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Neuroscience Of Pain Flashcards

1
Q

What is the difference between afferent and efferent information in the nervous system?

A

Afferent information carries signals from the body’s tissues about internal and external environments to the CNS, while efferent transmission sends directive signals from the CNS to body effectors.

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2
Q

What is the receptor type, stimulus, axon diameter, myelination, and conduction velocity for Ia fibers?

A

• Receptor Type: Muscle Spindle (Ia)
• Stimulus: Proprioception
• Axon Diameter: Largest
• Myelination: Yes
• Conduction Velocity: Fastest

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3
Q

What is the receptor type, stimulus, axon diameter, myelination, and conduction velocity for Beta fibers?

A

• Receptor Type: Meissner’s
• Stimulus: Touch
• Axon Diameter: Large
• Myelination: Yes
• Conduction Velocity: Fast

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4
Q

What is the receptor type, stimulus, axon diameter, myelination, and conduction velocity for A-delta fibers?

A

• Receptor Type: A-delta Nociceptor
• Stimulus: Tissue injury (mechanical, thermal)
• Axon Diameter: Small
• Myelination: Yes
• Conduction Velocity: Slower (fast pain, withdrawal reflex)

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5
Q

What is the receptor type, stimulus, axon diameter, myelination, and conduction velocity for C-PMN fibers?

A

• Receptor Type: C-PMN Nociceptor (polymodal)
•
Stimulus: Tissue injury (mechanical, thermal, algogenic chemicals in interstitial fluid)
• Axon Diameter: Smallest
• Myelination: No
• Conduction Velocity: Slowest (slow pain, chronic pain)

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6
Q

Which fibres are most prevalent and studied among nociceptors?

A

The free nerve endings of A-delta (Aδ) and C fibres are the most prevalent and studied.

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7
Q

Are all A-delta and C fibres nociceptors?

A

No, not all A-delta and C fibres are nociceptors, and not all nociceptors are A-delta or C fibres.

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8
Q

What type of receptors are A-delta and C fibres mostly classified as?

A

They are mostly high-threshold mechanoreceptors.

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9
Q

What function do C fibres have when innervating hair follicles?

A

These C fibres are slow-conducting and high-threshold but do not serve a nociceptive function. They detect stimuli from hair-to-hair over receptive fields and are also called C(aress) fibres.

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10
Q

How can A-Beta neurons respond to noxious stimuli?

A

When A-Beta neurons are not specialized, they can act as free nerve endings and respond to mechanical and noxious stimuli.

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11
Q

Which fibres are the fastest, and how fast are they?

A

Fat and myelinated fibres are the fastest, conducting signals at 80-120 m/s.

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12
Q

Which fibres are the slowest, and what is their conduction speed?

A

Thin, unmyelinated fibres, like A-delta (Aδ) and C fibres, are the slowest, conducting signals at 0.5-2 m/s.

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13
Q

What type of stimulation do A-delta (Aδ) and C fibres require to trigger a signal?

A

They need high-intensity mechanical stimulation, noxious heat, or noxious cold to trigger a signal.

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14
Q

Where are receptors located, and what is their role in sensory perception?

A

Receptors are located at the distal ends of afferent neurons (primary sensory neurons/first-order neurons) and are specialized to detect specific stimulus types.

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15
Q

Describe the path of an afferent signal from detection to processing in the brain.

A
  1. Stimulus detected by receptors.
  2. Signal travels to the dorsal root and dorsal horn of the spinal cord.
  3. Ascends via second-order neurons to the thalamus.
  4. Travels to the somatosensory cortex and other brain areas via third-order neurons for interpretation.
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16
Q

Besides the somatosensory cortex, what brain areas are involved in sensory processing?

A

Areas related to memory, emotion, cognition, and autonomics are also involved.

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17
Q

What is the path of an efferent signal?

A
  1. Signal travels down descending tracts to the ventral horn of the spinal cord.
  2. Travels through the ventral root to specific nerves.
  3. Reaches muscles or glands to produce a response.
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18
Q

What are the four stages between a stimulus and its perception?

A

Transduction, transmission, modulation, and perception.

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19
Q

What two events make up a nerve impulse?

A

An electrical event (action potential) and a chemical event (neurotransmitter release).

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20
Q

What happens during transduction?

A

Stimuli are converted into action potentials by sensory receptors.

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21
Q

What occurs during transmission?

