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Human basic neuroscience > Pain physiology > Flashcards

Pain physiology Flashcards

1
Q

Nociceptive pain

A

Due to damage to non-neural tissue and driven by activation of nociceptors

Examples: sprains, bruises, bone fractures, burns, inflammation (from e.g. an infection or arthritic disorder)

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2
Q

Neuropathic pain

A

Due to a lesion or disease of the somatosensory nervous system (peripheral or central nerves)Example: nerve trauma, carpal tunnel (nerve entrapment ), post herpetic neuralgia (viral), diabetic neuropathy (metabolic), chemotherapy-induced neuropathy (toxic)

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3
Q

Nociplasticpain

A

Altered nociception despite no clear evidence of actual or threatened tissue or nerve damage/disease. (Distrubance in central pain processing)

Example: fibromyalgia

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4
Q

Define peripheral nociceptors

A

Peripheral nociceptors are pseudo bipolar neurons with cell bodies located in ganglia

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5
Q
A

Multipolar neurons:Located in CNS (brain, spinal cord) and autonomic ganglia. More than two processes emanating from cell body. (e.g. interneurons)

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6
Q
A

Pseudobipolarneurons:(also called unipolar) Peripheral nociceptors, cell bodies located in spinal and cranial nerve ganglia (dorsal root ganglia and trigeminal ganglia, respectively)

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7
Q

Where are the cell bodies of peripheral nociceptors located?

A
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8
Q

Aß fiber mechanoreceptor

A

, myelinated, very fast

responds to touch, pressure, vibration, limb movement

senses touch, pressure, vibration, Discriminative touch

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9
Q

delta fibers:

Mechanoreceptors

Thermoreceptors

Chemoreceptors

A

Thinly myelinated, fast

responds to nocuous mechanical, thermal, chemical stimuli

Type I > 53◦C (medium mechanical)

Type II > 43◦C (high mechanical)

senses well localized, sharp, pricking pain, fast or 1st pain

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10
Q

C fiber:

Mechanoreceptors

Thermoreceptors

Chemoreceptors

A

Unmyelinated, slow

responds to nocuous mechanical, thermal, chemical stimuli

senses diffuse, dull, aching, burning pain

Slow or 2nd pain

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11
Q

Unimodal nociceptive afferent subtype

A

Mechanonosensitive – respond to intense mechanical stimulation that threaten to damage the tissue.

Thermosensitive – respond to temperatures >42 °C or <17 °C.

Chemosensitive –respond to the H+, K+, capsaicin, bradykinin etc

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12
Q

Polymodal nociceptive afferent subtype

A

Responds to several/all types of nociceptive stimuli

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13
Q

Silent nociceptive afferent subtype

A

Not responsive to mechanical or thermal stimuli during normal conditions, but activated during inflammation and then activated by mechanical and thermal stimuli

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14
Q

What is the primary neurotransmitter for nociception?

A

Glutamate

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15
Q

How is stimulation converted to pain signals? Give two common examples

A

“Transient receptor potential (TRP)” channels: ligand-gated ion channels responsive to heat, low pH, chemical and cold stimuli. (chili)

Acid-sensing ion channels (ASIC): responsive to chemical irritants, including low pH (e.g. during inflammation, ischemia.

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16
Q

Describe the route from heat stimuli to perception

A
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17
Q

Describe the route from chemical stimuli to perception

A
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18
Q

Describe the route from mechanical stimuli to perception

A
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19
Q

Describe the route from cold stimuli to perception

A
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20
Q

What are the central terminals of C-and A𝛿-fibers connect to dorsal horn cells

A
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21
Q

First-order neurons in the pain pathway

A

These are pseudounipolar neurons which have cells bodies within the dorsal root ganglion. They have one axon which splits into two branches, a peripheral branch (which extends towards the peripheries) and a central branch (which extends centrally into the spinal cord/brainstem).

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22
Q

Second-order neurons in the pain pathway

A

The cell bodies of these neurons are found in the Rexed laminae of the spinal cord, or in the nuclei of the cranial nerves within the brain stem. These neurons then decussate in the anterior white commissure of the spinal cord and ascend cranially in the spinothalamic tract to the ventral posterolateral (VPL) nucleus of the thalamus.

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23
Q

Third-order neurons in the pain pathway

A

The cell bodies of third-order neurons lie within the VPL of the thalamus. They project via the posterior limb of the internal capsule to terminate in the ipsilateral postcentral gyrus (primary somatosensory cortex). The postcentral gyrus is somatotopically organised. Therefore, pain signals initiated in the hand will terminate in the area of the cortex dedicated to represent sensations of the hand.

24
Q

What factors are released upon tissue damage which leads to the activation of nociceptors?

A

Arachidonic acid

Potassium

5-HT

Histamine

Bradykinin

Lactic acid

ATP

25
Q

Describe the pain pathway

A
26
Q

Dorsal horn interneurons

A

critical role in transmission and gating of nociceptive transmission

present in all lamina, but the majority are concentrated in lamina II

excitatory (glutamate) or inhibitory (e.g. GABA, glycine, enkephalin)

27
Q

Nociceptive primary afferents…

A

connect to projection neurons in lamina I and V, which cross the midline (decussate) and ascend in the spinothalamic (lateral) tract

28
Q
A

Dorsolateral tract of Lissauer (Lissauer’s tract) contain branches of the primary afferents that run 1-2 segments upwards or downwards before entering the grey matter of the dorsal horn

29
Q

Anterolateral system

A

Collection of ascending pathways that carry pain and temperature, as well as related touch, sensations from the spinal cord to the brainstem or thalamus.

