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Activity in Cerebral Palsy: How it helps muscles

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Title: Activity in Cerebral Palsy: How it helps muscles


1
Activity in Cerebral PalsyHow it helps muscles
( brains!)
Diane L. Damiano, PhD PT National Institutes of
Health Bethesda MD USA
2
TAKE HOME MESSAGE
  • Activity,
  • Activity,
  • Activity.

3
Activity and Cerebral Palsy
  • Those with CP have one of the most sedentary
    lifestyles among pediatric disabilities (Longmuir
    Bar-Or 2000)
  • Van den Berg-Emons et al (1995) estimated that
    average child with CP would need to exercise
    2.5 hours/day to reach activity levels of peers

4
Step Counts in CP by GMFCS LEVEL vs. Peers
(Bjornson et al 2007)
5
Outline
  • Discuss generalized effects of activity on muscle
    structure function and motor outcomes
    (optimizing physical rehabilitation)
  • Neurobiology of activity potential role of
    activity-based protocols for promoting neural
    recovery and restoration of function

6
  • Muscles now known to be one of the most
    plastic tissues in the body
  • Muscles respond in a fairly stereotypical
    manner to the amount and type of activity imposed
    upon them
  • Lieber et al, 2004

7
Muscle Myths
  • Previously thought that fiber types and of
    fibers determined genetically and could not
    change (marathon runners sprinters born, not
    made)
  • Rehabilitation of those with CP and other CNS
    disorders failed to include muscle strengthening
    or other intense training paradigms because it
    would gt spasticity.

8
How Do Muscles Adapt? (Harridge, Exp Physiol,
Review 2007)
  • Two basic mechanisms at the level of the muscle
    fiber (cell)
  • Change in mm size
  • Primarily by increase/decrease in fiber diameter
  • Mediated by satellite cells that repair or grow
    muscles (or replace themselves)
  • Change in size directly related to maximal force
    output
  • (In extreme cases (elite bodybuilders) perhaps
    normal development (Sjostrom, 1992) the number of
    fibers may increase)
  • Change in protein isoform (MHC) composition
  • affects maximal shortening velocity (faster if gt
    Type II)

9
How can muscle adaptations be indiced?
  • Decrease mm size
  • Immobilization
  • Decrease activity level (contractile activity)
  • Weightlessness
  • Increase mm size
  • Placing loads on muscles, e.g. progressive
    resistance exercise (PRE)
  • Change protein isoform (MHC) composition
  • High or low frequency electrical stimulation or
    high intensity (speed) voluntary training
  • Denervation

10
Muscle plasticity in adult developing skeletal
mm changes in MHC composition induced by
inactivity fast-type activity in Type I fibers
Schiaffino et al. Physiology 22 269-278 2007

11
What happens to muscles in CP?
  • From infancy on ( perhaps before) children w/ CP
    do not move as much as those w/o CP move
    differently
  • Muscles cells are not mature at birth therefore
    in CP, muscles may fail to develop properly
    from outset
  • If muscles are not used, they become
    progressively weaker then it becomes even harder
    to move
  • To what extent is this preventable or reversible?

12
What CP Care Environment Does to Muscles
  • Many treatments in CP weaken muscles
  • Muscle-tendon lengthenings ltforce-generation
    capability (Delp Zajac, 1992)
  • Orthoses can cause atrophy of calf mms
  • Botulinum toxin paralyzes one mm at a joint to
    allow gt stretch enhance opposite mm function
  • ITB depresses involuntary voluntary muscle
    activity
  • PT casting, splinting, restrictive garments,
    prior emphasis on movement quality vs. quantity,
    ban on strengthening can limit muscle development

13
Strength in CP vs. Non-CP Dominant Side
(Wiley Damiano, DMCN 1998)
14
Non-Dominant Side
15
Strength by GMFCS Level
16
Muscle Strengthening
  • Multiple reviews in CP other conditions showing
    that strength is predictably increased (Dodd,
    Tayl0r Damiano 2002 Taylor, Dodd Damiano
    2006)
  • Changes in gait speed other aspects of
    functioning noted often but not consistently
  • Depends on dose and duration. Must be done
    properly for sufficient time to achieve
    benefits
  • Must be maintained across lifespan

17
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20
Muscle Fatigue in CP
  • Fatigue is cited as main cause for decline or
    cessation in walking in CP (Bottos 2004)
  • Cardio-respiratory endurance lower in CP
  • No reports on voluntary muscle fatigue in CP
  • We hypothesized that those with CP would be more
    fatigable than age-matched peers, and that
    endurance would worsen with level of involvement

