2. Contain Introduction Normal physiology Pathophysiology
Assessment
3. Introduction Spasticity is a motor disorder that is
characterized by a velocity dependent increase in tonic stretch
reflexes (muscle tone) with exaggerated tendon jerks, resulting
from hyper excitability of the stretch reflex, as one component of
the upper motor neuron syndrome. American Academy of Neurology
(1990)
4. Why spasticity is important???? Because it often causes
disability and impairs functions of our patient. So based on that
we plan treatment.
5. Normal physiology Function of muscle spindle 1. It is
receptor organ for stretch reflex 2. It is play important role in
maintaining the muscle tone.
6. Muscle spindle
7. Innervation of the Spindles
8. Pathophysiology Immediately after scl, there are depressed
spinal reflexes during the state of spinal shock, followed by
development of hyperreflexia and spasticity over the following
weeks to month.
9. The pathophysiology of spasticity is not completely
understood; however, it is believed to arise primarily from loss of
the effect of numerous descending inhibitory pathways. These
include reciprocal 1a interneuronal inhibition, presynaptic
inhibition, renshaw-mediated recurrent inhibition, group II
afferent inhibition, and the Golgi tendon organs.
10. Axonal collateral sprouting and denervation super
sensitivity are change that may also play a role in the development
of spasticity. T
11. Let see normal physiology along with pathophysiology
12. The Monosynaptic (Stretch) Reflex Change in muscle length
can evoke a stretch reflex. Two type Nuclear bag fibers Nuclear
chain fibers Group la and 2 fibers
13. Reciprocal inhibition The la fibers also synapse on
interneurons that inhibit antagonist muscle groups, thereby
preventing contraction of antagonist muscle during activation of
agonist muscle groups; this inhibitory pathway is referred to as
reciprocal la inhibition and can be altered after SCI.
14. Clinically, reciprocal inhibition can be grossly observed
by eliciting monosynaptic muscle stretch reflexs: when tendon
tapped, a stretch is applied to the target muscle, which is
transmitted to the spinal cord through the la affrent fibers.
15. This reciprocal la inhibition after SCI may result in
simultaneous coactivation of agonist and antagonist muscle groups,
as is often seen in patients with spasticity.
16. Recurrent inhibition is mediated by Renshaw cells, which
are inhibitory interneurons located in the ventral horn of spinal
cord. Axon collaterals from alpha motor neurons synapse on and
activate the Renshwa cells,which in turn project inhibitory
impulses back to these motor neurons as well as to la inhibitory
interneurons.
17. Renshaw activity decreases the activity of the motor
neurons that were previously active and also inhibits la inhibitory
internurons. The level of recurrent inhibition has been explored in
patient with UMN lesions, and these individuals have been noted to
maintain normal recurrent inhibition during voluntary movement;
this may contribute to impaired motor function in these
patients.
18. There is evidence for increased recurrent inhibition in the
SCI population, which increases inhibition to the la interneurons.
This ultimately allows for cocontraction of agonist and antagonist
muscle groups due to the decreased la interneuron activity.
19. Reduction in presynaptic inhibition of afferent is another
potential contributor to the Pathophysiology of spasticity in SCI.
reciprocal inhibition was described by Sherrington in 1906, and
this process is responsible for relaxation of an antagonist muscle
during contraction of agonist.
20. in absence of reciprocal inhibition, cocontraction of
agonist and antagonist muscle groups is seen simultaneously,
interfering with intentional voluntary movement. GABA mediates
spinal inhibition both presynaptically and postsynapticaly.
presynaptic inhibition of Ia afferent occurs when the inhibitory
aminiacid GABA binds to receptors on the la terminals, which
subsequently increases the amount of input required to activate the
alpha motor neurons.
21. The decreased excitatory input to the alpha motor neurons
in turn depresses the monosynaptic stretch reflex. Postsynaptic
activation of GABA-A receptor can decrease the activity of motor
neurons and interneurons .afterSCI, the decrease in presynaptic
inhibition ultimately result in increased activity of the alpha
motor neuron; this may contribute to the hyper reflexiya and
spasticity seen in these individuals .it is possible to modulate
the presynaptic inhibition in individuals with SCI with the use of
GABA-Eergic medications including baclofen and diazepam.
22. GOLGI TENDON ORGAN Sensitive to intramuscular tension and
innervated by 1b sensory afferents. 1 or 2 g of tension is
sufficient to increase the firing rate of the spindle afferents.
But tendon organs don't register impulse conduction until the
tension reaches as high as 100 g.
