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Neuro Anatomy > Week 3 Learning Issues Part 2 > Flashcards

Week 3 Learning Issues Part 2 Flashcards

1
Q

motor neurons

A

axons form ventral root; somatic efferents and visceral efferents

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2
Q

somatic efferents

A

LMNs in VH

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3
Q

visceral efferens

A

preganglionic cell bodies in intermediate grey

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4
Q

interneurons

A

involved in local processing in spinal corx, short axons, can be inhibitory or excitatory and are important for information processing and modulating activity

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5
Q

projecting neurons

A

technically these are interneurons but they go long distances; these receive input from primary afferents or spinal cord interneurons and send axons up the spinal cord to brain via what matter

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6
Q

dorsal horn

A

sensory processing; interneurons and projecting neurons

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7
Q

ventral horn

A

motor processing; LMN

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8
Q

intermediate grey

A
  • sympathetic preganglinic neurons

- parasympathetic preganglionic neurons

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9
Q

sympathetic preganglionic neurons

A

in LH of thoracolumbar spinal cord segments

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10
Q

parasympathetic preganglionic neurons

A

found in sacral spinal cord intermediate grey; no LH

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11
Q

spinal cord grey matter can be divided into

A

horizontal laminae based on cytoarchitectural and connectional differences numbered D to V; spinal cord grey matter can also be divided into nuclei base don fx

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12
Q

fxs of nuclei of spinal cord grey matter

A

nociceptive afferents, nociceptive input, proprioception from hindlimbs; motor neuron pools (associated with specific muscles in VH), intermediolateral cell column (sympathetic preganglionic neurons)

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13
Q

white matter of spinal cord divided by

A

dorsolateral and ventrolateral sulci; divided into dorsal funiculus, lateral funiculus, and ventral funiculus

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14
Q

dorsal funiculus

A

contains ascending axons (sensory pathway carrying info to brain)

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15
Q

lateral funiculus

A

contains descending and ascending axons (motor and sensory)

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16
Q

ventral funiculus

A

contains predominantly descending axons (motor pathway carrying information to LMNs in spinal cord)

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17
Q

ascending and descending pathways

A

ascending: spinal cord -> brainstem -> cerebral cortex
descending: cerebral cortex -> brainstem -> spinal cord

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18
Q

ventral commissure

A

ventral to central canal, major site of decussation (crossing) of axons

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19
Q

propriospinal tract

A

axons from interneurons traveling btwn spinal cord segments to coordinate motor activity between segments (ex cutaneous trunci and withdrawal reflex)

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20
Q

primary afferent neurons

A

pseudounipolarl; central axonal process enters spinal cord via dorsal root and divides into multiple collateral branches which synapse on neurons in DH of spinal cord segment or adjacent pathways for further processing in brain

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21
Q

branches of primary afferent neuron central axonal process that mediate reflexes

A

synapse on interneurons in DH or LMNs in VH

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22
Q

categlories of afferent neurons

A
  1. Low threshold mechanoreceptors
  2. Nociceptors and thermoceptors
  3. Proprioceptors
  4. Visceral afferents
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23
Q

Low threshold mechanoreceptors respond to

A

touch, pressure, vibration

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24
Q

low threshold mechanoreceptors fiber types

A

Abeta fibers: large diameter, myselinated, fast conducting axons

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25
Q

How does CNS use mechanoreceptor information

A
  1. Locally in spinal cord (mediates reflexes and modulates activity in spinal cord)
  2. Travels to brain for conscious perception and motor fx (may take path that synapses in DH the takes different axon or may run thorugh white matter without synapsing and go straight to brain)
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26
Q

Nociceptors and Thermoceptors Receptor types

A

free nerve endings that respond to thermal, chemical, or intense mechanical stimulation

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27
Q

Nociceptors and thermoceptors fiber types

A

AS fibers (S is actually a greek letter see notes) and C fibers

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28
Q

AS fibers

A

(S actually greek symbol see notes); small diameter, lightly myelinated; mediate fast pain (first pain)= sharp and well localized; go to spinal cord then project to neuron and brain

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29
Q

C fibers

A

small diameter, unmyelinated; slow pain (second pain); throbbing/ burning ect; well localized; occurs after delay can persist for long time after injury

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30
Q

How does CNS use nociceptive information

A
  1. Locally in spinal cord (mediate reflexes, modulate activity in other spinal cord neurons)
  2. Travels to brain for conscious perception and emotional and autonomic responses to pain (increased HR ect)

