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Neurorehab > UMN and LMN system - Exam 3 > Flashcards

UMN and LMN system - Exam 3 Flashcards

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1
Q

Signs of lower motor neuron destruction

A
  1. Loss of reflexes
  2. Atrophy
  3. Flaccid paralysis
  4. Fibrillations
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2
Q

Causes of lower motor neurons

A
  1. Trauma
  2. Infection
  3. Disease
  4. Vascular disorders
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3
Q

Polio results in….

A

damage to muscle fibers

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4
Q

Polio infects and targets….

A
  1. Infects brain and spinal cord

2. Targets lower motor neurons

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5
Q

Types of polio…

A
  1. Subclinical
  2. Non-paralytic
  3. Paralytic
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6
Q

95% of all cases of polio are what type..

A

Subclinical

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7
Q

Symptoms of post-polio syndrome

A
  1. Onset of weakness in muscles
  2. Pain in joints and muscles
  3. Fatigue
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8
Q

What are PT treatments for polio?

A
  1. Appropriate exercise
  2. Energy saving techniques
  3. Joint protection
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9
Q

Symptoms of upper motor neuron syndrome…

A
  1. Paresis or paralysis
  2. Loss of fractionation movements
  3. Abnormal reflexes
  4. Velocity dependent hypertonia
  5. in specific types of UMN lesions:
    a. Abnormal contraction
    b. abnormal muscle synergies
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10
Q

What is paralysis?

A

Complete loss of voluntary control muscles

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11
Q

Paralysis occurs…

A

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

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12
Q

What causes loss of fractionation?

A

Caused by injury to lateral corticospinal tract

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13
Q

How is loss of fractionation demonstrated?

A

By fingers of involved hand acting as a single unit in the upper extremity

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14
Q

What causes babinski sign?

A

Occurs with damage to the corticospinal tract and you can use the Babinski sign test.

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15
Q

What causes muscle spasms?

A
  1. may occur in response to cutaneous stimuli…
  2. follows spinal shock
  3. abrupt flexion of LEs in response to gentle touch
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16
Q

Muscle stretch hyperreflexia…

A

Excessive muscle contraction when muscle spindles are stretched due to excessive firing of the LMNs

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17
Q

What is clonus?

A

Involuntary, repeating, rhythmic muscle contractions

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18
Q

What induces clonus?

A

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

  1. muscle stretch
  2. cutaneous and noxious stimuli
  3. attempts at voluntary movement
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19
Q

Hypertonia…

A

excessive resistance to stretch

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20
Q

What causes hypertonia?

A
  1. Myoplasticity

2. Overactive neural input to muscles

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21
Q

What is myoplasticity?

A

the ability of the muscle to make adaptive changes in response to neuromuscular activity level and prolonged positioning

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22
Q

What is neurospasticity?

A

Neuromuscular overactivity secondary to an UMN lesion and results in excessive active contraction

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23
Q

What causes spasticity?

A
  1. Hyperreflexia

2. Brainstem UMN overactivity

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24
Q

What are contractures?

A

The adaptive shortening of the muscles- tendon unit and soft tissues that cross or surround a joint resulting in significant resistance to passive or active stretch and limitation of ROM

