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Year 3 - Neurology (DP) > Neurophysiology > Flashcards

Neurophysiology Flashcards

1
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual tissue damage OR described in terms of such damage

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2
Q

What function does acute pain typically serve?

A

Protective

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3
Q

What is nociceptive pain?

A

An appropriate physiological response to painful stimuli via an intact nervous system

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4
Q

What is neuropathic pain?

A

An inappropriate response due to nervous system dysfunction

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5
Q

What is allodynia?

A

Pain from a non-noxious stimulus

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6
Q

What is hyeralgesia?

A

Excessive pain from a painful stimulus

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7
Q

Shingles, surgery, trauma, diabetes, amputation and idiopathic pain are what type - Nociceptive or Neuropathic?

A

Neuropathic

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8
Q

What is the first step of the WHO Analgesic Ladder?

A

Non-opioids:

  • NSAIDs
  • Paracetamol
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9
Q

What is the second step of the WHO Analgesic Ladder?

A 
Weak opioids:
- Codeine
- Tramadol
- Oxycodone (low dose)
\+/- Non-opioids
\+/- Adjuvants
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10
Q

What is the third step of the WHO Analgesic Ladder?

A 
Strong opioids:
- High dose morphine
- Fentanyl
\+/- Non-opioids
\+/- Adjuvants
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11
Q

What adjuvants are available for pain management?

A 
Antidepressants:
- Amitryptiline (1st)
- Duloxetine (3rd)
Anticonvulsants:
- Gabapentin (Alternative 1st)
- Pregabalin (2nd)
Topical analgesics:
- Capsaicin
- Lidocaine 5% plaster (4th)
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12
Q

What pain do NSAIDs mainly act on?

A

Nociceptive

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13
Q

What are the side effects of NSAIDs?

A

GI irritation/bleeding
Renal toxicity
Drug-drug interactions
CVS side effects (due to COX-2)

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14
Q

How does paracetamol work?

A

Inhibits central prostaglandin synthesis

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15
Q

What pain do opioids mainly act on?

A

Nocieptive

Some effect on neuropathic pain

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16
Q

What are the side effects of opioid analgesics?

A 
Nausea and vomiting
Constipation
Dizziness/Vertigo
Somnolence
Dry skin and pruritus
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17
Q

How do opioid analgesics work?

A
  • Stimulate limbic system receptors (eliminate subjective pain)
  • Affect descending paths that modulate pain
  • Decrease ascending pain signals
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18
Q

When are tricyclic antidepressants useful in pain management?

A

Neuropathic pain
Complex Regional Pain Syndrome
Tension headache

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19
Q

How do tricyclic antidepressants work?

A

Inhibit neuronal NA and 5-HT reuptake

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20
Q

What are the side effects of tricyclic antidepressants?

A 
Constipation
Dry mouth
Somnolence
HR and rhythm abnormalities
Insomnia
Increased appetite
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21
Q

Which is better in relieving neuropathic pain, SNRIs or SSRIs?

A

SNRIs

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22
Q

How do SNRIs and SSRIs work?

A

Selectively inhibit 5-HT and/or NA reuptake

Intensify descending inhibition -> Analgesia

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23
Q

What are the side effects of SNRIs and SSRIs?

A 
Nausea and vomiting
Constipation
Somnolence
Dry mouth
Increased sweating
Decreased appetite
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24
Q

How does gabapentin work?

A

Binds to presynaptic voltage-dependant calcium channels

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25
Q

How does pregabalin work?

A

Interacts with special N-type calcium channels

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26
Q

How does carbamazepine?

A

Blocks sodium and calcium channels (presynaptic)

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27
Q

What are the side effects of anticonvulsants in pain management?

A 
Sedation
Dizziness
Ataxia
Peripheral oedema
Nausea
Weight gain
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28
Q

How do topical analgesics work?

A

Reduce pain impulses transmitted by:

  • A delta fibres
  • C fibres
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29
Q

What are the side effects of topical analgesics?

A

Local:

  • Rash
  • Pruritus
  • Erythema
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30
Q

What is an opiate?

A

Substance extracted from opium or of a similar structure

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31
Q

What is an opioid?

A

ANY agent that acts upon an opioid receptor?

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32
Q

What brain regions are involved in pain perception and the emotional response that is projected to medulla and spinal cord?

A

Cortex
Amygdala
Thalamus and hypothalamus

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33
Q

What is the function of the periaqueductal grey (PAG)? What drugs can excite it?

A

Excitation produces profound analgesia
Enkephalins and morphine:
- Inhibit inhibitory GABAergic interneurones

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34
Q

What neurones compose the nucleus raphe magnus (NRM)?

A

Serotonergic and Enkephalinergic

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35
Q

What drug can excite the nucleus raphe magnus?

A

Morphine

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36
Q

What neurones compose the locus coeruleus (LC)?

A

Noradrenergic

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37
Q

How do the PAG, NRM and LC work?

A
  1. Electrical stimulation and opioids excite the PAG
  2. PAG excites NRM (as do opioids) and LC
  3. NRM and LC inhibit nociceptive transmission in dorsal horn
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38
Q

How do the axons of the NRM and LC project?

