Vestibular Pathologies

Original Editor - Jess Bell based on the course by Bernard Tonks
Top Contributors - Jess Bell, Kim Jackson, Lucinda hampton, Rucha Gadgil, Tarina van der Stockt and Olajumoke Ogunleye

Introduction[edit | edit source]

Vertigo is defined as the illusion of movement occurring in the environment. Acute vertigo can be caused by the following conditions:[1]

Unilateral Vestibular Lesion (UVL)[edit | edit source]

Vestibular Neuritis and Labyrinthitis[edit | edit source]

Vestibular neuritis and labyrinthitis are categorised as unilateral vestibular lesions (UVL). Other terms used include unilateral vestibular hypofunction (UVH) or unilateral vestibular dysfunction (UVD).[1] They are the second most common cause of vertigo. While there is little epidemiological data about labyrinthitis,[2] vestibular neuritis occurs in approximately 15 per 100,000 people in the US.[3]

Vestibular neuritis and labyrinthitis are believed to usually be caused by viral infections:[4]

  • In neuritis, the superior division of the eighth cranial nerve is commonly affected and hearing is preserved[5]
  • In labyrinthitis, the entire labyrinth is involved and there is hearing loss[1]

Acute versus Chronic UVL[edit | edit source]

In acute cases of UVL, symptoms include:

Physiotherapists do not often see patients in the acute stage. In chronic cases, symptoms include persistent dizziness and imbalance due to a lack of compensation.[1]

UVL Nystagmus[edit | edit source]

Vestibular neurons fire spontaneously at 100 AP/sec (i.e action potentials per second). A loss of input from one side and relative excitation of the intact side causes a mixed horizontal and torsional nystagmus.[1] The direction of nystagmus is labelled according to the quick phase:[1]

  • A right-sided lesion causes left beating and left torsional nystagmus

There is a torsional component to the nystagmus because the superior division of the nerve (which innervates the horizontal and anterior canals) is affected.[1]

Acute Symptoms or Vestibular Crisis[edit | edit source]

The acute stage, which usually lasts 2 to 3 days, is characterised by intense vertigo and nausea due to unequal vestibular input and disequilibrium. After a few days, acute symptoms resolve, but the patient is left with a dynamic deficit - i.e. dizziness and disequilibrium with rapid head movements. Vestibular rehabilitation plays an important role in the recovery of these dynamic deficits.[1]

Recovery[edit | edit source]

Spontaneous Recovery[edit | edit source]

Depending on the animal affected, symptoms from UVLs at rest (i.e. static symptoms / deficits) can normalise either partially or completely within the first week post-lesion due to vestibular compensation.[6] Nystagmus, skew-eye deviation and marked postural asymmetry recover spontaneously within 3 to 14 days. This recovery of function is due to the restoration of the tonic resting firing rates of the vestibular nuclei. This is achieved through the influence of the cerebellum and neurochemical changes at the level of the vestibular nuclei.[1]

Cellular Recovery[edit | edit source]

When there has been aminoglycoside (eg streptomycin and neomycin[7]) toxicity, it has been found that cellular recovery is possible for non-primate mammals (e.g. rodents[8]). It is not known if this recovery can occur in humans, but there is no evidence that regeneration of vestibular neurons occurs in primates.[1]

NB aminoglycosides are powerful broad-spectrum antibiotics that can adversely affect the kidney (nephrotoxicity), vestibular and auditory organs (ototoxicity), and the neuromuscular junction.[9]

Summary of UVL[edit | edit source]

  • Frequently caused by neuritis or labyrinthitis:
    • Neuritis – hearing is unaffected, vestibular impairment
    • Labyrinthitis – some loss of hearing, vestibular impairment
  • There is some evidence that corticosteroids can be helpful in the acute stage if they are given within 72 hours[10]
  • Recurrence is not common
  • Physiotherapists typically only see patients in the chronic phase - at this stage patients are generally functioning fairly well unless they move their heads too quickly
  • Patients in the chronic phase usually present with problems in one or more of the following domains:[1]
    • Gaze stability issues
    • Motion sensitivity
    • Compromised balance and postural control

Bilateral Vestibular Lesions (BVL)[edit | edit source]

BVLs are symmetrical and they are often due to ototoxicity, commonly related to aminoglycoside (gentamicin or streptomycin) use (see above).[11]

  • In high doses, these antibiotics consistently destroy the hair cells of the inner ear[1][12]
  • In normal doses, it has been found that ototoxicity occurs spontaneously in 3 percent of the population[1]

The following video provides more information on these antibiotics.


