Pain Flashcards
Definition of pain
The sensory and emotional experience associated with actual tissue damage.
Pain threshold
The point at which a stimulus is perceived as pain
Pain tolerance
The duration or intensity of pain one can tolerate before the start of overt pain responses
What is nociception and what can be said about nociceptors
Nociception is the sensory process of detecting tissue damage
Nociceptors: Free nerve endings of primary sensory neurons, afferent Adelta and C fibres. Located throughout the body and react to mechanical, chemical (excitatory NT’s, ischaemia, toxins) and thermal stimuli. Have a high threshold
What are the four main processes involved in nociception?
Transduction (conversion of pain t electrical signals by receptors), transmission, perception and modulation
C fibres vs A-delta fibres
C-fibres: most numerous, small diameter, unmyelinated (slow). Are polymodal. Pain is diffuse, dull, aching. Slow pain.
A-delta: medium diameter, myelinated. React to mechano-thermal stimuli. Well localised sharp fast pain
Transduction
The conversion of painful stimuli to electrical signals.
Transmission
Composed of electrical (AP’s) and chemical (NT) transmission.
Primary afferent to dorsal horn to brain stem to thalamus to sensory cortex
What are the two main classes of dorsal horn cells in relation to pain
1) Nociceptive specific in lamina’s 1 and 2. Activated by only noxious stimuli. A-delta and C
2) wide dynamic range in lamina 5. Activated by nociceptive and innocuous (touch), A-delta, C and A beta
What are the two divisions of the spinothalamic tract?
Neo-spinothalamic: Typically A-delta afferents (lamina 1) runs to PCG where pain is perceived
Paleo-spinothalamic: Typically C fibres, lamina 2 and 3, and takes info to reticular formation and limbic system. emotional part of pain
How is pain perceived?
Reticular formation: autonomic response and motor response
Limbic: emotional response
Somatosensory: interpretation of the pain
What is the transmitted signal liable to?
N.b a lot occurs in the dorsal horn
Dampening and amplificaton
How can pain be dampened?
- By segmental inhibition
- Descending inhibitory nerves
What is the gate control theory of pain (pain dampening)
premise
Three variables
Mechanism
- Based on the premise of a ‘gate’ in the dorsal horn modulating afferent nerve impulses.
- A-delta and C fibres open the gate; A-beta of light touch close the gate; brain messages can open or close gate
- Inhibitory interneurons in the dorsal horn keep gate closed by producing enkephalin (opiate like), stopping signals from A-delta and C fibres. The interneurons are stimulated by A-Beta fibres of touch, and descending inibitory information
E.g rub forehead when sore
Detail of descending inhibitory information
When pain signals pass through the midbrain, the periaqueductal area is stimulated causing neurons in the locus ceruleus(pons) and nucleus raphe magnus to transmit fibres to these interneurons and release serotonin or noradrenaline
Pain amplification and Windup (hypersensitivity)
Windup is the process of increased AP output from dorsal horn cells due to sustained low input from C fibres
Excessive calcium influx, lowering receptor threshold
Nociceptive pain
Tissue damage, opioid sensitive
Neuropathic pain
Damage to nerve fibres themselves. Opioid resistant.
Sensitive to membrane stabilisers (gabapentin, carbamazepine) ; tricyclics; spinal cord stimulators
Types of neuropathic pain
Peripheral: e.g diabetic neuropathy, trigeminal neuralgia. Described as burning tingling stinging
Central: spinal cord damage, thalamic pain syndrome
Complex regional pain syndrome
Can occur following injury major or minor, causing severe debilitating pain. Sympathetic NS also affected so abnormal circulation and increased temp. Loss of function
Inflammatory pain
divided into?
Post trauma pain associated with tissue damage and inflammatory mediators.
Neurogenic inflammation: release of neuropeptides from nerves C fibres (substance P etc). Axon reflex, cause more inflammatory mediator release (Primary hyperlagesia) and cause oedema and dilation. Can eventually cause WINDUP or central sensitisation (secondary hyperalgesia)
Non neurogenic inflammation: release of inflammatory substances from vessels and CT. peripheral sensitisation, primary hyperlagesia.
Both contribute to hyperalgesia (lowering pain threshold)
Primary and secondary hyperalgesia
Primary is peripheral sensitisation by inflammatory mediators lowering the pain threshold of the receptors.
Secondary is windup when afferents are constantly being stimulated so dorsal horn cells fire more, lower threshold due to excessive calcium
Chronic pain mechanism
Constant pain stimulation at dorsal horn causes excess NT to affect glial cells in the dorsal root. They release cytokines.
Causes more NT release. Can change physiology such that pain signal is generated in dorsal horn due to vicious circle
Associated with depression and bad sleep etc
