Exam II Flashcards

1
Q

Pyramidal system

A

Drive voluntary movements by activating ventral horn lower motor neurons directly, UMN pathways

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2
Q

Extrapyramidal system

A

Modulate voluntary movements by regulating the motor neurons indirectly, not part of the UMN pathways, tracts outside of the pyramids

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3
Q

Lateral MTs

A

innervate distal limb muscles for fine motor control and perform fractionated movements

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4
Q

Medial MTs

A

innervate axial/proximal girdle muscles to control posture and perform gross movements, involuntary coordinated responses that are mostly initiated in brainstem centers

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5
Q

Non-specific MTs

A

Do not activate or regulate any specific movements, activate during stress or emotions

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6
Q

Lateral corticospinal tracts

A

Most important tract controlling voluntary movements, unique ability to generate fractionated movements by using interneurons to inhibit unwanted neighboring muscles

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7
Q

Rubrospinal tracts

A

Arises in red nucleus in midbrain, decussates and descends to innervate contralateral motor neurons that activate wrist/finger extensors. In humans, it is small and makes minor contribution to control of distal upper limb muscles

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8
Q

Reticulospinal tracts

A

to regulate muscle activity in trunk and proximal limb muscles, help with gross movements needed during walking, help with automatic anticipatory postural adjustments during movements like reaching, carrying objects, control of autonomic functions

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9
Q

Medial vestibulospinal tract

A

Receives information about head position in space from vestibular nuclei, Regulates motor neurons bilaterally to control neck and upper back muscles (extensors)

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10
Q

Lateral vestibulospinal tract

A

Regulates motor neurons ipsilaterally to activate trunk paravertebrals and proximal LE extensors while inhibiting flexors to maintain upright antigravity posture within BOS

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11
Q

Medial/Anterior corticospinal tracts

A

activate neck, shoulder and trunk muscles, prepare the postural system for intended movements and coordinate posture with the other medial tracts

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12
Q

Nonspecific motor tracts

A

Facilitate all types of motor neurons across spinal cord, Activated during intense stress and emotions, involved in sending descending pain-regulating information

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13
Q

Corticobulbar (corticobrainstem) tracts

A

control of muscles in head, activate cranial motor nerve nuclei bilaterally that innervate muscles of face (except lower half muscles), mastication, tongue, pharynx, larynx, and some neck muscle (SCM/traps)

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14
Q

Cortical motor areas

A

Premotor and supplementary motor area plan for complex movements, in association with M1

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15
Q

Alpha (α MNs) motor neurons

A

large cell bodies, large myelinated axons – connect to extrafusal muscles

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16
Q

Gamma (γ MNs) motor neurons

A

medium cells bodies and myelinated axons – connect to intrafusal spindle muscle fibers

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17
Q

Synergy involving muscles at same joint

A

activate other muscles at same joints
Phasic synergy - modulated in both amplitude and timing
by Ia afferents
monosynaptic

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18
Q

Synergy involving muscles at neighboring joints

A

activate muscles at other neighboring joints
Tonic synergy - modulated only in amplitude
by II afferents
bisynaptic/polysynaptic

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19
Q

Hemiplegia or -paresis

A

(lesion of corticospinal tracts high up in the brain, may retain some voluntary control due to intact reticulospinal tracts) – stroke, TBI, CP

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20
Q

Quadriplegia or -paresis

A

(lesion of MTs in higher spinal levels) - SCI

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21
Q

Paraplegia or -paresis

A

(lesion of MTs in lower spinal levels) - SCI

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22
Q

Hypertonia

A

abnormal high resistance to passive stretch

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23
Q

Spasticity

A

velocity dependent – in UMN pyramidal/extrapyramidal MT lesions (stroke, SCI)

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24
Q

Rigidity

A

velocity-independent – in basal ganglia lesions (Parkinson’s disease)

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25
Q

Babinski’s sign

A

due to lack of inhibitory control by corticospinal tracts on withdrawal reflex receptive fields, normal till 6 months age as corticospinal tracts not myelinated by then.

