Physiology of pain 2 Flashcards
Acute pain
<3 months
Inflammatory (and nocioceptive)
- due to tissue injury or inflammation
e.g. following surgery, musculoskeletal injury, burn
Chronic pain
> 3 months
Affects 20-50% population
e.g. chronic back pain, cancer, carpal tunnel syndrome, arthritis, fibromyalgia, diabetes, migraine, post surgery, multiple sclerosis
Due to injury to nervous system
Peripheral sensitisation
Major mechanism of acute pain
Leads to pain hypersensitivity
Acute pain treatments sites of action
PNS (site of injury)
CNS
Both
Local anaesthetics
e. g. lidocaine, lignocaine
- topically applied to skin
Mechanism of action
- sodium channel blockers
Topical capsaicin treatment
TRPV1 channel agonist
Mechanism of action
- depletes substance P
- causes peripheral terminal to die back
Non-steroidal anti-inflammatory drugs
e.g. aspirin, ibuprofen
Mechanism of action
- reduces the inflammatory response by inhibiting prostaglandin synthesis
- prevents peripheral sensitisation
Cyclooxygenase inhibited ->
Prostaglandin synthesis reduced ->
Prevents decrease in Na+ channel threshold
Paracetamol/ acetominophen
Not NSAID
Mechanism of action
- inhibits cyclooxygenase enzymes
- acts on descending serotonergic pathways
Opioids
e.g. morphine, codeine, tramadol
Most effective pain relief but numerous side effects
Mechanisms of action
- agonists of the endogenous opioid system
- multiple sites of action (brainstem, spinal cord, peripheral)
Gate control theory
Modulation of pain at the spinal cord level
Pain evoked by nocioceptors can be reduced by simultaneous activation of low threshold mechanoreceptors
Rubbing/ blowing on the painful area can reduce the pain sensation
Stimulation of Aβ fibres in vicinity of injury activates interneurones in dorsal horn which inhibits spinothalamic neurones
Neuropathic pain mechanisms
Mechanisms are complex and involve both peripheral and central nervous systems
Spontaneous firing of nocioceptors
Following a peripheral nerve injury increase in axonal firing at the site of injury
Due to accumulation of ion channels at regenerating tip of axon
Responsible for spontaneous pain
Underlies central neuropathic pain mechanisms
Main peripheral mechanisms
Peripheral sensitisation
Spontaneous firing of nocioceptors
Central mechanisms
Central sensitisation
- with spinal cord
Changes in activation patterns/ cortical remapping
- within brain
Central sensitisation
Increase in the responsiveness of nocioceptive neurones within the CNS
Normal inputs begin to produce abnormal responses
Due to reduced threshold for activation of 2nd order neurones