Spasticity

OUTLINE
 Introduction- Historical aspects & Epidemiology
 Definition
 Overview of Pathophysiology
 Causes
 Assessment
 Management
 Conclusion

INTRODUCTION
 The term ‘Spasticity’ is derived from the Greek ‘Spasticos’ &
‘Spaon’ ( to draw or stretch)
 Term was first used in English by Good(1829)- describing
„spastic wryneck‟
 First recognized by Orthopedic surgeons- Stromeyer (1838)
performed subcutaneous tenotomy of contracted extremities
 First description given by Little(1843)
A F Thilmann et al. Spasticity: Mechanisms and management. Springer 1993

 William John Little himself suffered from Spasticity , treated by
Stromeyer
 Dedicated his dissertation “Symbolae ad talipedum varum
cognoscendum” to the surgeon
 Cerebral palsy now known as Little‟s disease
A F Thilmann et al. Spasticity: Mechanisms and management. Springer 1993

EPIDEMIOLOGY- Burden of the illness
 MS
 incidence is 4.2 cases per 100,000 and the prevalence is 0.9 per
1000
 affects between 37% and 78%
 SCI
 annual incidence of spinal cord injury (SCI) in the US is
approximately 11,000
 40%
http://www.mdvu.org/library/disease/spasticity

 Stroke
 the estimated annual incidence of ischemic and hemorrhagic
stroke is 183 per 100,000
 approximately 35%
 CP
 prevalence of CP as 3.6 per 1,000 children or about 1 in 278
children
 more than 90%
 TBI
 at least 5.3 million population, currently have a long-term or
lifelong need for help to perform activities of daily living as a
result of a traumatic brain injury
 ~ 50%
http://www.mdvu.org/library/disease/spasticity

DEFINITION
“Spasticity is a motor disorder characterized by a velocity dependent
increase in tonic stretch reflexes (muscle tone) with exaggerated
tendon jerks (phasic stretch reflexes), resulting from
hyperexcitability of stretch reflex, as one component of uppermotor
neuron syndrome” J.W.Lance(1980)
Lance JW (1980) Symposium synopsis. In: Feldman RG,Young RR,Koella WP (eds) Spasticity: disordered motor control. Year Book
Medical Publishers, Chicago

Spasticity- characterstic features
 Velocity dependence- increased tone of spasticity is velocity
dependent, that is, the faster the stretch, the greater the muscle
resistance
 ‘Clasp-knife’ phenomenon- spastic limb initially resists
movement and then suddenly gives way, like the resistance of a
folding knife blade
 Distribution- differential distribution with antigravity muscles
being more affected
Practical Neurology 2012;12:289–298

UMN Syndrome- accompaniments of Spasticity
 Positive features
 Clonus- involuntary rhythmic contractions, response to sudden
sustained stretch, alternate loading and off-loading of muscle
spindles
 Spasms- sudden involuntary movements involving multiple
muscle groups and joints, repetitive and sustained, represent an
exaggerated reflex withdrawal response to nociceptive stimuli
 Exaggerated tendon reflexes
 Babinski sign

 Spastic dystonia- tonic muscle overactivity that occurs without
any triggers, due to an inability of motor units to cease firing after
a voluntary or reflex contraction
 Characteristic postures of spastic dystonia
 shoulder adduction and internal rotation
 elbow flexion
 forearm pronation, wrist and elbow flexion
 hip adduction
 ankle plantar flexion and inversion
 can lead to contractures and deformities causing pain, discomfort

 Negative components
 Spastic co-contraction- inappropriate activation of antagonistic
muscles during voluntary activity. It is due to loss of reciprocal
inhibition during voluntary contraction
 Motor weakness
 Slowed movements
 Loss of dexterity

PATHOPHYSIOLOGY
 Muscle tone
 visco-elastic properties of muscle
 neural drive from spinal motor neurons
 Control
 Cortical- motor areas of the cortex facilitate ventromedial reticular
formation
 Supraspinal descending pathways
 Inhibitory pathway- dorsal reticulospinal tract, which arises in
the ventromedial reticular formation
 Excitatory pathways
1) Medial reticulospinal tract- arising in the bulbopontine
tegmentum, major pathway
2) Vestibulospinal tract
European Journal of Neurology 2002, 9 (Suppl. 1): 3–9

