#neurocentric

[wellandable]

Neurocentric Approach to Mechanical Pain - DNM in Vancouver, BC

It is a two-and-a-half-day workshop that will teach the philosophy, methods and techniques of DNM, which stands for Dermoneuromodulating. The course aims to help people understand pain and the nervous system and includes a hands-on, practical application.

Introducing DNM: Unlocking the Potential of Dermoneuromodulation. Are you an RMT looking to expand your skills, enhance your practice, and deliver exceptional results to your clients? Look no further; we are thrilled to present an exclusive opportunity for RMTs in beautiful Golden, BC, at 806 10th Ave S! DNM: The Complete Integration of Philosophy, Method, and Techniques We are excited to introduce DNM, also known as Dermoneuromodulation, a groundbreaking approach that can revolutionize how you treat your clients. Led by the esteemed Michael Reoch, RMT, our course will take you through the philosophy, method, and techniques of DNM, empowering you to achieve remarkable outcomes for your clients. Why DNM? Unleash Your Full Potential DNM is not just another technique; it's a comprehensive system that allows you to go beyond the ordinary and create profound changes in your client's well-being. Whether you are a seasoned practitioner or a fresh face in the industry, DNM has something unique to offer: 1. Holistic Philosophy: By understanding the intricate connections between the person, the dermis, the nervous system, and the musculoskeletal system, DNM gives you a holistic perspective that can lead to lasting results. 2. Effective Method: DNM revolves around the concept of gentle, intentional touch, helping you establish a deep connection with your clients and facilitating the body's natural healing mechanisms, ensuring that each treatment is uniquely designed for your client's needs. 3. Incorporate your already established Techniques: From myofascial release to neural mobilization, positional release, and sensory integration, DNM equips you with a robust philosophy of care that you can apply to your favourite techniques, allowing you to address a wide range of conditions and deliver exceptional outcomes that resonate with your clients. About Michael Reoch, RMT: You Instructor Leading this transformative course is none other than Michael Reoch, an RMT with extensive experience in DNM. Michael's passion for teaching and commitment to excellence have made him a trusted name in the industry. His expertise and dedication will ensure you receive the highest quality education and guidance throughout the course. Join Us in Kamloops, BC: Beautiful Surroundings for a Transformative Experience

Don't Miss Out - Secure Your Spot Today: Click the link below!

In the field of Manual Therapy, there are many techniques used to treat people in pain. These techniques involve pushing, pulling, and twisting skin and soft tissue. DNM uses techniques that change the state of the nervous system in the skin, spinal cord and brain to make it less painful and reactive.

Studies have demonstrated that touch has significant psychological and physiological impacts, with the nervous system regulating these effects. To effectively use Manual Therapy as a pain treatment, it's important to comprehend pain physiology through a social, biological, and psychological perspective. Research has indicated that establishing a non-threatening treatment environment for the patient is vital.

The skin is closely tied to the nervous system, which makes up around 2% of our body weight but uses 20% of our O2 and glucose at all times. Nerves do not respond well to sustained mechanical deformation, specifically compression and stretch. Dermoneuromodulating is a method that considers the nervous system of the patient to treat from "skin cell to sense of self." Techniques are usually light, and holds are slow.

DNM is a form of personalized manual care that targets nervous system signals to reduce discomfort and pain. This approach involves collaboration between therapist and patient to alleviate tenderness and improve well-being. Regardless of the damage in the affected area, DNM can effectively reduce pain.

The term DNM Stands for Dermo (skin), Neuro (nervous system) Modulation (a change from one state to another). It is a method of manual therapy/massage therapy used to change the state of the nervous system from a painful hyperactive state to a less painful and reactive one through receptors in the skin.

In Manual Therapy (MT), hundreds of techniques and methods attempt to approach treating people in pain. These maneuvers' speed, duration and force may differ, but the underlying mechanistic effects all follow the same rules. They can all agree that we push, pull and twist skin directly and soft tissue indirectly.

Lately, there has been considerable growth in research around the mechanisms of massage and other manual therapies, with a drift into the neuroscience involved in pain.

