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JMP Y2S1 > Week 43- Ascending Pathways and Sensation > Flashcards

Week 43- Ascending Pathways and Sensation Flashcards

1
Q

What is Nociception?

A

Signalling in the nervous system resulting from tissue damage

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2
Q

Is Nociception physiological or psychological?

A

Physiological

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3
Q

How does Nociception differ from pain?

A

It is physiological signalling in response to damage

Pain is a subjective feeling triggered by nociception signalling

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4
Q

Can there be nociception without pain?

A

Yes –> tissue damage triggers neural signals but no psychological distress eg anaesthesia , intoxication etc

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5
Q

Can there be pain without nociception?

A

Yes can be imagined pain and also hypnotised pain

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6
Q

What is the trigger for nociception?

A

Tissue damage/inflammatory response

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7
Q

What is the general pathway for nociception?

A

Tissue damage
Neural signal generation (nociceptors convert mechanical or chemical signals to neural)
Transmission –> ascending neural pathways to the brain
Perceptions/emotions/conceptualisations –> feed back to the transmission

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8
Q

What are the three classes of nociceptors?

A

Thermo
Chemo
Mechanical
–> Also polymodal –> nociceptors that react to multiple stimuli at once

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9
Q

What is the term for a pain producing chemical?

A

Algogenic

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10
Q

What is the Nociceptor reflex?

A

Reflex in which the body is able to move a limb out of harm without need of brain input

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11
Q

What is the steps in the nociceptor reflex?

A

Stimulus (e.g thermal receptor)
Afferent pathway to dorsal root ganglion and then to dorsal horn in spinal cord
Signals from afferent pathway travel ascending to brain as well as across to the ventral horn
Ventral horn efferent pathway
Effector organ targeted (muscle) –> response is movement (flexion away)

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12
Q

What is pain?

A

A defensive mechanism and a perceptual phenomenon

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13
Q

What is referred pain?

A

Pain perceived at a site that is different to the actual location of the nociceptive stimulus that is most commonly visceral

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14
Q

What is phantom pain?

A

The perception of pain in an absent leg –> possible mechanisms of activity in severed nerves

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15
Q

What are the different pain pathways?

A

Slow –> paleospino-thalamic

Fast –> neospino-thalamic

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16
Q

How does Slow and Fast pain pathways differ in fibre size?

A

Slow –> small fibres –> 0.2-5μm

Fast –> large fibres –> 6-20 μm

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17
Q

How does Slow and Fast pain pathways differ in sensation type?

A

Slow –> dull burning ache poorly localised

Fast –> sharp. Pricking well localised pain

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18
Q

How does Slow and Fast pain pathways differ in neurotransmitters?

A

Slow –> substance P

Fast –> glutamate

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19
Q

What location within the dorsal horn do slow and fast nociception pathways travel?

A

Slow –> deep dorsal horn

Fast –> superficial dorsal horn

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20
Q

What are the different types of pain?

A

Nociceptive
Inflammatory
Dysfunctional
Neuropathic

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21
Q

What is nociceptive pain?

A

Pain from legitimate noxious stimuli –> no nervous system lesion or inflammation

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22
Q

What are some features of nociceptive pain?

A

Evoked by high intensity stimuli
Pathway travels Painful stimulus –> nociceptor reaction Nociceptors –> nerves –> dorsal root ganglion, dorsal root, brainstem, thalamus, cortex

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23
Q

What is inflammatory pain?

A

Pain from active inflammation

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24
Q

What are some features of inflammatory pain?

A

Spontaneous and stimulus-dependant pain –> can happen with low and high stimuli
There is peripheral and central amplification

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25
Q

What is dysfunctional pain?

A

Pain but with no known structural nervous system lesion or active peripheral inflammation

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26
Q

What are some features of dysfunctional pain?

A

Spontaneous and stimulus dependant
Present with lack of stimulus
Peripheral and central amplification

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27
Q

What is neuropathic pain?

