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Neurological Conditions > Tone Abnormalities > Flashcards

Tone Abnormalities Flashcards

1
Q

What is muscle tone?

A

Muscle tone is underlying tension in the muscle

that serves as a background for contraction

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2
Q

What are some challenges to assessing muscle tone?

A

‒ Must be assessed when there is no active
resistance to the muscle stretch
‒ Changes with movement, posture, intention, and
environment

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3
Q

What is hypotonicity?

A

abnormally low tone (Down syndrome, poliomyelitis)

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4
Q

What is flaccidity?

A

total absence of tone

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5
Q

What is hypertonicity?

A

abnormally high tone

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6
Q

What is rigidity?

A

velocity independent resistance to stretch

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7
Q

What is spasticity?

A

velocity dependent resistance to stretch

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8
Q

What is clonus?

A

rhythmic oscillations or beats of involuntary

contraction in response to quick stretch

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9
Q

What is not muscle tone?

A

‒ Voluntary muscle contraction

‒ Posture

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10
Q

What are fluctuating abnormal tones?

A

Disorders with abnormal involuntary movements or

dyskinesias

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11
Q

What are quantitative measures?

A

‒ Dynamometer or Myometer
‒ Isokinetic testing systems
‒ Electromyography (EMG)
‒ Pendulum test

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12
Q

What are qualitative measures?

A

‒ Clinical tone scale
‒ Muscle stretch reflex test
‒ Ashworth and Modified Ashworth Scale

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13
Q

What is the clinical tone scale?

A 
Grade Description
 0        No tone
 1         Hypotonicity
 2        Normal tone
 3        Moderate hypertonicity
 4        Severe hypertonicity
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14
Q

What is the muscle stretch reflex test?

A 
Grade Description
 0        No reflex
 1+       Diminished reflex
 2+      Normal reflex
 3+      Brisker than average reflex
 4+      Very brisk or hyperactive reflex
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15
Q

What is the modified ashworth scale?

A 
Grade Description
 0        No ↑in muscle tone
 1         Slight ↑in muscle tone: catch
and release or min. resistance
at end ROM when moved in
flexion/extension
 1+        Slight ↑in muscle tone: catch
followed by min. resistance
throughout rest of ROM (< 1/2)
 2         More marked ↑in muscle tone
through most of ROM but
affected part(s) move easy
 3         Considerable ↑in muscle tone,
passive movement difficult
 4         Affected part(s) rigid in flexion
or extension
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16
Q

What are some general considerations when measuring muscle tone?

A

‒ Note positions of limb, body, neck, and head relative
to each other and gravity
‒ Muscle tone is most accurately measured in mid ROM
of muscle’s length
‒ Standardize touch
‒ Consider muscle strength
‒ Document what position muscle tone was measured

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17
Q

What can asymmetrical and symmetrical tonic neck reflexes influence?

A

tone of the flexors and
extensors depending on
position of the head

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18
Q

When do ATNR and STNR reflexes occur?

A

during infancy and in
subjects with
neurological deficits

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19
Q

What is muscle composed of?

A

contractile elements (myofilaments), cellular elements, connective tissue covering fibers and muscle, and tendons attaching muscle to bone

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20
Q

What are the cellular elements of muscle?

A

• Neural stimulation causes a release of calcium
• Allows formation of cross-bridges binding actin and myosin
proteins
• Energy from ATP breaks the cross-bridges so new bonds can
be formed
• As new bonds are formed and broken it changes the length
of the contractile unit: sarcomeres

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21
Q

What are neural contributions of muscle tone and activation?

A

‒ Neural inputs come from periphery, spinal cord, brain centers
‒ The alpha motor neuron is the final common pathway that
directly stimulates muscle contraction
• Generation, summation, and conduction of an activating signal

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22
Q

What may friction between connective tissue be affected by?

A

pressure on tissues and by the viscosity of fluids in which

tissue reside

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23
Q

What is elasticity?

