Somatosensory Cortex: An Overview (2023)

Secondary somatosensory cortex

The SII is located in the parietal operculum at the superior border of the Sylvian fissure and, although the functional specificities of pain processing are described, the SII has a clear role in cortex-mediated nociception. It is proposed that the SII is involved in the recognition of painful and thermal stimuli, in pain-related learning, and in the integration of tactile and nociceptive information. Most of the thalamic input to the SII comes from the CPI.¹¹³Individual neurons in IBS can be nociceptively specific and tend to have large receptive fields with contralateral or bilateral activation.¹¹⁴

The SII is consistently activated in imaging studies involving nociception. Its proximity to the temporal lobe has made it amenable to clinical research using implantable intracortical electrodes in patients with temporal lobe epilepsy, and a wealth of knowledge about function has been gained from such studies. With laser stimuli and implantable electrodes, SII responses were painful in gradations of stimulation intensity, from the lowest sensory threshold to stimulus recognition. What is interesting, however, is that the level of SII activation did not increase beyond the pain detection threshold with increasing stimulation intensity.¹¹⁵In another study, Frot et al.¹¹⁶using depth electrodes, demonstrated an increased latency in SII activation by tactile input compared to noxious stimuli, again supporting the idea of ​​SII involvement in integration and learning. In imaging studies, the SII is activated simultaneously with or even before the SI, indicating a parallel rather than a serial relationship between these two regions.¹¹⁷

Stimulation and injury studies are scarce due to difficulties in interpreting the location and because many ischemic injuries extend to other areas. Few stimulation protocols have specifically focused on IBS. Ostrowsky and colleagues^118.119reported that SII stimulation did not provoke painful sensations in humans, although this work focused mainly on the insula. In a systematic exploration of IBS stimulation, Mazzola et al.¹⁰⁷found responses to be a mixture of somatosensory, temperature, and pain sensations; the percentage of evoked pain sensations was the same as that produced by insula stimulation. Location difficulties have also impeded investigations of IBS injuries, although in general post-injury deficits in IBS support the idea of ​​direct involvement in pain processing. In one case with a purely sensory IBS-only effusion, the patient had limited contralateral deficits in light touch, pain, and temperature sensation.¹²⁰In other cases of IBS injury, investigators have reported central pain syndrome, hyperalgesia, and thermal and mechanical deficits; It is noteworthy, however, that such changes are not observed in parietal lesions without IBS.^121.122Despite some obstacles in the interpretation of data related to IBS injury, several lines of research clearly point to the involvement of this region in pain processing and in the integration of tactile and nociceptive signals.

Other afferents

Osomatosensory cortexreceives afferents from brain regions outside the thalamus. These include serotonergic inputs from the raphe nuclei (Kirifidesand others,2001), which play a role in the development of somatotopic organization (Boylanand others,2000). The locus coeruleus sends noradrenergic fibers to the somatosensory cortex which modulates synaptic input.Devilbiss e Waterhouse, 2000). There are also cholinergic inputs from Meynert's nucleus basalis (Baskervilleand others,1993), which modulate the plasticity of the somatosensory cortex (Zhu e Waite, 1998) and may serve to enhance the influence of extracortical inputs over intracortical afferents (Kimura, 2000). The somatosensory cortex also receives input from the zona incerta (Linand others,1997), but the role of this pathway is unclear.

The primary somatosensory cortex is located in the parietal lobe

Somatosensory information traveling rostrally in the medial lemniscus and spinothalamic tract is relayed in the ventral posterolateral (VPL) and ventral posteromedial (VPM) nuclei and projects through the posterior ramus of the internal capsule primarily to areas 3, 1, and 2. long, parallel bands of cortex that together occupy most of the postcentral gyrus; Most of area 3 is on the posterior wall of the central sulcus and most of area 2 is on the anterior wall of the postcentral sulcus. These areas are not only structurally separate, but also differ in their connections and properties; The body surface is mapped separately in each area, but as you go from area 3 to area 1 to area 2 the properties change from primarysomatosensory cortexto the beginning of the somatosensory association cortex (Abb. 22.15). Area 3 cells receive most of the thalamocortical projections from VPL and VPM; Cells in areas 1 and 2 receive progressively less information from the thalamus and progressively more from other cortical areas. Cells in area 3 have receptive fields that reflect the activity of certain types of receptors, while those in areas 1 and 2 have more complex receptive fields that respond to things like the position of the limbs or the shape of an object touching the skin. Strictly speaking, area 3 is the primary somatosensory cortex, but because the postcentral gyrus as a whole is the most prominent area dealing with somatic sensation, it is usually referred to as theprimary somatosensory area (first)(orS1).

