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Abstract:
We concur with Luis Garcia-Larrea9 that the article by Mandonnet et al.12 represents a valuable contribution to our understanding of the role of the insula for our pain perception, most critically because it conclusively shows in humans that the nociceptive input to the dorsal posterior insular cortex is not relayed there through other cortical regions, as was long suggested,13,16 but arrive through ascending fibers from the thalamus. However, this important contribution is, quite unnecessarily, tainted by the authors' failure to name the thalamic nucleus that projects to the posterior insula, writing instead that “it has been suggested that a subpart of the Po-SG specifically projects to an area in the posterior dorsal fundus in the insula,” despite the fact that this “subpart” was identified as a distinct nucleus several decades ago and was designated the VMpo (the posterior part of the ventromedial nucleus).6 It was given this name, which adheres to the commonly used nomenclature for the mammalian thalamus,10 because it lies adjacent (and posterior) to the VMb (the basal part of the ventromedial nucleus), together with which it provides a homeostatic afferent input to the insular cortex, that from VMpo arising from neurons in the spinal and trigeminal superficial dorsal horn and that from VMb from the nucleus of the solitary tract.3 Tract-tracing and electrophysiological recordings in macaque monkeys clearly identified VMpo, and neither the suprageniculate (SG) nor the posterior nucleus (Po), as the target of spinal lamina I projection neurons encoding pain and temperature modalities2,7 and as the source of thalamocortical projections to the dorsal posterior fundus of the insula.4 VMpo is readily identifiable in brain sections both from monkey and human thalamus1,2 (Fig. 1).
