Pain

Pain

A sensation that alerts us to damage to the body (internal & external)
1. Pain threshold= the level of stimulation at which an individual will begin to perceive pain
Proposed mechanism
1. LIMBIC SYSTEM (memory e.g. can influence concept of pain based on experiences)- PERIAQUEDUCTAL GREY (midbrain-releases enkephalins-natural pain killer- can decrease or inhibit pain signals-interact at NRM)-NUCLEUS RAPHE MAGNUS- causes release of 5HT to dorsal horns of spinal cord-causes inhibition of substance P (neurotransmitter for pain) release-pain ascending communication doesn't reach ventroposterior nucleus in thalamus- INTERNEURONES IN LAMINA II OF SPINAL CORD
  1. Primary sensory cortex is involved with the localisation of pain. (signals translated in somatosensory cortex, and percieved-site where stimulus can from (receptors))
  2. The thalmaus is the central switching station of the brain. It is multi nucleate- several nuclei are dedicated to pain. Medial nuclei (pain), lateral uclei (sensation/discrimination)
  3. Midbrain- most of the circuitry of the medulla is involved in pain. Extensive connections to the reticular brain stem- PAG (periaqueductal grey), NRM (nuclei raphe magnus)
  4. Aδ fibres
    1. Fast fibres, large, myelinated, large cell bodies
    2. A sharp pin prick- starts in superficial tissues-conducted by the fast fibres (10m/sec)-to the dorsal horn-they synapse & relay along the spinothalamic tract-terminate mainly in the thalamus projecting acrods the sensory cortex
  5. C fibres
    1. Slow, thin, unmyelinated, small cell bodies
    2. Aching pain from deep tissues-conducted by the slow fibres (1m/sec)- to the dorsal horn-they synapse & relay along the spinothalamic tract-terminate in the reticular nuclei in medulla, midbrain and thalamus- relayed across the sensory cortex, frontal lobes & limbic system
  6. Neurotransmitter for both fibres is substance P
Pain modulation
1. Integration of painful information occurs in the CNS- Opiods modulate pain transmission. Spinal cord is the first site of integration. Thalamus -dorsal horn neurons synpase onto projection neurone. Descending systems- ability to modulate and inhibit activity in the spinal cord.
Pain producing substances
1. Bradykinin, capsciacin (main constitute in chilli therefore stimulates temp fibres associated with pain-if over stimulate=sweat as body responding), substance P, Histamine & prostoglandins
2. Released from damaged cells so stimulating nocioceptors- vasoactive properties (increased circ & inflammation)
Endogenous opiods
1. Endorphins (neurohormones-psychological responses to pain), enkephalins (neurotransmitter, involved in analgesia), Dynorphins (analgesia & sedation)
Gate control theory
1. Melzack & Wall in 1968- rubbing injured region decreases pain sensation- details wrong but useful
2. Stimulated other receptors (not nocioceptors)-causing release of neurotransmitter etc has ability to inhibit signals from reaching the cortex
  1. Descending inhibition
    1. Touch- cortico-thalamic pathway (why we dont feel clothes)
    2. Pain (battle, sporting injuries, ecstasy)
    3. Microinjection of opiates into discrete regions of CNS (PAG, limbic system) promotes analgesia. Microstimulation tjere also produces analgesia. Opioid peptides are present there. Electrical stimulation of the PAG or NRM produces analgesia

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	Created by tanitia.dooley almost 11 years ago