Transcript dia's voor td - Maastricht UMC+

bed side examination of the dizzy patient
Herman Kingma, ORL-HNS department
history + bedside-examination + explanation
- 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
• 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: my tip
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
foot sole pressure
somatosensory
vision
gravitoreceptors
CNS
labyrinths
autonomic processes
blood pressure
heart beat frequency
respiration rate
interpretation
learning
adaptation
compensation
image stabilisation
hearing
circadian rhythm
spatial orientation
balance control
symptoms of vestibular dysfunction
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
patient with severe bilateral vestibular hyporeflexia
slow tandem walk
fast tandem walk
cortex
cgl
thal
mes
pons
cer
omn
vn
VOR: 8 msec
OKR and Smooth pursuit: >75 msec
simulation of oscillopsia  reduced dynamic visual acuity
in 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
5 major patterns
Bronstein and Lempert
”Dizziness”
• 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
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 fast
oculomotor
• gaze and fixation
• convergation / amblyopia / cover test / skew deviation
• pursuit and saccades
static 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 glasses
1.
observe patient’s gait / posture
2.
Romberg + tandem
if abnormal: past pointing test
3.
gaze and fixation
4.
convergence, amblyopia,
cover test, skew deviation
5.
pursuit
6.
saccades
specific bed-side examination
of the vestibular function
with Frenzel’s glasses
6.
spontaneous nystagmus
7.
Hallpike + HC-test
8.
3d VOR + OCR
9.
head shake nystagmus test
without Frenzel’s glasses
10.
head impulse test (H/V)
11.
fixation suppression test
12.
observe patient’s gait / posture
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
PC canalolithiasis or cupulolithiasis:
most common peripheral vestibular dysfunction
right
left
Hallpike
right PC-canalolithiasis
or cupulolithiasis
Hallpike
left PC-canalolithiasis
or cupulolithiasis
Hallpike
left or right AC
canalolithiasis
or cupulolithiasis
sidewards
or mid-Hallpike
right HC-canalolithiasis
right
Hallpike
left PC-canalolithiasis
Hallpike
left or right AC
canalolithiasis
or cupulolithiasis
sidewards
or Hallpike
sidewards
or Hallpike
left
right HC-canalolithiasis
geotropic
left HC-canalolithiasis
geotropic
sidewards
or Hallpike
right HC-cupulolithiasis
apo-geotropic
sidewards
or Hallpike
left HC-cupulolithiasis
apo-geotropic
right
left
Hallpike
right PC-canalolithiasis
Hallpike
left PC-canalolithiasis
Hallpike
left or right AC
canalolithiasis
or cupulolithiasis
sidewards
or mid-Hallpike
right HC-canalolithiasis
exclude neurological
origin of a down beat nystagmus
sidewards
or mid-Hallpike
left HC-canalolithiasis
sidewards
or mid-Hallpike
right HC-cupulolithiasis
sidewards
or mid-Hallpike
left HC-cupulolithiasis
normal tests:
if history points to deficit
manage patient
in 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