bed side examination of the dizzy patientHerman Kingma, ORL-HNS department

- history, examination and explanation require 20-30 minutes

- take the complaints of the patient seriously:

so, if you lack time ask patient to return for a special consultation

history + bedside-examination + explanation

• which complaints are related to vestibular deficits ?

• patients often do not know which complaints are

associated with peripheral vestibular dysfunction

• patients often think and are afraid that the complaints point

to a brain dysfunction

• complaints are frequently a complex mixture of acute ….

and sustained symptoms !!!

history

when taking the history assume that there were and are

acute transient and sustained vestibular complaints

untill you find out that that is not the case

history: my tip

image stabilisation

balance control

spatial orientation

interpretationlearning

adaptationcompensation

CNS

labyrinths

visiongravitoreceptors

hearing

somatosensoryfoot sole pressure

circadian rhythmautonomic processes

blood pressure heart beat frequency respiration rate

acute loss or fluctuating peripheral vestibular function

transient: vertigo, nausea, falling / imbalance

remaining peripheral vestibular function loss

sustained: - not feeling well, slight nausea- loss of balance at low speeds or complex situations- reduced dynamic visual acuity- reduced ability to discriminate between

self-motion and environmental motion- secondary: fear and fatigue

symptoms of vestibular dysfunction

patient with severe bilateral vestibular hyporeflexia

slow tandem walk fast tandem walk

cmesthal

cortex

pons cer

vn

omn

cgl

VOR: 8 msec OKR and Smooth pursuit: >75 msec

simulation of oscillopsia reduced dynamic visual acuityin case of bilateral vestibular areflexia

acute loss or fluctuating peripheral vestibular function

transient: vertigo, nausea, falling / imbalance

remaining peripheral vestibular function loss

sustained: - not feeling well, slight nausea- loss of balance at low speeds or complex situations- reduced dynamic visual acuity- reduced ability to discriminate between

self-motion and environmental motion- secondary: fear and fatigue

• single episode of prolonged vertigo + sustained complaints

• recurrent vertigo + sustained complaints

• recurrent dizziness + sustained complaints

• positional vertigo, less often sustained complaints

• chronic dizziness, impaired visual acuity, unsteadiness

5 major patternsBronstein and Lempert

”Dizziness”

a vestibular function loss implies

permanent impairment

analogue to hearing and visual losses

… and neuroplasticity differs per patient…!

bed-side examination

bed-side examination

balance• observe patient at entrance

Romberg eo/ec, tandem walk slow vs fastoculomotor• gaze and fixation• convergation / amblyopia / cover test / skew deviation• pursuit and saccadesstatic vestibulo-ocular stability• spontaneous nystagmus*positioning • Hallpike AD/AS * + barbecue AD/AS *VOR• head shake 3D VOR + OCR*• head shake nystagmus test*• head impulse test (H/V)additional• fixation suppression test• test for fistula and Tullio phenomenon * preferrably with

Frenzels glasses

without Frenzel’s glasses1. observe patient’s gait / posture2. Romberg + tandem

if abnormal: past pointing test3. gaze and fixation4. convergence, amblyopia,

cover test, skew deviation5. pursuit6. saccades

with Frenzel’s glasses6. spontaneous nystagmus7. Hallpike + HC-test8. 3d VOR + OCR9. head shake nystagmus test

without Frenzel’s glasses10. head impulse test (H/V)11. fixation suppression test12. observe patient’s gait / posture

specific bed-side examinationof the vestibular function

spontaneous eyes open nystagmus

vertical, horizontal symmetric or pendular

always central (acquired or congenital)

1st, 2nd or 3rd degree horizontal

mostly peripheral sometimes central

impact of visual fixation upon nystagmus

nystagmus increases by visual fixation

always central (acquired or congenital)

nystagmus decreases upon visual fixation

always peripheral

Hallpike

Hallpike

leftright

Hallpike

sidewardsor mid-Hallpike

right PC-canalolithiasis or cupulolithiasis

left PC-canalolithiasis or cupulolithiasis

left or right AC canalolithiasis or cupulolithiasis

right HC-canalolithiasis

sidewardsor mid-Hallpike

PC canalolithiasis or cupulolithiasis: most common peripheral vestibular dysfunction

Hallpike

Hallpike

sidewardsor Hallpike

left PC-canalolithiasis

left or right AC canalolithiasis or cupulolithiasis

right HC-canalolithiasis geotropic

left HC-canalolithiasis geotropic

right HC-cupulolithiasis apo-geotropic

left HC-cupulolithiasis apo-geotropic

sidewardsor Hallpike

sidewardsor Hallpike

sidewardsor Hallpike

right left

Hallpike

Hallpike

leftright

Hallpike

sidewardsor mid-Hallpike

right PC-canalolithiasis

left PC-canalolithiasis

left or right AC canalolithiasis or cupulolithiasis

right HC-canalolithiasis

left HC-canalolithiasis

right HC-cupulolithiasis

left HC-cupulolithiasis

sidewardsor mid-Hallpike

sidewardsor mid-Hallpike

sidewardsor mid-Hallpike

exclude neurological origin of a down beat nystagmus

normal tests: if history points to deficit

manage patientin line with the history

(but no ablative therapies)

optimal patient management: reality

• a vestibular deficit implies permanent function loss

• stimulation of neuroplasticity and use of rehabilitation exercises in natural environment improve function:

time is valuable: act fast

• frequently only the history points to a vestibular deficit

• explaining the relation between the deficit and the complaints forms the keystone of the therapy,

allowing the patient to cope with his or her problems