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Flashcards in Pain Pathways And Central Processing Of Pain Deck (10)

Encoding of the stimulus

Stronger stimuli-> larger receptor potentials-> higher frequency action potentials
Intensity-> number of responding receptors-> recruited in more intense stimuli



Majority respond to mechanical, thermal and chemical stimuli-> poly modal
-> selective in their response


Pain definition

Unpleasant sensory and emotional experience resulting from potential or actual tissue damage
Can suff serious injury without pain and feel pain without injury
Sensory discriminative component-> tells you that you have been hurt and the location
Emotional effective component-> association of unpleasant effects


A delta fibres

Fast conduction-> first pain
Synapse in intermediate lamina III and IV
Responses sensitive to glutamate receptor anatgonists (AMPA R)
Rapid sharp localised pain-> reflexive response


C fibres

Up myelinated fibres
Slower conduction-> second pain-> slow burning pain
Synapse in superficial lamina I and II
High receptor activating threshold
Responsive to glutamate receptor (AMPA and NMDA) and peptide receptor antagonists (intense pain only )
Visceral and cutaneous enter by same route-> gets confused


Spinal processing of pain

A delta and C fibres transmit noxious stimuli to spinal cord
Mainly lamina I and II -> substantial gelatinosa
Travel up spinothalamic tract
Also activate reflexive movement


Plasticity of spinal responses

Neural responses to repeated stimulation of c fibres are not always proportional to the intensity of the stimulus applied
Enhanced responses (wind up) are associated with elevated higher stimulation
Spinal neurones can become sensitised to the noxious stimulus
Hypeslgesia-> increased response to painful stimuli-> reduced threshold for pain, increased intensity of painful stimuli or spontaneous pain
-> primary in damaged tissue
-> secondary in surrounding tissue
Allodynia-> painful response to a normally innocuous stimuli


Brain stem involvement in pain

Spinoreticular tract-> same but to reticular fomation -> then to thamalus and hypothalamus
Activate brain stem systems
Changes in BP, rests, orientation towards stimulus
Emotional aspects of pain
Mid brain projections to peri aqueductal grey -> analgesia


Hypothalamus involvement in pain

Response to pain as a stressor
Neuroendocrine and behavioural responses


Descending inhibitory control of pain

PAG-> electrical stimulation from thalamus, hypothalamus and cortex -> analgesia
-> axons to nucleus raphe Magnus-> serotonin release
Nucleus reticularis paragiganto-> activated by ascending pain pathway-> axons to nucleus raphe Magnus
Locus coerulus-> directly inhibits pain by action on the spinal cord