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Health, healing or cure? The person-centred approach to treatment
Published in Rachel Freeth, Brian Thorne, Mike Shooter, Humanising Psychiatry and Mental Health Care, 2017
Rachel Freeth, Brian Thorne, Mike Shooter
So-called ‘hard determinists’ regard all events as caused or determined by antecedent conditions such that we cannot be responsible for our decisions, thinking and actions. In this camp are scientists such as Francis Crick who believe that there is a ‘neural correlate’ for ‘free will’ and that the seat of the ‘will’ is at or near the anterior cingulate sulcus in the brain (1994). For biological psychiatrists it is only a matter of time (or at least it is theoretically possible) before we understand the scientific laws that control all our brain processes - all our thoughts and decisions. Computer analogies of cognitive processes or the conditioning behavioural theories of BF Skinner, also suggests that we are more causally determined than we are free agents.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Most authors of recent textbooks in basic neuroanatomy describe the superior frontal gyrus as extending from the lateral surface of the cerebral hemisphere over the superomedial margin onto the medial surface, including cortex all the way to the cingulate sulcus (e. g., C&S. p. 33, Nolt, p. 14; a&b. p. so [Fig. 3–6]; w&G, p. 208 [Fig. 5–24]. n&d, p. 7, 484 [Fig. 16–4]). Several other authors, however, describe this area on the medial surface of each hemisphere, extending back to the paracentral sulcus and down to the cingulate sulcus, as a separate gyms, called the “medial frontal gyms” (B&K. p. 217. W&W, p. 986 989; M&M, p. 54; also, “Gyrus frontal is medialis” in IANC, p. A71). Al least two authors are inconsistent in this regard. On p. 130, Romero-Sierra (1986) states that “The cortex anterior to the paracentral sulcus and anterosuperior to the cingulate sulcus is part of the superior frontal gyrus”, however, in Fig. 8–5 (p. 130), he labels this area as “medial frontal gyrus.” Similarly, Snell states that “The cingulate gyrus is separated from the superior frontal gyrus by the cingulate sulcus” (1980, p. 236); but. in Fig. 14–3 (ibid.), he labels that area as the “Medial frontal gyms.”
Motor Areas in the Frontal Lobe: The Anatomical Substrate for the Central Control of Movement
Published in Alexa Riehle, Eilon Vaadia, Motor Cortex in Voluntary Movements, 2004
Richard P. Dum, Peter L. Strick
FIGURE 1.1 Identification of cortical areas in the macaque monkey. The cingulate sulcus (CgS), lateral sulcus (LS), and intraparietal sulcus (IPS) are unfolded and each fundus is indicated by a dashed line. The borders between cytoarchitectonic areas are delineated with dotted lines. M1 and the premotor areas are shaded. Abbreviations: AIP, LIP, MIP, VIP: anterior, lateral, medial, and ventral intraparietal areas; ArS: arcuate sulcus; CGp: posterior cingulate gyrus; CMAd, CMAv, CMAr: dorsal, ventral, and rostral cingulate motor areas; CS: central sulcus; F1 to F7: cytoarchitectonic areas in the frontal lobe according to Matelli et al.77248; FEF: frontal eye fields; Ig: granular insular cortex; M1: primary motor cortex; OFC: orbital frontal cortex; PMd: dorsal premotor area; PMv: ventral premotor area; PrCO: precentral opercular cortex; prePMd: pre-premotor area, dorsal; preSMA: presupplementary motor area; PS: principal sulcus; SEF: supplementary eye field; SI: primary somatosensory cortex; SII: secondary somatosensory cortex; SMA: supplementary motor area; PE, PEc, PEci, PF, PFG, PFop, PG, PGm, Pgop: parietal areas after Pandya and Selzer249; V6A, V6: posterior parietal areas after Galletti et al.177; 9m, 9l, 46d, 46v, 12l: prefrontal areas after Walker181 and Barbas and Pandya.186
Postoperative Focal Lower Extremity Supplementary Motor Area Syndrome: Case Report and Review of the Literature
Published in The Neurodiagnostic Journal, 2021
Nicholas B. Dadario, Joanna K. Tabor, Justin Silverstein, Xiaonan R. Sun, Randy S. DAmico
The supplementary motor area (SMA) is found bilaterally within the posterior frontal lobe in the medial frontal gyrus. The SMA is bordered posteriorly by primary motor cortex and inferiorly by the cingulate sulcus and cingulate, and the genu of the corpus callosum. Cortical models suggest that the SMA demonstrates extensive connections within and outside of the motor network and participates in a variety of functions Briggs et al. (2021). Primarily, the SMA is involved in the initiation and coordination of internal and externally cued movements – especially speech and bilateral motor control (Sheets et al. 2021; Vergani et al. 2014). Recent data suggest that the SMA is part of a prefrontal cognitive initiation “axis” in the medial frontal lobe where it coordinates with the default mode network and salience network to execute goal-directed behavior (Poologaindran et al. 2020).
Evaluation of Memory and Language Network in Children and Adolescents with Visual Impairment: A Combined Functional Connectivity and Voxel-based Morphometry Study
Published in Neuro-Ophthalmology, 2021
A Ankeeta, Rohit Saxena, S Senthil Kumaran, Sada Nand Dwivedi, Naranamangalam Raghunathan Jagannathan, Vaishna Narang
Activation of the cingulate sulcus and supplementary motor areas in both of these groups may be attributed to cognition, verb generation, attention and motor behaviour corresponding to their role in Braille reading and semantic retrieval.11,31,43 Activations in the prefrontal area, middle frontal gyrus (BA 9, 46) and inferior frontal gyrus (BA 45,47) in blind participants is indicative of word retrieval through the dorsal pathway with tactile and semantic encoding tasks44 and object naming31 associated with semantic language processes. Shifting of inferior frontal gyrus and increased BOLD responses in LB and EB adolescents may be due to lateralisation of the language areas. All participants may have been encoding the noun words (concrete or abstract nouns) into some object category followed by semantic processing. FC in EB and LB participants showed an increased range of connectivity with the hippocampus to language areas revealing the processing of Braille semantic and lexical components. The lateralisation of language processing is left lateralised and there is no change in this process.44
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.