A

taut tissues contribute to resistance of muscle

to stretch and slack tissues contribute very little

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24
Q

What happens when a muscle is stimulated in the shortened position?

A

there is a delay before movement can occur or force can

be generated

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25
Q

How can physical agents change muscle tone and activation?

A

‒ Heat ↑availability of ATP to myofilaments
‒ Heat and cold can change elasticity or friction of tissues
‒ ES can change amount of muscle fiber neural stimulation

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26
Q

What are structure and function of nerves?

A

‒ Dendrites receive stimulus; axons conduct stimuli toward destination
‒ Signals are conducted across synapses to other neurons using
neurotransmitters (acetylcholine, norepinephrine or serotonin

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27
Q

What are action potentials?

A

Depolarization and repolarization initiated by Na/K pumps that quickly
alter the charge of a neuron, creating a wave of activity

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28
Q

What is transmission?

A

Myelin insulation increases speed of action potential transmission
(up to 80m/sec)

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29
Q

What are the sources of neural stimulation of muscle (sensory organs)?

A

peripheral inputs (muscle spindles, golgi tendon organs, cutaneous receptors), spinal inputs, and supraspinal inputs (sensorimotor cortical contributions, cerebellum, basal ganglia, limbic system, vestibular system, reticular-activating system)

30
Q

What are peripheral inputs?

A

muscle spindles, golgi tendon organs, cutaneous receptors

31
Q

What is a muscle spindle?

A

located in muscle and senses when muscle

is stretched

32
Q

What are golgi tendon organs?

A

located in connective tissue between
muscle and tendon and senses maximal stretch (protective
mechanism)

33
Q

What are cutaneous receptors?

A

located in skin and senses interaction
with external world (temperature, texture, pressure, pain
and stretch)

34
Q

What are spinal inputs?

A

Located in the spinal cord and contribute to flexor or

extensor synergy patterns

35
Q

What are supraspinal inputs?

A

(originate above the spinal cord) sensorimotor cortical contributions, cerebellum, basal ganglia, limbic system, vestibular system, and reticular-activating system

36
Q

What are sensorimotor cortical contributions?

A

response to sensation,

idea, memory or external stimulus to move, act or respond

37
Q

What is the cerebellum?

A

registers any discrepancies between signals from
motor cortex and peripheral inputs and corrects for movement
errors or unexpected obstacles during movement

38
Q

What does the basal ganglia do?

A

modulates movement and tone (Parkinsonism)

39
Q

What are other descending inputs?

A

vestibular system, reticular-activating system

40
Q

What does the vestibular system do?

A

receives ongoing information about the head

position and movement

41
Q

What does the reticular-activating system do?

A

receives information from multiple
sensory systems (vision, auditory, vestibular, somatosensory, motor
cortex, and cerebellum)

42
Q

What does the limbic system do?

A

generates memories and attaches meaning to

changes in muscle tone or activation (activates SNS)

43
Q

What is an UE flexion synergy pattern?

A 
Scapular adduction
Scapular elevation (variable)
Shoulder external rotation
Shoulder abduction
Elbow flexion
Forearm supination
Wrist flexion
Finger/thumb response (variable)
44
Q

What is an UE extension synergy pattern?

A 
Scapular abduction
Shoulder internal rotation
Shoulder adduction
Elbow extension
Forearm pronation
Wrist extension
Finger/thumb response (variable)
45
Q

What is a LE flexion synergy pattern?

A 
Hip abduction
Hip flexion
Hip external rotation
Knee flexion
Ankle dorsiflexion
Toe extension(dorsiflexion)
46
Q

What is a LE extension synergy pattern?

A 
Hip adduction
Hip extension
Hip internal rotation
Knee extension
Ankle planter flexion
Ankle inversion
Toe flexion (planter flexion)
47
Q

What does normal muscle tone depend on?

A

Depends on normal composition and functioning of

muscles, the peripheral and central nervous systems

48
Q

What is required for normal muscle tone?

