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Theories and Procedures > Lecture 4: Muscle Tone > Flashcards

Lecture 4: Muscle Tone Flashcards

1
Q

What is Muscle tone?

A

“Underlying tension in the muscle serving as a background for contraction”

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2
Q

Essentials in Assessing Tone

A

No active contraction (pt must be relaxed)

No resistance to muscle stretch

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3
Q

Normal vs. Abnormal Tone

A

Normal: controllable range of tension that supports normal movement and posture
Abnormal: reduced ability to change tone at will for movement or holding

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4
Q

Low vs abnormally low

A

not abnormal if can change tone for movement or holding

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5
Q

High vs abnormally high

A

not abnormal unless intolerable (cramps, spasm) or when unable to control at will

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6
Q

Hypotonicity

A

“Decreased resistance to stretch when compared with normal”

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7
Q

Flaccidity

A

Total lack of tone (Type of hypotonicity)

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8
Q

Paralysis

A

complete loss of voluntary muscle contraction; not a tone disorder

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9
Q

Hypertonicity

A

Increased resistance to stretch compared to normal

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10
Q

Conditions associated with hypertonicity

A

RIgidity
Akinesia
Spasticity

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11
Q

Spasticity

A

A type of abnormal muscle tone (type of hypertonicity)

Velocity-dependent resistance to passive muscle stretch

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12
Q

What Spasticity is NOT

A

Paralysis
Abnormal posturing
A particular diagnosis or neural pathology
Hyperactive stretch reflex
Muscle spasm
Voluntary movement restricted to movement in flexor or extensor synergy

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13
Q

Rigidity

A

abnormal, hypertonic state in which muscles are stiff or immovable and resistant to stretch regardless of velocity

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14
Q

Akinesia

A

movement disorder, lack of movement typically associated with rigidity

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15
Q

Clonus

A

multiple rhythmic oscillations or beats of involuntary muscle contraction in response to a quick stretch, observed particularly with quick stretching of ankle PF’s or wrist flexors

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16
Q

Clasp-knife Phenomenon

A

initial resistance followed by sudden release of resistance in response to stretch of a hypertonic muscle; due to an upper motor neuron lesion

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17
Q

Muscle Spasm

A

involuntary, neurogenic contraction of a muscle, typically as the result of a noxious stimulus

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18
Q

Contracture

A

not necessarily a tone disorder(i.e if its a tight capsule); can be if it’s the muscle tendon unit (difference between a shortening and a contraction-must go through AROM assessment to differentiate the two)

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19
Q

Muscle Stretch Reflexes (DTRs)

A

Hyperactive DTRs present with spasticity and rigidity

Test done in order to determine if motor and sensory pathways are intact

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20
Q

Dyskinesia

A

Fluctuating Abnormal Tone

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21
Q

Ballismus

A

large throwing type movements

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22
Q

Tremor

A

involuntary oscillatory movement due to alternate contractions of opposing muscle groups

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23
Q

Types of Tremor

A

Intention (kinetic)- happens when trying to reach, do active movement
Postural (static)- occurs at rest

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24
Q

Athetosis

A

slow, involuntary, writhing, twisting, “worm like” movements

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25
Q

Chorea

A

dancelike, sharp, jerky movements

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26
Q

Dystonia

A

sustained involuntary contractions of agonist and antagonist muscles causing abnormal posturing or twisting movements

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27
Q

athetosis, chorea, dystonia are all what type of disorder

A

Basal ganglia disorders

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28
Q

Tremors are what type of disorder?

A

Cerebellar Disorder

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29
Q

Quantitative measures for Muscle Tone

A 
Passive manual stretch 
Dynamometer stretch 
Isokinetic testing 
EMG
Pendulum Test
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30
Q

EMG and its advantages/disadvantages

A

(measures resting tone, allows you to determine activity at rest)
Records electrical activity of the muscle
Advantages: Sensitive, very specific with muscle group
Disadvantage: Requires a needle, limited to local muscles, requires a lot of training to use

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31
Q

Pendulum Test

A

test for spasticity; not used often

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32
Q

Qualitative measures for Muscle tone

A 
Clinical tone scale (0 to 4+)
Muscle stretch reflex test (DTRs) (0 to 4+)
Ashworth and Modified Ashworth Scale
Scales of spasticity 
Tardieu Scale
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33
Q

Ashworth and Modified Ashworth Scale

A

Scales of spasticity
Limited to describing increased but NOT decreased muscle tone
Considerations: Test position, How much touch, & Muscle length

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34
Q

Muscular contributions to tone and activation coming from Components include

A

Myofilaments
Cellular structure
Connective tissue
Tendons

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35
Q

Muscular contributions to tone and activation coming from biomechanical properties

A

Length-tension
Friction
Elasticity

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36
Q

Physical Agents can alter muscle tone & activation how?