** nociceptive information is carried bilaterally in spinal cord and by more than one pathway. Only severe spinal cord lesions will block all pathways the mediate conscious awareness of pain**

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31
Q

Proprioceptors receptors

A

muscle spindles, golgi tendon organs, joint receptors

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32
Q

proprioceptor fiber types

A

A alpha fibers

large diameter, heavily myelinated, fast conducting, can be further subdivided based on conduction speed

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33
Q

How does CNS use proprioceptive information

A
  1. Locally in spinal cord
  2. Travel in DCML pathway to be used by cerebrum for conscious awareness of position/ coordinate cortically controlled motor fx
  3. travel in spinocerebellar pathways in lateral funiculus; to be used by cerebellum to regulate motor fx; cerebellar processing done w/o conscious awareness
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34
Q

afferent axon categlorizatoin

A

based on diameter; larger axon diameter conduct action potentials more rapidly and tend to be more heavily myelinated; diameter and degree of myelination of an axon can affect its susceptibility to damage and locally acting drugs

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35
Q

visceral afferents

A

includes chemoreceptors, thermoreceptors, mechanoreceptors; may get to CNS via autonomic pathways back to spinal cord or travling in vagus, glossopharyngeal or other CNs to brainstem
Primary afferents may synapse on interneurons in spinal cord to control reflexes or projecting neurons to carry information to the brain

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36
Q

LMN

A

usually used in terms of SEs; alpha-motor neurons and gama-motor neurons; motor pathways must contact both types of these for motor system to fx properly

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37
Q

alpha-motor neurons

A

innervate skeletal muscle fibers

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38
Q

gama-motor neurons

A

innervate intrafusal muscle fibers within muscle spindles (keep muscle spindle length in register with muscle length)
*muscle spiindles= sensory receptors that realy info about muscle length and tension to CNS

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39
Q

motor end plate

A

each muscle fiber (cell) contacted by one branch of an alpha motor neuron at motor endplate where axon divides forming up to 50 terminal buttons

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40
Q

terminal boutons

A

contact muscle cell membrane

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41
Q

neuromuscular junciton

A

where terminal boutons contact cell membrane (action potential crosses this)

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42
Q

single LMN typically innervates

A

multiple muscle fibers within a single muscle (a given muscle fiber will be innervated by only one LMN but one LMB will innervate multiple muscle fibers)

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43
Q

Motor unit

A

LMN and all the muscle fibers it innervates

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44
Q

smaller motor units

A

generally responisble for delicate less forceful movements; contain smaller motor neurons with smaller diameter axons with less myelin (slower conduciton)

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45
Q

larger motor units

A

usually repsonsible for rapid forceful mvoements; contain larger motor neurons with larger diameter axons with more myelin (faster conduction)

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46
Q

motor neuron pool

A

group of LMNs that innervate a given muscle; cell bodies of neurons within MNP grouped into longitudinal cluster (nucleus) within VH of spinal cord

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47
Q

LMNs controlled by

A

local reflex pathways and descending pathways from the brain

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48
Q

upper motor neurons

A

neurons in the brain that synapse on LMNs and control their activity

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49
Q

final common pathway in somatic motor system

A

LMNs; without them contraction of muscle does not occur

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50
Q

LMNs get input from

A

many different places

51
Q

interneurons can be

A

inhibitory or excitatory

52
Q

visceral effernts

A

autonomic nervous system (ANS) utilizes 2 or more efferent neurons to relay commands from CNS to effector organs (smooth and cardiac muscles, glands)

53
Q

cell body VE preganglionic neuron

A

located in the CNS either in the spinal cord or brainstem; in spinal cord in int grey; symp preganglionic neurons located in thoracolumbar spinal segments in lateral horn; parasympathetic preganglinic neurons in sacral spinal cord segments in int grey but no LHl parasympathetic preganglionc neurons also in located in brainstem nuclei

54
Q

preganglionic neurons in ANS

A

multipolar neurons that fx like somatic motor neurons; receive input from primary afferents, locate interneurons and descending projections from the brain; may be involved in simple reflexes or more complex processes controlled by higher centers in brainstem and hypothalamus