A

Nerve signals enter and ascend through the CNS using specific neural tracts.

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22
Q

What is modulation in the context of sensory processing?

A

Modulation alters sensory transmission intensity via inputs from touch or descending signals from the brain (e.g., emotions), either increasing or decreasing the signal.

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23
Q

What is perception in the sensory process?

A

Perception is the subjective experience of a stimulus, influenced by transduction, transmission, and modulation, and altered by factors like emotions and sleep.

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24
Q

How can emotions affect perception?

A

Emotions such as happiness, fear, or anger can significantly alter how a stimulus is perceived.

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25
Q

How does context change the perception of touch?

A

A touch during a happy moment feels different than the same touch during an argument, highlighting the role of perception and emotions.

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26
Q

What is the Gate Control Theory, and why is it useful for massage therapists?

A

The Gate Control Theory explains how touch and pressure stimuli (mechanoreceptors) can reduce pain signals (nociceptors) by modulating their transmission in the spinal cord.

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27
Q

What role do inhibitory GABA interneurons play in the Gate Control Theory?

A

GABA interneurons regulate whether second-order neurons in the spinothalamic tract fire, influencing pain transmission.

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28
Q

How do nociceptors affect the inhibitory interneuron in the Gate Control Theory?

A

Nociceptors inhibit the interneuron, preventing it from slowing or stopping the second-order neuron’s transmission, allowing pain signals to continue.

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29
Q

How do mechanoreceptors (A-beta fibres) influence the inhibitory interneuron?

A

Mechanoreceptors activate the interneuron, which slows or stops pain signal transmission along the pain pathway.

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30
Q

Why can mechanoreceptors “close the gate” before pain signals reach the brain?

A

Mechanoreceptors (A-beta fibres) transmit signals faster than nociceptors (A-delta/C fibres), allowing them to reach the dorsal horn first and activate the inhibitory interneuron to block pain signals.

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31
Q

What is the difference between ascending and descending modulation?

A

• Ascending modulation involves modifiers of sensory transmission in the dorsal horn (e.g., gating) and the thalamus (e.g., filtering).
• Descending modulation (central modulation) involves suppression or weakening of sensory experiences, including pain, by the CNS.

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32
Q

What are real-life examples of descending modulation in action?

A

Injured soldiers in combat or athletes during competition often feel little or no pain initially due to descending modulation suppressing sensory signals.

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33
Q

Why does the CNS suppress or weaken sensory experiences?

A

The CNS suppresses sensory input to prioritize attention to matters of greater importance or in the presence of distractions, reducing the value of the sensory experience.

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34
Q

Which brain areas collaborate to modulate sensory experience?

A

The cortex, thalamus, insula, amygdala, and hypothalamus work together to release chemicals like endorphins and enkephalins for pain modulation.

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35
Q

What endogenous chemicals are involved in descending modulation?

A

Endorphins, enkephalins, dopamine, serotonin (5-HT), norepinephrine (NE/NA), and endocannabinoids (e.g., anandamide).

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36
Q

Which brainstem structures are involved in descending modulation?

A

The periaqueductal gray (PAG) in the midbrain and the raphe nuclei in the brainstem release modulatory substances.

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37
Q

How do descending modulators affect the dorsal horn?

A

• Inhibit synapses where C and A-delta fibres try to activate second-order spinothalamic neurons (P/T cells).
• Activate local inhibitory neurons to “close the gate.”
• Directly inhibit the second-order neurons.

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38
Q

Which neurotransmitters are used by local inhibitory neurons in the dorsal horn?

A

GABA and glycine are the primary neurotransmitters used.

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39
Q

Where can endorphins and enkephalins act, and what is their role?

A

Endorphins and enkephalins act in the brain and spinal cord, reducing pain by inhibiting sensory transmission.

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40
Q

What is convergence in the context of central modulation?

A

Convergence occurs when multiple neurons send signals to a smaller number of second-order neurons, leading to confusion in the brain about the origin of pain.

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41
Q

How does convergence affect the brain’s ability to localize pain?

A

Convergence can make it unclear where pain originates because signals from different locations are interpreted as coming from the same second-order neuron.

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42
Q

Provide an example of how convergence can cause interpretation confusion.

A

In dental pain, convergence can make it difficult to identify which tooth is causing sensitivity or pain.

43
Q

What is referred pain?

