Lecture 13: Pain Flashcards

1
Q

What is pain?

A
    • Pain is “an unpleasant sensory and [or] emotional experience associated with actual or potential tissue damage…”
    • pathways responsible for bringing pain/sensory information to the brain are responsible for minimizing risk
    • Pain does not exist in your body, it can only exist in your brain. That is where you “feel” pain!
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2
Q

What are the different types of pain?

A

– Nociceptive pain: pain arising from tissue damage (aka adaptive pain because It has evolved to prevent us from situations that could harm us, it is a form of learning)
– Neuropathic pain: pain arising from damage to the damage-reporting system itself in the nervous system
Spontaneous generation of pain (no physical stimuli, but brain is reporting pain)
– Other pain: pain arising from neurological dysfunction, not damage. Ex. emotional pain

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3
Q

How does the pain reflex happen?

A

– when you respond to pain (ex. pulling away) before being consciously aware, that is when incoming afferent (sensory) information can directly synapse with interneurons which then activate those lower motor neurons and cause a reflex before the sensory information travels to the cortex

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4
Q

How do you perceive pain?

A
    • It starts with nociceptors which is a sensory neuron that responds to damaging stimuli (pain receptor)
    • Sends ”possible” threat signal to spinal cord and brain; doesn’t necessarily mean there is damage but that there is risk of damage
    • if activated then they send signals up the dorsal root (afferent/sensory information) and synapses with ascending spinothalamic fibers (brings up through spinal cord directly to thalamus)
    • nociceptors are being activated all the time, the thalamus and other brain regions will determine if activation of these nociceptors are credible threat and if thalamus should send this information to the cortex (if there is threat) or make a motor response
    • If the brain perceives this threat as credible, it will create the sensation of pain, and initiate a cascade of events to deal with the pain accordingly –> process is called nociception
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5
Q

What are the different types of nerve endings that respond to noxious stimuli?

A
    • Free nerve endings are embedded in the tissues (unencapsulated)
    • Encapsulated nerve endings synapse with tissues

Noxious stimulus = tissue injury ≠ pain (to feel pain, has to be processed by cortex to become conscious of it but this doesn’t always happen even if there’s tissue injury)

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6
Q

How do nociceptors get activated?

A
    • Noxious stimuli act on nociceptors to communicate information.
    • Ion channels in nerve endings; translate physical stimulus into electrical signal
    • Nerve endings may contain stretch sensitive Na+ channels;
    • Upon stretch, channels open which generates action potential; afferent sensory information
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7
Q

What are the different types of sensory fibers?

A
C Fibers
-- Small, unmyelinated;
-- Nociceptive (painful stimulus)
-- much less sensitive
Ab (beta) Ad (delta) Fibers
-- Medium, myelinated;
-- Nociceptive & non-nociceptive.
Aa (alpha) Fibers
-- Large, myelinated;
-- Light touch (ex. moving your arm), proprioception
-- Most sensitive because it has large, myelinated axons

these four different fibers don’t go all the way up to the brain, they go to the spinal cord

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8
Q

What fibers are involved in fast and slow pain?

A

C Fibers
– Aching, throbbing;
– Not localized (hurts around vicinity)
Ab, Ad Fibers
– Sharp pain;
– Localized
– Withdraw suddenly (spinal reflex -synapse with interneurons > LMN)
ex. slamming car door on fingers. Starts out with sharp, localized pain (Ab, Ad Fibers) and then it will become not localized, throbbing pain (c fibers). All fibers get activated, but the c fibers get activated later than the other three fibers (unmyelinated so it takes time for information to reach cortex and get processed) and when it does you get this throbbing pain

sometimes, the c fibers (much less sensitive) will get activated but not the Ab, Ad Fibers (much more sensitive) because the c fibers could have receptors for certain stimuli that the Ab, Ad Fibers do not have

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9
Q

What are the different types of pain?

A

Somatic Pain

    • Injury to skin, muscles, bone, joints, and connective tissues;
    • Very localized; Ab and Ad
    • Nociceptors are sensitive to temperature, chemical irritants, mechanical stresses (cutting, burning);
    • Both fast and slow pain (A and C fibers)

Visceral Pain

    • Results from the activation of nociceptors of the thoracic, pelvic, or abdominal viscera; ex. stomach pain
    • Poorly localized; C fibers
    • Slow pain only (C fibers)
    • Nociceptors sensitive to distention (stretch), ischemia and inflammation;
    • No receptors for cutting or burning;
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10
Q

What is the anterior horn?

A
    • spinal cord segment
    • Site where pain is modulated;
    • Afferent fibers sent to thalamus;
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11
Q

What are the different parts of the brain responsible in responding to pain?

A

Sensory Homunculus

    • Somatosensory cortex;
    • Where we consciously perceive localized pain; Ab/Ad activate specific neurons in the sensory homunculus (ex. activating neurons that are responsible for thumb, so you feel pain there)

Limbic System –> emotional arousal

Midbrain –> autonomic activation
- Increased HR, BP

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12
Q

What is the gate theory/gating?

A
    • Gating is one way in which humans modulate pain.
    • The gate theory of pain suggests that non-painful stimuli close the “gates” to painful input which prevents pain sensation from traveling to the brain; you overload it with other non-painful afferent sensory information (shaking hand) so that the brain does not know what to process so if it chooses to process the non-painful stimuli, then that’s what you feel instead of the noxious stimulus
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13
Q

How does the gating/gate theory work?

