L5 Flashcards

1
Q

muscle receptors are proprioceptors. signal?

A

signal position of body parts, movement and force

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2
Q

2 main proprioceptive organs

A

muscle spindles

golgi tendon organs

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3
Q

afferents in muscle spindles

A

Ia = fastest. 120 m/sec quadrapeds. 60 m/sec in human.

group II afferents = low conduction velocity.

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4
Q

afferents in GTO

A

Ib afferents = fast conduction ~60m/sec in human.

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5
Q

muscle spindles

  • structure.
  • what innervates them? purpose?
A

intrafusal muscle fibres, no contraction, produce no force. passive, measure muscle length changes.
- Gamma MN innervate : sensitize spindle to stretch. CNS downregulates

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6
Q

biasing firing rate

A

= change in firing rate from rest level.

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7
Q

4 hypotheses of g-MN action in normal movement

A

Y-loop hypothesis
servo-assistance
fusimotor set hypothesis
fusimotor prediction of intended movement

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8
Q

y-loop hypothesis

A
  • descending command from GMN to spindles, - info up to alpha MN= down to muscles = displacement info back to spindles.
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9
Q

servo-assistance hypothesis

A

a and g-mn are co-activated.
a cause muscle shorten
g keep spindle sensory region taught to maintain singalling of unplanned muscle length changes.
a = control, G = mediates, makes it easier

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10
Q

fusimotor set hypothesis

A

a and G activated independently.
- task-related setting of spindle sensitivity by g-mn action.
a can do muscle displacement on its own. g-mn chime in when behaviour is novel or difficult

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11
Q

fusimotor prediction of intended movement

A

static G increased and decreased according to expected muscle shortening and lengthening = activately changes activity throughout movement.
a - works on its own
g - chimes in whenever expected muscle length cahnge

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12
Q

2 pathways underlie stretch reflex

A
  1. sensory receptor monosynaptic connection to spinal cord

2. long loop - info goes up to brain stem, cerebellum, BG, thalamus, cortex

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13
Q

muscle stretch elicits firing in :

involving polysynaptic through interneurons = task-dependent.

A
  1. spindle - group Ia & II

2. GTO - Ib

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14
Q

monosynaptic (spinal) reflex

- tendon jerk response

A

rapid stretch by striking neurons. evoke Ia firing (MS) = activate a-MN of muscle = muscle contraction that resists length change.
- antagonist of this muscle inhibited by Ia afferent
GTO - respond to increase in force - disynaptically inhibit a- MN to resist change in force

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15
Q

length and force feedback “compete” during muscle stretch
- spindle-mediated reflex is strong =?
- GTO reflex is strong =?
GTO excitation in weight-bearing muscle = ?

A
Spindle = stiff spring
GTO = compliant spring

positive force feedback = increased stiffness of muscle

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16
Q

study at UBA of effect on stretch reflex on fear of heights

A
  • postural threat high = response doubled
    electrically stimulating spindle afferents did not change. = no muscle stretch, neither intrafusal nor spinle sensory was involved.
  • significant postural threat = increase G-MN activity enhances spindle sensitivity = enhances stretch - evoked reflex.
    a-MN excitability not elevated.
17
Q
interneuron function
- Ia inhibitory 
Renshaw
Ib inhibitory
interneurons of withdrawal reflex
A

1a = transmit spinle Ia input from agonist muscle to inhibit antagonist
renshaw: activated by a -mn. mediate recurrent inhibition back onto these and neighbouring agonist of a-MN. - inhibit self, to ensure it can keep firing with excess force = muscular wisdom
IB - GTO Ib input from agonist to inhibit agonist a-MN (feedback control of force)
interneuron ; nociceptive afferent. flex leg on pain, extend contralateral leg

18
Q

stretch EMG - short latency M1

long-latency M2 - long loop.

A

more stretch, bigger ratio btw M1 and M2. M1 gets bigger, M2 doesnt.

19
Q

anti-spastic drugs

A

GABA-A agonist = benzodiazapenes
DABA-B agonist = baclofen
A2 agonist: tizanidine & clonidine
cyproheptidine: ihibit 5HT mediated excitability.
botox & dentrolene = block NMJ
*also cause weakening, fatigeu and voluntary movement

20
Q

stretch reflexes increase after stroke and spinal cord injury

A

corticospinal tract lesion = opposite side body is weak/paralyzed
arm felxors = hyperreflexia due to increased sensitivity of stretch reflex pathway.

21
Q

evidence for transcortical pathway for longer-latency M2 component

A

klippel-feil syndrome