A

Pain from nervous system lesion or disease –> marked neuroimmune response

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28
Q

What are some features of neuropathic pain?

A

Evoked by low and high intensity stimuli

Peripheral amplification and central amplification and neuroimmune interactions in periphery and in CNS

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29
Q

What is neuropathic pain?

A

Pain from nervous system lesion or disease –> marked neuroimmune response
Neuropathic painispaincaused by damage or disease affecting the somatosensory nervous system.

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30
Q

What are some features of neuropathic pain?

A

Evoked by low and high intensity stimuli

Peripheral amplification and central amplification and neuroimmune interactions in periphery and in CNS

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31
Q

What is the pathway of nociceptive pain?

A

Nociceptor –> dorsal root ganglion –> 1st neuron (pseudo unipolar (DRG)) –> dorsal horn of spinal cord –> 2nd neuron –> ascending

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32
Q

What are the three branches of the trigeminal nerve and where do they sensory innervate the face?

A

Ophthalmic –> forehead eyes and nose
Maxillary –> upper jaw and cheeks
Mandibular –> lower jaw

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33
Q

What other structures apart from the face does the trigeminal nerve give sensory innervation?

A

Large cerebral vessels
Pial vessels
Large venous sinuses
Dura mater

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34
Q

How can the physiology of a migraine be described?

A

Vicious circle –> pain drives inflammation –> inflammation drives pain and back around

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35
Q

What is the difference between a headache and a migraine?

A

Headaches –> can include migraine, tension headaches, cluster headaches
Migraines –> neurovascular disorder –> starts in brain and moves to vessels –> has trigeminal involvement

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36
Q

What is the name for diseases of the peripheral nerves?

A

Neuropathies

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37
Q

How do neuropathies commonly clinically manifest?

A

Sensory or motor abnormalities

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38
Q

What is the 3 main pathological types of damage to peripheral nerves?

A

Primary axon degeneration

Primary demyelination

Destruction of both axon and myelin

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39
Q

What needs to remain for potential repair and regeneration of the peripheral axon and myelin?

A

The cell body (soma) of the nerve

40
Q

During axonal degeneration what happens to axon distal to point of transection?

A

They degenerate (Wallerian degeneration)

41
Q

What cell type is important for removing axon and myelin debris?

A

Macrophages

42
Q

What happens to the target tissue of damaged nerves?

A

It is denervated and commonly atrophies

43
Q

What is the general stages in nerve regeneration?

A

Regeneration starts at site of transection –> with formation of growth cone

Schwann cells guide the sprouting axons in the growth cone

Nerve cell body becomes swollen

Axon growth of 1-3mm per day

Tissue is reinnervated

Sprouting axons pruned to remove misguided branches

Schwann cells create new myelin sheaths around axons

44
Q

What is the growth cone in nerve regeneration?

A

Outgrowth of new branches from the stump of the proximal axon

45
Q

What determined if axon repair will be successful?

A

The distance between the 2 transected ends needs to remain in close proximity

46
Q

What is a Traumatic neuroma?

A

It is a nonneoplastic proliferation of axonal processes and associated Schwann cells –> results in a painful nodule

47
Q

What causes a traumatic neuroma?

A

Failure of the outgrowth axons to find their distal targets

48
Q

What happens during primary or segmental demyelination?

A

Schwann cells and myelin sheaths targets of damage –> axons relatively intact

Myelin sheaths degenerate

In response to damage Schwann cells and Schwann cell precursors proliferate

Repair is imitated through formation of new myelin sheaths

49
Q

What is needed for regeneration and recovery of nerves?

A

Cell bodies intact
No scarring of the nerve
Myelin is able to regenerate

50
Q

What is normally characteristic of regenerated myelin?

A

They tend to be shorter and thinner in comparison to the original
Leads to slower nerve conduction velocity

51
Q

What is wrong in mononeuropathy?

