Supplementary ‘diagnostic’
opportunities for assessing muscle tone
and muscle length & alternative focal
treatment approaches for consideration.
Presentation 3rd Feb 2017
It is sometimes quite difficult to distinguish between
severe spasticity and contracture formation.
To decide on an appropriate anti-spastic treatment
and determine realistic expectations, in some cases,
this distinction is very important.
Diagnostics: What are the benefits of assessing muscle tone
and muscle length under ‘GA’ as opposed to conscious?
• Establish neural (dynamic
element) v non neural (fixed
contracture)
• May use when cannot
differentiate if dynamic
aspect (gd 3+ on Ashworth
scale) or permanent
contracture/physical change
from fibrosis.
• Is it really that simple….
The use of Anaesthetics is complex …
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‘Type’ of anaesthetic may impact
‘true outcome’….??
Anaesthetics often a ‘cocktail’ of
meds which target different
components of muscle shortage.
Main aspect - sleep/anaesthetic
element - deep sleep is the
element for getting ‘floppy’.
Tone not dropped fully (individual
to person).
Up to anaesthetist to ‘juggle’ to get
it right to i.e.: get more relaxation.
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Conscious sedation/light sedation
(propofol/midazolam) preferred
over ‘full GA’ by medics - less
medical risks however also less
control of what ‘switching off’ - will
give ‘indicator’ re potential
spastic/dystonia component and
‘active’ element of resistance.
Muscle ‘relaxant’ (Ach receptors
agonists and antagonists, i.e.:
recuronium)–picture of
contracture, spasticity component
largely eliminated with deeper GA.
Analgesia component -pain
inhibition.
Challenges to putting someone under
anaesthetic
• Clinical risk - general health risk/ethics – risk v
benefits, is this truly necessary – most clinicians
take opportunity if linked to other procedures.
• Time
• Cost
• What is the clinical gain –would this truly give us
the answers that we are looking for?
Ask self
• Does clinical examination tell me enough?
• How long have symptoms been present – likelihood
of contracture?
• How does this link with patient goals?
• Risk/Benefits of additional information?
• Would outcome of Botox give the conclusion
anyway?
• Sleep – how is client positioned as REM sleep
induces muscle atonia.
What about more Regional Anaesthesia to
determine: contracture or spasticity ?
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Anaesthetic injection near a cluster of
nerves to numb/block the area of
body/specific nerve distribution:
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Epidural/Spinal Block
Diagnostic Peripheral Nerve Block with
local Analgesia
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The most common drugs include
lidocaine, ropivacaine, bupivacaine, and
mepivacaine, fentanyl.
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Nerve blocks with local
anaesthetics/analgesic which are
reversible and temporary are used as
diagnostic tests (Yalcin et al, 2014).
Reduced clinical risk.
Clinically used by some prior to Botox
ie.: they can be used to determine
which muscle is contributing to a
pathologic posturing, as in the case of
inversion of the foot.
Also resemble the effects of more
permanent motor blocks to determine
their potential effects.
Question?
When might you opt for:
• Spinal Block
• Diagnostic Peripheral Nerve Block with local
Analgesia
Spinal Nerve block & Diagnostic Peripheral Nerve
Block
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From focal/botox perspective – ? is it more valuable
to go as regional/territorial as possible and observe
effects.
Blocks can be more accurate on target areas ie.: in
what ‘switches off’.
Modulation of dose –pain will always go before
movement – can ask question how pain contributes
to spasm/changes in tone.
Diagnostic Nerve Blocks
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Tibial nerve block in lower limb equinovarus
deformity can be useful to establish if
contracture/spasticity.
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DTNB probably most useful, in situations where it is
uncertain if a more harm than good possible
particularly when significant function is based on
primitive motor behaviours or spasticity, or when
blocks may affect more than one aspect of a
function such as ambulation.
Eliminates spasticity within few mins and some hrs
later allowing Ax of contribution of different muscle
groups.
Utility – Inexpensive, easy to perform, low risk, can
do in any clinic setting, short Ax - numb within 5
min assess in 10, review if mobility improved after.
Needle for conduction, anaesthesia coupled with
portable electrical stimulator or emg (Deltombe et
al 2015) or use in conjunction with
ultrasonographaphy (Yalcin et al 2014).
BEST PRACTICE when considering equinus foot Selective rather than non selective diagnostic nerve
block of branches to identify spastic muscle.
(Deltombe et al 2015)
Treatment options
Dr M Sivan
Treatment: Focal Spasticity Management–
Is Botox our only option??
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Widespread use of botulinum toxin for focal spasticity has reduced the frequency of phenol
procedures, particularly in the upper limb where many situations call for the injection of smaller
muscles, which are eminently susceptible to botulinum toxin techniques (Roy C 2012).
Possible reasons to consider Phenol:
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Sensitivity/Previous reaction to Botox
Unsuccessful Rx with Botox
Poor tolerance to systemic muscle relaxants
Generally longer duration of effect
Large muscle groups that would exceed safe dose for Botox - Large dose range can be used
Cost reduction - typically, sufficient phenol to treat elbow flexors might cost 5% of the botulinum
dose required.