Unlike in UVLs, vertigo occurs infrequently in these patients because the acute vestibular loss is bilateral and symmetrical. Patients with BVLs primarily report:[1][14]

  • Balance problems during standing or walking
  • Oscillopsia (a visual disturbance in which objects appear to oscillate[15])
  • Disequilibrium and dizziness
  • Physical deconditioning

Age-Related Vestibular Changes[edit | edit source]

In individuals aged over 75 years, there is, on average, a 35 percent decrease in the vestibular system’s ability to encode faster head movements. This is why older adults have more difficulty moving quickly and tend to slow down their head movements. Older individuals can, therefore, be thought of as asymmetrical BVL patients.[1]

Perilymphatic Fistula[edit | edit source]

A perilymphatic fistula is a tear or defect in a membrane between the fluid-filled inner ear and middle ear. This causes pressure changes from the environment accessing the vestibular system and perilymphatic fluid might flow between the two compartments.[1][16] Causes of perilymphatic fistula include:[1][16][17]

  • Head trauma (most common)
  • Barotrauma (scuba diving, explosions)
  • Vigorous straining
  • Tumour in the middle ear
  • Chronic severe ear infections

Patients present with:[1][16]

  • Ringing or fullness in the ears, vertigo, imbalance and hearing loss
  • Tullio phenomenon - i.e. symptoms evoked by an auditory stimulus
  • Symptoms may increase with changes in altitude or air pressure (weather), exertion and activity

The diagnosis of perilymphatic fistula is controversial due to a lack of diagnostic tests. Medical management includes: bed rest, mild sedation and avoiding activities that could increase inner ear pressure. In severe cases, surgical grafting may be required.[1][17]

Meniere’s Disease and Endolymphatic Hydrops[edit | edit source]

Meniere’s disease or primary hydrops is a disorder of the inner ear that causes recurrent attacks of self limiting vertigo. Other associated symptoms are:[18]

  • Unilateral, fluctuating, low frequency sensorineural hearing loss
  • A sense of ear “fullness”
  • Tinnitus

While various theories have been proposed to explain its pathophysiology, Meniere’s disease is idiopathic - i.e. it has no known cause.[19][20]  It is believed that it may be due to the malabsorption of endolymph in the endolymphatic sac or duct, which causes pressure fluctuations in the inner ear.[1]

Secondary hydrops is related to a specific event or condition such as head trauma, infection, degeneration or tumour.[20]

Patients present with the following symptoms:[1][20]

  • Ear fullness, tinnitus, fluctuating hearing loss, vertigo and imbalance
  • In time, low-frequency sensorineural hearing loss develops
  • Vestibular function is episodic and the system may return to normal between episodes
  • Can last hours to a few days


Treatment[edit | edit source]

  • Dietary: decrease salt, alcohol, nicotine, and caffeine intake[1][22]
    • This may minimise any secondary fluctuations in the endolymph of the inner ear, and accordingly may reduce a patient’s dizzy spells
  • Vestibular rehabilitation (VR) does not appear to help, unless there is permanent loss of vestibular function in the later stages of the disease. However, more recently, some therapists are providing VR exercise-based treatment in an attempt to improve the final outcomes. While there is no research currently to support this, there is no harm in trying.[1]

Other Pathologies[edit | edit source]

Trauma (Labyrinthine Concussion)[edit | edit source]

A common cause of vestibular dysfunction in a younger population. It is usually caused by direct trauma to the vestibular system, but can also occur with abrupt changes in the head position not associated with impact.[1][23][24]

Acoustic Neuroma[edit | edit source]

