2.21 Motor System 3 Flashcards Preview

7303 Neuroanatomy > 2.21 Motor System 3 > Flashcards

Flashcards in 2.21 Motor System 3 Deck (37)
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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
2
Q

paresis

A

partial loss of voluntary contraction

3
Q

paralysis

A

complete loss of voluntary contraction

4
Q

types of muscle atrophy

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

disuse atrophy is the result of

A

lack of muscle use

6
Q

neurogenic atrophy is caused by

A

damage to nervous system

7
Q

What produces the most severe atrophy?

A

denervation of skeletal muscle

8
Q

What is essential for the health of skeletal muscle?

A

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

9
Q

spontaneous involuntary contractions include

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

hypotonia

A

abnormally low resistance to passive stretch

11
Q

two types of hypotonia

A
  • velocity-dependent

- velocity-independent

12
Q

velocity-dependent hypotonia

A

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

13
Q

velocity-independent hypotonia

A

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

14
Q

flaccidity

A

lack of resistance to passive stretch

15
Q

What can damage LMNs?

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

What does the loss of inhibitory corticospinal input combined with LMN and interneuron development of enhanced excitability result in?

A

excessive LMN response to afferent input from stretch receptors

26
Q

muscle stretch hyperreflexia: excessive muscle contraction occurs when

A

when spindles are stretched as a result of excessive LMN firing

27
Q

involuntary, repeating, rhythmic muscle contractions

A

clonus

28
Q

unsustained clonus

A

fades after a few beats, even with maintained muscle stretch

29
Q

sustained clonus is always

A

always pathologic in origin

30
Q

When is sustained clonus produced?

A

when lack of UMN control allows activation of oscillating neural networks in spinal cord

31
Q

When does clasp-knife response occur?

A

when paretic muscle is slowly and passively stretched and resistance drops at a specific point in the ROM

32
Q

clasp-knife response: the change in resistance similar to opening of a pocket knife

A

initial strong resistance to opening gives way to easier movement

33
Q

What afferents elicit the clasp-knife response?

A

type II

34
Q

problems with velocity dependent hypertonia

A
  • limits joint ROM
  • interferes with function
  • may cause deformity
35
Q

What is velocity dependent hypertonia caused by?

A

muscular changes (myoplasticity) and/or spasticity

36
Q

myoplasticity (velocity dependent hypertonia)

A

adaptive changes within a muscle in response to changes in NM

37
Q

spasticity (velocity dependent hypertonia)

A

NM overactivity, 2˚ to UMN lesion