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SPASTICITY
Spasticity
 Develops after spinal or cerebral lesions involving Upper Motor
Neurones of the corticospinal tracts, and is one part of the UMN
syndrome.
 A motor disorder characterised by an increase in muscle tone in
response to stretch of relaxed muscle.
 Unlike other types of hypertonia the response is velocity dependent
and is seen in the anti-gravity muscles, lower limb extensors, upper
limb flexors. This distinguishes spasticity from Parkinsonian rigidity.
 It results from a change in sensitivity of central reflex pathways, due
to enhanced motor neurone and interneurone excitability.
 Hypertonia is characterised by a velocity dependent increase in tonic
stretch reflexes with exaggerated tendon jerks, resulting from
hyperexcitability of the stretch reflex.
 It is length dependent, greater in the lower limb extensors when at a
shorter length, and the flexors when at a longer length. The opposite is
seen in the upper limb.
Upper motor neurone
 Neurones in any long descending tract that control or influence
movement and muscle tone, having a more or less direct influence upon
the excitability of the lower motor neurone (Anterior Horn Cell).
 Influence may be via direct synapse (corticospinal tract) or via the
interneural network.
Upper motor neurone syndrome
 This arises because of the interruption of supraspinal control.
 Negative phenomena are characterised by a reduction in motor
activity
 Positive phenomena are characterised by excessive motor activity.
Flexor spasms
 They occur spontaneously, or in response to cutaneous stimuli, which
need not be noxious.
 They are more common in spinal lesions, resulting in flexion of hip
and knee, with dorsi-flexion, and may also result in adduction and
internal rotation of the hip.
 They are due to lack of supraspinal inhibition of the flexor reflex
afferents, and disinhibition of the normal flexor withdrawal reflex.
Extensor spasms
 More common in incomplete spinal and cerebral lesions.
 Result in extension of hip and knee, with inversion and plantar
flexion.
 An example is the Positive Support Reaction, triggered by sensory
feedback from pressure on the ball of the foot as it touches the floor
when standing.
Associated Reactions
 Involuntary unnecessary activation of muscles remote from those
engaged in a task.
 They are triggered remotely, therefore motor activity in one part of
the body is associated with unintentional motor activity elsewhere.
 The severity increases with increased difficulty of the provoking
activity, and with an increase in effort.
Tendon Hyperreflexia
 Hyperactive reflexes which may occur independently of spasticity.
 May get radiation, due to muscle spindle sensitivity.
Clonus
 Occurs in the presence of exaggerated tendon reflexes.
 A sharp passive dosiflexion of the ankle causes a rhythmic contraction
of the plantarflexors, by eliciting a stretch reflex. The plantarflexors
contracting eliminates the stretch and the muscle relaxes. A rhythmic
tremor-like pattern of contraction and relaxation is set up.
Postural Tone
 The state of readiness of the body musculature in preparation for the
maintenance of a posture or the performance of a movement.
 Stabilisation of the limbs/trunk in optimal position for local
movement.
 A large supportive base of support is conducive to relaxation and a
general lowering of postural tone.
 An unstable, narrow base of support results in a heightening of
postural tone.
Muscle Tone
 The resistance felt to passive movement in a state of voluntary
relaxation.
 Normally no tonic stretch reflex is elicited, ie no muscle
contraction is produced.
Co-contraction
 Simultaneous contraction of agonists and antagonists, part of normal
reciprocal innervation providing postural fixation and stability.
 Dysfunction occurs in the UMN syndrome. Normally co-contraction
is activated and de-activated at cortical level and at spinal level by
reciprocal inhibition, but this is under supraspinal control. In UMN
syndrome, failure of normal reciprocal inhibition results in
inappropriate co-contraction, which inhibits normal modulation and
restricts movement and function.
Reciprocal Innervation
 Graded interaction of agonists, antagonists and synergists during
maintainence of a posture or performance of a movement.
 Essential for balance, maintaining the centre of gravity over the base
of support and providing body stability throughout postural
adjustments.
Clinical Consequences of the Positive Phenomena in UMN
Syndrome.
 3 main consequences:
Restrict movement
Cause excessive or inappropriate
movement.
Cause pain.
 Resulting clinical problems: Reduced function, both active
(patient’s voluntary function) and
passive (activities that are done
for the patient).
Interfere with physical therapies
Cause tissue damage
Produce soft tissue and joint changes.
 Muscles remaining in a shortened position result in soft tissue
damage.
 Attempted movements may be restricted due to the stretch reflex –
the patient is trying to move against their own hypertonia.
 Some EMG studies have shown that voluntary movement is often
too slow to elicit a stretch reflex.