Patients with acoustic neuroma most likely experience unilateral hearing loss or tinnitus.[25] A vague feeling of swaying or tilting is commonly the only manifestation of vestibular dysfunction.[1]

Ramsay Hunt Syndrome[edit | edit source]

Ramsay Hunt syndrome is usually caused by an activation of a latent herpes zoster infection in the lateral geniculate. In addition to vestibular symptoms, it often also causes facial paralysis.[1][26]

Otitis Media[edit | edit source]

 An inflammation of the middle ear and the tympanic membrane, which may be associated with vestibular symptoms in severe cases or when there are repeated infections.[1]

Superior Canal Dehiscence Syndrome[edit | edit source]

A condition where the bone overlying the superior aspect of the anterior canal is thin or absent. It can also affect the posterior canal. It can cause hearing and balance issues.[1]

Concussion / Mild Traumatic Brain Injury (mTBI)[edit | edit source]

Vestibular and ocular symptoms are common in patients who experience mTBI patients.[1][27] [28] These symptoms are typically caused by a combination of both central and peripheral conditions.[1] For some patients, symptoms associated with acute mTBI might resolve within days. However, for other patients, symptoms might persist for months post-injury, potentially lasting for more than a year - i.e. post-concussion syndrome (PCS).[29]

The National Collegiate Athletic Association Injury Surveillance System database (mTBI) found the following audio-vestibular symptoms in athletes: [30]

  • Dizziness (68 percent)
  • Balance problems (34 percent)
  • Noise sensitivity (29 percent)
  • Tinnitus (9 percent)

Marcus and colleagues screened major trauma ward admissions for adults and found that 87 percent of patients had subjective dizziness (i.e. the illusion of self-motion) and / or objective imbalance. Specific diagnoses given for this dizziness included:[31]

  • BPPV (38 percent)
  • Acute peripheral unilateral vestibular loss (19 percent)
  • Migraine phenotype headache (34 percent)

These symptoms are also common in children:

  • Ellis and colleagues found that 29 percent of children had visual and ocular symptoms acutely.  Of the children who developed chronic concussive symptoms, 63 percent had visual and ocular symptoms[32]
  • Master and colleagues found that 46 percent of children had more than one visual deficit after mTBI[33]
  • Reimer and colleagues found that of 115 paediatric patients with sports related concussion, 12 children (10.4%) were diagnosed with BPPV[34]


Vestibular dysfunction should, therefore, be considered in patients who, immediately after concussion, have dizziness and unsteadiness that gradually improves during the first few weeks post-injury.

NB patients may report that these symptoms are provoked by rapid head movements and that blurred vision also occurs during these movements - this suggests that the function of the vestibulo-ocular reflex (VOR) is altered.[1]

Assessment of the Vestibular System[edit | edit source]

For patients with vestibular symptoms, a vestibular assessment should include:[1]

  • Subjective history
  • VOR function
  • Static and dynamic balance / postural control
  • Assessment of nystagmus with and without fixation
  • Positional testing for BPPV (BPPV may occur in approximately 5 to 10 percent  of cases of persistent dizziness following concussion)[1]
  • Motion sensitivity
  • Cervical spine assessment
  • Screen of the vision system
  • Oculomotor control
  • Effects of visual motion
  • Pressure sensitivity
  • Infrared camera systems

Vestibular Rehabilitation[edit | edit source]

Vestibular rehabilitation (VR) may be of benefit for individuals with peripheral vestibular disorders (including BPPV), stable central vestibular disorders,[3][36] concussion[37][38] and post-concussion syndrome.[39][40]

Vestibular rehabilitation usually includes canalith repositioning manoeuvres (for BPPV) and individually targeted exercises aimed at facilitating sensorimotor compensation (including adaptation, habituation, substitution and standing and dynamic balance exercises).[38]

Evidence for Vestibular Rehabilitation for Post Concussion Syndrome (PCS)[edit | edit source]

More evidence is emerging to support the use of VR in patients who have PCS,[41] particularly interventions that include psychological, cervical and vestibular rehabilitation.[42]