Mechanisms at Various Levels
 Cortical & Supraspinal descending pathways
 Loss of cortical facilitation of the inhibitory pathway(dorsal
reticulospinal tract)
 Partial spinal cord lesion, which destroys the inhibitory
pathways but preserves the excitatory fibres
 Complete spinal cord lesion affecting both inhibitory and
excitatory pathways
 Spinal Cord
 Loss of recurrent inhibition- mediated by motor axon
collaterals and Renshaw cell
 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 neuron
 Denervation supersensitivity
 Collateral sprouting
 Muscles and joints
 Shortening of sarcomeres
 Loss of elastic tissue
 Fibro-fatty deposits in muscles and tendons

CAUSES
 Cerebral palsy
 Stroke
 Multiple sclerosis
 Traumatic Brain injury
 Spinal Cord Injury
 Anoxia
 Neurodegenerative

DISABILITY
 Orthopedic deformity such as hip dislocation, contractures, or
scoliosis
 Impairment of activities of daily living (eg, dressing, bathing,
toileting)
 Impairment of mobility (eg, inability to walk, roll, sit)

 Skin breakdown secondary to positioning difficulties and
shearing pressure
 Pain
 Sleep disturbance
 Depression secondary to lack of functional independence

Upper extremity patterns
 Adduction and internal
rotation of the shoulder
 Flexion of the elbow and
wrist
 Pronation of the forearm
 Flexion of the fingers and
adduction of the thumb
• PECTORALIS MAJOR
• LATISSIMUS DORSI
• TERES MAJOR
• BICEPS
• BRACHIORADIALIS
• BRACHIALIS
• PRONATOR TERES AND
QUADRATUS
• FLEXOR CARPI RADIALIS
AND ULNARIS
• FLEXOR DIGITORUM
PROFUNDUS AND
SUPERFICIALIS
• ADDUCTOR POLLICIS

Lower extremity patterns
 HIPADDUCTION AND
FLEXION
 KNEE FLEXION
 ANKLE PLANTAR FLEXION
OR EQUINOVARUS
POSITIONING
• ADDUCTOR MAGNUS
• ILIOPSOAS
• HAMSTRINGS (MEDIAL
MORE OFTEN THAN
LATERAL)
• TIBIALIS POSTERIOR
• SOLEUS
• GASTROCNEMIUS

Lower extremity patterns
 KNEE EXTENSION
 EQUINUS AND/OR
VALGUS ANKLE
 GREAT TOE
DORSIFLEXION
• QUADRICEPS
FEMORIS
• PERONEUS LONGUS
• EXTENSOR HALLUCIS
LONGUS

ADDUCTED/INTERNALLY ROTATED
SHOULDER
FLEXED ELBOW PRONATED FOREARM FLEXED WRIST
CLINCHED FIST THUMB IN PALM DEFORMITY STRIATAL TOE EQUINOVARUS
STIFF KNEE FLEXED KNEE ADDUCTED THIGHS

ASSESSMENT
 Ashworth and modified Ashworth scales
 most frequently used clinical methods for estimation of spasticity
G. R. Johnson. Outcome measures of spasticity. European Journal of Neurology 2002, 9 (Suppl. 1): 10–16

Bohannon and Smith found that many of their patients demonstrated levels of spasticity
towards the lower end of the scale
and included an extra category (1+) to render the scale more discrete.

 Advantages
 Simple
 requires no instrumentation
 is easy and quick to carry out
 Disadvantages
 interrater reliability
 worst for plantar flexors- to be due to a shorter lever arm at the
ankle to determine the resistance during the movement

Spasm frequency scores
 Created to follow the effect of intrathecal baclofen in patients
with spasticity caused by multiple sclerosis and SCL
 less optimal for other purposes
Spasticity-assessment: a review. Spinal Cord (2006) 44, 708–722

Journal of Neuroscience Methods. Vol 178, Issue 2, 15 April 2009, Pages 340–344
Waternberg Pendulum Test

