lecture 10 Flashcards

1
Q

what is gegenhalten seen in

A

severe dyspraxia/ apraxia `

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2
Q

spasticity is a ___ disorder characterized by a ____ depended _____ in ______ stretch reflexes with exaggerated _____ ______ resulting from ____________ of the stretch reflex

A
  • motor
  • velcoity
  • increase
  • tonic
  • tendon jerks
  • hyper excitability
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3
Q

if there is neural overactivity from an upper motor lesion and a spinal lesion happens what would be a results

A

hyperrefelxia bc alpha and gamma neurons are over stimulated

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4
Q

if there is neural overactivity from an upper motor lesion and a cerebral lesion happens what would be a results

A

excessive reticulospinal drive to motor neurons leading to muscle contractions

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5
Q

what is myoplasticity

A

contracture , atrophy, weak actin myosin binding

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6
Q

corticospinal tract from precentral cortex control what

A

voluntary mvmt

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7
Q

what are the 2 supra segmental contribution to spasticity

A

pyramidal tracts and extrapyramidal tracts

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8
Q

what is thought to help with some mvmt when CST is damaged

A

venteralmedial reticulospinal tract

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9
Q

what does isolated lesions of the primary motor cortex induce

A

weakness and decreased reflexes

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10
Q

what does the anterior limb of the internal capsule carry

A

sensory fibers

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11
Q

does the ventromedial reticulospinal tract cross

A

no

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12
Q

where does the ventromedial RST come from

A

pons

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13
Q

where does the dorsolateral RST come from and does it cross

A

medulla and yes it crosses (50% cross immediately and 50% does not cross)

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14
Q

where is the ventromedial reticular formation

A

in the medulla and it is an inhibitory area

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15
Q

what is the ventromedial reituclar formation closesly controlled by

A

premotr cortex / corticoreticular tract

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16
Q

what does renshaw cells inhibit

A

homonymous and synergisitic MNs

17
Q

when renshaw cells inhibit gamma MN and la interneurosn what is it called

A

recurrent inhibition

18
Q

what excites renshaw cells and what is the neurotransmitter

A

recurrent collaterals with ACH

19
Q

what is 1a reciprocal inhibition

A

1a afferents of agonist muscle inhibits alpha MNs of its antagonist muscle via interneurons

20
Q

what does 1a reciprocal inhibiton inhibit?

A

co contraction of agnoist and antagnoist mm

21
Q

basically what is recurrent inhibition

A

allows motor neurons to inhibit themselves

22
Q

1b autogenic inhibitoin is evoked by what

A

contraction of homoymous (same muscle that is being strecthed and contracted) m

23
Q

what is fuctional reorganization within spinal circuits

A

neuroplasticity

24
Q

what is most commonly used when measuring spasticity

A

moditifed ashworth scale (0- no muscle tone & 5 - rigitidy)

25
Q

what happens when deprived of supraspinal influences

A

collateral sprouting of axons
unmasking sensitivity of sensory receptors
heightened sensitivity of sensory receptors
enchanced cutaneous reflexes

26
Q

what contributes to the increased fusimotor drive

A

increased muscle spindle sensitivity resulting form hyperactivity of gamma MNs

27
Q

evidence from clinical observation for increased fusimotor drive is

A

“spinal shock” within 24 hours after SCI with no DTR able to be elicited during this time
exaggerated DTRs after spinal shock ends

28
Q

altered fusimotor drive can be due to long term neuromuscular adaptation including changes in muscle length and receptor sensitivity also called

A

myoplasticitiy