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632: Neuroanatomy-Neuroscience > UMN Circuits > Flashcards

UMN Circuits Flashcards

1
Q

UMNs provide all of the motor signals from where to where?

A

From the brain to the spinal cord and from the cerebrum to the cranial nerve lower motor neurons in the brainstem

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2
Q

What do medial UMNs signal?

A

LMNs that innervate postural and girdle muscles

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3
Q

The UMNs that synapse throughout the ventral horn contribute to what?

A

Background levels of excitation in the cord and facilitate local reflex arcs

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4
Q

Give an example in which the medial UMNs fire

A

If a loud noise occurs behind a person, the eyes and face turn toward the sound, before the person is consciously aware of the auditory stimulus

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5
Q

What are the 4 tracts that deliver signals that control posture and gross movements to medial LMN pools in the spinal cord? Where do each originate?

A
  • Reticulospinal (brainstem)
  • Medial vestibulospinal (brainstem)
  • Lateral vestibulospinal (brainstem)
  • Medial corticospinal (cerebral cortex)
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6
Q

The reticulospinal tract facilitates motor neurons where?

A

To bilateral postural muscles and to gross limb movement muscles of the entire body

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7
Q

Where do medial vestibulospinal tracts receive information from?

A

From the vestibular apparatus in the inner ear about head movement and position

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8
Q

The medial vestibulospinal tract facilitates motor neurons where?

A

to neck muscles

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9
Q

The lateral vestibulopsinal tract responds to what type of information?

A

Gravity information from the vestibular apparatus

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10
Q

How does the lateral vestibulospinal tract incorporate gravity information to postural muscles?

A

When a person is upright, the lateral vestibulospinal tracts are continuously active to maintain the center of gravity over the base of support, responding to the slightest destabilization

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11
Q

The medial corticospinal tract is a direct connection between what to things?

A

The cerebral cortex to the spinal cord

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12
Q

Medial corticospinal neurons synapse with LMNs that control what?

A

Neck, shoulder, and trunk muscles

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13
Q

What do lateral UMNs signal?

A

LMNs that innervate muscles used for fractioned movement and muscles in the face and neck

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14
Q

What is fractioning?

A

the ability to activate individual muscles independently of other muscles

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15
Q

What is fractioning essential for?

A

Normal movement of the hands, enabling us to button a button, press individual keyboard keys, or pick up small objects

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16
Q

Without fractioning, what would occur?

A

The fingers and thumb would act as a single unit, as they do when picking up a water bottle

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17
Q

What are the 2 UMN tracts that descend in the lateral spinal cord and synapse with laterally located LMN pools in the ventral horn?

A
  • rubrospinal

- lateral corticospinal

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18
Q

What is the most important pathway controlling voluntary movement?

A

the lateral corticospinal tract

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19
Q

How does the lateral corticospinal tract fractionate movement?

A

By activating inhibitory neurons to prevent unwanted muscles from contracting

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20
Q

The corticospinal tracts in the lower medulla form the pyramids and then continue down the brainstem, what occurs when they reach the junction between the medulla and spinal cord?

A
  • 88% of them cross over to the contralateral side and synapse with LMNs in the contralateral spinal cord
  • Only 10% travel ipsilaterally
  • The remaining 2% travel in the medial corticospinal tract
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21
Q

Where do lateral corticospinal tracts arise?

A

In the primary motor, premotor, and supplementary motor area

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22
Q

Where is the primary motor cortex located?

A

Anterior to the central sulcus, in the precentral gyrus

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23
Q

What does the primary motor cortex provide?

A

Precise, predominantly contralateral control of movements of the limbs

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24
Q

How are corticospinal cell bodies in the primary motor cortex arranged?

A

Somatotopically in an inverted homunculus

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25
Q

What are the 2 regions anterior to the primary motor cortex?

A
  • the premotor area

- the supplementary motor area

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26
Q

Where is the lateral premotor area located?

A

Anterior to the primary motor cortex on the lateral surface of the hemisphere

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27
Q

Where is the supplementary motor area located?

A

Anterior to the primary motor cortex on the superior and medial surface

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28
Q

Where do corticobrainstem fibers arise from and where do they project to?

A

They arise in the cerebral cortex and then project to cranial nerve nuclei in the brainstem

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29
Q

What do the corticobrainstem tracts facilitate?

A

Movements of facial, vocalizing, eating, and large superficial neck muscles via LMNs in cranial nerves

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30
Q

What are the 2 nonspecific UMN tracts?

A
  • ceruleospinal

- raphespinal

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31
Q

When active what do the ceruleospinal and raphespinal tracts facilitate?

A

LMNs to skeletal muscles

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32
Q

Disorders of the motor system may cause what 7 things?

A
  • Paresis and paralysis
  • Muscle atrophy
  • Involuntary muscle contractions
  • Abnormal muscle tone
  • Abnormal reflexes
  • Disturbances of movement efficiency and speed
  • Impaired postural control
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33
Q

What is paralysis?

A

the complete loss of voluntary contraction

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34
Q

What is paresis?

A

the partial loss of voluntary contraction

35
Q

What is hemiplegia?

A

Weakness affecting one side of the body

36
Q

What is paraplegia?

A

Weakness that affects the body below the arms

37
Q

What is tetraplegia?

A

Weakness that affects all four limbs

38
Q

What does a complete lesion of a peripheral nerve cause?

A

Paralysis because LMNs are the only pathway from the CNS to skeletal muscle

39
Q

What do UMN lesion cause?

A

Paresis because some of the descending motor tracts may be intact

40
Q

What is muscle atrophy?

