Vertigo Flashcards

1
Q

What is vertigo?

A
  • vertigo is an illusion of movement
  • includes sensation of rotation of self or of the environment as well as sensations of being pulled downwards/sideways or the room tilting - ie. ‘spinning’
  • always worsened by movement
  • often associated w/ difficulty in walking or standing with relief on lying or standing still
  • other common symptoms → nausea, vomiting, pallor, sweating
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2
Q

Dizziness is a generic term that may refer to lightheadedness, faintness, giddiness, swimming or floating sensation, unsteadiness, imbalance, mental confusion, minor seizures or even true vertigo.

What is the impact of dizziness?

A
  • 12x more likely to fall
  • falls commonest cause of accidental death in over 75s
  • psychological → dizziness increases anxiety + depression which interferes w/ recovery, reluctance to go out as unsteadiness mimics drunkenness
  • socio-economic → not able to go back to work, may not be able to do certain types of work, not able to drive in certain conditions, poor QoL
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3
Q

What are the causes of vertigo?

A
  • Otological → meniere’s disease, vestibular neuronitis, labyrinthitis, BPPV, cerumen impaction, perilymphatic fistula, trauma, infection
  • Central → CN VIII nerve disorders, MS, stroke, haemorrhage, migraine, acoustic neuroma, malignancy, trauma, infection, epilepsy
  • Other → DM, hypoglycaemia, alcohol, anaemia, dysrhythmias, iatrogenic, multisensory disease syndrome
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4
Q

The vestibular system aims to contribute to our balance system, maintain spatial orientation, stabilise vision and provide info related to movement and head position.

Give a brief overview of the structures involved in the vestibular system

A
  • otolith sits within vestibule - made up of saccule + utricle → for linear acceleration and deceleration, utricle is sensitive to change in horizontal movement where the saccule is sensitive to change in vertical acceleration
  • semicircular canals → for angular acceleration + deceleration, contain sensory hair cells activated by movement of inner ear fluid (endolymph), as head moves the hair cells in semicircular canals send nerve impulses to brain by way of acoustic nerve

Normally there is balanced input from both vestibular systems, vertigo develops from asymmetrical vesitbular activity. Abnormal bilateral vestibular activation results in truncal ataxia.

For more physiology see flashcards

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5
Q

What is vestibular nystagmus?

A
  • involuntary to and fro movement of eyes
  • has a fast + slow phase
  • direction of fast phase is direction of nystagmus
  • slow phase is produced by vestibular system
  • slow component usually ipsilateral to diseased structure
  • fast component due to cortical correction
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6
Q

Peripheral vertigo (85%) is the result of a problem with your inner ear or CN VIII, which controls balance. Central vertigo refers to problems within your brain or brainstem.

How do these present differently?

A
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7
Q

What is physiologic vertigo?

A
  • “motion sickness”
  • mismatch between visual, proprioceptive and vestibular inputs
  • not a diseased cochleovestibular system or CNS
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8
Q

What questions need to be asked in the vertigo history?

A
  • is it true vertigo?
  • autonomic symptoms?
  • pattern of onset and duration
  • auditory disturbances?
  • neurologic disturbances?
  • was there syncope?
  • unusual eye movements?
  • any past head or neck trauma
  • past medical history?
  • previous symptoms?
  • prescribed + OTC meds?
  • drug and alcohol intake?
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9
Q

What is involved in the examination of a vertigo patient?

A
  • otoscopy
  • full eye exam
  • tests of stance + gait → Romberg, Unterberger’s, tandem gait
  • cerebellar function
  • cranial nerves
  • positional tests
  • orthostatic vital signs
  • hearing test
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10
Q

What is the HiNTs Exam?

A
  • Head impulse, Nystagmus + Test of skew Deviation
  • screening tool to distinguish between central + peripheral vertigo
  • normal neurological exam cannot accurately exclude a central process
  • head impulse → pt relaxes head + maintain gaze on nose, gently move pts head to one side then rapidly move back to neutral - head impulse test is positive (consistent with peripheral vertigo) if there is a significant lag with corrective saccades
  • nystagmusunidirectional suggests peripheral but bidirectional nystagmus, I.E fast component to the right with rightward gaze and to the left with leftward gaze, is concerning for a central process, as is vertical nystagmus or pure torsional nystagmus
  • skew → pt gaze on nose, alternate covering of pt’s eyes, positive result = central vertigo
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11
Q

What is Benign Paroxysmal Positional Vertigo (BPPV)?

A
  • most common cause of vertigo (a peripheral cause)
  • acute attacks of transient vertigo lasting seconds-mins initiated by certain head position accompanied by torsional (rotatory) nystagmus
    • ​commonly occur on getting out of bed / looking up / rolling
  • causes: idiopathic (50%), head injury, whiplash, post-vestibular neuritis
  • in majority, self-limiting
  • dx → positive dix-hallpike manouvre + history
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12
Q

What is the Dix-Hallpike maneouvre?

A
  • rapidly moving pt from a sitting position to supine position
  • w/ head hanging over end of table, turned 45o to one side
  • hold for 15-20s to elicit nystagmus
  • onset of vertigo + rotatory nystagmus indicate positive test for dependent side
  • top pole of the eyes rotates towards the undermost (affected) ear
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13
Q

What is the pathophysiology BPPV?

A
  • due to otoliths
  • tiny crystals of calcium carbonate (normal part of inner ear) detach from otolithic membrane in utricle + collect in one of the semicircular canals (most commonly posterior)
  • head still → gravity causes otoliths to clump + settle
  • head moves → otoliths shift → stimulates cupula to send false signal to brain → vertigo and nystagmus occur
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14
Q

What is the treatment for BPPV?

