REVIEWS
Spasticity: pathophysiology,
1
Specialty registrar, Department
of Neurology, Royal Hallamshire
Hospital, Sheffield Teaching
Hospitals NHS Foundation Trust,
Glossop Road, Sheffield, UK
2
Department of Neurology, Royal
Hallamshire Hospital, Sheffield
Teaching Hospitals NHS
Foundation Trust, Glossop Road,
Sheffield, UK
Correspondence to
Dr Krishnan Padmakumari
Sivaraman Nair, Department of
Neurology, Royal Hallamshire
Hospital, Sheffield Teaching
Hospitals NHS Foundation Trust,
Glossop Road, Sheffield,
S10 2JF, UK;
siva.nair@sth.nhs.uk
Received 12 November 2011
Accepted 7 April 2012
evaluation and management
Ammar Kheder,1 Krishnan Padmakumari Sivaraman Nair2
Abstract
Spasticity is common in many neurological
disorders, such as stroke and multiple sclerosis.
It is part of the upper motor neurone syndrome
manifesting as increased tone, clonus, spasms,
spastic dystonia and co-contractions. The impact
of spasticity varies from it being a subtle
neurological sign to severe spasticity causing
pain and contractures. Existing spasticity can be
worsened by external factors such as
constipation, urinary tract infections or pressure
ulcers. Its management involves identification
and elimination of triggers; neurophysiotherapy;
oral medications such as baclofen, tizanidine and
dantrolene; focal injection of botulinum toxin,
alcohol or phenol, or baclofen delivered
intrathecally through a pump; and surgical
resection of selected dorsal roots of the spinal
cord. This article reviews the current
understanding of pathophysiology, clinical
features and management of spasticity.
Introduction
Spasticity is defined as ‘disordered sen-
sorimotor control resulting from an
upper motor neurone (UMN) lesion,
presenting as intermittent or sustained
involuntary activation of muscles’.1 It
is a frequent symptom of common
neurological disorders, such as mul-
tiple sclerosis and stroke. Spasticity
seldom exists in isolation and is usually
accompanied by one or more compo-
nents of UMN syndrome (table 1).
Spasticity varies from being a clinical
sign with no functional impact to being
a gross increase in tone interfering with
mobility, transfers and personal care.
Untreated, it can cause shortening of
muscles and tendons, leading to con-
tractures (figure 1). Some patients
depend on their spasticity to stand,
walk and transfer or sit upright. The
optimum management of spasticity
requires a co-ordinated approach with
rehabilitation professionals.
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Pathophysiology
Tone is the resistance of resting
muscle to passive movements. Normal
tone results from visco-elastic proper-
ties of muscle and neural drive from
spinal motor neurones. Viscosity is
the resistance of tissue to deforming
forces whereas elasticity is the ability
of a tissue to return to its original pos-
ition after being stretched. Viscosity
resists stretch; elasticity pulls the
muscle back to its original position.
When stretched, muscle spindle Ia
afferents excite spinal motor neu-
rones; this results in contraction of
agonist and relaxation of antagonistic
muscles. This stretch reflex is modu-
lated by supraspinal and spinal path-
ways, activity, posture and sensations.
Increased tone initially results from
the excessive neural drive of spinal
motor neurones, and later is partly
because of visco-elastic changes in
immobilised muscles and joints. In
spasticity, motor neurones respond to
stretch at a lower threshold than
normal, with long discharges: the
‘plateau potentials’.2 This results
from a change in balance between
inhibitory and excitatory inputs to
spinal motor neurones in favour of
excitation (table 2). After immobilisa-
tion, connective tissue and fat can
replace sarcomeres. Left unchecked,
this process can end in contractures
and permanent loss of joint mobility.3
As well as increased tone spasticity
has other features, such as clonus,
spasms, spastic dystonia and spastic
co-contractions.
Clonus is the phenomenon of
involuntary rhythmic contractions in
response to sudden sustained stretch.