A

Via the dorsolateral funiculus

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39
Q

Opioid action is mediated by what class of receptors?

A

G-protein coupled receptors (Gi/Go)

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40
Q

What opioids bind to opioid receptors, what occurs?

A

Postsynaptic potassium channels open

Hyperpolarisation and reduced excitability

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41
Q

What are mu opioid receptors responsible for?

A

Most analgesic action via opioids

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42
Q

What side effects do mu opioid receptors cause?

A

Respiratory depression
Constipation
Euphoria/Sedation/Dependence

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43
Q

What do delta opioid receptors do?

A

Contribute to analgesia

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44
Q

What is a side effect of delta opioid receptor binding?

A

Potentially pro-convulsant

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45
Q

What do kappa opioid receptors do?

A

Spinal and peripheral analgesia

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46
Q

What effect does the ORL1 receptor have?

A

Anti-opioid effect

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47
Q

When is morphine used?

A 
Acute severe pain (IV/IM/SC)
Chronic pain (PO)
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48
Q

When is diamorphine used?

A

Post-operative pain

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49
Q

When is fentanyl used?

A 
Maintenance analgesia (IV)
Chronic pain (transdermal patch)
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50
Q

When is buprenorphine used?

A

Chronic pain (patient-controlled injection systems)

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51
Q

When is pethidine used?

A

Acute pain esp. labour (IV/IM/SC)

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52
Q

What drugs can pethidine not be used with and why?

A 
Monoamine oxidase inhibitors
Can cause:
- Excitement
- Convulsions
- Hyperthermia
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53
Q

How does tramadol mainly work?

A

Potentiates NRM and LC systems

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54
Q

Apart from at the mu opioid receptor, where else does methadone work?

A

Potassium channels
NMDA receptors
Some 5-HT receptors

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55
Q

Why is methadone used to treat opioid (heroin) withdrawl?

A

Longer half-life and it is given PO (no need for injection)

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56
Q

When is etorphine used?

A

Veterinary medicine (large animal sedation)

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57
Q

When is naloxone used?

A

To reverse opioid overdose

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58
Q

How does naloxone work?

A

Competitive antagonist at mu-receptors

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59
Q

What are signs of opioid toxicity that would warrant naloxone used?

A

Respiratory and/or neurological depression

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60
Q

When might naloxone be given to a newborn?

A

Respiratory distress due to pethidone given during labour

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61
Q

Naloxone has a short half-life, why is this useful?

A

Helps avoid further toxicity

Easier to titrate dose and frequence

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62
Q

Etoricoxib, Celecoxib and Lumiracoxib are examples of what?

A

COX-2 selective inhibitors

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63
Q

What do COX-1 and COX-2 do?

A

Produce endoperoxides (Prostaglandin, Thromboxane-A2 and Prostacyclin [PGI2])

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64
Q

Which COX is induced in inflammation?

A

COX-2

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65
Q

How do COX-1 inhibitors cause GI toxicity?

A

Reduced production of PGE2 results in decreased protection against acid and pepsin

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66
Q

What is the analgesic effect of paracetamol due to?

A

N-acetyl-p-benzoquinoneimine

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67
Q

What are some serious side effects of COX-2 inhibitors?

A

Nephrotoxicity

Prothrombic

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68
Q

What subunit of the calcium channel to gabapentin and pregabalin effect?

A

Alpha-2-delta

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69
Q

What drugs can be used in migraine prophylaxis?

A

1st line:
- Amitryptiline OR
- Propanolol
2nd line is Gabapentin

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70
Q

What is the first line treatment for trigeminal neuralgia?

A

Carbamazepine

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71
Q

What is the perikaryon?

A

The soma/cell body of a neurone

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72
Q

What is the Nissl substance?

A

RER in a neurone

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73
Q

Where is the ‘all-or-nothing’ AP initiated?

A

Axon hillock

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74
Q

What viruses can exploit retrograde (presynaptic terminal to soma) transport to infect neurones?

A

Herpes
Polio
Rabies

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75
Q

What are the main structure type of neurones in the peripheral autonomic system?

A

Unipolar

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76
Q

What are the main structure type of neurones in the retinal system?

A

Bipolar

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77
Q

What are the main structure type of neurones in the dorsal root ganglia?

A

Pseudounipolar

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78
Q

What are the main structure type of lower motor neurones (motoneurones)?

A

Multipolar

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79
Q

What staining method allows visualisation of individual neurones?

A

Camillo Golgi’s

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80
Q

What are Golgi type i neurones?

A

Long axons (eg. Projection neurones from dorsal horn to brain)

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81
Q

What are Golgi type ii neurones?

A

Short axons (eg. Local interneurones in CNS)

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82
Q

What causes the upstroke in an AP?

A

Sodium influx

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83
Q

What is the typical membrane potential of threshold?

A

-60mV

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84
Q

What is the typical resting membrane potential?

A

-70mV

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85
Q

What is the typical membrane potential reached by overshoot?

A

+40mV

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86
Q

What causes the downstroke in an AP?

A

Potassium efflux

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87
Q

What is the typical membrane potential reached by undershoot?

A

-80mV

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88
Q

Membrane resistance (rm) aims to prevent what?