A

Affects single nerve:

Results in deficits in a restricted distribution dedicated by normal anatomy

52
Q

What is common causes of mononeuropathy?

A

Trauma
Entrapment
Infections

53
Q

What is wrong in polyneuropathy?

A

Generalised symmetrical involvement –> affects multiple nerves
Axons affected in length dependant fashion (deficits subsequently start in feet and ascend during disease progression)

54
Q

What is wrong in focal peripheral neuropathy/ mononeuritis multiplex?

A

Disease that affects peripheral nerves in a haphazard manner:
Mononeuropathy –> one nerve affected
Multi mononeuropathy –> asymmetrical disease of several nerves

55
Q

What is a common cause of peripheral neuropathy?

A

Vasculitis

56
Q

What is wrong in radiculopathy/polyradiculoneuropathies?

A

Disease affecting nerve roots as well as peripheral nerves –> leads to diffuse symmetric symptoms in proximal and distal parts of the body

57
Q

What is the result from a neuronopathies?

A

Destruction of neurons –> leads to secondary degeneration of axons

  • -> damage at level of the neuronal cell body
  • ->peripheral nerve dysfunction equally likely to affect proximal and distal parts of the body
58
Q

What are some examples of causes of neuronopathies?

A

Herpes zoster

Toxins like platinum compounds

59
Q

What are some examples of nutritional/metabolic neuropathies?

A

Diabetes Mellitus
Uraemia
Vitamin deficiencies –> Thiamine, Vit B6, Vit B12

60
Q

What are some examples of toxic neuropathies?

A

Drugs –> wide range

Toxic –> alcohol, lead, aluminium, arsenic, mercury, acrylamide

61
Q

What is the normal presentation of neuropathy in most toxins?

A

“Dying back” axonal neuropathy
Symmetrical sensory and motor neuropathy
“glove and stocking” distribution

62
Q

How does glucose impact peripheral nerves?

A

Thought to cause microvascular injuries to small blood vessels
These small blood vessels can no longer supply nerves

63
Q

What is the impact of alcohol on peripheral nerves?

A

Long term alcohol consumption can lead to malnutrition

Direct toxic affects –> acetylaldehyde, ethanol etc

64
Q

What is Paracetamol?

A

Weak COX inhibitor –> site of action in CNS

65
Q

What is the action of Paracetamol?

A

Good analgesic
Antipyretic
NO anti-inflammatory action

66
Q

What is the target of NSAIDs in pain management?

A

Prostaglandins sensitise nociceptive neurons –> lowering their threshold for activation
Prostaglandins also promote bradykinin release –> also activate nociceptive neurons
NSAIDs reduce prostaglandin production –> hence lower pain

67
Q

What is the mechanism of opioids in pain management?

A

Prevents AP generation
Activate PRE-synaptic u opioid receptors AND POST-synaptic u opioid receptors
PRE mechanism:

  1. Inhibits AdCy to reduce cAMP
  2. Inhibits voltage-gated Ca2+ channels
  3. Reduces synaptic vesicle mobilisation
  4. Reduces neurotransmitter release

POST mechanism:
1. Activates G protein to activate K+ channels

  1. K+ channels cause K+ efflux –> hyperpolarises cell
68
Q

How is neuropathic pain managed long term?

A

Treatment must involve constant reassessment of residual or on-going pain

69
Q

What are some options for invasive treatments for management of neuropathic pain?

A

Intrathecal opioids
Spinal cord stimulation
Deep brain stimulation
Neurosurgical techniques

70
Q

What is the mechanisms of tricyclic antidepressants?

A

Promotes activity of descending inhibitory pathways at the spinal cord
Reduces nociception = reduces pain

71
Q

What does Gabapentin and Pregabalin?

A

Reduces nociception –> reduces pain
BUT gabapentin appears to also increase GABA release
AND gabapentin prevents central sensitisation of nociception pathways

72
Q

What does carbamazepine and other anti-epileptic drugs do in pain management?

