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Neuro Anatomy > Week 6 Notes On Control Of Movement by Central Motor Pathways > Flashcards

Week 6 Notes On Control Of Movement by Central Motor Pathways Flashcards

1
Q

somatomotor pathways

A

originate from UMNs in cerebral cortex and brainstem; axons from UMNs travel to brainstem and spinal cord to influence activity in LMNs

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2
Q

role of descending somatomotor pathways

A
  • maintain appropriate body position (posture)
  • permit the animal to move around in their environment (locomotion)
  • control directed movement of the body relative to external environment
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3
Q

effective motor output acomplished

A

by coordination of efforts of multiple somatomotor pathways and cerebellum and basal ganglia which interact w/ somatomotor pathways to facilitate coordination

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4
Q

final common pathway for motor system

A

LMN in brainstem or spinal cord; LMN damaged UMN rendered useless

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5
Q

hierarchical organization of neural circuitry

A
  1. Spinal cord (lowest)
  2. Brainstem
  3. Motor cortex (highest)
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6
Q

spinal cord responsible for

A
  • most basic or automatic behaviors ie maintenance of muscle tone, reflexes, and v limited ability to generate some movement involved in locomition
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7
Q

sensory input to spinal cord

A
  • directly relayed to LMNs

- indirectly relayed via network of interneurons

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8
Q

which brainstem nuclei give rise to motor pathways

A

vestibular nuclei, red nucleus, UMNs of pontine and Medullary Reticular Formation and Rostral Colliculus

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9
Q

brainstem nuclei contain

A

UMNs which project to spinal cord or brainstem to influence LMNs or spinal cord reflex circuits

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10
Q

motor nuclei in brainstem receive and integrate info from

A

spinal cord, cerebellum, basal ganglia, thalamus, cortex, and special sense

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11
Q

without inputt from cerebral cortex brainstem can

A

mediate much more coordinated and useful motor fxs than spinal cord alone maintaining posture and basic locomotion

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12
Q

motor cortex location

A

frontal lobe of neocortex

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13
Q

motor cortex receives and integrates

A

highly processed information from association cortical areas, basal ganglia and cerebellum

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14
Q

descending pathways from motor cortex can

A

influence LMNs in brainstem and spinal cord for precise, specific movements

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15
Q

cortical UMNs can control movements by

A

influencing UMNs in Red Nucleus or Reticular formation of brainstem

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16
Q

UMNs in motor cortex required for

A

postural runs and complex highly coordinated and/ or visually guided movements

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17
Q

central motor pathways

A
  • corticospinal
  • rubrospinal
  • reticulospinal
  • vesitbulospinal
  • tectospinal
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18
Q

LMNs in brainstem in which nuclei

A
  • Trigeminal motor nucleus
  • Facial nucleus
  • Hypoglossal nucleus
  • Nuclei of CN III, IV, VI
  • axons from UMNs in motor cortex can terminate on these nuclei*
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19
Q

single UMN can accomplish useful combination of muscle activation

A

by synapsing on multiple LMNs

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20
Q

interneurons

A

allow UMNs to synapse on multiple LMNs

- also hardwire compensatory postural movements like crossed extensor reflex

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21
Q

what converge on spinal networks or directly on LMNs to control ovement

A

multiple descending somatomotor pathways along with local reflex pathways

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22
Q

postural rxns in spinal cord primarily facilitated by

A

vestibulospinal and reticulospinal tracts

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23
Q

various inputs to LMN

A
  1. Reticulospinal Tract
  2. Vestibulospinal tract
  3. contralateral interneurons
  4. Rubrospinal tract
  5. proprioceptive afferent
  6. nociceptor afferent
  7. corticospinal tract
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24
Q

reticulospinal tract

A

UMN activates LMNs for locomotion and postural compensation

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25
Q

vestibulospinal tract

A

UMN activates ipsilateral extensor LMNs for balance and posture

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26
Q

contralateral interneurons

A

involved reflex activity such as crossed extensor response

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27
Q

rubrospinal tract

A

UMN mediates cortically controlled movements and locomotion and modulates activity in reflex circuits via excitatory and inhibitory interneurons

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28
Q

proprioceptor afferent

A

ex. spindle afferents directly excite extensor LMNs to maintain muscle ton and weight bearing for postural compensation

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29
Q

nociceptor afferent

A

will excite ipsilateral flexor LMNs (not shown) and inhibit ipsilateral extensor LMNs via interneurons (withdrawal reflex)

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30
Q

corticospinal tract

A

UMN controls voluntary and complex movements of distal limbs and modulates activity in reflex circuits via excitatory and inhibitory interneurons