A
  • reassure patient that process resolves spontaneously
  • particle repositioning maneouvres
    • main aim → reposition the otoliths back to utricle
    • 3-step PRM / Epley manouvre
    • Semont manouvre
    • Brandt-Daroff exercise (by patient)
  • surgery for refractive causes
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15
Q

What is vestibular neuritis?

A
  • inflammation of the nerve - affects branch associated w/ balance, resulting in dizziness or vertigo but no change in hearing
  • sudden onset
  • only vestibular symptoms + worst symptoms in the beginning
  • prodromal viral URTI may be present
  • symptomatic recovery by central compensation
  • recovery influenced by age, vision, proprioception, mental health + medications
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16
Q

What is labyrinthitis?

A
  • commonly used to denote vestibular neuritis
  • labyrinth is structure in inner ear, consisting of semicircular canals, vestibule and cochlea
  • it is inflammation of the labyrinth
  • occurs when an infection affects whole structure of inner ear (labyrinth)
  • affects both vestibular apparatus AND cochlea
  • results in hearing changes as well as dizziness or vertigo
17
Q

Vestibular neuritis/labyrinthitis can occur as complication of acute/chronic otitis media, bacterial meningitis, cholesteatoma and temporal bone fractures. They normally are of viral origin (rubella, CMV, mumps, varicella zoster). Can result in meningitis as a complication.

How do you treat labyrinthitis?

A
  • Vestibular sedatives (benzos) should be used only for short duration
    • act by inhibiting normal side to reduce asymmetry
    • hence it interfered w/ central compensation
    • may prolong recovery from symptoms
  • vestibular rehabilitation exercises mainstay of treatment
  • anti-emetics for N+V
  • sudden hearing loss → steroids
  • IV antibiotics if bacterial
18
Q

What is Meniere’s disease?

A
  • AKA endolymphatic hydrops
  • idiopathic, XS endolymphatic fluid pressure
  • triad of fluctuating low freq hearing loss, severe vertigo + roaring tinnitus
  • RFs → high salt intake, caffeine, stress, nicotine, alcohol
  • recurrent episodes, initial episodes usually worse
  • preceding aural fullness common
  • occasionally bilateral
19
Q

What investigations are important to order for Meniere’s disease?

A
  • pure-tone air + bone conduction w/ masking
  • speech audiometry
  • tympanometry
  • oto-acoustic emissions
  • MRI internal auditory canals
20
Q

What is the management of Meniere’s disease?

A
  • life-style changes → limiting salt + caffeine
  • MEDICAL:
    • symptomatic relief of an acute attack → cinnarizine, prochloperazine, cyclizine
    • prophylactic preventive → betahistine, diuretics (bendroflumethiazide)
  • SURGICAL:
    • trans-tympanic treatment → gentamicin, steroids
    • endolymphatic sac surgery
    • vestibular neurectomy
    • labyrinthectomy
21
Q

What is migraine-related vertigo?

A
  • can mimic/co-exist w/ Meniere’s
  • usually has classical migraine + family history
  • episodic w/ symptom-free periods
  • can have other features of migraine
  • can be present +/- headache
  • Tx → same as migraine, common + under-diagnosed, consider in anyone w/ migraine + spontaneous episodic vertigo, often have motion sensitivity and AVOID opiates
22
Q

What is acute vestibular failure?

A
  • rapid onset of sustained + severe vertigo (abrupt onset or over few hrs)
  • often noticed first on waking
  • acute attack lasts 2-5 days then a steady resolution over 6-12wks
  • N+V, nystagmus
  • hearing unaffected (vestibular neuritis) but if cochlear involvement then hearing can be affected (acute labyrinthitis)
  • no neurological symptoms
  • causes: gentamicin toxicity, idiopathic, autoimmune
23
Q

What is post-traumatic vertigo?

A
  • often multiple contributors, changing over time
  • acute (concussion) - v common
    • 70% central vestibular gait apraxia
    • 40% BPPV
    • 30% vestibular migraine
  • persistent/chronic - NOT related to severity TBI/LoC
  • treat depending on primary contributor(s)
    • vestibular rehabilitation
    • Epley
    • migraine prophylaxis
24
Q

What is multisensory dizziness syndrome?

A
  • occurs when reduced inputs from more than 1 sensory system
  • particularly seen in elderly + those w/ systemic diseases such as DM
  • typical combo →
    • reduced visual acuity due to cataract/glaucoma
    • peripheral neuropathy resulting in reduced touch + proprioceptive input
    • impaired hearing
    • vestibular hypofunction
  • unable to adapt to familiar surroundings
  • made worse by side-effects of meds
  • Rx directed at improving sensory input
    • surgery for cataract, better DM control, hearing aids, use of cane/walker
    • avoidance of sedatives
25
Q

What is an acoustic neuroma (vestibular schwanomma)?

A
  • schwannoma of the vestibular portion of CN VIII
  • acoustic neuroma most common intracranial tumour causing SNHL + most common cerebellopontine angle tumour
  • starts in internal auditory canal + expands into cerebellopontine angle (CPA), compressing cerebellum and brainstem
  • presentation → unilateral SNHL or tinnitus, dizziness and unsteadiness may be present but true vertigo rare as tumour growth slow + compensation occurs
  • facial nerve palsy + trigeminal (V1) sensory deficit (corneal reflex) are late complications
26
Q

How is acoustic neuroma diagnosed and treated?

A
  • DIAGNOSIS
    • MRI w/ gadolinium
    • audiogram
    • poor speech discrimination relative to hearing loss
    • stapedial reflex absent or significant reflex decay
    • ABR - increase in latency of 5th wave
    • vestibular test → normal or asymmetric caloric weakness
  • TREATMENT
    • surgical exicison
    • other → gamma knife, radiation
27
Q

Summary of vertigo causes

A