In lesions below the mid-pons, a state of flaccidity, termed spinal shock, ensues immediately after injury with loss of all reflexes caudal to the injury. The resolution of spinal shock occurs gradually , taking weeks to months. The recovery from spinal shock is poorly understood and likely results from multiple, simultaneous adaptations in spinal processing that allow motor neuron to function independently from supraspinal control. Existence of spinal shock, followed by a gradual return of reflexes that eventually become hyperactive, suggests that spasticity is not just a result of a simple on/off switch triggered by an alteration in inhibitory and facilitative signals

1. Pathophysiology
of Spasticity
PRESENTED BY, DR JOE ANTONY
DEPT OF PMR
KGMU
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2. Contents
Definitions
Normal Physiology
Motor nerves
Proprioception
Muscle spindle
Golgi tendon organ
Stretch reflexes, lengthening reflex
Antagonist –agonist coordination
Reciprocal inhibition
Renshaw cell
Regulation of stretch reflex
Pathophysiology of spasticity
Post-stroke spasticity
Why spasticity is more in Flexors
Assessment scales of spasticity
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3. Definitions
Spasticity is defined as a velocity-dependent increase in muscle tone
Tone is defined as resistance offered to passive stretch of muscle
A motor disorder characterized by a velocity dependent increase in tonic and
phasic stretch reflex with exaggerated tendon jerks resulting from
hyperexcitability of stretch reflex.
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4. Contracture- Shortening of an elastic structure , which cannot be stretched with
clinically acceptable force
When there is severe spasticity, it is difficult to differentiate between spasticity and
contracture and will need examination under anesthesia to differentiate
Rigidity- Resistance to stretch that is not velocity dependent—the examiner
feels the same resistance to stretch irrespective of the velocity at which a muscle
muscle group is being stretched
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5. Normal Physiology of
stretch reflex
STRETCH REFLEX IS THE CORNER STONE OF PATHOPHYSIOLOGY OF
SPASTICITY
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6. Motor neurons
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7. Optimal Motor function depends on,
Proprioception
Stretching reflexes
Muscle agonist and antagonist coordination
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8. Propioception
Sense of relative position of body parts,
Muscle spindle
Golgi tendon Organ
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9. Muscle spindle and Golgi Tendon Body
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10. Muscle Spindle
Each muscle spindle has three essential elements:
1. Specialized intrafusal muscle fibers
◦ Nuclear bag fiber - Dynamic
◦ Nuclear chain fiber- Static
2. Large diameter myelinated afferent nerves
(types Ia and II) originating in the central
portion of the intrafusal fibers.
3. Small diameter myelinated efferent nerves
(gamma) supplying the polar contractile
regions of the intrafusal fibers .
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11. Muscle spindle
NUCLEAR CHAIN FIBER
Responsible for tonic phase of stretch
relflex
Persistent discharge even at sustained
stretch
Clinical importance- Spasticity
NUCLEAR BAG FIBER
Responsible for Phasic stretch reflex
Dischrage decreases during sustained
stretch
Clinical importance- Deep tendon reflex
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12. Stretch reflex (Myotactic Reflex)
Whenever a muscle is stretched suddenly,
excitation of the spindles causes reflex
contraction of the large skeletal muscle
fibers of the stretched muscle and also of
closely allied synergistic muscles.
Mono synaptic pathway Muscle
spindle
stretch
1a
nerve
fiber
Anterior
horn
neuron (
alpha
motor
neuron)
Same
muscle
Contraction
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13. Golgi tendon organ
 Placed in musculotendinous junction
Sensation of
Tension in muscle
Rate of tension in muscle
Projection into cerebellum and cerebrum
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14. Golgi tendon organ reflex
AKA,
Lengthening reflex
Inverse myotactic reflex
Autogenic inhibition
Clasped knife reflex
Clinical importance
Reason why persistent stretching is more
effective than pulsatile stretching
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15. Agonist and antagonist muscle
coordination
During every action there are 4 steps of muscle activity
Tone increases in both agonist and antagonist muscles in preparedness
Agonist muscle isometric contraction to do the action
Antagonist muscle do Eccentric contraction to control action, speed and stop at adequate moment
Coordination between two groups to prevent injury,
Achieved by Reciprocal Inhibition
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16. Reciprocal Inhibition
Simultaneous contraction of
antagonist muscles is normally
prevented by reciprocal inhibition of
the antagonist muscle motor neuron
pool within spinal cord, termed
reciprocal inhibition.
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17. Renshaw cell
Inhibitory neuron
Input from alpha motor neuron
Output into same neuron- Feedback
inhibition
Prevent Overactivity of Stretch reflex
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18. Spinal level
regulation of stretch
reflex
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19. Supra spinal regulation of stretch reflex
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20. Pathophysiology
Upper motor neuron syndrome
A collective term that refers to different types of motor behaviors produced by patients who have lesions
lesions proximal to the alpha motor neuron (spinal cord, brain), resulting in the loss of descending
inhibition and hypersensitivity of the reflex arc in the spinal cord
◦ Spasticity is only one component of UMNS
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21. Spasticity is characterized by an exaggeration of the stretch reflex
◦ Mechanism of which remains poorly understood
Likely due to abnormal intraspinal processing of afferent impulses,
Loss of descending inhibitory regulation of segmental reflexes,
Increased excitability of the motor neurons
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22. 22

