Tissue Specific Pain Flashcards
Can spinal pain arise from intrinsic structures of the vertebral column?
Yes, this is kellegrans first principle.
What might cause referred pain in the trunk and limbs?
Intrinsic structures of the vertebral column, kellegrans second principle.
Nerve root irritation is the only way referred pain can occur true false?
False, other mechanisms can, kellegrans third principle.
Referred pain in kellegrans principles is what type of nature?
Dull, aching, diffuse and hard to localise and perceived deeply. His fourth principle.
How is visceral and nerve root irritation pain defined apart from each other?
By calling it referred somatic pain. Kellegrans fifth principle. Meaning the type of pain is in the somatic tissues as opposed to viscera or nerves.
Explain the referred somatic pain pattern kellegrans mentioned?
He mentioned it does not follows dermatomal nature but a more segmental one. Stimulation of lower spinal segments produced pain in lower regions of the body wall or limb.
Overall kellegrans experiment was?
Stimulating with noxious stimuli, muscles and interspinous ligaments by injection of hypertonic saline, scratching and whatnot, producing referred pain in remote areas. Thoracic ligaments produced pain in anterior and posterior chest wall. Cervical and lumbar ligaments produced pain in the respective limbs.
Sensitivity of structures in order is? Most to least.
Periosteum, ligament, joint capsule, tendon, fascia, muscle
Referred pain maps linked to specific structures. Explain somatic referred pain map
Sclerotomes are suggested to be the reason for somatic referred pain. They are the regions of bones, joints and ligaments innverated by the same spinal cord segment.
Sclerotomes are realistic why why not?
The paper kellegrans presented was idealised sclerotomes and therefore not really based on quantitive data. Not good evidence.
What are muscle nociceptors activated by?
Pressing, squeezing, chemical stimulation like bradykinin and serotonin or potassium.
What evidence is there for chronic pain without inflammation?
There are no experimentally valid explanations of chronic muscle pain in the absence of inflammation
Explain what exhibits convergence and how it relates to referred pain?
Afferents converge and synapse onto second order Neurons that receive input from deep somatic tissues and the skin. When the dorsal horn neuron is stimulated pain is evoked but the neuron does not convey information as to where the source of pain came from. Pain comes from all structures
Theories of bone pain?
Capsular contracture (does not explain pain at rest) and intraosseous venous hypertension ( distension of veins proximal to obstruction)
Two calssifications of methods by which experimental muscle pain can be induced? Examples?
Endogenous and exogenous without and with external stimuli. Endogenous methods include is hernia and exercise and exogenous is intramuscular infusion of hypertonic saline,
Relationship between stimulus intensity, area, duration and pain intensity, area in local and referred pain?
Referred pain: felt approx 20 seconds after local pain and is diffuse and unpleasant.
Higher stimulus required to elicit referred pain compared to local.
What is another mechanism apart from convergence that may be involved in referred pain?
Spatial summation - involved in cutaneous, deep and visceral pain, the additional recruitment of nociceptors units that results in an increased barrage to dorsal horn and brain stem Neurons = increased local and referred pain
Qualities of referred muscle pain?
Diffuse, aching pain in muscle, pain referred to distant somatic structures and modifications in superficial and deep tissue sensibility in the painful areas
How might referred pain be related to Central sensitization?
Animals studies show new receptor fields to form via noxious muscle stimuli. Could be mechanism behind referred pain because of central hyperexcitability. It has been suggested to be the phenomenon of secondary hyperalgaesia in deep tissue
What might suggest role of central hyperexcitability (in relation to chronic musculoskeletal and drugs)
Patients given nmda receptor antagonists and responding better than when given morphine. Nmda receptor antagonist (ketamine) inhibit wind up and hyperalgaesia.
Hyperalgaesia for peripheral and Central sensitization in muscle pain?
Yes, maintained peripheral input can relate to both
Referred pain area was sprayed with anaesthic and reduced pain by up to 22% what does this suggest?
That referred pain may have involvement of cutaneous receptors but does not explain resting activity.
Referred pain requires what?
Intact peripheral nervous system and some spontaneous input,
Convergence projection theory, explain it
Afferent fibres from different tissues converge onto common spinal neuron, nociceptive activity at spinal cord confused
What doesn’t convergence projection theory explain?
The development of referred pain after local pain and its bidirectional nature, and threshold for local to referred is different.
What is the convergence facilitation theory?
Visceral organs insensitive to stimuli. Non nociceptive input created an irritable focus, which meant that some stimuli was perceived as referred pain. Recently this idea has been termed central sensitization. Non noxious stimuli can trigger
Axon reflex theory explain?
Axon reflex suggest that afferent fibre is bifurcated ( divided into two ), before connecting to dorsal horn. But doesn’t explain time delay of R pain, threshold differences or somatosensory sensibility changes in area of referred pain.
Hyperexcitability theory is?
That referred pain has no central mechanism. New receptive fields are created as a result of the opening of latent convergent afferent fibres in the dorsa, horn.
Thalamic convergence theory ?
Referred pain due to the summation of neural inputs in the brain as opposed to the spinal cord. From injured area and referred area.
Five cardinal characters of visceral pain?
- May not occur from all organs (no innverated or stimulus inappropriate)
- Not always linked with injury
- Referred to body wall
- Diffuse and poorly localised
- Accompanied by autonomic and motor reflexes.
What mechanisms produce visceral pain?
Spasm in smooth muscle in viscera
Contraction of smooth muscle against obstruction
Distension, tearing,
Ischemia
Inflammation of lining
Mech or chem stimulation of inflamed mucous membranes,
Traction or compression
What do not produce visceral pain?
Cutting, burning, pressure
What is the role of the vagus nerve in visceral pain?
Heart, lungs, Gi tract ( from oesophagus-transverse) all innverated by vagus nerve. Vagus modifies nociceptive processing in the spinal cord. Does not directly convey nociceptive signals.m
Splaninic nerve in visceral pain?
Chest, abdomin, pelvis viscera innverated by splanchinic nerves. Nociceptive afferents conveyed by splanchinic nerve.
High threshold visceral nociceptors found where and why? And respond to?
Respond only to noxious stimuli found in areas where pain is the dominant sensation such as heart and ureterer,
Low threshold why and where in viscera? Explain it in general.
Respond to intensity of stimulus by increasing their frequency of discharge from innocuous into the noxious range. Found predominantly in bowel and bladder which respond to both innocuous and noxious.
Why is visceral pain poorly localised?
Because it is diffusely innverated and the central pathways are poorly organised somatotopically. Meaning nervous system not wired to localise it accurately.
Why can visceral pain be felt in areas distant from the position of the organ?
Because segmental innveration is established early during development before viscera fully differentiated and before final topographic positions established.
Relationship between visceral pain and muscle spasm?
Muscles involved depend on both the spinal segments supplying the viscera and the intensity of stimulus. Muscles above and below involved segment of visceral pain usually recruited. This creates a muscle spasm which if on going can lead to chronic pain
Other sources of pain that may be associated with visceral pain?
Spread of infection or inflammation to involve parietal peritoneum of the abdominal wall, and invasion of visceral nerve plexus by spreading tumours. These secondary sources have their own mechanisms distinct from those of intrinsic visceral pain.
Convergence in visceral pain? Explain.
Afferents of viscera and from the body wall converge onto common Neurons in the dorsal horn. Convergence mainly at spinal level but can also occur at thalamus and even the cortex.
What is deep somatic pain?
Pain originating in the deep tissues, muscle, ligaments, joints, bones, tendon, fascia, periosteum
