53, 31 May 2013

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

Overview

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.

Classification

Distinguish Cause of Vertigo Based on:

  1. Time course
  2. Duration
  3. Recurrence

Lasting a Day or Longer

  • Vestibular neuronitis
  1. Onset over hours, peaks in first day, improves within days
  2. May recur episodically for weeks to months
  • Vertebrobasilar ischemia with labyrinth infarct
  1. Abrupt onset, improves within 1 week
  2. 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

Classification Based Upon Location of Dysfunction

Central vs. Peripheral

Central (20%):

Vertigo that arises from injury to the balance centers of the central nervous system (CNS), often from a lesion in the brainstem or cerebellum and is generally associated with less prominent movement illusion and nausea than vertigo of peripheral origin.[1] Central vertigo has accompanying neurologic deficits (such as slurred speech and double vision), and pathologic nystagmus (which is pure vertical/torsional).[2][1] Central pathology can cause disequilibrium which is the sensation of being off-balance. The balance disorder associated with central lesions causing vertigo are often so severe that many patients are unable to stand or walk.[2]

A number of conditions that involve the central nervous system may 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.[2] Central vertigo may not improve or may do so more slowly than vertigo caused by disturbance to peripheral structures.[2]


  • 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:
  1. Accounts for ½ of central causes
  2. Brainstem or cerebellar territory (anterior inferior cerebellar artery (AICA), posterior inferior cerebellar artery (PICA)) -> transient ischemic #ttack (TIA) or cerebrovascular accident (CVA)
  3. Associated diplopia, dysarthria, dysphagia, hemiparesis, etc.
  4. Cerebellar infarct may present with isolated vertigo
  5. Can have pontine lacunes, labyrinthine infarcts
  • Multiple sclerosis: associated brainstem symptoms may be subtle (facial numbness)
  1. Vertiginous symptoms may be sudden, transient, recurrent or persistent
  • Migraine: vertigo precedes headache and may last afterward
  1. Atypical form of migraine with aura -> may respond to migraine therapy
  • Drugs
  1. Sedatives, anticonvulsants may cause central vertigo in high/excess doses
  2. Anticonvulsants in prescription doses may cause nystagmus (phenytoin, carbamazepine)

Peripheral (80%):

Vertigo 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.[2] The most common cause is benign paroxysmal positional vertigo (BPPV), which accounts for 32% of all peripheral vertigo.[2] Other causes include Ménière's disease (12%), superior canal dehiscence syndrome, labyrinthitis and visual vertigo.[2][3] Any cause of inflammation such as common cold, influenza, and bacterial infections may cause transient vertigo if it involves the inner ear, as may chemical insults (e.g., aminoglycosides)[4] or physical trauma (e.g., skull fractures). Motion sickness is sometimes classified as a cause of peripheral vertigo.

Patients with peripheral vertigo typically present with mild to moderate imbalance, nausea, vomiting, hearing loss, tinnitus, fullness, and pain in the ear.[2] In addition, lesions of the internal auditory canal may be associated with ipsilateral facial weakness.[2] 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).[2]

  • 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
  1. Accounts for more than ½ of cases peripheral vestibular dysfunction
  2. Common in the elderly (patients usually > 60)
  3. Episodes of sudden onset, short duration -> condition often remits in 6 months
  4. Mechanism = stimulation of labyrinth by debris in posterior semicircular canal
  • Vestibular neuronitis
  1. Accounts for ¼ of cases peripheral vestibular dysfunction
  2. Isolated vertigo due to viral infection involving labyrinth (after URI)
  • Acute labyrinthitis
  1. Viral involvement of cochlea and labyrinth after upper respiratory infection (URI)
  2. Vertigo associated with tinnitus and hearing loss
  3. Symtpoms resolve completely within 3-6 weeks
  • Meniere’s disease
  1. Idiopathic endolymphatic hydrops -> damage to hair cells
  2. Tinnitus, ear pressure and hearing loss associated with vertigo
  3. Paroxysmal episodes lasting minutes to hours
  4. Frequency of episodes waxes and wanes over time
  5. Hearing loss can become permanent
  • Acoustic neuroma
  1. Benign tumor, but can cause brainstem compression if unprescribed
  2. Retrocochlear hearing loss, tinnitus, vague dizziness
  3. Very gradual symptom onset with progressive asymmetric hearing loss
  4. Vertigo not prominent because gradual time course allows central nervous system adaptation
  • Ototoxins: hearing impairment usually >> vestibular symptoms
  1. Gentamicin, streptamicin most injurious to vestibular portion of CN VIII

References

  1. 1.0 1.1 Dieterich, Marianne (2007). "Central vestibular disorders". Journal of Neurology. 254: 559–568. doi:10.1007/s00415-006-0340-7.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Karatas, M (2008). "Central Vertigo and Dizziness". The Neurologist. 14 (6): 355–364. doi:10.1097/NRL.0b013e31817533a3. PMID 19008741.
  3. Guerraz, M. (2001). "Visual vertigo: symptom assessment, spatial orientation and postural control". Brain. 124 (8): 1646&ndash, 1656. doi:10.1093/brain/124.8.1646. PMID 11459755.
  4. Xie, J; Talaska, AE; Schacht, J (2011). "New developments in aminoglycoside therapy and ototoxicity". Hearing research. 281 (1–2): 28–37. doi:10.1016/j.heares.2011.05.008. PMC 3169717. PMID 21640178.

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