1. Spasticity is a motor disorder characterized by increased muscle tone and exaggerated reflexes caused by hyper-excitability of the stretch reflex due to loss of inhibitory pathways in the spinal cord. 2. The pathophysiology of spasticity involves denervation supersensitivity, axonal sprouting, and loss of descending inhibition resulting in disinhibition of segmental reflexes. Changes in muscle properties also contribute to increased tone. 3. Spasticity is assessed using measures of physiology like reflexes, muscle tone, and stiffness scales; measures of voluntary movement; and functional measures of activities and quality of life.

1. By :-Heena
Moderator :-Dr.Dinesh Sir

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.
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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

14. 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.

15.  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.

17.  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.

18.  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.

19.  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.

20.  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.

21.  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.

22.  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.

23.  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.

24. 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.

25. GOLGI TENDON ORGAN

26.  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.

27.  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.

28.  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.

29.  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.

30.  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.

31.  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 .

32.  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.

33.  Phase 3 and 4 of Ditunno’s model describe early
hyperreflexia and later development of spasticity in
patient with SCI. the proposed physiologic mechanism
for both phases is axonal regrowth .

34.  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.

35.  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.

36.  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.

37.  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.

38.  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.

39.  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

40.  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.

41. Flexor and cross extensor reflex

42. Assessment
 In this we divide it in three category:
 Physiological measures
 Measures of voluntary activity
 Functional measures

43. 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

44. Measures of voluntary activity
 Isolated time movement tests
 Performance based measures
 Padobarography
 Detection of movement
 Gait
 Balance
 Body segment analysis

45. 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

46. Modified Asworth scale


47. 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.

48. 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
4 Unfatigable clonus (>10secs)
occurring at a precise angle
5. Joint Immobile
 Angle of muscle reaction (Y)

49.  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


50. 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

51. 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

52. Spasm frequency scale:
 Most commonly used Penn Spasm frequency scale
 It is modified by Priebe at al

53. 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.

54.  Spinal Cord Injury Spasticity Evaluation Total (SCI-
SET)
 Patient reported impact of spasticity measure.

55. 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

56.  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.