A

Current leaking from axon back to the extracellular space

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89
Q

What does membrane leakage generate?

A

Membrane potential change (delta-Vm)

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90
Q

The distance over which current spreads passively is know as the length constant (lambda). What does it depend on?

A

Membrane resistance (rm) and axial resistance of the axoplasm (ri)

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91
Q

How can we calculate the length constant?

A

Lambda = (rm/ri)^0.5

ie the square root of rm/ri

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92
Q

What does a longer length constant indicate?

A

Greater local current spread

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93
Q

How can we increase passive conduction?

A

Decreasing ri by increasing axon diameter

Increasing rm by insulatin axon with myelin

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94
Q

What cells produce myelin in the PNS? What axonal distribution do these have?

A

Schwann cells

Many around one axon

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95
Q

What cells produce myelin in the CNS? What axonal distribution do these have?

A

Oligodendrocytes

One around many axons

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96
Q

What does myelin result in?

A

Saltatory conduction

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97
Q

What channels are located in the Nodes of Ranvier?

A

Voltage-activated sodium channels

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98
Q

Give an example of a disease resulting in CNS demyelination?

A

MS

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99
Q

Give an example of a disease resulting in PNS demyelination? What can precipitate this?

A

Guillian-Barre:

  • Gastroenteritis
  • Respiratory tract infection
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100
Q

What is the most common CNS excitatory neurotransmitter?

A

Glutamate

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101
Q

What is the most common CNS inhibitory neurotransmitter?

A

GABA (or glycine)

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102
Q

What does glutamate activate?

A

Post-synaptive, cation-selective, ionotropic glutamate receptors

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103
Q

What does GABA activate?

A

Post-synaptic, anion-selective, ionotropic GABAa receptors

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104
Q

How wide is the typical synaptic cleft?

A

20-50nm

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105
Q

What is the diameter of a typical vesicle?

A

50nm

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106
Q

How can we differentiate between the pre-synaptic membrane and the post-synaptic membrane?

A

Pre:
- Active zones where vesicles cluster
Post:
- Postsynaptic density with neurotransmitter receptors

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107
Q

What is spatial summation?

A

Many inputs converge upon a neurone to determine its output

eg. 1 epsp + 2 ipsp = Net inhibition

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108
Q

What is temporal summation?

A

A single input can alter output by varying AP frequency

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109
Q

What are the three main amino acid neurotransmitters?

A

Glutamate
GABA
Gylcine

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110
Q

How can we tell if a neurotransmitter is an amine?

A

Typically ends in -ine (eg. Ach, dopamINE, histamINE, NA)

OR -in as in serotonIN

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111
Q

Apart from amino acids and amines, what other groups of neurotransmitter is there?

A

Peptides

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112
Q

What type of channels can glutamate, GABA, glycine, Ach and 5-HT activate? What speed of transmission does this permit?

A

Ionotropic, ligand-gated ion channels

Fast

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113
Q

What is the only neurotransmitter that cannot activate GPCRs? What speed of transmission do these receptors permit?

A

Glycine

Slow

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114
Q

What neurotransmitters are in all cells?

A

Glycine and glutamate

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115
Q

What neurotransmitters need to be specifically synthesised?

A

GABA and amines

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116
Q

What is the process by which peptide neurotransmitters are synthesised and stored?

A
  1. Precursor peptide synthesis by ribosomes at RER
  2. Precursor cleaved in Golgi - Active neurotransmitter
  3. Secretory granules bud off from Golgi
  4. Granules transported to terminal by fast axoplasmic transport along microtubules
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117
Q

What is the typical extracellular ion concentrations of the following:

  • Sodium
  • Potassium
  • Chloride
  • Calcium
A 
Sodium = 145 mM
Potassium = 4 mM
Chloride = 123 mM
Calcium = 1.5 nM
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118
Q

What is the typical intracellular ion concentrations of the following:

  • Sodium
  • Potassium
  • Chloride
  • Calcium
A 
Sodium = 12 mM
Potassium = 155 mM
Chloride = 14 mM
Calcium = 10^-7 M (0.0001 nM)
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119
Q

Ionotropic receptors allow for what type of gating?

A

Direct (receptor is also channel)

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120
Q

Metabotropic receptors allow for what type of gating?

A

Indirect (receptor and channel are distinct molecules)

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121
Q

Via what type of receptors can glutamate potentially be inhibitory?

A

Metabotropic

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122
Q

How can ionotropic glutamate receptors be classified?

A

Via their response to non-endogenous glutamate mimics

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123
Q

What can non-NMDA receptors bind?

A

Kainate and AMPA (agonists)

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124
Q

What do non-NMDA receptors permit?

A

Fast excitatory transmission via sodium and potassium channels

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125
Q

What do NMDA receptors permit?

A

Slow excitatory transmission via sodium, potassium and calcium

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126
Q

How can NMDA receptors promote neurotoxicity?

A

High calcium permeability

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127
Q

What can block NMDA receptors?

A

Ketamine and psychomimetric agents (eg. Phencyclidine)

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128
Q

What do GABAa receptors do? What type of receptor are they?