  • A retrospective study by Alsalaheen and colleagues looked at 114 patients referred for VR after concussion.[38] Patients most commonly reported the following symptoms:[38]
    • A sense of being off-balance (68 percent)
    • Lightheadedness (54 percent)
    • Spinning (46 percent)
    • Nausea (38 percent)
    • A sensation of motion (23 percent)
  • Overall, Alsalaheen and colleagues found that:[38]
    • Patients who had persistent dizziness and balance / gait dysfunction after concussion tended to improve after VR
    • Recovery occurred across a number of areas, including:
      • Dizziness Handicap Inventory
      • Activities-Specific Balance Confidence Scale
      • Functional balance performance
  • Schneider and colleagues studied the impact of VR on individuals who had persistent neck pain, dizziness and / or headaches post-sports related concussion:[43]
    • Both the treatment and control group received weekly physiotherapy sessions for 8 weeks or until the participant was medically cleared. Both groups received postural education, range of motion exercises, rest until asymptomatic, followed by a graded return to sport
    • The treatment group also received VR and cervical spine treatment
    • 73 percent of the intervention group were medically cleared at 8 weeks compared to only 7 percent of the control group
  • Brown and Camarinos found that symptoms such as headaches, dizziness, neck pain, gaze instability, balance dysfunction and fatigue can be improved with a multimodal approach that includes vestibular and cervicogenic rehabilitation, exertional training and education.[44]

Visual-Vestibular Mismatch[edit | edit source]

Visual-vestibular mismatch refers to visual-vestibular integration / processing impairments. It is quite common in the PCS population. It may be caused by dysfunctional sensory input and / or a disruption in CNS processing / sensory integration. Often visual and / or vestibular input are affected. Anxiety can also be a powerful disruptor of sensory integration.[1]

When a patient has a visual-vestibular mismatch, she / he might report the following:[1]

  • Frequent headaches
  • Feels unable to read, watch TV or work on computers for very long without symptoms
  • Dislikes being in busy environments (e.g. shopping)
  • Keeps bumping into walls / furniture
  • Feels nervous walking down the stairs
  • Feels "off" a lot of the time
  • Avoids going out - e.g. to the movies, out with friends, to restaurants or the theatre / concerts

Post Trauma Vision Syndrome (PTVS)[edit | edit source]

Post-trauma vision syndrome (PTVS) is characterised by binocular function problems.[45] Signs and symptoms of PTVS include:[1][46]

  • Eyes drifting outward
  • Eyes not working together
  • Double vision
  • Blurred vision
  • Light sensitivity
  • Functional visual field loss – testing for structural problems can be normal
  • Concentration difficulties
  • Symptoms provoked with reading
  • Poor spatial judgement / depth perception
  • Sense of visual midline is off

Evaluating mTBI and Dizziness[edit | edit source]

An assessment of clients who have head and neck trauma with or without a diagnosis of concussion should include an assessment of:[1]

  • Cervical spine
  • Vestibular system
  • Vision system
  • Sensory integration
  • Anxiety

This evaluation should also include an assessment of postural control and balance.

References[edit | edit source]

