Workshop in Cairo University - School of Medicine
Objectives:
Rehabilitation Process
Spasticity – Definition – Pathophysiology – Impact
Assessment of spasticity and ADL
Spasticity management options
Outcome measures – BTX injection sheet
Clinical cases – video
Gastric Cancer: Сlinical Implementation of Artificial Intelligence, Synergeti...
Spasticity Management, A rehab art. Hatem S. Shehata
1. HATEM SAMIR M. SHEHATA, M.D
PROFESSOR OF NEUROLOGY
CAIRO UNIVERSITY
SPASTICITY MANAGEMENT.
REHABILITATION ART
nt.
Faculty:
Prof. M Eltamawy
Prof. Hanan Amer
Prof Hatem Shehata
Prof. Nevin Shalaby
Prof. Amr Hassan
Prof. Sandra Ahmad
Dr. Shaimaa Al-Jaafary
Dr. Wael Ezzat
Dr. Haidy Shebawy
2. HATEM SAMIR MOHAMMED, M.D
OBJECTIVES
• Rehabilitation Process
• Spasticity – Definition – Pathophysiology – Impact
• Assessment of spasticity and ADL
• Spasticity management options
• Outcome measures – BTX injection sheet
• Clinical cases – video
2
3. HATEM SAMIR MOHAMMED, M.D
OBJECTIVES
• Rehabilitation Process
• Spasticity – Definition – Pathophysiology – Impact
• Assessment of spasticity and ADL
• Spasticity management options
• Outcome measures – BTX injection sheet
• Clinical cases – video
3
4. HATEM SAMIR MOHAMMED, M.D 4
GOALS
1. Optimizing social participation (considering persons’ wishes)
2. Minimizing distress of both patients and caregivers
3. Help patients to maximize behavioral repertoire
SPASTICITY. “HABILITATION/REHABILITATION”
• Rehabilitation is a long-term (may be life-long), problem-solving
process of recovery from an injury to obtain ‘optimum function’ despite of
residual disability
• It is the process by which physical, sensory, and mental capacities are
RESTORED or DEVELOPED in disabled patients
5. Change/abnormalities (molecular/cellular) - - organ (e.g.,
(cord malacia, hemorrhage, infarction, TBIDiseasePathology
(Change/abnormalities of whole body set (functional loss
S. & S.
((functional loss
Impairment
How impairment restricts the social tasks (roles). It is the
expression of the gap between a person's capabilities and
(the demands of the environment (environment interaction
Social Roles
((participation
Activity
((disability
TERMINOLOGIES SHOULD BE CHANGED
5
REHABILITATION MODEL (ICF-WHO)
HATEM SAMIR MOHAMMED, M.D
6. REAL CASE SCENARIO . . .
• 56 male patient, married (3 daughters), Banker ,
HTN, non diabetic
• 1 month ago right sided hemiplegia and dysphasia
• Assessment now: hemiparesis (G2 D, 3 P), mild
dysphasia
• Pathology: ICH
• Impairment: weakness +/- spasticity,
communication disorders
• Disability: toilet, dressing, hygiene, chocking,
decision making etc…
• Handicap: work / family / carer
6
What is the concern of his
primary physician ?
HATEM SAMIR MOHAMMED, M.D
7. HATEM SAMIR MOHAMMED, M.D
NEUROLOGICAL REHABILITATION
• Acute onset disability, with a phase of improvement followed by
relative stability: CVS, traumatic insults, infections, etc..