It is due to alternate loading and off-
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Table 1 Components of upper motor neurone syndrome
Positive components
Exaggerated tendon reflexes
Released reflexes
Babinski sign
Increased tone
Clonus
Spastic dystonia
Negative components
Spastic co-contractions
Motor weakness
Slowed movements
Loss of dexterity
Loss of selective motor control
loading of muscle spindles. A sudden stretch acti-
vates muscle spindles, resulting in the stretch
reflex. Tension produced by the muscle contrac-
tion activates the Golgi tendon organs, which in
turn activate an ‘inverse stretch reflex’, relaxing
the muscle. If the stretch is sustained, the muscle
spindles are again activated, causing a cycle of
alternating contractions and relaxations. It can be
triggered by active or passive stretch and can
interfere with walking, transfers, sitting and care.
Spasms are sudden involuntary movements that
often involve multiple muscle groups and joints.
They can be repetitive and sustained. These rep-
resent an exaggerated reflex withdrawal response
to nociceptive stimuli and are mediated by poly-
synaptic intersegmental spinal cord circuits.
Spastic dystonia is tonic muscle overactivity that
occurs without any triggers.4 It is due to an inabil-
ity of motor units to cease firing after a voluntary
or reflex contraction, resulting in sustained
muscle contractions. The postures characteristic
of spastic dystonia are shoulder adduction and
Figure 1 Spasticity resulting in flexion contractures of lower
limbs.
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Table 2 Pathophysiology of spasticity
Supraspinal pathways
Release of brain stem reflexes from cortical inhibition
Overactivity of non-adrenergic pathways from locus coeruleus
Overactivity of serotoninergic pathways from raphe nucleus
Spinal cord
Loss of recurrent inhibition, mediated by motor axon collaterals and
Renshaw cells
Loss of reciprocal inhibition, mediated by antagonistic muscle spindle
afferents
Reduced inverse stretch reflex, mediated by Golgi tendon organs
Reduced presynaptic inhibition of muscle spindle afferents
Spinal motor neurone
Denervation supersensitivity
Collateral sprouting
Muscles and joints
Shortening of sarcomeres
Loss of elastic tissue
Fibro-fatty deposits in muscles and tendons
internal rotation, elbow flexion, forearm prona-
tion, wrist and elbow flexion, hip adduction and
ankle plantar flexion and inversion. Spastic dys-
tonia can lead to contractures and deformities
causing pain, discomfort and high-care needs.
Spastic co-contraction is the inappropriate activa-
tion of antagonistic muscles during voluntary activ-
ity.4 It is due to loss of reciprocal inhibition during
voluntary contraction. Normal voluntary activity
involves selective and sequential contraction of
agonists and synergistic muscles, with antagonist
muscle inhibition. In spastic co-contraction, there
are instead mass contractions of both agonist and
antagonistic muscles, resulting in loss of dexterity
and slowed movements.
Clinical evaluation
Clinical assessment of spasticity includes the
following steps:
▪ Differentiation of spasticity from other causes of
increased tone
▪ Identification of potential triggers
▪ Measurement of spasticity
▪ Assessment of impact on function.
Complete assessment requires input from
patients, carers, therapists and other rehabilitation
professionals.
Is it spasticity?
Clinically, spasticity needs to be differentiated
from other causes of increased tone, such as
rigidity, catatonia, gegenhalten or contractures.
Spasticity has several characteristic features:
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▪ Velocity dependence: The increased tone of spasti-
city is velocity dependent, that is, the faster the
stretch, the greater the muscle resistance.
▪ ‘Clasp-knife’ phenomenon: This is where the
spastic limb initially resists movement and then
suddenly gives way, rather like the resistance of a
folding knife blade. During initial movement, the
tone is high due to overactive stretch. On sustained
movement, the inverse stretch reflex kicks in, relax-
ing the muscles with a ‘give away’ feel. In the later
stage, as contractures set in, this is replaced by a
non-elastic solid resistance.
▪ Stroking effect: Stroking the surface of the antag-
onistic muscle may reduce the tone in spasticity,
though it does not affect contracture.
▪ Distribution: Spasticity has a differential distribu-
tion with antigravity muscles being more affected.
Rigidity is a non-selective increased tone
throughout the range of muscle movements and
is not velocity dependent.
Gegenhalten, or ‘counter hold’ is an increase in
muscle tone proportional to the force applied.
