Spasticity and Rigidity
“Tone” refers to a relaxed muscle’s resistance to passive stretch/tension
The muscle resists the stretch through both active and passive mechanisms
The passive mechanisms refer to viscoelastic structures that are non-contractile.
Note
Forces created through passive mechanisms are invisible to EMGs
The active mechanisms refer to contractile motor units
These are controlled by spinal and supraspinal mechanisms
Note
Forces created through active mechanisms can be measured by EMGs
Intrafusal Fibers
Extrafusal Fibers
Tendon
Two types: Nuclear bag fibers and Nuclear chain fibers
Nuclear bag fibers:
Nuclear chain fibers:
Both Synapse onto Gamma motor neurons in Spinal Cord
Muscle spindles generate tone via the stretch reflex (dynamic or static):
Dynamic: sudden rapid stretch of a muscle → Ia → SC→ alpha motor neuron causes sudden contraction of muscle
Static: Sustained stretch→ type II → spinal cord → alpha motor efferents → cause asynchronous contraction of muscle fibers (motor units not all discharging together) = mild sustained contraction of these fibers as long as it is stretched.
This is the physiological basis of maintaining muscle tone
Muscle Stretches → Sensory info send to spinal cord → Muscle contracts to prevent overstretch damage
Patellar Tendon Reflex
Alpha motor neurons → Extrafusal fiber contracts to prevent overstretching Quadriceps contract
Within spinal cord, Ia & II afferents also synapse onto:
From dorsal horn to α-efferent
From dorsal horn to interneuron
This feedback loop helps regulate motor neuron activity, preventing excessive firing and contributing to the fine-tuning of motor control.
Found to be increased in those with SCI - Overexcitation1.
Important
VERY DEBATED IF INVOLVED IN SPASTICITY
Body needs to maintain stretch sensation when a muscle is contracting:
Tip
HYPOTHETICALLY if ONLY alpha-motor efferents are excited and Extrafusal fibers contract → reduces tension on muscle spindle → desensitization → decreased stretch proprioception info
HOWEVER this is not exactly what happens because the body needs to have stretch sensation during contraction/shortening!
To provide proprioception, the intrafusal fibers must contract and stretch in parallel with the extrafusal fibers MM Stretch → both intrafusal and extrafusal are stretched → type Ia/II → sensitive to stretch During a stretch, the stretch on the intrafusal fibers provide proprioceptive information of a muscle stretch MM Contraction → you would expect extrafusal contraction and intrafusal fibers to not contract However, not exactly the case;alpha gamma co-activation Alpha and gamma motor neurons contract in parallel in order to maintain tension on the intrafusal sensory fibers to provide proprioception during contraction
Golgi tendon organs (GTOs) are sensory organs found within tendons
These organs detect tendon stretch and send sensory signals via Type 1b afferents → spinal cord.
Muscle contraction → tendon lengthens → GTOs are proprioceptive/sense length → type 1b afferents → SC → DRG → synapses onto 2 interneurons:
Inhibitory interneuron
The inhibitory interneuron is activated which inhibits the alpha motor neuron to the bicep → Decreasing tension of agonist (bicep)
Excitatory Interneuron
Antagonist contraction to pull forearm in opposite direction Interneuron → alpha motor neuron → Excites antagonist (triceps)
Corticospinal Tract
see image on slide18
Where does it all go wrong?
Damage in Cerebrum:
MANY pathways are involved… medullary RST has a large effect on Hypertonia/Hyperreflexia
Studies show later on RST may take over more muscle mvmt to make up for dysfunctional CST in Spasticity (Sangari et al, 2019)
Reciprocal inhibition (which relaxes the antagonist muscle normally) is reduced with supraspinal lesions, leading to contract-relax cycles as muscles are stretched/contracted.
This heightened reflex activity can result in involuntary muscle spasms, which are sudden, often painful contractions of the muscle in response to stretch
Differentiating Points | Spasticity | Rigidity |
---|---|---|
Velocity dependency | Yes | No |
Resistance to movement | In one direction (flexion or extension) | In both directions |
Length dependency | Yes | No |
Type of hypertonicity | Clasp-knife | Lead pipe or Cog-wheel |
Grade | Criteria |
---|---|
0 | No resistance throughout the course of the passive movement |
1 | Slight resistance throughout the course of the passive movement, followed by release |
2 | Clear catch at precise angle, interrupting the passive movement, followed by release |
3 | Fatigable clonus <10 seconds when maintaining pressure occurring at precise angle |
4 | Infatigable clonus >10 seconds when maintaining pressure occurring at precise angle |
Why do we have them?
After UMN lesion
Synergies make MMTs inaccurate
Co-activation of other muscles makes it impossible to isolate 1 muscle
Not purely volitional movement, but rather more automatic driven (RST)Mooney2024?
Instead- staging with Brunnstrom post stroke can be helpful
Not always harmful!
However spasticity can interfere with functional activities which is when intervention is indicated…
Feature | Phasic Spasticity | Tonic Spasticity |
---|---|---|
Trigger | Rapid stretch | Sustained posturing |
Velocity-Dependent | Yes | No |
Neural Mechanism | Exaggerated stretch reflex (Ia afferents) → activates alpha motor neurons | Continuous excitation of α- and γ-motor neurons from Ia and II afferents |
Clinical Sign | Clonus, quick spasms | Constant stiffness, resistance to movement |
Spasticity is mostly due to dis-inhibition of the medullary (dorsal) Reticulospinal tract