Vertigo

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Not to be confused with acrophobia, an extreme or irrational fear of heights.
This article is about the medical condition. For other uses, see Vertigo (disambiguation).
Vertigo
Optokinetic nystagmus.gif

Horizontal optokinetic nystagmus, a symptom which can accompany vertigo.
ICD-10 H81, R42
ICD-9 438.85, 780.4
DiseasesDB 29286
eMedicine article/1159385
MeSH D014717

Vertigo /ˈvɜrtɨɡoʊ/ (from the Latin vertō "a whirling or spinning movement"[1]) is a subtype of dizziness in which a patient inappropriately experiences the perception of motion (usually a spinning motion) due to dysfunction of the vestibular system.[2][3][4] It is often associated with nausea and vomiting as well as a balance disorder, causing difficulties standing or walking. There are three types of vertigo. The first is known as objective[5][6] and describes when the patient has the sensation that objects in the environment are moving; the second is known as subjective[5][6] and refers to when the patient feels as if he or she is moving, and the third is known as pseudovertigo,[7] an intensive sensation of rotation inside the patient's head. While appearing in textbooks, this classification has little to do with the pathophysiology or treatment of vertigo.

Dizziness[8] and vertigo are common medical issues, affecting approximately 20%-30% of the general population.[9][10] Vertigo may be present in patients of all ages. The prevalence of vertigo rises with age and is about two to three times higher in women than in men.[4][9] It accounts for about 2-3% of emergency department visits.[4] The main causes of vertigo are benign paroxysmal positional vertigo,[8][11][12] Ménière's disease,[8][12] vestibular neuritis,[8][12] and labyrinthitis,[12] but may also be caused by a concussion[3] or a vestibular migraine.[12] Excessive consumption of ethanol (alcoholic beverages) can also cause symptoms of vertigo. Repetitive spinning, as in familiar childhood games, can induce short-lived vertigo by disrupting the inertia of the fluid in the vestibular system; this is known as physiologic vertigo.[13]

Classification of vertigo[edit]

Vertigo is classified into either peripheral or central depending on the location of the dysfunction of the vestibular pathway,[14] although it can also be caused by psychological factors.[15]

Peripheral[edit]

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.[5][16] The most common cause is benign paroxysmal positional vertigo (BPPV), which accounts for 32% of all peripheral vertigo.[16] Other causes include Ménière's disease (12%), superior canal dehiscence syndrome, labyrinthitis and visual vertigo.[16][17] 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)[18] 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.[16] In addition, lesions of the internal auditory canal may be associated with ipsilateral facial weakness.[16] 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).[16]

Central[edit]

Vertigo that arises from injury to the balance centers of the central nervous system (CNS), often from a lesion in the brainstem or cerebellum[5][8][19] and is generally associated with less prominent movement illusion and nausea than vertigo of peripheral origin.[20] Central vertigo has accompanying neurologic deficits (such as slurred speech and double vision), and pathologic nystagmus (which is pure vertical/torsional).[16][20] 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.[16]

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,[8][14] epilepsy,[2] cervical spine disorders such as cervical spondylosis,[14] degenerative ataxia disorders,[8] migraine headaches,[8] lateral medullary syndrome, Chiari malformation,[8] multiple sclerosis,[8] parkinsonism, as well as cerebral dysfunction.[16] Central vertigo may not improve or may do so more slowly than vertigo caused by disturbance to peripheral structures.[16]

Signs and symptoms[edit]

Vertigo is a sensation of spinning while stationary.[21] It is commonly associated with nausea or vomiting,[2] unsteadiness (postural instability),[19] falls,[22] and difficulties walking.[23] Recurrent episodes in those with vertigo are common and they frequently impair the quality of life.[4] Blurred vision, difficulty speaking, a lowered level of consciousness, and hearing loss may also occur. The signs and symptoms of vertigo can present as a persistent (insidious) onset or an episodic (sudden) onset.[24]

The characteristics of persistent onset vertigo is indicated by symptoms lasting for longer than one day[24] and caused by degenerative changes that affect balance as people age. Naturally, the nerve conduction slows with aging and a decreased vibratory sensation is common.[25] Additionally, there is a degeneration of the ampulla and otolith organs with an increase in age.[26] Persistent onset is commonly paired with central vertigo signs and systems.[24]

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.[24] 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[edit]

Motion sickness is one of the biggest symptoms of vertigo and it 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 characterized 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.