A

Referred pain occurs when sensory signals from deeper structures (like organs or muscles) are misinterpreted by the brain and felt on the body’s surface, often due to convergence in the nervous system.

44
Q

How does convergence contribute to referred pain?

A

Convergence happens when sensory signals from different areas (e.g., the heart and shoulder) share the same pathways to the brain, leading to misinterpretation of the source of pain.

45
Q

How does heart referral work as an example of referred pain?

A

Since the brain doesn’t often receive sensory signals from the heart, heart signals enter the spinal cord at the same levels as signals from the shoulder, chest, or arm, and are misinterpreted as coming from those areas, creating a heart referral pattern.

46
Q

How does referred pain change over time?

A

As the episode progresses, the pain intensity may increase, and additional tissues may contribute to the pain, allowing the brain to better identify the source of the pain.

47
Q

Why does referred pain typically come from deeper structures like viscera or muscles?

A

Deeper structures are less served by first-order neuron receptors and are not typically involved in day-to-day sensations, so the brain misinterprets converged signals from these structures as coming from the body surface.

48
Q

How do scleratomal sensations contribute to referred pain?

A

The diffuse nature of scleratomal sensation combined with convergence can create confusing referral patterns, which may be misinterpreted as visceral referral or trigger points.

49
Q

Can you provide an example of referred pain from cervical joints?

A

Ligament tears or facet joint issues in the cervical spine can cause referral pain patterns that may be mistaken for other causes, highlighting the complexity of referred pain.

50
Q

What is proximal depolarization?

A

Proximal depolarization occurs when neurons are activated by chemical, electrical, or mechanical means, but not at the usual receptor sites in the tissues, leading to misinterpretation of the pain location.

51
Q

How can neurons be activated in proximal depolarization?

A

Neurons can be activated through chemical, electrical, or mechanical means anywhere along their neurilemmas, not necessarily at the receptors in the tissues.

52
Q

How does proximal depolarization occur in thoracic outlet syndrome?

A

In thoracic outlet syndrome, muscle compression at the shoulder or neck level mechanically activates neurons that usually carry signals from the hand to the CNS, causing hand symptoms like numbness or pain despite no direct issue in the hand.

53
Q

How does proximal depolarization manifest in carpal tunnel and cubital tunnel syndromes?

A

In these conditions, nerve compression in tight passageways leads to symptoms like numbness, paraesthesia, and pain in the hand, following the nerve’s supply pattern despite the compression occurring at the wrist or elbow.

54
Q

Why is understanding proximal depolarization important for manual therapists?

A

It helps manual therapists assess and treat conditions effectively, as they need to understand how symptoms from compressed nerves can manifest in distant areas (like the hand, even if the issue is in the neck or spine).

55
Q

How does proximal depolarization occur in the spine?

A

Herniated discs, bone spurs, subluxation, and inflammation can impinge spinal nerves in the intervertebral foramen, creating symptoms in the tissues supplied by the affected spinal nerve(s).

56
Q

What is phantom limb sensation?

A

Phantom limb sensation is the experience of sensation or pain in a body part that is no longer present, often occurring after limb loss, but it can also occur after procedures like mastectomies.

57
Q

Is phantom limb sensation unique to limbs?

A

No, phantom sensation can occur in any body part, not just limbs. For example, it can be present following mastectomies.

58
Q

How can phantom sensation be initiated?

A

Phantom sensation can be initiated in two ways:
1. Proximal depolarization
2. Brain-generated phenomenon

59
Q

How does proximal depolarization contribute to phantom limb sensation?

A

After amputation, severed peripheral nerves in the stump can still transmit signals to their second-order neurons. Factors like clothing, therapy, or prostheses can irritate these nerve endings, causing them to depolarize and transmit signals to the brain, which interprets them as coming from the missing limb.

60
Q

How is phantom sensation a brain-generated phenomenon?

A

The brain continues to receive sensory information from the areas that previously corresponded to the missing body part. This stimulates the brain’s homunculus zones, sustaining recognition of the missing tissue.

61
Q

What role does the homunculus play in phantom limb sensation?

A

The homunculus is a representation of the body in the brain. In phantom limb sensation, the brain continues to stimulate the homunculus zones for the missing limb, contributing to the sensation of the limb being present.

62
Q

What is the “energy field” phenomenon in phantom sensations?

A

People with phantom sensations often feel aware of an “energy field” around the missing body part, like sensing someone moving through it.

