Pain is perceived when the stimulation of nociceptors is intense enough to activate Aδ fibers. It results in in a subjective experience of a sharp, prickling pain. With increase in stimulus strength, C fibers are recruited, and the person feels an intense, burning pain that continues after the stimulation ceases. The first phase, which is not particularly intense, comes immediately after the painful stimulus and is known as fast pain. The second phase, known as slow pain, is more unpleasant, less discretely localized, and occurs after a longer delay.
Peripheral nerve axons transduce the pain sensation resulting from the activation of nociceptors. The axons terminate in the dorsal horn of the spinal cord. Further, these impulses are relayed up the spinal cord and through the spinothalamic tract to output on the thalamus. Specifically, the pain pathways terminate in the ventral posterior lateral nucleus and the ventromedial nucleus. From these nuclei, nociceptive information is relayed to various cortical and subcortical regions, including the amygdala, hypothalamus, periaqueductal grey, basal ganglia, and regions of cerebral cortex.
Thalamic pain is a distressing and treatment-resistant type of central post-stroke pain. It is a severe pain and the lesions in the ventrocaudal regions of the thalamus carry the highest risk to develop pain.