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Flashcards in S3: Proprioceptors Deck (42)
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1
Q

What are Proprioceptors?

A

They are a type of sensory receptors that monitor the movements of your own body. They are found in muscles, tendons and joints.

2
Q

Two main functions of proprioceptors

A
  1. Allow you to know where your body is.

2. Provide vital feedback information for the control of our motor systems.

3
Q

Describe structure of motor unit

A
  • a-motor neurones innervate skeletal muscle (the extrafusal muscles) causing it to contract.
  • These have their cell bodies in the anterior horn of the spinal cord and their axons project out to muscle where they will give a single synapse to muscle fibres.
  • The a-motor neurone going down and innervating muscle fibres forms a muscle unit.
  • Each AP in that motor unit will produce an AP in the muscle fibres the neurone is innervating. This causes a transient twitch in the fibres (twitches are all or nothing events).
4
Q

Relationship between number of neurones to muscle fibre

A

A single neurone can innervate multiple muscle fibres but a single fibre can have only one nerve innervating it.

5
Q

How can the force of contraction of twitches can be modified by the brain?

A
  1. Change the frequency of action potential firing in the active motor units.
  2. Change the number of active motor units.
  3. Change the type of active motor units.
6
Q

Describe motor unit activity at rest

A

At rest, when relaxing there is a little activity going on in our muscle fibres. Small weak oxidative fibres are firing slightly producing some background tone in the muscle.
This is because there is activity in the smallest motor neurons that have the smallest and weakest motor units.

7
Q

What is the general rule about the size of a neurone cell body?

A

The general rule is that the bigger a neurons cell body, the bigger the stimulation you have to give it to get it up to fire an action potential.

  • So if there is weak excitatory input coming into a pool of motor neurones, only the smallest and weakest neurones are active.
  • So smaller cells are easier to activate than big cells.
8
Q

What does a pool of motor neurones mean?

A

A group of a-motor neurone cell bodies in the anterior horn that are involved in innervating a single muscle.

9
Q

Describe how force of contraction of twitches can be increased by increasing overall excitation of motor unit pool

A

Increasing the overall excitation of the motor unit pool means there will have more action potentials activating more muscle fibres. This means the next easiest (and larger) neurons will be activated.
- Middle neurones activated: These are more powerful, but more fatigable e.g. this is useful in long distance running
- Largest neurones activated: Maximum excitatory input coming to motor unit pool and there is activation of the biggest motor units. These innervate large powerful fibres e.g. throwing large things.
So if we grade muscle power by increasing the amount of excitatory input onto the a-motor neurone unit pool they will automatically activate from weakest to strongest.

10
Q

What 2 inputs affect whether a cell produces an AP or not?

A

Whether a cell produces an AP is based on the balance of excitatory and inhibitory inputs.
So if we want a weaker contraction we can have less excitation or more inhibition, this means it is a balance between excitation and inhibition.
More inhibition will switch off excitation, but if this inhibition is decreased, the smaller fibres will be first excited as they are more susceptible to being activated.
Importantly, it allows very fine control over movement.

11
Q

What two things do proprioceptors monitor?

A
  1. Changes in muscle length.

2. Tension in muscle tendon.

12
Q

Describe structure of muscle spindle and its fibres

A
  • Muscle spindle is in muscle
  • Spindle consists of a capsule and inside intrafusal muscle fibres
  • Surrounding the outside are normal muscle fibres called extrafusal fibres
  • Contractile portions are at end of intrafusal muscle fibres (actin and myosin) while the middle is just passive elastic fibres were afferent nerve fibres are found. It is stretch in the middle area that will activate the sensory afferents.
13
Q

How do intrafusal muscle fibres increase excitation of a-motor neurone pool?

A

Intrafusal fibres are associated with sensory afferents which project to the spinal cord and are able to increase excitation of that α-motor neurone pool!
- What occurs is when there is unintended stretch of a muscle, due to the muscle contracting too little (e.g. arm/leg sagging down). The spindle gets stretched (in middle) and this will cause the sensory afferents to send signals to the spinal cord and will increase excitation of the motor neurone pool innervating that same muscle. As a result there will be increased AP firing and contraction of more and bigger myofibres and the muscle will contract with more force allowing to maintain position. This allows control of posture.

14
Q

What is the difference between intrafusal muscles and extrafusal muscles?

A

Intrafusal muscles are those fibres inside the muscle spindle capsule which extrafusal muscles are the ordinary muscle fibres making up the bulk of the muscle.

15
Q

What controls our posture?

