Muscle Tone and Spasticity

Question 1

muscle tone

Answer 1

resistance to stretch

Question 2

muscle tone continuum

Answer 2

flaccidity
hypotonia
normal
hypertonia
- spasticity
- rigidity

Question 3

flaccidity

Answer 3

complete lack of resistance to passive stretch

Question 4

hypotonia

Answer 4

abnormally low/less than normal resistance to passive stretch

Question 5

hypertonia

Answer 5

abnormally strong resistance to passive stretch

Question 6

spasticity versus rigidity

Answer 6

spasticity: velocity dependent resistance to passive stretch
speed of movement

rigidity: non-velocity dependent resistance to passive stretch

Question 7

velocity dependent resistance

Answer 7

increased resistance to passive stretch that increases with speed of movement

Question 8

non-velocity dependent resistance

Answer 8

increased resistance to passive stretch that does not change with speed of stretch
- constant resistance

Question 9

flaccidity and hypotonia are _____ lesions

Answer 9

lower motor neuron

Question 10

cerebral/spinal shock

Answer 10

acute lesions to the motor tract cause cerebral/spinal shock
- temporary hypotonia with no motor activity below level of lesion

Question 11

hypertonia is a ________lesion

Answer 11

upper motor neuron
- stroke, SCI, brain injury, etc.

Question 12

relationship between spinal shock and hypertonia

Answer 12

hypertonia occurs during the months following spinal shocks because muscle tone increases due to neural/muscular changes

Question 13

2 mechanisms that cause UMN overactivity

Answer 13

absence of corticospinal/ reticulospinal inhibition to LMNS

brainstem

Question 14

cogwheel rigidity

Answer 14

start-stop resistance to movement as limb is moved passively though range of motion
- jerky, catch/release

Question 15

lead-pipe rigidity

Answer 15

constant resistance to movement throughout range of motion
- slow, stiff

Question 16

Gegenhalten rigidity

Answer 16

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.

Question 17

decerebrate rigidity/posturing

Answer 17

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

Question 18

decorticate rigidity/posturing

Answer 18

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

Question 19

clinical features of spasticity

Answer 19

• increased velocity dependent muscle tone
• hyperreflexia

Question 20

clasp knife phenomenon

Answer 20

initial resistance to passive stretch/movement, followed by sudden decrease in resistance as the movement continues

Question 21

muscle contractions due to spasticity can be beneficial in attempting to:

Answer 21

maintain
- postural control
- mobility
- muscle mass
- bone mineralization

reduce dependent edema
prevent DVTs

Question 22

supra-segmental contribution

Answer 22

descending pathways
- CST and RST

Question 23

what structures does the CST travel through before reaching the medulla?

Answer 23

motor cortices
corona radiata
internal capsule

Question 24

what is the difference between a primary motor cortex lesion and a premotor cortex lesion?

Answer 24

primary motor cortex lesion: weakness/reduced reflexes

premotor cortex lesion: SPASTICITY

Question 25

what happens if there are lesions to the corona radiate or internal capsule?

Answer 25

spasticity because the CST travels through here

Question 26

what is the difference between the lateral reticulospinal tract and the medial reticulospinal tract?

Answer 26

lateral: inhibitory --> alpha motor neuron -inhibits extensor tone medial: excitatory --> gamma motor neurons - facilitates extensor tone - along with vestibulospinal tract

Question 27

ventromedial reticular formation

Answer 27

-inhibitory system: inhibits stretch reflex via lateral reticulospinal tract

Question 28

bulbar medullary reticular formation

Answer 28

excitatory system: - facilitates spinal stretch reflex and extensor tone - inhibits flexors

Question 29

suprasegmental lesion: complete SCI

Answer 29

no inhibition coming down to muscles --> spasticity

Question 30

suprasegmental lesion: stroke (cortical)

Answer 30

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)

Question 31

segmental spinal contribution

Answer 31

reflex pathways

Question 32

how does an altered excitability of the spinal reflex lead to spasticity?

Answer 32

an UMN lesion disrupts the descending inhibitory control of the spinal reflexes, leading to hyperreflexia

Question 33

fusimotor drive

Answer 33

refers to the activity of gamma motor neurons that innervate the intrafusal muscle fibers of the muscle spindle.

Question 34

how does increased fusimotor drive lead to spasticity?

Answer 34

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

Question 35

Ia presynaptic inhibition

Answer 35

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

Question 36

Ia presynaptic inhibition dysfunction

Answer 36

↓ Presynaptic inhibition --> Hyperactive reflexes, ↑ tone

Question 37

1a reciprocal inhibition

Answer 37

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

Question 38

1a reciprocal inhibition dysfunction

Answer 38

↓ Inhibition (or reversed) --> Co-contraction, spasticity

Question 39

Ib non-reciprocal inhibition (autogenic inhibition)

Answer 39

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

Question 40

Ib non-reciprocal inhibition (autogenic inhibition) dysfunction

Answer 40

Ib inhibition reduced → the muscle doesn’t "shut off" properly under high force → ↑ tone and ↓ motor control

Question 41

Renshaw cell inhibition

Answer 41

Alpha motor neuron fires → activates Renshaw cell → Renshaw cell inhibits that gamma motor neuron, Ia interneuron → Keeps motor activity balanced and prevents over-firing

Question 42

Renshaw cell inhibition dysfunction

Answer 42

loss of inhibition on motor neurons → excessive muscle activity, spasms, spasticity, and poor motor control.

Question 43

non-neurological contributions

Answer 43

biomechanical factors - change in muscle tissue itself

Question 44

what do changes in soft tissue due to constant muscle activity result in?

Answer 44

contractures and altered muscle function → worsens spasticity

Question 45

what are common stimuli that trigger spasticity?

Answer 45

rapid stretch nociceptive: - painful stimuli - pressure ulcers non-nociceptive - touch, light pressure - bladder/bowel distension, infection, etc.

Question 46

what is the difference between the nerve conduction velocity results and EMG results for someone with spasticity?

Answer 46

NCV: NORMAL - peripheral nerves not damages EMG: INC activity - measures muscle contractions