• Fluctuating and/or unpredictable disability, often with some
progression: M.S
• Progressive, relatively predictable disability: MND
• Stable diseases present from childhood: C.P
– Categories of Neurological Conditions
7
8. HATEM SAMIR MOHAMMED, M.D
• A comprehensive service with a multidisciplinary team who should be
involved in an integrated program
• This team includes ‘a list of related specialties‘: Neurologist/Neurosurgeons/
Orthopedics/PMR/Therapists/ Occupational and Speech therapy/
Psychologists/Support workers
• Target: increase patients activities and reduce burden of the patient and
carers
8
STRATEGIES FOR NEURO-REHABILITATION
9. HATEM SAMIR MOHAMMED, M.D
Assessment (to collect data)
Identify problem
Genesis of problem
Prognostic factors
Expectations (patients / others)
Goals Setting (PLANNING)
Short term actions
Middle term directions
Long term goals
Interventons
Deliver treatment (alter natural Hx.)
Health education and support
Collect further data
Evaluations
Compare Goals vs. Set
Identify resolvable problems remain
9
REHABILITATION PROCESS
More Actions Needed
No Actions Needed
10. HATEM SAMIR MOHAMMED, M.D
OBJECTIVES
• Rehabilitation Process
• Spasticity – Definition – Pathophysiology – Impact
• Assessment of spasticity and ADL
• Spasticity management options
• Outcome measures – BTX injection sheet
• Clinical cases – video
10
11. HATEM SAMIR MOHAMMED, M.D 26/01/2016
SPASTICITY . . . DEFINITION
• One of the most specific
impairment that results in
muscle over activity resulting
from UMNL (++ tonic SR)
• It is one of positive UMNL signs
that involves a long-term
monitoring
11
Mild weakness, loss of ‘precision
grip’ which involves opposition
12. HATEM SAMIR MOHAMMED, M.D
• Spasticity is distinct from other motor disturbances:
• Sensori-motor disorder
• Velocity-dependent increase in tonic stretch reflex activity
• Length-dependent (clasp knife)
• State-dependent (variables)
• Usually seen in the anti-gravity muscles like the arm flexors and the leg
extensors
• Associated with high tone spasms and soft tissues changes
12
Pandyan et al., Disabil and Rehab, 2005
SPASTICITY . . . DEFINITION
13. HATEM SAMIR MOHAMMED, M.D
(1) Disability: weakness / dexterity
(2) Mask actions of antagonists
(3) Seating and postural problems
(4) Pains, stiffness and spasms (discomfort–
contractures–deformities)
(5) Hygiene and self care problems
(6) Mood changes and loss of self-esteem
(disfigurement–sexuality problems)
(7) Fatigue – Sleep disruption
Disability
Com
plications
13
SPASTICITY . . . CONSEQUENCES
14. HATEM SAMIR MOHAMMED, M.D
Loss of cortical drive after cerebral
or above lesion spinal insults
Loss of descending inhibitory spinal
circuits (Dorsal RST)
Increase muscle SR by intact Medial
reticulospinal and vestibulospinal tracts
Spastic hypertonia, spasms, and clonus
Greenwood, 1998
INCREASE MUSCLE
STRETCH REFLEX
14
SPASTICITY . . . PATHOPHYSIOLOGY
15. HATEM SAMIR MOHAMMED, M.D
• As a result neural pathways show
changes in their level of excitability:
• Altered α-motoneuron excitability
• Altered Ia and Ib inhibition
• Some studies also report changes in
the γ-motoneuron excitability (not
commonly accepted)
Voerman and Hermens, Disabil and Rehab, 2005
Spasticity (Pathophysiology)
15
16. HATEM SAMIR MOHAMMED, M.D
NEURAL AND NON-NEURAL COMPONENTS
OF SPASTIC LIMB DYSFUNCTION
• These two mechanisms are responsible for the clinically observed resistance to
passive movement associated with spasticity
• Muscle hyperactivity (muscle contraction and shortening)
• Bio mechanical changes (soft tissues; tendons, ligaments, joints):