When the limb is moved passively, the muscles
stiffen in proportion to the force applied, as if
the patient is actively opposing movement.
Catatonia is a neuropsychiatric syndrome
accompanying a wide range of psychiatric, neuro-
logical and medical conditions with motor,
behavioural, affective and autonomic features.5
The clinical features include abnormal posturing,
waxy flexibility and gegenhalten. In waxy flexi-
bility, patients maintain limbs in positions placed
by others for a long time.
Table 3 Diseases presenting predominately as spasticity
Spinal cord compression
Primary progressive multiple sclerosis
Motor neurone disease
Spinal vascular malforamtions
Hereditary spastic paraparesis
Subacute combined degeneration of the cord
Human T-lymphotropic virus myelopathy
Copper deficiency6
example, kyphoscoliosis, flexion contractures at
the elbow, hip and knee, or talipes equinovarus
at the ankle. Untreated, spasticity leads to con-
tractures, which are often difficult to correct
(figure 1). Spasticity affects positioning and
pressure area care, resulting in pressure ulcers
(figure 2). It makes hygiene tasks, especially clean-
ing of hands, axillae, elbows and genital areas par-
ticularly difficult. Spasticity can interfere with
bowel and bladder care and sexual relationships.
Spasticity is not always detrimental and has
some benefits. Trunk muscle stiffness helps with
sitting upright and with transfers. Spasticity of
hip and knee extensors aids standing, transfering
and walking. An overactive soleus facilitates toe
push-off and helps walking in children with cere-
bral palsy. Finger flexor spasticity enables people
to hold objects, such as cutlery and a toothbrush.
Clinicians must therefore weigh up the positive

What causes spasticity?

Neurologists encounter spasticity either as a pre-
senting feature of a neurological illness or as a
feature of an established condition. Spasticity
could be the initial manifestation of any path-
ology affecting UMN. Table 3 lists some condi-
tions that can present predominantly as spasticity.
Spasticity can worsen because of exacerbating
factors—nociceptive, visceral or somatic stimuli
—or it can increase through progression of the
underlying disease, through delayed complica-
tions of the primary pathology such as post-
traumatic syrnigomyelia, or through coincidental
new pathology.

What is the impact of spasticity?

Spasticity often causes discomfort. Any trivial
sensory stimulus may trigger painful spasms.
Spasticity restricts joint motion and limits mobil-
ity. The asymmetric pull of overactive muscles Figure 2 Sacral and bilateral ischial pressure ulcers in a patient
can alter posture and cause deformities, for with severe spasticity.

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and negative aspects of spasticity when advising Table 5 Modified Ashworth scale8
on its treatment. 0=No increase in muscle tone
1=Slight increase in muscle tone
Measurement of spasticity 1+=Slight increase in muscle resistance throughout the range
Before advising intervention, it is essential to 2=Moderate increase in muscle tone throughout the range of motion;
passive movement is easy
obtain a baseline measurement of the spasticity,
3=Marked increase in muscle tone throughout the range of motion;
to enable objective assessment of the impact of passive movement is difficult
treatment. Note that the degree of spasticity 4=Marked increase in muscle tone; affected part is rigid
varies with ambient temperature, time of the day,
fatigue, posture and position of the limb.4
Assessment of spasticity should include recording ▪ the patient’s need for mobility aids and assistive
of any exacerbating or relieving factors. There devices, such as wheelchairs, seats, hoists and orthoses.
are several scales that quantify different aspects
of spasticity, but no one scale is universally clinic-
Management
ally acceptable (table 4).
The modified Ashworth score is the most fre- The aim of management is to reduce the impact
quently used clinical measure (table 5). It is a of spasticity and to prevent secondary complica-
good clinical tool, especially for repeated mea- tions. The first step is to set treatment goals,
surements by the same assessor. It does not which must be agreed upon by the patient and
require any instruments and can be done easily the therapy team. Goals need to be meaningful
in different clinical settings. It is an ordinal scale for the patient and easily understood. Examples
but has several limitations.14 of spasticity management goals are the relief of
▪ It does not differentiate between spasticity and soft discomfort, improved sitting, standing and
tissue contractures. walking, facilitated activities of daily living,
▪ There is poor inter-rater reliability, as the applied reduced burden of care, improved body image
force varies between examiners. and self-esteem and prevention of complications.