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31
Q

medial pathways

A

include reticulospinal and vestibulospinal pathways

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32
Q

medial pathways primarily influence

A

axial and proximal limb muscles especially extensors

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33
Q

axons from medial pathways

A

descend spinal cord ipsilaterally or bilaterally in ventral white matter of spinal cord to influence LMNs in more medial aspect of VH (LMNs to proximal limb muscles)

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34
Q

UMNs medial pathways

A

often branch to terminate on many if not all spinal cord segments; not uncommon for some branches to cross midline and innervate contralateral LMNs

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35
Q

bilateral and far reaching projections of medial pathways permit

A

coordination of many muscles to maintain posture, regulate muscle tone, and control locomotion

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36
Q

lateral pathways

A

include corticospinal pathway and rubrospinal pathway

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37
Q

lateral pathways primarily influence

A

muscles of limb and distal limb especially flexors

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38
Q

axons from lateral pathways descend spinal cord in

A

dorsolateral funiculus

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39
Q

axons from lateral pathways synapse on

A

interneurons or directly on LMNs in lateral aspect of ventral horn
- these pathways have few synaptic interuptions

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40
Q

UMNs lateral pathways terminate

A

unilaterally on limited number of spinal cord segments

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41
Q

lateral pathways important for

A

voluntary directed movements of limbs for interacting with objects in the enivonrment; pattern of UMN projections and synapses on LMNs reflects their control of specific and limited muscle groups and therefore specific targeted movements

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42
Q

motor pathways that originate in cd brainstem

A

medial and lateral vestibulospinal pathways, pontine and medullary reticulospinal tracts, tectospinal tract, rubrospinal tract

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43
Q

rubrospinal tract UMNs and LMNs

A

UMNs in red nucleus; LMNs in spinal cord

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44
Q

rubrospinal pathway

A

afferent input to ipsilateral cerebellum -> decussate -> somatosensory cortex -> motor cortex -> red nucleus -> decussate -> reticulospinal UMNs -> LMNs to limbs

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45
Q

afferent input to rubrospinal pathway

A

DC-ML and spinocerebellar pathways

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46
Q

summarized pathway rubrospinal pathway

A
  1. UMNs in red nucleus in midbrain
  2. UMNs decussate in midbrain
  3. Descend the spinal cord in lateral funiculus
47
Q

Rubrospinal pathway controls

A
  • movements at various joints of limbs, excluding digits
  • voluntary targeted movements of limbs
  • red nucleus and midbrain motor circuits: important role in initiating and coordinating locomotion
48
Q

motor cortex and red nucleus

A

motor cortex synapses on red nucleus and exerts control over gait modification and postural rxn by synapsing on red nucleus

49
Q

resotral midbrain lesions that damage red nucleus can

A

result in contralateral gait and postural rxn deficits

50
Q

lesions where can interrupt rubrospinal tract to ipsilateral limb

A

lesions of cd midbrain, pons or medulla interrupt rubrospinal pathway to ipsilateral limb

51
Q

UMN deficits from lesion interrupting rubrospinal tract on ipsilateral side

A

spastic paresis +/- hyperreflexia

52
Q

corticosponal pathway (aka pyramidal tract) fx

A
  • predominant pathway for voluntary control of movement especially in distal limbs and digits in primaries not super important in cats and dogs we should not involve this for anything clinical
53
Q

coritcospinal pathway pathway

A
  1. motor cortex in frontal lobe
  2. UMNs travel in
    - Internal capsule
    - Crus Cerebri
    - Longitudinal fiber of the pons
    - pyramids
    3a. Cd medulla most axons decussate and descend spinal cord in dorsolateral funiculus
    4a. Synapse on interneurons or LMNs in lateral VH (where LMNs to distal limb muscles are located)
    3b. axons that did not decussate descend in ventral funiculus; will influence LMNs -> axial and ipsilateral proximal limb muscles (which play role in feed forward postural adjustments associated with voluntary movement)
54
Q

ischemic event knocking out motor cortex fx

A

acute loss of motor cortex function if ischemic event effects frontal lobe may produce clinical signs consistent with UMN lesion like contralateral spastic paresis, deficits in postural runs and sometimes hyper-reflexia but these are usually short lived b/c other pathways in motor system are able to compensate for loss of motor cortex; postural rxn deficits will persist

55
Q

animals with gradual progressive lesion of motor cortex

A

show little or no evidence of this lesion in its muscle tone, reflexes, or gait, unless gait is assessed on uneven terrain or with obstacles or if animal is circled; postural rxn deficits will persist

56
Q

corticospinal pathway UMNs and LMNs

A

UMNs- in cerebral cortex
LMNs- in spinal cord
* UMNs synapse directly on LMNs)
* can be contralateral or bilateral*