A

Heat: increases circulation → accessibility of ATP to the myofilaments
Heat and cold: alter elasticity or friction of the tissues
Electrical stimulation: alter amount of neural stimulation of muscle fibers

37
Q

Alpha Motor Neuron

A

Neural Contribution to tone and activation
Generation
Summation (spatial vs. temporal)
Conduction

38
Q

Neurotransmitters

A

Neural Contribution to tone and activation
Ach
Dopamine- deficits in dopamine result in rigidity, resting tremors, and difficulty initiating and executing movement (Parkinson’s Disease)

39
Q

Summary of Neural Transmission

A

Electrical signal down axon → release of neurotransmitters into synapse → summation of signals (spatial or temporal) → excitatory or inhibitory to postsynaptic cell → excitatory :action potential generated → membrane channels open → Na+ into cell (depolarization) → repolarization

40
Q

Action potential

A

Basic unit of nerve communication

41
Q

Resting membrane potential

A

Negative charge inside nerve > outside by 60-90 mV

Maintained by Na+ outside and K+ inside

42
Q

Depolarization

A

The reversal of the excitable cell membrane
Inside becomes + relative to the outside
Na+ channels open → membrane potential reversed to +30mV → K+ channels rapidly open

43
Q

Absolute refractory period

A

immediately after nerve depolarization when no AP can be generated

44
Q

Relative refractory period

A

after nerve depolarization in which the nerve is hyperpolarized and a greater stimulus than usual is required to produce an AP

45
Q

Nerve conduction factors

A 
Diameter of nerve (large diameter = faster)
Insulation (myelin = faster)
Temperature effects (heat = faster)
46
Q

Monosynaptic transmission

A

Stretch reflex: only one synapse between the sensory neuron receiving the stretch stimulus and the motor neuron transmitting the signal to the muscle fibers to contract

47
Q

Stimulation of the AMN (alpha motor neuron)

A

Signals from CNS → AMN → Axon branches innerve motor unit → muscle contraction

48
Q

Motor unit activation

A

Motor unit: muscle fibers innervated by all branches of a single AMN
All-or-none principle
Excitatory and inhibitory

49
Q

Input to AMN from peripheral receptors

A
  1. muscle spindles via 1a sensory neurons
  2. GTOs via 1b sensory neurons
  3. Cutaneous receptors via other sensory neurons
50
Q

Input to AMN from spinal sources

A

Propriospinal interneurons

51
Q

Input to AMN from supraspinal sources

A
  1. Cortex, basal ganglia via corticospinal tract
  2. Cerebellum, red nucleus via rubrospinal tract
  3. Vestibular system, cerebellum via vestibulospinal tracts
  4. Limbic system, autonomic nervous system via reticulospinal tracts
52
Q

Peripheral Nervous System Contents

A

AMNs that cause muscle contraction
Gamma motor neurons
Some autonomic nervous system effector neurons
All of the sensory neurons

53
Q

Gamma Motor Neurons

A

Innervate muscle spindles at the end regions
When stimulated, cause the equatorial region of the spindle to tighten
“Resets muscle spindles”
Increase spindle sensitivity → quick muscle response
Alpha-gamma coactivation

54
Q

Peripheral input

A

Protect the body
Counter obstacles
Adapt to unexpected occurrences in the environment during volitional movement

55
Q

Muscle Spindle: Reciprocal Inhibition

A

Receptors around spindle sense lengthening → AP sent through type 1a sensory neurons → to pool of AMN for the agonist muscle and pool for antagonic → if excitatory input sufficient, agonist contracts; inhibitory input to antagonist

56
Q

Golgi Tendon Organ

A

Detect and regulate active contraction
Transmit signals to the AMN pools of both the agonist and antagonist muscles via type 1b sensory neurons
Autogenic inhibition= stimulation of agonist, inhibition of antagonist

57
Q

Quick stretch vs Prolonged Stretch (Regarding Muscle spindles and GTO’s)

A

Quick: Spindle registers change in length → mm contracts
Prolonged:Initially facilitates but ultimately inhibits contraction
GTOs register tension at the tendons & inhibit the homonymous AMNs
Inhibits abnormally high tone in agonists
Facilitates antagonist

58
Q

Cutaneous receptors

A

Temperature, texture, pressure, pain, and touch
Spinal interneuron linkage
Painful stimuli
Crossed extension reflex

