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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
Chorea
dancelike, sharp, jerky movements
26
Dystonia
sustained involuntary contractions of agonist and antagonist muscles causing abnormal posturing or twisting movements
27
athetosis, chorea, dystonia are all what type of disorder
Basal ganglia disorders
28
Tremors are what type of disorder?
Cerebellar Disorder
29
Quantitative measures for Muscle Tone
``` Passive manual stretch Dynamometer stretch Isokinetic testing EMG Pendulum Test ```
30
EMG and its advantages/disadvantages
(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
31
Pendulum Test
test for spasticity; not used often
32
Qualitative measures for Muscle tone
``` Clinical tone scale (0 to 4+) Muscle stretch reflex test (DTRs) (0 to 4+) Ashworth and Modified Ashworth Scale Scales of spasticity Tardieu Scale ```
33
Ashworth and Modified Ashworth Scale
Scales of spasticity Limited to describing increased but NOT decreased muscle tone Considerations: Test position, How much touch, & Muscle length
34
Muscular contributions to tone and activation coming from Components include
Myofilaments Cellular structure Connective tissue Tendons
35
Muscular contributions to tone and activation coming from biomechanical properties
Length-tension Friction Elasticity
36
Physical Agents can alter muscle tone & activation how?
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
Alpha Motor Neuron
Neural Contribution to tone and activation Generation Summation (spatial vs. temporal) Conduction
38
Neurotransmitters
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
Summary of Neural Transmission
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
Action potential
Basic unit of nerve communication
41
Resting membrane potential
Negative charge inside nerve > outside by 60-90 mV | Maintained by Na+ outside and K+ inside
42
Depolarization
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
Absolute refractory period
immediately after nerve depolarization when no AP can be generated
44
Relative refractory period
after nerve depolarization in which the nerve is hyperpolarized and a greater stimulus than usual is required to produce an AP
45
Nerve conduction factors
``` Diameter of nerve (large diameter = faster) Insulation (myelin = faster) Temperature effects (heat = faster) ```
46
Monosynaptic transmission
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
Stimulation of the AMN (alpha motor neuron)
Signals from CNS → AMN → Axon branches innerve motor unit → muscle contraction
48
Motor unit activation
Motor unit: muscle fibers innervated by all branches of a single AMN All-or-none principle Excitatory and inhibitory
49
Input to AMN from peripheral receptors
1. muscle spindles via 1a sensory neurons 2. GTOs via 1b sensory neurons 3. Cutaneous receptors via other sensory neurons
50
Input to AMN from spinal sources
Propriospinal interneurons
51
Input to AMN from supraspinal sources
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
Peripheral Nervous System Contents
AMNs that cause muscle contraction Gamma motor neurons Some autonomic nervous system effector neurons All of the sensory neurons
53
Gamma Motor Neurons
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
Peripheral input
Protect the body Counter obstacles Adapt to unexpected occurrences in the environment during volitional movement
55
Muscle Spindle: Reciprocal Inhibition
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
Golgi Tendon Organ
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
Quick stretch vs Prolonged Stretch (Regarding Muscle spindles and GTO’s)
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
Cutaneous receptors
Temperature, texture, pressure, pain, and touch Spinal interneuron linkage Painful stimuli Crossed extension reflex
59
Modalities and Cutaneous receptors to Increase Tone
Quick, light touch Manual contact Brushing Quick icing
60
Modalities and Cutaneous receptors to Decrease Tone
Slow stroking Maintained holding Neutral warmth Prolonged icing
61
Spinal Sources of Input
Circuits of neurons in the spinal cord Circuits comprised of interneurons Propriospinal pathways Synergies
62
Supraspinal Sources: Descending Input
``` Corticospinal tract Basal Ganglia Rubrospinal tract (cerebellum, red nucleus) Vestibulospinal tracts Reticulospinal tract ```
63
Corticospinal Tract
Decision to move is initiated in the cortex Voluntary contraction Skilled, fine motor control, especially in distal limbs
64
Basal Ganglia
Modulates movement and tone
65
Rubrospinal Tract
Regulates movement, postural control, and muscle tone | Compares plans of intended movement from motor cortex with actual performance of segment
66
Vestibulospinal Tracts
Regulate posture from position of head and way in moves in space with respect to gravity
67
Reticulospinal Tracts
(Limbic System and ANS) Emotions, memories, motivation, alterness Regulate response to reflexes Affects muscle tone through influence on muscle spindle activity
68
Normal Tone Factors
Assuming motor units (AMN and mm fibers) are intact Normal function of muscles, PNS, and CNS Based on sum of input to AMN
69
ICF Model
Pathology→ impaired body structure and function→ impaired activity→ impaired participation
70
Low Muscle Tone
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
Damaged AMNs
``` Flaccid paralysis (all motor units of a muscle are involved) Denervation (no input to motor neuron) ```
72
Paresis
some of the AMNs are working, some are not
73
Recovery for Damaged AMNs
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
Rehab after AMN Damage
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
Consequences of Low Muscle Tone
Lack of force generation to maintain posture or movement | Poor posture and reliance on ligaments for support
76
Ways to Increase Tone
``` Quick stretch Tapping Resistive Exercises High frequency vibration Limb positioning ```
77
High Muscle tone
Result of abnormally high excitatory input compared to the inhibitory input to an otherwise intact alpha motor neuron
78
Consequences of High Muscle Tone
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
Hypertonicity due to pain, cold, stress results in
Muscle Guarding
80
Hyperonicity treatment
``` Remove the source of hypertonicity Neutral warmth/heat Stress reduction/relaxation techniques EMG biofeedback Hydrotherapy ```
81
SCI (Hypertonicity Condition)
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
Cerebral Lesions (Hypertonicity Condition)
develops over time due to change in input to AMNs
83
SCI Treatment
ROM, prolonged stretch, positioning, meds, surgery, FES (functional e-stim) Identify and remove painful stimuli to alleviate mm spasm
84
Cerebral Lesions Bobath theory
loss of inhibitory controls from higher centers; goal is to normalize hypertonicity
85
Cerebral Lesions Task-oriented approach
n.s. uses its remaining resources to perform tasks (adaptive response)
86
Course of Tone with CVA
Flaccid paralysis → voluntary movement in synergies → spasticity → controlled movement
87
Managing Hypertonicity after CVA
``` Prolonged icing Inhibitory pressure Prolonged stretch Inhibitory casting Positioning Biofeedback Task training Antagonist activation Neutral warmth Hydrotherapy ```
88
Rigidity (conditions like parkinsons)
Constant or intermittent Decorticate posture vs decerebrate posture Treatment considerations

Theories and Procedures (5 decks)

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