Sensory Pathways

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Sensory Pathways

• Pain and Temperature

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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 (Brodmanns areas
  3,1,2), as well as insular cortex.

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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.

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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.

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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.

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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.