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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
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

Neuro (23 decks)

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