Pain syndromes and the parietal lobe.

Abstract Pain was considered to be integrated subcortically during most of the 20 th century, and it was not until 1956 that focal injury to the parietal opercular-insular cortex was shown to produce selective loss of pain senses. The parietal operculum and adjacent posterior insula are the main recipients of spinothalamic afferents in primates. The innermost operculum appears functionally associated with the posterior insula and can be segregated histologically, somatotopically and neurochemically from the more lateral S2 areas. The Posterior Insula and Medial Operculum (PIMO) encompass functional networks essential to initiate cortical nociceptive processing. Destruction of this region selectively abates pain sensations; direct stimulation generates acute pain, and epileptic foci trigger painful seizures. Lesions of the PIMO have also high potential to develop central pain with dissociated loss of pain and temperature. The PIMO region behaves as a somatosensory area on its own, which handles phylogenetically old somesthetic capabilities based on thinly myelinated or unmyelinated inputs. It integrates spinothalamic-driven information – not only nociceptive but also innocuous heat and cold, crude touch, itch, and possibly viscero-somatic interoception. Conversely, proprioception, graphesthesia or stereognosis are not processed in this area but in S1 cortices. Given its anatomo-functional properties, thalamic connections, and tight relations with limbic and multisensory cortices, the region comprising the inner parietal operculum and posterior insula appears to contain a third somatosensory cortex contributing to the spinothalamic attributes of the final perceptual experience.