Vestibular (draft)

Overview

  • Dizziness caused by vestibular dysfunction is generally stimulated by changes to head or by position. Symptoms are usually relieved by remaining still.
  • Vestibular dysfunction may be due to central causes (eg TIA / stroke / vertebro-basilar insufficiency, MS, tumours) or peripheral causes (eg BPPV, vestibular neuritis / labyrinthitis / meniere’s).
  • Dizziness which does not significantly change with head / body movement is likely to be unrelated to the vestibular system
  • Certain medications, such as anti-hypertensives, anti-depressants, anti-convulsants and drugs used for Parkinson’s disease can also cause dizziness
  • Certain medical conditions (cardiac and otherwise) may cause collapse which may be preceded by dizziness
  • The duration of the vertigo, once stimulated, may provide information to the location:
    • In BPPV, the vertigo usually lasts less than one minute
    • In Meniere’s and migraine, the symptoms may last minutes to hours
    • For stroke and vestibular neuronitis, the symptoms may last 24 hours+
  • It is also necessary to consider other symptoms:
    • Deafness, tinnitus, ear fullness may suggest a labyrinthine cause (eg meniere’s)
    • Limb weakness / numbness, speech disturbance, headache, visual disturbance may suggest a neurological cause (eg TIA / CVA, tumour)
  • Nystagmus may also provide an indication to the level of pathology:
    • Purely vertical or torsional (head still, patient upright) nystagmus tends to indicate a central lesion
    • Mixed horizontal & torsional nystagmus tends to suggest peripheral dysfunction
    • Central nystagmus may present with directional change (such as beating to the right on movement to the right & beating to the left on movement to the left) while peripheral nystagmus beats in the same direction regardless of eye position

NOTE THAT SOME NYSTAGMUS MIGHT NOT BE VISIBLE TO THE NAKED EYE AND REQUIRES AN OTOSCOPE TO VIEW

Assessment

  • A thorough examination is required for patients who present with dizziness
  • Subjectively, symptoms should be explored:
    • Aggravating activities / positions
    • Duration of symptoms
    • Room spinning vs patient spinning vs ataxia/drunk feeling vs lightheaded
    • Other symptoms
  • Objectively this includes:
    • Neurological
    • Otological
    • Cardiovascular examination
      • Lying / standing blood pressure
    • Nystagmus (Horizontal gaze, Vertical Gaze)
      • Purely vertical or torsional (head still, patient upright) nystagmus tends to indicate a central lesion
      • Mixed horizontal & torsional nystagmus tends to suggest peripheral dysfunction
      • Central nystagmus may present with directional change (such as beating to the right on movement to the right & beating to the left on movement to the left) while peripheral nystagmus beats in the same direction regardless of eye position
    • Vestibulo-Ocular Reflex
      • Horizontal (fix gaze, turn head side to side 30 degrees)
      • Vertical (fix gaze, nod head up and down)
      • In a patient with labyrinthine dysfunction, the eyes will move with the head initially and then correct after a short delay
    • Vestibular Testing
    • Posterior Semi-Circular Canals
      • Hall Pike
        • Begin with the patient in long sitting
        • Turn the head 45 degrees to one side
        • Bring the patient back quickly, so that the trunk and neck are both extended
        • Watch the eyes for nystagmus and ask if the patient feels dizzy
        • Once symptoms have settled, repeat with the head rotated the other direction
        • The side with the most prominent nystagmus is considered to be the affected side
    • Horizontal Canals
      • Supine Head Roll
        • Begin with the patient in supine with a pillow
        • Turn the head to one side, observing for nystagmus
        • Turn the head back up and wait
        • Turn the head to the other side and observe
        • The side with the most prominent nystagmus is considered to be the affected side

Pathology

Benign Paroxysmal Positional Vertigo

Condition

  • Within the labyrinth of the inner ear lie collections of calcium crystals known as otoconia.
  • In patients with BPPV, the otoconia are dislodged from their usual position within the utricle and they move into one of the semicircular canals (the posterior canal is most commonly affected due to its anatomical position).
  • When the head is moved, the gravity-dependent movement of the heavier otoconial debris within the affected semicircular canal causes abnormal fluid endolymph displacement and a sensation of vertigo. This is known as canalithiasis.
  • In rare cases, the crystals themselves can adhere to a semicircular canal cupula rendering it heavier than the surrounding endolymph. Upon movement of the head, the cupula is weighted down by the dense particles thereby inducing an immediate and maintained excitation of semicircular canal afferents. This condition is termed cupulolithiasis.
  • The trigger is usually head or body movement, or change in surroundings relative to self
  • Symptoms may be related to change in barometric pressure or lack of sleep