Two processes seem to be apparent when we look at the research: 

First, the effects of touch have strong psychological and physiological effects. 

The nervous system controls these effects. 

If we use Manual Therapy as a treatment for pain resolution, we should look at understanding pain physiology within a social, biological and psychological framework. 

What we know from studying the non-specific effects of physical medicine is that we should strive for a treatment environment that creates the least amount of threat to the person being treated; therefore, We should act, dress and keep the treatment space in a way that won’t put the patient on the defensive. 

We know that we touch the skin primarily in manual therapy and that the skin is intimately tied into the nervous system embryologically as both arrive from the ectoderm. 

We know that the Nervous System makes up around 2% of our body by weight but uses 20% of our O2 and Glucose at all times.

The nervous system carries impulses from the peripheral (and from within), which are processed in the spinal cord and Brain to create an output response. If the impulses are deemed dangerous enough, the output is pain. 

We know that pain is a complex process that depends on contextual, psychological and biological factors that mostly happen without our conscious perception and that pain can’t happen without a nervous system. 

The human body has 72 kilometres of nerves, intimately connected to the vascular system millimetre by millimetre.

Nerves do not respond well to sustained mechanical deformation, specifically, compression more than stretch.

Dermoneuromodulating is a method that attempts to take these facts as an underlying framework for an interactive, hands-on approach to treating the experience of pain. It considers the nervous system of the patient to treat from “skin cell to sense of self.” Techniques are usually light, and holds are slow. Limbs and trunk are positioned to affect deeper nerve structures in combination with skin stretch. This is done to potentially shorten and widen a nerve's container, thus reducing mechanical deformation of the nerve. 

DNM is a method of manual care that puts the patient and their needs first. Instead of operating a recipe treatment, the treatment is an interaction between the patient and the therapist. The therapist and patient work together to find the areas that need attention and remove the tenderness and pain felt in that area. The focus is on changing the signalling within the nervous system to decrease discomfort. Pain does not happen in the muscles and other tissue but in the nervous system itself; therefore, whether or not the area of pain is damaged, we can reduce that pain with DNM.

[margbarcisforever]

everyone’s relationship with their body is gonna be different but god damn some of you are completely whipped by cartesian dualism and neurocentrism. cmon man.

[enactivewebs]

14.3

Phenomenality

Internalist, neurocentric approach to phenomenal experience

Non-conscious possibility

[theoldcurator]

Challenging Neurocentrism: Exploring the Limits of Neuroscience

Neurocentrism, the belief that all mental processes can be reduced to brain functions, has become a dominant paradigm in recent years. However, this reductionist approach to understanding human cognition and behavior has limitations that must be acknowledged. In this article, we explore the challenges of neurocentrism and discuss alternative approaches to studying the mind. One major limitation of neurocentrism is its focus on individual brains rather than social and cultural contexts. Human behavior is shaped by many factors beyond biology, including social norms, cultural traditions, and historical events. To fully understand human cognition and behavior, we must examine these broader contexts. Another challenge of neurocentrism is its reliance on reductionism. By breaking down complex phenomena into their constituent parts, reductionist approaches can overlook emergent properties that arise from interactions between those parts. For example, studies of brain activity may not capture the full complexity of human emotions or social interactions. Finally, neurocentrism can reinforce a deterministic view of human nature that undermines some ethical principles. If all mental processes are reducible to brain functions, then individuals may have less agency over their behavior than we typically assume. This could have implications for how we think about responsibility and accountability in legal contexts. In summary, while neuroscience has made significant contributions to our understanding of the mind and brain, it is important not to overstate its capabilities or overlook the limitations of a neurocentric approach. By taking into account broader social and cultural contexts and avoiding reductionist assumptions about complex phenomena, we can develop more nuanced and comprehensive models of human cognition and behavior. https://theoldcurator.beehiiv.com/subscribe Read the full article

[longhaulerbear]

Migraine is one of the most prevalent and disabling neurovascular disorders worldwide. However, despite the increase in awareness and research, the understanding of migraine pathophysiology and treatment options remain limited. For centuries, migraine was considered to be a vascular disorder. In fact, the throbbing, pulsating quality of the headache is thought to be caused by mechanical changes in vessels. Moreover, the most successful migraine treatments act on the vasculature and induction of migraine can be accomplished with vasoactive agents. However, over the past 20 years, the emphasis has shifted to the neural imbalances associated with migraine, and vascular changes have generally been viewed as an epiphenomenon that is neither sufficient nor necessary to induce migraine. With the clinical success of peripherally-acting antibodies that target calcitonin gene-related peptide (CGRP) and its receptor for preventing migraine, this neurocentric view warrants a critical re-evaluation. This review will highlight the likely importance of the vasculature in migraine.