55
Q

postganglionic cell bodies ANS

A

located in peripheral NS in peripheral ganglia

56
Q

myotactic or stretch reflex reflex center excitatory

A

spindle afferents synapse on alpha motor neurons that innervate same muscle and synergistic muscle; synapse is excitatory -> muscle contraction to -> original muscle length or desired position of limb
* this is monosynaptic*

57
Q

myotactic or stretch reflex center inhibitory

A

spindle afferents synapse on inhibitory interneurons that inhibit LMNs to antagonistic muscles to facilitate the return to normal position (antagonistic muscles relax making the movement easier)

58
Q

clinical test of myotactic reflex

A

tap on tendon of muscle or muscle itself so it stretches and stimulates muscle fibers (ex. patellar)

59
Q

what happens if you have a lesion cr to level of LMN cell bodies interrupting only the descending input to reflex center

A

if axons of descending UMNs eliminated then the reflex will not be eliminated or dimisined by may -> hyper-reflexia bc loss of descending inhibition

60
Q

myotactic reflex

A

provides a feedback system that monitors and maintains desired muscle length

61
Q

withdrawal reflex

A

aka flexor reflex; mediates withdrawal of limb from noxious stimuli; reflex center is polysynaptic

62
Q

withdrawal reflex reflex center

A

involves multiple segments of spinal cord b/c mult. muscles at mutt joints; afferent or interneuron axons may have to travel a few segments cr or cd in spinal cord; pinch skin at autonomous zone, ipsilateral limb flexes at all joints, in standing animal extensor tone will increase in contralateral limb for weight bearing bc of crossed extensor response

63
Q

withdrawal reflex effectors stimulated limb

A

stimulate limb -> ipsilateral flexors at all its excited (contracting) while all extensors are inhibited (and therefore relax) -> joints flex and limbs withdraw from painful stimuli

64
Q

withdrawal reflex contralateral limb

A

crossed extensor reflex; contraction of extensors in contralateral limb os it can support additional weight when one limb is flexed and lifted off the ground if animal Is standing; should not see this in standing animal; if you see this in recumbent animal most likely an interruption of descending pathways and UMN damage

65
Q

interneuron circuits mediating flexion/ crossed extensor reflex

A

also receive input from local circuits at level of spinal cord as well as descengin pathways that influence these circuits; normally spinal cord can’t mediate gait without input of UMNs in brainstem
- afferents such as cutaneous mechanoreceptors can stimulate the reflex (ie some animals will move foot if you touch paw)

66
Q

reflex loop

A

does not go directly to brain is locally in spinal cord

67
Q

cutaneous trunk reflex

A

segmental afferent neurons are stimulated when skin of trunk is pinched in thoracic and lumbar regions; afferents synapse in spinal cord on interneurons which ascending within spinal cord white matter to C8/ T1 spinal cord segments and synapse on LMNs that control cutaneous trunici muscle; these axons travel in lateral thoracic nerve and -> contraction of cutaneous muscles and -> a visible twitching of the skin

68
Q

perineal reflex loop

A

elicited by stimulating anus with mild noxious stimuli; should see contraction of anal sphincter and flexion of tail. Spinal cord segments S1-S3 provide afferent ascending pathway to perineal region and motor control of this region is controlled by pudendal nerve which is D1-S3

69
Q

maintenance of muscle mass

A

requires intact LMNs and local spinal cord circuits; if UMNs damaged then will see disuse atrophy but will see severe generation atrophy if LMNs damaged

70
Q

muscle tone and reflexes

A

maintinated by local spinal cord circuits connecting afferent and efferent neurons; influenced by UMNs but do not require UMN input to be present

71
Q

postural rxns

A

require afferent neurons, ascending sensory pathways to cerebral Cortex, descending motor pathways and LMNs in the spinal cord

72
Q

locomotion

A

intact LMNs and afferent feedback from sensory nerves, pathways between the spinal cord and brainstem and critical for normal locomotion, cerebellar cortex and cerebellum refine the movement; look for paresis and ataxia when assessing locomotion

73
Q

paresis/ paralysis

A

weakness/ lack of voluntary movement; typically interpreted in context of locomotion and weight bearing

74
Q

flacid paresis/ paralysis

A

LMN damage

75
Q

spastic paresis/ paralysis

A

UMN damage

76
Q

ataxia

A

uncoordinated movement bc loss of proprioceptive information input or processing

77
Q

voluntary movements

A

impossible to reliably asses in vet med; asses cortical fx by observing cortically controlled movements like postural rxns and animal’s ability to navigate obstacles or uneven terrain

