General Proprioception/UMN Flashcards

1
Q

what are the 3 components necessary for normal gait?

A
  1. LMN
  2. UMN
  3. general proprioception
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2
Q

what are lower motor neurons also called? what do they do? what are the two

A

general somatic efferent (GSE); innervate skeletal muscle and cause contraction; types:
1. cranial nerves (like those to the extraocular muscles)
2. spinal nerves: allow contraction of the flexors and extensors for movement of limbs

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3
Q

can LMN generate gait on their own?

A

NO!! they need upper motor neurons to tell them what to do

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4
Q

describe UMN (5)

A
  1. the central nervous system motor system
  2. responsible for gait generation: initiate movement and maintain tone for support against gravity (stand upright)
  3. act by influencing LMN
  4. facilitate AND inhibit extensor muscles/tone and flexor muscles
  5. control of the muscular activity associated with the visceral functions (respiratory, cardiovascular, and excretory)
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5
Q

what are the 2 aspects of gait generation, as controlled by the UMN?

A
  1. postural/stance phase: supports weight against gravity, establishes posture for initiation of gait
    -UMN recruit LMN
    -gravity stretches extensor muscles and neuromuscular spindles, afferent/sensory info travels to LMN in spinal cord, LMN contract extensor muscles and inhibit flexor muscles (extensor antagonists) (AKA PATELLAR REFLEX)
  2. swing phase/protraction: initiation of voluntary activity of the motor system
    -UMN responsible for facilitation of neurons that innervate the flexor muscles to initiate movement (pick up limb and advance)
    -then UMN shifts back to facilitation of neurons that innervate extensor muscles to complete the movement (to place limb back)
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6
Q

where are UMN located?

A

in various locations in the cerebrum and brainstem, with 4 tracts/groups (corticospinal, rubrospinal, reticulospinal, and vestibulospinal) that descend from the brainstem mainly in the lateral and ventral funiculus of the spinal cord

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7
Q

where is UMN gait generation mainly from in primetes? contrast to domestic animals

A

in primates, the UMN in the cerebrum is mainly responsible for gait generation; but in domestic animals/quadrupeds, the cerebrum is less essential for gait generation, it is actually the UMN in the brainstem that are most important for gait generation!

an exception to this rule for quadrupeds is that there is still a small contribution to gait generation by the UMN in the cerebrum, so acute lesions in the cerebrum/prosencephalon can still cause a gait deficit (but not paralysis like in primates)

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8
Q

what is proprioception?

A

the perception of body position and movement in the absence of vision (knowing where your limbs are in space/relative to your body)

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9
Q

describe the general proprioception system (2)

A
  1. a sensory system that detects the state of the position and the movement in muscles and joints
  2. proprioceptors sensitive to movement are diffusely located in the internal mass of the body in muscles, tendons, joints, and inner ear and are sensitive to stretch
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10
Q

describe the general somatic afferent system (2)

A
  1. sensory for touch, temperature, and nociception
  2. mechanoreceptors, thermoreceptors, and nociceptors receive stimuli by physical contact with the external environment
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11
Q

how are general proprioception fibers and general somatic afferent fibers carried to the central nervous system?

A

by sensory (afferent) nerves

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12
Q

what are the 2 basic pathways of general proprioception?

A
  1. conscious
  2. unconscious
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13
Q

describe the unconscious pathway of general proprioception (5)

A
  1. unconscious transmission to the cerebellum
  2. cerebellum modifies movements but
  3. cerebellum needs to know where the limb/body is before you move it (via sensory input) so that it can modify that movement
  4. cerebellum modifies movement by influencing UMN in the brain the generate gait
  5. this pathway modifies gait generation
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14
Q

describe the conscious pathway of general proprioception

A
  1. GP information goes to the cerebral cortex for conscious recognition of body position (this is how, when you close your eyes, you are aware of where your body is located “I moved my arm and I know I moved my arm”)
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15
Q

what are the 4 big changes seen on a neuro exam with LMN disease?