thixotropy, intra-articular adhesions
(Gracies, 2005)
16
17. HATEM SAMIR MOHAMMED, M.D
PRO / CONS
POSSIBLE BENEFITS OF SPASTICITY
• A common argument
• > 38% of stroke survivors affected by spasticity
☞ May help patients to walk, stand or transfer (e.g., stand pivot transfers)
☞ May assist in maintaining muscle bulk (inherently prevents atrophy)
☞ May assist in preventing DVTs
☞ May assist in preventing pressure ulcer formation over bony prominences
• No positive overall benefit to spasticity in an individual at any stage of life
17
18. HATEM SAMIR MOHAMMED, M.D
OBJECTIVES
• Rehabilitation Process
• Spasticity – Definition – Pathophysiology – Impact
• Assessment of spasticity and ADL
• Spasticity management options
• Outcome measures – BTX injection sheet
• Clinical cases – video
18
19. HATEM SAMIR MOHAMMED, M.D
ASSESSMENT TOOLS
• Clinical Assessment: subjectivity - inter-rater variability
• Neurophysiological
Voerman et al., 2005
Neurophysiological response to electric stimulation
•(H / M reflex)
Evoked potentials
•(motor and sensory evoked potentials)
19
20. HATEM SAMIR MOHAMMED, M.D 20
Muscle Tone
ADL Barthel index, Others QoL tests
Sensory
Gait
assessment
Other tools
MAS, Tardeau scale, Bilateral adductor tone
VAS: for pain and dyasthesia
Cramps (Spasms)– Spasms Frequency Scale
Gait analysis laboratory
Timed-TMWT
Goal Attainment Scale ‘the most difficult’
ROM ‘the easiest – don’t forget’
Assessment Axes
21. HATEM SAMIR MOHAMMED, M.D
Q: WHICH TOOL WILL YOU USE ??
A: THAT HELPS TO ASSESS THE TARGETED OUT COME
Impairment related measures
Spasticity
Range of movement
Functional measures
Reduction of pain
Ease of applying splint/orthosis
Ease of maintaining hygiene
Ease of dressing
Improved seating position
Improved gait pattern
Improved gait efficiency
MAS / Tardeu scale / dynamic EMG
Goniometry
Suggested outcome measure
Visual analogue scale/Spasm Frequency Scale
Timing of tasks/number of helpers/carer rating scale
Timing of tasks/number of helpers/carer rating scale
Timing of tasks/number of helpers/carer rating scale
Photographic record/measurement i.e. pelvis level
Video analysis/10 meter walk test
Video analysis/patient rating/energy cost assessment
21
22. HATEM SAMIR MOHAMMED, M.D
CLINICAL SCALES
It measures Stiffness not Spasticity – No Speed of Movement is Specified
Modified Ashworth Scale
22
23. HATEM SAMIR MOHAMMED, M.D
Measurements take place at 3 velocities
Responses are recorded at each velocity as X/Y, with X
indicating the 0 to 5 rating, and Y indicating the degree of
angle at which the muscle reaction occurs.
Patient position:
supine, with head in midline
Tardieu Scale
23
26. HATEM SAMIR MOHAMMED, M.D
VAS: a subjective pain measure, ranged from 0
(no pain) to 10 (unbearable pain).
The patients mark the point that represents their
perception of the current status
Horizontal line
100 mm in length
Visual Analogue Scale (VAS)
No spasms0
One spasm or less a day1
One to five spasms a day2
Five to nine spasms a day3
Ten or more a day4
Spasm Frequency Scale
How many spasms occurred in the
affected muscles or extremities during the
last 24 hours ?
26
Clinical Scales (Cont’d)
27. HATEM SAMIR MOHAMMED, M.D
TIMED 10-METER WALKING TEST (TMWT)
• Patient walks with/without assistance 10 meters (32.8 feet) and the time is measured for the
intermediate 6 meters (19.7 feet)
• Start timing when the toes of the leading foot crosses the 2-meter mark
• Stop timing when the toes of the leading foot crosses the 8-meter mark
• It can be performed at preferred walking speed or fastest speed possible (preferred vs.