A

Operate a chloride channel

Ionotropic

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129
Q

What do GABAb receptors do? What type of receptor are they?

A

Operate a potassium channel

Metabotropic

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130
Q

How do benzodiazepines work?

A

Positive allosteric modulators of GABAa:

  • Enhance chloride entry
  • Hyperpolarisation
  • Even further enhancement in presence of GABA
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131
Q

How do barbituates work?

A

Similar to benzodizapeines

Potentiate effect of GABA at GABAa

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132
Q

How does baclofen work?

A

GABAb agonist:

  • Enhances potassium efflux
  • Hyperpolarisation
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133
Q

How does glycine work?

A

Acts on an ionotropic glycine receptor:

- Gates a chloride channel

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134
Q

Where is glycine released and what neurones does it usually affect?

A

Interneurones in spinal cord

Inhibits antagonistic muscle motoneurones

135
Q

What do ionotropic receptors essentially act as?

A

ON-OFF switches

136
Q

What is a quanta?

A

The amount of transmitter in 1 vesicle

137
Q

How can we increase quanta release?

A

Extensive innervation:
- eg. Purkinje cell (Inferior Olivary Neurone Synapse_
- eg. Inhibitory basket cell (Cerebellum, hippocampus, cortex)
Mega humongous presynapse:
- eg. Calyx of Held synapse

138
Q

What are Hermann currents and what do they trigger?

A

Local current flow

Trigger -all-or-nothing’ APs

139
Q

What do low threshold mechanoreceptors mediate?

A

Touch
Vibration
Pressure

140
Q

What do low threshold thermooreceptors mediate?

A

Cold and cool
Indifferent
Warm and hot

141
Q

What do thermal nociceptors respond to?

A

Extreme temperatures:

  • > 45 degrees celcius
  • 10-15 degrees celcius
142
Q

What do chemical nociceptors respond to?

A

Substances found in tissues in inflammation

143
Q

What info do slowly adapting tonic/static adaptation responses provide? What is this important in?

A

Position
Stretch
Force
Important in posture

144
Q

What info do rapidly adapting phasic/dynamic adaptation responses provide? What is this important in?

A

Detect changes in stimulus strength eg. rate of motion
Examples:
- Some muscle spindle afferents
- Hair follicle afferents

145
Q

What info do very rapidly adapting very phasic/dynamic adaptation responses provide? What is this important in?

A

Respond only to very fast movements eg. Rapid vibration

Eg. Pacinian corpuscle

146
Q

Which axon types have the thickest myelin and the biggest diameter from the skin and their equivalent from muscles/tendons?

A

A-alpha

Group i

147
Q

Which axon types have the thinest myelin and the second smallest diameter from the skin and their equivalent from muscles/tendons?

A

A-delta

Group iii

148
Q

Which axon types are unmyelinated and have the smallest diameter from the skin and their equivalent from muscles/tendons?

A

C

Group iv

149
Q

What is the function of A-alpha fibres?

A

Proprioception of skeletal muscle

150
Q

What is the function of A-beta fibres?

A

Mechanoreceptors of skin

151
Q

What is the function of A-delta fibres?

A

Pain and temperature

152
Q

What is the function of C fibres?

A

Temperature, pain and itch

153
Q

What is the receptive field (RF)?

A

The RF of an afferent neurone is the region that, when stimulated, adequately causes a response in that neurone.
The peripheral terminal of primary afferent neurones

154
Q

How is the size of an RF evidenced?

A

By two point discrimination:

  • ~2mm on fingertips
  • ~10mm on palms
  • ~40mm on forearms
155
Q

How does decreasing the RF size affect discriminative capacity?

A

Increases it

156
Q

Where are Meissner’s corpuscles most abundant and absent?

A

Most abundant where 2 point discrimination highest

Absent in hairy skin

157
Q

Where are Merkel’s discs most abundant and present?

A

Similar distribution as Meissner’s corpuscles and some present in hairy skin

158
Q

How are Merkel’s discs grouped?

A

In Iggo domes:

  • Multiple discs innervated by a single myelinated fibre
  • Both cell and fibre are mechanosensitive
159
Q

What do both the cell and fibre express in Merkel’s discs?

A

Piezo2

160
Q

Where are Krause end bulbs found?

A

At border of dry skin and mucous membranes

161
Q

Where are Ruffini endings found?

A

Within dermis and joint capsules

162
Q

Where are Pacinian corpuscles found?

A

Within dermis and fascia

163
Q

What cutaneous receptors are encapsulated?

A

Meissner’s corpuscles
Ruffini endings
Pacinian corpuscles

164
Q

What fibre group do Meissner’s corpuscles transmit to and what modality does it detect?

A

A-beta

Stroking/Flutter (rapidly adapting)

165
Q

What fibre group do Merkel disc receptors transmit to and what modality does it detect?

A

A-beta

Pressure and texture (slowly adapting)

166
Q

What fibre group do Pacinian corpuscles transmit to and what modality does it detect?

A

A-beta

Vibration (very rapidly adapting)

167
Q

What fibre group do Ruffini endings transmit to and what modality does it detect?

A 
A-beta
Skin stretch (slowly adapting)
168
Q

What fibre group do Hair (G) guard (long) transmit to and what modality does it detect?