Measurement of spasticity
Measurement of spasticity is difficult because of its complex, multifactorial and fluctuating nature. It is influenced by both neural and
non-neural factors, for example:
Noxious stimuli
The position of the limb against gravity
The degree of co-contraction of the antagonist muscle
The extent of available voluntary control in the limb
Constipation
Bladder problems
Medication
Mental/emotional state – fear, anxiety
Room temperature
Time of day
Speed of movement
Fatigue
Tone of voice
Measurement of resistance to passive movement and available joint
range in a limb will provide some measure of spasticity, but this will
not distinguish between the neural and biomechanical components.
Ashworth Scale
Originally designed to study an anti-spastic drug in the treatment of
spasticity in adults with MS. It has been found to have good reliability
for elbow flexor tone. However, there is lack of standardisation of
technique, for example the velocity of the movement, the number of
repetitions, and the testing position used.
Measurement of the common consequences of spasticity and the
UMN syndrome.
Pain – Visual analogue scale, Pain rating scale.
Abnormal limb posture (spastic dystonia) – video, photos.
Associated reactions – mild, moderate, severe.
Joint range – goniometry
Medical and surgical treatment of spasticity
The importance of physiotherapy and patient education in the
management of increased tone is essential. Medical and surgical
treatments of varying efficacy and invasiveness are available, but to
be effective they should be used in conjunction with physiotherapy.
Medical Management
The functioning of the spinal reflexes and the supraspinal pathways
are mediated by neurotransmitters, of which there are many, both
excitatory and inhibitory.
Anti-spastic drugs are based on the pharmacological manipulation of
the action of neurotransmitters.
Baclofen
Gamma-aminoburtyric acid (GABA) is a major inhibitory
neurotransmitter in the CNS. Baclofen binds to GABA receptors and
has therefore a pre-synaptic inhibitory effect on the release of
excitatory neurotransmitters. It also acts post-synaptically and reduces
the firing of the motor neurones.
It is effective mostly in the treatment of SCI and MS, especially in the
reduction of flexor spasms. It is also beneficial in spasticity due to
cerebral lesions, although less so, and with increased side effects.
The dose is titrated to achieve optimum level, starting with 5mg twice
daily, up to a maximum of 60mg daily. Occasionally it is given up to
80mg or even 120mg daily for very severe cases, but this could result
in toxic confusional state.
Side effects include drowsiness, muscle weakness, nausea and fatigue.
Large doses in cerebral lesions may result in general depression of the
CNS, sedation, ataxia and cardiorespiratory depression. In the elderly
it may lead to hallucinations, confusion and increased frequency of
seizures in epileptic patients.
It shouldn’t be stopped suddenly as this may result in spasms,
hallucinations and seizures.
Diazepam
Diazepam acts by facilitating GABA mediated inhibition, therefore
increasing pre-synaptic inhibition and reducing post-synaptic
responses to the excitatory neurotransmitter Glutamate. It can be used
alone or in combination. In spinal pathology, both trauma and MS, it
is less effective than Baclofen for intermittent flexor spasticity, but
effective for more continuous hypertonia. It is not as effective as
Baclofen for cerebral lesions. The dose starts at 2mg twice daily,
increasing by 2mg every few days, until side effects become
troublesome. The maximum dose is 60mg daily. Particular care
should be taken with the elderly and those with cerebral lesions.
Side effects include dizziness, fatigue, imbalance, muscle weakness,
and overdose can lead to coma and respiratory depression.
Paradoxical reactions can also occur, such as insomnia, anxiety,
hostility, hallucinations and increased spasticity. It can produce
physical addiction, and abrupt withdrawal can lead to seizures.
Dantrolene (Dantrium)
This is unique amongst anti-spasticity drugs as it acts peripherally. It
inhibits the release of calcium ions from sarcoplasmic reticulum in
muscle therefore preventing activation of the contractile apparatus and
diminishing the force of the muscle contraction. It has a generalised
effect on striated muscle. It can be given in conjunction with centrally
acting drugs but may exacerbate their side effects eg drowsiness and
dizziness.
The dose starts at 25mg daily and is increased by a further 25mg
every few days to a maximum of 400mg daily.
Side effects include an increase in nausea, vomiting and muscle
weakness as the dose is increased. The main side effect is irreversible
liver damage (10% of patients), therefore liver function tests should
be closely monitored, especially for women and the elderly.
Tizanidine (Zanaflex)
This has only become available more recently in the UK, and is
mainly used in the treatment of MS. It acts pre-synaptically having an
inhibitory effect on spinal interneurones, depressing polysynaptic
reflexes. It also has an effect on the excitability of the alpha motor
neurone and the descending noradrenergic pathways. It also reduces
the synaptic transmission of nociceptive stimuli in the spinal
pathways.
Side effects include sedation, dry mouth, bradycardia and
hypotension, although it is reported to produce less muscle weakness
than Baclofen and less sedation than Diazepam. It is contraindicated
in patients receiving anti-hypertensive therapy.