▪ It is a six-level ordinal scale that is not sensitive to Goal attainment scaling is a measure of the
change. extent to which treatment goals are achieved.
The intended outcome is graded as12
Documentation of spasticity assessment should ▪ −2: much worse than expected
also include: ▪ −1: somewhat worse than expected
▪ assessment of other UMN syndrome components, ▪ 0: achieved the expected outcome
such as weakness and loss of dexterity ▪ +1: somewhat better than expected
▪ the response to antispasticity drugs, and their ▪ +2: much better than expected outcome.
adverse effects The patient is actively involved in setting goals
▪ contractures, as these do not respond to pharmaco- and in measuring the outcome of interventions.
logical interventions Some key elements of spasticity management
are identification and elimination of triggers, non-
Table 4 Measurement of spasticity pharmacological interventions and medications.
Clinical neurophysiolgical measures7
H reflex Identifying and eliminating triggers and aggravating
T reflex factors (table 6)
F-waves Common causes of spasticity exacerbation are
Measures of increased tone urinary tract infections and constipation. Bladder
Modified Ashworth scale8 stones may rarely present through worsening of
Tardieu scale9 spasticity (figure 3). Patient and carer education
Pendulum test10 to recognise these triggers is an important part of
Spasm frequency management.
Penn spasm frequency score11
Measures of focal spasticity
Non-pharmacological interventions
Leeds arm spasticity impact scale12
Passive movements
Adductor spasticity score13
Passive stretching decreases the excitability of
Patient reported scales
motor neurones and maintains the visco-elastic
Visual analogue scale12
properties of muscles and joints.15 Manual

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Table 6 Factors aggravating spasticity
Pressure ulcers
Ingrown toenails
Skin infections
Injuries
Constipation
Urinary tract infection
Urinary tract calculi
Deep vein thrombosis
Improper seating
Ill-fitting orthotics
Post-traumatic syringomyelia
stretching delivered by therapists, therapy assis-
tants or carers is time and labour intensive. The
intensity of force applied, the duration of a
stretch and the number of repetitions per session
may vary with the person applying stretch and
within and between treatment sessions. Machines
such as the isokinetic dynamometer deliver stan-
dardised passive stretches. However, they are
expensive and not widely available. Muscles and
joints can be kept stretched for hours or days
using casts or splints, sometimes used together
with botulinum toxin injections. Prolonged
stretching can help to treat contractures. Patients
often report exacerbation of spasticity on waking
up: stretching and taking a morning dose of anti-
spasticity medication before getting out of bed
may help to reduce this. However, a recent sys-
tematic review failed to show evidence for
regular stretching in neurological conditions.16
The effect of stretching on spasticity and contrac-
tures is still largely evidence free; however, there
is no evidence that it is harmful.
Exercises
Exercises improve motor control and cardiovas-
cular fitness in people with UMN disorders.
Figure 3 Calculi in urinary bladder causing exacerbation of
spasticity.
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Strong trunk, pelvic and shoulder girdle muscles
provide stability required for accurate control of
the distal movements.17 Whereas exercises
improve strength and overall function in people
with spasticity, there is only very limited evi-
dence that they directly reduce spasticity.18
Exercises that help people with spasticity include
cycling, strengthening exercises and treadmill
training.18–20 In contrast to previous ideas, exer-
cises do not aggravate spasticity.18 Exercises may
be inappropriate if patients are not otherwise
fit, have osteoporosis, coagulation disorders or
severe limitation of passive range of movement,
or in the immediate postoperative period.17
Biofeedback uses visual or auditory cues to help
patients judge their performance. This technique
helps patients to recognise and promote muscu-
lar activity that is not otherwise obvious to
them. It also helps to avoid unwanted activity
such as spastic co-contractions.15
Posture and standing
Standing for about half an hour a day may help
to reduce spasticity.21 As well as its effect on
spasticity, weight bearing and standing also help
to improve psychological wellbeing, to improve
bone mineral density, facilitate pulmonary drain-
age and helps bowel and bladder functions. Tilt
tables and standing frames help with proper posi-
tioning of the joints and trunk while standing.
