Vertigo = rotational dizziness

• implies disturbance of semicircular canals or their central pathways
  • ‘giddy’ and ‘light-headed’ is often used by patients in the improving, post-acute phase
  • but also used by patients with general medical conditions
    • anaemia
    • hypoglycaemia
  • and patients with haemodynamic problems
    • orthostatic hypotension
    • pre-syncope (cardiovascular)
  • and also patients with psychological problems
    • imbalance and unsteadiness
  • consider also sensori-motor disorders of the lower limbs
    • Parkinsonism
    • gait ataxia
    • spinal cord syndromes

It can sometimes be helpful to ask the following questions:

• Do you feel the problem is with your legs or in your head?
• Do you feel like you are about to faint? (pre-syncope)
• Do you feel like you are on a merry-go-round or on a boat? (vestibular)

Physical Examination

Unidirectional nystagmus — the direction (but not the intensity) of the nystagmus is unaffected by changes in the direction of gaze

• slow phase in the direction of the defunct labyrinth
• fast phase beating to the contralateral side
• intensity will be most visible when looking in the direction of the fast phase, less so in the midline, and least in the opposite direction
• confirms nystagmus is “vestibular” in origin and while typical for a peripheral lesion, this can also be seen in central vestibular lesions involving the brainstem (where additional signs make localisation relatively easy)

The vestibule-ocular reflex (VOR) is impaired in peripheral vestibular loss (but maintained in central vestibular loss).

• Demonstrated when head moved in the direction of the damaged labyrinth (or vestibular nerve)
• The method of choice in clinically assessing the integrity of the VOR in the acute phase
• Suppression of nystagmus
  • suppression of unidirectional vestibular nystagmus when visual fixation is allowed is a key sign of “peripheral” vestibular dysfunction
  • conversely without visual fixation, as in the dark, the nystagmus intensity is increased (that is, faster slow-phase velocity)
  • the ability to suppress spontaneous nystagmus in the light suggests intact central (mainly cerebellar) mechanisms
  • Frenzel’s glasses, an ophthalmoscope, or even observing the nystagmus beating behind closed eyelids can be used to examine the effect of loss of visual fixation on nystagmus intensity
• Neurological examination
  • any clear-cut central neurological signs in the presence of a neuro-otological syndrome make lesion localisation relatively easy, particularly when there is brainstem involvement
    • isolated cerebellar strokes, however, may mimic a peripheral vestibular syndrome
• General examination
  • focused general examination is important
  • peripheral neuro-otological syndrome: examine external auditory meatus for local pathology — cholesteatoma, eardrum perforation, discharge, vesicles of Ramsay-Hunt syndrome
  • stroke: careful cardiovascular examination — e.g. AF

Acute Isolated Vertigo

• Acute Idiopathic Unilateral Peripheral Vestibulopathy (Labyrinthitis)
• Cerebellar Stroke
• Migrainous vertigo
• Missed BPPV
• Bilateral vestibular failure

Acute Idiopathic Unilateral Peripheral Vestibulopathy (Labyrinthitis)

• Commonest cause of vertigo lasting > 24 hours during which there are symptoms and signs of unilateral vestibular hypofunction
• Typically, subacute onset over hours of spinning vertigo
• Sensation of vertigo is intense and almost always associated with nausea and vomiting
• Patients see the visual world spinning around them, mainly in a horizontal direction
• Sense of self-movement is present with the eyes closed and is made worse by any head movement and reduced (but rarely fully suppressed) by keeping the head absolutely still
• Generally, the nystagmus settles over several days (because of brainstem plasticity while recovery of function in the affected ear takes weeks to months)

Differential Diagnosis

• Cerebellar stroke — Head Impulse Test, positive neuroimaging
• Migrainous vertigo — Past History, negative neuroimaging

Investigation: Caloric test

Treatment: Corticosteroids

Cerebellar stroke

Acute vertigo plus any one of new-onset (occipital) headache, central neurological symptoms and signs, acute deafness, and intact head impulse test, require neuroimaging.

