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Neuro > Tone > Flashcards

Tone Flashcards

1
Q

Ia

A

Innervate bag and chain

respond to length of muscle –> dynamic (velocity)

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2
Q

II

A

innervate chain
not velocity dependent
sensitive to absolute length

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3
Q

gamma motor neurons

A

dynamic and static

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4
Q

IIb: GTO

A

located in musculotendinous junction
in series with extrafusal fibers
can inhibit alpha motor neurons in response to tension

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5
Q

Phasic Reflexes (Twitchy)

A
  • response to a change in the level of sensation to a specific receptor
  • brief depression of muscle activity gives appearance of twitch
  • all monosynaptic reflexes are phasic
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6
Q

Tonic Reflex

A
  • emerge in response to change in level of stimulus
  • sustained contraction and relatively smooth movement
  • all are polysynaptic
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7
Q

Is stretch reflex modifiable?

A
  • yes

- performance outcome is dependent on context

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8
Q

Acute damage to cerebellum results in:

A
  • transient hypotonia

- improves gradually in parallel to recovery of muscle spindle sensitivity

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9
Q

anterior lobe damage

A

disruption in regulation of muscle spindle sensitivity, reactions to cutaneous stimuli, proprioceptive supporting reactions

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10
Q

Cerebellar sign

A

many more swings in pendular reflex

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11
Q

What causes clasp knife phenomena?

A

lesion to descending pyramidal motor system

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12
Q

what is clasp knife phenomena attributed to?

A

change in balance of reflex effects coming from muscle spindles (resist motion) and GTOs (suppress resistance)

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13
Q

what is spasticity manifested as?

A

velocity and muscle length dependent increase in resistance to externally imposed muscle stretch

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14
Q

What does spasticity result from?

A

hyper excitable descending excitatory brainstem pathways and from the resultant exaggerated stretch reflex response
reduced threshold of spinal stretch reflex

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15
Q

motor impairments related to but distinct from spasticity

A

abnormal synergies
inappropriate muscle activation and co-activation
all share similar pathophysiological signs

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16
Q

is spasticity manifested in active muscles?

A

no

only resting muscles

17
Q

What can cause medial reticulospinal pathways to become hyper-excitable?

A
  • disinhibition/ unmasking mechanisms
  • unopposed excitatory descending inputs to spinal stretch reflex circuit (elevated activity of spinal motor neurons and reflex circuit OR velocity and length dependent increase)
18
Q

median time to detect spasticity post-stroke

A

34 days

19
Q

does spasticity spontaneously resolve?

A

rarely

20
Q

what is acute spasticity ( <4 weeks) an important predictor for?

A

severe spasticity at 6 and 12 months

21
Q

proportional recovery of spasticity

A

severity predicts the amount of recovery expected after stroke

22
Q

what happens if spasticity is suppressed or treated aggressively during early stages of recovery ?

A

there is no correlated functional improvement in a later stage

23
Q

spasticity is “blank” and tone is “blank”

A

spasticity is neural

tone is multifactorial

24
Q

Neural factors of tone

A
  • balance of descending facilitory and inhibitory influences of segmental spinal processes
  • peripheral afferent processes
  • predictive abilities to set gain and threshold for larger loop stretch reflexes
  • orientation in space –> righting reflex
25
Q

Biomechanical factors of tone

A
  • length of muscle, length tension relationship (torque/angle = stiffness)
  • visco-elastic properties of muscle and connective tissue (intrinsic muscle/ ct properties)
  • speed of lengthening
  • physical inertia of extremity
26
Q

behavioral factors of tone

A

arousal, fear, pain

27
Q

Negative signs

A
  • address first

- weakness, lack of dexterity, fatiguability

28
Q

positive signs

A
  • address second
  • flexor and extensor spasm
  • conus
  • babinski
  • exaggerated cutaneous reflex
  • clasp knife
  • autonomic hyper reflexia
  • elements of dystonia
29
Q

what is the primary basis for disorders following CNS lesions?

A

inadequate recruitment of agonist motor neurons (negative sign)

30
Q

What affects “ true” motor recovery in early stages of post cortical lesion

A
  • spasticity and related neuromusculature impairments emerge and evolve from the same pathophysiological process of abnormal neuroplasticity
  • no effective treatment to correct abnormal neuroplasticity
31
Q

when is spastic functional recovery achievable?

A

when motor impairments are managed

  • strengthen weak muscles throughout entire course of recovery
  • manage spasticity in chronic stage when it impedes function

Neuro (12 decks)

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