L34. Activation of Muscle Flashcards

1
Q

What are some observable signs of faulty motor control? [7]

A
  • Paralysis and weakness
  • Stiffness (either passive or while moving)
  • Increased reactivity
  • Ticks, twitches and jerks
  • fibrillations and fasiculations
  • loss of coordination and smoothness
  • loss of effectiveness of movements
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2
Q

Define the term “sign” in the context of motor control

A

An observable or measurable motor abnormality or the absence of normal motor actions

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3
Q

Define the term “symptom” in the context of motor control

A

problems of motor function as reported by patients

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4
Q

Define the term “syndrome” in the context of motor control

A

Associated or clustered signs and symptoms (this grouping of signs/symptoms are often due to a single underlying process)

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5
Q

Describe motor neurons and where their cell bodies (soma) reside

A

Motor neurons are large cholinergic neurons that form clusters in the grey matter of the ventral horn of the spinal cord

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6
Q

What is the anatomical and functional relationship between motor neurons and muscles?

A

Each muscle is innervated by hundreds/thousands of motor neurons (called the motor pool) of that muscle.

And the level of activation (the number of neurons in that motor pool that are being activated) determines the state of contraction of that muscle

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7
Q

Describe conduction through the motor neuron and how this is achieved. What is the relationship of a single motor neuron with muscle fibres.

A
  • Muscle neurons are large caliber, fast conducting through a myelinated axon
  • The muscle fibre makes a large synapse with the muscle in a structure called the Neuromuscular junction

One neuron innervates several fibres within the muscle

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8
Q

What is the motor unit of a muscle fibre?

A

The motor unit is the distribution of muscle fibres that a single muscle neuron innervates. There are hundreds and thousands of these motor units in a single muscle.

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9
Q

Describe the concept of the most basic level of muscle control

A

The state of contraction/activity of a single muscle depends on…

  1. The activation of motor units (ie. the number of motor units involved in the action)
  2. The frequency of stimulation of each of these motor units.
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10
Q

What is the approximate speed of electrical conduction through motor neurons?

A

Approximately 30 m/s

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11
Q

How are muscles activated?

A

There is an incremental nature of muscle activation

This means that the action potential and subsequent muscle fibre activity of a neuron is ALL-OR-NONE and thus the control depends on the number of fibres involved

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12
Q

If muscle fibres are controlled by an all-or-none concept (ie. active or not active, there is no in between), how is the control of muscle contraction by a single motor unit achieved?

A

Variations in frequency, not amplitude

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13
Q

What is Henneman’s size principle of motor neuron pool recruitement in muscle activation?

A

There is an order of recruitment of different motor units (size/fibre types/force) as force increases in a muscle

It states that under load, motor units are recruited from smallest to largest.

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14
Q

How is maximal force achieved in a muslce?

A

The activation of 100% of the motor neuron pool of that muscle - which means the large motor neurons are involved

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15
Q

Describe the order of recruitement from lowest force to maximal force of muscle fibres

A
  1. Slow-twitch, low-force, fatigue resistant and Small fibres
  2. Fast-twitch, low-force,fatigue-resistant medium fibers
  3. Fast-twitch, high-force, less fatigue-resistant and Large muscle fibers
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16
Q

There are muscles are almost constitutively active to maintain postural tone. Describe their biochemical profile compared to other muscles

A

They have a sustained capability to generate contraction (able to undergo anaerobic metabolism) to generate sufficient amounts of ATP and thus fatigue very slowly

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17
Q

What happens when one action potential reaches the muscle fibre at the neuromuscular junction

A

There is a 1:1 relationship between action potential:muscle activation (1 synapse per muscle cell)

The arrival of a nerve impulse to the post-synaptic cell (the muscle) results in a complete activation of the muscle

(Compared to other neurons where a there a multiple synapses onto the post-synaptic cell and there is an additive effect of all the inputs - There is always a threshold reached to cause muscle activation)

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18
Q

What is the safety margin of the neuromuscular junction?

A

It refers to the ability of neuromuscular transmission to remain effective under various physiological conditions and stresses.