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 1.34 1.35 1.36 Tonks B. Vestibular Pathologies Course. Plus , 2021.
  2. Barkwill D, Arora R. Labyrinthitis. [Updated 2021 Jan 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
  3. 3.0 3.1 Hall CD, Herdman SJ, Whitney SL, Cass SP, Clendaniel RA, Fife TD et al. Vestibular rehabilitation for peripheral vestibular hypofunction: An evidence-based clinical practice guideline: FROM THE AMERICAN PHYSICAL THERAPY ASSOCIATION NEUROLOGY SECTION. J Neurol Phys Ther. 2016;40(2):124-55.
  4. Smith T, Rider J, Cen S, et al. Vestibular Neuronitis. [Updated 2020 Jul 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
  5. Gacek RR. A perspective on recurrent vertigo. ORL J Otorhinolaryngol Relat Spec. 2013;75(2):91-107.
  6. Peusner KD, Shao M, Reddaway R, Hirsch JC. Basic concepts in understanding recovery of function in vestibular reflex networks during vestibular compensation. Front Neurol. 2012;3:17.
  7. merriam webster aminoglycoside Available: (accessed 5.9.2021)
  8. Burns JC, Stone JS. Development and regeneration of vestibular hair cells in mammals. Semin Cell Dev Biol. 2017;65:96-105.
  9. Xie J, Talaska AE, Schacht J. New developments in aminoglycoside therapy and ototoxicity. Hear Res. 2011;281(1-2):28-37.
  10. Goudakos JK, Markou KD, Psillas G, Vital V, Tsaligopoulos M. Corticosteroids and vestibular exercises in vestibular neuritis. Single-blind randomized clinical trial. JAMA Otolaryngol Head Neck Surg. 2014;140(5):434-40.
  11. Petersen JA, Straumann D, Weber KP. Clinical diagnosis of bilateral vestibular loss: three simple bedside tests. Ther Adv Neurol Disord. 2013;6(1):41-5.
  12. Huth ME, Ricci AJ, Cheng AG. Mechanisms of aminoglycoside ototoxicity and targets of hair cell protection. Int J Otolaryngol. 2011;2011:937861.
  13. JJ Medicine. Aminoglycosides | Bacterial Targets, Mechanism of Action, Side Effects. Available from: [last accessed 20/6/2021]
  14. Kingma H, Felipe L, Gerards MC, Gerits P, Guinand N, Perez-Fornos A et al. Vibrotactile feedback improves balance and mobility in patients with severe bilateral vestibular loss. J Neurol. 2019;266(Suppl 1):19-26.
  15. Merriam Webster oscillopsia Available: (accessed 5.9.2021)
  16. 16.0 16.1 16.2 Kita AE, Kim I, Ishiyama G, Ishiyama A. Perilymphatic fistula after penetrating ear trauma. Clin Pract Cases Emerg Med. 2019;3(2):115-8.
  17. 17.0 17.1 Sarna B, Abouzari M, Merna C, Jamshidi S, Saber T, Djalilian HR. Perilymphatic fistula: A review of classification, etiology, diagnosis, and treatment. Front Neurol. 2020;11:1046.
  18. Meniere’s disease. BMJ 2014;349:g6544
  19. Oberman BS, Patel VA, Cureoglu S, Isildak H. The aetiopathologies of Ménière's disease: a contemporary review. L’eziopatogenesi della Sindrome di Ménière: stato dell’arte. Acta Otorhinolaryngol Ital. 2017;37(4):250-63.
  20. 20.0 20.1 20.2 Gürkov R, Pyykö I, Zou J, Kentala E. What is Menière's disease? A contemporary re-evaluation of endolymphatic hydrops. J Neurol. 2016;263 Suppl 1:S71-S81.
  21. Vestibular Disorders Association. Meniere's Disease. Available from: [last accessed 18/6/21]
  22. Sharon JD, Trevino C, Schubert MC, Carey JP. Treatment of Menière's Disease. Curr Treat Options Neurol. 2015;17(4):341.
  23. Choi MS, Shin SO, Yeon JY, Choi YS, Kim J, Park SK. Clinical characteristics of labyrinthine concussion. Korean J Audiol. 2013;17(1):13-17.
  24. Bartholomew RA, Lubner RJ, Knoll RM, Ghanad I, Jung D, Nadol JB Jr et al.. Labyrinthine concussion: Historic otopathologic antecedents of a challenging diagnosis. Laryngoscope Investig Otolaryngol. 2020;5(2):267-77.
  25. Foley RW, Shirazi S, Maweni RM, Walsh K, McConn Walsh R, et al. Signs and symptoms of acoustic neuroma at initial presentation: An exploratory analysis. Cureus. 2017;9(11):e1846.