63
Q

How does the brain reconcile cognitive awareness with phantom sensation?

A

The brain knows the body part is gone but still experiences sensory transmissions and emotional responses, leading to vivid dreams and emotions related to the missing part.

64
Q

How does the sensory cortex adapt after limb loss?

A

Adaptations in the sensory cortex occur for the missing part, causing a shift in the sense of its existence and altering the interpretation of afferent signals from the stump.

65
Q

What is the “telescoping” phenomenon in phantom sensations?

A

Telescoping is the perception that the amputated part is moving closer to the stump, often as the brain tries to solve the “problem” of the missing limb.

66
Q

Do people born without body parts experience phantom sensation?

A

Yes, people born without body parts may still experience phantom sensation, but it is less developed compared to those who lost limbs.

67
Q

What percentage of amputees experience chronic phantom limb pain (PLP)?

A

50-85% of amputees experience disturbing or painful phantom sensations that become chronic.

68
Q

What causes chronic phantom limb pain (PLP)?

A

PLP is thought to arise from a combination of stump afferentation, neurophenomena in the spinal cord and brain, and brain “confusion” about the status of the missing limb.

69
Q

How effective are traditional medical treatments for phantom limb pain (PLP)?

A

Traditional medical approaches only provide relief for 10%-12% of individuals with PLP.

70
Q

How effective is mirror therapy for treating phantom limb pain (PLP)?

A

Mirror therapy has shown success in treating PLP, particularly for soldiers who have lost limbs in recent wars.

71
Q

What does central sensitization refer to?

A

Central sensitization refers to a state where physical and/or emotional trauma leads to heightened pain responses, reduced effectiveness of descending modulation, and long-term changes in neuron function and neurochemical production.

72
Q

How does central sensitization affect neurons?

A

Over time, central sensitization causes altered neuron health and function, dysfunctional synapses, and changes in neurochemical production, leading to chronic pain syndromes.

73
Q

What is somatization in the context of central sensitization?

A

Somatization occurs when mental or emotional distress is expressed as physical symptoms, complicating central sensitization and pain experiences.

74
Q

How are anxiety, pain, and depression connected?

A

Anxiety, pain, and distress contribute to depression by depleting key neurochemicals like serotonin, dopamine, endogenous opioids, and norepinephrine, which are involved in mood regulation.

75
Q

How does depression contribute to its own cycle?

A

Depression depletes serotonin, dopamine, endogenous opioids, and norepinephrine, which worsens mood and reduces the effectiveness of descending modulation, exacerbating pain and physical discomfort.

76
Q

How does depression affect descending modulation?

A

Depression reduces the effectiveness of descending modulation because it depletes the neurochemicals involved in pain modulation, resulting in heightened pain sensitivity and physical discomfort.

77
Q

How does an individual’s history affect how they interpret pain?

A

The chronicle of sensations experienced by an individual influences how the brain interprets incoming pain signals, potentially leading to misinterpretations (e.g., heart dysfunction causing shoulder pain to be perceived as heart-related).

78
Q

How can previous trauma affect pain perception?

A

Previous trauma can lead to hypersensitivity in affected tissues or desensitization in other areas, sometimes creating dissociative sensations, which massage therapists may encounter.

79
Q

How does an individual’s history affect referred pain?

A

Sensation patterns like referred pain can be customized by the brain based on individual history, making assessment more challenging.

80
Q

Why does pain vary from person to person?

A

Pain varies because each person’s life experiences, beliefs, stressors, support systems, and other factors influence how they interpret stimuli, including noxious stimuli. Two people with the same pathology may experience completely different pain outcomes.

81
Q

What is the biopsychosocial model of pain?

A

The biopsychosocial model suggests that pain is influenced by three main pillars: biology, psychology, and social factors, all of which can affect how much pain an individual experiences.

82
Q

How does damage or disease affect sensory perception?

A

Damage or disease can affect sensory perception by disrupting normal functioning in the peripheral and central nervous systems, leading to challenges in interpreting sensory information.

83
Q

What factors can make it difficult for the brain to interpret sensory information in the case of damage or disease?

A

Factors include neuron loss/scarring (lowering firing rates), inflammation, edema, and chemicals released by damaged tissues, which can cause intense and irritable firing patterns along sensory pathways.

84
Q

How does damage pathology contribute to proximal depolarization confusion?