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25
Contractures result from...
1. loss of sarcomeres 2. Interarticular pathology (joint adhesions, osteophytes...) 3. Fibrous changes in connective tissue
26
What is paresis?
Decreased ability to generate the level of force required for a task.
27
What is a complete spinal cord injury?
Loss of all descending neuronal control below the level of the lesion
28
What is an incomplete spinal cord injury?
1. Functioning of some ascending and/or descending fibers are preserved 2. Reduction of type 1 muscle fibers and predominance of type IIb fibers
29
Clinical signs of spinal spasticity...
1. Velocity dependent increase in tonic stretch reflexes 2. Brisk deep tendon reflexes 3. Involuntary flexor and extensor spasms 4. Clonus 5. Hyperreflexia
30
What is used to decrease excessive muscle tone produced by hyperreflexia?
Baclofen
31
What does Baclofen causes?
Causes inhibition in spinal cord stretch reflex pathways
32
Benefits of Baclofen...
1. Decrease spasms 2. Decrease pain 3. Decrease sleep disturbance 4. Increase bladder function 5. Increase mobility
33
Treatments used to active neuromuscular system below level of lesion.
1. Treadmill training with body weight support and FES, which can activate stepping pattern generators and elicit a walking EMG pattern at hips and knees
34
Stroke occurs...
Typically in the middle cerebral artery, resulting in damage to the corticospinal, corticreticular, and corticobrainstem tracts
35
Myoplasticity post stroke...
Paretic muscles exert excessive resistance to muscle stretch due to changes in the muscle... 1. contracture 2. increased weak binding of actin and myosin
36
After a CVA, what factor limits UE activity?
Weakness...
37
After a CVA, what provides voluntary control of the paretic limb?
the reticulospinal tract and it mainly afffects the proximal joints
38
Interventions Post CVA...
1. Movements against resistance 2. Bicycling 3. Functional retraining 4. partial body weight support gait training 5. constraint induced movement 6. Botox injections
39
What is spastic cerebral palsy?
1. Abnormal supraspinal influences | 2. Failure of normal neuronal selection
40
What impairs UE function for CP pts?
1. Poor Coordination 2. Hyperreflexia 3. Contracture
41
Interventions for CP
1. Task oriented gait training 2. selective dorsal rhizotomy in some cases 3. Constraint-induced movement therapy (constraining the less involved UE) 4. Botox injections 5. Functional training
42
Amyotrophic lateral sclerosis destroys...
1. UMNs | 2. Brainstem and spinal cord LMNs bilaterally
43
Amytrophic lateral sclerosis leads to...
1. Paresis 2. Myoplastic hypertonicity 3. Hyperreflexxia 4. Babinski sign 5. Atrophy 6. Fasciculations 7. Fibrillations
44
What are common characteristic of UMN lesions?
The force exerted by a muscle is produced by intrinsic, passive, and active factors... 1. Paresis 2. Abnormal cutaneous reflexes 3. Abnormal timing of muscle activity 4. Myoplastic hypertonicity
45
What are uncommon characteristics of UMN lesions?
1. Hyperreflexia 2. Clonus 3. Clasp-Knife Phenomenon 4. Reflex Irradiation 5. Abnormal co-contraction of antagonists
46
Three types of polio...
1. Spinopolio 2. Bulbarpolio 3. Spinobulbar polio
47
UMN project from and to...
Project from cortical and brainstem centers to LMN and to interneurons in the brainstem and spinal cord
48
What do upper motor neurons do?
Provides all the motor signals from the brain to the spinal cord and from the cerebrum to the cranial nerve LMNs in the brainstem
49
Where do UMN synapse in the medial/lateral/ and ventral horn?
Read and discover in the book..... need answer
50
Postural and gross movements begin...
in the brainstem and proceed to the LMNs
51
What are the tracts of the medial upper motor neuron tracts?
1. Medial reticulospinal tract 2. Medial vestibulospinal tract 3. Lateral vestibulospinal tract 4. Medial corticospinal tract
52
Funiculi....
a small bundle of nerve fibers in the spinal cord
53
Describe the medial reticulospinal tract process.
1. Begin in the reticular formation 2. Project ipsilaterally and contralaterally throughout spinal cord 3. Synapses with LMNs to postural and gross limb movements
54
Function of reticulospinal tracts
1. Coordination of trunk and postural muscles when walking 2. Aids in directing head movement in response to audio or visual stimulation 3. Anticipatory postural adjustments and reaching
55
Describe the medial vestibulospinal tract process