Therapists often use tilt tables to initiate standing
and than progress to standing frames.
Proper positioning of limbs and trunk during
standing, sitting or lying is essential to prevent
aggravation spasticity and development of con-
tractures. Incorrect standing, for example, with
ankles plantar flexed, knees flexed and hip flexed
and adducted, can facilitate spasticity and con-
tractures. Devices such as T-rolls and splints help
to position limbs properly and thereby prevent
contractures. A wheelchair and seating assessment
also help to position the trunk and limbs prop-
erly during sitting and is an essential component
of management of late stage spasticity. Splints
such as wrist–hand orthosis and ankle–foot orth-
osis may help in managing spasticity. They
provide a prolonged stretch and inhibit motor
neurone excitability. However, there is little evi-
dence to support their ability to inhibit motor
neurones.22
Physical modalities
Physical modalities used to treat spasticity
include ultrasound, cryotherapy (application of
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cold), vibration, shockwave therapy, magnetic
stimulation, transcutaneous electrical nerve
stimulation (TENS) and functional electrical
stimulation. These physical modalities work
through either modulating the visco-elastic prop-
erties of muscles and tendons (cryotherapy, ultra-
sound and shock wave therapy), inducing
long-term depression at the spinal level, stimulat-
ing cortico-cortical inhibitory pathways (mag-
netic stimulation), inducing short-term plasticity
in injured spinal motor systems or activation of
proprioceptive inputs (TENS).15 There is only a
limited evidence base to support the use of these
modalities and no current guidance about their
use in clinical practice.
Medications
Before starting antispasticity drugs, it is essential
to decide the treatment goals: for example, to
reduce pain and discomfort, to facilitate a good
night’s sleep, to achieve proper position on the
chair or in bed, to facilitate hygiene or to
improve functions such as gait. The choice of
treatment and the timing of doses depend largely
on these goals. Weakness is a side effect of all
antispasticity drugs, usually due to unmasking of
underlying UMN weakness, rather than from a
direct drug effect. Inappropriate dose escalation
often leads to side effects and hence to poor
compliance. A ‘start low and go slow’ policy
limits these unwanted functional effects.
Spasticity is often undertreated. Drugs are too
quickly labelled as ineffective without a fair trial
of maximal tolerated doses. It is essential to try to
reach the maximal tolerated dose for a sufficiently
long period before stopping a drug. Patients not
responding to one drug may respond to another.
Sudden stopping of even an apparently ‘ineffect-
ive’ drug may cause a rebound increase in spasti-
city. It is better to taper initial drug while
simultaneously introducing the second drug.
A combination of two drugs should be tried if
the spasticity does not respond to a single agent,
or if the patient can tolerate only low doses. It is
important to time the doses according to the
patient’s activity, care and therapy. Ambulant
patients often require lower doses during the
daytime as they may be using spasticity to facilitate
their walking. A dose may be required immediately
after awakening in the morning to facilitate care.
Oral agents
The commonly used antispasticity drugs are
those acting on a gamma aminobutyric acid
294 Practical Neurology 2012;12:289–298. doi:10.1136/practneurol-2011-000155
(GABA)ergic system (baclofen, gabapentin and
benzodiazepines), α-2 adrenergic system (tizani-
dine) and those that block calcium release into
the muscles (dantrolene). Even though these
drugs have been used for several decades, there
are no evidence-based guidelines for the choice,
titration rates and withdrawal of these drugs.23
Our recommendations (below) are based on both
a literature review and clinical pragmatism.
Baclofen
Baclofen is the most widely used oral antispasti-
city drug. It is a GABA-B receptor agonist.
