1. Improving life and end-of-life care in advanced neurological conditions: Spasticity Management Rory O’Connor MD Consultant Physician in Rehabilitation Medicine Airedale General Hospital

2. Overview What is spasticity? Epidemiology Current spasticity treatment Pharmacotherapy

3. What is Spasticity?

4. Spasticity Diagnosis Central nervous system lesion –Motor and sensory loss Increased muscle tone –Especially rate dependent increase in tone Provoked or unprovoked spasms

5. Consequences of Spasticity Contractures Skin breakdown Pain and discomfort Impairments Restricted participation Caregiver strain

6. Spasticity

7. What is Spasticity?

8. Supraspinal Input Supraspinal or higher spinal lesion results in a net loss of inhibition below lesion –Dorsal Reticulospinal tract ( - ) –Medial Reticulospinal tract (+) –Corticospinal tract (+) –Vestibulospinal tract (+) –Coerulospinal tract (+)

9. Spinal Input 1.Reflex disinhibition –Nociceptive reflex: flexor withdrawal –Propriospinal phasic reflex: tendon reflex 2.Primitive reflex release –Cutaneous: extensor plantar response –Proprioceptive: positive support reaction 3.Tonic stretch reflex

10. Tonic Stretch Reflex No reflex activity in response to muscle stretch in a relaxed normal person Mediated via 1a afferents from muscle spindle Length dependent –Reflex inversely related to muscle length

11. Loss of Supraspinal Input Uncontrolled efferent drive –Hemiplegic posture Associated reaction –Failure to inhibit spread of motor activity Disordered muscle control –Co-contraction

12. Neurotransmitters Gamma amino butyric acid (GABA) –Inhibition of motor neurons Glutamate –Excitation of motor neurons Alpha-2 adrenergic –Spinal interneuron inhibition

13. Soft Tissues in Spasticity Muscle biochemical changes: thixotropy –Stiffness –Contracture –Fibrosis –Atrophy Tendon changes Joint changes

14. What is Spasticity? An increased tonic stretch reflex resulting in velocity- and length-dependent hypertonia due to abnormal spinal processing of proprioceptive input

15. Epidemiology of Spasticity

16. Spinal –Traumatic spinal cord injury60% –Non-traumatic spinal cord injury Supraspinal –Stroke20% –Multiple Sclerosis 30% –Cerebral Palsy50% –Traumatic Brain Injury 19%*

17. Current Spasticity Treatment

18. Reduction of noxious stimuli Multidisciplinary programme Pharmacotherapy –Generalised, regional, focal Surgery

19. Spasticity Treatment Cost may inhibit decision to treat –Time-consuming and multidisciplinary –Expensive equipment and seating systems But untreated spasticity –May mask voluntary movement –Result in permanent contractures –Window of opportunity may be small

20. Reduction of Noxious Stimuli

26. Multidisciplinary Teamwork Careful positioning throughout 24-hours –Maintaining muscle length –Reducing deformity Regular stretching Splinting and orthoses All act to reduce the tonic stretch reflex

27. Seating

28. Pharmacotherapy

29. Pharmacotherapy Follow-up No point in pharmacotherapy without –Avoidance of precipitating factors –Adequate therapy/splinting/orthosis –Appropriate seating review

30. Pharmacotherapy Generalised –Oral baclofen, dantrolene, tizanidine Regional –Intrathecal baclofen or phenol Focal –Intramuscular botulinum, phenol neurolysis

31. Generalised

32. Reduce excitatory neurotransmitters –Tizanidine Facilitate inhibitory neurotransmitters –Baclofen Inhibit skeletal muscle contraction –Dantrolene

33. Regional

34. Intrathecal Baclofen Test dose to screen for effectiveness Non-destructive and reversible Dose titratable Reduction of side effects compared to oral baclofen –1% of oral dose

35. Intrathecal Pump Abdominal pocket for pump Intrathecal catheter tunnelled subcutaneously

36. Intrathecal Phenol Severe lower limb spasticity affecting care, positioning or causing pain Generalised treatments ineffective or causing side effects Other regional and focal treatments inappropriate Bowel, bladder and sexual dysfunction

37. Modified Right Lateral Position Spinal fluid 30 o

38. Modified Right Lateral Position

39. Injection of Phenol

40. Spinal fluid

41. Injection of Phenol

42. End Result Spinal fluid

43. Unexpected Findings

44. Final Outcome

45. Focal

46. Phenol Nerve Blocks Non-selective denervation –Protein denaturation –Destruction of nerve axons Effect apparent immediately and diminishes with time Injection of mixed nerves will cause anaesthesia as well as paralysis

47. Commonly Blocked Nerves Musculocutaneous –Biceps brachii, brachialis Obturator –Hip adductors Sciatic –Hamstrings Posterior tibial –Gastrocnemius, soleus

48. Botulinum Botulinum exotoxin –Types A and B available commercially Intramuscular injection –Endocytosed in pre-synaptic neuron –Cleaves acetylcholine –Neuromuscular junction function inhibited Axon sprouting terminates effect 2-6 months

49. EMG Guidance

50. Botulinum - FDS

51. Botulinum - FDP

52. Botulinum - Hypersalivation

54. Take Home Message I Spasticity limits activities in two ways –Inhibiting muscle power and coordination –“Masking” profound muscle weakness But anti-spasticity agents produce muscle weakness

55. Take Home Message II Spasticity is the result of –Neural –Non-neural } abnormalities

56. Take Home Message III Multidisciplinary treatment must comprise –Neural –Non-neural } modalities