5. Spasticity causes and neurosurgical management .pptx

Spasticity causes and neurosurgical management

1. Spasticity causes and neurosurgical management

2. Spasticity Spastikos - “to draw or tug” Motor disorder Velocity-dependent increased resistance to passive stretch Exaggerated tendon jerks Hyperexcitability of the stretch reflex - James Lance (1980)

3. Pathophysiology of Spasticity Theory Imbalance between excitatory and inhibitory impulses to the alpha motor neuron Due to a lack of descending inhibitory input to the alpha motor neuron Descending Inhibition Sensory Excitation

4. Pathophysiology of Cerebral Origin Spasticity Inhibitory signals modulate reflex signals–tone remains normal Lack of neural inhibition leads to spasticity Normal brain delivers inhibitory neural signals to the spinal cord Damaged brain fails to generate or sends inadequate inhibitory signals

5. Pathophysiology of Spinal Origin Spasticity Inhibitory signals modulate reflex signals–tone remains normal Lack of neural inhibition leads to spasticity Inhibitory neural signals sent to the alpha motor neuron Damaged spinal cord fails to relay adequate inhibitory signals Normal Damaged

6. Factors aggravate spasticity Age and Ageing 2013; 42: 435–41.

7. Causes BMJ 2014;349:g4737 doi : 10.1136/bmj.g4737 (Published 5 August 2014)

8. Characteristics of Spasticity Hyperactive stretch reflex Increased resistance to passive movement Posturing of extremities Stereotypical movement synergies Spasticity of arm showing excessive flexion of elbow, wrist, and fingers BMJ 2014;349:g4737 doi : 10.1136/bmj.g4737 (Published 5 August 2014)

9. Clinical features of spasticity Clonus Involuntary rhythmic contractions triggered by stretch; these can interfere with walking, transfers, sitting, and care Spasms Sudden involuntary movements that often involve multiple muscle groups and joints in response to somatic or visceral stimuli Spastic dystonia Tonic muscle overactivity without any triggers owing to the inability of motor units to cease firing after a voluntary or reflex activity; results in characteristic limb postures and contractures Spastic co-contraction Inappropriate activation of antagonistic muscles during voluntary activity due to lack of reciprocal inhibition causing a loss of dexterity and slowness in movements BMJ 2014;349:g4737 doi : 10.1136/bmj.g4737 (Published 5 August 2014)

10. Possible Advantages of Spasticity Maintains muscle tone Helps support circulatory function May prevent formation of deep vein thrombosis May assist in activities of daily living

11. Consequences of Spasticity May interfere with mobility, exercise, joint range of motion May interfere with activities of daily living May cause pain and sleep disturbance Can make patient care more difficult

12. Measuring Spasticity Ashworth and Modified Ashworth scales Spasm and reflex scales Passive quantitative tests Active tests of movement

13. Differential diagnosis Contractures Rigidity Catatonia

14. Goals of Spasticity: Management Decrease spasticity Improve functional ability and independence Decrease pain associated with spasticity Prevent or decrease incidence of contractures Improvement of posture Facilitation of sitting, standing, and walking Reduction in burden of care Improvement of hygiene in areas such as palm, axilla , and groin Improvement in body image and self esteem Prevention of complications such as pressure ulcers Facilitate hygiene Ease rehabilitation procedures Save caregivers’ time BMJ 2014;349:g4737 doi : 10.1136/bmj.g4737 (Published 5 August 2014)

15. Spectrum of Care for Management of Spasticity Injection Therapy Neurosurgery Orthopedic Treatments Rehabilitation Therapy Prevent Nociception Intrathecal Baclofen (ITB™) Therapy Oral Drugs Patient

16. Traditional Step-Ladder Approach to Management of Spasticity Neurosurgical Orthopedic Neurolysis Oral medications Rehabilitation Therapy Remove noxious stimuli

17. Rehabilitation Therapy Stretching Weight bearing Inhibitory casting Vibration of the antagonist Pool therapy EMG biofeedback Electrical stimulation Positioning and rotary movements

18. Correct positioning in side lying Age and Ageing 2013; 42: 435–41.

19. Correct Wheelchair Positioning Age and Ageing 2013; 42: 435–41.

20. Pharmacological Intervention [Ward (2002)] Generalized spasticity Oral agents Regional spasticity Intrathecal baclofen phenol nerve block Focal Spasticity Botulinum toxin phenol block

21. Pharmacological Intervention Oral Medications Baclofen Dantrolene Sodium Tizanidine Gabapentin Diazepam

22. Pharmacological Intervention Oral agents… BMJ 2014;349:g4737 doi : 10.1136/bmj.g4737 (Published 5 August 2014)

23. Pharmacological Intervention Regional Spasticity Intrathecal Drug Therapy - administered directly into subarachnoid space of CNS with a programmable pump Intrathecal Baclofen , Morphine Sulphate ( Infumorph ), Fentanyl . Improvement in walking speed, functional mobility without impairing uninvolved extremity. Fewer systemic side effects because not circulating in blood stream. Infection, impaired wound healing, pump malfunction, and catheter dislocation in 20-25% of cases.

24. Pharmacological Intervention: Focal Spasticity Chemical Neurolytics - destruction of a portion of the nerve. Phenol Injections - causes chemical (Wallerian) denervation. Dose dependent, hit proximal muscles first. Works at alpha motorneurons directly. Pain at administered site, causalgia w/ sensory nerve injury. Botulinum Toxin - binds to presynaptic cell and prevents NT release. Begins 3-7 days and last 2-6 months, specific muscles. May have diminishing returns (A &B), small muscles..