78
Q

conscious awareness of stimuli

A

observe cortically controlled responses to stimuli (ex crying); ascending sensory pathway transverses the spinal cord, brainstem, and cerebrum; must be intact for animal to demonstrate conscious awareness; cortically controlled responses include vocalization, and targeted movements to eliminate stimulus

79
Q

division of spinal cord into 4 regions for localizing lesion

A

C1-C5: segments cr to cervical enlargement
C6-T2: cervical enlargement; associated with brachial plexus; sensory and motor to thoracic limb; motor to cutaneous trunk muscle (C8/T1); motor to phrenic nerve (C5,C6,C7)
T3-L3: between cervical and lumbar enlargements
L4-S3: lumbosacral plexsus

80
Q

L4-S3

A

lumbosacral plexus; can be divided into L4-S1 (lumbar enlargement) and S1-S3 (sacral spinal cord segments)

81
Q

L4-S1 lesion

A

may damage LMNs to the muscles of pelvic limbs, the circuitry associated with pelvic limb reflexes and the origin of the ascending sensory pathways from pelvic limb

82
Q

Lower motor neuron deficits L4-S1 muscle tone

A

decreased to absent in pelvic limbs (chronic lesion may -> dramatic muscle atrophy)

83
Q

Lower motor neuron deficits L4-S1 reflexes

A

decreased (hyporeflexia) or absent in pelvic limbs

84
Q

Lower motor neuron deficits L4-S1 postural reactions

A

decreased or absent in pelvic limb

85
Q

Lower motor neuron deficits L4-S1 locomotion/ voluntary movement

A

paresis or flaccid paralysis

86
Q

sensory deficits deficits L4-S1

A

reduced or absent pain perception to pelvic limbs; incoming sensory info and origin of ascending pathway may be interrupted so loss of proprioceptive input form limb may -> ataxia

87
Q

lesion affecting S1-S3

A

may damage LMNs and VE neurons that supply bladder, external uretheral sphincter and anal sphincter, and origin of ascending pathway from perineum

88
Q

Motor deficits lesion s1-s3

A
  • muscle ton in detrusor, external uretheral and anal sphincters: decreased to absent (inability to empty bladder effectively and completely, atonic bladder, urine dribbling)
  • perineal reflex: decreased to absent (pudendal nerve)
  • voluntary control of micturition and defication: decreased to absent
  • may cause weak withdrawal reflex, mild ataxia, paresis of pelvic limb bc S1 controls sciatic nerve
89
Q

sensory deficits lesions s1-s3

A

reduced or absent pain perception when noxious stimuli applied to perineum

90
Q

lesions T3-L3

A

damage ascending sensory pathways form lumbar enlargement and sacral spinal cord to brain and descending motor pathways from brain to lumbar enlargement and sacral spinal cord. These pathways = essential for postural rxns, locomotion, conscious perception of stimuli and micturition

91
Q

Upper motor neuron defiicits T3-L3

A

damage to UMNs descending from brain to lumbar enlargement (pelvic limb( and sacral spinal cord (lower urinary tract fx)

92
Q

muscle tone UMN deficitis T3-L3

A

normal or increased (hypertonia) in pelvic limbs since reflex circuitry that controls tone is intact but dissociated form brain regulation which is mostly inhibitory

93
Q

reflexes UMN deficitis T3-L3

A

normal or increased (hyperreflexia) +/- crossed extensor response bc loss of UMN inhibition

94
Q

postural rxns UMN deficitis T3-L3

A

slow or absent in pelvic limb

95
Q

locomotion UMN deficitis T3-L3

A

paresis or spastic paralysis of pelvic limb

96
Q

urinary tract UMN deficitis T3-L3

A

increased tone in urinary sphincters -> inability to empty bladder; can also -> abolished conscious control of urination bc interruption of ascending and descending pathways associated with urinary fx (requires severe/ bilateral lesion)

97
Q

sensory decificts T3-L3

A

lesions between cervical and lumbar enlargements may interrupt ascending pathways traveling to brain

  • may have reduced to absent pain perception when noxious stimulus applied to pelvic limbs, perineum, rump, or cd trunk (won’t turn to look at stimulus)
  • interruptions of proprioceptive pathways from pelvic limb to brainstem, cerebellum, and cerebrum
98
Q

interuptions proprioceptive pathways form pelvic limb to brainstem, cerebellum, and cerebrum

