Improving life and endoflife care in advanced neurological conditions: Spasticity Management

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Improving life and end-of-life care in advanced
neurological conditionsSpasticity Management

• Rory OConnor 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

• Reflex disinhibition
• Nociceptive reflex flexor withdrawal
• Propriospinal phasic reflex tendon reflex
• Primitive reflex release
• Cutaneous extensor plantar response
• Proprioceptive positive support reaction
• 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
30o
Spinal fluid
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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