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Neuroscience (BMS109) > Pain > Flashcards

Pain Flashcards

1
Q

What is allodynia?

A
  • Neurons become sensitve to non-nociceptive inputs

- Painful response to normally innocuous (non-painful) stimuli

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2
Q

What is referred pain thought to reflect?

A

Convergence of visceral afferent neurons onto similar pathways as the skin afferents in the CNS

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3
Q

What is hyperpathia?

A
  • Fibre or axonal loss
  • Raises the detection threshold
  • Need greater stimulus before pain is detected

BUT when threshold reached - explosive pain

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4
Q

Evidence AGAINST the specificity theory?

A

1) Pain perceived not always proportional to intensity of stimulus
2) Modulation by other stimuli (eg. acupuncture)
3) Perception if pain in severed limbs
4) Referal of pain from viscera –> skin
5) Placebo effect

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5
Q

What can cause central sensitistion?

A
  • Local release of prostaglandins from nociceptive dorsal horn neurons causing hyperalgesia
  • Damage to central pathways (diabetes, shingles, MS, stroke)
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6
Q

What does bradykinin do?

A

Lowers the threshold of nociceptive molecular fibres (TRPV1)

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7
Q

What does the placebo effect prove?

A

That voluntary or involuntary mechanisms can overcome severe pain

(soldiers can have severe wounds with no pain)

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8
Q

What is another name for the spinothalamic tract?

A

The anterolateral system

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9
Q

How does stimulation of the periaqueductal grey (in the midbrain) provide pain relief?

A
  • Activates brainstem nuclei (raphe) which modulates the activity of the dorsal horn neurons
  • Dorsal horn decending inputs activate enkephalin-releasing interneurons
  • Inhibits C fibres
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10
Q

What does capsican do and what does this show?

A
  • Mimics endogenous vanilloids released from stressed cells

- Nociceptors may also detect release of chemicals from stressed cells

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11
Q

Where does the affective-motivational pathway input to?

A
  • Limbic system (emotional)

- Hypothalamus (homeostasis)

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12
Q

What do prostaglandins do?

A
  • Lower the action potential threshold for pain

- Some painkillers act on the COX enzyme involved in prostaglandin synthesis

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13
Q

Which fibres are nociceptive?

A

Aδ and C

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14
Q

What is fast pain?

Which fibres?

A
  • The first pain felt
  • Sharp, immediate
  • Mimicked by direct stimulation of Aδ nociceptive fibres
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15
Q

What causes hyperalgesia?

A

Release of inflammatory substances bradykinin and prostaglanids when tissue is damaged

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16
Q

What other areas of the brain are activated in response to pain?

A
  • Insula

- Cingulate cortex

17
Q

What does the parabrachial nucleus respond to?

A
  • Painful stimuli ANYWHERE on the surface of the body

- In the affective-motivational tract

18
Q

What does measurements in the activity of the somatosensory cortex indicate?

A
  • Somatosensory cortex responds to painful stimuli and intensity of painful stimuli (in the same place as non-painful stimuli in the same location)
  • Pain is spatially mapped
  • Spinothalamic tract projections preserve topography
19
Q

How prove cellular receptors are specific to pain?

A

1) Non-nociceptive fibres are already saturated before pain is perceived
Nociceptive fibres fire when pain is percieved

2) If block C fibres, only immediate pain felt
- If block Aδ fibres, only slow pain is felt
- If stimulare Aα or Aβ fibres (non-nociceptive) no pain is felt

20
Q

How does rubbing an area relieve pain?

A
  • Relay of nociceptive signals by the projection neuron is gated by the activity of an inhibitory interneuron
  • C fibres usually inhibit the interneuron but Aβ activate it
  • Mechanoreceptors Aβ locally inhibit nociceptive C inputs to the spinal chord
21
Q

What is the specificity theory of pain?

A
  • Pain is a DISTINCT sensation

- Detected and transmitted by specific receptors and pathways to distinct pain areas of the brain

22
Q

What is slow pain?

Which fibres?

A
  • The second pain felt
  • Delayed but longer lasting
  • Diffuse
  • Mimicked by direct stimulation of C nociceptive fibres
23
Q

What are the 2 components of the central pain pathways?

A

1) Sensory discrimitive
- Signals location, intensity and type of stimulus
- Through the spinothalamic tract

2) Affective-motivational
- Signals ‘unpleasantness’ of pain

24
Q

What is pain?

A
  • An enigmatic sensation
  • Graded motivation
  • Discrimitive sensation (different to different people)
  • Can be intolerable
25
Q

What is ‘referred pain’?

A

Pain due to damage of internal organs perceived as coming from locations on the skin

26
Q

How prove molecular receptors are specific to pain?

A
  • TRPV1 (capsican receptor) in Aδ and C fibres is activated by capsican in chillies and by temperatures of 45 degrees
  • Other TRV receptors are only activated in Aδ alone at higher temps (52 degrees)
  • Different fibres allow sensation of a more intense pain
27
Q

Evidence FOR the specificity theory?

A

1) Receptors (cellular and molecular) respond SPECIFICALLY to pain
2) Specific pathways that convey pain
3) Regions of the CNS are specifically and distinctly activated in response to pain

28
Q

What are the mystifying symptoms of pain?

A
  • Emotional variability (what people think pain in)
  • Radiation over wide regions
  • Referral (from deep tissue –> skin)
  • Persistent after sensations
29
Q

What is the convergence theory of pain?

A
  • Pain is a integrated, plastic state

- Pain is a CONVERGENT somatosenssory activity within a distributed network of neuormatrix (neurons)

30
Q

What is hyperalgesia?

A
  • An increased repsonse to a painful stimuli which is normally tolerable
  • As a result of lowered nociceptor theresholds
31
Q

Describe the affective-motivational pathway

A
  • Shares some paths with the spinothalamic tract but branches off differently
  • Little/ no topographic mapping (parabrachial nucleus)
32
Q

What does phantom limb pain suggest?

A
  • Pain may be centrally represented
  • In part may be a central representation of what we expect pain to be
  • Central maps may partly be preformed (children born without limbs can suffer)

Neuroscience (BMS109) (23 decks)

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