25. Pharmacological Intervention Oral Drugs Diazepam Brainstem reticular formation and spinal polysynaptic pathways Fatigue; reduced motor coordination, intellect, attention, memory Dantrolene Sodium Skeletal muscle calcium stores Hepatotoxicity, generalized muscle weakness Oral Baclofen GABA-b receptors Drowsiness, confusion, headache, lethargy Tizanidine Hydrochloride a2-adrenergic receptors Dizziness, sedation, dry mouth Intrathecal Drugs Intrathecal Baclofen Gaba-b receptors Pump malfunction/ dislocation Focal Drugs Phenol Injection Neuromuscular junction Causalgia with sensory nerve injury, pain at injection site, hematoma Botulinum Toxin Nerve Injection site pain, muscle weakness in injected muscle, hematoma, muscle necrosis, phlebitis [ Gallichio , (2004)] Drug Site of Action Adverse Effects

26. Neurosurgery Surgical Treatments Neurodestructive Procedures Selective Dorsal Rhizotomy (SDR) Rhizotomy Neurectomy Myelotomy Cordectomy

27. SDR: The Basics First performed in 1913, but did not become popular until 1970’s Dorsal rhizotomy became selective and outcomes evaluated since 1987 SDR involves cutting sensory nerve roots that when stimulated, trigger exaggerated motor responses as measured by EMG intraoperatively

28. SDR: Procedure Multilevel laminectomy vs. minimally invasive approaches L1 – S1 sensory roots are identified and divided into 3-5 rootlets Each rootlet is stimulated and responses are measured via EMG Rootlets with the most abnormal signal are cut Surgery takes about 4 hours

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33. SDR: Potential Complications Paralysis of legs Neurogenic bladder Sensory loss or dysethesias Wound infection CSF leak

34. SDR: Outcomes of Metanalysis Children with diplegic CP (GMFCS II-III) received SDR + PT, or PT w/o SDR. Concluded that SDR + PT is efficacious in reducing spasticity and has a small effect on gross motor function McLaughlin J et al. Dev Med Child Neuro 2002, 44: 17-25.

35. SDR versus ITB 1-year outcomes of 71 children who underwent SDR before 1997 versus 71 children with ITB, matched by GMFCS and age Both interventions significantly decreased Ashworth scores, increased PROM, improved function and resulted in high parental satisfaction Compared with ITB SDR provided greater improvements in muscle tone, PROM, and gross motor function Fewer patients in the SDR group required subsequent orthopedic procedures No difference between the degree of parents’ satisfaction Kan P et al. Childs Nerv Syst. 2007 Sep 5.

36. SDR: Outcomes Short and long term outcomes demonstrate: Decreased spasticity Improved or unchanged strength Improved gait pattern Decreased oxygen cost Improved overall function including decreased use of walking aids

37. SDR: Candidacy Determinations Pre-term birth Imaging consistent with PVL Primarily spastic tone Evidence of fair selective motor control Demonstrated ability to cooperate and follow through with rehabilitation program Patient selection Red flags Hyperextension at the knee in gait Multiple orthopedic procedures Generalized lower extremity/trunk weakness Poor incorporation of trunk in gait Poor isolated control of lower extremity movement Poor rehab potential (behavior, sensory issues, cognition, social)

38. Surgical Intervention [Lazorthes et al. (2002)] Neurosurgery - severe and painful spasticity, irreversible. Dorsal rhizotomies - Regional spasticity . Cut dorsal cords and grey mater ( gelatinosa area). Can cause decrease in voluntary mobility, sepsis, decreased lemniscal sensitivity, and death. Peripheral neurotomies - Focal spasticity. Used if botulinum toxin failed. Done distally only reducing the myotatic reflex. Cervical Spinal Cord Stimulation - reversible. E Stim administered directly to spinal area. Intrathecal Baclofen is more commonly used.

39. Orthopedic Surgeries Soft Tissue Procedures Tendon lengthening Tendon transfers Tenotomy Myotomy

40. Surgical Intervention [Woo (2001)] Tendon Lengthening - preferred method Allow full passive range with some residual muscle tension. Muscle must be immobilized under tension. Tendon Transfer - used on children (Shriner’s) Gait analysis with dynamic electromyographic monitory helps reduce common errors associated with this procedure. Osteotomy - for skeletal deformity Restore boney architecture, muscle-length can be improved. Used along with tendon lengthening. Artrhodesis - joint fusion When the above are prohibited. Stabilize unstabel joints (subtalar, thumb, wrist).

41. Conclusion Spasticity is a frequent and debilitating feature of common neurological conditions such as stroke, multiple sclerosis, and traumatic brain and spinal cord injuries The disorder is often associated with pain and discomfort and increased care needs Spasticity is difficult to manage and requires a collaborative approach involving multiple disciplines The evidence for both drug and non-drug treatments of spasticity is limited More research is required to determine the effectiveness of various treatments of spasticity

42. References Woo, R. Spasticity: Orthopedic Perspective. Journal of Child Neurology. 2001; 16(1): 47-53 Barnes, M. Management of Spasticity. Age and Ageing. 1998;27:239-245 Gallichio , Joann E. Pharmacologic Management of Spasticity Following Stroke. Physical Therapy Journal . 2004; 84: 973-981 Lazorthes , Y., Sol, J-C., Verdie , S., & J-C. The Surgical Management of Spasticity. European Journal of Neurology. 2002; 9(1): 35-41 Ward A. B. A Summary of Spasticity Management - a Treatment Algorithm. European Journal of Neurology . 2002; 9: 48-52