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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.