21
Methods
  • Subjects 18 w/ CP 15 controls (ages 10-23y)
  • Fatigue Protocol
  • Biodex isokinetic dynamometer
  • Consecutive, maximal, (concentric)
  • reciprocal knee extension/flexion reps
  • 35 repetitions at 60 deg/s
  • Instructions Push all the way up as hard and
    fast as possible pull down.
  • Verbal encouragement each repetition

22
Methods
  • Computed slope of the decline in torque
    (normalized to peak torque) in the quadriceps
    hamstrings mms

23
Results for the Quadriceps
24
Correlation of Slope GMFCS
Spearman (r) -0.50, p .035
25
RESULTS
  • Group w/ CP had greater endurance in their
    quadriceps than controls hamstrings not
    different in CP
  • Stackhouse et al. 2005 evaluated fatigue with
    electrically elicited contractions found
    quadriceps (but not triceps surae) to be less
    fatigable in CP
  • We further found that the less functional (and
    weaker) they were, the greater their endurance
    tended to be
  • HOW DO YOU EXPLAIN THIS?

26
FATIGUE PARADOX
  • Stronger individuals may fatigue more rapidly
    (inconsistent)
  • Muscles in CP have predominance of Type I fibers
    (Rose 2001)
  • The subjective complaint of fatigue is likely due
    to weakness. Individuals with CP are working at
    higher of maximum, so this makes them feel more
    tired during a similar task - same thing happens
    in elderly
  • Loss of strength with age increases fatigue even
    more
  • Suggests that the most effective long term
    strategy to avoid fatigue is to maintain/increase
    strength to lessen relative effort

27
In Vivo Evidence of Muscle Plasticity
28
THIGH CT SCANS IN TWO MATCHED PATIENTS WITH
COMPLETE SCI (n56)
TRADTIONAL PT CONTROL 6
MOS. OF FESCYCLING
(Sadowsky, McDonald, Damiano et al)
29
Introduction to Muscle Architecture
  • Fascicle geometry
  • Fascicle Length (FL)
  • Fascicle Angle (FA)
  • FL MT / sin (FA) (Shortland et al, 2002)
  • Muscle size
  • (2D) Muscle thickness (MT)
  • (3D) Cross-sectional area (CSA)
  • (3D) Muscle volume
  • (3D) Muscle length

30
RECTUS FEMORIS 3D US
Longitudinal ?
RF
Axial ?
31
Relationship of muscle size to strength in CP
  • Ohata et al (2004, 2006) suggested that muscle
    thickness could be used as a surrogate measure of
    strength in CP, especially for those who are too
    young, too cognitively impaired or lack
    sufficient motor control.

32
MUSCLE THICKNESS IN ADULTS WITH CP (Ohata et al,
Phys Ther 2006)
BY STANDING ABILITY
BY GMFCS LEVEL
33
Muscle Ultrasound (US)
  • GE VOLUSON730 E linear (2D) volume (3D) probes
  • PARTICIPANTS18 w/CP (12 ambulators), 20
    Controls 11 measured before after intense
    summer sports camp
  • METHODS
  • Muscles
  • Rectus Femoris (RF)
  • Vastus lateralis (VL)
  • Position Supine with hips knees in extension
  • Measurements
  • RF 50 of ASIS to Patella
  • VL 50 of GT to lateral femoral condyle

34
Relationship of Muscle Thickness to Peak Torque
VL MT (mm)
ISOMETRIC PEAK TORQUE (N.m)
p lt 0.05 p lt 0.01
35
Rectus Femoris Cross-Sectional Areain CP by
GMFCS Level and vs. Control
GMFCS X Normalized Cross-Sectional Area r
0.50, p .05
36
RECTUS FEMORIS THICKNESS
CONTROL (23kg) RFT20.0 mm
GMFCS II (21kg) RFT13.3 mm
GMFCS III (25.6kg) RFT105 mm
GMFCS IV (28.4kg) RFT10.4 mm
37
CHANGE IN RECTUS CROSS SECTIONAL AREA (CSA) BY
WEEKS IN SPORTS CAMP
Does intense and prolonged physical activity gt mm
size in CP? (new evidence suggesting this is
possible in as few as 3 weeks)
38
NEUROBIOLOGY OF ACTIVITY
  • Over the past 40 years, considerable data have
    been accumulated on the beneficial physiological
    effects from physical activity
  • We are now becoming aware what activity does for
    the brain (e.g. it decreases depression slows
    cognitive decline in Alzheimer's)