This is a result of the

  • Amount of transmitter released per impulse being greater than that required to trigger an action potential in the muscle fibre.
  • Large number of receptors on the post-synaptic membrane
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19
Q

How does Myasthenia Gravis affect the safety margin of the neuromuscular junction?

A

MG is an autoimmune disease that attacks and reduces the number of Nicotine receptors (AChR) on the postsynaptic membrane and inability of ACh to activate receptors.

This erodes (significantly narrows) the safety margin to the point where the impluse may no longer enough to generate threshold and muscle twitch

20
Q

What two physcial factors help to increase the efficiency of NMJ effectiveness (and thus increase the safety margin)

A
  1. Varicosities at the end of the NMJ (the tips of the axon) increase the surface area of the synaptic ACh release site = more ACh release
  2. The post-synaptic membrane has folds to further increase surface area to allow for more receptors to be expressed = more receptor activation
21
Q

What happens if muscles remain unactivated? (Eg. if they lose or have reduced innervation)

A

They attempt to increase their excitability by producing more ACh receptors at the NMJ. These may even spread to have expression beyond the junction boundary (extrajunctional activation).

This means that their sensitivity to very small amounts of ACh is markedly increased in attempt to get some muscle activation

22
Q

Describe muscle fibrillations and how they occur

A

Fibrillations are tiny contractions caused by the activity of a single muscle cell caused by non-synpatic means (ie. ACh floating around, not from an axon causes excitation of single muscle cells)

They can be due to:

  • hypersensitivity by increased AChR expression

Because it is a single cell, they cannot be measured on the surface (require extracellular electrodes)

23
Q

Describe muscle fasciulations and how they occur

A

Fasiculations are groups of muscle fibres (ie a whole motor unit) contracting involuntarily as a result of spontaneous activation of a degenerating MN/axon.

The degenerating motor neuron has some small levels of activity but are completely uncoordinated and thus as it degenerates it spontaneously attempts to send signals resulting in isolated fasiculations).

They can be measured on the surface

24
Q

What happens to a muscle after long term denervation?

A

Atrophy and degeneration

Atrophy can occur in catabolic states and denervation as a result of lack of nourishment and electrical activity to the muscle.

Complete denervation will lead progressively to irreversible muscle loss

25
Q

Is there a risk of atrophy and degeneration as a result of basic muscle inactivity (ie. not denervation)?

A

Muscles are rarely inactive

Muscles have a resting tone/state of contraction (thought to be set by the cerebellum) that makes them ready to carry out any voluntary movement (except during REM sleep).

This means that muscles are always receivng some basal level of excitation preventing atrophy and degeneration

26
Q

What causes an involuntary muscle activation (ie. the sensory reflex)

A

There is an afferent component to muscle activity (ie sensory inputs) that help coordinate and control muscle movement.

Muscle sense and spinal reflex organisation through:

  • Intrafusal muscle fibres (spindles) encoding length
  • Golgi tendon organs encoding force
27
Q

Describe the monosynaptic reflex

A
  1. Small pulls (by a tendon tap) sends an afferent action potential through the mechanosensory fibres of the intrafusal muscle fibres
  2. Synaptic connections are made to the ventral horn (motor neuron) to cause a contraction of the muscle
28
Q

Why is the monosynaptic stretch reflex (deep tendon reflex) considered a negative feedback reflex?

A

Because the muscle senses a stretch/lengthening signalling it is too long and the monosynaptic stretch pathway causes the muscle to contract back to its normal state

29
Q

What happens when the peripheral motor system (Lower motor neuron) components are damaged? Why? [6]

A
  1. Weakness or paralysis (due to lost innervation)
  2. Decreased superficial reflexes (lost sensory innervation like pain and temperature)
  3. Hypoactive deep reflexes (due to impaired efferent muscle innervation)
  4. Decreased tone (decreased level of electrical activity)
  5. Fasciulations and fibrilations (signs of denervation and hyperexcitability of the muscle)
  6. Severe muscle atrophy (due to denervation and lack of electrical activity)
30
Q

How are voluntary movements elicited?

A

Upper motor neurons from the cortex travel down the spinal cord white matter and then synapse with the alpha motor neuron in the ventral horn (usually through interneurons)

31
Q

What is the common final pathway?

