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Neuro > Chapter 10 Part 2 > Flashcards

Chapter 10 Part 2 Flashcards

1
Q

What can disorders of the motor system cause?

A 
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
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2
Q

What is paresis?

A

the partial loss of voluntary contraction

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3
Q

What is paralysis?

A

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

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4
Q

What is muscle atrophy?

A

loss of muscle bulk

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5
Q

What is disuse atrophy a result of?

A

lack of muscle use

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6
Q

What causes neurogenic atrophy?

A

caused by damage to the nervous system

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7
Q

What causes the most severe atrophy?

A

denervation of skeletal muscle

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8
Q

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

A

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

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9
Q

What are examples of involuntary muscle contractions?

A 
muscle spasms
cramps
fasciculations
myoclonus
tremors
fibrillations
abnormal movements generated by dysfunction
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10
Q

Muscle spasms:

A

sudden involuntary contractions of muscle

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11
Q

Cramps

A

severe and painful muscle spasms

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12
Q

Fasciculations:

A

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

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13
Q

Myoclonus

A

brief, involuntary contractions of a muscle or group of muscles

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14
Q

Tremors

A

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

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15
Q

Fibrillations

A

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

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16
Q

What conditions are pathologic?

A

fibrillations and abnormal movements generated by dysfunction of basal ganglia

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17
Q

What is muscle tone?

A

the resistance to stretch in the resting muscle

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18
Q

How is muscle tone classified?

A 
rigidity
spasticity
normal
hypotonia
flaccidity
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19
Q

What is rigidity?

A

hypertonia (abnormally strong resistance to passive stretch

velocity independent

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20
Q

What is spasticity?

A

hypertonia

velocity dependent; sign of UMN lesion

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21
Q

What is hypotonia?

A

an abnormally low resistance to passive stretch

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22
Q

What is flaccidity?

A

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

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23
Q

What can damage LMNs?

A

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

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24
Q

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

A

Loss of reflexes
Atrophy
Flaccid paralysis
Fibrillations

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25
Q

What changes can UMN lesions produce?

A 
changes in movement control
Paresis or paralysis
Loss of fractionation of movement
Abnormal reflexes
Velocity-dependent hypertonia
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26
Q

What are signs and symptoms of UMN syndrome?

A 
weakness
spasticity (increased tone, hyperactive reflexes)
clonus
babinski's sign
loss of fine voluntary movements
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27
Q

What are signs and symptoms of LMN syndrome?

A 
weakness or paralysis
decreased superficial reflexes
hypoactive deep reflexes
decreased tone
fasciculations and fibrillations
severe muscle atrophy
28
Q

What is fractionation?

A

the ability to activate individual muscles independently of other muscles

29
Q

What does loss of fractionation interfere with?

A

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

30
Q

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

A

dorsiflexing the ankle

31
Q

What is Babinski’s sign?

A

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

32
Q

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

A

muscle stretch hyperreflexia
clonus
clasp-knife response

33
Q

What does excessive muscle contraction occur?

A

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

34
Q

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

A

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

35
Q

What is unsustained clonus?

A

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

36
Q

What is sustained clonus?

A

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
Q

When does the clasp-knife response occur?

A

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

38
Q

What elicits the clasp-knife response?

A

type II afferents

39
Q

What does spasticity do?

A

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

40
Q

What is UMN hypertonia caused by?

A
  1. myoplasticity

2. spasticity

41
Q

Myoplasticity:

A

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

42
Q

Spasticity:

A

is neuromuscular overactivity, secondary to an UMN lesion

43
Q

What happens by age 4 in normal development?

A

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

44
Q

What does damage to the corticospinal tracts during development cause?

A

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

45
Q

What are mechanisms of spasticity?

A
  1. developmental spasticity
  2. adult-onset cerebral spasticity
  3. spinal spasticity
46
Q

What does a typical stroke interrupt?

A

corticospinal and corticoreticular tracts on one side of the brain

47
Q

Reticulospinal tract overactivity is the primary cause of what?

A

stoke spasticity due to diminished cortical inhibition

48
Q

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

A

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

49
Q

What can hyperreflexia limit?

A

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

50
Q

Common impairments in UMN lesions?

A 
Abnormal synergy
Abnormal contracture
Hyperreflexia
Hypertonia 
Muscle contracture
Muscle tone
Muscle overactivity
Myoplasticity
Paresis
Spasticity
51
Q

What are some measuring tools for hypertonia?

A

Ashworth Scale or modified AS
EMG
Torque/force resistance

52
Q

What is an EMG used to determine?

A

which factors are contributing to movement impairment

53
Q

What factors can contribute to movement impairment?

A

hyperreflexia
contracture
cocontraction
inappropriate timing of muscle activity

54
Q

What are types of UMN lesions?

A 
Spastic cerebral palsy (CP)
Stroke or cerebrovascular accident (CVA)
Spinal cord injury (SCI)
Traumatic brain injury (TBI)
Multiple sclerosis (MS)
Tumors
55
Q

What leads to movement dysfunction?

A

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

56
Q

What is included in motor disorders in spastic CP?

A

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
Q

What is the most frequently affected region in a stroke?

A

MCA (middle cerebral arterty)

58
Q

What does a stroke cause damage to?

A

damage to corticospinal, corticoreticular and corticobrainstem neurons

59
Q

What connections does a stroke disrupt?

A

cortical connections with the spinal cord, brainstem and cerebellum

60
Q

What are motor disorders after a MCA the consequence of?

A

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

61
Q

What does the reticulospinal tract provide?

A

voluntary movement of the paretic limbs.

62
Q

Complete SCI:

A

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

63
Q

Incomplete SCI:

A

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

64
Q

After SCI, what produces excessive resistance to muscle stretch?

A

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

65
Q

In people with SCI, what limits movement?

A

hyperreflexia and contracture

Neuro (23 decks)

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