Chapter 10 Part 2 Flashcards Preview

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Flashcards in Chapter 10 Part 2 Deck (65):
1

What can disorders of the motor system cause?

Paresis and paralysis
Muscle atrophy
Involuntary muscle contractions
Abnormal muscle tone
Abnormal reflexes (see UMN syndrome)
Disturbances of movement efficiency and speed
Impaired postural control

2

What is paresis?

the partial loss of voluntary contraction

3

What is paralysis?

the complete loss of voluntary contraction (such as complete SCI)

4

What is muscle atrophy?

loss of muscle bulk

5

What is disuse atrophy a result of?

lack of muscle use

6

What causes neurogenic atrophy?

caused by damage to the nervous system

7

What causes the most severe atrophy?

denervation of skeletal muscle

8

Why does denervation of skeletal muscle cause the most severe atrophy?

because frequent neural stimulation, even at a level inadequate to produce muscle contraction, is essential for the health of skeletal muscle

9

What are examples of involuntary muscle contractions?

muscle spasms
cramps
fasciculations
myoclonus
tremors
fibrillations
abnormal movements generated by dysfunction

10

Muscle spasms:

sudden involuntary contractions of muscle

11

Cramps

severe and painful muscle spasms

12

Fasciculations:

quick twitches of muscle fibers of a single motor unit visible on the skin surface

13

Myoclonus

brief, involuntary contractions of a muscle or group of muscles

14

Tremors

resting or intention) – involuntary rhythmic movements of a body part

15

Fibrillations

brief contractions of single muscle fibers not visible; result from UMN or LMN lesions

16

What conditions are pathologic?

fibrillations and abnormal movements generated by dysfunction of basal ganglia

17

What is muscle tone?

the resistance to stretch in the resting muscle

18

How is muscle tone classified?

rigidity
spasticity
normal
hypotonia
flaccidity

19

What is rigidity?

hypertonia (abnormally strong resistance to passive stretch
velocity independent

20

What is spasticity?

hypertonia
velocity dependent; sign of UMN lesion

21

What is hypotonia?

an abnormally low resistance to passive stretch

22

What is flaccidity?

the lack of resistance to passive stretch (complete loss of muscle tone)

23

What can damage LMNs?

Trauma, infection (e.g., poliomyelitis), degenerative or vascular disorders, and tumors

24

What can the affected muscles undergo when the LMN cell bodies or axons are destryoed?

Loss of reflexes
Atrophy
Flaccid paralysis
Fibrillations

25

What changes can UMN lesions produce?

changes in movement control
Paresis or paralysis
Loss of fractionation of movement
Abnormal reflexes
Velocity-dependent hypertonia

26

What are signs and symptoms of UMN syndrome?

weakness
spasticity (increased tone, hyperactive reflexes)
clonus
babinski's sign
loss of fine voluntary movements

27

What are signs and symptoms of LMN syndrome?

weakness or paralysis
decreased superficial reflexes
hypoactive deep reflexes
decreased tone
fasciculations and fibrillations
severe muscle atrophy

28

What is fractionation?

the ability to activate individual muscles independently of other muscles

29

What does loss of fractionation interfere with?

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

30

What does loss of fractionation in a lower limb interfere with?

dorsiflexing the ankle

31

What is Babinski's sign?

the extension of the great toe, accompanied by fanning of the other toes

32

What are the three most common abnormal reflexes in those with chronic SCI?

muscle stretch hyperreflexia
clonus
clasp-knife response

33

What does excessive muscle contraction occur?

when spindles are stretched as a result of excessive firing of the LMNs

34

What results in excessive LMN response to afferent input from stretch receptors?

Loss of inhibitory corticospinal input combined with LMN and interneuron development of enhanced excitability

35

What is unsustained clonus?

fades after a few beats, even with maintained muscle stretch.

36

What is sustained clonus?

is always pathologic in origin and is produced when a lack of UMN control allows the activation of oscillating neural networks in the spinal cord

37

When does the clasp-knife response occur?

Occurs when a paretic muscle is slowly and passively stretched and resistance drops at a specific point in the range of motion

38

What elicits the clasp-knife response?

type II afferents

39

What does spasticity do?

Limits joint range of motion, interferes with function, and may cause deformity

40

What is UMN hypertonia caused by?

1. myoplasticity
2. spasticity

41

Myoplasticity:

adaptive structural changes within a muscle in response to changes in neuromuscular activity level and to prolonged positioning

42

Spasticity:

is neuromuscular overactivity, secondary to an UMN lesion

43

What happens by age 4 in normal development?

a corticospinal axon that previously synapsed with LMNs to antagonist and synergists will only synapse with LMN to the agonist

44

What does damage to the corticospinal tracts during development cause?

causes persistence of inappropriate connections and abnormal development of spinal motor centers= abnormal cocontraction

45

What are mechanisms of spasticity?

1. developmental spasticity
2. adult-onset cerebral spasticity
3. spinal spasticity

46

What does a typical stroke interrupt?

corticospinal and corticoreticular tracts on one side of the brain

47

Reticulospinal tract overactivity is the primary cause of what?

stoke spasticity due to diminished cortical inhibition

48

What happens when UMN tracts are severed in the spinal cord?

disinhibited LMN and interneurons below the lesion develop enhanced excitability, causing hyperreflexia

49

What can hyperreflexia limit?

limit walking speed, interfere with positioning, mobility, hygiene, comfort, and sleep

50

Common impairments in UMN lesions?

Abnormal synergy
Abnormal contracture
Hyperreflexia
Hypertonia
Muscle contracture
Muscle tone
Muscle overactivity
Myoplasticity
Paresis
Spasticity

51

What are some measuring tools for hypertonia?

Ashworth Scale or modified AS
EMG
Torque/force resistance

52

What is an EMG used to determine?

which factors are contributing to movement impairment

53

What factors can contribute to movement impairment?

hyperreflexia
contracture
cocontraction
inappropriate timing of muscle activity

54

What are types of UMN lesions?

Spastic cerebral palsy (CP)
Stroke or cerebrovascular accident (CVA)
Spinal cord injury (SCI)
Traumatic brain injury (TBI)
Multiple sclerosis (MS)
Tumors

55

What leads to movement dysfunction?

Abnormal supraspinal influences, failure of normal neuronal selection, and consequent aberrant muscle development

56

What is included in motor disorders in spastic CP?

Problems with coordination
Abnormal tonic stretch reflexes both at rest and during movement
Reflex irradiation – spread of reflex activity (e.g., tapping of biceps induces finger flexor activity)
Lack of postural preparation before movement
Abnormal cocontraction of muscles

57

What is the most frequently affected region in a stroke?

MCA (middle cerebral arterty)

58

What does a stroke cause damage to?

damage to corticospinal, corticoreticular and corticobrainstem neurons

59

What connections does a stroke disrupt?

cortical connections with the spinal cord, brainstem and cerebellum

60

What are motor disorders after a MCA the consequence of?

the consequences of paresis, decreased fractionation of movement, and myoplasticity.

61

What does the reticulospinal tract provide?

voluntary movement of the paretic limbs.

62

Complete SCI:

All descending neuronal control is lost below the level of the lesion

63

Incomplete SCI:

Function of some ascending and/or descending fibers is preserved within the spinal cord

64

After SCI, what produces excessive resistance to muscle stretch?

excessive stretch reflexes, muscle contracture, and increased cross-bridge binding

65

In people with SCI, what limits movement?

hyperreflexia and contracture