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

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

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

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

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 30 o

Modified Right Lateral Position

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

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