Intracranial vessel dilation has been implicated in migraine, specifically meningeal arteries. In one study, during experimental induction of migraine, dilation of both middle meningeal and middle cerebral arteries was observed.

Using the vascular hypothesis as inspiration, several studies have shown that migraine attacks were associated with release of vasoactive peptides. The vasodilatory peptides calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating polypeptide (PACAP-38), as well as the neurotransmitter nitric oxide (NO), are all potent vasodilators implicated in migraine pathophysiology.

CGRP is a multifunctional neuropeptide found on sensory nerve fibers (Russell et al., 2014). These fibers innervate vessels where CGRP receptor activation can cause both smooth muscle-dependent and endothelium-dependent activation (Wang et al., 1991; Raddino et al., 1997; Brain and Grant, 2004). Infusion of CGRP in migraine patients results in a delayed migraine-like headache, occurring around 1–5 h after treatment. However, this study also reported a decrease in blood pressure following infusion of CGRP that returned to levels similar to baseline within 60 min of administration (Lassen et al., 2002). To understand the mechanisms of migraine, several studies have induced migraine-like behavior via administration of CGRP.

Although most studies focus on vasodilatory agents implicated in migraine, the role of vasoconstrictors must not be ruled out. There have been observations that plasma levels of endothelin-1 (ET-1), a potent vasoconstrictor, were increased during early stages of a migraine attack, but rapidly decreased at the onset of the headache (Kallela et al., 1998). ET-1 is an important regulator of cerebral blood flow and its receptors are found in endothelium and vascular smooth muscle cells of the arterial system and throughout the CNS (Arai et al., 1990; Sakurai et al., 1990). Kallela et al. (1998) observed that even though ET-1 was elevated during early phases of the migraine attack, the cubital vein blood pressure measurements were unchanged. ET-1 levels rapidly decline approximately 3–4 h after the initiation of the attack, which coincides with reports of headache onset (Kallela et al., 1998). However, the authors did not report the actual blood pressure values and the observation time points are unclear.

It is important to note that ET-1 has the ability to either induce vasoconstriction or an initial vasodilation followed by vasoconstriction depending on whether it is activating endothelin type A receptor (ETA) or endothelin type B (ETB). ETA activation causes sustained vasoconstriction via smooth muscle and can inhibit NO synthesis (Arai et al., 1990; Ikeda et al., 1997) however, ETB activation initially increases release of NO and prostacyclin, which are known vasodilators, followed by sustained vasoconstriction via endothelial cells (de Nucci et al., 1988; Hoffman et al., 1989; Winquist et al., 1989; Sakurai et al., 1990). Furthermore, the non-specific endothelin receptor (A/B) antagonist bosentan inhibits neurogenic inflammation but not vasoconstriction and is not effective for the treatment of migraine (May et al., 1996). However, the ability of bosentan to act on the initial vasodilation that occurs with ETB activation was not assessed. This, along with other studies showing inhibition of neurogenic inflammation is not enough to abort migraine, supports a possible vascular role in migraine. Future studies dissecting the temporal relationship among the release of vasoactive agents such as CGRP, NO and ET-1 in migraine patients are necessary.

Vascular inflammation is a mechanism that may contribute to migraine pathogenesis. Dural vessels are thought to contribute to neurogenic inflammation, an event that activates sensory neurons and is characterized by vasodilation, plasma extravasation, and release of pro-inflammatory molecules from mast cells (Raddant and Russo, 2011). These non-vasomotor roles may involve all three layers of vessels: the inner endothelium layer, the middle smooth muscle layer and the outermost adventitia layer of fibroblasts and connective tissue.

