Muscle Tone Flashcards

1
Q

What is tone?

A

The amount of resistance to passive stretch in a resting muscle.

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2
Q

What are the two components of tone?

A

Mechanical

Neural

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3
Q

Mechanical component of tone is?

A

The inherent/intrinsic physical properties of the tissues that make up the muscle.

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4
Q

Neural component of tone is?

A

The number of active motor units at a given time.

-The number of active motor units can be altered by the brain/brainstem to adjust to the environment.

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5
Q

Fact of Tone are?

A

-Always have tone even at rest.

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6
Q

What is the Gamma (Y) Loop?

A

Not a reflex but one means of many of adjusting muscle tone.

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7
Q

The gamma motor neuron is?

A

The motor neuron innervating the contractile component of the muscle spine.

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8
Q

What happens with hypotonicity?

A

Completely atonic - flaccid

Typically due to damage to lower motor neuron innervating skeletal muscle in either the CNS (soma) or in the PNS (axon).

-Fewer motor units able to contract

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9
Q

Hypotonicity is associated with?

A

An acute injury

  • Nervous system shock
  • Persists with a chronic upper motor neuron injury.
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10
Q

Hypotonicity without an AP reaching the axon terminal to release ACh at the?

A

Neuromuscular junction the motor unit cannot contract.

  • Cannot contract voluntarily
  • Cannot contract involuntarily
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11
Q

Hypotonicity - Fewer weak actin-myosin bonds are associated with?

A
  • Reduced or lost deep tendon reflex
  • -Disruption of the reflex arc
  • Paresis/paralysis
  • -Loss of innervation to the muscle fibers
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12
Q

Hypertonicity is?

A

Upper motor neuron damage

-Injuries in the brainstem and spinal cord

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13
Q

Hypertonicity is often accompanied by?

A

An exaggerated deep tendon reflex and presence of a tonic stretch reflex (hyperreflexia)

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14
Q

What is spasticity - Velocity Dependent - Myoplastic changes are?

A
  • Contracure

- Increased weak actin-myosin bonds

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15
Q

What is spasticity - Velocity Dependent - Neural changes are?

A

Neuromuscular overactivity causing too many active motor units

Chronic upper motor neuron injuries

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16
Q

Spasticity - Possible neural mechanisms are?

A
  • Loss of cortical inhibition of excitatory brainstem upper motor neuron tracts = overactivity of lower motor neurons and abnormal muscle systems
  • Decreased activation threshold of lower motor neuron = enhanced excitability of lower motor neurons
17
Q

Spasticity - Possible neural mechanisms are - Underactivity of?

A

inhibitory upper motor neuron on stretch reflexes

-Disinhibition of interneurons and reflex arc (hyperreflexia)

18
Q

Spasticity - Possible neural mechanisms are - Decreased activation threshold of?

A

Lower motor neuron = enhanced excitability of lower motor neuron

19
Q

Spasticity - Possible neural mechanisms are - other theorized contributors are?

A

Impaired reciprocal inhibition

  • Abnormal co-contraction
  • Injury to immature nervous system
  • Loss of fractionation in mature system
20
Q

Hypertonicity - Rigidity is?

A

Velocity independent

-Basal nuclei (ganglia) disorder (ex: Parkinson disease)

21
Q

Hypertonicity - Decerebrate posture - Caudal midbrain injury is?

A

-Extension of limbs and trunk with upper extremity internal rotation and ankle plantarflexion

22
Q

Hypertonicity - Decorticate posture - Injury rostral midbrain or bilateral injuries superior to midbrain is?

A

Extension of lower extremity and trunk with upper extremity flexion at elbow and wrist, and ankle plantarflexion