06-09-23 – Neurophysiology Revisions Flashcards

1
Q

Learning outcomes

A
  • Revise and understand how nerves work in both the central and peripheral nervous systems
  • Understand the basics of nerve conduction studies, detecting common nerve and neuromuscular junction problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Label the parts of a neuron (in picture).

Describe the 4 steps in the transmission of information along a neuron.

A
  • Parts of a neuron (in picture).
  • 4 steps in the transmission of information along a neuron:

1) Excitable cells

2) Information arrives at the cell body via dendrites where it is assimilated and processed

3) Processed information is then digitised into APs which are transmitted along the axon

4) At the end of the axon the information is passed to the target (muscle or neuron) at boutons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does diameter and surface area of an axon affect movement of charge along the axon?

What are the characteristics of an unmyelinated axon a balance between?

A
  • The larger the diameter of the axon, the lower the resistance is.
  • Passive movement of charge along the axon is easier with less resistance
  • Larger axons have faster passive charge movement
  • The more surface area there is on an axon, the higher its capacity to store charge across its membrane
  • The higher the capacitance the harder it is for charge to cross over the membrane, i.e. to overcome the repellent force of charge accumulated there.
  • The characteristics of an unmyelinated axon are a compromise between these two factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the 4 actions of the Voltage dependent sodium channels during the stages of an action potential

A
  • 4 actions of the Voltage dependent sodium channels during the stages of an action potential:

1) At resting potential Na+ channels are closed - the activation gate is closed

2) Depolarization opens the activation gate and Na+ flows into the cell along its electrochemical gradient

3) A delayed component of voltage dependent activation is the blocking of the channel by the inactivation gate (after about 0.5ms)

4) Repolarization of the cell re-sets the two gates to their equilibrium positions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does information transmit along axons?

What is the voltage for resting potential?

What is the threshold voltage for action potentials?

Describe 3 features of action.

Describe the voltage graph for an action potential (in picture)

A
  • Information transmits along axons via action potentials
  • The resting membrane potential is -70Mv
  • The threshold potential for action potentials is -55mV
  • 3 features of action potentials:
    1) Self-propagates
    2) Travels in one direction
    3) No volume control – Just ON and OFF
  • Voltage graph for an action potential (in picture)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the 6 different stages of an action potential (in picture)

A
  • 6 different stages of an action potential (in picture)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is myelin?

What is it used for?

What cells provide myelination in the CNS and PNS?

How many axons do these cells provide myelination for?

A
  • Myelin is a fatty sheath
  • It is used to insulate axons in order to increase the diameter of axons, therefore increasing the speed of transmission
  • Oligodendrocytes provide myelination in the CNS (Multiple axons each)
  • Schwann cells provide myelination in the PNS (One axon each)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are nodes of Ranvier?

What is their purpose?

What is Saltatory conduction?

What is the benefit of saltatory conduction?

A
  • Nodes of Ranvier are the periodic gaps between myelin sheaths along the axon
  • They exchange ions in order to regenerate the action potential (action potentials occur at the nodes of Ranvier)
  • Saltatory conduction is the propagation of action potentials along myelinated axons
  • By saltatory conduction, currents can travel farther and faster with less energy wasted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does diameter affect conduction in unmyelinated nerve fibres?

How does myelination affect speed of conduction?

What is slowing of conduction consistent with?

Why are most fibres in the nervous system myelinated?

How fast is normal conduction velocity?

How fast is conduction velocity in alpha motor neurons?

A
  • For unmyelinated nerve fibres, larger diameter = faster conduction
  • Myelination is responsible for enhancing the speed of conduction, so any slowing of the speed of conduction is consistent with demyelination
  • To keep the nervous system compact, most fibres are myelinated, so small diameter myelinated fibres can conduct faster than large unmyelinated ones
  • Normal conduction velocity = 50-60 meters/second
  • The fastest alpha motor neurons can conduct at 120 m/s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do neurons communicate between each other?

What is the synaptic cleft?

How large is he synaptic cleft?

What is the bouton of a presynaptic cell?

How are neurotransmitters released from the presynaptic cell membrane?

Where do they diffuse to?

How are neurotransmitters inactivated?