A

can -> ataxia, uncoordinated gate, in pelvic limbs

99
Q

how to more accurately localize lesions in thoracic and cr lumbar regions

A

cutaneous trunci reflex

100
Q

Lesions damaging c6-t2

A

can produce LMN signs in thoracic limb, UMN signs in pelvic limb and loss sensory pathways to brain from thoracic and pelvic limbs

101
Q

LMN signs in thoracic limbs

A

include loss muscle tone (+/- atrophy), decreased or absent reflexes, slow or absent postural rxns and paresis or flaccid paralysis of locomotion

102
Q

sensory pathway damage to thoracic limb

A

reduced or absent pain perception in thoracic limb and ataxia in thoracic limb if damage to sensory pathways that originate in these segments

103
Q

lesion affecting LMNs in segments in C8/T1

A

cutaneous trunci reflex can be absent with lesions affecting cutaneous trunci LNs in segments C8/T1

104
Q

lesion affecting LMNs c5-C7

A

respiration may be compromised by lesions affecting LMNs of segments c5-c7 bc phrenic nerve

105
Q

UMN signs pelvic limb

A

reduced or absent pain perception and ataxia bc interruption of same descending and ascending pathways that produced these signs with lesions in T3-L3 range

106
Q

UMN urinary tract with damage to C6-T2

A

present similar to lesion in T3-L3 lesion (ie increased tone in urinary sphincters -> inability to empty bladder; can also -> abolished conscious control of urination bc interruption of ascending and descending pathways associated with urinary fx (requires severe/ bilateral lesion)

107
Q

lesions affecting T1 and T2

A

can -> Horner’s syndromes bc symp trunk is T1-L4

108
Q

lesions c1-c5

A

lesions here are cr to cervical enlargement and don’t interfere with LMNs or local reflex circuits for limbs; deficits caused by interruption of ascending and descending pathways involved in postural rxn, locomotion, conscious perception, respiration, and micturition

109
Q

pelvic limb and urinary tract deficits C1-C5 lesions

A

same as T3-L3 lesions but cutaneous trunci reflex won’t help further localize lesions in this region bc not cutaneous trunci in this part of the neck

110
Q

thoracic limb signs C1-C5 lesion

A

may include hyper-reflexia, hypertonia, slow or absent postural reactions, spastic paresis, ataxia and decreased pain perception when noxious stimuli applied to thoracic limb

111
Q

severe lesions in c1-c5

A

interrupt descending pathways that control respiration and can -> death

112
Q

voluntary movement evaluation animals

A

generally we evaluate locomotion/ gate and postural rxns to asses UMNs in animals bc can’t ask them to move something; postural rxns require forebrain (cerebral cortex) processing, basic locomotion coordinated by brainstem does not asses forebrain fx unless the animal is presented with locomotion challenges

113
Q

paresis

A

weakness in context of voluntary motor fx and or locomiton

114
Q

paralysis

A

complete loss of voluntary motor fx and or locomotion

115
Q

flaccid paralysis

A

lacking muscle tone and reflexes as observed with LMN damage

116
Q

spastic paralysis

A

muscle tone and reflexes persist as observed with UMN damage

117
Q

LMN damage -> paralysis

A

presents more dramatically as difficulty during weight bearing phase of gait. Will bear weight on affected limb for shorter duration of time

118
Q

UMN damage -> paresis

A

presentes more dramatically as delayed protraction of limb as if muscles (LMNS) not getting signals to imitate stride

119
Q

mono paresis/ plegia

A

1 limb affected

120
Q

paraparesis/plegia

A

pelvic limbs are affected

121
Q

quadraparesis/plegia (tetra paresis/plegia)

A

all 4 limbs affected

122
Q

ataxia

A

lack of coordination that occurs when processing proprioceptive info is disrupted w/o norma proprioceptive information receipt and processing CNS can’t coordinate or adjust movements appropriately. Spinal cord lesions interrupt ascending proprioceptive patwhays to brainstemand cerebellar circuits that are critical for gate

123
Q

3 types ataxia

A
  1. Interruption of proprioceptive pathways to brain -> lesion blocking ascending path from spinal cord to brain -> general proprioceptive ataxia unocridanted gate due to interruption of proprioceptive pathway to brain can be in spinal cord or brainstem usually (lesion)
  2. Cerebellar dys fxn
  3. Vestibular dys fx

Neuro Anatomy (17 decks)

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