Pain and temperature information from the face and head, as well as from the body, follows similar pathways in the central nervous system. Neurons in the descending trigeminal nucleus transmit this information to specific nuclei (VPM, VPI) of the opposite thalamus through the ventral trigeminothalamic tract, which runs closely with the medial lemniscus. The descending nucleus also projects to the intralaminar complex and other thalamic nuclei, similar to the spinothalamic tract. The thalamic nuclei then send this information to the somatosensory cerebral cortex for sensory discrimination of pain and temperature, as well as to other cortical regions responsible for emotional responses.

Interrupting the spinothalamic tract and damaging the thalamus results in the loss of both the sensory-discriminative and motivational-affective aspects of pain on the opposite side of the body. This led to the development of a surgical procedure called anterolateral cordotomy, used to treat pain, especially in cancer patients. However, this procedure is now rarely performed due to advancements in drug therapy and the possibility of pain returning later. The return of pain may indicate disease progression or the development of a central pain state. In addition to pain, anterolateral cordotomy also causes loss of cold and warmth sensation on the opposite side of the body. While there may be a minimal deficit in tactile sensation, the intact sensory pathways in the dorsal part of the spinal cord provide sufficient tactile information to make the loss insignificant.

Destruction of the VPL or VPM nuclei reduces sensation on the opposite side of the body or face. The lost sensory qualities are those transmitted primarily through the dorsal column–medial lemniscus pathway and its trigeminal equivalent. The sensory-discriminative aspect of pain is also lost. However, the motivational-affective aspect of pain remains if the medial thalamus is intact. This suggests that pain persists due to projections from the spinothalamic and spinoreticulothalamic pathways to this part of the thalamus. In some cases, a lesion in the somatosensory thalamus leads to a central pain state known as thalamic pain. Patients with thalamic pain report experiencing pain even with the slightest touch, although the intensity of the touch is below the pain threshold. This increased pain sensitivity is believed to result from sprouting of low-threshold dorsal column system fibers after the lesion, which synapse with surviving thalamic neurons that normally only mediate pain. Lesions in the brainstem or cortex can also produce pain indistinguishable from thalamic pain.

Neuropathic pain, which occurs without nociceptor stimulation, may arise after damage to peripheral nerves or CNS structures involved in transmitting nociceptive information. Peripheral neuropathic pain follows damage to a peripheral nerve, while central neuropathic pain can occur after CNS damage.
Pain and temperature information originating from the face and head is conveyed along analogous ascending central pathways, as is such information from the body. Neurons in the descending trigeminal nucleus transmit pain and temperature information to specific nuclei (VPM, VPI) of the contralateral thalamus via the ventral trigeminothalamic tract, which runs in close association with the medial lemniscus. The descending nucleus also projects to the intralaminar complex and other thalamic nuclei in a fashion similar to that of the spinothalamic tract. The thalamic nuclei in turn project to the somatosensory cerebral cortex for sensory discrimination of pain and temperature and to other cortical regions responsible for motivational-affective responses.
Effects of Interruption of the Spinothalamic Tract and Lesions of the Thalamus on Somatosensory Sensation
When the spinothalamic tract and accompanying ventral spinal cord pathways are interrupted, both the sensory-discriminative and the motivational-affective components of pain are lost on the contralateral side of the body. This result motivated development of the surgical procedure known as anterolateral cordotomy, which was used to treat pain in many individuals, especially those suffering from cancer. This operation is now used infrequently because of improvements in drug therapy and because pain often returns months to years after an initially successful cordotomy. Return of pain may reflect either extension of the disease or development of a central pain state. In addition to loss of pain sensation, anterolateral cordotomy produces loss of cold and warmth sensation on the contralateral side of the body. Careful testing may reveal a minimal tactile deficit as well, but the intact sensory pathways of the dorsal part of the spinal cord provide sufficient tactile information that any loss caused by interruption of the spinothalamic tract is insignificant.
Destruction of the VPL or VPM nuclei diminishes sensation on the contralateral side of the body or face. The sensory qualities that are lost reflect those that are
CHAPTER 7 The Somatosensory System transmitted mainly by the dorsal column–medial lemniscus pathway and its trigeminal equivalent. The sensory-discriminative component of pain sensation is also lost. However, the motivational-affective component of pain is still present if the medial thalamus is intact. Presumably, pain persists because of the spinothalamic and spinoreticulothalamic projections to this part of the thalamus. In some individuals a lesion of the somatosensory thalamus results in a central pain state known as thalamic pain. Patients with thalamic pain report that even the slightest touch feels painful, although the intensity of the touch is lower than the threshold of any pain receptor. It is thought that their pain sensitivity is due to a post-lesion sprouting of low-threshold dorsal column system fibers that synapse onto surviving thalamic neurons that normally mediate only pain. Pain that is indistinguishable from thalamic pain can also be produced by lesions in the brainstem or cortex.
Pain sometimes occurs in the absence of nociceptor stimulation. This type of pain is most likely to occur after damage to peripheral nerves or to parts of the CNS that are involved in transmitting nociceptive information. Pain caused by damage to neural structures is called neuropathic pain. Neuropathic pain states include peripheral neuropathic pain, which may follow damage to a peripheral nerve, and central neuropathic pain, which sometimes occurs after damage to CNS structures.