In supplement to Botox where total dose required excessive
Gaid 2012
Phenol nerve blocks
• Treatment of efferent component of reflex arc
• Conversion of UMNS to LMNS via “partial denervation of
nerve”/ chemical neurolysis
• Carbolic Acid (from Benzene)
• Soluble in water (<6.7%)
• 1-‐2% local anaesthetic
• >5% Denatures protein/ tissue necrosis
• Injection -Inflammatory reaction –Nerve destruction –
Wallerian degeneration –Fibrosis and re-‐innervation
sprouting
The safer and more common use of
phenol infiltration at the peripheral
• Max 1 Gm (20 Ml of 5% phenol)
nerve level is now more accepted
• Duration 6 Months-1 year
for brain injury and spinal cord
injury patients (Botte et al 1995).
Phenol nerve blocks
• Painful dysesthesia (due to mixed nerve nature) (0-‐32%)–Higher
incidence with tibial nerve, median and ulnar nerve; lower incidence
with musculocutaneous and obturator nerve
• Motor point blockade - Injecting motor points rather than nerve trunks
are that individual muscles can be targeted. The absence of sensory
fibres reduces the chance of dysaesthesia following injection.
• Muscle atrophy/ fibrosis
• DVT if vessel involvement
• Swelling (sympathetic involvement)
• Reversal of muscle imbalance, weakness in muscle, muscle or ligament
sprains can occur after nerve blocks caused by loss of reflexive
protection against overstretching the muscle in which spasticity has
been relieved, changes in the dynamics of ambulation, or loss of
reflexive support for other soft tissues.
Phenol Nerve Block
Lower Limb can do:
• OBTURATOR NERVE BLOCK –
ADDUCTORS.
• SCIATIC NERVE – HAMSTRINGS
• FEMORAL NERVE – QUADRICEPS
• TIBIAL NERVE – EQUINOVARUS
DUE TO INCREASED TONE OF
SOLEUS, TIBIALIS POST AND
TIBIALIS ANT.
(Gaid 2012)
• Wichers 1991 - Partial blocking of the
tibial nerve with phenol as a
treatment of gait disorders due to
pes equinus in central paralysis.
• May be valuable in improving
walking.
• Only done after trial block with
anaesthesia.
• Functional results linked to levels of
activity pre nerve block, sitters and
hardly walkers less favourable.
Results ascribed to better possibility
to actualise future muscle balance
improved by block. May be useful
early phase.
Phenol Nerve Block
• Obturator nerve block is used to treat hip joint pain and in the
relief of adductor muscle spasm associated with hemi-or
paraplegia.
• With the introduction of modern nerve stimulators, selective
blockade of the obturator nerve has become more reliable and
has seen a resurgence of interest in recent times.
• Neurolytic blockades with alcohol or phenol, performed with the
help of a nerve stimulator and/or radioscopy, result in a costeffective and effective reduction of muscle spasms.
• The main drawback is its temporal duration and the need to
repeat the blockade when the previous block wears off (New
York School of Anaesthesia).
Phenol block versus botulinum toxin
Phenol nerve block
Botulinum toxin injection
Immediate action
Delay > 5 days
Longer duration of action >6 months
Shorter duration up to 3months
Can be repeated immediately
Ideally not repeated within 3 months
Targets multiple muscles
Localised effect
Cheap <£1
Expensive >£100
Possible sensory side effects
No sensory side effects
Requires more technical skills, can be done
at bedside, or in a clinic or office, and
general anaesthesia is rarely required.
EMG/ USS guided
Easier to perform, can be done at bedside,
or in a clinic or office, and general
anaesthesia is rarely required.
Anatomy/EMG/ USS guided
Dr M Sivan
Permanent Solution? Neurotomy
Fouad (2011)
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Selective peripheral neurotomy of tibial nerve
indicated for Rx spastic foot in well selected cases.
Retrospective study 16 pts Grade 3,4 modified
Ashworth.
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Variable SPN Tibial nerve neurotomy undertaken
when spasticity localised to specific muscle or muscle
group or few easily accessible peripheral nerves.
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SPN - supresses spasticity without excessively
impacting motor power - if this is goal at least
1/5motor fibres preserved.
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Soleus reported to be exclusively involved in 75% of
cases in some studies.
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Operative planning essential with detailed
assessment of each spastic muscle to determine
where to section.
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Differentiation between spasticity and contracture
essential before deciding options.
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SPN considered after perioperative motor blocks
/possible trial with botox.
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Need post op rehabilitation.
Deltombe et al (2015)
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Compare diagnostic tibial nerve block with
anaesthetics followed by STN in equinovarus.
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Test spasticity using ashworth, gait - video and
distance, passive df, mrc strength.
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Decrease spasticity, improved kinematics at 2
months and 2 yrs.
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Both reduce spasticity equally.
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Diagnostic nerve block valuable screen before
neurotomy.
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Deformity mainly caused by triceps surae
(soleus/gastroc) and tib posterior.
