118 SECTION2Berne & Levy Physiology •Fig. 7.6 Featureextractionbycorticalneurons.Theresponseswererecordedfromaneuroninthesomatosensorycortexofamonkey.Thedirectionofastimuluswasvaried,asshownbythearrowsinthedrawing.NotethattheresponsesweregreatestwhenthestimulusmovedinthedirectionfromUWtoRFandleastfromRWtoUF.F,fingers;R,radialside;U,ulnarside;W,wrist.(FromCostanzoRM,GardnerEP.J Neurophysiol 1980;43:1319.)R W F UW RF RW UF U R U R F U W UF RW F W RF UW 1 second
Effects of Lesions of the Somatosensory Cortex
A lesion of the S-I cortex in humans produces sensory changes similar to those produced by a lesion of the somatosensory thalamus. However, usually only a part of the cortex is involved, and thus the sensory loss may be confined, for example, to the face or to the leg, depending on the location of the lesion with respect to the sensory homunculus. The sensory modalities most affected are discriminative touch and position sense. Graphesthesia and stereognosis (i.e., the ability to recognize objects such as coins and keys as they are handled) are particularly disturbed. Pain and thermal sensation may be relatively unaffected, although loss of pain sensation may follow cortical lesions. Conversely, cortical lesions can result in a central pain state that resembles thalamic pain (see “
Effects of Interruption of the Spinotha lamic Tract and Lesions of the Thalamus on Somatosensory
The sensations of pain and temperature are related and often grouped together because they are mediated by overlapping sets of receptors and are conveyed by the same types of fibers in the PNS and the same pathways in the CNS. One consequence of these labeled lines is that pain sensations in particular are not due to stronger activation of touch pathways, as might naively be thought. This difference is borne out experimentally because if SA afferents, for example, are stimulated more and more frequently, the sensation of tactile pressure becomes stronger but not painful.
The axons that carry painful and thermal sensations are members of the relatively slowly conducting Aδ and C classes. However, not all Aδ and C axons carry pain and temperature information; some respond to light touch in a manner similar to what was described for low-threshold mechanoreceptors.
Unlike the case for low-threshold mechanoreceptors in which morphologically distinct receptors correspond to response properties, the Aδ and C axons conveying pain and temperature information appear to originate mostly as “free nerve endings.” (This description is not entirely accurate; the endings are mostly but not entirely covered by Schwann cells.) Despite the lack of distinct morphological specialization associated with their endings, Aδ and C axons constitute a heterogeneous population that is differentially sensitive to a variety of tissue-damaging or thermal stimuli (or both). This ability to sense tissue-damaging stimuli (mechanical, thermal, or chemical) is mediated by what are called nociceptors. These receptors share some features with low-threshold mechanoreceptors but are distinct in many ways, such as the ability to become sensitized (see later). Indeed, there appear to be a significant number of C fibers that are silent or unresponsive to any stimuli until first sensitized.
The first functional distinction that may be made in the pain system is between Aδ and C axons. Aδ axons conduct signals faster than C fibers do and are thought to underlie what is called first pain, whereas C fibers are responsible for second pain. Thus after a damaging stimulus, one first feels an initial sharp, pricking, highly localized sensation (first pain) followed by a duller, more diffuse, burning sensation (second pain). Experiments in which Aδ or C fibers were selectively activated demonstrated that activity in Aδ fibers produces sensations similar to first pain and that activity in C fibers produces second pain–like sensations.