A

It is our muscle spindles rather than brain! We don’t have to think about how hard it is to contract our muscles in order to control a limb in one position. We also have to make exactly the right number of motor neurones fire the right number of AP to keep a posture and it is our spindles that control this.

16
Q

Describe reciprocal inhibition in the control of posture

A

An example is our arm:

  • Biceps and triceps muscles present. a-motor neurone activates biceps.
  • The muscle spindle has its afferent which makes a monosynaptic connection with the motor neurone, so if you have unintended stretch of the muscle it will reflex contract (if contraction becomes too weak to support the mass and arm sags down which stretches the muscle).
  • The afferent also activates an inhibitory interneurone which suppresses activity in the motor neurone driving the antagonistic muscle - inhibits stretch reflex in anatagonist muscle.
  • Therefore, when we have the unintended stretch of the biceps, the spindle will detect the stretch of muscle and send a signal to the spinal cord which increases excitation to the α-motor neurone pool (via the afferents) to the biceps to increase contraction and at the same time activate inhibitory interneurones that inhibit the α-motor neurones to the triceps, which relaxes it.
  • This is because if we a reflexively contracting the biceps, the triceps need to be relaxed to allow this movement.
17
Q

Mechanism of interneurones allowing reciprocal inhibition

A

The interneurons are glycinergic and act through inotropic receptors (LGICR) on the motor neurone. They open up and allow Cl- to flow in (for example) which hyperpolarises the cell decreasing AP firing.
- Because of this, reciprocal inhibition is rapid in onset, short lasting and relatively weak (what we would expect from LGIC inhibition).

18
Q

Why is presynaptic inhibition important?

A

The motor system needs a way to suppress the muscle spindle input, to allow voluntary movements to take place (muscle spindles can prevent muscles from stretching).

19
Q

Describe presynaptic inhibition

A

Using the arm as an example:
- The triceps naturally also have muscle spindles which have monosynaptic connections with their own a-motor neurones.
- As we can see, the bicep afferents make synaptic connections with inhibitory interneurons that inhibit release of neurotransmitter from the antangonist spindle afferents. This prevents the triceps afferent from exciting its motor neurones when it’s stretched.
This is presynaptic inhibition which has switched off the triceps reflex arc and this is what we want because if we are contracting the bicep we want the triceps to relax.

20
Q

Mechanism of interneurones allowing presynaptic inhibition

A

The interneurones here are GABAergic and works through GABAb on the axon terminals which are metabatropic.
- Because of this presynaptic inhibition is slow in onset but long-lasting and more powerful because it is switching off the reflex arc at the synapse. Preventing the α-motor neurones from even being stimulated.

21
Q

Difference between presynaptic inhibition and reciprocal inhibition

A
  • Presynaptic is through G-couples receptors while reciprocal is through ligand gated.
  • Presynaptic switches off the reflex arc at the synapse while reciprocal only inhibits it.
  • Presynaptic prevents a-motor neurones from being activated while reciprocal decreases the AP firing.
22
Q

What neurones control extrafusal and intrafusal fibres?

A
  • a-motor neurones control extrafusal fibres

- y-motor neurones control poles of intrafusal muscle fibres

23
Q

When are the sensory stretch afferents in elastic central part of intrafusal fibres activated? Why does this need to be controlled?

A

the afferents will only be activated if this bit stretches.
So if the central elastic bit of the muscle spindle stretched at the same time as every time we stretched a muscle, e.g. at a deliberate movement the spindles would be activated and try stop it happening. To try and stop this happened, presynaptic inhibition occurs.

24
Q

How to poles help prevent centre of intrafusal fibres stretching?

A

One way is that the poles of the intrafusal fibres are innervated by γ- motor neurones. This allows control of the length of those contractile pole regions of the intrafusal fibres.
The γ- motor neurones do this in such a way that if we are doing a voluntary movement, then if everything goes to plan, the centre of the intrafusal fibres will not change length if we stretch the muscle (or contract it). All the length will be taken up by the poles, therefore the afferents won’t be activated. There will be no activity in the central region so it remains at same length under tension and sensitive to being stretched.
This is the way brain gets to turn off this reflex, by ordering the gamma motor neurones to get the length to be taken up by the poles.

25
Q

Examples of poles in intrafusal fibres during contraction and stretch

A

Muscle contraction:
- a-MN contracting extrafusal fibres and gamma-MN contracting poles of intrafusal fibres so they take up length and central portion does not change.

