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The cortical processing of pain
Published in Camille Chatelle, Steven Laureys, Assessing Pain and Communication in Disorders of Consciousness, 2015
Several studies have attempted to record nociceptive LFPs in other regions of the awake human brain. In a recent study, Liu et al. (2010) showed that laser stimuli elicit consistent bilateral responses in the amygdala. Using subdural grids, Lenz et al. (1998) obtained reproducible biphasic responses in the mid portion of the anterior cingulate in three epileptic patients when stimulating the face at a location compatible with Brodmann area 24. However, they were unable to explain why they failed to elicit similar responses when stimulating the upper limb. Frot et al. (2008) reported that laser stimulation of the upper limb elicits consistent responses in the posterior midcingulate cortex.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Even though much of the orbital surface of the frontal lobe lies far anterior, making up most of Brodmann areas 11–12, some authors exclude the orbitofrontal cortex from their prefrontal area (e.g., prefrontal vs. limbic association cortex: K&S, p. 215, 674 (Table 51–11; DSR&W, p. 392). By reading the relevant material in the texts just cited, one sees that this exclusion results from data strongly linking the orbitofrontal cortex anatomically with the so-called limbic system. Such narrowing of the definition of prefrontal cortex, as a portion of it comes to be identified with a more specific anatomic-physiologic system, may represent a natural step in its semantic evolution. As might be anticipated when a term is defined in so many different ways, several authors are inconsistent in their usage. This is related particularly to the practice of assigning Brodmann-area designations to the prefrontal cortex. For example, Snell includes in his prefrontal cortex “the greater parts of the superior, middle, and inferior frontal gyri, the orbital gyri, most of the medial frontal gyrus, and the anterior half of the cingulate gyrus,” but he assigns to all of these only Brodmann areas 9–12 (1980, p. 264). There is a gross discrepancy here, for several additional areas (at least 24, 32–33, and 46–47) are included in the gyri he describes. Similarly, Gilman and Newman describe the “prefrontal region” as consisting of “The large remaining part of the frontal lobe lying rostral to the motor and premotor areas,” but they, too, assign to that region only Brodmann areas 9–12 (1987, p. 208).The most inconsistencies I noted are in a textbook by Noback and Demarest (1981). Their broadest definition of the “prefrontal cortex” is “The portion of the frontal lobe located rostral to the precentral sulcus” (p. 5). In other words, it would correspond closely to Brodmann areas 6, 8–12, 32, and 44 47; but it would not include areas 24 and 33, since the latter are in the cingulate gyrus, which Noback and Demarest define as being outside the frontal lobe (in the separate “limbic lobe”—e.g., p. 8 [including Fig. 1–8], 473). On p. 12, however, they define the prefrontal cortex more narrowly, excluding the “premotor area”—i.e., Brodmann areas 6, 44, and 45 (see, also, p. 2 [Fig. 1–2]). A third and even narrower definition of prefrontal cortex is used on p. 473, 511, and 515, where Noback and Demarest exclude not only Brodmann areas 6 and 44 45. but also Brodmann area 85 and the “orbitofrontal cortex” (which they equate with Brodmann areas 11–12, p. 511). In this definition, they also explicitly include Brodmann area 24 (p. 473, 515). This is inconsistent with their statements that the prefrontal cortex is part of the frontal lobe (e.g., p. 5, 12, 511), for area 24 lies wholly within the limbic lobe, which Noback and Demarest define as separate from the frontal, parietal, temporal, and occipital lobes (p. 8 [including Fig. 1–8]).
MRS and DTI evidence of progressive posterior cingulate cortex and corpus callosum injury in the hyper-acute phase after Traumatic Brain Injury
Published in Brain Injury, 2019
Tim P. Lawrence, Adam Steel, Martyn Ezra, Mhairi Speirs, Pieter M. Pretorius, Gwenaelle Douaud, Stamatios Sotiropoulos, Tom Cadoux-Hudson, Uzay E. Emir, Natalie L. Voets
The grey-white matter junction and midline brain structures have been reported as particularly vulnerable in TBI. The corpus callosum (CC), a white matter tract critical for interhemispheric communication, is reported to be frequently impacted (20,21) and CC damage could offer an anatomical imaging correlate of injury severity (22). Injury to the posterior cingulate cortex (PCC), a highly anatomically connected region forming part of the posterior medial cortex (23), has also been shown to predict outcome following TBI (24,25). The PCC plays an important role in health and disease, and abnormal function following TBI is thought to result in attentional deficits (26). The PCC is bounded superiorly by the marginal ramus of the cingulate sulcus, posteriorly by the parieto-occipital sulcus, anteriorly by Brodmann area 24 and inferiorly by the corpus callosum (26). The cingulum bundle (CB) provides structural connection between the PCC, the medial temporal lobes and the ventromedial prefrontal cortex (27). Damage to functional networks that converge on midline areas vulnerable to TBI are thought to be associated with persistent post-traumatic complaints (28). Alterations in imaging parameters within inter-related cortical and white matter regions susceptible to injury may, therefore, shed light on the metabolic disruption that underpins DAI. To the best of our knowledge, the relationship between metabolic disruption in cortical regions and injury of white matter tracts that link them at a network level has not been investigated, in humans, in the first 24 h following TBI.