A

A-beta

Stroking/Flutter

169
Q

What fibre group do Hair (D) down (short) transmit to and what modality does it detect?

A

A-delta

Light stroking

170
Q

What fibre group do C mechanoreceptors transmit to and what modality does it detect?

A

C

Stroking, social and erotic touch

171
Q

What are the grey matter subdivisions?

A

Horns (dorsal and ventral)

10 distinct Laminae of Rexed

172
Q

In which laminae do nociceptors (A-delta/C fibres) terminate in the spinal cord?

A

Laminae i and ii

173
Q

In which laminae do low threshold mechanoreceptors (A-beta) terminate in the spinal cord?

A

Laminae iii, iv, v and vi

174
Q

In which laminae do proprioceptors (A-alpha) terminate in the spinal cord?

A

Laminae vii, viii and ix

175
Q

What sensations does the Dorsal Column Medial Lemniscus (DCML) pathway transmit?

A

Discriminatory touch
Pressure
Vibration
Conscious proprioception

176
Q

What sensations does the Spinothalamic Tract (STT) transmit?

A 
Pain (lateral)
Thermosensation (lateral)
Crude touch/Pressure (ventral)
Itch (ventral)
Tickle (ventral)
177
Q

Where does the Dorsal Column Medial Lemniscus decussate?

A

Brainstem (great sensory decussation)

178
Q

Where do the first order neurones of the DCML end?

A

Brainstem

179
Q

Where do the second order neurones of the DCML ascend and end?

A

Medial lemniscus to ventral posterolateral nucleus of thalamus

180
Q

Where do the third order neurones of the DCML end and via where?

A

Primary sensory cortex (S1) via posterior internal capsule

181
Q

Where does the Spinothalamic Tract decussate?

A

At each level of the spinal cord (anterior white commissure) close to point of entry via Lissauer’s Tract

182
Q

Where do the first order neurones of the STT end?

A

Ipsilateral spinal cord (at each level)

183
Q

Where do the second order neurones of the STT end?

A

Thalamus

184
Q

Where do the third order neurones of the STT end?

A

Primary sensory cortex

Also cingulate and insular cortices

185
Q

What sensations does the Spinocerebellar Tract transmit?

A

Proprioceptive info from:

  • Muscle spindle (dorsal)
  • Golgi tendon organs (ventral {and dorsal])
186
Q

In what part of the DCML do sensations from the lower limb (up to T6) travel?

A

Fasciculus gracilis (gracile tract) - more medial

187
Q

In what part of the DCML do sensations from the upper limb (above T6) travel?

A

Fasciculus cuneatus (cuneate tract) - more lateral

188
Q

Where are the soma of trigeminal sensory neurones?

A

Trigeminal sensory ganglion

189
Q

Where do the 2nd order neurones of the trigeminal system start?

A

Either the:

  • Chief sensory nucleus (general tactile)
  • Spinal nucleus (pain and temperature)
190
Q

Where do the 2nd order neurones of the trigeminal system decussate and project to?

A

Ventroposteriomedial nucleus of thalamus via trigeminal lemniscus

191
Q

Where do the 3rd order neurones of the trigeminal system relay info to?

A

Cortex via thalamocoritcal neurones

192
Q

Where is the primary sensory cortex (S1) located?

A

Post-central gyrus of the parietal cortex

193
Q

What is the primary sensory cortex immediately posterior to?

A

Central sulcus (SI)

194
Q

What is the primary sensory cortex adjacent to?

A

Posterior parietal cortex (S2)

195
Q

What Brodmann areas makes up the primary sensory cortex?

A

3a, 3b, 1 and 2 (from anterior to posterior)

196
Q

Where do inputs to the primary sensory cortex come from?

A

Venteroposterior thalamus:

  • ~70% to Brodmann areas 3a and 3b
  • ~30% to Brodmann areas 1 and 2
197
Q

What sensory input does Brodmann area 3a deal with?

A

Proprioception

198
Q

What modality sensitivity is Brodmann area 3a responsible for?

A

Body position

199
Q

What sensory inputs does Brodmann area 3b deal with?

A

Cutaneous (Merkel’s and Meissner’s) AND

Brodmann area 3a

200
Q

What modality sensitivity is Brodmann area 3b responsible for?

A

Touch (texture, shape, size)

201
Q

What sensory inputs does Brodmann area 1 deal with?

A

Cutaneous (rapid mechanoreceptors)

Brodmann area 3b

202
Q

What modality sensitivity is Brodmann area 1 responsible for?

A

Texture discrimination

203
Q

What sensory inputs does Brodmann area 2 deal with?

A

Joint afferents
Golgi tendon organs
Deep tissues
Brodmann areas 3a and 3b

204
Q

What modality sensitivity is Brodmann area 2 responsible for?

A

Object perception (size and shape - Stereognosis)

205
Q

In what cell layer of the somatosensory cortex do thalamic inputs mainly terminate in?

A

iv - Lamina granularis interna

206
Q

From superficial to deep, what are the six cell layers of the somatosensory cortex?