Wartenberg Pendulum Test
 The patient is seated or lying with the lower leg hanging over the
end of a couch. The examiner then extends the leg to the
horizontal position, while the patient is told to relax. The leg is
then released and allowed to swing freely under the action of
gravity. With the use of electrogoniometers,the swing of the leg
about the knee joint may be evaluated
 In individuals with spasticity, a reduction of the swing is
generally found
 the ratio between the initial flexion and the final position of the
knee joint measured by goniometers, when the leg has come to a
rest

 ratio shows a clear correlation to the severity of spasticity as
evaluated by the AS
 The advantage of the pendulum test is its simplicity, and the more
refined quantification of the severity of spasticity that is obtained
compared to the AS
 Drawbacks- depends crucially on how the person is seated and
the ability of the person to relax fully. Furthermore, it may only
be used to evaluate spasticity in the knee muscles and it seems not
to give any useful information in severe spasticity

Powered oscillation system

Powered oscillation system
 Developed by Walsh (1996)
 The patient held a simple handle attached to a newly developed
electric motor
 motor produced flexion/extension of the joint and the apparatus
also measured EMG
 Walsh showed that, the ability to measure different amplitude and
natural frequency of oscillation depending upon joint stiffness

MANAGEMENT
 When to treat
 Not all spasticity requires treatment- inappropriate treatment of
spasticity may lead to loss of function, when spasticity is
counterbalancing the effects of paresis
 may need to be treated when it causes
 Pain
 Difficulty performing ADL
 Impaired mobility, whether related to ambulation or transfers
 Poor joint positioning
 An increased risk for the development of contracture
 Skin breakdown

 Aims
 to reduce the impact of spasticity
 to prevent secondary complications
 Goals
 relief of discomfort
 improved sitting, standing and walking, facilitated activities of
daily living
 reduced burden of care
 improved body image and self-esteem
 prevention of complications

 Goal attainment scaling
 measure of the extent to which treatment goals are achieved
 intended outcome is graded as
 −2: much worse than expected
 −1: somewhat worse than expected
 0: achieved the expected outcome
 +1: somewhat better than expected
 +2: much better than expected outcome

Factors influencing treatment
 Duration of spasticity
 Severity of spasticity
 Distribution of spasticity
 Success/failure of prior interventions
 Current functional status and future goals
 Patient's age, preferences, and ability to comply with treatment
 Availability of support/caregivers and follow-up therapy
Richard D. Zorowitz et al. Spasticity: A Clinical Review. www.medscape.org

MANAGEMENT- KEY ELEMENTS
 Identification and elimination of triggers
 Non pharmacological interventions
 Passive movements
 Exercises
 Posture & Standing
 Physical modalities
 Medications
 Oral
 Injectables
 Surgical

Identification and elimination of triggers
 Patient and carer education to recognise these triggers is an
important part of management
 Pressure ulcers
 Ingrown toenails
 Skin infections
 Injuries
 Constipation
 Urinary tract infection
 Urinary tract calculi
 Deep vein thrombosis
 Improper seating
 Ill-fitting orthotics

Passive movements
 Passive stretching decreases the excitability of motor neurones
and maintains the visco-elastic properties of muscles and joints
 Prolonged stretching can help to treat contractures
 Stretching can be facilitated by using casts or splints, sometimes
used together with botulinum toxin injections
 No conclusive evidence whether therapy is effective but no
evidence that it is harmful

 Exercises
 improve motor control and cardiovascular fitness in people with
UMN disorders
 Posture and standing
 Standing for about half an hour a day may help to reduce
spasticity
 weight bearing and standing also help to improve psychological
wellbeing, to improve bone mineral density, facilitate pulmonary
drainage and helps bowel and bladder functions
 Proper positioning of limbs and trunk is essential to prevent
aggravation spasticity and development of contractures
 Devices such as splints help to position limbs properly

 Physical modalities
 These physical modalities work through either modulating the
visco-elastic properties of muscles and tendons
 Ultrasound
 Cryotherapy
 Vibration
 Shockwave therapy
 Magnetic stimulation
 Transcutaneous electrical nerve stimulation (TENS)
 limited evidence base to support the use

Medications
 Principles of drug therapy
 Weakness is a side effect of all antispasticity drugs, usually due
to unmasking of underlying UMN weakness
 A „start low and go slow‟ policy limits these unwanted functional
effects
 reach the maximal tolerated dose for a sufficiently long period
before stopping a drug and labeling it as ineffective
 Patients not responding to one drug may respond to another

