One practical conclusion to be reached from anatomic and physiologic studies is that, at thalamic levels, fibers and cell stations transmitting nociceptive impulses are not organized into discrete loci. In general, as one ascends from peripheral nerve to spinal, medullary, mesencephalic, thalamic, and limbic levels, the predictability of neuron responsivity to noxious stimuli diminishes. Thus it comes as no surprise that neurosurgical lesions that interrupt afferent pathways at progressively higher levels of the brainstem and thalamus become decreasingly successful.
Both ventroposterior nuclei project to two main cortical areas: the primary sensory (postcentral) cortex (a small number terminate in the precentral cortex) and the upper bank of the sylvian fissure. The thalamic projection to the primary sensory cortex that is distributed mainly along the postcentral gyrus of the anterior parietal lobe is shown in Fig. 8-6 (the “sensory homunculus”). The cortical representation allows for accurate localization of the site of origin of a painful stimulus but the notion that thalamic projections terminate solely in this region is an oversimplification. These cortical projections are described more fully in Chap. 8 but it can be stated that they are concerned mainly with the reception of tactile and proprioceptive stimuli and with all discriminative sensory functions, including pain. However, stimulation of these (or any other) cortical areas in a normal, alert human being does not produce pain, for which reason the extent to which cortical areas are directly activated by thermal and painful stimuli remains uncertain.
The intralaminar nuclei, which also project to the hypothalamus, amygdaloid nuclei, and limbic cortex, probably mediate the arousal and affective aspects of pain and autonomic responses. Thalamic and cerebral cortical localization of visceral sensation is not well known. However, cerebral-evoked potentials and increased cerebral blood flow (by positron emission tomography [PET] studies) have been demonstrated in the thalamus and preand postcentral gyri of patients undergoing rectal balloon distention (Silverman et al; Rothstein et al).
The discovery of a system of descending fibers and way stations that modulate activity in nociceptive pathways has proved to be a major addition to our knowledge of pain. The endogenous pain control system that has been studied most extensively emanates from the frontal cortex and hypothalamus and projects to cells in the periaqueductal region of the midbrain and then passes to the ventromedial medulla. From there it descends in the dorsal part of the lateral fasciculus of the spinal cord to the posterior horns (laminae I, II, and V; see further discussion under “Endogenous Pain-Control Mechanisms”). Several other noradrenergic and serotonergic descending pathways, which arise in the locus ceruleus, dorsal raphe nucleus, and nucleus reticularis gigantocellularis, are also important modifiers of the nociceptive response. The clinical significance of these pain-modulating pathways, still under study, is discussed further on.