1) The document discusses spasticity, specifically the pathophysiology and assessment of spasticity. It covers topics like the stretch reflex, muscle spindles, golgi tendon organs, spinal interneurons, and supraspinal influences on spasticity. 2) Key points include that spasticity is a velocity-dependent increase in muscle tone caused by hyperexcitability of the stretch reflex. It can be assessed by measuring the exaggeration of the stretch reflex at different velocities. 3) Spasticity is caused by abnormal processing in the spinal cord that leads to excessive reflex activation of motor neurons in response to input from muscle spindles. Supraspinal pathways like the reticulo

1. SPASTICITY
PATHOPHYSIOLOGY &
ASSESSMENT
DR. SOUVIK BHATTACHARJEE
JUNIOR RESIDENT
DEPARTMENT OF PHYSICAL MEDICINE & REHABILITATION
AIIMS, BBSR

2. INDEX
• INTRODUCTION
• STRETCH REFLEX
• MUSCLE SPINDLE & GOLGI TENDON ORGAN
• ABNORMAL STRETCH
• INTRINSIC HYPERTONIA
• STIFFNESS
• EXAGGERATION OF STRETCH REFLEX
• SPINAL INTERNEURONS
• SUPRASPINAL INFLUENCES
• PROBLEMS
• ASSESSMENT

3. INTRODUCTION
• “Spasticity is a motor disorder characterised by a velocity dependent
increase in tonic stretch reflexes (muscle tone) with exaggerated
tendon jerks, resulting from hyperexcitability of the stretch reflex, as
one component of the upper motoneuron syndrome”
• Besides the dependence from velocity, spasticity is also a length-
dependent phenomenon. In the quadriceps, spasticity is greater
when the muscle is short than when it is long. This is probably one of
the mechanisms underlying the so called clasp knife phenomenon.

4. INTRODUCTION
• Spasticity is more often found in the flexor muscles of the upper limb
(fingers, wrist, and elbow flexors) and in the extensor muscles of the
lower limb (knee and ankle extensors). However, there are several
exceptions. For example, we observed patients in whom spasticity is
prevalent in extensor muscles of the forearm.

5. STRETCH REFLEX
• Stretch reflexes are mediated by
excitatory connections between Ia
afferent fibers from muscle spindles
and 𝛼-motoneurons innervating the
same muscles from. which they arise.
• Passive stretch of the muscle excites
the muscle spindles, leading Ia fibers
to discharge and send inputs to the 𝛼-
motoneurons through mainly
monosynaptic, but also oligosynaptic
pathways.
• The 𝛼-motoneurons in turn send an
efferent impulse to the muscle,
causing it to contract.

6. MUSCLE SPINDLE AND GOLGI TENDON ORGAN
• The muscle spindle plays a critical role
in the provision of necessary
information for proper motor control.
• It is attached in parallel to the main
muscle mass, and it contains afferent
type Ia and II fibers that communicate
information concerning position and
rate of change of a muscle to the
spinal column.
• The g motor neuron is an integral
component of the muscle spindle.
During normal motor function, the g
motor unit coactivates with the a
motor neuron and maintains the
spindle tension and efficiency.

7. MUSCLE SPINDLE AND GOLGI TENDON ORGAN
• Found within the muscle
tendons, through the Ib fibers
and their related interneurons,
the Golgi tendon organs limit
muscle contraction by
facilitating antagonists and
inhibiting agonists. Thus, they
serve to impose a ceiling effect
on muscle contraction and
prevent musculotendinous
injury.

8. EMG OF NORMAL STRETCH REFLEX
• Surface EMG recordings in a normal subject at rest clearly show that
passive muscle stretches, performed at the velocities used in the
clinical practice to assess muscle tone, do not produce any reflex
contraction of the stretched muscle.
• Recording the EMG of elbow flexors during imposed elbow extension,
no stretch reflex appears in the biceps when the passive displacement
occurs at the velocities usually used during the clinical examination of
muscle tone (60∘ –180∘ per second). It is only above 200∘ per second
that a stretch reflex can be usually seen.

9. ABNORMAL STRETCH
• When the passive stretch is slow, the stretch reflex tends to be small
(low amplitude) and the tone may be perceived relatively normal or
just increased.
• When the muscle is stretched faster, stretch reflex increases and the
examiner detects an increase in muscle tone. Therefore, spasticity is
due to an exaggerated stretch reflex.
• Although spasticity is velocity-dependent, surface EMG recordings
show that in many cases if the stretch is maintained (velocity = 0),
the muscle still keeps contracting, at least for a time.

10. INTRINSIC HYPERTONIA
• Spasticity is responsible for the velocity-dependence of muscle
hypertonia in patients with UMNS. However, it must be stressed that
in such patients muscle hypertonia is a complex phenomenon, where
spasticity represents only one aspect.
• Hypertonia in patients with UMNS, therefore, can be divided into two
components: hypertonia mediated by the stretch reflex, which
corresponds to spasticity, and hypertonia due to muscle contracture,
which is often referred as nonreflex hypertonia or intrinsic
hypertonia.