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26
Q

Signs of motor cortex/tract lesions (UMN lesions)

A

Paresis/paralysis
Abnormally high tone
Abnormally high reflex activity
Loss of fractionated movements
Abnormal synergies
Myoplasticity
Abnormal co-contractions – CP

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27
Q

Signs of motor neuron lesions (LMN lesions)

A

Paralysis or paresis - flaccidity
Decrease in muscle tone – hypotonia/flaccidity
Decrease or loss of reflexes (hyporeflexia)
Neurogenic atrophy – due to lack of trophic support to muscles

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28
Q

Clonus

A

Involuntary reflexive repeating contractions of a single muscle group in response to quick stretch – a manifestation of hyper-reflexia

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29
Q

Cause of Clonus

A

lack of descending MT control, allowing activation of oscillating neural networks in spinal cord

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30
Q

Myoplasticity

A

Adaptive changes in muscles in response to changes in neuromuscular activity level, occurs due to increased number of weak actin-myosin bonds, contracture.

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31
Q

feedforward mechanism

A

Anticipatory use of sensory information

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32
Q

feedback mechanism

A

Use of sensory information during and after movement to make corrections/adjustments

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33
Q

Mechanoreceptors

A

Touch, pressure, stretch, vibration

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34
Q

Thermoreceptors

A

respond to heating/cooling

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35
Q

Chemoreceptors

A

respond to chemicals

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36
Q

Somatosensations from skin (cutaneous)

A

touch, temperature, nociception

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37
Q

Somatosensations from MSK system

A

proprioception, nocioception

38
Q

Tonic receptors

A

Pressure receptors – therapeutic touch

Stretch receptors in muscle

39
Q

Phasic receptors

A

Tendon stretch receptors
Pressure receptors
Thermoreceptors

40
Q

Nuclear bag fibers

A

more elastic – stretch quickly

41
Q

Nuclear chain fibers

A

less elastic – stretch slowly

42
Q

Ia muscle spindle

A

responds better to quickly-changing muscle length using ‘phasic’ discharge pattern – velocity-dependent discharge - dynamic sensitivity

43
Q

II muscle spindle

A

responds better to slowly-changing muscle length using ‘tonic’ discharge pattern – not dependent on velocity of change in muscle length - static sensitivity

44
Q

Gamma dynamic

A

activate bag fibers

45
Q

Gamma static

A

activate both bag and chain fibers

46
Q

Axons for DC/ML pathways

A

stay on same side of spinal cord and travel up to medulla

47
Q

Axons for AL (ST/Divergent) pathways

A

enter the spinal cord and synapses with the 2nd order neuron right away (which crosses over)

48
Q

Dorsal column/medial lemniscus sensations

A

Light touch, proprioception, vibration

49
Q

Anterolateral columns (spinothalamic + divergent pathways)

A

Convey nociception/pain, temperature and crude touch information to brain

50
Q

Spinothalamic pathway

A

fast, discriminative pain and temperature and crude touch, somatotopic arrangement in S1, 3 neuron pathways

51
Q

Divergent pathways

A

slow, non-specific, crude nociception – no somatotopy, 2 or 3 neuron pathways, more associated with chronic pain

52
Q

Primary somatosensory area (S1)

A

somatotopic arrangement of sensory information (touch, proprioception, nociception, temperature)

53
Q

Secondary somatosensory area

A

further processing of S1 information by sending to association/cognitive areas to provide ‘perception’ to incoming sensory information

54
Q

1st order neuron

A

C fibers, Synapse with interneurons in dorsal horn, Interneurons release substance P, Can get sensitized by repeated stimulation during chronic injury

55
Q

2nd order ascending neurons

A

Spinoreticular, Spinomesencephalic, Spino-emotional

56
Q

3rd order neurons (only for spino-emotional)

A

To wide areas in cortex – anterior cingulate, insula, amygdala, dorsal prefrontal cortex