fast)
• Collect 3 trials and calculate
the average of the three trials
Acceleration Deceleration
27
28. HATEM SAMIR MOHAMMED, M.D
• 3 components:
• Kinematics: analysis of
body positions, angles,
velocities, accelerations of
body segments and joints
during motion)
• Kinetics: analysis of forces
• EMG
28
Gait Analysis
Assessment Tools (Cont’d)
30. HATEM SAMIR MOHAMMED, M.D
PATHOMECHANICS OF HEMIPLEGIC GAIT
• Reduced knee flexion in swing phase (stiff-legged gait)
• Equinus (excessive ankle plantar flexion) which leads to: increase
energy required to initiate swing period of gait cycle
• Gait asymmetry, short step length, speed reduction and longer gait cycle
• Mass limb movement pattern: on the paretic side requiring
compensatory pelvic adjustment in non-paretic side
• Defective “body image”
30
31. HATEM SAMIR MOHAMMED, M.D
OBJECTIVES
• Rehabilitation Process
• Spasticity – Definition – Pathophysiology – Impact
• Assessment of spasticity and ADL
• Spasticity management options
• Outcome measures – BTX injection sheet
• Clinical cases – video
31
33. HATEM SAMIR MOHAMMED, M.D
SPASTICITY MANAGEMENT OPTIONS
Physical therapy
Regular exercises
Physiotherapy
Surgery
Severe spasticity
Medical
therapy
Generalized
Oral agents
Regional
Intra-thecal baclofen
Focal
BTX-A injection
Phenol blockade
Consider each in combination with others
33
34. HATEM SAMIR MOHAMMED, M.D
PHARMACOLOGIC MANAGEMENT
• Systemic
• Baclofen (30-90 mg/d), diazepam (5-15 mg/d), dantrolene sodium
(100-400 mg/d), clonidine (0.3-0.9 mg/d), tizanidine (< 36 mg/d),
carbamates (methocarbamol 3–6 g, carisoprodol), endocannabinoids
(Sativex)
• Limitations: non-selective; large dosages often required which may
result in intolerable side effects (sedation, weakness, GIT disturbances
and hepatotoxicity)
34
35. HATEM SAMIR MOHAMMED, M.D 35
ECB.
‘Retrograde’ inhibition of nerve impulse transmission
1. Action potential at the presynaptic
2. Neurotransmitter (NT) release
3. Glutamate and GABA
4. Binding to GABA-R and iGlu-R
5. Inhibitory …………… Excitatory
6. Activated Glu
7. Increase Calcium
8. ECBs bind to pre-synaptic cannabinoid
receptors (CB1-R)
9. Net result is inhibition of further Ca
influx, and so inhibition of NT release
stimulates
endocannabinoid
(ECB) synthesis
36. HATEM SAMIR MOHAMMED, M.D
• Local treatment options.
• Motor point and nerve blocks: aqueous phenol (Neurolysis by coagulate
proteins)
Limitations: tissue necrosis, pain and dysesthesia; variable duration of effect;
often irreversible
• Local injections of BTX-A
36
Pharmacologic Management (Cont’d)
37. Indications: generalized moderately severe spasticity
(not adequately treated with oral medications and
BTX).
The spasticity reduction in LL (+/-) UL depends on the
catheter position in the spinal fluid.
Low catheters (T 10-12): improve mainly the legs.
Higher catheters (T 1-2): arm spasticity is targeted.
■ Regional treatment options. Intra-thecal Baclofen (ITB)
37
Pharmacologic Management (Cont’d)
HATEM SAMIR MOHAMMED, M.D
38. Test dose: 50 ug baclofen injection in spinal fluid. Then
evaluate for 4-8 hours (response)
Pump is inserted under abdominal muscles
A catheter is inserted through a needle intrathecally and is
threaded upward
Catheter is tunneled under the skin to the abdomen and is
connected to the pump
The pump filled with baclofen is programmed by a
computer to continuously release a specified dose
38
Pharmacologic Management (Cont’d)
HATEM SAMIR MOHAMMED, M.D
39. HATEM SAMIR MOHAMMED, M.D
SURGICAL MANAGEMENT
• Selective dorsal rhizotomy
• Selective Neurotomy: partial section of motor nerve branches
• Orthopedic surgery as tendon release (depending on age of patient)
Limitations: invasive; irreversible; parathesia; effectiveness varies
39
40. Selective Dorsal Rhizotomy (SDR)
1. Exposing LL nerve roots through a midline lumbar
incision.
