VRT Theory and Practice.

1. VRT Theory and Practice. Dr. Mohammad Shafique Asghar Au.D, (USA). American Board of Audiology, (Board certified audiologist). M.Sc Audiological Medicine,(UK). MCPS (ENT), M,B.B,S (Pb).

2. The reality; • Pharmacology and surgery have not been the solution for most patients with UVD/BVD or BPPV. • So VRT has emerged over several years as an exciting and successful alternative treatment for patients with chronic non resolved motion intolerance and imbalance problems.

3. VRT: Definition • VRT can be described as systematic repetitive exercises and protocols which extinguish or ameliorate patient’s motion provoked symptoms as well as enhancing postural stability and equilibrium.

4. History of VRT • VRT is not new. • Cawthorne (1944) and Cooksey (1946) were the the first who discussed the benefits of active eye and head movement exercises for the patients with chronic labyrinthine problems. • Brandt Daroff (1980) and Norre & De Werdt (1980) reported treatment protocols and efficacy of VRT for patients with peripheral vestibular dysfunction.

5. H/O VRT. • Horak, Shumway-cook, Beckers, Heardman, Shepherd, Telian, and SmithWheelock are some of other names who contributed a lot for VRT in mid and late eighties. • Semont, Freyss and Vitte (1988) introduced Liberatory maneuver for BPPV. • Epley (1993) and Parnes and Price-Jones (1993) introduced Canalith repositioning Maneuver for BPPV.

6. How Does VRT work? • The underlying physiological bases For VRT is “Plasticity of the CNS”. • VRT does not work by regeneration or treatment of the damaged vestibular end organs. • It works by allowing the CNS to acclimate or adapt to asymmetrical/conflicting input from the vestibular mechanism.

7. How does VRT work • Normally the CNS compensates within 90 days following dysfunction or loss of the vestibular system. • But certain vestibular lesions, particularly those that occur with rapid onset, do not benefit from compensation phenomenon.

8. How does VRT work • The reasons for failure of compensation. • Reluctance of the patients to do any activities involving active head movements which produce symptoms of dizziness. • “The brain cannot fix what the brain cannot see”. • Drugs like Meclizine, Valium and Stugron which either suppress CNS or peripheral vestibular function also hamper central compensation.

9. Role of Vest, Visual and somatosensory Systems • The primary roll of vestibular system is to tell the brain where the head is. So it acts as an internal reference to tell the brain how the head is oriented in space. • The visual and somatosensory systems are the external references, providing the brain with the information about the movement and stability of the world around us. • Working together in harmony they help us maintain a normal equilibrium.

10. Candidacy for VRT • VRT works best for the patients who are not in acute phase of the disease. (Symptoms no longer have the acute labyrinthine storm with debilitating vertigo accompanied by nausea, vomiting and diaphoresis). • Patients with End stage Meniere's disease who do not have any active diseases, but have signs and symptoms of vestibulopathy and patients with Labyrinthitis, Vestibular neuritis, vertibrobasilar and labyrinthine ischemia.

11. Signs and symptoms of patients for VRT • Symptoms are provoked by head movement, • Particular frequency of motion and in particular direction. • There may be significant visual provocation. • Sense of motion sickness while looking at certain patterns of floor tiles or wallpapers. • Difficulty in walking down the aisle of a grocery store while turning their head side to side and up and down while shopping.

12. VRT. Strategies • Adaptation • And substitution protocols

13. Diagnosis based strategies • To obtain maximum outcome the correct therapeutic strategies must be used. • Strategies may be combined. • Adaptation Or Substitution • Adaptation and Substitution • Repositioning /Liberatory

14. Diagnosis based strategies. Dx Category: • High frequency non compensated. • Vestibulopathy w/o unsteadiness • Vestibulopathy w/ unsteadiness. • Bilateral loss/CNS • BPPV Strategy: • Adaptation • Adaptation • Adaptation and Substitution • Substitution • Repositioning/Liberatory

15. Diagnosis based strategies (Diagnostic categories) • High frequency non-compensated weakness in one or both systems, provoked with dynamic movements (Peripheral vestibular). • Unilateral vestibular loss or distortion (peripheral) without unsteadiness.

16. Diagnostic categories (cont).. 3. Unilateral vestibular loss or distortion (peripheral) with unsteadiness. 4. Bilateral vestibular loss (peripheral)

17. Diagnostic categories (cont).. 5. Central dizziness (central motor or movement coordination deficit).May involve neurologic or vascular components, e.g., Cerebellar infarct or peripheral neuropathy (feet). 6. BPPV (peripheral).

18. Diagnostic categories. • Brief description of causes, symptoms and signs of each diagnostic category.

19. Vestibulopathy • The first three categories can be attributed to a vestibulopathy. • Vestibulopathy may be described as a change or reduction in the function of one or both of the peripheral vestibular mechanisms. • The actual pathophysiology is less important than the provoking stimuli of the symptoms. • So whatever the cause is (Meniere’s disease, vestibular neuritis or a surgical procedure, it is the manifestation of the dysfunction that will be treated.

20. Vestibulopathy Within vestibulopathy there are three main categories. • Non compensated high frequency type lesion. (Ear analogy of frequency). • Symptoms/signs. • C/O not being right, when turning their heads. • Almost oscillopsia type f symptoms related to head movement.

21. Vestibulopathy • This is because of asymmetrical input from both vestibular systems. • This asymmetrical signal causes a defect in either the gain or phase of the VOR. • The patient only has symptoms at high frequency of head movements. • ENG and Calorics are often normal • Only diagnosed with HFHS test or VAT.

