Pain Mechanism Flashcards
The perception of injurious stimulis is called []
The perception of injurious stimulis is called nociception
What is the difference in acute and chronic pain (with regards to usefulness)
When can pain be regarded as chronic? [1]
Acute pain: protects body from further damage by warning that there is threat to the system
Chronic: tells us that damage has occured but serves no useful function; required for 3 months to be chronic
Where is the first neuron for pain mechansim located? [1]
Dorsal horn (then decussates & ascends in the spinothalamic tract)
What is neuropathic pain? [1]
chronic maladaptive pain after TBI or spinal cord injury
What is labelled line neural coding? [2]
there are specific neuronal circuits transmitting specific sensory information from the skin to the brain.
generation of specific sensations often involves crosstalk among distinct labeled lines
What is functional pain? [2]
no underlying lesion found despite investigation
pain is disproportionate to the degree of any clinically discernable tissue injury
How should we regard chronic pain?
Chronic pain cannot be regarded merely as a symptom; it is a “disease” in its own right, which demands treatment !!
Referred pain
Severe pain down a leg (sciatica) may be caused by a []
Hip problem may give rise to []
Gall bladder pain may be felt in the []
severe pain down a leg (sciatica) may be caused by a slipped disk in the back
a hip problem may give rise to knee pain
gall bladder pain may be felt in the right shoulder
[] & [] are the most common mental disorders associated with chronic pain.
What are the NTs that are involved in these mental disorders and how do the influence pain? [3]
Depression & anxiety are the most common mental disorders associated with chronic pain
Serotonin (5HT) & Norepinephrine (NE); generally suppress sensations of normal bodily functions
Dopamine (DA); modulates pain perception & dampens pain
What is the pain matrix?
The pain matrix is a fluid system composed of several interacting networks. A nociceptive matrix receiving spinothalamic projections (mainly posterior operculoinsular areas) ensures the bodily specificity of pain and is the only one whose destruction entails selective pain deficits.
What are the 3 types of pain? [3]
- NOCICEPTIVE PAIN
- NEUROPATHIC PAIN
- FUNCTIONAL PAIN
Afferent sensory fibers
Label the axon type [A-C] and the sensations they produce
A: Abeta; touch
B: Adelta; pain & temp
C: C; pain; temp; itch; chemoreception
Afferent sensory fibers
What is the difference in afferent fibres that project first pain and secondary pain? [2]
First pain: Aδ fibre
Secondary pain: C fibre
Nociceptors
Name the channel that tranduces heat information [1]
Name the channel that tranduces cold information [1]
TRP: heat
TRPM8: cold
Nociceptors
Name some inflammatory mediators that are released by tissue damage that can transduce chemical nociceptors [4]
prostaglandins; proteases; histamine; serotonin; H+; K+
(Inflammation soup)
Peripheral sensitization
How does Capsaicin reduce pain?
The relief of pain that may follow this topical treatment is thought to be related to the temporary deactivation of heat-sensitive epidermal nociceptors expressing the Transient Receptor Potential Vanilloid 1 (TRPV1)
Capsaicin excites pain and heat rececptors; but then desensitization the receptors and reduces pain
Explain the mechanism that causes peripheral sensitisation to pain
Primary afferent attracts substance P
Substance P attracts mast cells or neutrophils & releases histamines
Histamines, alongside other chemicals like prostaglandins, ATP, 5-HT, bradykinin
Substance P also dilates the blood vessels
This will excite the pain terminals
The nociceptor terminals become more sensitive to the same quantity of the chemical mediators.
Describe the characteristics of primary erythromelalgia [2]
What is the pathophysiology of behind primary erythromelalgia? [2]
Primary erythromelalgia is a rare autosomal dominant neuropathy characterized by the combination of recurrent burning pain, warmth and redness of the extremities.
It is a channelopathy (genetic etiology) caused by mutations ofSCN9A, the encoding gene of the voltage-gated sodium channel subtype Nav1.7 - causes the channel to open with less depolarisation
.
Describe the difference in path between DCML and spinothalamic pathways [2]
Spinothalamic: secondary neuron decussates at level of spinal cord immediately; ascends contralatery
DCML: ascends on ipsilateral side and decussates at level of medulla
Label A & B [2]
A: C fibre
B: Adelta fibre
Explain the mechanism of how sensing pain in the face occurs
spinal trigeminal nucleus in the lateral medulla of the brainstem
Incorporates sensory information principally from the three extracranial divisions of the trigeminal nerve (V1, ophthalmic; V2, maxillary; V3, mandibular)
The SN projects both contralaterally and ipsilaterally to the ventral posteromedial nucleus of the thalamus (via the ventral and dorsal trigeminothalamic tracts)
This sensory information will be relayed from the thalamus to the primary motor cortex via the primary sensory cortex, allowing response to stimuli of the face
(instead of the DRG, face uses trigeminal nucleus to conduct pain)
Explain what phantam pain is and how occurs [2]
If lost limb, can still feel pain in that limb
Due to second neuron still being present, just lost primary afferent
Which type of receptors is the midbrain periaqueductal gray full of? [1]
Which nuclei does this receptor type influence? [4]
Opoid receptors - influences the:
- parabrachial nucleus
- medullary reticular formation
- locus coerruleus
- raphe nuceli
Describe the distribution of endocannabinoid receptors [3]
in the pain pathway at the peripheral and central (spinal and supraspinal) levels
in areas of the brain and brainstem nuclei involved in nociceptive perception as thalamus, amygdala, and periaqueductal grey matter.
Both CB1and CB2receptors have been detected in non-neuronal cells participating in immune and inflammatory processes in the proximity of the primary afferent neurons nerve terminals.
Explain the main function of the endocannabinoid receptors
Activate Via retrograde transmission:
- Post synaptic neuron sends a message to pre-synaptic neuron to stop release of GABA and glutamate (e..g if GABA activated - will stop release of glutamate)
E.g. Activation of GABA receptor causes release of endocannabinoid, which goes retrogradly (to the pre-synaptic terminal) and decrease release GABA)
