Katrina Buchanan - Spasticity Management in MS: A team approach

1. Katrina Buchanan
Consultant Physiotherapist, Spasticity Service, NHNN
Spasticity Management in MS:
A team approach
MS Trust. 5th November 2018

2. Plan
§ What is spasticity?
§ Impact on the person with MS
§ Assessment
§ Interventions and team management
§ Case studies

3. Spasticity Definitions
‘ a motor disorder characterised by
a velocity dependent increase in
tonic stretch reflexes, with
exaggerated tendon jerks,
resulting from hyperexcitability of
the stretch reflex, as one
component of the upper motor
neurone syndrome’
Lance
1980
‘disordered sensori-motor control,
resulting from an upper motor
neurone lesion, presenting as
intermittent or sustained
involuntary activation of muscles’
SPASM 2005
Narrow Broad

4. Upper Motor Neurone Syndrome
§ Spasticity
§ Spasms:
Ø Flexor
Ø Extensor
Ø Adductor
§ Increase in tendon
reflexes
§ Extensor plantar
responses
§ Clonus
§ Positive support reaction
• Weakness
• Fatigue
• Loss of Dexterity
This is a syndrome that develops over time, not a direct or
immediate effect of a pyramidal tract or cortical lesion

5. Why does spasticity occur?
§ Our understanding of spasticity it derived from animal
models and experimental studies on people with
spasticity
§ Spasticity develops over time and seems to require
several factors to occur
§ A lesion to upper motor neurone pathways
§ A reduction in inhibition in spinal cord circuits
§ Adaptive changes in the properties of the motor
neuron and spinal interneurons

6. UMN lesion
§ Essential for spasticity to occur
§ Descending tracts modulate activity in the spinal
cord circuits and affect processing in these circuits
when damaged.
§ Theory that there is a reduction in descending
inhibitory input to the SC
§ Parapyramidal pathways and serotenergic
pathways have also been implicated in the
evolution of spasticity

7. Reduction in inhibitory SC circuits
§ Several inhibitory spinal cord circuits show reduced
activity in human subjects including;
§ Presynaptic inhibition
§ Reciprocal inhibition
§ Recurrent (Renshaw inhibition)
These reductions are not uniformly seen, seen in
adult stroke patients but not CP or childhood brain
lesions

8. Adaptive Changes in MN’s and spinal
interneurons
§ Animal models demonstrate a reduction in
inhibitory GABAergic synaptic boutons and a
shrinkage of GABAergic cell bodies after SCI
lesion
§ In humans after SCI reciprocal inhibition (ankle
DF’s to PF’s) can decrease and change to
activation instead of inhibition
§ Over months plateau potentials develop, that
prolong motor neurone discharge and thus
contraction

9. Non Neural / Biomechanical
• Muscles, tendons, ligaments
and joints can become stiff when
movement is impaired and lead to
contractures
• This stiffness is felt as resistance
to passive movement.
• This contributes to the
hypertonia of the UMN syndrome

10. How many patients with MS are affected by
spasticity and spasms
Can you estimate how many MS patients will experience
symptoms of spasticity and spasms
§ A. 25 %
§ B. 48%
§ C. 72%
§ D. 84%

11. How many patients with MS are affected by
spasticity and spasms
§ North American Research Committee on MS survey of
18,727 patients with MS
§ 84% some spasticity
§ 30% moderate to severe spasticity
§ Spasticity and spasms impacted on sleep, comfort,
caused reduced mobility and pain and a reduced
quality of life.

12. Impact of spasticity and spasms
Safety
Mood
Negative Positive
Body Image
Remember spasticity can also be useful..
Transfers
Maintains vascular
flow, prevent DVT
Sexual activity
Relationships
Maintains muscle bulk
Likes movement
associated with
spasms
Washing
Feeding
Posture
Uses spasms to
assist mobility
Bladder & Bowel
Dressing
Mobility

13. Spasticity assessment
§ Process starts from referral
§ Appropriate team member contacts person, referrer, local
community team etc.
MDT Clinic – Dr, nurse, physio, if needed OT
Nursing telephone assessment
PT appointment
MDT clinic
§ Expertise of team
§ ‘One stop shop’
§ Sharing and learning for person and team
§ Good practice for invasive procedures decision making

