Pain Flashcards
What is allodynia?
- Neurons become sensitve to non-nociceptive inputs
- Painful response to normally innocuous (non-painful) stimuli
What is referred pain thought to reflect?
Convergence of visceral afferent neurons onto similar pathways as the skin afferents in the CNS
What is hyperpathia?
- Fibre or axonal loss
- Raises the detection threshold
- Need greater stimulus before pain is detected
BUT when threshold reached - explosive pain
Evidence AGAINST the specificity theory?
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
What can cause central sensitistion?
- Local release of prostaglandins from nociceptive dorsal horn neurons causing hyperalgesia
- Damage to central pathways (diabetes, shingles, MS, stroke)
What does bradykinin do?
Lowers the threshold of nociceptive molecular fibres (TRPV1)
What does the placebo effect prove?
That voluntary or involuntary mechanisms can overcome severe pain
(soldiers can have severe wounds with no pain)
What is another name for the spinothalamic tract?
The anterolateral system
How does stimulation of the periaqueductal grey (in the midbrain) provide pain relief?
- Activates brainstem nuclei (raphe) which modulates the activity of the dorsal horn neurons
- Dorsal horn decending inputs activate enkephalin-releasing interneurons
- Inhibits C fibres
What does capsican do and what does this show?
- Mimics endogenous vanilloids released from stressed cells
- Nociceptors may also detect release of chemicals from stressed cells
Where does the affective-motivational pathway input to?
- Limbic system (emotional)
- Hypothalamus (homeostasis)
What do prostaglandins do?
- Lower the action potential threshold for pain
- Some painkillers act on the COX enzyme involved in prostaglandin synthesis
Which fibres are nociceptive?
Aδ and C
What is fast pain?
Which fibres?
- The first pain felt
- Sharp, immediate
- Mimicked by direct stimulation of Aδ nociceptive fibres
What causes hyperalgesia?
Release of inflammatory substances bradykinin and prostaglanids when tissue is damaged
What other areas of the brain are activated in response to pain?
- Insula
- Cingulate cortex
What does the parabrachial nucleus respond to?
- Painful stimuli ANYWHERE on the surface of the body
- In the affective-motivational tract
What does measurements in the activity of the somatosensory cortex indicate?
- 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
How prove cellular receptors are specific to pain?
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
How does rubbing an area relieve pain?
- 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
What is the specificity theory of pain?
- Pain is a DISTINCT sensation
- Detected and transmitted by specific receptors and pathways to distinct pain areas of the brain
What is slow pain?
Which fibres?
- The second pain felt
- Delayed but longer lasting
- Diffuse
- Mimicked by direct stimulation of C nociceptive fibres
What are the 2 components of the central pain pathways?
1) Sensory discrimitive
- Signals location, intensity and type of stimulus
- Through the spinothalamic tract
2) Affective-motivational
- Signals ‘unpleasantness’ of pain
What is pain?
- An enigmatic sensation
- Graded motivation
- Discrimitive sensation (different to different people)
- Can be intolerable
What is ‘referred pain’?
Pain due to damage of internal organs perceived as coming from locations on the skin
How prove molecular receptors are specific to pain?
- 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
Evidence FOR the specificity theory?
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
What are the mystifying symptoms of pain?
- Emotional variability (what people think pain in)
- Radiation over wide regions
- Referral (from deep tissue –> skin)
- Persistent after sensations
What is the convergence theory of pain?
- Pain is a integrated, plastic state
- Pain is a CONVERGENT somatosenssory activity within a distributed network of neuormatrix (neurons)
What is hyperalgesia?
- An increased repsonse to a painful stimuli which is normally tolerable
- As a result of lowered nociceptor theresholds
Describe the affective-motivational pathway
- Shares some paths with the spinothalamic tract but branches off differently
- Little/ no topographic mapping (parabrachial nucleus)
What does phantom limb pain suggest?
- 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)