• Vertigo is commonest symptom in cerebellar stroke
  • cerebellar hemispheric stroke without brainstem involvement may complain of vertigo without any other symptoms
  • rarely, there may be no nystagmus or on-the-couch ataxia of the limbs
    • hyperacute onset of vertigo, occipital headache, profound gait ataxia are red flags
    • Head Impulse Test is intact
    • CT will diagnose some ischaemic strokes and virtually all cerebellar haemorrhages, but MRI is more sensitive, particularly with diffusion weighting

Migrainous vertigo

• Diagnosis requires clinical suspicion and is one of exclusion
• Typically a migraineur with recent increase in headache frequency develops, over the same period, vestibular episodes (but with headache and vertigo not occurring together)
• non-headache migrainous symptoms e.g. photophobia (i.e. patients may have only isolated vertigo)
• some patients may have symptoms and signs (including nystagmus) suggestive of central dysfunction and neuroimaging may be required on first presentation

Missed BPPV

• commonest cause of acute vertigo
• clinical diagnosis usually straightforward
• typical history — position-induced vertigo lasting seconds, typically on lying down and turning over in bed
• typical findings — torsional nystagmus beating towards the lower ear during the Hallpike manoeuvre
• Epley manoeuvre is effective (medium-term) treatment

More recently Dr. Carol Foster, at the University of Colorado School of Medicine, developed a “half-somersault” technique to treat BPPV and it seems to be preferred by patients.

Bilateral vestibular failure

• By far the commonest cause of in-hospital bilateral vestibular failure is aminoglycoside toxicity
  • gentamycin and streptomycin are primarily vestibulotoxic while amikacin and neomycin are predominantly cochleotoxic
    • the typical patient will have been in critical care, often with renal failure
    • consider in critically ill patients with “dizziness”
    • diagnose clinically with Head Impulse Test
    • confirm with Caloric Testing

Acute Vertigo With Deafness (Meniere’s disease)

• commonest cause of acute vertigo with deafness
• clinical diagnosis relies on a constellation of symptoms, signs and confirmatory testing
• typical attacks start with a feeling of fullness in one ear, leading to progressive tinnitus, ipsilateral fluctuating hearing loss and severe vertigo
• examination during an attack shows a peripheral vestibular nystagmus with the head impulse test lateralising the vestibular hypofunction to the symptomatic ear
• over time there is progressive audiovestibular loss and as this happens, the severity of the acute attack peters out
• rarely, patients may develop very sudden drop attacks without other acute symptoms of Meniere’s disease at the same time

Vertebrobasilar ischaemia

• hearing loss, usually peripheral (occasionally a central lesion affecting crossing auditory pathways (lateral lemniscus) of the contralateral dorsolateral upper pons (bilateral hearing loss has been reported with vertebrobasilar ischaemia)
  • almost always accompanied by vertigo
  • associated brainstem signs
  • overall good prognosis for some degree of hearing recovery — 80% in the long term
  • brief (minutes), isolated audiovestibular episodes (mainly vertigo) before a vertebrobasilar stroke can occur

Acoustic neuroma

• typically present with gradually progressive unilateral hearing loss and tinnitus
• vertigo is rare in uncomplicated acoustic neuroma because the insidious onset allows brainstem mechanisms to almost fully compensate for the progressive peripheral (vestibular) deficit
• rarely, haemorrhage into an acoustic neuroma withy vertigo has been reported

Labyrinthine haemorrhage

Causes:

• infants with perinatal distress
• pancytopenic leukemic patients
• antiplatelet or anticoagulation therapy
• cocaine ingestion
• SLE

[Imaging shows hyperintense signal in the membranous labyrinth and cochlea on T2-weighted MRI with no change in signal on contrast administration. Hearing loss and vestibular canal paresis are usually severe and permanent.]

Reference

• Seemungal BM, Bronstein AM. A practical approach to acute vertigo. Pract Neurol 2008; 8:211-221
• Half Somersault Canalith Repositioning – YouTube