14. History
§ What is the main problem?- open question
Ø Spasms, stiffness, pain, disturbed sleep, difficulty with
walking or transferring
Remember all components of the UMN syndrome
§ Terminology!
Ø Stiff or heavy?
Ø Spasms or lancinating neuropathic pain?
§ How does spasticity/ spasms impact on daily life
Ø 24 hour routine
Ø Partners, carers, families perspective
Ø Positive and negative aspects

15. History cont.
§ Previous and current interventions:
Ø Therapy, drugs, seating, orthotics
Ø Is there a home exercise programme?
§ Consider mood, self image, motivation, hopes,
expectations, fears
(tone of voice, emotions, non-verbal clues)

16. Consider
§ Are there trigger or aggravating factors?
§ Is pain related to spasticity or other cause?
Ø Neuropathic, musculoskeletal
§ Is the spasticity helpful for function?
§ Is it focal or generalised?
§ What is the individuals level of knowledge about
spasticity?
§ What interventions have they tried already and what
was the outcome?

17. Sensory Stimuli
Infection
Posture
and
Position
Patterns of
Movement
Emotional issues
Depression
Change in
Physical Function
Trigger and aggravating factors

18. Assessment- Hands on
§ Observe-posture, movement
§ Feel resistance to passive movement
§ ?determine biomechanical component
§ Underlying weakness
Does the spasticity need treating?

19. Outcome Measures
1. Resting position/posture:
§ description, picture,
photograph, video
2. Muscle tone/resistance to
passive movement:
§ Ashworth
§ Hip adductor tone rating
(Snow et al, 1990)
(Consider balance between
neural and non-neural
changes)
3. Passive joint range of
movement:
§ Goniometer, tape measure
4. Active limb and trunk
movement:
§ Goniometer
§ Muscle testing (Oxford
Scale)
5. Spasms
Spasm frequency scale (Priebe et al
2007)
Clonus and spasm score (Smith
1994)
6. Seating posture
Alignment, tolerance, support
required
7. Function – e.g. walking, transfers, UL
function, speech
10 metre timed walk
9 hole peg test
Speech comprehension score
8. Subjective rating scales
Visual Analogue - pain, stiffness,
comfort
MSS-88
ArmA, ArmB, LegA, LegB
9. Goal attainment

20. Ashworth scale
Affected part(s) rigid in flexion or extension4
Considerable increase in tone; passive movement difficult3
More marked increase in tone, but affected part(s) easily flexed2
Slight increase in tone giving a catch1
No increase in tone0
Criteria (degree of muscle tone)Score
Muscle tone
Ashworth B. Practitioner 1964;192:540-2.

21. Spasm Frequency Scale (Priebe et al 2007)
Spasms occurring more than 10 times per hour4
Spasms occurring more than once per hour3
Infrequent full spasms occurring less than once an hour2
Mild spasms induced by stimulation1
No spasms0
Spasm FrequencyScore
Penn RD, et al. New Engl J Med 1989;320:1517-21.
Score Spasm Severity
1 Mild
2
2
Moderate
Severe

22. Goal

23. Primary
Options for spasticity management
Ongoing Medical, Therapy & Nursing
Oral
Medication
Focal
Treatments
Intrathecal
Baclofen
Intrathecal
Phenol
Inpatient
Rehabilitation
MILD
SPASTICITY
SEVERE
SPASTICITY
Surgical
Options
Teamwork
Intermediate
Secondary

24. Spasticity management
Oral
Medication
Botulinum
Toxin
Intrathecal
Baclofen
Intrathecal
Phenol
Inpatient
Rehabilitation
Surgical
Options

25. Individualised treatment plan
§ Education
§ What is spasticity?
§ Contribution of spasticity to current problems/ function
§ Management of trigger factors
§ Physical management programme
§ Positioning, Seating, Standing, Stretches, Strengthening
§ Pharmacological treatment
http://www.uclh.nhs.uk/OurServices/ServiceA-
Z/Neuro/SPAS/Pages/Home.aspx

26. Physical Management
§ Maximise use of weakened muscles.
§ Maintain / improve soft tissue length.
§ Remove physical trigger factors.
§ Determine if spasticity is being used for function.
§ If needed for function prevent contracture and
overuse of spasticity.
§ If not needed re-educate movement patterns.