22. Vestibulopathy (cont)… 2. Unilateral vestibular loss without unsteadiness. Symptoms/signs. • Present with more acute symptoms, sometimes mimic like BPPV • May C/O motion intolerance • A common complaint is the inability to look down while riding on a down escalator, but do not have a complaint while going up.

23. Vestibulopathy (cont)… • Significant weakness on Calorics • Direction fixed nystagmus (beating towards better ear) on many of the gaze and positional tests.

24. Vestibulopathy (cont)… 3. Unilateral vestibular loss with unsteadiness. • Symptoms/signs. • All the symptoms of Vest. W/O unsteadiness and. • Loss of surefootedness. • Patient will adapt compensatory strategies by touching the walls or furniture as they walk. • Some C/O as if walking drunk and cannot walk in a straight line.

25. Vestibulopathy (cont)… • Significant weakness on Calorics • Direction fixed nystagmus (beating towards better ear) on many of the gaze and positional tests. • Posturography with and without computer will reveal a visual and surface dependence with poor stability on vestibular only sensory condition.

26. Dysequilibrium • This may be either because of: • Bilateral peripheral vestibular loss. • CNS origin.

27. Bilateral Peripheral vestibular loss. • Symptoms/signs. • Patient cannot maintain balance with their eyes closed. • May also occur in elderly because of changes in vascular supply to the vestibular systems as occur in presbyacusis.

28. CNS related. • Causes. • Cerebellar infarcts, • Brainstem small vessel ischemia, • Age related Cerebellar atrophy, • Diseases causing peripheral neuropathy like diabetes and vascular diseases. • The term Presbyastrasia is often used to describe these age related equilibrium deficits.

29. CNS related (cont)… • Signs/symptoms • Loss of surefootedness. • Patient will adapt compensatory strategies by touching the walls or furniture as they walk. • Some C/O as if walking drunk and cannot walk in a straight line.

30. CNS related (cont)… • ENG abnormalities on voluntary ocular motor tasks. • Low intensity (3-5 deg/sec) direction fixed nystagmus will be present. • Nystagmus never changes or enhances with dynamic movements or high frequency head shake test.

31. CNS related (cont)… • Calorics may be robust and normal. • Functional abnormalities are most prominent on Posturography showing high degree of instability, even on easier sensory conditions.

32. Why VRT works • Adaptation: • Exercises which extinguish symptoms through repetition of provoking type activities. • Enhance recovery of VOR function. • Occurs due to plasticity of the CNS.

33. Adaptation protocols. • Easy - static. • Difficult – Dynamic. • This protocol: Reduce retinal slippage. And enhance gaze stabilization.

34. Adaptation maneuver

35. Why VRT works • Adaptation. CNS and vestibular system learn to adapt to imbalanced signal coming from peripheral vestibular sensory receptor. Role of VOR: VOR is mediated by vestibular system. In case the signals from the two internal head sensors are asymmetrical the result is a sense of “after motion” with head motion.

36. Adaptation (cont…) • So in case of peripheral vestibulopathy the VOR is disturbed. • Gaze stabilization exercises work to return the VOR to eliminate the retinal slippage and patients perception of after motion.

37. Substitution Method • Strengthens weakened system to return to function by challenging remaining ones. • Forces remaining systems to become more trustworthy when others are lost.

38. Substitution Method • Easy – Static with Eyes open/closed. • Difficult- Dynamic, Eyes open/closed

39. Substitution Maneuver

40. (VRT) Substitution method. • The principal involved is compensatory shift. • If a sense is lost, the individual simply learns to utilize other senses more efficiently.

41. Building protocols. • Start with the protocols which are easier to perform and then work to more difficult ones. • It is helpful to plan the protocols two to three sessions ahead.

42. Liberatory/Repositioning and Desensitization For the treatment of BPPV • Brandt Daroff Maneuver. • Semont’s Liberatory Maneuver. • Epley’s Maneuver.

43. Therapy models. • Self directed exercises. • Clinician directed exercise. • Balance retraining. • Repositioning/Liberatory maneuvers.

44. Self Directed Exercises. • This model is suitable for the patients who.. • Do not require supervision during exercises. • Are not in acute phase • The people who cannot travel so frequently. • Each program is individually tailored based on the test results and the situations which provoke symptoms.

45. Self Directed Exercises (cont)… • Patients attends a one hour instructional session at clinic. • Then patient is provided with a set of protocols within a self directed program. • For best results patient has to at least 20-30 min/session 2-3 times a day. • Most patients improve within 3-4 wks treatment span.

46. Clinician directed exercises: • This model is suitable for the patients… • Whose symptoms may be sever or relatively acute • And require supervision during exercises.

47. Clinician directed exercises (cont)… • Therapy session involves use of special vestibular therapy apparatus. • There is also emphases on fall prevention. • Usually patient participates in one or two 60 min sessions/wk. • Average program length is 8-10 sessions. • As patients progress this exercise protocol is supplemented with self directed exercises.

48. Balance retraining • This model is suitable for the patients… • Who have loss of balance, • Unsteadiness, • Loss of surefootedness. • These patients do not have dizziness or motion intolerance.

49. Balance retraining (cont)… • An emphases is placed on practical solutions to the common problems of getting around in the dark and walking on uneven surfaces such as thick carpets, thick grass and moving on ramps and stairs. • Fall prevention, • Movement coordination and improved participation in everyday activities are the hallmark of the program.

50. Balance retraining