Overview of the control of movement 02.03.23 Flashcards

1
Q

How does a movement begin?

A

In the motor cortex then it is sent down the UMN to the LMN pathway which will activate the muscle.
Crosses the neuromuscular junction to activate the muscle

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2
Q

How do we smoothen the execution of muscle movement?

A

Via the extra pyramidal pathway

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3
Q

How is feedback then sent back to the brain?

A

By the afferent - sensory nerves
Brain receives this feedback and co-ordinate the movement

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4
Q

What projections does the primary motor cortex have?

A

Primary motor cortex projects long axons through internal capsule and brainstem into the spinal cord and will terminate in an area called the anterior horn cell of the spinal cord (2nd order neuron)

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5
Q

What are 3 features of the UMN disorders?

A
  • Spasticity
  • Spastic weakness/ pyramidal weakness
  • Brisk reflexes
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6
Q

What are the common causes of UMN disorders?

A
  • Brain/brain stem - Strokes, Tumours, Demyelination (MS)
  • Spinal cord – MS, cord compression, spinal cord degenerative causes- Hereditary spastic paraparesis (partially able to move leg), Vit B12 deficiency
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7
Q

Where do the neurons sit in the spinal cord for LMNs?

A

In the anterior part of the spinal cord (peripheral)
They project out axons from here to muscles

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8
Q

What are the features of the LMN disorder?

A
  • Flaccid weakness
  • Reduced tone
  • Muscle wasting (fasciculations - twitching)
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9
Q

What is the deep tendon reflex arc? (sensory)

A
  • Knee jerk
  • Tap patella tendon in the knee
  • Tendon gets stretched when we tap on it
  • Muscle spindles sense this stretch
  • Stretch receptors send signal to spinal cord (sensory)
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10
Q

What is the deep tendon reflex arc? (motor)

A
  • Signals enter into the dorsal root ganglion which projects onto spinal cord
  • anterior horn cell sends signal down motor neuron to effector muscle to contract the muscle
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11
Q

What information do muscle spindles send?

A

Afferent information - lots of it that needs to be processed

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12
Q

What are some causes of the LMN injury?

A
  • At the neuron: MND, Polio
  • At the roots: radiculopathy
  • At the nerves: neuropathies
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13
Q

What are 3 causes of peripheral nerve damage?

A
  1. Diabetes
  2. Idiopathic (spontaneous)
  3. Alcohol/ toxins/ drugs
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14
Q

What stimulates the vesicles to exocytosis?

A

Calcium causes vesicles to release the ACh to the synapse for it to bind to the ACh receptors on the post-synaptic neuron

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15
Q

What does binding of the ACh to the receptors cause

A
  • Opens the intrinsic ion channel, resulting in a cation entering
  • This results in a local depolarisation of the sarcolemma
  • This results in opening of the sodium channels causing an influx of Na+
  • depolarisation of the sarcolemma that travels
    down the t-tubules and ultimately causes the
    release of Ca2+ from the sarcoplasmic reticulum - CONTRACTION.
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16
Q

What happens to unbound ACh in synaptic cleft?

A
  • Unbound ACh in synaptic cleft defuses away or is
    hydrolysed (inactivated) by acetylcholinesterase
    (AChE)
17
Q

What is the structure of the skeletal muscle?

A
  • Lots of muscle fibres make a muscle cell - bundles
  • muscle fibres are made of myofibrils
  • These myofibrils are made of units called sarcomeres
18
Q

What is the structure of a sarcomere?

A
  • Sarcomeres are made of thick and thin filaments
    – Z line is the end of the sarcomere
    – Thick and thin filaments slide over one another to
    shorten the muscle during contraction
19
Q

What is the sliding filament theory?

A
  • During contraction thin filaments slide over thick
    filaments
  • Thick filaments= myosin and have “heads”
  • Thin filaments = actin, these slide
  • Ca and ATP required for sliding and attachment