27. Physical management -
Therapeutic interventions to consider
Active
exercise
Standing
Functional
electrical
stimulation
Balance
between
movement and
positioning
Wheelchair
posture and
seating
Passive
movement
Splinting and
the use of
orthotics
Stretches
CONSIDER
From: Spasticity Management: A practical multidisciplinary guide.
Eds: Stevenson, V and Jarrett, L. Taylor Francis 2016.

28. Pharmacological therapies
§ Generalised
§ Baclofen, Tizanidine, Dantrolene,
Benzodiazepines, Gabapentin,
§ Canabinoids
§ Focal
§ Botulinum toxin
§ Regional nerve blocks
§ Intrathecal
§ Baclofen
§ Phenol

29. Oral agents for spasticity
Drug Dose Action Side effects
Baclofen 5 – 40mg tds GABA - B Sedation, weakness
Gabapentin 100 – 1200mg tds VGCCh
?GABA
Sedation, poor
concentration,
unsteadiness
Tizanidine
*LFT monitoring
2 – 12 mg tds α adrenergic
antagonist
Sedation, dry mouth,
hypotension
Dantrolene
*LFT monitoring
25 – 100mg qds Ca2+ release Sedation,
GI upset
Liver failure
Benzodiazepines
Clonazepam
Diazepam
Drug dependent
0.25-0.5mg nocte
GABA - A Sedation,
dependence

30. Optimisation
Getting the most out of the drugs
§ Timing
§ Tablets on waking.. Not with breakfast
§ Adjust to activities eg. Car travel, work patterns, therapy,
sexual activity
§ Drug choice
§ Take advantage of other drug actions
§ Clonazepam and sedation- for nocturnal spasms
§ Gabapentin- for neuropathic pain
§ ? Sativex for pain, bladder dysfunction, poor sleep
§ Mechanism for monitoring effect and adjusting dose
§ Patient and carer education, treating therapists, GP

31. Issues with oral drugs
§ Side effects
§ Blood monitoring
§ Exposing weakness
Ø Trunk and lower limbs, occ UL’s
§ Mechanism for monitoring effect and adjusting dose
Remember- the aim is to improve function and minimise
complications, not simply to reduce spasticity

32. Sativex [Δ9-tetrahydrocannabinol (THC) and
cannabidiol (CBD)]
§ Combination of the cannabis extracts Δ9-
tetrahydrocannabinol (THC) and cannabidiol (CBD)
§ Several studies have shown a small benefit or trend in
reducing spasticity (50% responder rate)
§ Generally well-tolerated
§ Side effects (mostly psychotropic effects of
cannabis), seem to be dose related
§ Granted UK license in June 2010 as an
add on therapy in MS
§ Not currently NICE approved, except in Wales
§ Access via specialist centres only
Sativex- Eur J Neurol 18:1122-31, 2011

33. Combining drugs
Start low and go slow
§ Start first choice drug
Ø Increase according to effect or tolerance
Ø Stop titration when desired effect achieved or side
effects occur
Ø If no effect at full tolerated dose, withdraw
§ Add in 2nd drug
Ø Repeat process

34. What if the drugs don’t work?
Ø Review trigger factors and physical management
programme before escalating therapy
Ø Consider other treatment options:
§ Focal treatments
§ Chemical neurolysis or botulinum toxin
§ Intrathecal baclofen
§ Intrathecal phenol
§ Surgery

35. Focal intervention- Botulinum toxin
§ Focal spasticity
§ Neural component - Neuromuscular blockade
§ Weakens the targeted muscle
§ Targeted follow up post injection
*Without therapy input probably pointless..

36. INTRATHECAL TREATMENTS

37. § Concentration of GABA receptors at dorsal horn of laminae 1- 4
- Intrathecal infusion is therefore delivered direct to site of action
Individuals who may be helped by ITB are:
§ Those with severe lower limb spasticity or spasms
§ Those in whom oral medication, therapy and nursing
interventions are no longer managing their spasticity effectively
§ Responsive to ITB
§ Have realistic, appropriate and achievable goals
§ In agreement with treatment goals and to be responsible for pump
follow up (individual or carer)
Intrathecal Baclofen

38. Patient selection for ITB therapy
§ Patients are selected for ITB Therapy following unsuccessful
(or intolerable) treatment with oral antispasticity agents
•Physical
therapy
•Oral
antispastic
agents in
mono-therapy
or combination
therapy
•ITB screening •response
•Other options,
eg intrathecal
phenol
•Patients with
hypertonicity
arising from
severe non-
focal spasticity
causing
significant
functional
impairment
•positive
•negative
•ITB Therapy