A 
Lamina i - Lamina molecularis
Lamina ii - Lamina granularis externa
Lamina iii - Lamina pyramidalis externa
Lamina iv - Lamina granularis interna
Lamina v - Lamina pyradmidalis interna
Lamina vi - Lamina multiformis
207
Q

What does the posterior parietal cortex do?

A

Receives and integrates info from S1 and other cortical areas (visual, auditory) and sub-cortical areas (thalamus)

208
Q

Damage to the posterior parietal cortex causes what symptoms/signs?

A

Agnosia
Asterognosia
Hemispatial neglect syndrome

209
Q

Where are upper motor neurones found?

A

Within the brain

210
Q

Where are the lower motor neurones found?

A

Soma in the brain stem

Some in ventral column of spinal cord

211
Q

Apart from UMNs, where else do LMNs receive inputs from?

A

Proprioceptors and interneurones

212
Q

What do LMNs command?

A

Muscle contraction

213
Q

What neurones comprise LMNs? What are their functions?

A

Alpha-motor neurones:
- Innervate the bulk of muscle fibres that generate force
Gamma-motor neurones:
- Innervate muscle spindles

214
Q

Where are there more motor neurones? Why?

A 
Cervical enlargements (C3-T1) for arms
Lumbar enlargement (L1-S3) for legs
215
Q

What is the motor unit comprised of?

A

The alpha-motor neurone and all the muscle fibres it supplies

216
Q

What is a motor neurone pool?

A

The collection of alpha-motor neurones innervating a single muscle

217
Q

Force of contraction of a muscle is graded by what 2 main principles?

A
  • AP frequency of alpha-motor neurones (each cause a twitch)

- Recruitment of synergistic motor units

218
Q

Are LMNs innervating axial muscles located more medially or laterally to those supplying distal muscles?

A

Medially

219
Q

Are LMNs innervating flexors located more dorsally or ventrally to those supplying extensors?

A

Dorsally

220
Q

What are the three inputs to an alpha-motor neurone?

A

Central terminals of dorsal root ganglion cells
UMNs
Spinal interneurones

221
Q

For fine movements, what is the size of a motor unit? Where might these units be present?

A

Small (few fibres)

Extraocular eye muscles

222
Q

For postural muscles, what is the size of a motor unit? Where might these units be present?

A

Large (100s - 1000s)

Leg muscles

223
Q

How are alpha-motor neurones innervating fast motor units different to those innervating slow units?

A

Larger

Faster conducting axons

224
Q

Usually, there is one motor axon endplate (NMJ) per muscle fibre. Where is this untrue?

A

Extraocular eye muscles

225
Q

Where are motor axon endplates usually located on a fibre?

A

Near centre

226
Q

There are fast and slow skeletal muscle types. How do they differ?

A

How fast myosin ATPase splits ATP to provide energy for cross-bridge recycling

227
Q

Where do Type i (slow-oxidative) fibres get ATP from?

A

Oxidative phosphorylation

228
Q

Why are Type i fibres fatigue resistant?

A

Slow contraction and relaxation

229
Q

Why are Type i fibres red?

A

Rich in myoglobin

230
Q

Where do type iia (fast) fibres get ATP from?

A

Oxidative phosphorylation

231
Q

Are Type iia fibres fatigue resistant or not?

A

They are

232
Q

What colour are Type iia fibres?

A

Red

233
Q

Where do Type iib/x fibres get ATP from?

A

Glycolysis

234
Q

Are Type iib/x fibres fatigue resistant or not?

A

They aren’t

235
Q

What colour are Type iib/x fibres?

A

Pale

236
Q

What are the features of a fast-fatiguing motor unit?

A

Very high tension
Large alpha-motor neurones
Type iib/x fibres

237
Q

What are the features of a fatigue resistant motor unit?

A

High tension
Intermediate alpha-motor neurones
Type iia fibres

238
Q

What are the features of a slow motor unit?

A

Low tension
Small alpha-motor neurones
Type i fibres

239
Q

How does increasing the muscle load affect the contraction velocity?

A

It decreases it

240
Q

What is the Henneman Size Principle?

A

The susceptibility of an alpha-motor neurone to discharge an AP is a function of its size

241
Q

Which alpha-motor neurones are more easily activated and trained?

A

Smaller alpha-motor neurones

242
Q

What is the myotatic reflex?

A

When a skeletal muscle is pulled, it pulls back

243
Q

Change in length (and rate of change) of a muscle is registered by what structure? What does this contribute to?

A

Muscle spindle

Non-conscious proprioception

244
Q

What does a muscle spindle consist of?

A

A fibrous capsule
Intrafusal muscle fibres
Sensory afferents:
- Type ia class (myelinated and very fast)
Gamma-motor neurone efferents (innervate intrafusal fibres)

245
Q

What is the process by which a muscle responds to stretch?

A
  1. Muscle spindle stretches
  2. Activation of Ia afferents
  3. Excitatory transmission in spinal cord (glutamate)
  4. Activation of alpha-motor neurone (extrafusal fibre innervation)
  5. Homonymous muscle contraction
246
Q

What type of reflex in the myotatic reflex?

A

Monosynaptic (only one in the body)

247
Q

In what muscles in the myotatic reflex more prominent?