Affect emotions, behavior, personality

57
Q

Unconscious Spinocerebellar pathways

A

Convey information needed to monitor and adjust movement coordination to cerebellum

dorsal SC: stays ipsi
ventral SC: crosses over twice

58
Q

Fidelity

A

determine precision of location, intensity, timing

59
Q

High-fidelity information

A

light touch, proprioception, sharp discriminative pain/temperature

60
Q

Low fidelity information

A

aching pain, itch

61
Q

Conscious relay pathways

A

light touch, proprioception, discriminative pain/temperature - high fidelity

62
Q

Conscious divergent pathways

A

info conveyed to many higher locations – conscious and emotional levels - low fidelity – aching pain/chronic pain

63
Q

Non-conscious pathways

A

proprioceptive info to cerebellum for postural control

64
Q

Pre-embryonic timeline

A

conception to day 14

65
Q

Embryonic timeline

A

Day 15 to end of wk 8

66
Q

Fetal timeline

A

Start of 9th wk to birth

67
Q

Pre-embryonic stage

A

Starts with repeated cell division, solid sphere, cavity opens, development of embryonic disc

68
Q

Embryonic stage

A

all organs are formed

69
Q

Ectoderm

A

epidermis, sensory organs, the Nervous System

70
Q

Mesoderm

A

dermis, muscles, skeleton, excretory, circulatory systems

71
Q

Endoderm

A

gut, liver, pancreas, respiratory system

72
Q

Neural tube

A

primordium of the CNS (brain and spinal cord)

73
Q

Neural crest

A

group of cells that break off of the tube, forms much of PNS (DRGs, sensory CNs, ANS, schwann cells, endocrine organs etc).

74
Q

Hindbrain

A

medulla, pons, cerebellum, 4th ventricle

75
Q

Midbrain

A

Midbrain

76
Q

Forebrain

A

diencephalon and telencephalon

77
Q

Telencephalon

A

cerebral hemispheres and basal ganglia

78
Q

Diencephalon

A

thalamus, hypothalamus

79
Q

Sensory loss may proceed in the following order of descending diameter

A

Sensory loss may proceed in the following order of descending diameter

  1. Conscious proprioception/light touch
  2. Cold
  3. Fast nociception (sharp pain)
  4. Heat
  5. Slow nociception (aching pain, tingling, prickling sensations)

During recovery, sensation returns in the reverse order

80
Q

Referred pain mechanism

A

Occurs when branches of nociceptive fibers from internal organs (autonomic) and branches of nociceptive fibers from skin (somatosensory) converge on same 2nd order neuron in dorsal horn or thalamus, and those pathways become sensitized

81
Q

Motor pools

A

cluster of motor neurons that connect to single muscle belly

82
Q

Withdrawal reflex

A

Reflexive withdrawal from stimulus

Elicited by painful cutaneous stimuli

Needs synaptic interactions between neurons at various spinal cord levels

83
Q

Crossed extension reflex

A

Reflexive extension of the other LE to support posture and prevent falling

84
Q

Reciprocal inhibition

A

During agonist muscle contraction or reflex activity, inhibition of antagonist is achieved by activating inhibitory interneurons in spinal cord that inhibit motor neurons of the antagonist group.

85
Q

Sensory nerve conduction velocity (NCV) studies

A

to test the integrity of peripheral nerves following injuries

86
Q

Main factors that limits functional activities after stroke

A

paresis, loss of fractionated movement, hypertonia, abnormal synergies and myoplastic changes

87
Q

Main factors that limit functional mobility after SCI

A

paresis/paralysis, stretch hyperreflexia and myoplastic changes

– sometime hyperflexia can be useful for SCI patients

88
Q

Light touch

A

via A beta afferents, skin pressure (light), vibration, skin stretch

89
Q

Coarse touch

A

by free nerve endings via Aδ and C afferents

Pleasant touch
Pressure (firm/deep)
Tickle/itch
Nociception (pinch)

90
Q

Spinoreticular

A

to reticular formation – arousal, attention changes due to pain

91
Q

Spinomesencephalic

A

to superior colliculus (via PAG) –turning head/eye towards painful stimuli

92
Q

Spino-emotional

A

to midline/intralaminar nuclei in thalamus