Vestibular Pathologies
Introduction[edit | edit source]
Vertigo is defined as the illusion of movement occurring in the environment. As will be discussed in this page, acute vertigo can be caused by the following conditions:[1]
- Cerebrovascular accident - posterior circulation strokes
- Neurological disorders - e.g. multiple sclerosis
- Endolymphatic hydrops - e.g. Meniere’s disease
- Migraine associated vertigo (also known as vestibular migraine)
- Vestibular neuritis and labyrinthitis
- Head trauma (occasionally)
- BPPV
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). They may also be referred to as 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]
They are believed to usually be due to viral infection:[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:
- Nystagmus
- Nausea
- Vomiting
- Imbalance
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. A loss of input from one side and relative excitation of the intact side results in a mixed horizontal and torsional nystagmus.[1] The direction of nystagmus is labelled according to the quick phase:[1]
- Right-sided lesion = 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
Acute Symptoms or Vestibular Crisis[edit | edit source]
The acute stage, which lasts for 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]
Nystagmus, skew-eye deviation, and marked postural asymmetry recover spontaneously within 3 to 14 days. These are termed static deficits. 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]
It has been found that cellular recovery is possible for non-primate mammals following aminoglycoside toxicity. It is not known if this can occur in humans, but there is no evidence of regeneration of vestibular neurons in primates.[1]
NB aminoglycosides are powerful broad-spectrum antibiotics, but they can adversely affect the kidney (nephrotoxicity), vestibular and auditory organs (ototoxicity), and the neuromuscular junction.[6]
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
- During the acute phase (which usually lasts less than 2 to 3 days) there is some evidence that corticosteroids can be helpful if given within 72 hours[7]
- Recurrence is not common
- Physiotherapists often only see patients in the chronic phase when patients generally function fairly well unless they move their heads too quickly
- Patients in the chronic phase typically present with problems in one or more of the following domains:[1]
- Gaze stability issues
- Motion sensitivity
- Compromised balance and postural control
References[edit | edit source]
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 1.9 Tonks B. Vestibular Pathologies Course. Physioplus, 2021.
- ↑ Barkwill D, Arora R. Labyrinthitis. [Updated 2021 Jan 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560506/
- ↑ 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.
- ↑ 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: https://www.ncbi.nlm.nih.gov/books/NBK549866/
- ↑ Gacek RR. A perspective on recurrent vertigo. ORL J Otorhinolaryngol Relat Spec. 2013;75(2):91-107.
- ↑ Xie J, Talaska AE, Schacht J. New developments in aminoglycoside therapy and ototoxicity. Hear Res. 2011;281(1-2):28-37.
- ↑ 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.