A
  • Neurons communicate via synapse and neurotransmitters
  • The synaptic cleft is the gap between the pre and postsynaptic cell
  • The synaptic cleft is approximately 20 nanometres
  • The bouton of a presynaptic cell is a swelling
  • Neurotransmitters are released from the presynaptic cell membrane by exocytosis
  • Neurotransmitters diffuse to the postsynaptic membrane where they bind to receptors
  • Neurotransmitters are then inactivated by diffusion, re-uptake or enzymal inactivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 2 ways receptors are classified?

A
  • 2 ways receptors are classified:

1) How they are activated:
* Ionotropic (directly gate ion flow) or
* Metabotropic (indirectly gate ion flow or activate other pathways)

2) Positive/negative effects:
* Excitatory or inhibitory depending on the ions they let into/out of the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the 6 steps involved from neurotransmitter release to formation of an action potential (in picture)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does each receptor type possess?

What are generator potentials used for?

How does strength of external signals affect AP frequency in axons?

A
  • Each receptor type (e.g touch) has a modality and feeds information about modality to the CNS
  • Generator potentials are used by receptors to code the duration and magnitude of external signals
  • This means stronger external signals result in a higher frequency of APs in the axon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a neuromuscular junction? What happens when an AP reaches the neuron terminus?

What is released?

What does this stimulate?

How does botulinum toxin affect this process?

A
  • The neuromuscular junction is a chemical synapse between a motor neuron and a muscle fibre
  • When an action potential reaches the neuron terminus, this activates voltage-gated calcium channels
  • Acetylcholine is released and attaches to nicotinic- acetylcholine receptors on the postsynaptic surface
  • This process stimulates muscle contraction
  • Botulinum toxin works by stopping acetylcholine from being released from the end motor neuron, hence stopping muscle contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What type of condition is Myasthenia Gravis (MG)?

What is it caused by?

What does MG present with?

What does Mg usually begin with?

What is MG treated with?

How often does Myasthenic crisis occur?

What can this lead to?

A
  • Myasthenia Gravis (MG) is an autoimmune disease of the neuromuscular junction
  • It is caused by antibodies blocking / destroying post-synaptic acetylcholine receptors
  • MG presents with painless weakness with fatiguability (hallmark of MG)
  • MG usually begins with oculomotor weakness in one or both eyes
  • Treatment usually acetylcholinesterase inhibitors and immunosuppressants
  • Myasthenic crisis can occur in about 20% of patients, which leads to acute respiratory failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the purpose of stretch reflexes?

What are they mediated by?

How are muscle spindles arranged?

A
  • Stretch reflexes enable muscles to oppose external forces that tend to elongate them
  • Stretch reflexes are mediated by sense organs within muscles known as muscle spindles
  • Muscle spindles are mounted in parallel to the extrafusal muscle fibres
16
Q

Describe the 3 different portions of spindle fibres (in picture).

What does the sensory afferent to the spinal cord provide?

What is the role of the gamma motor neuron efferent from the spinal cord?

A
  • 3 different portions of spindle fibres (in picture)
  • The sensory afferent to the spinal cord provides information on stretch
  • The gamma motor neuron efferent from the spinal cord regulates the degree of contraction in a muscle
17
Q

Describe the mechanisms involved in muscle stretch reflexes

A
  • The mechanism involved in muscle stretch reflexes are feedback loops
  • There are positive signals that result in the contraction of the agonistic muscle to protect overstretching (e.g biceps)
  • There are negative signals to promote relaxation in the antagonistic muscles (e.g triceps)
18
Q

Summary of muscle spindle involvement in muscle contraction

A
19
Q

What is the purpose of nerve conduction studies?

What type of fibres do these studies look at?

Which fibres do they not look at?

How does large/small nerve fibre disease tend to present?

How can these symptoms be tested in other ways?

A
  • The purpose of nerve conduction studies is to Test conduction in peripheral nerves, giving evidence for any axonal injury or demyelinating disease
  • Nerve Conduction Studies looks at large fibres only
  • Do not test a single nerve fibre but rather a sum of action potentials from a bundle of nerve fibres
  • Can test sensory fibres – which travel up to the level of the dorsal root ganglion in the spinal cord
  • Can test motor fibres which travel from the anterior horn cell
  • Large nerve fibre disease tends to present with negative symptoms e.g. loss of motor power or sensory numbness/ loss of proprioception
  • Small nerve fibre disease tends to present as positive symptoms e.g. chronic pain, burning, allodynia. (pain due to a stimulus that does not normally provoke pain)
  • These are tested in other ways e.g. Sympathetic skin response (SSR) tests, thermal thresholds etc.
20
Q

Nerve conduction study: motor study.