Baclofen reduces calcium influx and suppresses
release of excitatory neurotransmitters, including
glutamate and aspartate. It down-regulates activity
of 1a sensory afferents, spinal interneurones and
motor neurones. The usual starting dose is 5 mg
thrice daily, increased by 5–10 mg weekly, until
there is an optimal effect. The maximum dose is
90–120 mg per day. Its side effects include weak-
ness, drowsiness and dizziness; some people
report sexual dysfunction and urinary incontin-
ence. Baclofen can reduce the seizure threshold
and should be used with caution in people with
seizures. Stopping baclofen can provoke rebound
spasticity within 48 h, though it usually settles
after another 48 h. Sudden withdrawal may also
cause seizures and hallucinations. Baclofen should
be used with caution during pregnancy: although
there are no reports of baclofen directly causing
human fetal malformations, animal studies using
high doses show that it causes impaired sternal
ossification and omphalocele.24 Withdrawal from
maternal baclofen occasionally provokes neonatal
convulsions25 and so newborns of mothers taking
baclofen should receive oral baclofen 0.5 mg per
kg per day, weaned off over 9 days.26 Baclofen
appears in breast milk and this must be considered
when advising mothers about breast feeding.
Benzodiazepines
Benzodiazepines act on GABA-A receptors. They
have similar efficacy to other antispasticity drugs,
but more troublesome side effects. Drowsiness
and behavioural side effects limit its use during
the daytime. They are particularly useful to treat
spasticity that interferes with sleep. Clonazepam
is particularly useful to treat nocturnal spasms.
The usual starting dose is 500 mg at night, with a
maximum dose of 1 mg.
Gabapentin and pregabalin
A few small trials show the efficacy of these
GABAergic drugs in treating spasticity.27 28 They

are particularly useful as adjuncts in treating
spasticity associated with pain. Their side effects
include weight gain, gastro-intestinal distur-
bances, confusion, depression, hostility and sleep
disturbance. Gabapentin should start at 300 mg
once daily on day 1, 300 mg twice daily on day 2,
then 300 mg thrice daily on day 3, then increased
according to the patient’s response in steps of
300 mg every 2–3 days to maximum of 3600 mg
daily. The dose of pregabalin is 75 mg twice a day
and it can be titrated up to 300 mg twice daily.
Tizanidine
Tizanidine is an α-2 receptor agonist which
enhances noradrenergic activity in the spinal
cord and brain. It inhibits excitatory spinal inter-
neurones and tracts from locus coeruleus. Its side
effects include dry mouth, gastrointestinal dis-
turbance, hypotension and acute hepatitis. It is
essential to monitor liver enzymes during the
first 4 months of treatment. Sudden stopping of
tizanidine can lead to a hyperadrenergic syn-
drome, characterised by anxiety, tremor, hyper-
tension and tachycardia. The usual starting
dosage is 2 mg at bedtime, increased by 2 mg
weekly to a maximum of 36 mg, divided into 3–
4 daily doses.
Dantrolene
Dantrolene blocks calcium release from the
sarcoplasmic reticulum and interferes with excita-
tion–contraction coupling of the skeletal muscle.
Unlike other antispasticity drugs, it acts directly
on the muscle and so is less sedative. The starting
dose is 25 mg daily for the first week, increased
in steps of 25 mg per week to a top dose of
100 mg 3–4 times daily. The most important side
effect is hepatotoxicity, and so liver function
must be monitored carefully.
Cannabinoids
There are cannabinoid receptors in dorsal spinal
cord, basal ganglia, hippocampus and cerebel-
lum, and these modulate spasticity.29
Tetrahydrocannabinol, an agonist of cannabinoid
1 and 2 receptors, reduces spasticity but causes
sedation and psychotropic side effects.
Cannabidiol has lower affinity for both these
receptors and reduces the psychotropic and seda-
tive effects of tetrahydrocannabinol. Recently,
nabiximols (Sativex) oromucosal spray, a 1:1
mixture of 9-δ-tetrahydrocannabinol and canna-
bidiol, was licensed for use in spasticity in mul-
tiple sclerosis in the UK. An independent review
noted improvement in patient reported outcome
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measures, but found no significant reduction in
objective measures of spasticity.30 Side effects
include taste disturbance, dry mouth, oral ulcers,
dizziness, depression, mood changes, cognitive
impairment, drowsiness, dysarthria and blurred
vision.29 30 Nabiximols currently has only a
limited role in managing treatment-resistant spas-
ticity. It may be worth trying a 4-week trial in
patients with spasticity from multiple sclerosis
who are not responding to a combination of two
drugs in adequate doses. As only 30–40% of
people show a response, the treatment effect
should be reviewed at 4–6 weeks and continued
only if there is an objective improvement. There
are still concerns about its long-term effects on
cognition, behaviour and mental health.
