Pain

Question 1

Define Pain

Answer 1

Unpleasant sensory & emotional experience associated with actual or potential tissue damage or described in such terms of damage (however pain does not always equal damage)

*Pain is registered by nociceptors - somatosensory receptors found in skin/muscle/joint capsules/visceral organs/periosteum

Question 2

What fibres detect pain

Answer 2

A delta - small/medium diameter

         - transmit 'fast' pain ie sharp/stabbing pain
         - highly myelinated 

C fibres - un-myelinated

          - 'slow' pain - burning/aching/dull
          - v. small diameter * Other fibres  - A alpha fibres - fast conducting 
                       - proprioceptive info - A beta - mechanical stimuli e.g touch/temperature

Question 3

What is the pain pathway from PNS to CNS

Answer 3

> Threat = detected at nociceptor
Travels via 1st order (afferent) neuron to spinal cord
delivered to laminae rexed 1 & 2 (where a delta and c fibres are) on tip of dorsal horn (also where substantia gelatinosa - important nuclei of cell bodies are found)
synapses with 2nd order neuron (via neurotransmitters glutamate = a delta + substance p = c fibres)
2nd order neuron then crosses to contralateral side ventral horn and ascends to thalamus (synapses with 3rd order)
3rd order then delivers signals to somatosensory cortex

Question 4

What are the main pain pathways

Answer 4

> Lateral spinothalamic tract: main pain signals
: has midbrain projection to
peri-aqueductal grey matter
Spinoreticular tract: connects with reticular formation
in brainstem
: memory + emotional component
of pain
(brain receives info, processes it + determines response)

Question 5

What are the main components in registering pain

Answer 5

1. Thalamus - sorting office - sends signals to right place
2. Limbic system - emotional link to pain - may affect intensity
3. Somatosensory cortex - locates pain
   - determines severity
   - executes response
   * also linked to autonomic response - more blood to area to boost healing or release pain modulators to reduce pain signals arriving

Question 6

How do reflexes work?

Answer 6

> Not always time to wait for brains response
integration in spinal cord grey matter can occur = reflex arc pathway
where 1st order neuron synapses with interneuron instead of 2nd order
interneuron then synapses with motor neuron for quick response

Question 7

Describe the descending pain pathways and their role

Answer 7

Role: control and inhibit pain signals of ascending pathways
> key areas = periaqueductal grey matter - brainstem
= Nucleus raphe magnus - medulla
> signals from PAG to NRM then to interneuron at synapse of 1st order neuron
- inhibit substance p - signal doesn’t cross synapse
- or stimulates substantia gelatinosa to release an opioid which prevents messages in 2nd order neuron from transmitting to brain

Question 8

Describe pain gate theory

Answer 8

Method of pain inhibition
> Rub it better (ascending inhibition)
- mechanoreceptors (A beta fibres) transmit faster than c fibres
- if activated they reach gate with c fibres first - reduce amount of pain signals that reach brain as they take priority
> Descending inhibition: mid-brain axons descend to posterior horn of spinal cord to stop transmission (see descending pathways)

Question 9

What effects the pain gate

Answer 9

> state of mind - anxiety causes brain to open gate to c fibres
endorphins/encephalins - greater number - closes pain gate (released in exercise + acute trauma)
Central control - memories/past experiences + response strategies can affect if gate opens

Question 10

Pain types

Answer 10

• Acute - less than 3 months
• Chronic - > 3 months + persistent
• Nociceptive pain - stimulated nociceptors in soft tissue (somatic = joint/muscle etc. visceral = pelvic/thoracic/abdominal organs)
• Neuropathic pain - damage to nervous system (usually felt as burning or altered sensation)
• Psychogenic pain - affected by psychological factors

Question 11

Describe chronic pain

Answer 11

> Lasts beyond time of healing so cause may be unknownor may be due to ongoing damage e.g arthritiscan also be due to hypersensitivity - dysfunctional nociceptive system where CNS becomes more sensitive to pain- peripheral sensitisation: increased sensitivity to afferent nerve stimuli = localised - Central sensitization: wind up (persistent state of high reactivity)
: pain occurs in unaffected areas of body

Question 12

What is central sensitization and why does it occur

Answer 12

• Persistent state of high reactivity due to:
• Persistent nociceptive input to CNS causes changes in brain and spinal cord
  > pain is then amplified
  > descending pathways become less effective - can’t modulate pain as well
• Can lead to:
  > hyperalgesia = overreaction to stimuli
  > allodynia = pain to non-painful stimuli
  > chronic pain state