Another somatosensory association area calledsecond somatosensory area (S2)was also described; it receives input not only from S1 but also, to a lesser extent, directly from NPV and VPM. It occupies part of the parietal operculum, most of it buried in the lateral sulcus and possibly extending to the insula. S2 is also organized somatotopically, but its order is reversed to that of S1; That is, the facial areas of both maps are contiguous and the remainder of the S2 map extends to the lateral sulcus. Cells in S2 usually have bilateral receptive fields, so they are activated by touching either of two symmetrically located sites.

Stimulation of the postcentral gyrus in conscious humans produces sensations usually described as tingling or numbness in a contralateral body part whose position is related in an orderly manner to the stimulated site (seeAbb. 3.30). The sensations generally do not resemble those produced by natural stimuli, such as bending a hair or touching the skin, presumably because electrical stimulation of the cortex is a poor imitation of the pattern of activity produced by natural stimuli. Interestingly, pain sensations can rarely be extracted from the postcentral gyrus, instead the concept of a pain matrix arises, in which disparate regions of the cerebral cortex form a network dedicated, at least in part, to the perception of pain. . Large lesions affecting the entire postcentral gyrus cause significant impairment in the finer aspects of somatic sensation (e.g., judging the precise location or intensity of a stimulus) and a serious deficit in the sense of position and movement of the affected parts, but this damage does not occur. it does not negate the tactile sensation or the sensation of pain. In the few cases where removal of the postcentral cortex has been attempted as a treatment for intractable pain, the patient's pain has usually been relieved only partially and briefly, and a hyperpathic state similar to thalamic pain often ensues. In contrast, small lesions that affect only the portion of the postcentral gyrus adjacent to the central sulcus do not cause loss of pain and temperature sensitivity, but cause difficulty in localizing painful stimuli to the somatotopically appropriate region of the body on the contralateral side. Consistent with this clinical observation, neurons that respond specifically to pain stimuli have been found in the somatosensory cortex of monkeys at approximately the junction between areas 3 and 1. However, processing pain information is not the exclusive domain of S1. Pain-sensitive neurons have also been found in S2 and other areas, and functional imaging studies have shown increased blood flow in S1, S2, part of the insula, and in the anterior cingulate cortex in response to painful stimuli. S1 is thought to be important for the localization of painful stimuli, and the other areas (particularly the insula and cingulate gyrus) are blamed for pain discomfort.

7.7 Conclusion

primarysomatosensory cortexit is an excellent model system for understanding the development and function of cortical circuits. Its somatotopic organization and well-defined receptive field properties have been used effectively for decades to study the role of molecular mechanisms and neural activity in circuit formation and function in adults. Due to the large number of cell types in neocortical areas, a complete understanding of the specific circuits underlying these phenomena has been delayed. In this chapter, we provide an up-to-date picture of the circuitry elements of the somatosensory cortex, the specificity of their connections, and the changes in their connectivity during development. Although much has become clear in recent decades, significant efforts are still needed to understand the range of mechanisms by which plasticity can arise.are implemented in these circuits and the extent to which this plasticity affects certain elements of the circuit. As new tools are developed for labeling individual circuit components and for studying function and connectivity, it can be expected that more detailed insights into the development of cortical circuits will emerge.