A
    • C fibers and A fibers synapse with the projection neuron (spinothalamic tract) and excite it
    • When a projection neuron gets excitatory stimulation, it will fire an action potential so you feel pain because it will send it directly to the thalamus.
    • A and C fibers synapse and excite inhibitory interneuron. This inhibitory interneuron is synapsed with the projection neuron. So, when A and C fibers are activated, they send excitatory signals to the interneuron, which has an inhibitory effect on the projection neuron.
    • If you rub/shake your hand after feeling pain, you stimulate these A and C fibers which can stimulate the projection neurons and it can stimulate and activate the inhibitory interneurons. If you activate inhibitory interneurons, they release GABA and inhibit the projection neurons and interrupt it from sending signals up to thalamus.
    • Stimulation by non-noxious input suppresses pain; changes the firing rate of the projection neuron which will confuse the thalamus when determining if the activation is painful or not (blunts the painful stimuli)
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14
Q

How does the descending pain pathway work?

A
    • In response to this noxious stimulus, the brain will activate descending neural pathways to dampen afferent signaling
    • the midbrain (tegmentum - periaqueductal gray matter specifically) releases dopamine and norepinephrine and the Raphe Nuclei releases 5-HT (serotonin) which then causes the release of cannabinoids and opioids
    • cannabinoids and opioids inhibit firing of afferent neurons in spinothalamic tract so signal doesn’t get through.
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15
Q

What is inflammation?

A
    • You need an ongoing signal to persist in order to tell you to rest your body
    • Inflammation is the bridge from acute painful stimulus to chronic.
    • Inflammation is a localized physical condition in which part of the body becomes reddened, swollen, hot, and often painful, especially as a reaction to injury or infection.
    • Chronic pain leads to inflammation which causes sensitization of nerves
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16
Q

How does inflammation/sensitization occur?

A
    • Broken/damaged cells release pro-inflammatory cytokines (e.g. prostaglandin, bradykinins)
    • Prostaglandin and bradykinin upregulate glutamate receptors on nerve terminals; leads to hyper-excitability > CNS sensitization;
    • Post-synaptic membranes is hyper-excitable so that even normal stimulus will come through, but is perceived as noxious.
    • Also attracts neutrophils (clear debris), causes blood vessels to swell, area gets red, etc.
17
Q

What are NSAIDs?

A
    • Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin;
    • Stops/interrupts inflammatory cascade (anti-inflammatory)
18
Q

What is hyperalgesia and allodynia?

A

Hyperalgesia

    • Stimulus that should be a little bit painful is very painful;
    • Pain is out of proportion with stimulus;
    • Hyperactivation of peripheral nerve fibers > C-fiber overactivity.

Allodynia

    • Stimulus that should not be painful is painful;
    • A-fiber mediated
19
Q

What are inhibiting and sensitizing factors that influence pain?

A
    • Anticipation of relief from pain (placebo); Expectation/anticipation of pain (nocebo)
    • Distraction from pain; Attention to pain (being distracted from the pain helps because the thalamus receives other information to relay so the pain signals are blunted because the thalamus is working on other distracting information)
    • Positive outlook; Anxiety, depression
    • Cognitive contextualisation of the painful stimulus -understanding why you are feeling pain (ex. knowing it’s for research); Lack of understanding or context for painful stimulus
20
Q

What is neuropathic pain?

A
    • Neuropathic pain is the generation of painful signals due to damage to the central (or peripheral) nervous system (not in response to any external stimuli or damage of tissue)
    • Typically caused by upregulated or dysfunctional ion channels (e.g. sodium channels that open when they shouldn’t, or stay open for too long, or are sensitive to too many things, etc);
  • -> Can occur on damaged nerves or nearby undamaged nerves;
  • -> Leads to hyperexcitability;
21
Q

What are some pharmacological pain management?

A

Locally acting agents:

    • Local anesthetics (e.g. lidocaine, solarcaine); cocaine/amphetamines blocks sodium ion channels which can prevent pain signals (action potentials)
    • Topical NSAIDs (stops inflammatory cascades)

Non-opiates

    • COX inhibitors (e.g. ibuprofen, naproxen); COX (cyclooxygenase) is an enzyme that produces prostaglandin (cytokine). COX inhibitors can prevent the production and stop the inflammatory cascade (swelling, hypersensitization)
    • Acetaminophen (works in the brain only)
    • Neuropathic agents (e.g. gabapentin); gabapentine mimics gaba (inhibitory) which will stop action potentials and prevent pain signals
    • Cannabinoids (stop NTs from being released)
    • Antidepressants (e.g. SSRI, TCAs)
Opiates 
-- Codeine
-- Morphine
-- Hydromorphone Fentanyl
-- Methadone
opiates stops neurons from communicating
22
Q

What are some non-pharmacological pain management?

A

Local

    • Fixation of tissue;
    • Surgical excision of mass;
    • Physiotherapy/massage;
    • Compresses (hot, cold); gating hypothesis
    • Exercise.

Central

    • Psychosocial/spiritual support;
    • Stress management;
    • Distraction;
    • Deep brain stimulation; Exercise, physiotherapy