1. Begins at the medial vestibular nuclei 2. Axons project to spinal cord, ipsilaterally and contralaterally 3. Those that crosses, crosses at the level of nuclei 4. Axons descend int he cervical spinal cord and terminate on LMNs in the ventral horn at the cervical and thoracic levels
56
Function of vestibulospinal tract
Adjust the position of the head in response to changes in posture
57
Describe the lateral vestibulospinal tract
1. Begins at the lateral vestibular nucleus 2. Axons project ipsilaterally 3. Descend the entire length of the spinal cord 4. Terminates on interneurons that facilitate LMNs innervating extensor muscles WHILE inhibiting LMNs to the flexors
58
Function of lateral vestibulospinal tract
Maintain COG over BOS and to respond to any type of destablization
59
Describe medial (anterior) corticospinal tract
1. Descends from the motor cortex through the pyramids to the spinal cord 2. Ipsilateral tract 3. Synapse in the cervical and thoracic spinal cord
60
Function of medial (anterior) corticospinal tract
Convey information to LMNs that control the neck, shoulder, and trunk muscles
61
Tracts that coordinate fractionation and fine movements
1. Lateral corticospinal 2. Rubrospinal 3. Corticobrainstem
62
Process of lateral corticospinal tract
1. Begins at the cerebral motor cortex 2. Projects through the internal capsule, cerebral peduncles, anterior pons and pyramids down the lateral funiculus of the entire spinal cord 3. Cross in the pyramids 4. End in the lateral and dorsal horns
63
Function of lateral corticospinal tract
1. Control of voluntary movement | 2. Fractionation in distal limbs
64
What is the considered the most important pathway controlling voluntary movement?
Lateral corticospinal tract
65
Of all the corticospinal fibers... 90% are where
Lateral tracts
66
Process of rubrospinal tract
1. Begins at the red nucleus 2. Crosses the midbrain 3. Project through pons, medulla, and spinal cord 4. Ends in the lateral funiculus where it synapses with LMN of UE flexion
67
Function of rubrospinal tract
1. Primarily involved in the upper extremities | 2. Assists with contralateral UE flexion, inhibits UE extension
68
Describe the corticobrainstem tracts (corticobulbar, corticonuclear tracts)
1. Begins in the primary motor cortex | 2. Projects to cranial nerve nuclei in the brainstem (V, VII, IX, X, XI, XII)
69
Function of corticobrainstem
Facilitates LMNs innervating muscles of face, tongue, pharynx, and larynx, trapezius, and SCM
70
What are non-specific UMNs?
Two tracts descending from bilateral nuclei in the brainstem 1. Raphespinal tract 2. Ceruleospinal tract
71
Function of non-specific UMN
To enhance activity of interneurons and motor neurons in the spinal cord
72
Raphespinal tract function
releases serotonin to modulate activity of the LMN in the spinal cord
73
Ceruleospinal tract function
releases norepinephrine which facilitates activity in the spinal cord
74
When are non-specific UMN activated?
During excessive limbic activity
75
What are signs of motor neuron lesions?
1. Paresis or paralysis 2. Muscle atrophy 3. Involuntary muscle contraction 4. Abnormal muscle tone
76
Hemiplegia
Loss of strength on one side of body
77
Paraplegia
Loss of strength below the arms
78
Tetraplegia (Quadriplegia)
Loss of strength in all four limbs
79
Tremors
Involuntary, rhythmic movements of a body part
80
Fibrillations
Brief contractions of single muscle fibers not visible on skin Rapid, irregular, and unsynchronized contraction of muscle fibers
81
Tone
Resistance to passive stretch
82
Hypotonia and flaccidity
Low or absent resistance to passive stretch
83
What causes hypotonia and flaccidity?
1. LMN lesions 2. Acute UMN lesions 3. Developmental disorders
84
Hypertonia
Abnormally strong resistance to passive stretch
85
Types of hypertonia
1. Velocity dependent (spasticity) | 2. Velocity independent (rigidity)
86
Types of rigidity
1. Decerebrate | 2. Decorticate
87
Decerebrate rigidity and cause
Extensor posturing Caused by severe midbrain lesion a. damage below red nucleus b. Rubrospinal tract wiped out
88
Decorticate rigidity and cause
Upper extremity flexor posturing Caused by severe lesions superior to the midbrain a. Disruption of the corticospinal tract b. Red nucleus is disinhibited
89
During "shock"...
Stretch reflexes cannot be elicited and muscles are hypotonic
90
Following "shock"...
Muscle tone increases as a result of neural changes. | Interneurons and LMNs resume activity

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