A

The alpha motor neuron beginning in the ventral horn of the spinal tract descending down to the NMJ is the final common pathway.

It is called this because both voluntary and reflex movements (ie. all motor control) has to pass through this pathway to elicit any sort of muscle activity

32
Q

Through what tract does descending motor control go through in the spinal cord?

Where is the location of this tract?

A

The corticospinal tract

It has an lateral and a ventromedial component to it

33
Q

Describe the difference between the lateral corticospinal tract and the ventrolateral spinal tract?

A

The lateral white matter tracts mainly innervate the distal muscles, thus mainly concerned with dextrous movements

The venteromedial white matter tract innervates the proximal muscles and thus innervate muscles more concerned with postural tone

34
Q

Does the corticospinal tract decussate? Where does it do this?

A

The two parts of the corticospinal tract decussate in different areas.

85% of the corticospinal tract fibres travel in the lateral brainstem. And these decussate in the caudal medulla at the decussation of pyramides.

The rest of the tract (ventromedial corticospinal tract) travels ipsilaterally through the spinal cord and provides bilateral innervation at the spinal cord level.

35
Q

Describe the pathway of the main corticospinal tract from the primary motor cortex to the spinal cord

A
  • It travels through the white matter of the internal capsule
  • It descends into the brain
  • It synapses in the brainstem and sends projections through the reticular formation travelling ventromedially to supply the proximal muscles
36
Q

Explain the names extrapyramidal and pyramidal motor tracts

A

The pyramidal are those that come from the primary motor cortex (like corticospinal and some corticobulbar)

Extrapyramidal tracts are chiefly found in the reticular formation of the pons and medulla, and target neurons in the spinal cord involved in reflexes, locomotion, complex movements, and postural control: reticulospinal, colliculospinal, etc

37
Q

Describe the path of the lateral corticospinal tract from the primary motor cortex to the spinal cord

A
  • From the motor cortex it projects through the white matters of the internal capsule
  • Fibres relay to the branstem and decussate at the decussation of pyramids
  • Projections travel down to the lateral region of the spinal tract
  • They either synapse with interneurons or directly on the alpha motor neurons
38
Q

What is the reticulospinal tract?

A

An extrapyramidal motor tract that descends from the reticular formation in two tracts to act on the motor neurons supplying the trunk and proximal limb muscles.

  • Important for initiating movement (tone and posture)
39
Q

What is the colliculospinal tract?

A

A tract from the superior colliculus of the brainstem to lower motor neurons

Involved in involuntary adjustment of head position in response to visual information.

40
Q

What happens to locomotion when the brain can no longer influence the spinal cord in humans?

A

The spinal locomotor circuits can not be activated in any way possible (the brain is critical to activate walking)

41
Q

What happens to the activity of the motoneurons if the brain is no longer able to influence their function (ie UMN lesion)?

A

The brain is normally inhibitory on the spinal cord and rather than being less excitable, the motorneurons exhibit a Hyperexcitability with hyperreflexia and hypertonia

42
Q

What are the main signs and symptoms observed in UMN lesions? Explain them [5]

A
  1. Weakness (due to a reduced activation)
  2. Spasticity - increased tone due to lost net inhibitory input from the UMN
  3. Spaciticity - hyperreflexia and clonus (where the movement can’t be stopped)
  4. Babinski sign
  5. Loss of fine voluntary movements
43
Q

Why are reflexes and gait always examined in neurological clinical exams?

A

Because they involve all levels of the motor control system: the brain, spinal cord and the periphery. These movements of walking and reflex action interogate the entire nervous system.

44
Q

What is the difference between a spinal reflex and a segmental reflex?

A

Spinal Reflex: a reflexive action mediated by cells in the spinal cord, bypassing the brain altogether. Eg. knee jerk

Segmental Reflex: a reflexive action mediated by neurons in several segments of the spinal cord. Eg. withdrawl reflex

45
Q

Describe what an exaggerated segmental reflex would mean compared to an abnormal spinal reflex

A

An exaggerated segmental reflex means the inhibitory control of brain is lost and hence is an UML sign. An abnormal spinal reflex tells you the brain isn’t responding correctly (can also be an UML)

46
Q
A