Spasticity is a motor disorder characterized by velocity-dependent increase in muscle tone and exaggerated reflexes resulting from hyper-excitability of the stretch reflexes as part of the upper motor neuron syndrome. It is caused by interruption of descending inhibitory pathways and alteration of central inhibitory commands leading to rearrangement of spinal cord circuitry and peripheral changes in the muscle over time. Spasticity is not a single symptom but part of a movement disorder defined by features like hypertonia, abnormal reflexes, dystonia, resistance to movement, and abnormal posturing affecting coordination and mobility. A multifaceted approach is needed for management including prevention, physiotherapy, pharmacological and surgical interventions to address both neural and non-neural factors.

1. What is Spasticity?
Spasticity is a TRIAD of painful mass muscle spasms,
rigid posturing of limbs, and increased reflexes.
Most common definition to be found in literature:
It is a motor disorder characterized by a velocity-
Dependent increase in tonic stretch reflexes with
exaggerated tendon jerks, resulting from hyper
excitability
of the stretch reflex, as one component of the upper
motor neuron syndrome.
Lance, 1980
Muscle hypertonia as a result of
Exaggerated reflexes

2. • Reflex in general is a stereotyped movement or response elicited by a standard
stimulus
• Stretch Reflex - Is the simplest monosynaptic reflex or the two-neuron reflex, an example of which is the tendon jerk
reflex or tendon tap reflex
• Skeletal muscles contains specialized proprioceptors called muscle spindles. These receptors sense a change in muscle
length and send excitatory impulses to the alpha motor neurons in the spinal cord. Stimulated alpha motor neuron fires
back and shortens the muscle thus releasing the tension and signalization from its spindles…
Can It be that simple…?

3. 1. Level of complexity:
Inhibitory interneurons
mediating reciprocal
innervation
Activation of agonists is linked to
inhibition and relaxation of
antagonists

4. 2. Level of complexity:
Fusimotor system where muscle spindles sensitivity and so the sensitivity of the stretch reflex itself is adjusted by
the activity of Gama motor neuron system

5. Gamma-motor neurons regulates the sensitivity of the stretch reflex by adjusting the level of tension in the intrafusal
muscle fibers of the muscle spindles. This helps to regulate muscle length and tone. Stimulation of a γ-motor neuron
contracts the ends of the intrafusal fibres and consequently stretches the middle part of the muscle spindle. This part of
the spindle is innervated by type Ia sensory fiber that go on to synapse with alpha-motoneurons, completing the
GAMMA LOOP

6. 3. Level of complexity:
Alpha motor neurons are involved in other major spinal cord reflexes
Stretch
reflex
Golgi
tendon
reflex
Withdrawal
reflex
Crossed
extensor
reflex

7. 4. Level of complexity:
Alpha and Gama motor neurons are influenced by sensitive stimulation

12. 5. Level of complexity: Spinal neuronal network is influenced by all higher
neural structures involved in the control of movement
Motor Cortex
Planning and
Directing voluntary movement
Brainstem Centers
Basic movements and
Postural control
BASAL GANGLIA
Initiation
Of movement
BASAL GANGLIA
Initiation
Of movement
CEREBELLUM
Sensory motor
coordination
CEREBELLUM
Sensory motor
coordination
Local circuit neurons
Reflex coordination
Local circuit neurons
Reflex coordination
Motor neuron pools
Lower motor neurons
Motor neuron pools
Lower motor neurons
SKELETAL MUSCLESSKELETAL MUSCLES
Brain stem
tracts
Brain stem
tracts Coticospinal
tracts
Coticospinal
tracts

13. 6. Complexity can be beautiful…

17. 7. The structure is all alive
• It means
dynamic
• Not only moving
but also changing
in time
• And some kind of
software is
running on it…
That is changing
too