59
Q

Modalities and Cutaneous receptors to Increase Tone

A

Quick, light touch
Manual contact
Brushing
Quick icing

60
Q

Modalities and Cutaneous receptors to Decrease Tone

A

Slow stroking
Maintained holding
Neutral warmth
Prolonged icing

61
Q

Spinal Sources of Input

A

Circuits of neurons in the spinal cord
Circuits comprised of interneurons
Propriospinal pathways
Synergies

62
Q

Supraspinal Sources: Descending Input

A 
Corticospinal tract  
Basal Ganglia 
Rubrospinal tract (cerebellum, red nucleus)
Vestibulospinal tracts
Reticulospinal tract
63
Q

Corticospinal Tract

A

Decision to move is initiated in the cortex
Voluntary contraction
Skilled, fine motor control, especially in distal limbs

64
Q

Basal Ganglia

A

Modulates movement and tone

65
Q

Rubrospinal Tract

A

Regulates movement, postural control, and muscle tone

Compares plans of intended movement from motor cortex with actual performance of segment

66
Q

Vestibulospinal Tracts

A

Regulate posture from position of head and way in moves in space with respect to gravity

67
Q

Reticulospinal Tracts

A

(Limbic System and ANS)
Emotions, memories, motivation, alterness
Regulate response to reflexes
Affects muscle tone through influence on muscle spindle activity

68
Q

Normal Tone Factors

A

Assuming motor units (AMN and mm fibers) are intact
Normal function of muscles, PNS, and CNS
Based on sum of input to AMN

69
Q

ICF Model

A

Pathology→ impaired body structure and function→ impaired activity→ impaired participation

70
Q

Low Muscle Tone

A

Loss of normal AMN input to otherwise normal muscle fibers or Neural Stimulation
Insufficient activation of the motor units to prepare for holding or movement

71
Q

Damaged AMNs

A 
Flaccid paralysis (all motor units of a muscle are involved)
Denervation (no input to motor neuron)
72
Q

Paresis

A

some of the AMNs are working, some are not

73
Q

Recovery for Damaged AMNs

A

Rearborizing - remaining AMN increase number of muscle fibers innervated by increasing number of axonal branches
Regrowth of axons through remaining myelin sheaths (extremely slow)

74
Q

Rehab after AMN Damage

A

Goal: activate AMNs
Physical agents: hydrotherapy, quick ice, e-stim
Other: ROM, ther ex, orthotic devices
Casting- can be used to decrease hypertonicity
Head injury/stroke- progression from hypo to hypertonic

75
Q

Consequences of Low Muscle Tone

A

Lack of force generation to maintain posture or movement

Poor posture and reliance on ligaments for support

76
Q

Ways to Increase Tone

A 
Quick stretch 
Tapping 
Resistive Exercises 
High frequency vibration 
Limb positioning
77
Q

High Muscle tone

A

Result of abnormally high excitatory input compared to the inhibitory input to an otherwise intact alpha motor neuron

78
Q

Consequences of High Muscle Tone

A

Discomfort or pain from muscle spasms, contractures, abnormal posture, skin breakdown, increased effort by caregivers to assist with bathing, dressing, transfers, development of stereotyped movement patterns that may inhibit development of movement alternatives, may inhibit function

79
Q

Hypertonicity due to pain, cold, stress results in

A

Muscle Guarding

80
Q

Hyperonicity treatment

A 
Remove the source of hypertonicity 
Neutral warmth/heat 
Stress reduction/relaxation techniques 
EMG biofeedback 
Hydrotherapy
81
Q

SCI (Hypertonicity Condition)

A

AMN’s below lesion lack both excitatory and inhibitory input to AMN’s form supraspinal sources
Still get propriospinal input
Spinal shock- flaccid tone, absent DTRs followed by hypertonicity

82
Q

Cerebral Lesions (Hypertonicity Condition)

A

develops over time due to change in input to AMNs

83
Q

SCI Treatment

A

ROM, prolonged stretch, positioning, meds, surgery, FES (functional e-stim)
Identify and remove painful stimuli to alleviate mm spasm

84
Q

Cerebral Lesions Bobath theory

A

loss of inhibitory controls from higher centers; goal is to normalize hypertonicity

85
Q

Cerebral Lesions Task-oriented approach

A

n.s. uses its remaining resources to perform tasks (adaptive response)

86
Q

Course of Tone with CVA

A

Flaccid paralysis → voluntary movement in synergies → spasticity → controlled movement

87
Q

Managing Hypertonicity after CVA

A 
Prolonged icing 
Inhibitory pressure
Prolonged stretch 
Inhibitory casting 
Positioning
Biofeedback 
Task training 
Antagonist activation 
Neutral warmth 
Hydrotherapy
88
Q

Rigidity (conditions like parkinsons)

A

Constant or intermittent
Decorticate posture vs decerebrate posture
Treatment considerations

Theories and Procedures (5 decks)

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