Botulinum toxin
All therapeutically used botulinum toxins are pre-
pared from the bacterium Clostridium botuli-
nium, which causes botulism, a potentially fatal
neuromuscular paralysis. The heavy chain of
botulinum toxin binds to and becomes interna-
lised into presynaptic nerve endings. There, it
degrades synaptosomal-associated protein 25, a
protein required for fusion of acetylcholine vesi-
cles to the presynaptic membrane. This inhibits
release of acetylcholine, thereby blocking neuro-
muscular transmission. The effect is reversed by
nerve sprouting and reinnervation which devel-
ops over a few months. When injected into skel-
etal muscle, botulinum toxin causes selective
weakness of the target muscle. It is particularly
useful in the treatment of focal spasticity. It has
the advantage of achieving selective reduction in
spasticity without the side effects of global weak-
ness or sedation.
Before considering botulinum toxin, it is
important first to address all triggers factors have
and to ensure that there are no significant con-
tractures. The next step is to agree with members
of the multidisciplinary team the treatment goals,
the target muscles and postinjection interven-
tions. Before giving the injections, these goals
and the treatment plan must be discussed and
agreed with the patient and carer, with informed
consent. Electromyography, nerve stimulator or
ultrasound can be used to identify the target
muscle. Postinjection interventions such as
physiotherapy, splinting and serial casting help to
maximise benefits of botulinum toxin injections.
The patient should be reassessed 4–6 weeks after
the initial injections to assess the efficacy of the
injections and whether the treatment goals have
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been attained. If required, further injections
should be planned after 3–4 months.12 Adverse
events of botulinum toxin include respiratory
tract infections, muscle weakness, urinary incon-
tinence, falls, fever and pain.31 Rarely, the toxin
can cause transient dysphagia, even requiring
nasogatric feeding.
Intrathecal baclofen
Oral baclofen has only very low bioavailability to
GABAergic neurones in the spinal cord. When
administered intrathecally, however, a relatively
small dose of baclofen can give a high concentra-
tion of drug within the spinal cord. This helps to
achieve good muscle relaxation and to avoid
troublesome side effects. Intrathecal baclofen
(ITB) is relatively well-tolerated and is effective
in spasticity secondary to spinal cord disorders,
stroke, cerebral palsy and multiple sclerosis.32–35
It is indicated for significant lower-limb spasticity
which persists despite adequate treatment with at
least two oral antispasticity drugs concomitantly.
A recent review in multiple sclerosis suggested
that ITB pumps were under used.36
The ITB system comprises a subcutaneous
pump which stores and delivers programmable
doses of baclofen through a catheter into the
spinal subarchnoid space (figure 4). The pumps
can be adjusted to vary the doses delivered,
depending on the level of patient activity and
needs. Although ITB has a greater effect on
lower-limb spasticity and spasms, it also helps to
reduce upper-limb tone. ITB is usually first tested
using a temporary catheter with an initial test
dose is 50 mg, and subjects are monitored for
side effects and efficacy. One should proceed to
baclofen pump implantation if the screening test
succeeds in meeting the goals previously agreed
with the patient and multidisciplinary team.
Patients must be warned about potentially life-
threatening complications and the need for
regular long-term monitoring. Implants may lead
to procedure related complications such as infec-
tion, skin erosions, cerebrospinal fluid leak and
seroma formation around the pump. The fre-
quency of complications varies from zero to 2.24
per implant.37 Abruptly stopping ITB can cause
high fever, confusion, rebound spasticity and
muscle rigidity, similar to neuroleptic malignant
syndrome. Common causes include pump failure,
battery failure, catheter block and non-
adherence. Patients who cannot attend regular
monitoring visits should not be offered this inter-
vention. Treatment of acute ITB withdrawal
296 Practical Neurology 2012;12:289–298. doi:10.1136/practneurol-2011-000155
Figure 4 X-ray showing intrathecal baclofen pump.
should be aimed at reducing muscle tone and
treating central nervous system (CNS) effects
such as delirium and seizures. If possible, ITB
should be restarted with a temporary external
catheter at the same dose and rate. Large oral
doses of baclofen, for example, 120 mg per day
are often used, but may still not be adequate, as
the penetration into CNS is poor and oral baclo-
fen takes as it takes 3–4 days to become effective.