23. GOLGI TENDON ORGAN
24. If tension is generated beyond capacity there is sudden
relaxation to prevent possible damage to tendon. . This sudden
relaxation of a muscle in the face of dangerously high tension is
called the lengthening reaction or the "clasp-knife" reflex because
of its similarity to the way a pocketknife suddenly snaps closed
when the blade is moved to a certain critical position.
25. Nonreciprocal lb inhibition is another mechanism that may
play a role in development of spasticity of supraspinal origin but
does not appear to be involved in spasticity related to SCI, Golgi
tendon organs, which are contraction sensitive receptors, have
group I afferents and lb inhibitory interneurons that projects to
the spinal cord and are involved in preventing antagonist muscles
from firing while the agonist is firing.
26. There is evidence for replacement of lb inhibition with
facilitation in hemiplegic individual with supraspinal lesions,
leading to simultaneous cofiring of agonist and antagonist muscle
groups: however, studies in individuals with SCI have shown that lb
inhibition is unaltered.
27. Two additional mechanisms that play role in the development
of spasticity after SCI are axonal sprouting and denervation
supersensitivity . Ditunno et al describe the transmition from
spinal shock immediately after SCI the development of spasticity
and hyperreflexia 1 to12 months later. in their proposed 4-phase
model of spinal shock.
28. There is observation of areflexia or hyporeflexia , as well
as paralysis and muscle flaccidity for initial 0 to 24 hours
postinjury. These findings are due to loss of excitatory input from
supraspinal pathways, including vestibulospinal and reticulospinal
pathways, among others.
29. Loss of descending inhibitory input to spinal inhibitiory
interneurons may cause further hyporeflexia. In the second phase of
spinal shock, there is return of the H reflex 1 to 3 days after
injury, although muscle stretch reflexs are still absent. This
likely due to denervation supersensitivity, which causes increased
neuronal firing in response to neurotransmitters and has been
reported to occur in the brain and spinal cord .
30. The denervation supersensitivity may be due to decreased
reuptake of excitatory neurotransmitters, up-regulation of
receptors on the postsynaptic membrane, or alteration of
degragation and synthesis of receptors.
31. Phase 3 and 4 of Ditunnos model describe early
hyperreflexia and later development of spasticity in patient with
SCI. the proposed physiologic mechanism for both phases is axonal
regrowth .
32. new synapse are formed by spinal afferents and interneurons
as well as spared supraspinal descending pathways. Axonal sprouting
of spared descending motor tracts may result in motor recovery,
whereas axonal sprouting of the neurons involved in segmental
reflexes may produce less desirable effects, such as the
development of hyperreflexia and spasticity.
33. Intrinsic changes within muscle may also play role in the
development of increased muscle tone. These mechanical changes may
include loss of sarcomeres, increased stiffness of muscle fibers,
altered muscle fiber size and distribution of fiber types, and
changes in collagen tissue and tendons.
34. The work of Kamper et al in stroke patients demosttrated
that muscle fiber played some part in phenomenon of spasticity as
decresing the initial length of tested spastic metacarpophalangeal
fibers reduced muscle stiffness suggesting that the biomechanical
quality of muscle fibers play some part in the development of
spasticity.
35. These changes in spastic muscle may be a result of the
development of subclinical contracture rather than true reflex
hyperexitibility or be an intrinsic property of the changes in
biomechanical property of the muscle.
36. A strong, painful, or potentially damaging stimulus
delivered to cutaneous or joint receptors can reflexly cause a
sudden bodily withdrawal away from the stimulus. Stepping on a tack
is a good example of this reflex in action. The person will
typically flex (withdraw) the stimulated foot and leg while
extending the other leg in order to propel the body away from the
tack.. At the same time, inhibitory interneurons ipsilaterally
inhibit extenders of the stimulated limb while contralaterally
inhibiting flexors of the opposite limb.
37. This is a polysynaptic, bilateral reflex incorporating both
excitatory and inhibitory interneurons. Delivery of the stimulus to
the receptors in a limb increases the firing rate of pain-carrying
group III and IV afferents into the posterior horn. where they
synapse with interneurons. Excitatory interneurons ipsilaterally
stimulate alpha motor neurons to the flexors in that limb while
contralaterally stimulating extenders in the opposite limb - thus
the term flexor-crossed-extensor reflex
38. This reflex is often intersegmental. This should not be
surprising when one considers that many muscles are involved in
such movements. In the cat, for example, a painful stimulus
delivered to one hind leg will not only reflexly withdraw that leg,
but will extend to both hind legs and forelegs on the opposite side
as well. This means that the group III and IV afferents not only
stimulated interneurons at the same segmental level at which they
entered the cord, but activated synapses at higher and lower cord
levels as well. The ascending and descending collaterals travel in
the fasciculus proprius (ground bundles) of the white matter. The
fibers in these tracts carry intersegmental connections.
