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

Overview

What is spasticity?

Epidemiology

Current spasticity treatment

Pharmacotherapy

What is Spasticity?

Spasticity Diagnosis

Central nervous system lesion– Motor and sensory loss

Increased muscle tone– Especially rate dependent increase in tone

Provoked or unprovoked spasms

Consequences of Spasticity

Contractures

Skin breakdown

Pain and discomfort

Impairments

Restricted participation

Caregiver strain

Spasticity

What is Spasticity?

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 (+)

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

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

Loss of Supraspinal Input

Uncontrolled efferent drive– Hemiplegic posture

Associated reaction– Failure to inhibit spread of motor activity

Disordered muscle control– Co-contraction

Neurotransmitters

Gamma amino butyric acid (GABA)– Inhibition of motor neurons

Glutamate– Excitation of motor neurons

Alpha-2 adrenergic– Spinal interneuron inhibition

Soft Tissues in Spasticity

Muscle biochemical changes: thixotropy– Stiffness– Contracture– Fibrosis– Atrophy

Tendon changes

Joint changes

What is Spasticity?

An increased tonic stretch reflex resulting in velocity- and length-dependent hypertonia due to abnormal spinal processing of proprioceptive input

Epidemiology of Spasticity

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%*

Current Spasticity Treatment

Current Spasticity Treatment

Reduction of noxious stimuli

Multidisciplinary programme

Pharmacotherapy– Generalised, regional, focal

Surgery

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

Reduction of Noxious Stimuli

Reduction of Noxious Stimuli

Reduction of Noxious Stimuli

Reduction of Noxious Stimuli

Reduction of Noxious Stimuli

Reduction of Noxious Stimuli

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

Seating

Pharmacotherapy

Pharmacotherapy Follow-up

No point in pharmacotherapy without– Avoidance of precipitating factors– Adequate therapy/splinting/orthosis– Appropriate seating review

Pharmacotherapy

Generalised– Oral baclofen, dantrolene, tizanidine

Regional– Intrathecal baclofen or phenol

Focal– Intramuscular botulinum, phenol neurolysis

Generalised

Generalised

Reduce excitatory neurotransmitters– Tizanidine

Facilitate inhibitory neurotransmitters– Baclofen

Inhibit skeletal muscle contraction– Dantrolene

Regional

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

Intrathecal Pump

Abdominal pocket for pump

Intrathecal catheter tunnelled subcutaneously

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

Modified Right Lateral Position

Spinal fluid

30o

Modified Right Lateral Position

Injection of Phenol

Injection of Phenol

Spinal fluid

Injection of Phenol

End Result

Spinal fluid

Unexpected Findings

Final Outcome

Focal

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

Commonly Blocked Nerves

Musculocutaneous– Biceps brachii, brachialis

Obturator– Hip adductors

Sciatic– Hamstrings

Posterior tibial– Gastrocnemius, soleus

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

EMG Guidance

Botulinum - FDS

Botulinum - FDP

Botulinum - Hypersalivation

Botulinum - Hypersalivation

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

Take Home Message II

Spasticity is the result of– Neural– Non-neural

} abnormalities

Take Home Message III

Multidisciplinary treatment must comprise– Neural– Non-neural

} modalities