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Anatomy of the head and neck
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
On the lateral surface, a horizontally aligned lateral sulcus separates the frontal lobe from the temporal lobe. By retracting the lips (known as the opercula) of the lateral sulcus, the insula can be exposed. This effectively lies deep to the temporal lobe and is invisible from the surface. A parieto-occipital sulcus posteriorly separates the parietal lobe from the occipital lobe.
Give an account of the structure and function of the primary visual cortex and its neuronal connections
Published in Nathaniel Knox Cartwright, Petros Carvounis, Short Answer Questions for the MRCOphth Part 1, 2018
Nathaniel Knox Cartwright, Petros Carvounis
The primary visual cortex (PVC) or Brodman area 17 is situated either side of the calcarine sulcus on the medial aspect of the occipital lobe of both cerebral hemispheres. It extends from the parieto-occipital sulcus anteriorly to just posterolateral to the occipital pole.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
The “calcarine sulcus” was probably named thus originally because its floor bulges into the ventricular system, forming an elongated elevation—the “calcar avis”—in the ventricular wall (e.g., W&G, p. 212, C&S, p. 45). Since the calcar avis underlies the sulcus anterior to its junction with the parieto-occipital sulcus (w&w, p. 989), historic and gross anatomic consistency would be served by continuing to consider that sulcus as part of the calcarine sulcus. Cytoarchitectural and functional considerations, however, provide a rationale for describing the sulcus anterior to the point of union of the parieto-occipital and calcarine sulci as a continuation of the parieto-occipital sulcus. The cytoarchitectural areas below this continuation are the same as those below the parieto-occipital sulcus more posteriorly—Brodmann areas 17, 18, 19 (e.g., C&S, p.652 [Fig. 19–5B]), universally described as the “visual” areas (e.g., w&w, p. 1017 [Fig. 7.136B])—and none of these areas extend above the parieto-occipital sulcus nor above the sulcus which continues anteriorly from the point of union of the parieto-occipital and calcarine sulci (e.g., the illustrations just cited).
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.