2.21 Motor System 3 Flashcards

1
Q

What may disorders of the motor system cause?

A
  • paresis and paralysis
  • muscle atrophy
  • involuntary muscle contractions
  • abnormal muscle tone
  • abnormal reflexes
  • disturbances of movement efficiency and speed
  • impaired postural control
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2
Q

paresis

A

partial loss of voluntary contraction

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3
Q

paralysis

A

complete loss of voluntary contraction

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4
Q

types of muscle atrophy

A
  • disuse atrophy
  • neurogenic atrophy
  • denervation of skeletal muscle
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5
Q

disuse atrophy is the result of

A

lack of muscle use

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6
Q

neurogenic atrophy is caused by

A

damage to nervous system

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7
Q

What produces the most severe atrophy?

A

denervation of skeletal muscle

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8
Q

What is essential for the health of skeletal muscle?

A

frequent neural stimulation, even at a level inadequate to produce muscle contraction

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9
Q

spontaneous involuntary contractions include

A
  • muscle spasms
  • cramps
  • fasciculations
  • myoclonus
  • tremors
  • fibrillations
  • abnormal movements generated by dysfunctional basal ganglia
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10
Q

hypotonia

A

abnormally low resistance to passive stretch

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11
Q

two types of hypotonia

A
  • velocity-dependent

- velocity-independent

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12
Q

velocity-dependent hypotonia

A

amount of resistance to passive movement depends on velocity of the movement

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13
Q

velocity-independent hypotonia

A

resistance to passive movement remains constant, regardless of speed of force application

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14
Q

flaccidity

A

lack of resistance to passive stretch

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15
Q

What can damage LMNs?

A
  • trauma
  • infection
  • degenerative disorders
  • vascular disorders
  • tumors
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16
Q

if LMN cell bodies and/or axons are destroyed, then affected muscles can undergo:

A
  • loss of reflexes
  • atrophy
  • flaccid paralysis
  • fibrillations
17
Q

UMN lesions can produce several changes in movement control, including:

A
  • paresis or paralysis
  • loss of fractionation of movement
  • abnormal cutaneous reflexes
  • velocity dependent hypertonia
18
Q

paralysis in UMN syndrome

A

occurs in muscles innervated by LMNs below the level of a complete spinal cord lesion

19
Q

paresis in UMN syndrome

A
  • occurs in UMN lesions as a consequence of inadequate facilitation of LMNs
  • common after stroke, in spastic CP, TBI, and incomplete SCI
20
Q

UMN syndrome and loss of fractionation

A

interferes with fine movements, including fastening buttons or picking up coins, because the fingers of the involved hand act as a single unit

21
Q

UMN syndrome and loss of fractionation: LE

A

in a lower limb, loss interferes with dorsiflexing the ankle

22
Q

UMN syndrome: abnormal cutaneous reflexes

muscle spasms

A
  • in people with SCI, muscle spasms may occur in response to cutaneous stimuli
  • spasms begin after recovery from spinal shock
23
Q

3 most common abnormal reflexes in those with chronic SCIs

A
  • muscle stretch hyperreflexia
  • clonus
  • clasp-knife response
24
Q

muscle stretch hyperreflexia

A
  • loss of inhibitory corticospinal input combined with LMN and interneuron development of enhanced excitability
25
What does the loss of inhibitory corticospinal input combined with LMN and interneuron development of enhanced excitability result in?
excessive LMN response to afferent input from stretch receptors
26
muscle stretch hyperreflexia: excessive muscle contraction occurs when
when spindles are stretched as a result of excessive LMN firing
27
involuntary, repeating, rhythmic muscle contractions
clonus
28
unsustained clonus
fades after a few beats, even with maintained muscle stretch
29
sustained clonus is always
always pathologic in origin
30
When is sustained clonus produced?
when lack of UMN control allows activation of oscillating neural networks in spinal cord
31
When does clasp-knife response occur?
when paretic muscle is slowly and passively stretched and resistance drops at a specific point in the ROM
32
clasp-knife response: the change in resistance similar to opening of a pocket knife
initial strong resistance to opening gives way to easier movement
33
What afferents elicit the clasp-knife response?
type II
34
problems with velocity dependent hypertonia
- limits joint ROM - interferes with function - may cause deformity
35
What is velocity dependent hypertonia caused by?
muscular changes (myoplasticity) and/or spasticity
36
myoplasticity (velocity dependent hypertonia)
adaptive changes within a muscle in response to changes in NM
37
spasticity (velocity dependent hypertonia)
NM overactivity, 2˚ to UMN lesion