23. Non neuronal mechanisms of spasticity
In addition to these neuronal disturbances, limb immobilization, disuse, and denervation lead
to changes in muscle properties, termed rheologic properties.
Alterations in tendon compliance and physiological changes in the muscle fiber cause increased
mechanical resistance of the muscle.
 Other changes that can increase muscle resistance in the absence of electromyographic
muscle activity include muscle atrophy and shortening, loss of sarcomeres, and muscle
infiltration with connective tissue and fat.
These changes in muscle properties further exacerbate impairment in motor control caused by
spasticity.
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24. In lesions below the mid-pons, a state of flaccidity, termed spinal shock, ensues immediately
after injury with loss of all reflexes caudal to the injury.
 The resolution of spinal shock occurs gradually , taking weeks to months.
 The recovery from spinal shock is poorly understood and likely results from multiple,
simultaneous adaptations in spinal processing that allow motor neuron to function
independently from supraspinal control.
Existence of spinal shock, followed by a gradual return of reflexes that eventually become
hyperactive, suggests that spasticity is not just a result of a simple on/off switch triggered by
an alteration in inhibitory and facilitative signals
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25. Pathophysiology of post stroke spasticity
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26. Brunnstorm stages of recovery from stroke
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27. Why spasticity is more in PFs,Knee Flexors,Hip
flexors,Elbow flexors, Wrist flexors etc
Evolutionarily and embryologically they are the stronger group
of muscles, has basic functions and has more representation
higher centers.
Physiological withdrawal response is flexor response. Loss of
spinal regulation causes exaggeration of withdrawal response
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28. Clinical Assessment Scales
Ashworth Scale: It was first described in 1964 in a study that
evaluated medication effectiveness in MS.
In the Ashworth Scale, the level of resistance of limb passive ROM
is measured on an ordinal scale.
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29. Modified Ashworth Scale (MAS)
The Ashworth scale was later expanded as the Modified Ashworth
Scale (MAS) which is more commonly used in clinical practice.
But MAS has not demonstrated good intra- or interrater reliability for
spasticity assessment.
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30. Modified Modified Ashworth Scale (MMAS)
Because the reliability of the MAS has been questioned, a Modified
Modified Ashworth Scale (MMAS) was developed, which eliminates the
1+ grade and adjusts the definition of grade 2 to attempt to create a more
ordinal relationship .
MMAS has demonstrated possible improvements in interrater reliability
compared to the MAS.
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31. Tardieu Scale
Evaluating muscles moving at different velocities helps
distinguish musculotendinous stiffness from spasticity
For each muscle group tested, the joint is moved at three
different velocities (V1, V2, V3). The quality of muscle reaction
and angle at which muscle reaction occurs are recorded.
Velocities:
V1—Joint is moved as slow as possible
V2—Speed of limb segment falls with gravity
V3—Joint is moved as fast as possible
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32. TARDIEU SCALE CONTD.
Muscle response quality:
0—No resistance through range of motion (ROM)
1—Slight resistance throughout ROM, no clear catch
2—Clear catch interrupting passive movement, followed by release
3—Fatigable clonus (<10 seconds)
4—Non fatigable clonus (>10 seconds)
5—Joint is immovable
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33. Modified Tardieu Scale:
R1 and R2 components added to Tardieu Scale
– R1 is defined as the angle at which muscle reaction occurs during V3
(fastest velocity).
– R2 is defined as the angle at which muscle reaction occurs during V1
(slowest velocity).
– A large difference between R1 and R2 indicates that velocity-dependent
tone (i.e., spasticity) is predominant, while a small difference between R1
and R2 indicates that velocity-independent tone (such as from muscle
contracture) is predominant.
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35. Point to remember- Tardieu angle is not
clinical ROM angle we regularly use
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36. 36

37. Thank you
References
1. Braddoms 6th edition
2. Spinal cord medicine,Krishbaun
3. Delisas physical medicine and rehabilitation 5th edition
4. Guyton and hall 12 th edition
5. Trompetto C, Marinelli L, Mori L, Pelosin E, Currà A,
Molfetta L, Abbruzzese G. Pathophysiology of spasticity:
implications for neurorehabilitation. Biomed Res Int.
2014;2014:354906. doi: 10.1155/2014/354906. Epub
2014 Oct 30. PMID: 25530960; PMCID: PMC4229996.
6. Tardieu scale training manual
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