 Sudden stopping of even an apparently „ineffective‟ drug may
cause a rebound increase in spasticity. 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
 It is important to time the doses according to the patient‟s activity,
care and therapy

Oral agents
 Gamma aminobutyric acid (GABA)ergic system
 Baclofen
 Gabapentin
 Benzodiazepines
 α-2 adrenergic system
 Tizanidine
 Block calcium release into the muscles
 Dantrolene
 Cannabinoids

BACLOFEN
 most widely used oral antispasticity drug
 Mechanism
 GABA-B receptor agonist
 reduces calcium influx
 ↓s release of excitatory neurotransmitters(glutamate & aspartate)
 down-regulates activity of 1a sensory afferents, spinal
interneurones & motor neurones
 Dose
 starting - 5 mg thrice daily
 Maintenance- ↑d by 5–10 mg weekly, until there is an optimal
effect
 Max- 90–120 mg per day

 Adverse effects
 weakness, drowsiness and dizziness
 sexual dysfunction& urinary incontinence
 reduces seizure threshold
 Abrupt stoppage can provoke rebound spasticity within 48 h
 Sudden withdrawal may also cause seizures and hallucinations
 Caution pregnancy- animal studies show impaired sternal
ossification and omphalocele

Benzodiazepines
 act on GABA-A receptors
 Drowsiness and behavioural side effects limit its use during the
daytime
 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
 useful as adjuncts in treating spasticity associated with pain
 Gabapentin - 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
 Pregabalin- 75 mg twice a day and it can be titrated up to 300 mg
twice daily
 Adverse effects- weight gain, gastro-intestinal disturbances,
confusion, depression and sleep disturbance

Tizanidine
 Mechanism
 α-2 receptor agonist
 It inhibits excitatory spinal interneurones and tracts from locus
coeruleus
 Dose
 Starting dosage is 2 mg at bedtime, increased by 2 mg weekly to
a maximum of 36 mg, divided into 3–4 daily doses
 Adverse effects
 dry mouth, gastrointestinal disturbance, hypotension and acute
hepatitis
 Sudden stopping of tizanidine can lead to a hyperadrenergic
syndrome, characterised by anxiety, tremor, hypertension and
tachycardia

Dantrolene
 Mechanism
 blocks calcium release from the sarcoplasmic reticulum and
interferes with excitation–contraction coupling of the skeletal
muscle
 acts directly on the muscle and so is less sedative
 Dose
 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
 Adverse effects
 most important side effect is hepatotoxicity, and so liver function
must be monitored carefully

Cannabinoids
 Cannabinoid receptors in dorsal spinal cord, basal ganglia,
hippocampus and cerebellum, and these modulate spasticity
 Cannabidiol & Nabiximols limited role in managing treatment-
resistant spasticity
 may be worth trying in patients who are not responding to a
combination of two drugs in adequate doses
 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
 concerns about its long-term effects on cognition, behaviour and
mental health

Botulinum toxin
 Prepared from the bacterium Clostridium botulinium
 Mechanism
 heavy chain of binds to and becomes internalised into presynaptic
nerve endings
 degrades synaptosomal-associated protein 25, a protein required
for fusion of acetylcholine vesicles to the presynaptic membrane.
 Inhibits release of acetylcholine, thereby blocking neuromuscular
transmission
 Reversal
 effect is reversed by nerve sprouting and reinnervation which
develops over 3-4 months

 Usage
 Particularly useful in the treatment of focal spasticity. Achieves
selective reduction in spasticity with little side effects
 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
 patient should be reassessed 4–6 weeks after the initial injections
to assess the efficacy of the injections
 If required, further injections should be planned after 3–4 months
 Adverse effects
 muscle weakness, urinary incontinence, falls, fever and pain.
Rarely, the toxin can cause transient dysphagia, even requiring
nasogatric feeding

Phenol
Injection of phenol guided by nerve stimulation for
obturator nerve for treatment of adductor spasticity

