Defining and Measuring Spasticity

Transcription

Defining and Measuring Spasticity
Defining and Measuring
Spasticity
Anand D Pandyan
(behalf of a much bigger team)
Professor of Rehabilitation Technology
School of Health and Rehabilitation
Keele University, UK
Motor control / capacity …
Lost/disordered control after an UMN
lesion…
UMN lesion
Independence
threshold
0
Life span (years)
Twilight zone
The paradoxical symptoms
Increased activity
Reduced activity
•Increased reflexes
•Weakness
•Spasticity
•Fatigueability
•Altered tone
•Loss of fine
•Spasm & Clonus
motor control
•Abnormal
movement patterns &
co-contraction
A brief history
1. 1st occurrence - Spastic Paralysis (this is a term
I have seen in the literature since 1890’s)
2. Spasticity then used in the context of the
positive symptoms (Sherrington & Hughlings
Jackson)
3. First form of a clinical definition produced by
Denny-Brown 1960’s
4. The Lance definition of the 1980’s
The Lance definition….
A motor disorder characterised by a velocity
dependent increase in the tonic stretch reflex
(muscle tone) with exaggerated tendon
reflexes, resulting from the hyper-excitability of
the stretch reflex, as one component of the
upper motor neurone syndrome.
Lance (1980): 51-55, 185 – 204, 485-494.
Malhotra et al 2009 Clin Rehbail
Lance
31%
Muscle
Tone
35%
None
31%
Other
3%
clinician
Nurse
Therapist
Carer
Patient
Researcher
Spasticity
There was an attempt at splitting
• Spastic hypertonia: Velocity dependent
increase in hypertonia with a catch when
a threshold is exceeded. (no abnormal
resting position)
Dystonic hypertonia: After testing the limb will return to fixed resting
posture that can vary with state of mind or attempted movement.
(stiffness is independent of direction)
• Rigid hypertonia: Resistance to passive movement is not velocity
dependent and no consistent abnormal posture is observed.
(stiffness is independent of direction)
•
Sanger et al 2003 Paediatrics – North American Task Force
Updating the definition
(SPASM - consortium)
Disordered sensori-motor control,
resulting from an upper motor
neurone lesion, presenting as
intermittent or sustained
involuntary activation of muscles
Pandyan et al 2005 Disabili & Rehab – SPASM consortium
The obvious first step
Spasticity
Increased activity
•Increased reflexes
•Increased reflexes
•Altered tone
•Spasticity
•Spasm & Clonus
•Altered tone
•Abnormal
•Spasm & Clonus
movement
•Abnormal
movement patterns patterns & cocontraction
& co-contraction
The splitting
Spasticity
•Increased reflexes
•Altered tone/Stretch induced muscle
activity
•Spasm
•Clonus
•Abnormal movement patterns & cocontraction
The splitting
Spasticity
•Increased reflexes (Not necessarily
abnormal but modulation may be altered)
•Altered tone/Stretch induced muscle
activity
•Spasm
•Clonus
•Abnormal movement patterns & cocontraction
The splitting
Spasticity
•Increased reflexes
•Altered tone/Stretch induced muscle
activity
•Spasm
•Clonus
•Abnormal movement patterns & cocontraction
Altered tone
1. Resistance one feels when
stretching the joint
This is a confounded measure so
cannot contribute to a definition
2. Readiness of the muscle to act
This is reduced and is no different
to the definition of paralysis or
weakness – so there is a problem
Stretch induced muscle activity
Increase in the gain
and/or reduction in
threshold velocity
dependent responses to
a stretch
Velocity response is nonstationary and its
influence on stiffness is
variable
The start of the splitting
Spasticity
•Increased reflexes
•Altered tone/Stretch induced muscle
activity
•Spasm
•Clonus
•Abnormal movement patterns & cocontraction
The start of the splitting
Spasticity
•Stretch induced muscle activity
•Spasm
•A transient but continuous muscular
contraction (cutaneous/visceral triggers)
•Clonus
•Abnormal movement patterns & cocontraction
The start of the splitting
Spasticity
•Stretch induced muscle activity
•Spasm
•Clonus
•A transient but intermittent / rhythmic
/ cyclical muscle contraction
(proprioceptive and/or cutaneous)
•Abnormal movement patterns & cocontraction