A

the loss of muscle bulk

41
Q

What is the difference between disuse and neurogenic atrophy?

A
  • Disuse atrophy is the result of a lack of muscle use

- Neurogenic atrophy is caused by damage to the nervous system

42
Q

What produces the most severe atrophy and why?

A

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

43
Q

What are 7 types of spontaneous involuntary contractions?

A
  • Muscle spasms
  • Cramps
  • Fasciculations
  • Myoclonus
  • Tremors
  • Fibrillations
  • Abnormal movements generated by dysfunctional basal ganglia
44
Q

What is a muscle spasm?

A

sudden involuntary contractions of muscle

45
Q

What is a muscle cramp?

A

severe and painful muscle spasms

46
Q

What are fasciculations?

A

quick twitches of muscle fibers of a single motor unit visible on the skin surface (eye twitches with anxiety)

47
Q

What is myoclonus?

A

brief, involuntary contractions of a muscle or group of muscles (hiccups, head bob while falling asleep, etc.)

48
Q

What are tremors?

A

involuntary rhythmic movements of a body part

49
Q

What are fibrillations?

A

brief contractions of single muscle fibers not visible on the surface of the skin

50
Q

What are fibrillations a result of?

A

UMN or LMN lesions

51
Q

Which of the involuntary movements are always pathologic?

A

Fibrillations

52
Q

What is muscle tone?

A

the resistance to stretch in resting muscle

53
Q

What is the difference between hypotonia and flaccidity?

A
  • Hypotonia is an abnormally low resistance to passive stretch.
  • Flaccidity is the lack of resistance to passive stretch (complete loss of muscle tone)
54
Q

What 3 things can cause hypotonia or flaccidity?

A
  • LMN lesions
  • acute UMN lesions
  • developmental disorders, usually caused by brain hypoxia/ischemia, intracranial hemorrhage, or genetic/metabolic disorders
55
Q

What are the 2 types of hypertonia?

A
  • spasticity

- rigidity

56
Q

In spasticity, the amount of passive movement depends on what?

A

The velocity of movement

57
Q

Spasticity is usually a sign of what?

A

UMN lesion

58
Q

In rigidity, resistance to passive movement is _____, regardless of the speed of the force application

A

constant

59
Q

Describe decerebrate rigidity position

A

The limbs and trunk are extended, the limbs are internally rotated, and the feet are plantarflexed

60
Q

Describe decorticate rigidity position

A

The upper limbs are flexed and the lower limbs are extended with the feet plantarflexed

61
Q

Describe spinal/cerebral shock

A

This condition occurs when an acute UMN lesion interrupts descending motor commands, which means the LMNs affected become temporarily inactive owing to loss of descending facilitation and edema affecting the area of the lesion

62
Q

What types of things can damage LMNs?

A
  • trauma
  • infection
  • degenerative or vascular disorders
  • tumors
63
Q

What occurs if LMN cell bodies and/or axons are destroyed?

A

Muscles undergo:

- loss of reflexes
- atrophy
- flaccid paralysis
- fibrillations
64
Q

How are UMNs damaged?

A
  • SCI
  • spastic CP
  • MS
  • TBI
  • stroke
65
Q

What 4 things are the result of UMN lesions?

A
  • paresis or paralysis
  • loss of fractionation of movement
  • abnormal reflexes
  • spasticity
66
Q

Paresis occurs in UMN lesions as a consequence of what?

A

inadequate facilitation of LMNs

67
Q

Paresis is common in what type of patients?

A
  • stroke (CVA)
  • spastic CP
  • TBI
  • incomplete SCI
68
Q

Where does paralysis occur in UMN lesions?

A

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

69
Q

Loss of fractionation interferes with what?

A

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

70
Q

In the lower limb, the loss of fractionation interferes with what?

A

dorsiflexing the ankle

71
Q

What type of abnormal cutaneous reflexes occur in UMN lesions?

A

Babinski’s sign which is extension of the great toe accompanied by fanning of the other toes when the bottom of the foot is firmly stroked

72
Q

In people with SCI what may occur in response to cutaneous stimuli?

A

muscle spasms that begin after recovery from spinal shock

73
Q

What are the 3 most common abnormal reflexes in those with chronic SCIs?

A
  • Muscle stretch hyperreflexia
  • Clonus
  • Clasp-knife response
74
Q

What is muscle stretch hyperreflexia?

A

Loss of inhibitory corticospinal input combined with LMN and interneuron development of enhanced excitability results in excessive LMN response to afferent input from stretch receptors

75
Q

What is the result of muscle stretch hyperreflexia?

A

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

76
Q

What is clonus?

A

involuntary, repeating, and rhythmic muscle contractions

77
Q

What type of clonus is always pathologic?

A

sustained clonus

78
Q

When is sustained clonus produces?

A

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

79
Q

Describe the clasp-knife response

A

When a paretic muscle is slowly and passively stretched, resistance drops at a specific point in the ROM, this is called the clasp-knife response

80
Q

What afferent fibers elicit the clasp-knife response?

A

Type II

81
Q

What are the adverse side effects of velocity-dependent hypertonia?

A
  • limits joint ROM
  • interferes with function
  • may cause deformity
82
Q

Velocity-dependent hypertonia is caused by what?

A

muscular changes (myoplasticity) and/or spasticity

83
Q

What is myoplasticity?

A

Adaptive structural changes within a muscle in response to changes in neuromuscular activity level and to prolonged positioning (i.e. contractures)

84
Q

What is spasticity?

A

Neuromuscular overactivity, secondary to an UMN lesion

632: Neuroanatomy-Neuroscience (26 decks)

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