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6BBYN302 Perspectives on Pain and Nervous System Disorders > Neuropathic Pain > Flashcards

Neuropathic Pain Flashcards

1
Q

What are the two main categories of analgesics used for pain management?

A
  • NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)
  • Opioids
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2
Q

What are the primary types of sensory nerve fibers in the peripheral nervous system?

A
  • Abeta fibers (large, innervate sensory mechanoreceptors)
  • Adelta fibers (thinly myelinated)
  • Unmyelinated C fibers (thermoreceptors/nociceptors)
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3
Q

Describe the path of nociceptor activity from peripheral nerves to the brain.

A
  • Nociceptor activity travels through pathways in the spinal cord, brain stem, and terminates in various cortical areas of the brain
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4
Q

What are the clinical challenges in pain management?

A
  • Chronic pain is a widespread unmet need
  • Medications often offer inadequate pain control
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5
Q

What is the pain stimulus and mechanism for nociceptive pain?

A
  • Pain Stimulus: Tissue damage
  • Mechanism: Activation of nociceptors
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6
Q

What is the pain stimulus and mechanism for inflammatory pain?

A
  • Pain Stimulus: Inflammatory mediators
  • Mechanism: Involves both peripheral and central sensitization
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7
Q

What is the pain stimulus and mechanism for neuropathic pain?

A
  • Pain Stimulus: Nerve injury
  • Mechanism: Includes ectopic activity, neuro-immune interactions, and central sensitization
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8
Q

What is the pain stimulus and mechanism for dysfunctional pain?

A

Pain Stimulus: Not known
Mechanism: Not known

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9
Q

What is the characteristic feature of dysfunctional pain?

A

-Characteristic Feature: Dysfunction in the central organization generating pain signals in the absence of tissue damage in the periphery.

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10
Q

How is neuropathic pain defined?

A
  • Pain that arises as a direct consequence of a lesion or disease affecting the somatosensory system
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11
Q

What are the various types of receptors in the somatosensory system?

A

Thermoreceptors, photoreceptors, mechanoreceptors, and chemoreceptors.

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12
Q

Name some examples of conditions or pathologies that can lead to neuropathic pain.

A

-HIV infection
- metabolic/nutritional issues (e.g., diabetic and alcoholic neuropathy),
- neurotoxicity (e.g., from drugs like cisplatin and taxol)
- traumatic injury (e.g., surgical damage)
- central lesions (e.g., spinal cord injury & stroke)

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13
Q

What is a common issue in neuropathic pain, especially in conditions like diabetes?

A

-Spontaneous pain

  • which can be persistent and exist even when patients cannot sense direct tactile stimulation.
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14
Q

What is postherpetic neuralgia, and what is its association with varicella-zoster virus?

A
  • It’s chronic neuropathic pain that persists in some individuals who have had shingles, caused by the varicella-zoster virus.
  • This virus lives in the DRG, becoming activated in the DRG, and can lead to pain related to damage to central fibers
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15
Q

How are animal models of diabetic neuropathy typically induced, and what is their purpose?

A
  • Induction of Diabetic Neuropathy: Animal models of diabetic neuropathy are often induced by using streptozotocin (STZ), a drug toxic to the insulin-producing beta cells in the pancreas.
  • Purpose: replicate the neuropathic pain associated with diabetes & study potential treatments
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15
Q

What are some common models for studying neuropathic pain in animals, especially involving damage to peripheral nerves?

A
  • Common Models:
    Inducing injury to large peripheral nerves like the sciatic nerve.
  • Examples include loosely tying sutures around the nerve to cause swelling and partial nerve degeneration.
  • Other models include the chronic restriction injury, where half of the sciatic nerve is affected.
15
Q

What is a common model for studying neuropathic pain that doesn’t damage the sciatic nerve itself but the roots connecting it to the dorsal root, and what advantage does this model offer?

A
  • One common model involves damaging the roots that connect the sciatic nerve to DRG rather than the sciatic nerve itself.
  • Advantage: In this model, all the damaged cells are located in 1 DRG, which allows for separate study of these cells.
  • In contrast, other models result in scattered damaged nerve fibers throughout the nerve, making it harder to isolate & study them.
16
Q

What happens to damaged nerve fibers in neuropathic pain, particularly in terms of gene expression?

A
  • Phenotypic Shift: Damaged nerve fibers undergo a dramatic shift in their phenotype.
  • Gene Expression: thousands of genes dysregulated following nerve injury & this is likely to impact nerve’s function.
  • Ectopic Activity: Nerve fibers disconnected from peripheral targets may generate spontaneous AP which CNS interprets as pain
16
Q

In neuropathic pain, how does the processing of somatosensory information in the spinal cord change, and are the mechanisms well understood?

