Physiology of Proprioception Flashcards

1
Q

Which muscle fibres are recruited for contraction?

How does the brain maintain accuracy in movement?

A
  • • Red fibres are recruited/activated first; small, easily excited
    • Increased excitatory input increases and more White fibres are recruited/activated; large, strong
  • Brain tells the muscles about the changes in muscle length and the amount of tension produced
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2
Q

What do muscle spindles consist of?

What are the 2 types of muscle spindles?

What do the spindle afferents do?

What are the 3 stages in which the muscle spindles control Posture e.g. holding a cup?

What does the brain do to your arm during intended movement of it?

Which motor neurons activate the contractile spindle poles?

What happens to the muscle spindles during contraction?

How are the spindle poles then made sensitive to stretch again?

What happens to the muscle spindles during relaxation?

How is the muscle intentionally stretched?

A
  • Intrafusal (spindle) muscle fibres; stretchy, passive centre with contractile poles at each end
  • • Nuclear Chain type; nuclei sitting in a flat centre
    • Nuclear Bag type; nuclei sitting in a bulbous centre
  • Sends information to the brain and ventral horn of the spinal cord; provides a boost to the excitation of the muscle
    1. Muscle stops producing enough force to support the cup
      1. Spindles in bicep stretch as the arm begins to drop
      2. Afferent signals sent to spinal cord to increase excitation of motor neurons
  • Signals from brain activates the antagonist motor neurons to contract the tricep and stretch the bicep
  • γ motor neurons
  • During passive shortening, the α motor neurons contract the muscle by its stretchy centre area; centre becomes insensitive to stretch
  • γ motor neurons intentionally contract the poles
  • During passive stretch, both the centres and poles are stretched
  • Brain switches off both sets of neurons to allow the poles to stretch a lot while the centre doesn’t
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3
Q

What occurs in Pre-synaptic Inhibition? What type of inhibition occurs?

What occurs in Post-synaptic Inhibition? What type of inhibition occurs?

How does the brain maintain accuracy of movement e.g. grabbing a cup?

A
  • GABAergic (metabotropic) interneurons inhibit neurotransmitter release from antagonist afferents
    o Slow, Long-lasting, Specific
  • Glycinergic (ionotropic) inhibits the antagonistic motor neurons directly
    o Fast, Short lasting, Non-specific
    1. Brain signals activate α and γ neurons, but the cup is heavier than expected
      1. Muscles shorten too slowly, but end-poles contract as expected
      2. Spindle is activated
      3. Reflex increases excitation of muscle and corrects movement
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4
Q

Golgi Tendon Organs:
What is their structure?

Where are they found?

What is their function?

What happens when the tendon is stretched?

How do they control muscle tension? What is this called?

What occurs to the spindle reflexes and extensor tendon organs to help initiate the contraction phase?

What can a loss of proprioceptors lead to?

A
  • 1b sensory nerve endings wound around collagen fibres
  • Within the capsule of tendon fibres
  • Measures tension generated by muscle contraction
  • Collagen fibres squash the 1b nerve endings to activate them
  • Tension in extensor inhibits extensor motor neurons during standing = Non-reciprocal Inhibition
  • Spindle reflexes are dis-inhibited just before a muscle goes from stretching to contraction, Extensor tendon organs switch form inhibiting to exciting muscle contraction to boost contraction phase
  • Weakness of gait
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5
Q

UMN Lesions:
What is lost?

What are the symptoms? Why do they occur?

How can Spasticity and Hypertonia be treated?

LMN Lesions:
What is lost?

What are the symptoms?

A
  • Loss of control of α, γ and interneurons
  • • Weakness; no signal to contract
    • HYPERTONIA, ↑reflexes; brain can’t control reflex
    • NO WASTING; muscles remain active due to reflex input
  • • Both reduced by a non-specific increase in spinal cord inhibition; Oral Benzodiazepines boost the effectiveness of GABAergic inhibition
    • Spasticity reduced by suppressing the Type Ia reflex; Intrathecal Baclofen activates GABA receptors on Ia afferent synapses to reduce neurotransmitter release
    • Spasticity associated with muscle spasms; IM Botox given to weaken the neuromuscular synapses
  • Loss of α motor neuron
- • Denervated muscle = Flaccid Paralysis
• Weakness
• WASTING
• FASICULATIONS
• Loss of reflexes
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6
Q

Type Ia afferents:
What are their axons like?

What connection do they have to α motor neurons?

What do they affect?

What are they important for?

What can a loss of UMN control to their reflexes cause?

Type II afferents:
What are their axons like?

What connection do they have to α motor neurons?

What do they affect?

What are they important for?

What can a loss of UMN control to their reflexes cause?

A
  • Thick, Fast axons
  • Monosynaptic
  • SPEED OF MUSCLE STRETCH
  • Correcting rapid, unintended movements e.g. in gait
  • SPASTICITY
  • Thin, Slow axons
  • Indirect
  • AMOUNT OF MUSCLE STRETCH
  • Maintaining limb position, posture, muscle tone
  • HYPERTONIA
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