The initial dose is 2mg daily, gradually increasing by 2 to 4mg every
2 to 4 days, to a maximum of 36mg daily.
Clonidine
This is an antihypertensive drug. It is effective in reducing flexor
spasms in spinal and brain stem spasticity.
L-threonine
This is an amino acid related to glycine, an important post-synaptic
inhibitory neurotransmitter in the spinal cord. It is used in the
treatment of familial spastic paraparesis and MS, with some success.
Gabapentin
Originally an anti-epileptic drug, it enhances inhibitory GABA-ergic
transmission in the CNS. It has been shown to have modest effect on
traumatic spinal spasticity and in MS. The dose used is 400mg twice
daily.
Vigabatrin
Another anti-epileptic drug, with similar action to Gabapentin. It
reduces spinal spasticity, having a similar effect to Baclofen.
Surgical Management
Phenol
Phenol impairs nerve conduction when injected in close proximity to
peripheral nerves. It has immediate effect, lasts longer than Botox,
and may be permanent. The injections damage motor and sensory
nerves. Undesirable effects are painful and variable, with an
unpredictable duration of effect.
Phenol can be given intrathecally, but it has been shown to damage
sacral nerves, resulting in faecal and urinary incontinence, and to
damage sympathetic nerves, resulting in pressure sores.
Lignocane/Ethanol
Intramuscular Lignocane/Ethanol is used to induce blockade of 1a
muscle afferent fibres, arising from the muscle spindle. Duration of
effect is initially very short – less than 24 hours, but is prolonged to
several weeks with repeated injections.
Dorsal Rhizotomy
Microsurgical lesions of the dorsal root entry zone of the lateral root
remove input from nociceptors and muscle spindles, therefore
reducing flexor and stretch reflexes without complete limb deafferentation. It is irreversible, and there is a surgical risk.
Botulinum Toxin
Botox denervates a muscle through neuromuscular junction blockade
and is used to treat focal muscle hyperactivity. It was originally used
for focal dystonias. There are no adverse CNS side effects. The effect
lasts for 3 to 4 months. The Botox is taken up by the presynaptic
nerve terminal where it prevents binding of Acetylcholine vesicles to
the presynaptic membrane, inhibiting their release. This results in
denervation of the muscle. Recovery from the blockade occurs via
sprouting of new axons from adjacent nerves, and from pre-terminal
portions of the affected nerves. During this 3 month period there will
be muscle weakness and atrophy.
The likelihood of showing a functional gain from Botox will depend
upon whether or not the assumption that the motor overactivity being
treated was contributing to the functional loss was correct. Patient
selection is the key to success.
1. Baclofen
 Binds to the inhibitory neurotransmitter GABA to
increase inhibition of excitatory neurotransmitters
pre-synaptically.
Acts post-synaptically to decrease the firing of
motor neurones.
Side Effects – drowsiness, muscle weakness, nausea,
fatigue, general CNS depression, ataxia, sedation.
In the elderly – hallucinations,confusion and seizures.
2. Diazepam
 Facilitates GABA mediated inhibition, therefore increasing
pre-synaptic inhibition.
 Reduces post-synaptic responses to the excitatory
neurotransmitter Glutamate.
 Side effects – Dizziness, fatigue, imbalance, muscle
weakness, physical addiction. Overdose can lead to coma
and respiratory depression.
3. Dantrolene
 Acts peripherally to inhibit the release of calcium ions and
therefore diminish the force of muscle contraction.
 Side effects – nausea, vomiting, muscle weakness,
irreversible liver damage (10% of patients)
4. Tizanidine
 Pre-synaptic inhibitory effect on spinal interneurones,
depressing polysynaptic reflexes.
 Reduces excitability of alpha motor neurones.
 Reduces synaptic transmission of nociceptive stimuli in
spinal pathways.
 Side effects – bradycardia, sedation, dry mouth,
hypotension
5. Other interventions
 Clonidine
 L-threonine
 Gabapentin
 Vigabatrin
 Phenol – injected peripherally to impair nerve conduction.
Can be given intrathecally.
 Lignocane/Ethanol – intramuscular blockade of muscle
afferent fibres arising from the muscle spindle.
 Dorsal Rhizotomy – Microsurgical lesion of the dorsal root
entry zone of the lateral root to remove input from
nociceptors and muscle spindles.
6. Botulinum Toxin
 Injected at the neuromuscular junction to produce muscle
denervation and therefore reduce focal spasticity.
 BTX is taken up into the nerve cell and prevents binding of
Acetylcholine vesicles to the pre-synaptic membrane,
inhibiting their release.
 Recovery occurs after 3 months due to axonal sprouting,
therefore need repeat injections to maintain the effect.