Muscle stretch:

  • When muscle is stretched voluntarily a-MN are not active as muscle is not contracting but it is being stretched.
  • gamme-MN are also switched off allowing poles to stretch and take up length so central portion does not change length.
26
Q

Inhibition of stretch reflex

A
  1. Post synaptic: The reciprocal inhibition neurones can be activated by the brain as well as the muscle spindles afferents.
  2. Pre synaptic : Contact the terminals of muscle spindle afferents rather than motor neurone.
  3. Inhibition of a-MN pool : Descending control system pathways from the brain travel down to activate inhibitory interneurons. If we increase the inhibition of the motor neurone pool we will decrease the contraction of the muscle as a whole.
27
Q

How do we maintain accuracy of movement? Use an example with lifting cup

A

To learn a new movement an maintain accuracy, the motor systems need constant feedback about the movement they are generating.
- E.g. pick up cup, heavier than expected than for movement planned but we still lift it accurately.
- As we lift the cup, it takes more contraction in our muscles to lift the mug as heavier weights slow down muscle contraction unless power is increased.
- So as we start to lift the mug, our alpha MNs fire but our muscle shortens slower than intended because the weight is heavier.
- The muscle spindles however are not attached to the tendons and are not carrying any weight themselves, so the intrafusal fibres receive their impulse from the gamma motor neurones and contract at the normal, expected speed (faster than main muscle).
- So as a result the muscle as a whole is contracting more slowly while the intrafusal fibres contract normally.
- This actually results in the centres of the intrafusal fibres stretching, so the afferents get activated and go on to excite the alpha motor neurone pool with more frequency which recruits more motor units increasing the contraction of the muscle. So in this case, our muscle spindle reflex has corrected the movement (contract more strongly to overcome extra weight). In this way our spindles allow us to perform movements accurately e.g. touch nose with finger when eyes closed.

28
Q

What do lower motor neurones mean in musculoskeletal system?

A

The a-motor neurones

29
Q

Describe lower motor neurone lesions

A
  • LMN can be in cell body itself or section of nerve preventing signal from reaching muscle.
  • Lesions prevents excitatory signals from reaching the muscle, hence muscle fibres have lose innervation causing flaccid paralysis. The muscle is no longer capable of contraction as efferent part of reflex has been lost. Overtime due to absence of contraction, the actin and myosin will breakdown and gradually the muscle will waste away into connective tissue.
  • Fasciculations may be seen where muscle fibre has been denervated and they send out signals to attract surviving MN to innervate it. So the surviving MN will grow out and re-innervate and everytime this neurone fires the fibres will twitch.
  • Fibrillations is when the denervated muscle fibres start to twitch automatically.
30
Q

What are upper motor neurones?

A

UMN have their cell bodies in the brain and carry signals down from the brain to the spinal cord.

31
Q

Where may upper motor neurone lesions be found?

A
  • UMN control all facets of spinal motor circuits. An UMN lesion may be at the cell body in brain but could be a lesion in the spinal cord that cuts through the axon and prevents the signal from getting down to the motor circuitry.
32
Q

Consequences of upper motor neurone lesions

A
  • The UMNs connect onto the α-motor neurones, so you lose the ability to contract the muscle so the person becomes weak, the muscle itself hasn’t wasted away so is still strong in itself (due to intact reflex arc), but you are unable to voluntarily have strength over your muscle and use the strength.
  • The UMNs also control the gamma motor neurones of the reflex arc, so if the brain cannot do this (fire gamma motor neurones properly) it means that you have uncontrolled reflexes. This is because the centre of your intrafusal fibres will keep stretching as no longer being taken up by the poles.
  • As well as this the UMNs have control over the inhibitory interneuones, so if these cannot be excited it means that the signals to α-motor neurones cannot be dampened down so you get increased tone and reflexes even on voluntary movement. E.g. bicep starts stretching voluntarily but due to lesion there is no inhibition so bicep contracts reflexively = stiff.
  • There is no wasting as muscles remain active due to reflex input.
33
Q

What are the two types of intrafusal muscle fibre?

A

Contained within our capsule we can have around 6 intrafusal fibres. The intrafusal fibres can be divided into two classes:

  1. The “nuclear bag” fibres are associated with type Ia afferents
  2. The “nuclear chain fibres” which are associated with type II afferents.

There are some in the middle (associated with both), but these are two extremes.
Both these afferents (and hence fibres) produce slightly different reflexes and they can be controlled separately by the brain as there are different y motor neuron inputs.