The start of the splitting
Spasticity
•Increased reflexes
•Altered tone/Stretch induced muscle
activity
•Spasm
•Clonus
•Abnormal movement patterns & cocontraction There is a need to resolve the
pathology and physiology
conundrum
SWING PHASES
Unimpaired
walking
Gastroc-soleus muscles
Anterior tibial
? Spastic
response
Newcastle 2004 - SPASM
EMG Walk 3 - Right
12
Walk 1 - Left
R Rectus
2.0
L Rectus F
V
V
-2.0
-12
12
R Vastus
2.0
L Vastus L
V
V
-2.0
-12
12
2.0
L Vastus M
R Hamstrings
V
V
-2.0
2.0
-12
12
R Peroneus L
V
-2.0
V
2.0
-12
10
L Hams L
R Tib Ant
L Hams M
V
-2.0
4.0
V
L Tib Ant
V
-10
12
R Gastroc
-4.0
4.0
L EDL
V
V
-12
12
R Soleus
-4.0
4.0
V
L EHL
V
-4.0
-12
Child with CP
Normal
Attempt 1
50
10
0.1
5
0
0
0
0
2.742
5.484
8.226
10.968
0
- 0.1
13.71
Time (s)
Grip (Kg)
Extensor EMG (mV)
Flexor EMG (mV)
Stroke patient – ipsilateral
Non-impaired adult is similar
0.2
40
30
0.1
EMG activity
0.2
Grip Strength
Grip (Kg)
15
-5
Muscle activity in the contralateral arm
0.3
maxrc1a
EMG activity (mV)
20
20
10
0
0
- 10
- 0.1
15
20
25
Time (s)
Grip Strength (Kg)
Arm Flexor EMG
Arm Extensor EMG
Elbow Flexor EMG
Elbow Extensor EMG
Non-impaired adult
contralateral
Current “state of the art”
Spasticity
•Spasm
•Clonus
•Stretch induced muscle activity
•Abnormal movement patterns & cocontraction still remain unresolved
A brief introduction to
measurement & classification
Stiffness
not spasticity!
Neural
Spasticity
Voluntary
In-voluntary*
(SPASTICITY)
Non-neural
Contracture
Current “state of the art”
Spasticity
•Spasm
•Clonus
•Stretch induced muscle activity
•Abnormal movement patterns & cocontraction still remain unresolved
Score
Penn spasm frequency
scale
Spasm frequency score
0
No spasms
No spasms
1
Mild spasms at stimulation
One or fewer spasms per day
2
Irregular strong spasms
less than one time/hour
Between one and five spasms per
day
3
Spasms more often than
one time/hour
Five to less than 10 spasms per day
4
Spasms more than 10
times/hour
Ten or more spasms per day, or
continuous contraction
Source of information: Penn RD et al 1989 Intrathecal baclofen for severe
spinal spasticity. N Engl J Med, 320: 1517 – 1521. Snow BJ et al 1990
Treatment of spasticity with botulinum toxin: a double blind study. Ann
Neurol, 28: 512 – 515. Biering-Sørensen et al 2005 Spasticity-assessment:
a review. Spinal Cord, 44: 708 – 722.
Current “state of the art”
Spasticity
•Spasm
•Clonus
•Stretch induced muscle activity
•Abnormal movement patterns & cocontraction still remain unresolved
Measuring Clonus – the original
Tardieu classification method
Held & Pierrot-Deseilligny (1969)
No resistance throughout the course of the passive
movement
Slight resistance throughout the course of the passive
movement, with no clear catch at precise angle
Clear catch at precise angle, interrupting the passive
movement, followed by release
Fatigable clonus (< 10 seconds when maintaining
pressure) occurring at precise angle
Infatigable clonus (> 10 seconds when maintaining
pressure) occurring at precise angle
Current “state of the art”
Spasticity
•Spasm
•Clonus
•Stretch induced muscle activity
•Abnormal movement patterns & cocontraction still remain unresolved
Biomechanical &
Neurophysiological
Force to move limb
Measuring stretch induced muscle
activity
EMG
EMG
Joint Angle
Displacement
Muscle activity extensors
Muscle activity flexors
Force/Moment
Outcome
Threshold
angle
Wartenberg
Spasticity may be a potential
epiphenomenon
Evidence for an epiphenomenon
NF
Muscle
activity at
a slow
F
stretch
NF
Muscle
activity at
a fast
F
stretch
W0 W6 W12 W24 W32
1.1
0.97 0.73 0.74 0.7
(0.2) (0.3) (0.2) (0.2) (0.1)
1.1
(0.4)
1.2
(0.3)
1.0
(0.4)
1.1
(0.5)
1.1
(0.3)
1.3
(0.6)
1.4
(0.6)
0.9
(0.2)
1.3
(0.7)
0.82
(0.2)
0.7
(0.1)
1.1
(0.3)
1.7
(0.6)
0.8
(0.1)
1.9
(0.7)
Are you as
confused as I?
My funders
Action Medical Research, N.Staffs
Medical Institute, EU, DoH (NIHR),
Biometrics Ltd, Allergan.
My many colleagues
Garth, Chris, Hermie, Caroline,
Sybil, Sandra, Rasheed, Venu
My many students
Jose, Liz, Shweta, Leanne,
Cameron