Adjuvant drugs to treat acute baclofen with-
drawal include dantrolene, benzodiazepines, pro-
pofol, tizanidine and cyproheptadine.38
Phenol
Phenol injected directly into peripheral nerves
cause destruction of neural tissue by protein
coagulation. This chemical neurolysis has long
been in use to treat spasticity.39 Muscle near the
injection site is usually damaged along with the
target nerves. These agents are effective in treat-
ing spasticity that occurs in large, powerful
muscle groups close to the trunk, such as the
thigh adductors. The most commonly applied
blocks are to the medial popliteal muscles to aid
spastic foot drop, or obturator nerve blocks
either in patients with scissoring gait or to
improve perineal hygiene and seating posture. It
should be done only under the guidance of an
ultrasound scan or nerve stimulator (figure 5).
Nerve sprouting may lead to recurrence of spasti-
city. A single injection often has effects lasting
many months and can be repeated if necessary.
The most trouble some side effect is pain and
dysaesthesia; it is therefore used usually only in
people with loss of sensation. Other side effects
are peripheral oedema, skin sloughing and
wound infection.39 Phenol also increases the risk
of deep venous thrombosis and leukaemia.

Figure 5 Injection of phenol guided by nerve stimulation for
obturator nerve for treatment of adductor spasticity.
However, there are no reports of leukaemia in
those who received it as spasticity treatment.
In selected people whose spasticity is resistant
to conventional treatment, intrathecal injection
of 0.5–4.0 ml of 5% phenol in glycerine may be
an alternative.40 As phenol indiscriminately
damages motor and sensory nerve roots, it
should be reserved for people who have no func-
tional movement in their legs, lost bladder and
bowel functions and lost sensation to their legs.
Selective dorsal rhizotomy
This procedure involves a surgical section of
dorsal nerve roots of the lumbosacral spinal
cord. This reduces the sensory input into spinal
motor neurone pools, reducing their excitability.
It is usually used to treat spasticity associated
with cerebral palsy, with good long-term out-
comes.41 Patients with spastic dystonia or
co-contractions are unlikely to benefit from this
procedure. It is an invasive surgical procedure
and requires multiple-level laminectomies and
must be followed by an intensive rehabilitation
programme. Side effects include sensory loss,
urinary incontinence, low-back pain and spinal
deformity. Recently, less invasive percutaneous
radiofrequency ablation of dorsal root ganglion
showed promising results.42
Summary
Spasticity is one component of UMN syndrome
and its effects are often compounded by other
deficits in motor function. The impact of spasti-
city varies between patients. Treatment strategies
should be selected keeping in mind the useful
effects of spasticity. Untreated, it can cause sig-
nificant discomfort and problems to mobility and
care. An important aspect of management is
to eliminate trigger factors and to try non-
pharmacological approaches. Oral antispasticity
REVIEWS
drugs should be started at a low dose and grad-
ually titrated. Once started, no single drug
should be discarded until its maximum dose is
reached or if patient develops intolerable side
effects. In patients whose spasticity is resistant to
oral treatments, surgical interventions such as
ITB pump should be tried.
Acknowledgement Authors would like to thank Mr Martin
McClleland, Consultant in Spinal Injuries, Princess Royal Spinal
Injuries and neurorehabilitation Centre, Northern General
Hospital, Sheffield for permission to reproduce figures 2, 3 and 5.
Contributors Both Dr A Kheder and Dr KPS Nair made
substantial contributions to this article; Dr Ammar Kheder:
Literature search, review of literature, writing; Dr KPS Nair:
Idea, review of literature, writing, correspondence.
Competing interests KPSN was a site investigator for a clinical
trial of Sativex for spasticity funded by GW Pharma Ltd UK.
Provenance and peer review Commissioned. Externally peer
reviewed. This paper was reviewed by Diane Playford,
London, UK.
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