The Good Doctor

Tag: vertigo

  • When the Patient says: “I Feel Dizzy, Doctor.”

    When the Patient says: “I Feel Dizzy, Doctor.”

    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