39. ITB therapy
ITB Therapy provides baclofen continually
to the cerebral spinal fluid (CSF), and hence
the receptors, via a pump and catheter
system
• Slide courtesy of Medtronic

41. Intrathecal dose is approx. 1% of oral equivalent
0
10,000
20,000
30,000
40,000
50,000
60,000
Oral Intrathecal
60,000
600
1.240
0
0.2
0.4
0.6
0.8
1
1.2
1.4
Oral Intrathecal
•µgofbaclofen
•µgpermillilitreofCSF
Daily dose Therapeutic dose
•Avoids systemic side effects

42. Contraindications to ITB therapy
§ Known allergy to baclofen (need to have tried it orally
prior to ITB)
§ IV drug user
§ Concomitant significant sepsis
- Chronic pressure sores not a contraindication
§ Psychological issues
- Needle phobia, lack of commitment, body image
issues
§ ? Precarious ambulation

43. Not contraindications…
§ Pregnancy or potential pregnancy
§ MRSA colonisation
§ Spinal fusion (cervical approach can be used if
necessary)
§ Epilepsy
§ LP or VP shunts
§ Malnutrition
§ Need for MRI scans (MS patients)
§ Walking!

44. National ITB document- May 2010
§ Intrathecal baclofen treatment
§ Assessment for ITB treatment
§ Role of physiotherapy
§ Trial of ITB
§ Pump implantation – operative technique
§ Long term follow-up
§ Complications related to ITB therapy
§ Transition from paediatric to adult services
§ Education on ITB for medical and allied healthcare
professionals
§ Audit of complications in the UK and future research
§ Evidence base to support commissioning of ITB services
§ Recording and sharing data
§ Building a national dataset
Consensus document:
§ Neurologists,
Neurosurgeons,
§ Rehab physicians,
Paediatricians,
§ Nurses, Physios

45. How is it done?
Aspects of ITB service:
§ MDT spasticity assessment & measures
- Patient selection
§ Trial
§ Implant
§ Discharge planning
§ Long term follow up
- Pump refill and dose titration
- 24 hour help-line

46. Trial procedure
§ Need ITU/ anaesthetic availability
§ Continue normal oral medication
§ Define goals of treatment and of trial
§ Perform outcome measures pre and post
§ Bolus or continuous infusion
- LP’s or temporary catheter
- Children may have GA for catheter placement
- Monitor vital signs every 30 mins

47. Areas goal set
§ Improve transfers 9
§ Relieve pain 8
§ Improve sitting 7
§ Use standing equipment 4
§ Improve perineal access 3
§ Improve sleep 2
§ Lower oral drugs 1
34 goals set in 17 patients
Managing spasticity in people with multiple sclerosis. A goal orientated approach to intrathecal
baclofen therapy. L. Jarrett et al. (2001) International Journal of MS Care, 3(4),2-11.

48. Intrathecal baclofen injection/ bolus:
Onset of action
Onset à ½ - 1 hour after bolus
Peak à 4 hours after bolus
Duration à 4 - 8 hours after bolus

49. Screening test flow chart
•In children < 25kg or walkers use 25 mcg, occasionally lower
Not a Candidate
•Source: Medtronic; Indications, drug stability and emergency procedures reference manual
•Day 1
•Bolus: 50 mcg
Day 2: 24 hrs after
Bolus: 75 mcg
Day 3: 24 hrs after
Bolus: 100 mcg
•+
-
•+ -
•+
-
= Positive Response
“Implant”
= Negative Response
additional bolus or “No Implant”
•+
-

50. Pump implant
Pump Pocket:
Abdominal incision usually, but
can be chest, gluteal, thigh…
Intrathecal Catheter: Lumbar
Incision

51. Summary of implant procedure

52. Programming
•Computer print
out- for medical
notes and
patient hand
held record
Pump- Stores and infuses
prescribed drug. Stores all relevant
patient and system data
Programmer- External device that
allows precise and adjustable
dosing via telemetry

53. Dosing patterns
•Time
•Increasin
g dose

54. Evidence base
§ First used in 1985 for spinal cord injury1
§ Shown to be effective in;
§ Spinal cord and brain injury
§ Multiple sclerosis
§ Stroke
§ Cerebral palsy
§ Benefit sustainable over time2
§ More recently used in dysautonomias, dystonias
• 1. Penn RD, Kroin JS. Continuous intrathecal baclofen for severe spasticity. Lancet 1985;ii:125–7.
• 2. Zahavi A, Geertzen JHB, Middel B et al. Long term effect (more than five years) of intrathecal baclofen
on impairment, disability and quality of life in patients with severe spasticity of spinal origin. J Neurol
Neurosurg Psychiatry 2004;75:1553–7.

