1. bed side examination of the dizzy patient Herman Kingma, ORL-HNS department

2. - 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

3. 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

4. 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

5. image stabilisation balance control spatial orientation interpretation learning adaptation compensation CNS labyrinths vision gravitoreceptors hearing somatosensory foot sole pressure circadian rhythm autonomic processes blood pressure heart beat frequency respiration rate

6. 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

7. patient with severe bilateral vestibular hyporeflexia slow tandem walk fast tandem walk

8. c mes thal cortex pons cer vn omn cgl VOR: 8 msec OKR and Smooth pursuit: >75 msec

10. simulation of oscillopsia  reduced dynamic visual acuity in case of bilateral vestibular areflexia

11. 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

12. 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 patterns Bronstein and Lempert ”Dizziness”

13. a vestibular function loss implies permanent impairment analogue to hearing and visual losses … and neuroplasticity differs per patient…!

14. bed-side examination

15. 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

16. 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 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 specific bed-side examination of the vestibular function

17. spontaneous eyes open nystagmus vertical, horizontal symmetric or pendular always central (acquired or congenital) 1 st, 2 nd or 3 rd degree horizontal mostly peripheral sometimes central

19. impact of visual fixation upon nystagmus nystagmus increases by visual fixation always central (acquired or congenital) nystagmus decreases upon visual fixation always peripheral

20. Hallpike left right Hallpike sidewards or mid-Hallpike right PC-canalolithiasis or cupulolithiasis left PC-canalolithiasis or cupulolithiasis left or right AC canalolithiasis or cupulolithiasis right HC-canalolithiasis left HC-canalolithiasis right HC-cupulolithiasis left HC-cupulolithiasis sidewards or mid-Hallpike sidewards or mid-Hallpike sidewards or mid-Hallpike PC canalolithiasis or cupulolithiasis: most common peripheral vestibular dysfunction

21. Hallpike left right Hallpike sidewards or Hallpike right PC-canalolithiasis 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 sidewards or Hallpike sidewards or Hallpike sidewards or Hallpike right left

22. Hallpike left right Hallpike sidewards or 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 sidewards or mid-Hallpike sidewards or mid-Hallpike sidewards or mid-Hallpike exclude neurological origin of a down beat nystagmus

23. normal tests: if history points to deficit manage patient in line with the history (but no ablative therapies)

24. 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