A
  • Processing Amplification: In neuropathic models, the processing of somatosensory info in spinal cord is amplified by several mechanisms
  • Mechanism Variability: It’s not entirely clear which mechanisms are most important & there may be variations in their importance in different categories of patients
16
Q

What happens to nerve fibers in damaged nerves, and how does this relate to neuropathic pain?

A
  • Nerve Damage: In damaged nerves, Wallerian degeneration occurs, where the nerve fibers undergo degeneration.
  • Pain Connection: This partial innervation of target tissue resulting from Wallerian degeneration believed to contribute to neuropathic pain.
    note: Many factors released during Wallerian degeneration, which can act on the spared nerve fibers and potentially drive neuropathic pain
17
Q

What is a Remak bundle?

A
  • consists of C fibers grouped together, where unmyelinated Schwann cells bundle axons closely by surrounding them, keeping them from touching each other
18
Q

how does a Remak bundle change in neuropathic pain?

A
  • these bundles are reduced in size due to axon degeneration
  • the remaining axons are located in partially deinnervated Schwann cells, which respond to nerve damage by releasing numerous injury factors
  • remaining fibers are exposed to these factors, potentially leading to abnormal activity
19
Q

How does nerve injury impact gene expression?

A
  • Nerve injury can lead to the dysregulation of thousands of genes
20
Q

What are the functional consequences of gene expression changes after nerve injury?

A
  • Nerve injury-induced gene expression changes can result in production of novel NTs & disrupt genes related to nociceptive properties
21
Q

How does nerve injury affect opioid receptors in neuropathic pain patients?

A
  • can lead to downregulation of opioid receptors that are usually present on C fibers
22
Q

How does the onset of activity relate to altered behaviour in neuropathic pain?

A
  • onset of spontaneous activity in nerve fibers correlates with onset of altered behavior in neuropathic pain
23
Q

what happens to both damaged and non-damaged neurons in neuropathic pain?

A
  • Both damaged and non-damaged neurons display ectopic (abnormal) activity in neuropathic pain
24
Q

What is a distinguishing feature of neuropathic pain compared to other types of pain?

A
  • isolated neurons themselves become sources of ectopic firing

(has been demonstrated in humans by applying a needle into the nerve to measure the activity)

25
Q

How does blocking spontaneous activity affect neuropathic pain behavior?

A
  • reverses neuropathic pain behaviour, providing a potential therapeutic approach
26
Q

What is the role of Nav1.8 Na channel in neuropathic pain?

A
  • found only in nociceptors
  • suggested to play a role in neuropathic pain
27
Q

How was the role of Nav1.8 Na channel initially studied, and what were the results?

A
  • antisense sequences used to target the Nav1.8 Na channel
  • & it appeared to have a role in neuropathic behaviour recovery
28
Q

What did the discovery of a Nav1.8 knockout (KO) animal reveal about its role in neuropathic pain?

A
  • found that a Nav1.8 KO animal could still display neuropathic pain,
    (casting doubt on channel’s exclusive involvement)
29
Q

What other Na channel was upregulated in neuropathic pain?

A
  • Nav1.3 Na channel
  • potentially to increase excitability of damaged nerve fiber
30
Q

How does the presence of a Nav1.3 KO mouse impact neuropathic pain?

A
  • Even though Nav1.3 was upregulated, presence of a Nav1.3 KO mouse also developing neuropathic pain …suggests that this channel may not be the sole cause
31
Q

What is another possible mechanism for neuropathic pain related to nerve excitability?

A
  • Downregulation of K+ channels, which hyperpolarize and dampen neuronal excitability, may contribute to neuropathic pain.
  • Many K+ channels are downregulated in neuropathic pain models
32
Q

How did a study involving the KCNS1 gene support the role of K channel downregulation in neuropathic pain?

A
  • Individuals with mutation in the KCNS1 gene, which encodes a K channel are more susceptible to neuropathic pain
  • and downregulation of K channels can induce a neuropathic pain state (Costigan et al 2010).
33
Q

What are some potential issues associated with studying neuropathic pain and these changes in connectivity?

A
  • Statistical power could be an issue in studies related to neuropathic pain and its connectivity changes
34
Q

What is the debate between peripheral and central causes of neuropathic pain?

A
  • debate regarding whether neuropathic pain primarily arises from peripheral or central causes
  • however, noted that persistent peripheral drive is common in neuropathic pain
35
Q
A

6BBYN302 Perspectives on Pain and Nervous System Disorders (11 decks)

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