Functional reorganization of the somatosensory cortex

Human EEG and MEG studies have advanced our understanding of cortical reorganization in phantom limb pain. Animal experiments have shown that the receptive fields of neurons in S1 that respond to harmless stimuli migrate to neighboring areas of the skin when nerve damage or amputation interrupts their original input. This reorganization of the receptive fields of deafferent neurons was originally thought to be a protective mechanism against the development of phantom sensations. However, when this prediction was tested in human amputees, the opposite relationship was observed: the level of phantom limb pain was positively correlated with the level of cortical reorganization determined by the use of harmless somatosensory stimuli (Floret al. 1995,Montoya and others, 1998,Grusser and ai. 2001,Karl u. a. 2001). This observation is consistent with findings that more damage to somatosensory pathways is associated with more pain, such as B. in syringomyelia and postherpetic neuralgia (Fields and others. 1998,Hatemal. 2010,Petersen and Rowbotham 2010). Interestingly, however, the positive correlation between S1 reorganization and pain in amputees is maintained during pharmacological pain relief.Birbaumer et al., 1997,Huseet al. 2001), suggesting that the extent of damage to somatosensory afferents is not the only factor driving this relationship. Consequently, a similar maladaptive plasticity in S1 and reversal with successful treatment for chronic non-specific low back pain has been described (Floret al. 1997) and complex regional pain syndrome (CRPS) type 1 (Maihofner et al. 2003, 2004,Promise to 2006), Conditionsno detectable nerve damage. Primate data support an effect of nociceptive afferent inputs on S1 processing of harmless stimuli associated with an intact somatosensory system and suggest modulation of the response of rapidly adapting neurons in area 3b/1 by γ-aminobutyric acid (GABA) released after activation of suggestive nociceptive neurons in area 3a as a possible mechanism (Whitselet al. 2010). In contrast, the inverse relationship - the pathophysiological contribution of S1 reorganization to pain - is still not well understood. However, treatment approaches aimed at improving and correcting sensorimotor input have resulted in pain relief in patients with CRPS.Promise to 2005,Moseleyet al. 2008) and amputees in whom concomitant normalization of S1 maps to non-harmful input was observed (Lotze and have. 1999,MacIver et al. 2008).

4.24.2.6.5 The somatosensory cortex

Osomatosensory cortexhas been the focus of interest after injuries to the somatosensory pathways.Qi et al., 2014;Kaaset and others, 2008), and historically was early work on cortical map changes after nerve injury (Merzenich et al., 1983,1984), which helped lay the groundwork for decades of work on somatosensory plasticity. Since the primary somatosensory cortex (in primates S1 = Areas 3a, 3b, 1 and 2) receives sensory information from the periphery, all deafferentation injuries remove cortical information and alter the corresponding cortex. The extent of the change depends on what was removed and whether or not there is an alternative route for the same or similar information to the cortex.

In short, DRLs that remove all sensory information from, say, D1-D3 in one hand immediately "swap" the corresponding region of S1 in monkeys (Darian-Smith e Brown, 2000). In the first 3 to 4 months after injury and as long as input to the affected hand is sufficiently spared, most of the original cortical map reappears despite permanent loss of input. When the lesion is slightly larger and deafferentiation is complete for one of the involved fingers, adjacent finger entries expand into the original map, but corresponding "silent" regions are also typically present in the cortical map of the hand. In more extreme studies of dorsal root lesions, input from the adjacent face map can expand into the original "hand" region over many months, and over many years, cortex that remains inactive tends to atrophy. After a combined DRL/DCL lesion in which the DCL is confined to the cuneiform fasciculus of the dorsal column, the cortical map responds apparently identically to the DRL alone, presumably because the DCL comprises primarily sensory fibers already cut by the DRL (Darian-Smith et al., 2014;Darian-Smith e Fisher, 2019). This contrasts with the different responses of the corticospinal tract after these two injuries.Darian-Smith et al., 2014;Fisher and others, 2018).

Studies examining spinal cord injuries in monkeys show less severe behavioral disturbances and therefore a more complete recovery. This results in a more complete cortical map of Area 3b at 6 weeks post-injury (Reed and others, 2016) than that seen after a DRL or DRL/DCL, and reflects the fact that DCL does not affect the spinothalamic, spinocervical, or other dorsolateral fiber pathways (seeAbb.1). When the DCL is complete (Reed and others, 2016) the reorganization of the cortical "hand" map was more dramatic, but surprisingly reactivated, presumably by pathways that cross the spinal cord outside the dorsal columns.

4.23.3.2 Arrival of thalamocortical and other afferents in the somatosensory cortex

The primarysomatosensory cortexreceives input from a variety of sources, such asD'Amato et al., 1987;Bennett-Clarke and others, 1991;Simpson and others, 2006). Afferents from the dorsal thalamus, as well as projections from the cortical raphe, show patterns in the barrel cortex. Noradrenergic inputs are not structured according to cytoarchitectural landmarks.

