UMN Syndrome; Muscle Tone Flashcards
(34 cards)
Muscle performance is mostly concerned with ___ neurons. With pathology, what is its definition?
LMN
Inability to generate force on muscle in primary disorder.
Motor control is usually a(n) ___ disorder. Name 4 components of motor control.
UMN
- Dexterity
- Coordination
- Agility
- Fractionated movement
What is a classic sign of UMN syndrome?
Loss of fractionated movement (being able to move a single muscle group independently).
With UMN syndrome, there is typically increased muscle tone, what’s happens to the reflexes?
Hyperreflexia.
What is a movement synergy?
Trying to move your hand and the whole limb moves in flexion or ext.
Why can’t a person with a cortical stroke move?
UMN’s can’t recruit LMN for movement because higher centers can’t generate APs.
With paresis, there is decreased activation of the antagonist or agonist?
Antagonist.
With an UMN injury, is muscle atrophy greater or lesser than LMN injury?
Less.
What is learned non-use?
Not using a limb that works resulting in negative neuro-plastic changes.
Which spinal tract activates muscles that control individual joint movements?
Cortical spinal.
What area of the brain would you cut to eliminate fractionated movement alone?
Pyramids in the rostral medulla (corticospinal tract).
What spinal tract is the hand mostly innervated by?
Lateral corticospinal.
What does the bulbar-spinal tract control?
Gross movements of the trunk and girdle muscles.
Is a DTR polysynaptic? T/F
False, monosynaptic.
What is diaschiasis and what is its relationship with DTRs and why?
Spinal shock lasting hours to days after injury. It can result in hyperative reflexes due to:
- Upregulation on neurotransmitters
- Loss of UMN control of inhibitory circuits
Rehabilitation after nerve injury is optimal in the sub acute phase. What is the goal?
To drive neuroplasticity, specifically competition-driven collateral growth from IA afferents of LMN onto the alpha MN. You want the UMN to produce more collaterals than the IA afferent.
What is the mathematical relationship between DTRs and muscle strength?
Inversely related.
What is a practical use of the tonic stretch reflex?
Can give insight into the level of spasticity of a muscle, as this reflex is not usually seen.
When would you see a clasp knife reflex?
Only with UMN lesion.
- resistance drops off after a break point, like a jack knife.
- only with slow, passive stretch
What types of receptors are responsible for tonic reflexes (incl jack knife)?
Type II afferents, joint capsule and touch receptors.
How is muscle tone defined?
Resistance to passive stretch.
What are the factors that contribute to muscle tone?
- Active factors, like UMN firing
- Instrinsic factors like weak actin myosin bonds at rest
- Passive factors: titin - keeps the ends of sarcomeres together.
Is there a neural component to the slow stretch reflex in a normal person?
No, tonic, slow stretch reflex is inhibited. Most resistance is from titin, the passive element.
How do you lose sarcomeres?
Contractures from immobility.
- also lose titin
- more actin-myosin bonds at rest (why you get stiffer)