Spinothalamic tract

Spinoreticular tract

Spinotectal tract

30
Q

Spinothalamic tract

A

(lateral and anterior) destined for thalamus, important for localization of painful stimuli and thermal stimuli

31
Q

Spinoreticulartract

A

destined for reticular formation, causes alertness and arousal in response to painful stimuli

32
Q

Spinotectaltract

A

destined for tectum, orient eyes and head towards stimuli

33
Q

What are the two main pathways that carry nociceptive signals to higher centers in the brain?

A

The spinothalamic and the spinoreticulartracts

34
Q

What is the difference between the two adjacent spinothalamic tract pathways: anterior and lateral.

A

Lateral: information about pain and temperature

Anterior: information about crude touch.

35
Q

Describe the ascending visceral pathway for pain

A
36
Q

Name the three types of opioid receptors which regulate the neurotransmission of pain signals

A

These receptors are called mu, delta, and kappa opioid receptors.

They are all G protein-coupled receptors and their activation leads to a reduction in neurotransmitter release and cell hyperpolarisation, reducing cell excitability.

37
Q

Name the three types of endogenous opioids:

A

Β-endorphins – which predominately binds to mu opioid receptors

Dynorphins – which predominately bind to kappa opioid receptors

Enkephalins – which predominately bind to delta opioid receptors

38
Q

General definition of pain sensitization

A

Increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of response to normally subthreshold inputs.

39
Q

Hyperalgesia

A

An increased response to a stimulus which is normally painful

40
Q

Allodynia

A

Pain due to a stimulus that does not normally provoke pain.

41
Q

Mechanisms for peripheral activation and sensitization of nociceptors during inflammation

A
42
Q

Describe the role of antidromic axon reflexes in neurogenic inflammation

A

antidromic axon reflexes induce release of neuropeptides from peripheral terminals

43
Q

Primary hyperalgesia (including allodynia)

A

Increased sensitivity to pain at the site of injury due to sensitization of peripheral nerve endings (peripheral sensitization)

44
Q

Secondary hyperalgesia (including allodynia)

A

Increased sensitivity to pain at locations adjacent or remote from the site of injury due to changes in the spinal cord and higher brain areas (central sensitization).

45
Q

Central sensitization

A

Definition: Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input Note: This may include changes in endogenous descending pain control systems.

46
Q

Processes leading to central sensitization (facilitation)

A

Sustained release of glutamate and neuropeptides (e.g. substance P) →increased activation of their respective postsynaptic receptors

Removal of NMDA receptor Mg+block →increases influx of calcium →activation of many intracellular pathways that contribute to reduction of threshold for activation of postsynaptic neuron (e.g. modified ion channel responsiveness and increased expression of ion channels and receptors)

Altered activity in interneurons (increased activity in excitatory interneurons, decreased activity in inhibitory interneurons)

47
Q

Central sensitization: Secondary hyperalgesia

A

Facilitation: Impulses from the injured area cause a state of stimulation in the central neurons with increased excitability -> magnification of the pain impulses arising from the area of secondary hyperalgesia

Convergence: Afferent from the healthy area converge on the same second order neurons that receive pain signals from the injured area

48
Q

”Gate control -theory”

Observation: •Rubbing a jammed finger reduces the pain i.e. activation of low-threshold mechanoreceptors reduce sensation of sharp pain

A

Explanation:

Mechanoreceptive afferents activate local neuronal inhibitory circuits in the dorsal horn (“closing the gate”)•In “competition” with nociceptors that inactivates the inhibitory neurons (“opening the gate”)A likely mechanism behind the pain relieving effect of transcutaneous electrical nerve stimulation (TENS)

49
Q

Functional endogenous pain modulation

A
  1. ACC –endogenous opioids or opioid drugs activate descending pain inhibition
  2. RVM –Cholecystokinin (CCK) antagonizes opioid-induced analgesia
50
Q

Dysfunctional pain modulation in chronic pain, example from fibromyalgia (FM)

A
  1. ACC and 2. Thalamus not activated normally during pain in FM.

Association between:

1) Reduced ACC activation
2) reduced availability of opioid receptors in ACC
3) pain intensity

FM patients with longer FM duration has

Smaller ACC volume

Reduced placebo response

51
Q

Pharmacological pain treatment to nociceptive pain

A

Paracetamol/acetaminophen

NSAIDs

opioids

tramadol

SNRIs?

52
Q

Pharmacological pain treatment to Neuropathic pain

A

amitryptilin

SNRIs

gabapentin

pregabalin

tramadol

opioids

Topical: lidocain, capsaicin

53
Q

Pharmacological pain treatment to Nociplasticpain

A

amitryptilin

SNRIs

gabapentin

pregabalin

tramadol

54
Q

Projected pain

A

pain projected from a damaged structure in the peripheral or central nervous system. Projectedpain is neuropathic.

55
Q

Referred pain

A

pain felt in a part of the body other than its actual source (distant to the site of injury). Referred pain is nociceptive.

56
Q

Referred pain clinical picture

A

Diffuse and variable

Distribution related to pain intensity

Distribution lacks neuroanatomic correlate

No pathognomonic sensory abnormalities

Anaesthetic blocks of primary pain focus can normalize sensitivity

57
Q

Projected pain (peripheral) clinical picture

A

Distinct

Distribution relatively stable over time

Distribution in accordance with nerve root or nerve

No pathognomonic sensory abnormalities

Anaesthetic blocks do not normalize sensitivity

Human basic neuroscience (68 decks)

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