A
  1. gait: LMN paresis, ambulatory or no, paresis or paralysis, short and choppy gait!! because limbs can’t support weight long enough for a full stride
  2. reflexes: decreased
  3. muscle tone: decreased (flaccid)
  4. muscle mass: decreased
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16
Q

describe the patellar reflex (LMN) (2)

A
  1. tap patellar tendon, should see extension of the stifle via the quadriceps muscle
  2. tests sensory and motor to the femoral nerve located L4-L6 (LFour, LFive, and LFsix)
17
Q

describe pelvic limb withdraw

A
  1. tests sensory and motor of the sciatic nerve
  2. sciatic located L6-L7 and S1 (LSix, LSeven, S1)
18
Q

describe thoracic limb withdraw

A
  1. tests sensory and motor to spinal cord segments C6-T2
  2. sensory depends on the area stimulated (example: lateral digit tests sensory to ulnar +/- median nerve)
  3. motor relies on many nerves within C6-T2
    3a. shoulder flexion: axillary, radial, thoracodorsal
    3b. elbow flexion: musculocutaneous
    3c. carpal and digit flexion: median and ulnar
19
Q

how is muscle tone usually assessed for LMN exam? (2)

A
  1. typically evaluated standing, as tone can decrease if relaxed when laying down
  2. flex limb and see how much/easily can bounce back/extend
  3. if have LMN disease, can’t contract muscles!
20
Q

when can atrophy be observed with LMN disease? in small animals versus large animals

A

atrophy after 5-7 days with small animals
atrophy after 1-2 weeks with large animals

21
Q

what happens if you damage UMN? (4)

A
  1. no longer affecting ability to contract extensor and flexor muscles, so LMN technically okay but
  2. there are now no signals from the brain to tell the LMN what to do with their muscles
  3. this can lead to paresis, spasticity, hyperreflexia, but NO muscle atrophy!
22
Q

describe the gait of an animal with UMN

A

UMN can still say lift limb, but damage will cause a pause before UMN can say advance the limb, then another pause before can bring limb back, so will see a long and lopey stride, potentially with knuckling and scuffing, floating, overreach

23
Q

what is spasticity?

A

increased extensor tone

24
Q

how does UMN cause spasticity?

A

UMN facilitate and inhibit extensor and flexor muscles, and most lesions that affect UMN release antigravity extensor muscles from inhibition , leading to increased extensor tone/hypertonia (spasticity of the extensor muscles) versus LMN lesions that cause muscles to be flaccid

25
Q

describe reflexes in UMN disease (3)

A
  1. most commonly see normal reflexes
  2. but may occasionally see hyperreflexia, most commonly of the patellar tendon reflex, will see this reflex more brisk than usual and sometimes repetitive, and may see deficits in crossed extensor reflex
  3. generally describe reflexes as normal to increased with a UMN lesion
26
Q

describe the crossed extensor reflex and how it relates to UMN damage (3)

A
  1. when an animal is standing, noxious stimulus to one paw causes withdrawal of ipsilateral limb and concurrent extension of contralateral limb to maintain standing
  2. when an animal is lying down, descending UMN from brain inhibit the crossed extensor reflex because it is not needed
  3. if this reflex occurs in an animal in recumbency, the UMN inhibitory pathways are damaged, indicating a lesion/damage in UMN tracts
27
Q

how do we assess proprioception? (2)

A
  1. gait
  2. postural reactions
28
Q

what kind of gait is observed with damage to the general proprioception system?

A

long and lopey/hypermetria with some scuffing,

also known as the same as UMN damage gait; this is known as GP ataxia and looks the same as UMN damage

but slightly characteristic to GP ataxia, the animal may also circumduct and place limbs too lateral or may place limbs too medial and cross over midline

29
Q

why do UMN paresis and GP ataxia look the same?

A

the tracts are next to each other so they are affected together, therefore there is a lot of overlap in resultant clinical signs

30
Q

describe how postural reactions test everything (3)

A
  1. receptor (proprioceptor) conveys sensory information proximally along peripheral nerve
  2. sensory info ascends in spinal cord (unconsciously to the cerebellum and then consciously to the cerebrum)
  3. UMN from the brain descend the spinal cord to tell LMN to flip paw back over
31
Q

do postural reactions only test proprioception?

A

no! need both proprioception and a functioning LMN unit for normal postural reactions; so you can use this to tell if something is neuro or not neuro

32
Q

can you differentiate between conscious and unconscious proprioception?

A

nope!!