55. ITB as 1st line treatment- cost?
§ Mathematical modelling of effectiveness and cost of
disabling (non ambulant) spasticity management (ITB
vs conventional) in France
§ Conventional- physical therapy, followed by oral
meds, then either 1) neurosurgery +nursing, 2) ITB,
3) focal treatment, followed by neurosurgery+
nursing.
§ Results- ITB 1st line was more effective (78% vs
59%) and cheaper (E59,391 vs E88,272)
Bensmail et al. Neurorehabilitation and Neural Repair 2009
23(6);546-552.

56. Pros and cons of ITB
Pros
§ Extremely effective
§ Flexible dosing
§ No systemic side effects
(particularly CNS)
§ Consistent treatment
§ No drug interactions
§ Allows reduction of oral
medications
Cons
§ Surgical procedure
§ Risk of complications
§ Catheter issues, infection
§ Potential risks (can be fatal)
§ Overdosing
§ Withdrawal (missed refill apt)
§ Limited battery life
§ Minimal effect on upper limbs
§ May compromise walking
§ Body image issues

57. Intrathecal Phenol
§ Protein coagulation & necrosis
§ Axonal degeneration
§ Indiscriminate destruction of motor and
sensory fibres

58. Selection criteria
§ Severe lower limb spasticity
§ Oral medication, physiotherapy, nursing no longer
effective
§ ITB not appropriate or Phenol preferred
§ Bladder & bowel dysfunction with effective management
programme in place
§ Aware of potential sexual dysfunction
§ Sensory impairment of lower limbs
§ Patient aware of irreversibility (stem cell treatment…)

59. Efficacy
25 patients
§ Goals of treatment;
§Increase ease of care
§Comfort
§Positioning in bed or wheelchair
§ Marked reduction in tone, pain, spasm intensity and
frequency. Increased ease in positioning, hoisting,
hygiene and dressing
Managing Severe Lower Limb Spasticity - Can Intrathecal Phenol still
have a role? Jarrett L et al. (2002) J Neurol, Neurosurg & Psychiatry.
73(6):705-9.

60. Aspects of IP service
§ Spasticity assessment & measures
§ Expert injector
§ Local anaesthetic trial as inpatient
§ Nursing, physio and wheelchair service follow
up
§ Repeat injections may be necessary

61. Lumbar spinal anatomy
Cerebrospinal fluid
Front
Motor nerves
Sensory nerves

62. Right lateral position
Front
90o
Motor nerves
Sensory nerves

63. Lumbar puncture
Front

64. Modified right lateral position
Front
30o

65. Insertion of Phenol
Front

66. End result
Damaged
motor nerve

67. Neurosurgery
§ Peripheral Neurotomies
§ Microsurgical technique; preservation of ~1/4
fibres prevents excessive weakness and
wasting
§ Selective Dorsal Root Rhizotomy (SDR)
§ Predominantly children with cerebral palsy
§ Selection of rootlets divided
§ MicroDREZotomy (DREZ- dorsal root entry zone)
§ Microsurgical incisions, 2-3mm in depth, 35-45
degree angle
§ Useful for pain

68. Orthopaedic procedures
• Consider only after spasticity treated and goal
orientated
§ Tendon lengthening
§ Aim; to achieve a more functional position of limb
§ Tendon transfer
§ Used to normalise articular orientation
§ E.g. distal tendon of peroneus brevis onto the tibialis anterior
for equinavarus foot
§ Osteotomies
§ Correct bony deformity from abnormal childhood growth
§ Articular surgery (arthrodesis)
§ Last resort and never in growing children

69. Acknowledgements
§ To all of the patients who consented to their photos and
videos being used to help with education and training of
health professionals
§ To you all for coming to this session today