57
Q

vestibulospinal pathway

A
  • important for maintaining muscle tone, balance, and posture
58
Q

vestibulospinla pathway activity

A

depends predominantly on input from vestibular apparatus and cerebellum
- medial and lateral vestibulospinal tracts

59
Q

cerebral cortex and vestibulospinal pathway

A

cerebral cortex has no direct control over activity in vestibulospinal pathway

60
Q

medial vestibulospinla pathway projection

A

-bilateral projection to cervical spinal cord via MLF and ventromedial funiculus

61
Q

medial vestibulospinal pathway provides innervation to

A

neck muscles controlling head position, therefore controls movements of head for maintaining posture and balance

62
Q

lateral vestibules spinal pathway projects

A

mostly ipsilaterally to all levels of spinal cord via ventromedial funiculus

63
Q

Lateral vestibulspinal pathway excites and inhibits

A

LMNs to ipsilateral axial and proximal limb extensors, inhibits LMNs innervating ipsilateral flexors

64
Q

activity in lateral vestibular nucleus

A

on either side; pushes body in opposite direction

65
Q

lateral vestibulospinal pathway facilitates and inhibits

A

facilitates ipsilateral stretch reflex for extensor muscles and inhibits contralateral stretch reflex therefore lesions involving vestibular nuclei can affect general muscle tone and stretch reflexes

66
Q

vestibulospinal pathway UMNs and LMNs

A

UMNs in rostral medulla

LMNs in spinal cord

67
Q

if ____bulbar pathway not ____spinal pathway

A

then LMNs are in brainstem if bulbar in spinal cord if spinal

68
Q

pontine and medullary reticulospinal tracts fx

A

posture and locomotion; particularly controlling axial and proximal limb muscles

69
Q

reticulospinla tracts and cortical input

A

get cortical input but don’t require it to stimulate locomotion; getting pushed or pulled can -> locomotion
- motor cortex UMNs control locomotion circuits that reaction to conscious awareness of wanting to move toward something like a cookie ect.

70
Q

medullary reticulospinal UMNs

A

largely facilitate flexor muscles; receive signficiant amount of excitatory input form motor cortex and red nucleus

71
Q

pontine reticulospinal UMNs

A

facilitate extensor muscles
- these neurons important in support phase of locomotion of in stabilizing posture via ipsilateral extensors during a movement of contralateral limb

72
Q

neurons of pontine reticulospinal UMNs receive input from

A
  • can be corticaly controlled by UMNs for anticipatory postural adjustments
  • also receive input including input from spinal cord proprioceptive afferents and vestibular afferents and are v active in absence of cortical input
73
Q

motor cortex projects onto pontine and medullary reticulospinal tract to

A

control activity in reticulospinal UMNs to

  1. Make gate adjustments based on visually detected obstacles or terrain irregularities
  2. control postural rxns
  3. mediate “voluntary” directed locomotion such as approaching a visual stimulus
    * motor cortex tells reticulospinal neurons what it wants to accomplish and reticulospinal neurons create motor pattern required for locomotion*
74
Q

lesions affecting reticulospinal UMNs in brainstem or spinal cord

A

produce ipsilateral spastic paresis or paralysis which will be manifested in gait

75
Q

Tectospinal tract arises from

A

rostral colliculus and controls muscles in neck

76
Q

tecetospinal tract important for

A

orienting movement

77
Q

isolated lesions of rostral colliculus

A

would affect tectospinal tract but isolated lesions of rostral colliculus are rarely observed clinically but may result in ipsilateral turning and circling

78
Q

tectum projects to

A

brainstem circuitry that controls eye movements which must be coordinated with movements of head when animal is turning to look at something

79
Q

rubrospinal tract midbrain lesion ipsi or contralateral

A

could affect both sides bc a lot of decoration here

80
Q

rubrospinal tract motor cortex and red nucleus

A

contralateral then decoration in midbrain then ipsilateral

81
Q

sensory circuits going through cerebellum vs those going through cd brainstem

A

can knock out the ones in cd brainstem and everything is fine bc ones going to cerebellum sufficient but if knock out ones in cerebellum will have deficits bc ones in cd brainstem are not sufficient

82
Q

red nucleus

A

can control input from cortico-rubrospinal tract; red nucleus gets a lot of input from cerebellum

83
Q

motor cortex is essential for

A

certain limb movements including postural runs, navigating obstacles or uneven terrain during locomotion, and making targeted movements of limbs

84
Q

to coordinate movements of limbs motor cortex is essential for

A

axons from UMNs in motor cortex can terminate on UMNS in brainstem

85
Q

cortical UMNs can synapse in reticular formation to

A

influence reticulospinal tracts for voluntary locomotion and feed forward implementation of postural adjustments

86
Q

in domestic animals motor cortex exterts control of

A

motor function predominantly by synapsing on UMNs of rubrospinal and reticulospinal tracts rather than by making direct synapses on LMNs via corticospinal tract

