The Evolutionary Development of the Brain As It Pertains to Neurosurgery

Basma, Jaafar; Guley, Natalie; Michael, L Madison; Arnautović, Kenan I.; Boop, Frederick A.; Sorenson, Jeff

doi:10.7759/cureus.6748

Cited by 5 publications

(7 citation statements)

References 21 publications

(26 reference statements)

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“…In rodents, there is no formation of a telencephalic flexure, but, as in humans, their primary visual cortex lies on the dorsomedial aspect, rostral to the occipital pole. Furthermore, there is no looping of the stria terminalis, and the hippocampus extends all the way to the posterior hemisphere ( 14 ). Animals that do form a telencephalic flexure include all primates, dogs, whales, cats, cows, horses, and pigs ( 8 ).…”

Section: Discussionmentioning

confidence: 99%

Cadaveric White Matter Dissection Study of the Telencephalic Flexure: Surgical Implications

et al. 2022

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Neurosurgery has traditionally been overtly focused on the study of anatomy and functions of cortical areas with microsurgical techniques aimed at preserving eloquent cortices. In the last two decades, there has been ever-increasing data emerging from advances in neuroimaging (principally diffusion tensor imaging) and clinical studies (principally from awake surgeries) that point to the important contribution of white matter tracts (WMT) that influence neurological function as part of a brain network. Major scientific consortiums worldwide, currently working on this human brain connectome, are providing evidence that is dramatically altering the manner in which we view neurosurgical procedures. The development of the telencephalic flexure, a major landmark during the human embryogenesis of the central nervous system (CNS), severely affects the cortical/subcortical anatomy in and around the sylvian fissure and thus the different interacting brain networks. Indeed, the telencephalic flexure modifies the anatomy of the human brain with the more posterior areas becoming ventral and lateral and associative fibers connecting the anterior areas with the previous posterior ones follow the flexure, thus becoming semicircular. In these areas, the projection, association, and commissural fibers intermingle with some WMT remaining curved and others longitudinal. Essentially the ultimate shape and location of these tracts are determined by the development of the telencephalic flexure. Five adult human brains were dissected (medial to lateral and lateral to medial) with a view to describing this intricate anatomy. To better understand the 3D orientation of the WMT of the region we have correlated the cadaveric data with the anatomy presented in the literature of the flexure during human neuro-embryogenesis in addition to cross-species comparisons of the flexure. The precise definition of the connectome of the telencephalic flexure is primordial during glioma surgery and for disconnective epilepsy surgery in this region.

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Section: Discussionmentioning

confidence: 99%

Cadaveric White Matter Dissection Study of the Telencephalic Flexure: Surgical Implications

et al. 2022

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“…Spreading neuronal activation throughout the brain induced Acad upregulation in the paralimbic and limbic areas regardless of treatment type. The limbic and paralimbic areas are well-developed in the early stages of evolution (Basma et al, 2020;Bloch et al, 2019;MacLean, 1954;Mega et al, 1997), suggesting that neurons in phylogenetically primitive regions potentially express Acad.…”

Section: Discussionmentioning

confidence: 99%

Comparative distribution ofArcadlin/Protocadherin‐8mRNA in the intact and ischemic brains of adult mice

Inoue

Sawano

Yamaguchi

et al. 2022

J of Comparative Neurology

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The structural plasticity of dendritic spines serves as the adaptive capabilities of the central nervous system to various stimuli. Among these stimuli, cerebral ischemia induces dynamic alterations in neuronal network activity. Arcadlin/Paraxial protocadherin/Protocadherin-8 (Acad), a regulator of dendritic spine density, is strongly induced by activating stimuli to the neurons. However, the detailed distribution of Acad in normal and ischemic adult brains remains unclear. We comprehensively described Acad expression patterns in normal and ischemic adult brains by in situ hybridization histochemistry. We found that intact adult brains expressed Acad in the piriform cortex, dentate gyrus, hippocampal CA3, entorhinal cortex, amygdala, and hypothalamus. Acad expression was dramatically upregulated in the piriform cortex, olfactory area, dentate gyrus, entorhinal cortex, prefrontal cortex, insular cortex, amygdala, and septohippocampal nucleus 4 h after cerebral ischemia.

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“…The modern images in the modern conscious brain are produced by large interconnected ensembles of neocortical neurons. This probably did not challenge the ancestral, hippocampus-destined reptilian medial cortical pallium, which was as large or larger than the connected tiny dorsal cortical pallium and the then larger olfactory lateral cortical pallium [ 176 , 177 , 178 , 179 , 180 , 181 , 182 ]. The brains of our reptilian ancestors had no mammalian-strength neocortex.…”

Section: Where Does Ad Start?mentioning

confidence: 99%

“…This created the four modern neocortical visual pathways, which included the OT ‘What’ pathway in the occiptotemporal pathway [ 183 , 184 ]. The medial pallium eventually became the hippocampal conformation, and its archaic lateral and dorsal pallial connections became, in part, the small LEC super-hub [ 178 , 181 ].…”

Section: Where Does Ad Start?mentioning

confidence: 99%

“…The current enormous 6-layer cortex is the product of a 3-layer reptilian-like brain consisting of periventricular sheets known as medial, dorsal, lateral, and ventral pallia, each with only one layer of pyramidal neurons [ 177 , 178 , 179 , 180 , 181 , 194 , 197 , 198 ]. Between the medial and lateral pallia was a narrow wedge of dorsal neuropil with an immense World-changing future—the enormous human neocortex.…”

Section: Originsmentioning

confidence: 99%

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Alzheimer’s Disease and Its Possible Evolutionary Origin: Hypothesis

Whitfield

Rennie

Chakravarthy

2023

Cells

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The enormous, 2–3-million-year evolutionary expansion of hominin neocortices to the current enormity enabled humans to take over the planet. However, there appears to have been a glitch, and it occurred without a compensatory expansion of the entorhinal cortical (EC) gateway to the hippocampal memory-encoding system needed to manage the processing of the increasing volume of neocortical data converging on it. The resulting age-dependent connectopathic glitch was unnoticed by the early short-lived populations. It has now surfaced as Alzheimer’s disease (AD) in today’s long-lived populations. With advancing age, processing of the converging neocortical data by the neurons of the relatively small lateral entorhinal cortex (LEC) inflicts persistent strain and high energy costs on these cells. This may result in their hyper-release of harmless Aβ1–42 monomers into the interstitial fluid, where they seed the formation of toxic amyloid-β oligomers (AβOs) that initiate AD. At the core of connectopathic AD are the postsynaptic cellular prion protein (PrPC). Electrostatic binding of the negatively charged AβOs to the positively charged N-terminus of PrPC induces hyperphosphorylation of tau that destroys synapses. The spread of these accumulating AβOs from ground zero is supported by Aβ’s own production mediated by target cells’ Ca2+-sensing receptors (CaSRs). These data suggest that an early administration of a strongly positively charged, AβOs-interacting peptide or protein, plus an inhibitor of CaSR, might be an effective AD-arresting therapeutic combination.

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The Evolutionary Development of the Brain As It Pertains to Neurosurgery

Cited by 5 publications

References 21 publications

Cadaveric White Matter Dissection Study of the Telencephalic Flexure: Surgical Implications

Cadaveric White Matter Dissection Study of the Telencephalic Flexure: Surgical Implications

Comparative distribution ofArcadlin/Protocadherin‐8mRNA in the intact and ischemic brains of adult mice

Alzheimer’s Disease and Its Possible Evolutionary Origin: Hypothesis

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