Differential diagnosis[edit]

A number of specific conditions can cause vertigo. In the elderly, however, the condition is often multifactorial.[4]

Benign paroxysmal positional vertigo[edit]

Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder[9] 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.[8][12] Patients with BPPV may experience brief periods of vertigo, usually under a minute,[8] which occur with change in position.[27] It is the most common process of vertigo.[4] It occurs in 0.6% of the population yearly with 10% having an attack during their lifetime.[4] It is believed to be due to a mechanical malfunction of the inner ear.[4] BPPV may be diagnosed with the Dix-Hallpike test and can be effectively treated with repositioning movements such as the Epley maneuver.[4][11][27][28]

Vestibular migraine[edit]

Vestibular migraine is the association of vertigo and migraines and is one of the most common causes of recurrent, spontaneous episodes of vertigo.[4][9] The etiology of vestibular migraines is currently unclear;[9] however, one hypothesized cause is that the stimulation of the trigeminal nerve leads to nystagmus in individuals suffering from migraines.[12] Other suggested causes of vestibular migraines include: 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.[2] Vestibular migraines are estimated to affect 1-3% of the general population[4][12] and may affect 10% of migraine patients.[12] Additionally, vestibular migraines tend to occur more often in women than in men and rarely affect individuals after the sixth decade of life.[9]

Ménière's disease[edit]

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).[12] However, this idea has not been directly confirmed with histopathologic studies but electrophysiologic studies have been suggestive of this mechanism.[29] 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.[8][24][29] As the disease worsens, hearing loss will progress.

Vestibular neuritis[edit]

Vestibular neuritis presents with severe vertigo[4] with associated nausea, vomiting, and generalized imbalance and is believed to be caused by a viral infection of the inner ear though several theories have been put forward and the etiology remains uncertain.[8][30] Individuals with vestibular neuritis do not typically have auditory symptoms but may experience a sensation of aural fullness or tinnitus.[30] Persisting balance problems may remain in 30% of people affected.[4]

Pathophysiology[edit]

The neurochemistry of vertigo includes six primary neurotransmitters that have been identified between the three-neuron arc[31] that drives the vestibulo-ocular reflex (VOR). Glutamate maintains the resting discharge of the central vestibular neurons, and may 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 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. Dopamine, histamine, serotonin, and acetylcholine are neurotransmitters thought to produce vomiting.[8] It is known that centrally acting antihistamines modulate the symptoms of acute symptomatic vertigo.[32]

Diagnostic approach[edit]

Tests for vertigo often attempt to elicit nystagmus and to differentiate vertigo from other causes of dizziness such as presyncope, hyperventilation syndrome, disequilibrium, or psychiatric causes of lightheadedness.[12] Tests of vestibular system (balance) function include: electronystagmography (ENG),[12] Dix-Hallpike maneuver,[12] rotation tests, head-thrust test,[8] caloric reflex test,[8][33] and computerized dynamic posturography (CDP).[34] CT scans or MRIs are sometimes used by physicians when diagnosing vertigo.[2]

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.[34]

Pharmacologic treatment of vertigo[edit]

Definitive treatment depends on the underlying cause of the vertigo.[8] Ménière's disease patients have a variety of treatment options to consider when receiving treatment for vertigo and tinnitus including: a low-salt diet, intratympanic injections of the antibiotic gentamicin, a benzodiazepine such as diazepam to reduce vertigo by sedating the vestibular system,[35] or surgical measures such as a shunt or ablation of the labyrinth in refractory cases.[36] Other treatment options for vertigo may include:[37]

See also[edit]

References[edit]