A

Extensor muscles

248
Q

The supinator (wrist) reflex assesses what spinal levels?

A

C5-C6

249
Q

The biceps (elbow) reflex assesses what spinal levels?

A

C5-C6

250
Q

The triceps (elbow) reflex assesses what spinal levels?

A

C7

251
Q

The quadriceps (knee) reflex assesses what spinal levels?

A

L3-L4

252
Q

The gastrocnemius (ankle) reflex assesses what spinal levels?

A

S1

253
Q

What part of muscle spindle intrafusal fibres do Ia sensory neurones innervate?

A

A non-contractile equatorial region

254
Q

What part of muscle spindle intrafusal fibres do gamma-motor neurones innervate?

A

Contractible polar ends

255
Q

Where are the cell bodies of gamma-motor neurones located?

A

Ventral horn

256
Q

What does gamma-motor neurone stimulation result in?

A

Spindle contraction

257
Q

Why is the muscle spindle kept taut?

A

Maintains its sensitivity

258
Q

What are dynamic/bag 1 nuclear bag fibres responsible for?

A

Very sensitive to rate of muscle length change

259
Q

What are static/bag 2 nuclear bag fibres responsible for?

A

More sensitive to overall muscle length

260
Q

What are chain fibres sensitive to and what innervates them?

A

Absolute muscle length

Static gamma-motor neurones

261
Q

What do type Ia afferents form around an intrafusal fibre?

A

A primary annulospiral nerve winding around the centre

262
Q

What do type II afferents form on an intrafusal fibre?

A

Flowerspray endings (except on dynamic bags)

263
Q

Type Ia afferents are more sensitive to what?

A

Rate of length change

264
Q

Type II afferents are more sensitive to what?

A

Absolute intrafusal fibre length

265
Q

Only static gamma-motor neurones are activated during what activities?

A

Where muscle length changes slowly and predictably:

  • Sitting
  • Standing
  • Slow walking
266
Q

When are both dynamic and static gamma-motor neurones activated?

A

Where muscle length changes rapidly and unpredictably

267
Q

Where are Golgi tendon organs located?

A

Muscle-tendon junctions

268
Q

What do Golgi tendon organs do?

A

Monitor muscle tension (in series with extrafusal fibres)

269
Q

What fibres innervate Golgi tendon organs?

A

Ib sensory afferents

270
Q

What is the function of Golgi tendon organs?

A

Regulate muscle tension in order to:

  • Protect muscle from overload
  • Keep tension in an optimal range
271
Q

What is the course of a group Ib afferent?

A

Enter spinal cord
Synapse with inhibitory interneurones:
- Synapse upon alpha-motor neurones of same muscle

272
Q

What reflex is the result of group Ib afferent firing?

A

Inverse myotatic reflex - Muscle relaxation

273
Q

Where are free nerve endings located in joints?

A

Capsule

Connective tissue

274
Q

Where are Golgi type units located in joints?

A

Ligaments

275
Q

Where are Paciniform endings located in joints?

A

Periosteum near articular attachments

Also in fibrous part of capsule

276
Q

Where are Ruffini endings located in joints?

A

Joint capsule

277
Q

What are the most numerous sensory units in joints?

A

Free nerve endings

278
Q

What is the function of free nerve endings in joints? What is the threshold and adaptation rate of these?

A

Nociceptive

High-threshold and slowly-adapting

279
Q

What is the function of Golgi type units in joints? What is the threshold and adaptation rate of these?

A

?Protection

High-threshold and slowly-adapting

280
Q

What is the function of Paciniform endings in joints? What is the threshold and adaptation rate of these?

A

Detect acceleration

Low-threshold and slowly-adapting

281
Q

What is the function of Ruffini endings in joints? What is the threshold and adaptation rate of these?

A

Static position and movement speed

Low-threshold and slowly-adapting

282
Q

What do inhibitory interneurones mediate?

A

Inverse myotatic reflex

Reciprocal inhibition between extensor and flexor

283
Q

What is reciprocal inhibition?

A

Voluntary contraction of an extensor stretches the antagonising flexor - Myotatic reflex

284
Q

What do the descending paths of reciprocal inhibition do?

A

Activate extensor alpha-motoneurones
Inhibit flexor alpha-motoneurones
Results in unopposed extension
(The opposite can occur)

285
Q

What do excitatory interneurones mediate?

A

Flexor reflex

Crossed extensor reflex

286
Q

What is the flexor reflex?

A

Flexion due to noxious stimuli

287
Q

What is the crossed extensor reflex?

A

Extension due to noxious stimuli

288
Q

What is the function of the crossed extensor reflex?

A

Enhances postural support:

- When injured foot withdraws, supporting leg extends to prevent falling over

289
Q

What activity do excitatory interneurones display

A

Oscillatory/Pacemaker

290
Q

In a simplistic motor control hierarchy, what is the function of the highest levels?

A

Strategy (what is the aim of the movement)

291
Q

What do the highest levels in a simplistic motor control hierarchy involve?

A

Neocortical association areas

Basal ganglia

292
Q

In a simplistic motor control hierarchy, what is the function of the middle levels?

A

Tactics (sequence of extension and flexion)

293
Q

What do the middle levels in a simplistic motor control hierarchy involve?