39. Flexor and cross extensor reflex
40. Assessment In this we divide it in three category:
Physiological measures Measures of voluntary activity Functional
measures
41. Measure of physiological activity Measure utilizing nerve
conduction Tendon reflex Measure passive activity Ashworth scale
Tardieu scale Range of motion Stiffness and muscle tone Stretch and
stretch reflexes Pendulum test model Reflex threshold angle
42. Measures of voluntary activity Isolated time movement tests
Performance based measures Padobarography Detection of movement
Gait Balance Body segment analysis
43. Functional mesures Visual analoge scale and likert scale
Timed ambulation tests Functional performance mesures The pediatric
evaluation of disability inventory Qality of life mesures 36 item
short from healthy survey Satsfaction with life scale Euro QOL
44. Modified Asworth scale
45. TARDIEU SCALE This scale quantifies muscle spasticity by
assessing the response of the muscle to stretch applied at
specified velocities. Grading is always performed at the same time
of day, in a constant position of the body for a given limb. For
each muscle group, reaction to stretch is rated at a specified
stretch velocity with 2 parameters x and y.
46. Velocity to stretch (V) Quality of muscle reaction (X) V1
As slow as possible V2 Speed of the limb segment falling V3 As fast
as possible (> natural drop) with no clear catch at a precise
angle V1 is used to measure the passive range of Motion. (PROM).
Only V2 and V3 are used followed by release to rate spasticity ) 0
No resistance throughout passive movement 1 Slight resistance
throughout, 2 Clear catch at a precise angle, Motion. (PROM). 3
Fatigable clonus (10secs) occurring at a precise angle 5. Joint
Immobile Angle of muscle reaction (Y)
47. Angle of muscle reaction (Y) Measure relative to the
position of minimal stretch of the muscle (corresponding at angle)
Spasticity Angle R1 Angle of catch seen at Velocity V2 or V3 R2
Full range of motion achieved when muscle is at rest and tested v1
velocity
48. Testing Positions Upper Limb To be tested in a sitting
position, elbow flexed by 90 at the recommended joint positions and
velocities. Shoulder Horizontal Adductors V3 Vertical Adductors V3
Internal Rotators V3 Elbow Flexors V2 Shoulder adducted Extensors
V3 Shoulder abducted Pronators V3 Shoulder adducted Supinators V3
Shoulder adducted Wrist Flexors V3 Extensors V3 Fingers Angle PII
of digit III- MCP Palmar Interossei V3 Wrist resting position +
FDS
49. Lower Limb To be tested in supine position, at recommended
joint positions and velocities Hip Extensors V3 Knee extended
Adductors V3 Knee extended External Rotators V3 Knee flexed by 90
Internal Rotators V3 Knee flexed by 90 Knee Extensors V2 Hip flexed
by 30 Flexors V3 Hip flexed Ankle Plantarflexors V3 Knee flexed by
30
50. Spasm frequency scale: Most commonly used Penn Spasm
frequency scale It is modified by Priebe at al
51. Spinal cord assessment tool for spasticity Develop by Benz
et al measure spasticity in spinal cord injury. Flexor spasm and
clonus score of it correlate with PSFS. Not widely used.
52. Spinal Cord Injury Spasticity Evaluation Total (SCI- SET)
Patient reported impact of spasticity measure.
53. References:- Rehabilitation medicine: principles and
practice third addition edited by joel A.DeLisa Neurological
rehabilitation , third addition Darcy ann Umphred Spasticity
diagnosis and its manegment Ditunno et al describe the transmition
from spinal shock immediately after SCI the development of
spasticity Kamper et al in stroke patients demosttrated that muscle
fiber played some part in phenomenon of spasticity
54. Elovic EP, simone lk ,zaftonte r outcome and assessment for
spasticity in patient with traumatic brain injury:the state of the
art j head truama rehabili 2004. Lieber rl ,steinman s brash ia et
al. structural and functional changes in spastic skeletal muscle
.muscle nerve 2004 . RymerWZ powers rk pathophysiology of muscular
hypertoniyain spasticity neurosurg art rev.