Immunohistochemical localization of serotonin (5-HT) combined with autoradiographic images of serotonin uptake sites in newborn rat somatosensory cortex revealed dense transient serotonergic innervation with dense spots over the cortical barrels.D'Amato et al., 1987).

Subsequent studies confirmed the origin of these endpoints from the raphe nuclei and suggested the possibility that serotonergic input could aid TCAs in barrel-specific patterning. A double labeling study with lipophilic markers in fixed embryonic brains showed that thalamic afferents reach the somatosensory cortex well before these projections from the raphe nuclei (Erzurumlu e Jhaveri, 1992). Thus, it became clear that TCAs are the first corticopetal projections to reach the somatosensory cortex and transmit peripherally related patterns (Erzurumlu e Jhaveri, 1990,1992). Dual labeling experiments have further demonstrated that the pattern of TCAs in rodent somatosensory cortex predates other afferent terminals and extracellular matrix patterns seen in the developing barrel cortex (Blue and others, 1991;Jhaveri et al., 1991).

4.14.7.1 Pain perception and the somatosensory cortex

5.05.4.1 The primary somatosensory (SI) cortex

The primarysomatosensory cortex(SI) is located in the anterior part of the parietal lobe, where it forms the postcentral gyrus. It consists of Brodmann's areas 1, 2, 3a, 3b. Areas 3b and 1 receive cutaneous tactile information, areas 3a and 2 proprioceptive information.

Nociceptive input to the SI monkey has been demonstrated anatomically. The SI receives direct spino-thalamic-cortical input from the ventrobasal nuclei, specifically the ventro-posterolateral VPL nucleus (Gingold et al., 1991). Nociceptive neurons in SI are found in clusters, raising the possibility that SI may contain specific nociceptive columns (Lamouret al., 1983). Due to the lack of evidence of nociceptive neurons in the most superficial cortical layers, this hypothesis has not yet been confirmed. Nociceptive neurons are rare in SI monkeys and have been identified primarily in area 1 (Kenshallo and others, 2000), while optical imaging methods also suggested a nociceptive input into area 3a (Tommerdahlet and others, 1996). Thus, nociceptive signal processing within the SI may differ spatially from tactile signal processing, which is mainly directed to area 3b. There is also some human EEG and MEG evidence that nociceptive areas may be more medial within the SI than tactile areas with the same receptive fields, suggesting that processing of nociceptive and tactile signals may occur in different subareas of the SI (Ploner et al., 2000;Schlereth and others, 2003). Nociceptive input to the human SI was confirmed by subdural recordings (Kanda et al., 2000;Ohara et al., 2004). About 75% of PET and fMRI studies reported SI activation (Bushnell and others, 1999;Apkarian and others, 2005).

Nociceptive neurons in SI have small receptive fields arranged somatotopically and are therefore ideal for encoding the location of nociceptive stimuli.Kenshalo and Isensee, 1983). The somatotopy of nociceptive processing in the human SI has been confirmed by EEG and PET studies (Tarkka und Treede, 1993;Anderson and others, 1997). Action potential discharges from SI nociceptive neurons in monkeys are modulated by the intensity of mechanical and thermal stimuli, and their discharges correlate with speed of recognition.Kenshallo and others, 1988). These results suggest that SI nociceptive neurons are involved in encoding pain intensity. This conclusion was confirmed by a PET study of hypnotic modulation of perceived pain intensity, which also modulated IS perfusion (Hofbauer and others, 2001) and by correlation analysis (Timmerman and others, 2001).

Summary

Optical imaging studies ofsomatosensory cortex(SI) in primates has led to a reassessment of our understanding of cortical functional organization. This chapter describes findings that show that somatosensory topography, long a basis of cortical function, may not be as accurate in awake monkeys, suggesting a reassessment of the relationship between topographic representation and sensory accuracy. Optical maps of the haptic funnel illusion, which show a map of how tactile stimuli are perceived rather than a skin topography map, require a reassessment of the topographic representation in the SI as a body map. With regard to the representation of sensory submodalities, optical images of vibrotactile pressure, vibration, and vibration domains show notable similarities and differences between modality maps in the visual and somatosensory cortices.