2. Sensory roots are divided into 3 – 5 rootles, that
are electrically stimulated to identify and cut nerves
with abnormal responses.
Commonly in young patients with LL spasticity (with
relative good strength and good back extensors
power) or (to improve hygiene).
Prerequisites: No contractures.
Complications rate: 5 – 10%
PT should start after a month (1-2 times/wk)
if the goal is to improve ROM; and (4-5/wk)
if the goal is to improve strength
40HATEM SAMIR MOHAMMED, M.D
41. HATEM SAMIR MOHAMMED, M.D
Orthopedic Surgery
• Indications:
(1) ease care, (2) improve function, (3) cosmetics
• Both bony and soft tissue surgeries
• The major soft tissue procedure involves lengthening the muscle-tendon unit
(tenotomy) – and (tendon transfer)
• Other surgeries include:
• Capsulotomy
• Fascial arthroplasty
• Removal of excessive callus formation
41
42. HATEM SAMIR MOHAMMED, M.D
OVERVIEW OF REHABILITATION INTERVENTION
• Early start – better outcome.
• Positioning ‘bed, wheelchair, splinting, casting, AFO)
• Joints stretching and PROM to prevent contractures or shortening
• Full stretch for 2 hours / 24 hours (Medical Disability Society, 1988)
• Re-educate ‘Relearning’ and facilitate balance/equilibrium
• Gait training
• In advanced spasticity, (Biomechanical hypertonia) resistant disability
▪ Not velocity-dependent and poor response to antispastic agents.
▪ The only treatment: stretching, positioning, splinting and casting
42
43. HATEM SAMIR MOHAMMED, M.D
DOES REHABILITATION WORK ???
ROLE OF NEURONAL PLASTICITY
• Late recovery (neuronal plasticity) is
proposed to underlie cortical map
reorganization following neurological
insults
• The undamaged regions of the brain can
progressively adopt the function of the
lesioned area by neuronal sprouting and
synaptogensis leading to change in
cortical representations (maps)
This can be enhanced by
enriched environment,
structured physiotherapy and
TMS
43
44. HATEM SAMIR MOHAMMED, M.D
OBJECTIVES
• Rehabilitation Process
• Spasticity – Definition – Pathophysiology – Impact
• Assessment of spasticity and ADL
• Spasticity management options
• Outcome measures – BTX injection sheet
• Clinical cases – video
44
45. HATEM SAMIR MOHAMMED, M.D
NOW . . . I DECIDED TO INJECT BTX
WHY ?? HOW ??
• Selection criteria for injection (identify the problem precisely):
(1) Preserved functionality (type of spasticity) , (2) Others
• Understanding and expectations of treatment by patient and caregiver
• Dosage and site of injection
45
46. HATEM SAMIR MOHAMMED, M.D
PREPARATORY STEPS
• Before injection: Checklist
• Complete examination
• Goal determined: a contract with patient
• Take into account patients on anti-coagulants
• Muscles to inject
• Muscle localization
• Techniques of injection
• Evaluation after 2-4-6 weeks
46
47. HATEM SAMIR MOHAMMED, M.D
PROBLEM DISTRIBUTION GOAL SETTING
Regional
Multifocal
(generalized with focal problems)
Focal
47
48. HATEM SAMIR MOHAMMED, M.D
COMMON CLINICAL PATTERNS – UPPER LIMB
Adducted/internally
rotated shoulder
Flexed wrist Pronated forearm
Clenched fist Flexed elbow Thumb in palm
Courtesy WE MOVE, 2006
48
50. HATEM SAMIR MOHAMMED, M.D
COMMON CLINICAL PATTERNS – LOWER LIMB
Equinovarus
Striatal toe
Stiff knee Flexed knee Adducted thighs
50
Courtesy WE MOVE, 2006
51. HATEM SAMIR MOHAMMED, M.D
WHICH MUSCLES TO TREAT ?