  1. ^ "Definition of vertigo". Merriam-Webster Online Dictionary. Retrieved 2007-09-19. 
  2. ^ a b c d e Taylor, J; Goodkin, HP (2011). "Dizziness and vertigo in the adolescent.". Otolaryngologic clinics of North America 44 (2): 309–321. doi:10.1016/j.otc.2011.01.004. PMID 21474006. 
  3. ^ a b Scherer, MR; Schubert, MC (2009). "Traumatic brain injury and vestibular pathology as a comorbidity after blast exposure". Physical therapy 89 (9): 980–992. doi:10.2522/ptj.20080353. PMID 19628578. 
  4. ^ a b c d e f g h i j k l m Neuhauser HK, Lempert T (November 2009). "Vertigo: epidemiologic aspects". Semin Neurol 29 (5): 473–81. doi:10.1055/s-0029-1241043. PMID 19834858. 
  5. ^ a b c d U.S. National Library of Medicine (2011). "Vertigo-associated disorders". National Institutes of Health. Retrieved 2 January 2013. 
  6. ^ a b Berkow R., ed. (1992). The Merck manual of diagnostics and therapy. Rahway: Merck & Co Inc. p. 2844. 
  7. ^ Ropper, AH; Brown RH (2005). Adams and Victor’s Principles of Neurology (eighth ed.). NY, Chicago, San Francisco. p. 1398. 
  8. ^ a b c d e f g h i j k l m n o p q r Kerber, KA (2009). "Vertigo and dizziness in the emergency department". Emergency medicine clinics of North America 27 (1): 39–50. doi:10.1016/j.emc.2008.09.002. PMC 2676794. PMID 19218018. 
  9. ^ a b c d e f von Brevern, M; Neuhauser, H (2011). "Epidemiological evidence for a link between vertigo and migraine.". Journal of vestibular research: equilibrium & orientation 21 (6): 299–304. doi:10.3233/VES-2011-0423. PMID 22348934. 
  10. ^ Chu, YT; Cheng, L (2007). "[Vertigo and dizziness].". Acta Neurologica Taiwanica 16 (1): 50–60. PMID 17486734. 
  11. ^ a b Alvarenga, GA; Barbosa, MA; Porto, CC (2011). "Benign paroxysmal positional vertigo without nystagmus: diagnosis and treatment". Brazilian journal of otorhinolaryngology 77 (6): 799–804. PMID 22183288. 
  12. ^ a b c d e f g h i j k l m Post, RE; Dickerson, LM (2010). "Dizziness: a diagnostic approach". American Family Physician 82 (4): 361–369. PMID 20704166. 
  13. ^ a b Fauci, Anthony S.; Daniel L. Kasper, Dan L. Longo, Eugene Braunwald, Stephen L. Hauser, J. Larry Jameson (2008). Chapter 22. Dizziness and Vertigo Harrison's Principles of Internal Medicine (17th ed. ed.). New York: McGraw-Hill. ISBN 978-0-07-147691-1. 
  14. ^ a b c Wippold 2nd, FJ; Turski, PA (2009). "Vertigo and hearing loss.". AJNR. American journal of neuroradiology 30 (8): 1623–1625. PMID 19749077. 
  15. ^ "Chapter 14: Evaluation of the Dizzy Patient". Retrieved 2009-08-06. 
  16. ^ a b c d e f g h i j Karatas, M (2008). "Central Vertigo and Dizziness". The Neurologist 14 (6): 355–364. doi:10.1097/NRL.0b013e31817533a3. PMID 19008741. 
  17. ^ Guerraz, M. (2001). "Visual vertigo: symptom assessment, spatial orientation and postural control". Brain 124 (8): 1646–1656. doi:10.1093/brain/124.8.1646. PMID 11459755. 
  18. ^ 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. 
  19. ^ a b Jahn, K; Dieterich, M (December 2011). "Recent advances in the diagnosis and treatment of balance disorders.". Journal of neurology 258 (12): 2305–2308. doi:10.1007/s00415-011-6286-4. PMID 22037955. 
  20. ^ a b Dieterich, Marianne (2007). "Central vestibular disorders". Journal of Neurology 254: 559–568. doi:10.1007/s00415-006-0340-7. 
  21. ^ "Vertigo: Dizziness and Vertigo: Merck Manual Home Edition". 
  22. ^ Vieira, ER; Freund-Heritage, R; da Costa, BR (September 2011). "Risk factors for geriatric patient falls in rehabilitation hospital settings: a systematic review". Clinical rehabilitation 25 (9): 788–799. doi:10.1177/0269215511400639. PMID 21504956. 