A

Motor cortex

Cerebellum

294
Q

In a simplistic motor control hierarchy, what is the function of the lowest levels?

A

Execution (activate motor pools - movement)

295
Q

What do the lowest levels in a simplistic motor control hierarchy involve?

A

Medulla

Spinal cord

296
Q

Where are the cell bodies of the corticospinal (pyramidal) tracts located?

A

Motor cortex (~2/3):
- Brodmann areas 4 and 6
Somatosensory areas of parietal cortex (~1/3):

297
Q

Where do axons of the corticospinal tract course after leaving their site of origin?

A

Base of medulla - Medullary pyramid

298
Q

Where do the fibres of the corticospinal tract decussate? What tracts do these form?

A 
Pyramidal decussation:
- 75-90% of fibres
- Lateral corticospinal tract
More caudally (in spinal cord):
- 10-25% of fibres
- Initially stay ipsilaterally as the ventral corticospinal tract
299
Q

What is the function of the lateral corticospinal tract?

A

Controls fine movement of limbs

300
Q

Damage above the pyramidal decussation will cause what lateral corticospinal deficits?

A

Contralateral motor deficits

301
Q

Damage below the pyramidal decussation will cause what lateral corticospinal deficits?

A

Ipsilateral motor deficits

302
Q

What is the function of the ventral corticospinal tract?

A

Axial muscles of the trunk

303
Q

Where does the rubrospinal tract originate?

A

Magnocellular red nucleus

304
Q

Where does the rubrospinal tract receive inputs from?

A

Motor cortex

Cerebeullum

305
Q

Where do axons of the rubrospinal tract decussate?

A

Ventral tegmental decussation

306
Q

Where does the rubrospinal tract descend in relation to the lateral corticospinal tract?

A

Ventrolateral

307
Q

What is the function of the rubrospinal tract?

A

Controls flexors

308
Q

What are the lateral descending spinal tracts?

A

Corticospinal tract

Rubrospinal tract

309
Q

Generally, what do lesions of the lateral tracts result in?

A

Loss of ‘fractioned’ movements:
- ie. Shoulder, elbow, wrist and fingers can’t move independently
Slowing and impairment of accuracy of voluntary movements

310
Q

What do lesions of the lateral tracts have little effect on?

A

Posture

311
Q

The rubrospinal tract, if not damaged, can take over some functioning of the lateral corticospinal tract if lesioned. What functioning can’t it restore?

A

Distal flexors

Independent finger movements

312
Q

Where do the soma of the vestibulospinal tracts reside?

A

Vestibular nuclei

313
Q

Where do the soma of the vestibulospinal tracts receive input from?

A

Vestibular labyrinths via CN VIII

Also cerebellum

314
Q

Where does the lateral vestibulospinal tract originate from?

A

Lateral vestibular nucleus (Deiter’s nucleus)

315
Q

Does the lateral vestibulospinal tract descend ipsilaterally or contralaterally?

A

Ipsilaterally

316
Q

What is the function of the lateral vestibulospinal tract?

A

Help with posture:

  • Facilitate extensor motor neurones
  • In antigravity muscles (eg. legs)
317
Q

Where does the lateral vestibulospinal tract end (roughly)?

A

Lumbar spinal cord

318
Q

Where does the medial vestibulospinal tract originate from?

A

Medial vestibular nucleus

319
Q

Where does the medial vestibulospinal tract end (roughly)?

A

Cervical spinal cord

320
Q

What is the function of the medial vestibulospinal tract?

A

Control neck and back muscles:

- Head movements

321
Q

Where do the soma of the tectospinal tracts reside?

A

Superior colliculus (aka optic tectum)

322
Q

Where does the tectospinal tract receive inputs from?

A

Direct input from retina
Input also from:
- Visual cortex
- Afferents conveying somatosensory and auditory info

323
Q

Where do the axons in the tectospinal tract decussate?

A

Dorsal tegmental decussation

324
Q

Is the tectospinal tract more medial or lateral?

A

Medial (close to midline)

325
Q

Where does the tectospinal tract end?

A

Cervical spinal cord

326
Q

What is the function of the tectospinal tract?

A

Influences muscles of the:

  • Neck
  • Upper trunk
  • Shoulders
327
Q

Where do the reticulospinal tracts originate?

A

Reticular formation

328
Q

Where is the origin of the reticulospinal tracts located?

A

Along the length and at the core of the medulla

329
Q

Does the pontine (medial) reticulospinal tract descend ipsilaterally or contralaterlly?

A

Ipsilaterally

330
Q

What is the function of the pontine (medial) reticulospinal tract?

A

Enhances postural neck reflexes
Maintains standing posture:
- Helps facilitate lower limb extensor contraction

331
Q

Does the medullar (lateral) reticulospinal tract descend ipsilaterally or contralaterlly?

A

Neither - Bilaterally

332
Q

What is the function of the medullar (lateral) reticulospinal tract?

A

Opposes actions of pontine tract

Helps relax antigravity muscles

333
Q

What controls both reticulospinal tracts?

A

Descending signals from cortex

Year 3 - Neurology (DP) (5 decks)

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