11. INTRINSIC HYPERTONIA
• In a clinical setting it can be difficult to distinguish reflex and
nonreflex contributions to muscle hypertonia, especially when
muscle fibrosis occurs without shortening of the muscle.
Biomechanical measures combined with EMG recordings can be
helpful in this attempt.
• The two components of hypertonia are likely to be intimately
connected. The reduced muscle extensibility due to muscle
contracture might cause “any pulling force to be transmitted more
readily to the spindles,” thus increasing spasticity .

12. STIFFNESS OF THE MUSCLE
ACTIVE STIFFNESS
• Accumulation of hyaluronan
• Immobilization or paresis
decrease normal turnover
• Increase molecular weight and
macromolecular crowding
• Increase fluid viscosity,
decreases gliding and lubrication
between the layers of collagen
and fibers.
PASSIVE STIFFNESS
• Due to immobilization, spastic
muscle rests in a shortened
length (fibers becoming more
stiff)
• In chronic phase , collagen
deposition occurs in between
muscle bundles. Leading to
fibrosis within muscle
• Increased passive mechanical
stiffness

13. EXAGGERATION OF STRETCH REFLEX
• The exaggeration of the stretch reflex in patients with spasticity could
be produced by two factors
1. The first is an increased excitability of muscle spindles. In this case,
passive muscle stretch in a patient with spasticity would induce a
greater activation of spindle afferents with respect to that induced
in a normal subject.
2. The second factor is an abnormal processing of sensory inputs
from muscle spindles in the spinal cord, leading to an excessive
reflex activation of 𝛼-motoneurons

14. EXAGGERATION OF STRETCH REFLEX
• Studies in the decerebrate cat suggest that 𝛾- motoneurons
hyperactivity and subsequent muscle spindle hyperexcitability have
a role in producing hypertonia.
• Studies in humans suggest that fusimotor dysfunction probably
contributes little to exaggerated stretch reflex.
• the commonly accepted view, therefore, is that spasticity is due to an
abnormal processing in the spinal cord of a normal input from the
spindles.

15. EXAGGERATION OF STRETCH REFLEX
• The velocity-dependence of spasticity can be attributed to the
velocity sensitivity of the Ia afferents.
• several studies suggest that II afferent fibers from muscle spindles are
also involved in spasticity activating the 𝛼-motoneurons through an
oligosynaptic pathway.
• It has been suggested that II afferent fibers, which are length-
dependent, could be responsible for the muscle contraction in
isometric conditions often seen after the dynamic phase of the
stretch reflex in patients with spasticity.

16. SPINAL INTERNEURON
• The effects of the Ia and Ib fibers are often
mediated through and with the help of
interneurons called Ia and Ib interneurons,
respectively. Other interneurons, including
the Renshaw cell and the propriospinal
interneurons,
• The type Ia interneurons receive activation
from the type Ia neurons from the muscle
spindle. When activated, the Ia interneurons
facilitate agonist activity and reciprocally
inhibit antagonist muscles, preventing the
futility of co-contraction. Ia interneurons are
also under supraspinal influence, and this
plays a critical role in strengthening of
reciprocal inhibition by the type Ia
interneuron. The loss of supraspinal
influence on the Ia interneurons plays a
critical role in co-contraction and cerebral
origin spasticity.

17. SPINAL INTERNEURON
• The Ib afferents from these organs connect to
their respective Ib interneurons. These
interneurons also receive supra- and propriospinal
influences from above that facilitate antagonists
and inhibit the firing of agonist muscles
• The process of recurrent inhibition involves the
Renshaw cell, which receives input directly from
the a motor neuron. This process shuts off agonist
activity by its direct effect on the a motor neuron,
in addition to facilitation of antagonist function
mediated via the antagonist muscle’s Ia
interneuron.
• Tight motor control requires the function of the
Renshaw circuit, and a loss of its function may
greatly compromise movements. Like many other
neurons, spinal and supraspinal input influence
Renshaw cell function. Renshaw cell inhibition is
increased in SCI.

18. SUPRASPINAL INFLUENCES
• In the human motor system, there are five important descending
pathways: corticospinal, reticulospinal, vestibulospinal, rubrospinal,
and tectospinal.
• The CST originates from the cerebral cortex and is primarily involved
in voluntary movement. Isolated lesions in the corticospinal pathway
produce weakness, loss of dexterity, hypotonia, and hyporeflexia,
instead of spasticity.
• The other four descending pathways originate from the brain stem.