39
PROMOTING ACTIVITY
  • Activity should be done early and often
    parents can have the largest effect on this in
    infancy
  • In addition to physical changes, personality,
    cognitive social development may also be
    affected by early activity (or lack thereof)

40
Activty-Based Exercise Programs
  • Catch-22 Those with CP need intense exercise to
    improve motor function, but they lack the motor
    function to exercise intensely.
  • Therapeutic approach Use of devices that force
    or enable person to exercise beyond their
    voluntary capabilities
  • Body-weight supported treadmill training
  • Lokomat and other motor driven gait devices
  • FES and motor-assisted cycles

41
RANDOMIZED TRIAL OF TREADMILL TRAINING IN
INFANTS WITH DOWN SYNDROME (Ulrich
DA, Ulrich BD, Angulo-Kinzler RM, Yun J 2001)
Description 30 infants with DS assigned to
control or home treadmill training beginning at
independent sitting. Followed until onset of
independent walking.
42
RESULTS
43
Review of BWSTT in Pediatric Rehabilitation
(Damiano DeJong, 2008 in press)
  • Shown to be efficacious (RCT) in Down Syndrome to
    accelerate motor milestone acquisition more
    intense training seems to increase activity
    levels at 2 years
  • Pediatric SCI prolonged training in a few
    individual cases with impressive anecdotal
    results in most (children can be taught to step
    even if they cannot move voluntarily)
  • CNS impairments 17 studies (no RCT) suggesting
    that this improves gait speed and GMFM DE. No
    comparison to alternatives (e.g. over ground
    training)

44
RESULTS BWSTT ICF ACTIVITY
45
Potential Benefits of Treadmill Training in CP
  • Strengthen anti-gravity muscles (by adjusting BWS
    or adding weights)
  • Increase gait speed (gt belt speed)
  • Improve gait symmetry (e.g. elongating shorter
    strides)
  • Improve interlimb coordination (through
    appropriate sensory inputs practice)
  • Increase endurance aerobic training)
  • Combinations of above

46
Motor-Assisted Cycling
  • BWS treadmill training labor cost intensive,
    difficult for therapist/ family
  • External assistance needed for those who cannot
    cycle on their own due to paresis or lack of
    motor control (FES-cycles or new motor assist
    devices)
  • Cycling can be performed in home with little or
    no assistance, trunk balance or WS
  • Form of locomotion similar in phasing frequency
    to walking (Ting, 2002)
  • Evidence of shared neural circuitry similar
    reflex modulation in walking cycling (Brooke
    1997)

47
Current Cycling Trial
  • PARTICIPANTS 10 children w/ CP, ages 5-17,
    GMFCS III/IV
  • PROTOCOL All perform 50RPM passive or
    active-assisted cycling 30 min/day for 5
    days/week X 3 mos
  • GOAL improve lower extremity coordination
  • PRIMARY OUTCOMES Changes in comfortable as
    fast as possible cadence, variability in
    cadence, EMG reciprocation vs. synchronization
  • SECONDARY OUTCOMES 1) changes in spasticity 2)
    Changes in cortical activation in response to a
    sensory stimulation using fMRI none able to be
    still enough

48
Case study from motor-assisted cycling study
  • 5 ½ yo boy with spastic diplegia
  • GMFCS III ambulates w/ post walker
  • Ashworth 3 (0-4) in quadriceps hamstrings
    (strong catch in first half of motion)
  • Had adapted cycle, but needed assist from parents
    to ride
  • He was able to cycle with the device part of the
    time (no resistance)

49
Cortical Plasticity
  • The brain is also use-dependent
  • Dramatic changes in the PNS produce dramatic
    changes in brain (e.g. SCI amputation)
  • Spinal circuits can be accessed and trained
    effects may be specific and localized
  • Spinal circuits may be used to drive cortical
    changes that may be more generalized
  • How do we help the brain recover?

50
What type of activity does brain like?
  • Intense (amount, speed, mm activation)
  • Some imposed rhythm but variable (more neural
    control)
  • Complex or interesting solving problems
  • Electrical stimulation (other sensory
    stimulation)
  • Locomotor training (loading/ proprioceptive
    input)

51
Conclusions
  • Those with motor disorders need to be active
    their whole life to minimize negative plasticity
    in mm (e.g. atrophy) optimize positive
    plasticity (e.g. gtfiber size)
  • Increasingly obvious that we have been
    under-rehabilitating people with CP other motor
    disorders
  • Potential for exercise and activity to restore
    neural function and connectivity just beginning
    to be realized, Muscle activation (electrical
    activity) appears necessary to drive cortical
    plasticity

52
THANK YOU
NIH CLINICAL CENTER
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