87
Q

When evaluating patients consider lesions of

A
  • cerebral cortex
  • midbrain
  • pons
  • medulla
  • spinal cord zone
  • L vs R side
88
Q

ability to asses motor fxs test

A
  1. Muscle tone
  2. Reflexes
  3. Postural rxns
  4. Locomotion (looking for paresis/ paralysis)
89
Q

most fundamental nervous system requirement for muscle contraction and therefore movement of anytype

A

LMN

90
Q

if LMNs damaged in CNS, ventral roots, or peripheral nerves animal will demonstarate

A

decreased or absent muscle tone, reflexes, and postural runs as well as flaccid paresis/ paralysis; muscle will also undergo profound atrophy

91
Q

damage to UMNs in spinal cord

A
  • results in normal or increased muscle tone/ reflexes

- postural rxn deficits and spastic paresis or paralysis of gait

92
Q

damage to lesion in c1-c5 spinal cord vs in brain

A

c1-c5 lesion may impact all UMNs thet control a limb but lesions in brain may spare some UMNs depending on how far rostral lesion is

93
Q

lesion in cd medulla vs in pons

A

lesion in cd medulla has potential to impact all UMNs to the limbs; lesion in pons will impact many UMNs but leave those that originate cd to lesion intact

94
Q

cortical UMNs originate

A

in motor cortex in cerebral hemisphere contralateral to the limb

95
Q

acute lesion of the of motor cortex may result in

A

transient hypertonia and hyperreflexia and spastic hemiparesis. but not complete paralysis of contralateral limbs

96
Q

animal in lesion with motor cortex paralysis

A

an animal with a lesion in motor cortex will never be completely paralyzed bc brainstem UMNs are able to mediate gait and some other movements without cortical input

97
Q

acute forebrain lesion

A

will lead to tone, reflex, and gait deficits; usually these are relatively mild and resolve quickly as intact elements of somatomotor system reorganize to compensate

98
Q

cortical lesions may cause enduring deficits in

A

locomotion in face of obstacles or on irregular terrain and will cause permanent deficits in ability to perform postural rxns b/c motor cortex is required for performing these tasks and brainstem UMNs cannot “learn” to compensate

99
Q

rostral midbrain lesions

A
  • damaging red nucleus and descending pathways from motor cortex will manifest as UMN deficits in contralateral thoracic and pelvic limns
  • lesions more severe and enduring than cortical lesions bc both cortical and rubrospinal UMNs are impacted by the lesion and the red nucleus and surrounding midbrain plays important role in locomotion
100
Q

lateralized lesion spanning rostral to cd extent of midbrain

A

UMNs to both ipsilateral and contralateral limbs will be impacted (bc decoration of rubrospinal tract) and UMN signs will be seen in the limbs on both sides

101
Q

unilateral lesion of pons or medulla

A

will manifest as hypertonia, hyperreflexia, postural rxn deficits and spastic hemiparesis, or hemiplegia of ipsilateral limbs; similar to lesions of C1-C5 spinal cord segments

102
Q

medullar lesion severity

A

medullary lesions can produce most severe UMN deficits of all regions of brain bc all UMN pathways are present in medulla

103
Q

lesion that is large or affects both sides of brainstem will affect

A

motor function of limbs on both sides

104
Q

vestibulospinal pathway extensors or flexors

A

generally largely extensors

105
Q

organization of motor pathways

A

they are topographically organized; can be seen in md to lat organization of VH in every tract and nucleus up to cortex; neurons that are adjacent to each other influence the same or nearby muscles and muscles of body are represented in spatially continuous way across nucleus or axon tract

106
Q

paresis

A

weakness to generate voluntary movement

107
Q

paralysis

A

inability to generate voluntary movement

108
Q

locomition

A

fx that minimally requires brainstem UMN control of spinal cord LMNs

109
Q

spastic paresis/ paralysis

A

occurs when UMNs in cervical or lumbar enlargement damaged; muscle ton present or even increased bc LMNs in myotactic reflex loops in tact -> characteristic of opacity

110
Q

spastic hemiparesis could be caused by

A

lesion in pons, medulla, or C1-C5 spinal cord lesion ipsilateral to affected limb

111
Q

flaccid paresis/ paralysis

A

occurs when LMNs are damaged; muscle tone is decreased or absent bc LMNs are damaged

112
Q

no lmn

A

no lmm -> no muscle contraction -> no muscle tone

113
Q

flaccid paresis/ paralysis most easily IDed in gait as

A

decreased or lack of ability to bear weight on limb

114
Q

in locomotion flaccid paresis manifests

A

similar to lameness affected limb demonstrating shortened weight bearing phase

Neuro Anatomy (17 decks)

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