19. SUPRASPINAL INFLUENCES
• The tectospinal tract originates from the tectum (superior colliculus)
in the midbrain and contributes to visual orientation.
• The reticulospinal tract (RST) and the vestibulospinal tract (VST)
provide balanced excitatory and inhibitory descending regulation of
spinal stretch reflex.
• The rubrospinal pathway emanates from the lateral brain stem and is
almost absent in humans.
• Imbalance of these descending inhibitory pathways, along with
facilitatory influences on stretch reflex, are thought to be the cause
of spasticity.

20. SUPRASPINAL INFLUENCES
• The dorsal RST , which originates from the ventromedial reticular
formation in the medulla, provides a powerful inhibitory effect on
the spinal stretch reflex.
• The medullary reticular formation receives cortical facilitation from
the motor cortex via corticoreticular fibers, which act as the
suprabulbar inhibitory system.
• Corticospinal and corticoreticular tracts run adjacent to each other in
the corona radiata and internal capsule. Below the medulla, the
dorsal RST and the lateral CST descend adjacent to each other in the
dorsolateral funiculus.

21. SUPRASPINAL INFLUENCES
• The medial RST and VST exert excitatory effects on spinal stretch reflexes.
• The medial RST has a diffuse origin, mainly in the pontine tegmentum, and
has efferent connections passing through and receiving contributions from
the central gray and tegmentum areas of the midbrain, and the medullar
reticular formation (distinctly different from the inhibitory area).
• In contrast to the dorsal RST, the medial RST is not affected by stimulation
of the motor cortex or internal capsule.
• The VST originates from the lateral vestibular nucleus and is virtually
uncrossed. Both the RST and VST descend onto the ventromedial cord,
anatomically distant from the lateral CST and dorsal RST in the dorsolateral
cord.

22. SUPRASPINAL INFLUENCES
• Excitability of the spinal stretch
reflex arc is maintained both by
descending regulation from the
inhibitory dorsal RST and
facilitatory medial RST and VST, and
intraspinal processing of the
stretch reflex.
• Recent reports suggest that
abnormalities in the supraspinal
pathways predominate, whereas
intraspinal mechanisms represent
secondary plastic rearrangements
responsible for the development of
spasticity.

24. MECHANISM OF SPASTICITY
1. AT CORTICAL LEVEL : loss of cortical facilitation of inhibitory DRST
2. AT THE LEVEL OF SPINAL CORD : reduction of presynaptic inhibition,
Ib facilitation, II facilitation, reduced reciprocal inhibition.
3. AT SPINAL MOTOR NEURON LEVEL : dennervation supersensitivity
and collateral sprouting.
4. AT THE LEVEL OF MUSCLE : shortening of sarcomeres and lost of
elastic tissue

25. PROBLEMS
Postural Abnormalities :
• They are manifestations of imbalance of agonist and antagonist
strength and hypertonia.
• Thus, a flexed elbow posture is not necessarily as a result of flexor
muscle group hypertonia solely, but may be a combination of
hypertonic flexors and weak extensors; or it could also be that both
flexor and extensor muscle groups are both hypertonic, but the
former predominates.

28. PROBLEMS
• Impaired Movement
Similar to abnormal postures, impaired movements usually result
from the interaction among spasticity, weakness, and other features
of the UMN syndrome, such as loss of coordination and dexterity, and
dystonia, or sustained contraction of muscles.
• Functional Limitation: Activity limitation is even more complex
because the causes of impaired movement. Tactile and proprioceptive
sensory loss, visual field cut and hemineglect, and cognitive
difficulties, such as learning a novel task and procedural sequencing,
can magnify the motor challenges imposed upon by spasticity and
weakness.

29. BENEFITS
• Helps in ambulation, standing and transfers (stand pivot transfers)
• Maintains muscle bulk due to muscular contractions
• Prevents DVT by providing improved venous flow secondary to
muscle contraction.
• May prevent osteoporosis
• Diagnostic tool

30. COMPLICATIONS
• Interferes with function
• Discomfort or pain in patients with intact or abnormal sensation
• Interferes with hygiene and nursing care
• Contractures and disfigurement
• Decubitus ulcers
• Bone fractures, malunion
• Joint subluxation and dislocation
• Acquired peripheral or entrapment neuropathy.

31. MEASURES OF SPASTICITY

32. MODIFIED ASHWORTH SCALE

33. ASHWORTH SCALE

34. TARDIEU METHOD

35. SPASM FREQUENCY SCALES

36. ADDUCTOR TONE SCORE
SCORE FINDINGS
0 No increase in tone
1 Increased tone
Hips are easily moved by one person upto 45°
2 Hips are abducted to 45° by one person with mild effort
3 Hips are abducted to 45° by one person with moderate effort
4 Two persons are required to abduct the hip to 45°

37. OTHER METHODS
• Dynamic multichannel EMG
• Computerised gait analysis
• The pendulum test
• Temporary anaesthetic nerve block
• Electrophysiological testing.

38. BRUNNSTROM STAGES OF MOTOR RECOVERY
AFTER STROKE

39. THANK YOU