L5 Flashcards
muscle receptors are proprioceptors. signal?
signal position of body parts, movement and force
2 main proprioceptive organs
muscle spindles
golgi tendon organs
afferents in muscle spindles
Ia = fastest. 120 m/sec quadrapeds. 60 m/sec in human.
group II afferents = low conduction velocity.
afferents in GTO
Ib afferents = fast conduction ~60m/sec in human.
muscle spindles
- structure.
- what innervates them? purpose?
intrafusal muscle fibres, no contraction, produce no force. passive, measure muscle length changes.
- Gamma MN innervate : sensitize spindle to stretch. CNS downregulates
biasing firing rate
= change in firing rate from rest level.
4 hypotheses of g-MN action in normal movement
Y-loop hypothesis
servo-assistance
fusimotor set hypothesis
fusimotor prediction of intended movement
y-loop hypothesis
- descending command from GMN to spindles, - info up to alpha MN= down to muscles = displacement info back to spindles.
servo-assistance hypothesis
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
fusimotor set hypothesis
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
fusimotor prediction of intended movement
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
2 pathways underlie stretch reflex
- sensory receptor monosynaptic connection to spinal cord
2. long loop - info goes up to brain stem, cerebellum, BG, thalamus, cortex
muscle stretch elicits firing in :
involving polysynaptic through interneurons = task-dependent.
- spindle - group Ia & II
2. GTO - Ib
monosynaptic (spinal) reflex
- tendon jerk response
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
length and force feedback “compete” during muscle stretch
- spindle-mediated reflex is strong =?
- GTO reflex is strong =?
GTO excitation in weight-bearing muscle = ?
Spindle = stiff spring GTO = compliant spring
positive force feedback = increased stiffness of muscle
study at UBA of effect on stretch reflex on fear of heights
- 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.
interneuron function - Ia inhibitory Renshaw Ib inhibitory interneurons of withdrawal reflex
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
stretch EMG - short latency M1
long-latency M2 - long loop.
more stretch, bigger ratio btw M1 and M2. M1 gets bigger, M2 doesnt.
anti-spastic drugs
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
stretch reflexes increase after stroke and spinal cord injury
corticospinal tract lesion = opposite side body is weak/paralyzed
arm felxors = hyperreflexia due to increased sensitivity of stretch reflex pathway.
evidence for transcortical pathway for longer-latency M2 component
klippel-feil syndrome