A

Multiple sources of neural input (both excitatory and

inhibitory) are required

49
Q

What determines the amount of muscle tone or activation?

A

Sum of all the input determines the amount of muscle

tone or activation

50
Q

What may result in abnormalities in muscle tone in activation?

A

Abnormalities in muscle tone and activation may result
when pathology or injury affect
– Muscles
– Alpha motor neurons
– Any other source of input to alpha motor neurons

51
Q

What is low muscle tone (hypotonicity)?

A

insufficient
activation of the motor units to prepare for holding or
movement

52
Q

What does hypotonicity cause?

A

poor posture, difficulty in movements, and pain

53
Q

What causes alpha motor neuron damage or denervation?

A

poliomyelitis, demyelinating

diseases (MS), trauma to nerves, nerve compression

54
Q

What is rehabilitation like after alpha motor neuron damage?

A

‒ Regrowth is generally slow and can occur only at a limited
distance
‒ Electrical stimulation (ES), hydrotherapy, and quick ice
have been used for rehabilitation of alpha motor neuron
damage

55
Q

What causes insufficient excitation of alpha motor neurons?

A

• Prolonged immobilization with a cast for fracture healing
• Stroke, multiple sclerosis, or head injury also alters the
balance of excitatory and inhibitory inputs

56
Q

What is some rehabilitation to increase tone?

A

‒ Physical agents are not often used after stroke, head injury,
or other supraspinal lesions
‒ ES, hydrotherapy, and quick ice may be used as an adjunct
to therapeutic exercises, orthotics, and functional training
of traditional rehabilitation

57
Q

What is high muscle tone (hypertonicity)?

A

abnormally high

excitatory input to an intact alpha motor neuron

58
Q

What are some associated effects to hypertonicity?

A
  • Muscle spasms
  • Contractures
  • Abnormal postures leading to skin ulcers
  • Difficulty with assisted dressing, transfers, hygiene
  • May inhibit functioning
59
Q

What is high muscle tone aggravated by?

A

pain, cold, or stress

60
Q

What are spinal cord injuries?

A

Initial flaccidity is followed by spasticity

– Frequently, greater on one side

61
Q

What is management for SCI?

A

Selective ROM exercises, prolonged stretch,

positioning or orthotics, medications, and surgery

62
Q

What are cerebral lesions?

A

Stroke, Parkinson’s disease, multiple sclerosis

63
Q

What is management for cerebral lesions?

A

Prolonged stretch or icing, inhibitory pressure or
casting, continuous passive motion, biofeedback, and
task training

64
Q

What is spasticity?

A 
Primary impairment or adaptive response?
• Develops some time after injury
• Recovery follows a predictable course
• Voluntary motor output limited to movement in flexor or
extensor patterns (synergies)
65
Q

What is rigidity?

A

‒ Consequence of central nervous system pathology
• Parkinson’s, stroke, head injury, multiple sclerosis
‒ Posturing
• Decorticate posture
• Decerebrate posture

66
Q

What is decorticate posture?

A

(above the brain stem) hypertonicity of neck and back extensors; hip extensors,
adductors, and internal rotators; knee extensors; ankle planter flexors
and invertors; wrist flexors; and finger flexors, elbow FLEXORS

67
Q

What is decerebrate posture?

A

(below the brain stem) hypertonicity of neck and back extensors; hip extensors,
adductors, and internal rotators; knee extensors; ankle planter flexors
and invertors; wrist flexors; and finger flexors, elbow EXTENSORS

68
Q

What is basal ganglia disease?

A

Parkinson’s disease

• Parkinson’s disease is a resting tremor that fluctuates

69
Q

What is cerebral palsy?

A

‒ Involuntary writhing (wriging of wrists, etc.)

• Self-inflicted injuries are possible

70
Q

what is management for cerebral palsy?

A

positioning, ROM

interventions, and neutral warmth

Neurological Conditions (5 decks)

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