19. What is Spasticity?
• Lance’s definition has been criticized for being too narrow by
describing spasticity as being only a form of reflex hypertonia
• But the increase of stretch reflexes is not the only reason of
muscles thightness. It is one of multiple factors on the neural
part of the Upper motor neuron syndrome
• The non-neural effects can add significantly to the neural
mechanism as the fixed static state of muscles and joints
further interferes with modulation of tonus by alteration of
the feedback
• Immobilization in spastic position leads to sensory deficits
and contributes to development of pain
• The factor of time with structure remodelation is important
for the clinical picture and therapy

20. Other definitions of Spasticity
• Factors which can lead to a mechanical resistance in movement are the
reduced elasticity of the tendons and the biomechanical changes of
muscle fibers
Dietz 1992
• Excessive activation/co contraction: Too many muscles with
inappropriate force
Sarmann 1977
• Altered sequence of muscle firing
Dewald 2001
• Loss of central command to generate and sustain force, with no loss of
contractile capacity
Sarmann 2002
• Delayed initiation and termination of muscle contraction
Chae 2002
• Change in muscle function caused by hypertonia resulting from upper
motor neuron syndrome and leading to spastic movement disorder
Jiri 2011

21. UMN LESION
Non-neural Neural
Flaccidity
Mal-alignment
Length changes
Flaccidity
Mal-alignment
Length changes
Biomechnical changesBiomechnical changes
Mass PatternsMass Patterns
HypertoniaHypertonia
Poor voluntary activity
With poor specificty
Poor voluntary activity
With poor specificty
Neuralshock
Diaschisis
Plasticity
Neuralshock
Diaschisis
Plasticity
Loss of pre-synaptic control
Loss of recurrent inhibition
Loss of reciprocal inhibition
Novel connections(SP cord)
Loss of pre-synaptic control
Loss of recurrent inhibition
Loss of reciprocal inhibition
Novel connections(SP cord)
Peripheral input gains control of SCCPeripheral input gains control of SCC
Inc Hyper-reflexia and AR’sInc Hyper-reflexia and AR’s
Loss of Golgi activity
During voluntary movement
Loss of Golgi activity
During voluntary movement

22. Pathophysiology of Impairment
After a Central Nervous System Lesion
Gracies et al., 1997

23. Spastic muscles EMG

24. So what causes a muscle to become
spastic?
• Not completely understood, despite
considerable investigation
• Interruption of descending inhibitory
pathways or alteration of central inhibitory
commands
• Rearrangement of spinal circuitry and changes
in the muscle itself occurring with time

25. Characteristics of Spasticity
Rather then being a uniform specific symptom it is a part
of upper motor neuron syndrome with:
• Hyperactive stretch reflex
• Abnormal cutaneous reflexes
• Spastic dystonia with imbalance between flexors and extensors leading to
slow effortful movement
• Increased resistance to passive movement
• Abnormal posturing of extremities leading to muscle shortening
• Stereotypical movement synergies and uncoordinated movements
• Clonus
• Abnormal antagonist contraction during voluntary agonist effort
• Extra-segmental co-contraction with abnormal contraction distant from
the muscles involved in a voluntary effort
Leading to SPASTIC MOVEMENT DISORDER

27. Management of Spasticity
1. Prevention of exacerbating factors:
Increased nociceptive input: Infection, Pressure
sores, Bladder stones, Urine retention, Fecal
impaction, Injuries, Soft tissue stretch by wrong
position or forced movement, Fatigue and stress
Medication
2. Physiotherapy: Intelligent cooperation with
organism adaptation and self repairing ability

28. 3. Pharmacological Intervention:
• Generalized Spasticity: Oral Agents
– Baclofen
– Dantrolene Sodium
– Tizanide Hydrochloride
Side effects limiting dosage
• Regional Spasticity: Intrathecal Baclofen
• Focal Spasticity: Botulinum Toxin injection

29. 4. Surgical Intervention
Neurosurgery
Dorsal rhizotomies
Peripheral neurotomies
Orthopedic surgery
Tendon Lengthening
Tendon Transfer
Osteotomy - for skeletal deformity
Arthrodesis - joint fusion
Despite all therapeutic options our effort only rarely meets full
success…