• Elbow flexion:
• Biceps brachii, brachialis, brachioradialis, pronator teres
• Spastic hand:
• FCR, FCU, FDS, FDP, FPL, interosseii, opponens
• Stiff knee gait:
• Rectus femoris, hamstrings
• Equinovarus:
• Triceps sure, tibialis posterior
• Toe flexion:
• Flexor digitorum longus and brevis, FHL
• Muscle treated frequently depends on patient condition and practitioner
personal experience,
51
52. HATEM SAMIR MOHAMMED, M.D
WHAT IS THE BEST DILUTION ?
• 1 or 2, or 5 ml / 100 U BOTOX ®
• High volume dilution and end-plate targeting achieve greater muscle
blockade
• Low volume for small muscles - - - Large volume for large muscles
52
53. HATEM SAMIR MOHAMMED, M.D
WHAT IS THE BEST INJECTION
TECHNIQUE AND SITE?
• The best technique is the one you feel confident with
• Blind technique:
• Poor accuracy / not to recommend
• Risk to inject ‘between’ muscles
• Unrelated to injector experience
• In one study assessed 121 practitioners injected cadaver muscles, 43%
succeeded and 57% failed
• EMG if large and superficial
• ES if small and deep
• U/S-guided: if deep or failed to be stimulated
53
54. HATEM SAMIR MOHAMMED, M.D
BTX INJECTION SHEET . . . .
• Signed consent: information – patient and caregivers
• Agent used: . . . . . Dilution: (. . . units / ml saline)
• Muscle identification: palpation / EMG / Others
• Muscle injected Units:
………………… ……..
• Appointment date for splinting (type, method of applications, review appointment)
• Appointment date for further review (2-4-6 wks):
• Response to injection ?
• Has functional goal been achieved ?
• Is further injection needed at current time ?
54
56. HATEM SAMIR MOHAMMED, M.D
DIAGNOSTIC NERVE BLOCK WITH ANAESTHETICS
• Lidocaine injection (1 ml) at the level of motor nerve branches
innervating spastic muscles
• Immediate and transient spasticity reduction
• Determine the respective responsibility of spasticity, contracture and
weakness
• Evaluation of function without spasticity
56
68. CASE VIDEOS
Disability:
(1) weak back extensors
(2) flexed posture (overacting left
iliopsoas) – left loin pain
(3) overacting adductors
(4) co-contraction (hamstrings/
quadriceps F)
(5) left talipus eq varus
(6) disabling spontaneous clonus
Plan:
(1) BoNT injection: Iliopsoas (left):
50. Quadriceps (rectus femoris – vastus medialis):
25 X 2 (small doses to minimize clonus).
Hamstrings: 50 X 2. Adductors (bilateral), left
gracilis: 50 X 2. Left Gastromedialis & lateralis:
30. Left tibialis posterior: 50
(2) Stretching of injected muscles
(3) Strengthening of back extensors
(4) Then gait and balance ex
A.S, 36-yr, SPMS. Diagnosed 10 yr ago
Wheel-chair: 18 mo
On CPM (9 mo)
This patient was subjected to 3 injection sessions
4 mo apart
18 Sep 2011
68
69. 3 WEEKS AFTER 1
ST
INJECTION
(DECREASED HAMSTRINGS OVERACTIVITY
– KNEE EXTENDED)
STILL BACK EXTENSORS (WEAK)
LEFT LOIN PAIN DISAPPEARED
8 weeks after 2nd injection
(Back extensors can support walking)
69
20 Mar 2012
16 Oct 2011