lecture 10 Flashcards
what is gegenhalten seen in
severe dyspraxia/ apraxia `
spasticity is a ___ disorder characterized by a ____ depended _____ in ______ stretch reflexes with exaggerated _____ ______ resulting from ____________ of the stretch reflex
- motor
- velcoity
- increase
- tonic
- tendon jerks
- hyper excitability
if there is neural overactivity from an upper motor lesion and a spinal lesion happens what would be a results
hyperrefelxia bc alpha and gamma neurons are over stimulated
if there is neural overactivity from an upper motor lesion and a cerebral lesion happens what would be a results
excessive reticulospinal drive to motor neurons leading to muscle contractions
what is myoplasticity
contracture , atrophy, weak actin myosin binding
corticospinal tract from precentral cortex control what
voluntary mvmt
what are the 2 supra segmental contribution to spasticity
pyramidal tracts and extrapyramidal tracts
what is thought to help with some mvmt when CST is damaged
venteralmedial reticulospinal tract
what does isolated lesions of the primary motor cortex induce
weakness and decreased reflexes
what does the anterior limb of the internal capsule carry
sensory fibers
does the ventromedial reticulospinal tract cross
no
where does the ventromedial RST come from
pons
where does the dorsolateral RST come from and does it cross
medulla and yes it crosses (50% cross immediately and 50% does not cross)
where is the ventromedial reticular formation
in the medulla and it is an inhibitory area
what is the ventromedial reituclar formation closesly controlled by
premotr cortex / corticoreticular tract
what does renshaw cells inhibit
homonymous and synergisitic MNs
when renshaw cells inhibit gamma MN and la interneurosn what is it called
recurrent inhibition
what excites renshaw cells and what is the neurotransmitter
recurrent collaterals with ACH
what is 1a reciprocal inhibition
1a afferents of agonist muscle inhibits alpha MNs of its antagonist muscle via interneurons
what does 1a reciprocal inhibiton inhibit?
co contraction of agnoist and antagnoist mm
basically what is recurrent inhibition
allows motor neurons to inhibit themselves
1b autogenic inhibitoin is evoked by what
contraction of homoymous (same muscle that is being strecthed and contracted) m
what is fuctional reorganization within spinal circuits
neuroplasticity
what is most commonly used when measuring spasticity
moditifed ashworth scale (0- no muscle tone & 5 - rigitidy)
what happens when deprived of supraspinal influences
collateral sprouting of axons
unmasking sensitivity of sensory receptors
heightened sensitivity of sensory receptors
enchanced cutaneous reflexes
what contributes to the increased fusimotor drive
increased muscle spindle sensitivity resulting form hyperactivity of gamma MNs
evidence from clinical observation for increased fusimotor drive is
“spinal shock” within 24 hours after SCI with no DTR able to be elicited during this time
exaggerated DTRs after spinal shock ends
altered fusimotor drive can be due to long term neuromuscular adaptation including changes in muscle length and receptor sensitivity also called
myoplasticitiy