  23. ^ Ricci, NA; Aratani, MC; Dona, F; Macedo, C; Caovilla, HH; Gananca, FF (2010). "A systematic review about the effects of the vestibular rehabilitation of middle-age and older adults". Revista brasileira de fisioterapia 14 (5): 361–371. PMID 21180862. 
  24. ^ a b c d e Strupp, M; Thurtell, MJ; Shaikh, AG; Brandt, T; Zee, DS; Leigh, RJ (July 2011). "Pharmacotherapy of vestibular and ocular motor disorders, including nystagmus". Journal of neurology 258 (7): 1207–1222. doi:10.1007/s00415-011-5999-8. PMID 21461686. 
  25. ^ Kaneko, A; Asai, N; Kanda, T (2005). "The influence of age on pressure perception of static and moving two-point discrimination in normal subjects". Journal of hand therapy: official journal of the American Society of Hand Therapists 18 (4): 421–424. doi:10.1197/j.jht.2005.09.010. PMID 16271689. 
  26. ^ Kutz Jr, JW (September 2010). "The dizzy patient.". The Medical clinics of North America 94 (5): 989–1002. doi:10.1016/j.mcna.2010.05.011. PMID 20736108. 
  27. ^ a b MedlinePlus (2011). "Benign positional vertigo". U.S. National Institutes of Health. Retrieved 2 January 2013. 
  28. ^ Prim-Espada, MP; De Diego-Sastre, JI; Perez-Fernandez, E (June 2010). "[Meta-analysis on the efficacy of Epley's manoeuvre in benign paroxysmal positional vertigo].". Neurologia 25 (5): 295–299. PMID 20643039. 
  29. ^ a b Semaan, MT; Megerian, CA (April 2011). "Ménière's disease: a challenging and relentless disorder.". Otolaryngologic clinics of North America 44 (2): 383–403. doi:10.1016/j.otc.2011.01.010. PMID 21474013. 
  30. ^ a b Goddard, JC; Fayad, JN (2011). "Vestibular Neuritis". Otolaryngologic Clinics of North America 44 (2): 361–365. doi:10.1016/j.otc.2011.01.007. 
  31. ^ Angelaki, DE (July 2004). "Eyes on target: what neurons must do for the vestibuloocular reflex during linear motion". Journal of neurophysiology 92 (1): 20–35. doi:10.1152/jn.00047.2004. PMID 15212435. 
  32. ^ Kuo, CH; Pang, L; Chang, R (June 2008). "Vertigo-part 2-management in general practice". Australian family physician 37 (6): 409–413. PMID 18523693. 
  33. ^ "Core Curriculum: Inner Ear Disease — Vertigo". Baylor College of Medicine. 23 January 2006. Archived from the original on 2007-06-30. Retrieved 19 September 2007. 
  34. ^ a b "Diagnosis: How are vestibular disorders diagnosed?". Vestibular Disorders Association. 2013. Retrieved 9 January 2013. 
  35. ^ Mayo Clinic Staff (2012). "Treatment and Drugs". Mayo Clinic. Retrieved 2 January 2013. 
  36. ^ Huon, LK; Fang, TY; Wang, PC (July 2012). "Outcomes of intratympanic gentamicin injection to treat Ménière's disease.". Otology & Neurotology 33 (5): 706–714. doi:10.1097/MAO.0b013e318259b3b1. PMID 22699980. 
  37. ^ Huppert, D; Strupp, M; Muckter, H; Brandt, T (March 2011). "Which medication do I need to manage dizzy patients?". Acta oto-laryngologica 131 (3): 228–241. doi:10.3109/00016489.2010.531052. PMID 21142898. 
Outer ear
Middle ear
and mastoid
Inner ear and
central pathways
Common pathway
Equilibrioception
Hearing
Hearing impairment
Excessive response
Deafblindness
Other

M: EAR

anat (e/p)/phys/devp

proc, drug (S2)
Cognition
Alteration of
consciousness
Fainting/Syncope
Other
Emotional state
Behavior
Perception/
sensation
disorder

M: PSO/PSI

dsrd (o, p, m, p, a, d, s), sysi/epon, spvo

proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D)

M: TST

–
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