Greg Detre
18/11/99
somatosensory: first to be studied to give insight into micro-structure
all cortical areas � share input output properties
maps of the body in the somatosensory thalamus (VPL, VPM) + cerebral cortex
can map receptive fields electrophysiologically
primate somatosensory cortex � post-central gyrus
4 cortical areas � each has 4 discrete maps
3b = primary target of thalamus for somatosensory, including all sensory dimensions (pain, hot etc.)
labelled line persists
columnar orgnaisation in 3b relfects that within a single map
how reconcile quality of sens + location???
1. proprioceptors vs cutaneous � different cortical areas
2. different input � same cortical area � add together, give more sophisticated discrimination
complicated pattern of connections between thalamus + cortex (4 areas PL gyrus)
each area: separate body surface map
distorted � reception
columnal superimposed submodalities
complex interaction of cortical areas ������ 1+2 more complex���������� texture, stereoagnosia
processing of fine discriminatory touch � straightforward
pain:
sensation varied��������� � intensity
can modulate the sense of pain
pathways from free nerve endings in skin �/span> cortex��� ����� spinal cord
antero-lateral pathway in the spinal cord
through dorsal roots, synapse, cross at the level entering midline to opposite side then up � brain
nociceptors (noxious)
axons: thin, unmyelinated � very slow compared to cutaneous Ad and C-fibres � conduct sense of pain
terminals in skin respond to high threshold, mechanical distortions of skin or neural damage, heat
stimuli = usually tissue damage
one thermo-receptor optimal respond = heat
or chemical capsaysin(???) = found in chili peppers
a dull sense of localised pain � conduction velocities
tissue damage � many chemicals released which � neuron fire
pain can either travel from skin � spine
also goes back down a side-branch to sensitise a large area around, hyperalgesia, to protect the damaged area
Ad and C-fibres terminate in restricted regions of dorsal horn (outer layers) then cross mid-line
(= an area rich in neurotransmitter for change pain)
then run up antero-lateral tract
pain fibres can synapse in (areas of the brain specific for terminating):
1. the thalamus - spino-thalamic tract
2. mid-brain (periaqueductal grey spino� tract)
can diminish the sense of pain
relay station for modulating pain
transmission of pain � cortex: gate
morphine receptors in the brain
\ analogues = endogenous morphine-like = endorphins
= natural opiate-releasing cells inhibit transmission of pain
now looking for naturally-occuring endogenous analogues � cannaboids + maybe alcohol reception too
subst P = prolongs post-synaptic � - pain lasts longer
can burn out
3. lower down, in the brain stem
reticular = most caudal � behavioural compensation activates the cortex � arousal then � to cortex processing then � to spine for mechanical reflexes
�
Gate theory of pain � Melzack + Wall
at the spinal level, mod nos transmission by � normal cutaneous input
argument: dock leaves on nettle = similar mechanical stimulation of rubbing
using sensory input to gate pain sensation
maybe evolved to ignore pain in areas with lots of contact
cortex:
how pain is represented in cortex������ use functional imaging
difficult to investigate in animals � ethics
it seems to me that the gate theory won't have an adaptive explanation � epiphenomenal?