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Pain Mechanisms

A presentation ton the history, physiology and mechanisms of pain
by

Ajit Panickar

on 21 February 2011

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Transcript of Pain Mechanisms

PAIN MECHANISMS
Ajit Panickar
definition
pathways
types
mechanisms
neuropathic
pain depends on the stimulus

pain also depends on where you apply the stimulus
somatic nerves
skin, muscle, joints, ligaments, bones
stimuli=heat/cold, stretch, inflammation

visceral nerves
internal organs: pelvis, thorax, abdomen
stimuli=stretch, inflammation, ischaemia
PAIN IS ALWAYS
Sensory
Subjective
Emotional
PAIN IS NOT ALWAYS
the result of tissue damage
Historical context
"Pain is what the patient says it is"
The subjectivity of experience
nociceptors
A nerve is a wire
fast pain
SLOW PAIN
A-delta
Discriminative
"Where? What? How bad?"
Sharp, short, localised
Reflex withdrawal
Not abolished by morphine
C fibre
Affective & arousal
Emotional & sympathetic response
Dull, diffuse, prolonged
Spasm & guarding
Abolished by morphine
the dorsal horn
Where peripheral becomes central
The gate control theory
descending modulation
Extracts from ‘Gunshot Wounds and Other Injuries':

“The last of the immediate symptoms of grave lesions of nerves is pain, elsewhere than in the wound..(in some) the pain was of that strange burning nature...it was rare to observe this peculiar and agonizing form of suffering among the immediate consequences of a nerve wound.

The seat of burning pain is very various. Its favourite site is the foot and hand. Its intensity varies from the most trivial burning to a state of torture. The part itself becomes exquisitely hyperaesthetic so that a touch or a tap of the finger increases the pain. Exposure to the air is avoided by the patient with a care which seems absurd and most bad cases keep the hand constantly wet, finding relief in the moisture.

As the pain increases, the general sympathy becomes more marked. The temper changes and grows irritable, the face becomes anxious and has a look of weariness and suffering. The sleep is restless. At last the patient grows hysterical. He walks carefully, carries the limb tenderly with the sound hand, is tremulous, nervous and has all kinds of expedients for lessening his pain.”
features of neuropathic pain
Second order neurone
third order neurone
the brain
Medial: discriminative
Lateral: affective

No single pain center
Medial system
LATERAL SYSTEM
Lateral thalamic nuclei & somatosensory cortices
Fast & discriminative
"Where? How bad? How long?"

Medial thalamic nuclei, anterior cingulate gyrus,
prefrontal cortices, amygdala (fear)
Slow & affective
"Fear? Emotion?"

Experimental lesion: no pain perceived
Experimental lesion:
pain perceived but no longer bothersome

Effect of opioids
burning/electrical/tingling/pricking/"pins & needles"
spontaneous/paroxysmal
may follow nerve distribution
ALLODYNIA: non-painful stimulus is painful
HYPERALGESIA: mildly painful stimulus is very painful
change in skin colour/temperature
mechanisms of neuropathic pain
examples
diabetic neuropathy
trigeminal neuralgia
CRPS
Post-herpetic neuralgia
ACUTE
chronic
Easy to recognize
"Useful"
Physiological signs
Arbitrarily >3 months
Useless - "a malefic force"
No physiological signs
Difficult to believe in?
A Case of Phantom Limb Pain
plasticity vs elasticity
elasticity
plasticity
injury or experience
can change the way pain is felt
"Pain changes the way we feel pain"
windup
HARD-WIRED SYSTEM
Same stimulus produces the same response
soft-wired/plastic system
Repeated identical stimuli
produce increasing response
central sensitization
IN SUMMARY..........
CLASSIFICATION
rEYNOLD AND HIS RATS
Surgery on unanaesthetized rats
by stimulating the PAG
Pain as punishment
WHO ANALGESIC LADDER
ADJUVANT ANALGESICS
ROLE OF THE ANAESTHETIST
Surgery
CHRONIC PAIN
LABOUR ANALGESIA
MBBS MRCP(UK) FRCA
Pain Fellow & Specialist Registrar in Anaesthesia
West of Scotland Deanery
Biopsychosocial model
HOW IS CHRONIC PAIN DIFFERENT?
SPECIAL INTERVENTIONS
ANTIDEPRESSANTS
ANTICONVULSANTS
LOCAL ANAESTHETICS
VENOMS
CAPSAICIN
KETAMINE
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