Phenol
 Chemical neurolysis
 5% concentration
 injected directly into peripheral nerves cause destruction of
neural tissue by protein coagulation
 Usage
 effective in treating spasticity that occurs in large, powerful
muscle groups close to the trunk- thigh adductors
 blocks 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
 A neurostimulator with a Teflon-coated needle electrode is used
for guidance

 often has effects lasting many months(~6mths) and can be repeated
if necessary
 Nerve sprouting may lead to recurrence of spasticity
 Adverse effects
 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.
 Phenol also increases the risk of deep venous thrombosis and
leukaemia

Intrathecal baclofen
 Indication-
 for significant lower-limb spasticity which persists despite
adequate treatment with at least two oral antispasticity drugs
concomitantly
 Principle-
 Oral baclofen has only very low bioavailability to GABAergic
neurones in the spinal cord
 administered intrathecally, a relatively small dose of baclofen can
give a high concentration of drug within the spinal cord
 Patients should initially be screened using a temporary catheter
with an initial test dose is 50 mg

 Device
 comprises a subcutaneous pump which stores and delivers
programmable doses of baclofen through a catheter into the spinal
subarchanoid space
 can be adjusted to vary the doses delivered, depending on the level
of patient activity and needs
 Complications
 procedure related complications- infection, skin erosions,
cerebrospinal fluid leak and seroma formation around the pump
 Abruptly stopping ITB can cause high fever, confusion, rebound
spasticity and muscle rigidity, similar to neuroleptic
malignantsyndrome

Neurosurgical management
 for severe spasticity following the failure of noninvasive
management (adequate medical and physical therapy)

PERIPHERAL NEUROTOMY
 Indications

 Procedure
 It involves microdissection guided by neuro-stimulation at low
intensity
 Extent of the nerve resection- must be limited to a maximum to
4/5 fibres,over a length of 5 mm, to prevent any regrowth
 Care must be taken with the sensory fibres, if too many cut in
the sensory peripheral nerve, may induce neurogenic pain
 Results(Mertens et al., 180 pts)
 reduction of spasticity in 82% of cases, with recurrence in only
8%
 reduction in pain 85%, and a reduction in cutaneous lesions
78%
 10% functional improvement, recovery of some ability to walk
European Journal of Neurology 9 (Suppl. 1), 35–41

Microsurgical DREZotomy
 Principle
 Modern dorsal rhizotomy is a hyper-selective rhizotomy
 At the periphery, the nerve fibres are mixed
 Technique of Dorsal Root Entry Zone-otomy (DREZotomy)
consists of selective cutting of fibres at the dorsal root zone,
including a large area up to the superfcial layers of the posterior
grey matter

 Technique was especially developed for treating neurogenic
pain
 Spasticity- selectively suppress the nociceptive afferent
discharges to the spinal cord
 Indication
 severe and regional spasticity, possibly associated with
chronic intractable pain
 Procedure
 Lesion, max depth 3mm is placed 45 in the ventromedial
direction at dorsal radicular spinal junction

 Results (Mertens and Sindou (1998) )
 n =151 patients with lower limb spasticity, follow-up 5.6 yrs
 Decreased hypertonia - 78% Ashworth < 2
 Decreased spasms - 88%
 Increased voluntary mobility - 11%
 Decreased pain - 82%

Spinal cord stimulation
 Principle
 selective stimulation of the larger fibres in order to inhibit the
activity of the smaller nociceptive fibres and so to decrease the
nociceptive input at the level of the spinal cord
 level of stimulation was dependent on the topography of the
spasticity
 electrode must be placed in the posterior epidural space in order to
stimulate the dorsal columns
 Various authors report improvement varying from 50% to 80%
over a period of 2 to 5 yrs, some report no significant
improvement
 Currently considered as an alternative only if other conservative
and surgical treatments do not work

Stratified management approach
European Journal of Neurology 2002, 9 (suppl. 1): 48–52

CONCLUSION
 Spasticity is one component of UMN syndrome
 Impact of spasticity varies between patients
 Not all cases require treatment, useful effects of spasticity must be
kept in mind before beginning treatment
 Untreated, it can cause significant discomfort and problems to
mobility and care
 Elimination of triggers and supportive physiotherapy are an
important aspect of management

 Oral medications should be started at a low dose and gradually
titrated
 No single drug should be discarded until its maximum dose is
reached or if patient develops intolerable side effects
 Intervention to be considered in patients with Spasticity resistant
to oral medications

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