What do axons and myelin give rise to?

A
  • Nerve conduction study: motor study
  • The axons give rise to the amplitude of the action potential (CMAP – Compound Motor Action Potential)
  • Myelin gives rise to the conduction velocity (MNCV – Motor Nerve Conduction Velocity)
  • Remember speed = distance/ time
21
Q

Nerve conduction study: sensory study.

What do axons and myelin give rise to?

How can the superficial radial nerve be stimulated?

How can the action potentials be recorded?

A
  • Nerve conduction study: sensory study
  • Again, the axon gives rise to the amplitude of the action potential (SNAP – sensory nerve action potential)
  • Myelin gives rise to conduction velocity (SNCV – sensory nerve conduction velocity)
  • The superficial radial nerve can be stimulated using electrodes placed around the thumb
  • The radial nerve sensory action potential can be recorded using surface electrodes at the wrist
22
Q

What are 3 abnormal patterns that can be seen on nerve conduction studies?

A
  • 3 abnormal patterns that can be seen on nerve conduction studies:

1) Axon loss
* When axons are lost, there are fewer excitable axons, and therefore fewer muscle cells are excited, resulting in a lower compound muscle action potation (CMAP)

2) Diffuse demyelination
* For diffusely disrupted myelin, distal latency is prolonged, and the conduction velocity is slow but the CMAP retains normal amplitude

3) Focal demyelination
* Signals are slowed, with some not getting through at all

23
Q

When are nerve conduction studies indicated?

What are they less useful for?

What are 3 limitations of nerve conduction studies?

A
  • Nerve conduction studies are indicated for any focal sensory or motor symptoms
  • They are less useful in polyneuropathies, but sometimes still used
  • 3 limitations of nerve conduction studies:

1) Not suitable for testing small fibres

2) Often not diagnostic on their own, but can be useful as part of a work-up of history taking, neurological examination and further tests/ imaging

3) Results less reliable in elderly patients

24
Q

What are 4 focal neuropathies nerve conduction studies (NCS) are used for?

What are 4 polyneuropathies nerve conduction studies (NCS) are used for?

A
  • 4 focal neuropathies nerve conduction studies (NCS) are used for:
    1) Traumatic nerve injury
    2) Carpal tunnel syndrome
    3) Ulnar neuropathy
    4) Radiculopathy (can identify root level and severity)
  • 4 polyneuropathies nerve conduction studies (NCS) are used for:

1) Diabetes mellitus (may present with axon-loss peripheral neuropathy)

2) Motor Neuron Disease (can be a mix of upper and lower motor lesions so NCS useful for assessing lower motor neurons)

3) Demyelinating Polyneuropathies
* Charcot-Marie-Tooth disease
* Guillain-Barré syndrome

4) Disorders of the Neuromuscular Junction e.g. Myasthenia Gravis

25
Q

What type of condition is Charcot-Marie Tooth Disease?

What type of neuropathy does it cause?

When does it present?

What are 4 symptoms and signs of Charcot-Marie Tooth Disease?

A
  • Charcot-Marie Tooth Disease is a hereditary demyelinating polyneuropathy
  • It causes cause sensory and motor peripheral neuropathy
  • It typically presents in childhood or early adulthood
  • 4 Symptoms and signs of Charcot-Marie Tooth Disease:

1) Difficulty walking

2) Foot drop

3) High arched feet and hammertoe

4) If motor power loss, then legs often resemble an inverted champagne bottle

26
Q

What type of condition is Guillain-Barré syndrome?

How fatal is this condition?

How do patients usually present with Guillain-Barré syndrome?

What can occur if symptoms are left untreated?

How is it treated?

How long can recovery take?

A
  • Guillain-Barré syndrome is an autoimmune, rapidly progressive demyelinating polyneuropathy
  • This condition can be life-threatening
  • Patients with Guillain-Barré syndrome usually present with progressive peripheral neuropathy
  • If left symptoms can deteriorate until the respiratory muscles are paralysed
  • Treatment consists of IVIG (Intravenous immunoglobulin), analgesia, and if needed ventilatory support.
  • Guillain-Barré syndrome can have long recovery with need for rehabilitation