Sensory Pathways
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Transcript Sensory Pathways
Sensory Pathways
Pain and Temperature
I. General Organization of the
Anterolateral System (ALS)
1st Order Neuron is the dorsal root ganglion (DRG)
cell.
2nd Order Neuron is the spinothalamic neuron. Cell
body is in the dorsal horn of spinal cord. Axon
terminates in the VPL nucleus of the thalamus.
3rd Order Neuron is the thalamocortical neuron. Cell
body is in the VPL nucleus. Axon terminates in the
somatosensory cortex (Brodmann’s areas 3,1,2), as
well as insular cortex.
II. First Order Neuron
Peripheral process of dorsal root ganglion cell is incorporated into
receptor (free nerve endings for both nociception and
thermoception). Central process enters the spinal cord in the Zone
of Lissauer (posterolateral funiculus) by way of the lat. div. of dorsal
root and terminates in the dorsal grey horn.
Thinly myelinated (Ad) fibers (for fast sharp pain) and unmyelinated
(C) fibers for slow burning pain. Glutamate and substance P,
respectively mediate these responses.
Referred pain (from viscera to body wall or soma) is due to
convergence of sensory and visceral nerve impulses onto the same
second order sensory neurons.
“Gate theory of pain” proposes that nociceptive activity can be
blocked at the level of the spinal cord by activation of low-threshold
mechanoreceptors (Ab) fibers which facilitate inhibitory
interneurons that induce suppression of firing of 2nd order neurons
transmitting pain.
III. Second Order Neuron
Cell body located in the dorsal horn of the spinal cord.
Axon crosses midline obliquely at the ant white commissure and joins the ALS approx
I segment above the cell body of origin.
Syringomyelia (cavitation of the cord around the area of the central canal) results in
destruction of the ant white commissure which produces bilateral loss of pain and
temperature over one or more dermatomes beginning 1 spinal segment below the
cavitation.
Cordotomy (sectioning the ALS) results in contralateral loss of pain and temperature
of all dermatome beginning with the dermatome 1 segment below the level of
cordotomy.
Throughout brainstem ALS ascends just lat to the medial lemniscus. Lesioning the
ALS at the level of brainstem causes contralat loss of pain and temperature over
dermatomes C1-S5.
Unilateral lesion of dorsolateral medulla may include both ALS and 1st order
trigeminal system fibers resulting in loss of pain and temp on the ipsilateral face and
contralateral body.
Lesion of VPL may result in the “thalamic pain syndrome”.
Collateral branches off the ALS activate reticular centers for arousal.
IV. Third Order Neuron
The axon of VPL neurons ascend through the
internal capsule and terminates in the
ipsilateral somatosensory cortex (areas
3,1,2).
Lesioning 3,1,2 spares pain perception but
not the ability to localize it on the contralateral
side of the body.
Insular (aka interoceptive) cortex detects
tissue and organ homeostasis.
V. Experience of Pain and Temperature – Beyond
ALS
Pain varies according to the emotional state of individual.
Reticular formation relays pain impulses to:
Autonomic centers and hypothalamus (for autonomic and
endocrine integration)
Ant cingulate gyrus and limbic system (for integration with
emotions).
Intralaminar thalamus and basal ganglia (motor integration
and arousal).
Reticular centers feedback (serotonin and nor-epi fibers) to dorsal
horn of spinal cord to excite enkephalin (opioid) inhibitory
interneurons in the substantia gelatinosa. The feedback ultimately
supresses pain input from the periphery.