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Partial sectioning of motor nerve branches- spare
sensory fibres to avoid neuropathic pain and
sensory deficit.
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Benefit long lasting.
Selective Peripheral Tibial Neurotomy
Bollens et al (2011)
Kim et al (2010)
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Effects of tibial nerve neurotomy (TNN) as a
treatment for adults presenting with spastic
equinovarus foot: A systematic review
Use controversial, review based on case
studies/series no rct.
Partial and selective sectioning of motor nerve
braches to selective muscles sectioning afferent
fibres to sc lead to decrease in myotactic reflex
gain.
Efferent extensive denervation of
corresponding muscle.
Collateral sprouting of axons in next month
leads to widening of persisting motor units thus
recovery of pre op motor strength.
Can have positive effect gait based on study
findings.
Neurotomy old technique rx adduction via
obturator.
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Long term results of microsurgical tibial
neurotomy of spastic foot comparison of adult
and child
Selective neurotomy generally safe and
effective long lasting with equinovarus
deformity
Can recalibrate balance agonist and antagonist
when other approaches unsuccessful/ reduces
focal spasticity
Side effects – possible sensory - normally FDL
and occ Tibialis Post
Sectioning needs to be sufficient to prevent reoccurrence
Cannot replace surgery of contracture, perform
before fixed deformity develop
Similar outcomes in adults and children
Satisfaction higher in children than adults.
Pain most often transient.
Post op rehab needed.
Treatment of spasticity in children
• It is not common place for children to be put under
anaesthetic as an assessment procedure
• For the treatment of localized or segmental spasticity,
botulinum toxin is recommended as an effective and
generally safe treatment.
• For more generalized spasticity, a number of useful oral
agents and intrathecal baclofen are available, each with
their positive and negative attributes
Treatment of focal/segmental
spasticity
• Two strategies are in current use: perineural injection of phenol or ethyl
alcohol and intramuscular injection of botox
• Although the use of botox has grown exponentially and has substantially
replaced phenol and alcohol, all 3 techniques are used for focal spasticity
and addressing specific muscles in generalized spasticity.
• Botox provides a specific presynaptic neuromuscular junction blockade
but does not injure the nerve or muscle.
• Phenol and alcohol are effective by providing neural and, at times, muscle
destruction.
• The common denominator of these medications is the blockade of the
agonist muscles allowing increased stretch and resting length while the
antagonist muscles continue activity and strengthen. The goal is a more
appropriate balance between the agonists and antagonists with prolonged
improvement.
Botulinum toxin type A for treating children and
young people with spasticity – Nice pathways
Consider botulinum toxin treatment in children and young
people in whom focal spasticity of the upper limb is :
• Impeding fine motor function
• compromising care and hygiene
• causing pain
• impeding tolerance of other treatments, such as orthoses
• causing cosmetic concerns to the child or young person.
• Consider botulinum toxin treatment where focal
spasticity of the lower limb is :
• Impeding gross motor function
• compromising care and hygiene
• causing pain
• disturbing sleep
• impeding tolerance of other treatments, such as orthoses
and use of equipment to support posture
• causing cosmetic concerns to the child or young person.
Botulinum toxin treatment , including
assessment and administration, should be
provided by healthcare professionals within
the network team who have expertise in
child neurology and musculoskeletal
anatomy.
Administering botulinum toxin :
• To avoid distress to the child or young person undergoing treatment
with botox think about the need for:
• topical or systemic analgesia or anaesthesia
• sedation (see the NICE pathway on sedation in children and young
people).
• Consider ultrasound or electrical muscle stimulation to guide the
injection of botulinum toxin type A.
• Consider injecting botulinum toxin type A into more than one
muscle if this is appropriate to the treatment goal, but ensure that
maximum dosages are not exceeded.
Treatment of generalized spasticity
• For individuals who have generalized spasticity, oral
or enteral medications can provide systemic
symptom relief. Advantages include the relative ease
of use and the lower cost compared with other
interventions, but each of these drugs carries with it
risks of side effects and a fairly limited base of
research on therapeutic efficacy in children.
• these agents may be attractive as a convenient initial
treatment, as a means to help with sleep, and/or in
combination with focal treatments for spasticity in
children
Intrathecal baclofen
• ITB requires surgical implantation and carries with it
a moderate risk of complications
• Complications may involve overdosing, under dosing
with or without withdrawal, catheter malfunction,
wound infections, or fluid collections around the
pump and occur at varying rates but may be more
frequent in younger patients or those with greater
spasticity
• For best results, spasticity treatment should be part
of an integrated therapeutic approach in which
patients, caregivers, therapists, physicians, and
surgeons have an open and clear communication
about the overall rehabilitation process of the
patient.
Conclusion
Diagnosis
• Use of ‘GA’ likely for very few.
• Regional diagnostic nerve block in some cases may have
a place for consideration.
Treatment/Management focal spasticity
• There may be a place to consider alternative options
than Botox in selected cases.
• Clear clinical reasoning essential to select cases and
support care planning.