Vestibular Pathologies

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

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Introduction

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:

• 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)

Vestibular Neuritis and Labyrinthitis

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). They are the second most common cause of vertigo. While there is little epidemiological data about labyrinthitis, vestibular neuritis occurs in approximately 15 per 100,000 people in the US.

They are believed to usually be due to viral infection:

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

Acute versus Chronic UVL

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.

UVL Nystagmus

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. The direction of nystagmus is labelled according to the quick phase:

• 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

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.

Recovery

Spontaneous Recovery

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.

Cellular Recovery

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.

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

Summary of UVL

• 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
• 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:

• • Gaze stability issues
  • Motion sensitivity
  • Compromised balance and postural control

Bilateral Vestibular Lesions (BVL)

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

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

Unlike in UVLs, Vertigo occurs infrequently in these patients because the acute vestibular loss is bilateral and symmetrical. Patients with BVL primarily report:

• Balance problems during standing or walking
• Oscillopsia
• Disequilibrium and dizziness
• Physical deconditioning

Age-Related Vestibular Changes

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.

Perilymphatic Fistula

A perilymphatic fistula is a tear or defect in a membrane between the fluid-filled inner

and middle ear. This causes pressure changes from the environment accessing the vestibular system and there can be a flow of perilymphatic fluid between the two compartments. Causes of perilymphatic fistula include:

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

Patients present with:

• 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 and treatment of perilymphatic fistulas is controversial due to a lack of diagnostic tests. Medical management includes: bed rest, mild sedation, avoiding activities that will increase inner ear pressure. In severe cases, surgical grafting may be required.

Meniere’s Disease and Endolymphatic Hydrops

Meniere’s disease or primary hydrops is a disorder of the inner ear, that results in recurrent attacks of self limiting vertigo. Other associated symptoms are: unilateral fluctuating low frequency sensorineural hearing loss, a sense of ear “fullness” and tinnitus.

Meniere’s disease is idiopathic - i.e. it has no known cause.  Various theories have been proposed about the pathophysiology of Meniere’s Disease. It is possibly due to the malabsorption of endolymph in the endolymphatic sac or duct, which causes pressure fluctuations in the inner ear fluid.

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

Patients present with the following symptoms:

• 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

• Dietary: decrease salt, alcohol, nicotine, and caffeine intake
  • This may minimise any secondary fluctuations in the endolymph of the inner ear, which may significantly 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.