Symptoms

  • In BPPV, vertigo is the main presenting symptom on head movement, along with nystagmus
  • Vertigo typically lasts less than a minute
  • There may also be associated nausea / vomiting
  • Limb weakness / paraesthesia or speech / swallowing disturbance would indicate a likely neurological cause (possibly the region supplied by the posterior circulation) and is NOT characteristic of BPPV

Treatment

Posterior Canal

  • Most common by far
  • Epley’s manoeuvre (reported to be successful in 80% of cases in one treatment)
  • Semont manoeuvre (>60% after 1, >80% after 2 sessions, >95% after 4)
  • Of those successfully treated, 44% redevelop symptoms within 2 years
  • Brandt-Daroff exercises may reduce the rate of recurrence of BPPV (conflicting data). If used acutely as treatment, these exercises can eliminate symptoms in 25-85% of patients (ie less successful than other two)
  • Habituation exercises
    • Desensitize vestibular system, with the idea to elicit vertigo mildly, then stop and wait for the symptoms to pass, and repeat for a set period
    • Eye exercises (as in assessment)
      • Fixed head, shift gaze side to side, up and down
      • Fixate on object in front, shift head from side to side, up and down
    • Brandt Daroff exercises may also be considered desensitization

Horizontal Canal

  • Represents 10-17% of all BPPV
  • Positive supine roll test
  • Presents with horizontal nystagmus that changes direction depending on the side that is down
  • Usually resolves spontaneously within a week
  • No controlled studies on Rx fo horizontal canal
  • Rx based on theory

Anterior Canal

  • Very rare, may present as a result of Epley or Semont
  • Diagnosed based on downbeating or torsional nystagmus on Hall-Pike
  • Usually resolves spontaneously inside 1 week

Meniere’s Disease

Background

  • ENDOLYMPH, a fluid which fills the membranous labyrinth, is probably produced by the secretory cells in the epithelium surrounding the sensory epithelia, and by the stria vascularis, the epithelium lining of the upper part of the cochlear duct. It drains into the venous sinuses of the dura mater through the endolymphatic duct.
  • An abnormal increase in the amount of endolymph, whether by overproduction or failure to eliminate, leads to a condition called Meniere’s disease.
  • The excess fluid produces recurrent vertigo (dizziness) and a sensation of fullness in the affected ear, which is accompanied in later stages by tinnitus (jingling in the ears), and deafness.
  • The pathological changes resulting from dilation of the endolymphatic system are degeneration of the hair cells in the maculae of the vestibule and in the spiral organ, which give rise to both auditory and vestibular dysfunction.
  • In most cases only one ear is involved, but both ears may be affected in about  15% of patients. Meniere’s disease typically starts  between the ages of 20 and 50 years. Men and women are  affected in equal numbers.

Cause

  • It is not entirely understood as to what causes Meniere’s disease, however, it has been linked to infection, (bacterial, viral, symphilitic, Herpes) allergy and autoimmune response, although most cases are classified as idiopathic.
  • Diet may also play a large part, with suggestion that abnormal glucose metabolism and high plasma lipid concentration may affect. Some foods have been identified as likely triggers (see below).

Symptoms

  • This disease is characterised by transient attacks of dizziness or vertigo that are so severe that the afflicted individual cannot stand or walk, which may last from 20 minutes to 2 hours.
  • There is persistent sense of disequilibration for days after an acute episode.
  • Nausea, vomiting, abnormal eye movements (nystagmus) and a sensorineural hearing loss also occur.
  • The transient character of the symptoms may be a consequence of changes in fluid pressure within the labyrinth.

Treatment

  • Medical treatment consists of diet modification to avoid possible trigger factors, such as salt, caffeine, smoking alcohol and stress.
  • Anti inflammatories, such as corticosteroids, diuretics, vestibular suppressants and vasodilators are used to reduce symptoms.
  • Surgery may be indicated in extreme cases.