Muscle Tone and Spasticity Flashcards
muscle tone
resistance to stretch
muscle tone continuum
flaccidity
hypotonia
normal
hypertonia
- spasticity
- rigidity
flaccidity
complete lack of resistance to passive stretch
hypotonia
abnormally low/less than normal resistance to passive stretch
hypertonia
abnormally strong resistance to passive stretch
spasticity versus rigidity
spasticity: velocity dependent resistance to passive stretch
speed of movement
rigidity: non-velocity dependent resistance to passive stretch
velocity dependent resistance
increased resistance to passive stretch that increases with speed of movement
non-velocity dependent resistance
increased resistance to passive stretch that does not change with speed of stretch
- constant resistance
flaccidity and hypotonia are _____ lesions
lower motor neuron
cerebral/spinal shock
acute lesions to the motor tract cause cerebral/spinal shock
- temporary hypotonia with no motor activity below level of lesion
hypertonia is a ________lesion
upper motor neuron
- stroke, SCI, brain injury, etc.
relationship between spinal shock and hypertonia
hypertonia occurs during the months following spinal shocks because muscle tone increases due to neural/muscular changes
2 mechanisms that cause UMN overactivity
absence of corticospinal/ reticulospinal inhibition to LMNS
brainstem
cogwheel rigidity
start-stop resistance to movement as limb is moved passively though range of motion
- jerky, catch/release
lead-pipe rigidity
constant resistance to movement throughout range of motion
- slow, stiff
Gegenhalten rigidity
involuntary resistance to passive movements
- catch and release
- feels like the patient is “helping” or resisting variably—almost as if they’re not cooperating, but it’s not voluntary.
decerebrate rigidity/posturing
cause: damage of brainstem between midbrain and pons
positioning: extension of arms
- rigid extension of limbs/trunk
- plantarflexion
- internal rotation of shoulders, wrist/finger flexion
decorticate rigidity/posturing
cause: damage to superior midbrain or cerebral cortex
positioning: flexion of arms
- rigid extension of limbs/trunk
- plantarflexion
- internal rotation of shoulders, wrist/finger flexion
clinical features of spasticity
- increased velocity dependent muscle tone
- hyperreflexia
clasp knife phenomenon
initial resistance to passive stretch/movement, followed by sudden decrease in resistance as the movement continues
muscle contractions due to spasticity can be beneficial in attempting to:
maintain
- postural control
- mobility
- muscle mass
- bone mineralization
reduce dependent edema
prevent DVTs
supra-segmental contribution
descending pathways
- CST and RST
what structures does the CST travel through before reaching the medulla?
motor cortices
corona radiata
internal capsule
what is the difference between a primary motor cortex lesion and a premotor cortex lesion?
primary motor cortex lesion: weakness/reduced reflexes
premotor cortex lesion: SPASTICITY
what happens if there are lesions to the corona radiate or internal capsule?
spasticity because the CST travels through here
what is the difference between the lateral reticulospinal tract and the medial reticulospinal tract?
lateral: inhibitory –> alpha motor neuron
-inhibits extensor tone
medial: excitatory –> gamma motor neurons
- facilitates extensor tone
- along with vestibulospinal tract
ventromedial reticular formation
-inhibitory system: inhibits stretch reflex via lateral reticulospinal tract
bulbar medullary reticular formation
excitatory system:
- facilitates spinal stretch reflex and extensor tone
- inhibits flexors
suprasegmental lesion: complete SCI
no inhibition coming down to muscles –> spasticity
suprasegmental lesion: stroke (cortical)
since L. CST originates in the cortex, it is not working, therefore it is not inhibiting the reticulospinal tract
since the reticulospinal tract originates in the brainstem, it is up-regulated, causing excessive extensor and flexor tone (spasticity)
segmental spinal contribution
reflex pathways
how does an altered excitability of the spinal reflex lead to spasticity?
an UMN lesion disrupts the descending inhibitory control of the spinal reflexes, leading to hyperreflexia
fusimotor drive
refers to the activity of gamma motor neurons that innervate the intrafusal muscle fibers of the muscle spindle.
how does increased fusimotor drive lead to spasticity?
hyperactive gamma motor neurons increase the sensitivity of muscle spindles (la fibers) to stretch, making the muscle more likely to contract in response to even small stretches
Ia presynaptic inhibition
the reduction of neurotransmitter release from Ia afferent terminals onto alpha motor neurons, controlled by inhibitory interneurons—before the signal even reaches the synapse –> Smooth, coordinated motion
Ia presynaptic inhibition dysfunction
↓ Presynaptic inhibition –> Hyperactive reflexes, ↑ tone
1a reciprocal inhibition
Ia reciprocal inhibition is the process where stretching (activation) of a muscle causes inhibition of its antagonist, allowing for smooth, coordinated movement.
- inhibits co-contraction of agonist/antagonist muscles
1a reciprocal inhibition dysfunction
↓ Inhibition (or reversed) –>
Co-contraction, spasticity
Ib non-reciprocal inhibition
(autogenic inhibition)
It’s a spinal reflex where Ib afferents from Golgi tendon organs (GTOs) inhibit the same muscle (the agonist) to protect it from excessive force or tension.
- doesn’t directly affect antagonist
Ib non-reciprocal inhibition
(autogenic inhibition) dysfunction
Ib inhibition reduced → the muscle doesn’t “shut off” properly under high force → ↑ tone and ↓ motor control
Renshaw cell inhibition
Alpha motor neuron fires → activates Renshaw cell → Renshaw cell inhibits that gamma motor neuron, Ia interneuron → Keeps motor activity balanced and prevents over-firing
Renshaw cell inhibition dysfunction
loss of inhibition on motor neurons → excessive muscle activity, spasms, spasticity, and poor motor control.
non-neurological contributions
biomechanical factors
- change in muscle tissue itself
what do changes in soft tissue due to constant muscle activity result in?
contractures and altered muscle function → worsens spasticity
what are common stimuli that trigger spasticity?
rapid stretch
nociceptive:
- painful stimuli
- pressure ulcers
non-nociceptive
- touch, light pressure
- bladder/bowel distension, infection, etc.
what is the difference between the nerve conduction velocity results and EMG results for someone with spasticity?
NCV: NORMAL - peripheral nerves not damages
EMG: INC activity - measures muscle contractions