  26. Gondivkar S, Parikh V, Parikh R. Herpes zoster oticus: A rare clinical entity. Contemp Clin Dent. 2010;1(2):127-9.
  27. Ellis MJ, Leddy J, Cordingley D, Willer B. A physiological approach to assessment and rehabilitation of acute concussion in collegiate and professional athletes. Front Neurol. 2018;9:1115.
  28. Benson BW, Meeuwisse WH, Rizos J, Kang J, Burke CJ. A prospective study of concussions among National Hockey League players during regular season games: the NHL-NHLPA Concussion Program. CMAJ. 2011;183(8):905-11.
  29. Grandhi R, Tavakoli S, Ortega C, Simmonds MJ. A review of chronic pain and cognitive, mood, and motor dysfunction following mild traumatic brain injury: complex, comorbid, and/or overlapping conditions? Brain Sci. 2017;7(12):160.
  30. Chorney SR, Suryadevara AC, Nicholas BD. Audiovestibular symptoms as predictors of prolonged sports-related concussion among NCAA athletes. Laryngoscope. 2017;127(12):2850-3.
  31. Marcus HJ, Paine H, Sargeant M, Wolstenholme S, Collins K, Marroney N et al. Vestibular dysfunction in acute traumatic brain injury. J Neurol. 2019;266(10):2430-3.
  32. Ellis MJ, Cordingley D, Vis S, Reimer K, Leiter J, Russell K. Vestibulo-ocular dysfunction in pediatric sports-related concussion. J Neurosurg Pediatr. 2015;16(3):248-55.
  33. Master CL, Scheiman M, Gallaway M, Goodman A, Robinson RL et al. Vision diagnoses are common after concussion in adolescents. Clin Pediatr (Phila). 2016;55(3):260-7.
  34. Reimer K, Ellis V, Cordingley DM, Russell K, Ellis MJ. Benign paroxysmal positional vertigo after pediatric sports-related concussion. Clin J Sport Med. 2020;30(4):412-5.
  35. Vestibular Disorders Association. Youth Concussion - The Vestibular Connection. Available from: [last accessed 18/6/2021]
  36. Bhattacharyya N, Gubbels SP, Schwartz SR, Edlow JA, El-Kashlan H, Fife T et al. Clinical practice guideline: benign paroxysmal positional vertigo (update). Otolaryngol Head Neck Surg. 2017;156(3_suppl):S1-S47.
  37. Schneider KJ, Meeuwisse WH, Nettel-Aguirre A, Barlow K, Boyd L, Kang J et al. Cervicovestibular rehabilitation in sport-related concussion: a randomised controlled trial. Br J Sports Med. 2014;48(17):1294-8.
  38. 38.0 38.1 38.2 38.3 38.4 Alsalaheen BA, Mucha A, Morris LO, Whitney SL, Furman JM, Camiolo-Reddy CE et al. Vestibular rehabilitation for dizziness and balance disorders after concussion. J Neurol Phys Ther. 2010;34(2):87-93.
  39. Murray DA, Meldrum D, Lennon O. Can vestibular rehabilitation exercises help patients with concussion? A systematic review of efficacy, prescription and progression patterns. Br J Sports Med. 2017;51(5):442-51.
  40. Schneider KJ, Meeuwisse WH, Barlow KM, Emery CA. Cervicovestibular rehabilitation following sport-related concussion. Br J Sports Med. 2018;52(2):100-1.
  41. Mucha A, Fedor S, DeMarco D. Vestibular dysfunction and concussion. Handb Clin Neurol. 2018;158:135-44.
  42. McCrory P, Meeuwisse W, Dvořák J, Aubry M, Bailes J, Broglio S et al. Consensus statement on concussion in sport-the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017;51(11):838-47.
  43. Schneider KJ, Meeuwisse WH, Nettel-Aguirre A, Barlow K, Boyd L, Kang J et al. Cervicovestibular rehabilitation in sport-related concussion: a randomised controlled trial. Br J Sports Med. 2014;48(17):1294-8.
  44. Brown L, Camarinos J. The Role of Physical Therapy in Concussion Rehabilitation. Semin Pediatr Neurol. 2019;30:68-78.
  45. Padula WV, Argyris S, Ray J. Visual evoked potentials (VEP) evaluating treatment for post-trauma vision syndrome (PTVS) in patients with traumatic brain injuries (TBI). Brain Inj. 1994 ;8(2):125-33.
  46. Hudac CM, Kota S, Nedrow JL, Molfese DL. Neural mechanisms underlying neurooptometric rehabilitation following traumatic brain injury. Eye Brain. 2012;4:1-12.