34
Q

Describe group II afferents (role and structure)

A
  • At low length there is periodic firing, but as it increases to longer length there is more firing, more length = more firing.
  • These group II afferents are encoding different lengths of muscle, a simple relationship between muscle length and firing. The fibres respond (fire) in proportion to the length of muscle and are important in maintaining limb position, posture and resting muscle tone. Important for slow changes in position.
  • Group II afferents generally have thinner, slower axons and form mainly indirect connections to α-motor neurones (i.e. they synapse onto interneurones first).
35
Q

How will loss of UMN input affect group II afferents?

A

A loss of an upper motor neurone input to group II reflexes will cause the reflex to run out of control causing hypertonia (increased tone).
This is increased resistance to moving it, the muscle will be more stiff. But it will be equal at all velocities.
f you have an improperly controlled type II arc, it is said that hypertonia can be treated by suppressing the group II reflex with α2 agonists (e.g. tizanidine).
It appears boosting noradrenergic transmission.

36
Q

Describe group Ia afferents (role and structure)

A
  • Type Ia afferents fire rapidly when the muscle is changing length rapidly, but once it reaches a given length it quickly goes back to the original level. It responds in proportion to the velocity of the muscle stretch.
  • Ia afferents respond to the rate of change in length (i.e. the velocity of movement) and are important for correcting rapid unintended movements. To test these afferents we would hit the tendon with tendon hammer and we would see a short sharp change in the muscle. They help correct pertubations in gait (e.g. high heel slip to the side and making the foot straight again).
  • Group Ia afferents have thicker, faster axons and make monosynaptic connections to α-motor neurones.
37
Q

How will loss of UMN input affect group Ia afferents?

A

A loss of upper motor neurone input to group Ia reflexes causes velocity-dependent increase in tone (this is called spasticity).
This is because of the lack of control over the α-motor neurones.
This is because afferent stimulates the α-motor neurones of the agonist (e.g. bicep) and also the triceps get stretched which causes their own reflex arc. Usually the antagonist α-motor neurones will be inhibited by descending fibres (as well as the afferent of the agonist) but because the inhibition isn’t there on both α-motor neurones, both contract hard = spasticty.

38
Q

How to treat spasitity (UMN symptoms)?

A
  • This can be done by a non-specific increase in spinal inhibition. However, this is a problem because you will end up hyperpolarising a-MN so they don’t fire.
  • Boost the effectiveness of GABAa receptors, you can use benzodiazepines.
  • More specifically by mimicking the effect of presynaptic inhibition. Activate GABAb receptors on the muscle spindle afferent terminal, we do this by using baclofen. Because the GABAb receptors are located on the synaptic terminal of the Ia afferent, their excitation with baclofen will dampen down firing.
    Therefore the Ia afferent will not be able to stimulate the α-motor neurone to contract, so we don’t get these strong contractions in the agonist and antagonist, preventing spasticity. By targeting the Ia afferent specifically we are not making the α-motor neurones any less excitable and therefore not interfering with the patients ability to voluntarily activate their α-motor neurones.
  • Botox - suppress unwanted reflexes by reducing stretch of motor neurone input to muscle fibres by it weakening the NMJ of that muscle. Doesn’t help with loss of movement but reduces spasticity.
39
Q

Describe golgi tendon organ structure

A
  • There is then a special encapsulated bit of tendon and these are joined to 1b sensory afferent fibre which are fast and fat. They have sensory nerve endings in the tendon.
  • Within the capsule there are collagen fibres which link the muscle to the bone and wrapped within this collagen are the 1b sensory afferent endings.
    If the muscle contracts it will pull on the tendon and squash these sensory endings between the collagen fibres, causing them to depolarise and produce APs.
    The harder the muscle contracts the more tension produced in the tendon and so more APs will be fired!
40
Q

Role of golgi tendon organ

A

Golgi tendon organs measure tension generated by active muscle contraction, because if you passively stretch the muscle you don’t produce enough tension to cause these fibres to fire.
GTO afferents activate two pathways that control the strength of muscle contraction and it is the upper motor neurones (descending pathways) that dictate which is active at any moment.

41
Q

How can golgi tendon organ control muscle tension?

A
  • If contraction is ramping up too high, the Golgi tendon organ will dampen it down, acting like a negative feedback e.g. to stop muscle spindles from overcorrecting movement.
  • In dynamic situations (e.g. walking) there will be particular moments in the gait cycle where the pattern generator in the spine will activate the positive feedback loop from the Golgi tendon organ to the muscle. This will ramp up the power of the muscle briefly.
42
Q

What happens with loss of golgi tendon organ?

A
  • Hypertonia in static situations e.g. standing as there is no negative feedback to stop leg muscles contracting more than needed.
  • Weakness in dynamic situations (e.g. gait, when walking). They will have excess tone (stiff) legs when standing and weak walking.