A

Block action potential generation –> hence reduces nociception and pain

73
Q

What is the gold standard for trigeminal neuralgia?

A

Carbamazepine

74
Q

What is the mechanism of Ketamine?

A

Polyamine –> competitive antagonist

75
Q

How does Capsaicin work for pain management?

A

Agonist at transient receptor potential vanilloid type 1 (TRPV1 receptor)
–> ligand gated non-selective cation channel (Ca2+ and Na+)
–> initial activation leads to drainage of substance P
Analgesic duration depends on rate of replacement of substance P

76
Q

Why can capsaicin be more effective post nerve injury?

A

TRPV1 receptors are upregulated following peripheral nerve injury

77
Q

How does Lignocaine function for nerve damage?

A

It is a voltage-gated sodium channel blocker

Reduce nociception

78
Q

How can lidocaine be administered?

A

IV or spinally

79
Q

What is the idea behind the WHO ladder for pain management?

A

Assess pain first
THEN choose drug from appropriate level
–> do not start from the bottom option and work up to success

80
Q

What is the normal clinical pattern of sensory loss in glove and stocking distributions?

A

Sensory loss starts normally in the toes –> feet –> distal legs and fingers –> wrist –> forearm etc

81
Q

What is the clinical pattern of sensory loss with specific peripheral nerves?

A

There is sensory loss in the areas in which only that nerve innervates (can be both muscular and sensory depending on nerve)

82
Q

What is normally the clinical pattern of sensory loss within specific dermatomes?

A

There is usually a sensory loss in corresponding dermatomes to where there has been a nerve root lesion –> eg herniation of a vertebrae –> will lead to the dermatome for that vertebrae to losing sensory information

83
Q

What happens to sensory information in complete spinal cord transection?

A

The dermatomes of the level and below of the transection will lose sensory information

84
Q

What is the effect on sensory ability in a stroke?

A

Contralateral sensory loss

85
Q

What is the pattern of sensory loss in Mononeuropathies?

A

Localised sensory disturbance in the area supplied by the damaged nerve.

86
Q

What is the pattern of sensory loss in Peripheral neuropathy?

A

Symmetrical sensory deficits in a ‘glove and stocking’ distribution in the peripheral limbs.

87
Q

What are the most common causes of peripheral neuropathies?

A

diabetes mellitus and chronic alcohol excess.

88
Q

What is the pattern of sensory loss in Radiculopathy?

A

occurs due to nerve root damage (e.g. compression by a herniated intervertebral disc), resulting in sensory disturbances in the associated dermatomes.

89
Q

What is the pattern of sensory loss in Spinal cord damage?

A

Sensory loss both at and below the level of involvement in a dermatomal pattern due to its impact on the sensory tracts running through the cord.

90
Q

What is the pattern of sensory loss in Thalamic lesions(e.g. stroke)?

A

Contralateral sensory loss.

91
Q

What is the pattern of sensory loss in Myopathies?

A

Often involve symmetrical proximal muscle weakness.

92
Q

What are some red flags for clinical presentation of back pain for possible fracture?

A

major trauma

minor trauma in elderly/osteoporotic

93
Q

What are some red flags for clinical presentation of back pain for possible tumour/infection?

A 
age (<20 or >50)
Hx of cancer
Fever
weight loss
recent bacterial infection
immunosuppression
pain worse at night/when supine
94
Q

What are some red flags for clinical presentation of back pain for possible neurological deficit?

A

severe/progressive sensory loss/weakness

bladder or bowel dysfunction

95
Q

What is trigeminal neuralgia?

A

It is pain caused by disruption of the trigeminal nerve which supplies facial sensation
Pain can be caused by even mild stimulation of the face

96
Q

What is the causes of trigeminal neuralgia?

A

Nerve compression –> vascular, tumour
Demyelination –> MS
Brain lesion –> surgical trauma, stroke, facial trauma

JMP Y2S1 (24 decks)

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