A

Damage along sensory pathways can lead to confused interpretation of sensory signals, especially when the firing patterns become irritable or misfiring due to inflammation and tissue damage.

85
Q

What is causalgia, and what causes it?

A

Causalgia is a specific symptom caused by peripheral nerve damage, most often related to median, sciatic (tibial), and C8/T1 spinal nerve injuries, involving damage to sympathetic vasomotor neurons.

86
Q

What are the primary symptoms of causalgia?

A

The primary symptom is intense “burning” pain with a “shooting” quality, often accompanied by erythema (reddening) of the skin. Pressure, temperature (especially heat), and almost any stimulus can trigger causalgia.

87
Q

What triggers or aggravates causalgia symptoms?

A

Strong emotional states, pressure, temperature changes (especially heat), and guarding postures or behaviors can trigger or worsen causalgia symptoms.

88
Q

What is reflex sympathetic dystrophy (RSD)?

A

Reflex sympathetic dystrophy is a variant of causalgia, with similar symptoms but potentially differing in underlying pathophysiology.

89
Q

What is neuropathic pain?

A

Neuropathic pain occurs due to irritation or damage in the sensory nervous system, either in the peripheral nerves or the central nervous system (CNS).

90
Q

What are some common causes of neuropathic pain?

A

Causes include peripheral nerve damage (e.g., trauma, neuralgias, shingles, amputation) and CNS damage (e.g., transverse myelitis, spinal stenosis, multiple sclerosis, stroke), or a combination (e.g., alcoholism, diabetes, chemotherapy).

91
Q

What are some specific factors that can contribute to neuropathic pain?

A

Possible contributing factors include ascending and descending abnormalities in nerve pathways, which can be influenced by conditions like trauma, infections, or diseases affecting the nervous system.

92
Q

What are the common symptoms of neuropathic pain?

A

Symptoms can range from numbness and tingling to “burning,” “electric shock,” or “stabbing” sensations. It can also present as more typical pain and may be triggered by non-nociceptive stimuli.

93
Q

How does the presentation of neuropathic pain vary?

A

Neuropathic pain can be continuous or episodic, and its intensity can vary significantly, often making it very challenging to live with.

94
Q

What factors can make neuropathic pain worse?

A

Fatigue, illness, intense emotional states, anxiety, and depression can exacerbate neuropathic pain.

95
Q

What treatment approaches are recommended for neuropathic pain?

A

Treatments include anticonvulsant, analgesic, and antidepressant medications, physiotherapy, massage therapy, psychotherapy, acupuncture, and relaxation practices.

96
Q

What is anaesthesia?

A

Anaesthesia is the absence of any sensation, where the stimulus does not produce any expected sensory response. It can be induced, such as with a nerve-blocking agent in dental work.

97
Q

What is hypaesthesia?

A

Hypaesthesia is diminished sensation, where the stimulus is experienced, but with less intensity than expected. It is often referred to as numbness and can be a side effect of medical conditions.

98
Q

What is hyperaesthesia?

A

Hyperaesthesia is heightened or exaggerated sensation, where the response to a stimulus is stronger than expected. It can be caused by neuronal irritation or damage, and sometimes psychoemotional factors.

99
Q

What is paraesthesia?

A

Paraesthesia refers to abnormal sensations, such as “pins and needles,” “prickling,” or the feeling of “bugs crawling on the skin.” It occurs when the stimulus creates irritation or alters perception, and may also occur with reduced blood flow to a nerve.

100
Q

What is dysaesthesia?

A

Dysaesthesia occurs when a paraesthesic sensation is painful, such as “hot pokers,” “electric burning,” or “feeling like it’s on fire.” These are strange and painful sensory experiences.

101
Q

What is allodynia?

A

Allodynia occurs when an innocuous (non-painful) stimulus results in pain, often a “regular” type of pain such as achy or sharp pain. It can be caused by nerve damage, CNS issues, or poor central modulation.

102
Q

What is hypalgesia?

A

Hypalgesia is a weak response to a nociceptive (painful) stimulus, where the sensation is less intense than expected due to reduced sensitivity to pain.

103
Q

What is hyperalgesia (hyperalgia)?

A

Hyperalgesia is heightened sensitivity to painful stimuli, where the pain intensity is unexpectedly strong, often accompanied by prolonged pain and a strong emotional response.

Pain (4 decks)

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