2. Muscle and bone plasticity
after spinal cord injury:
Review of adaptations to disuse and
electrical muscle stimulation
Group C

3. Introduction
 The paralyzed musculoskeletal system retains a
remarkable degree of plasticity after spinal cord
injury (SCI)
 Muscles and bones show different changes and
adaptations after the spinal cord has been
injured.

4.  Muscles atrophy and shift toward a fast-fatigable
phenotype arising from numerous changes in
histochemistry and numerous enzymes.
 Bone mineral density (BMD) decreases as neurogenic
osteoporosis occurs in paralyzed limbs. The primary
adaptations of bone to reduced use are demineralization
of epiphyses and thinning of the diaphyseal cortical wall.
 However electrical stimulation of paralyzed muscle
markedly reduces deleterious post-SCI adaptations.
 Physiological levels of electrically induced muscular
loading hold promise for preventing post-SCI bone mass
density decline

5. Muscle adaptations to spinal cord
injury
 Muscle fibres contain slow and fast muscle fibres depending on their
function.
 Slow fibres (Type 1): Can perform prolonged work and are resistant
to fatigue.
 Fast fibres (Type 2): Can perform rapid action but fatigue quickly.
 After SCI, muscles shift from slow to fast fibres.
 Histochemistry shows major changes in:-
• Myosin Heavy chain isoforms (MHC)
• Sarcoplasmic reticulum Ca+2 ATPase isoforms (SERCA)
 These changes are consistent with fast twitch muscle fibres.

6.  The timeline of both these changes plus muscle atrophy
vary but overall the shift supports the fast twitch fibres.
 Atrophy may be faster than the transformation of the
isoforms.
 Timeline:
• After 6 weeks lower limb muscles were 45% smaller
than controls.
• A complete transformation of Myosin Heavy Chains is
complete by 17 months.
• SERCA protein isoforms begin to adapt quickly and
transform gradually over time.

7. Muscle response to training
 Electrical muscle stimulation to paralyzed muscles show
the evidence of their increased use via hypertrophy and
improvements in fatigue resistance by increasing their
oxidative capacity and glycolytic capacity.
 Low frequency(15 to 50Hz) repetitive stimulation is more
advantageous while high frequency (greater than 50) is
known to compromise with neuromuscular junction
hence not recommended
 Load offers during electrically elicited contraction also
improve the training related changes
 high resistance training shows more resistance against
fatigue and metabolic adaptation by phosphocreatine
recovery than the low resistance training..

8.  Innervated and denervated muscles
 Muscle transformation
 Factors effecting hypertrophy of muscle
 Muscles load effects on bones

9. Bone adaptations to SCI
 As muscle is the primary deliverer of loads to the skeletal
system, the bones of paralyzed limbs lack an important
stimulus for maintenance of bone density
 When weight-bearing and muscular contraction diminish
or cease after SCI, the loss of mechanical loading yields
an imbalance between osteoclastic and osteoblastic
activity.
 Bone resorption outpaces bone formation eventually
leading to neurogenic osteoporosis

10.  Mechanism:
Within a few months after SCI, BMD starts to decline.
Trabaculae in the epiphysis become fewer in number or
may become perforated.
Disuse remodeling replaces trabecular lattice with fatty
marrow.
Bone mass at the site of long diaphyses is lost via
thinning of the cortical wall, reducing the bone’s bending
stiffness.
As a result overall bone strength decreases.

12. Bone response to training
 Biochemical stresses effect structure of skeletal
system
 loads applied to bone create stress.
 change in length of bone is shear
 max. shear in young lamellar bone is 2.5% change
in length
 remodeling on trabecular surface due to very low
strain levels or disuse leads to demineralization

13.  Animal studies have shown adaptive capacity of bone to
mechanical loading at a high rate
 Non-SCI animal models have pattern of bone loss
resembling that of human bone loss after SCI
 results showed potential usefulness of re-introduction of
load after disuse-related BMD(bone mineral density) loss
 In humans with SCI,DEXA(dual-energy X-ray
absorptiometry)-based studies revealed no BMD effects
with low level electrical stimulation and electrically
stimulated cycling
 Bloomfield and colleagues showed that unlike low
intensity, high intensity work showed small BMD
increases at distal femur a trabecular bone
 Mohr and colleagues showed that SCI subjects who
increased their cycling work over 1 year, experienced
10% increase in proximal tibia, a trabecular bone

14.  3-dimensional densitometeric technique like peripheral
quantitative computed tomography p-QCT was used to
clarify the growth of trabecular bone from non
responding cortical bone
 recent work on SCI subjects had 3 years of unilateral
soleus stimulation.Trabecular BMD at distal tibia was
31% higher in trained than in untrained limbs
 parts of the same limb without training experienced post-
SCI demineralisation.

15. Neural contributions to
musculoskeletal deterioration
 Bone has an extensive sympathetic sensory nerve
supply, particularly in metabolically active regions.
 These nerve fibers may sense local mechanical loads or
may stimulate bone remodeling via neuropeptides, and
because these nerves accompany intraosseous blood
vessels, they may also allow a communication between
the autonomic and skeletal systems.
 Although a link between autonomic disruption,
intramedullary venous stasis and osteoporosis has been
hypothesized, little is known about the underlying
mechanism.

16. Conclusion
 Rehabilitation specialists in the next decade will have an
important goal to minimize the deleterious metabolic
chaos that results to the musculoskeletal system after
SCI
 New electrical stimulation technologies designed to
capitalize on the extensive plasticity of paralyzed bones
and muscle must emerge
 These technologies must be feasible so that an
individual with SCI can comply with them and live a
better life.