improving life and end-of-life care in advanced neurological conditions: spasticity management rory...
TRANSCRIPT
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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
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Overview
What is spasticity?
Epidemiology
Current spasticity treatment
Pharmacotherapy
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What is Spasticity?
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Spasticity Diagnosis
Central nervous system lesion– Motor and sensory loss
Increased muscle tone– Especially rate dependent increase in tone
Provoked or unprovoked spasms
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Consequences of Spasticity
Contractures
Skin breakdown
Pain and discomfort
Impairments
Restricted participation
Caregiver strain
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Spasticity
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What is Spasticity?
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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 (+)
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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
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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
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Loss of Supraspinal Input
Uncontrolled efferent drive– Hemiplegic posture
Associated reaction– Failure to inhibit spread of motor activity
Disordered muscle control– Co-contraction
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Neurotransmitters
Gamma amino butyric acid (GABA)– Inhibition of motor neurons
Glutamate– Excitation of motor neurons
Alpha-2 adrenergic– Spinal interneuron inhibition
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Soft Tissues in Spasticity
Muscle biochemical changes: thixotropy– Stiffness– Contracture– Fibrosis– Atrophy
Tendon changes
Joint changes
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What is Spasticity?
An increased tonic stretch reflex resulting in velocity- and length-dependent hypertonia due to abnormal spinal processing of proprioceptive input
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Epidemiology of Spasticity
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Epidemiology of Spasticity
Spinal– Traumatic spinal cord injury 60%– Non-traumatic spinal cord injury
Supraspinal– Stroke 20%– Multiple Sclerosis 30%– Cerebral Palsy 50%– Traumatic Brain Injury 19%*
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Current Spasticity Treatment
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Current Spasticity Treatment
Reduction of noxious stimuli
Multidisciplinary programme
Pharmacotherapy– Generalised, regional, focal
Surgery
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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
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Reduction of Noxious Stimuli
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Reduction of Noxious Stimuli
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Reduction of Noxious Stimuli
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Reduction of Noxious Stimuli
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Reduction of Noxious Stimuli
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Reduction of Noxious Stimuli
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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
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Seating
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Pharmacotherapy
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Pharmacotherapy Follow-up
No point in pharmacotherapy without– Avoidance of precipitating factors– Adequate therapy/splinting/orthosis– Appropriate seating review
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Pharmacotherapy
Generalised– Oral baclofen, dantrolene, tizanidine
Regional– Intrathecal baclofen or phenol
Focal– Intramuscular botulinum, phenol neurolysis
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Generalised
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Generalised
Reduce excitatory neurotransmitters– Tizanidine
Facilitate inhibitory neurotransmitters– Baclofen
Inhibit skeletal muscle contraction– Dantrolene
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Regional
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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
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Intrathecal Pump
Abdominal pocket for pump
Intrathecal catheter tunnelled subcutaneously
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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
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Modified Right Lateral Position
Spinal fluid
30o
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Modified Right Lateral Position
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Injection of Phenol
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Injection of Phenol
Spinal fluid
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Injection of Phenol
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End Result
Spinal fluid
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Unexpected Findings
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Final Outcome
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Focal
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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
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Commonly Blocked Nerves
Musculocutaneous– Biceps brachii, brachialis
Obturator– Hip adductors
Sciatic– Hamstrings
Posterior tibial– Gastrocnemius, soleus
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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
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EMG Guidance
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Botulinum - FDS
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Botulinum - FDP
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Botulinum - Hypersalivation
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Botulinum - Hypersalivation
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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
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Take Home Message II
Spasticity is the result of– Neural– Non-neural
} abnormalities
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Take Home Message III
Multidisciplinary treatment must comprise– Neural– Non-neural
} modalities