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Somatic Sensation: Pain :face_with_head_bandage: (Headache (Causes of…
Somatic Sensation: Pain :face_with_head_bandage:
Dual pathway of pain transmission
A-delta fibres
Fast-sharp pain
Via neospinothalamic tract
Mainly to thalamus and lesser degree to brain stem (reticular system)
Highly localised pain (specific sensation)
C fibres
Slow-chronic pain
Paleothalamic tract
Mainly to brain stem (75-90%) and lesser to thalamus
Pain poorly localised (nonspecific sensation)
Sudden onset of pain stimulus
Produces dual pain sensation
Fast, sharp pain
Followed by slow, burning pain a second later
If one pathway is blocked, the other still functions (C fibres via LA)
Pain control/Analgesia system
Brain control over input of pain signals to CNS
3 Components
Periaqueductal gray matter
Innervating midbrain and upper pons
Enkephalinergic neurons
Raphe magne nucleus
Innervating lower pons and upper medulla
Serotonergic neurons
Pain inhibitor complex
Dorsal horns of spinal gray matter
Enkephalinergic neuron
Blocks pain signal before it is even relayed to brain
Electrical stimulation of PGM and RMN are able to inhibit completely very strong pain signals from the dorsal horns of the spinal cord
Prolonged blockade
Analgesia last for many minutes to hours
Minute amounts of morphine injected into periaqueductal gray matter and periventricular nuclei cause EXTREME analgesia
Important opiates
Endorphins
Beta-endorphins
Found in thalamus and pitiutary gland
Dynorphins
Found in minute amounts
However, EXTREMELY strong opiate
200x stronger than morphine when injected directly into the analgesia system
Enkephalins
Met-enkephalin
Leu-enkephalin
Secreted by nerve endings of PGM in the raphe magne nucleus and pain inhibitory complex
Causes presynaptic inhibition of both A-delta and C-fibres signals upon synapse - prevents the relay of signals and release of substance P
Possible MOA - blocking Ca channel blockers
C fibres release Substance P on stimulation
Slow to accumulate and degraded, responsible for slow-chronic pain
Tactile sensory signals
Activation of large sensory fibres
by peripheral tactile receptors
Depresses stimulation of pain from the same area of the body
Local lateral inhibition
Rubbing skin near itchy or painful areas relieves the itch
Pain relief by acupuncture
Referred pain
When tissue damage to a certain organ causes pain in a location remote from the original source of damage
Of clinical importance as the only cardinal sign of any visceral inflammation or damage
Pain is initiated in a visceral organ and referred
To a skin surface far from the organ
To another deep area of a different location
Stimulation of visceral pain receptors trigger pain signals
Pain signals travel through the receptor, synapse occurs with the SAME second order neurons receiving pain fibres from the skin
Pain signals travel through the same neurons conducting pain signals from skin
Visceral pain
Viscera only has nociceptors
Pain from viscera on abdomen or chest the only method to gauge visceral damage and inflammation
Highly localised damage - not much pain stimulated
eg: gut cut into two, no significant pain as few pain fibers involved
Diffuse damage stimulating many pain fibers across a large surface - severe pain
Ischemia - blood vessel blocked in a large area of gut causes stimulation of multiple nerve fibers at once
Poorly localised
Pain in two places
Cause of pain affects both viscera and parietal wall of visceral cavity
True visceral pain pathway
Transmitted via ANS
Referred to a surface of skin far away from damaged tissue
Ie in appendicitis - pain is referred via sympathetic visceral fibers into visceral chain
Referred to area near the umbillicus - aching, cramping pain
Parietal pain pathway
Transmitted via local spinal nerves from pleura, pericardium, parietal peritoneum
Referred to surface area directly above the damaged area
I.e in appendicitis, pain impulses comes from the parietal peritoneum where the inflamed appendix touches
Sharp pain of irritated peritoneum above the lower right area
Causes
Ischemia
Formation of acidic end products or tissue degenerating substrates ie bradykinins and enzymes
Chemical stimuli
Leakage from GIT into peritoneum
Rupture of gastric and duodenal ulcer - severe pain
Hollow viscus spasm
Due to ischemia or mechanical stimulation
Gut, ureter, bile duct, gall bladder
Rhythmic spasm
Overdistention
Overfilling causes overstretching
Ischemia occurs
Headache
Referred pain from deeper structures to the surface of head
Can be intracranial or extracranial in origin
Intracranial headaches
Rarely caused by damaged to the brain itself as the brain is almost completely insensitive to pain
Venous sinuses, tentorium, blood vessels of the dura, middle meningeal artery
Causes of headaches
Meningitis
Most severe headache
Affects all parts of the head
Caused by inflammation of all meninges
Low CSF
Decreased floatation of the brain in the CSF
Weight of brain causes the extension of various dural surfaces
Migraine
Special headache of unknown causes
Alcoholic headache
Alcoholic is toxic to tissues and causes irritation to meninges, leading to intracranial headache
Constipation
Toxic products absorbed from GIT
Divided into
Cerebral vault headache
Brainstem and cerebellar vault headache
Temperature
Body can experience diverse gradation of cold and heat
Due to three receptors
Cold receptors
8-43C
Warmth receptors
(30-50C, peak at 45)
Pain receptor
Extreme cold (<15)
Extreme heat (>45)
Can adapt rapidly and extensively but never completely
A cold receptor will react strongly to a sudden fall in temperature initially
However, stimulation fades rapidly in the first few seconds and progressively slower in the next few hours
Allows the body to respond markedly to sudden changes as well as steady states in temperature
Temperature of skin falls
Person feels colder than when temperature of skin is normal
Other examples: Sauna, shower room, human freezer
Mechanism of stimulation
Changes in metabolic rate
For every 10 degrees celcius the metabolic rate is altered by 2x multiplier
Is based on spatial summation as there are few thermal receptors in a single area
Transmission of stimulation
In almost parallel, but not the same pathways as pain signals