The endothelium can both send and respond to signals via release of vasoactive substances to maintain vessel homeostasis (Tomiyama and Yamashina, 2010; Jacobs and Dussor, 2016). For example, when perturbed, cells of the vasculature can release ATP, consequently activate purinergic receptors, stimulate release of NO and pro-inflammatory mediators from endothelial cells (Burnstock, 2016; Jacobs and Dussor, 2016). Endothelium-induced NO release is then capable of sensitizing nearby afferents and possibly contributing to pain experienced during migraine. Two studies reported migraineurs have a decreased count of circulating endothelial progenitor cells (Hill et al., 2003; Rodríguez-Osorio et al., 2012). These cells are a marker of endothelium integrity and function, and a reduction suggest endothelial cell dysfunction (Hill et al., 2003). Additionally, there is mounting evidence of circulating endothelial microparticles in female migraine patients, particularly those diagnosed with migraine with aura (Liman et al., 2015). Tietjen et al. (2009) concluded that decreased concentrations of urinary NO stable metabolites in migraineurs in between migraine attacks compared to control subjects was indicative of endothelial cell dysfunction. Reports from the Levine lab suggest that vascular endothelial cells play a role in enhanced peripheral hyperalgesia via endothelin-1 and both β-adrenergic antagonist ICI-118551 and sumatriptan, both which have receptors on endothelial cells, attenuated endothelin-induced enhancement of hyperalgesia (Joseph et al., 2013). These findings suggest that anti-migraine drugs can produce anti-nociceptive effects by actions on endothelial cells. Conversely, Napoli et al. (2009) concluded that endothelial cells were properly functioning in migraineurs, however, smooth muscle cells failed to function properly following a diminished response to NO. Thus, there is evidence of endothelial dysfunction in migraine, although it is not without controversy.

Smooth muscle cells are of particular interest in migraine although studies that focus on their non-vasomotor contributions are limited. However, one promising area is the ability of NO to activate soluble guanylyl cyclase (sGC) in vascular smooth muscle cells. Recently sGC has been implicated in migraine pathogenesis (Ben Aissa et al., 2017). sGC is a major NO receptor and has been reported as a mediator of nitroglycerin-induced migraine pain (Ben Aissa et al., 2017). While NO induction of sGC causes vasodilation, it can influence dural nociceptors via the NO-cGMP pathway (Levy and Strassman, 2004). More recently Zhang et al. (2013) showed that this NTG infusion has been shown to cause delayed meningeal inflammation via vascular phosphorylated ERK expression. These data, though few, warrant more comprehensive studies to determine the role of smooth muscle activation in migraine models.

Finally, an unexpected contribution of the fibroblasts has recently been suggested by the Dussor lab (Wei et al., 2014). Cultured fibroblasts from the dura are capable of releasing mediators that sensitize dural afferents and induce-migraine-like behavior in rodents (Wei et al., 2014). These cells release IL-6 which is elevated during migraine attacks.

One theory is that neurogenic inflammation caused by activated mast cells can sensitize nociceptors and thus trigger headache (Theoharides et al., 2005; Waeber and Moskowitz, 2005; Levy, 2009). While direct evidence is lacking, clinical studies have reported increased circulating intracranial inflammatory mediators during an attack (Sarchielli et al., 2006; Goadsby and Edvinsson, 1993). Moreover, activated mast cells release histamine, prostaglandins and a host of pro-inflammatory peptides (Roberts et al., 1979; Heatley et al., 1982; Lewis et al., 1982; Tetlow et al., 1998; Theoharides et al., 2005; Aich et al., 2015). Specifically, tryptase and histamine release have been reported to release neuropeptides from proximal nerve endings and contribute to hyperalgesia (Kleij and Bienenstock, 2005; Aich et al., 2015). This along with the ability of mast cells to increase pERK, cfos, and excitation of meningeal nociceptors provide insight into a mechanism of how mast cells might contribute to peripheral sensitization.

Histamine has been reported to be increased in plasma levels during a migraine attack (Heatley et al., 1982; Moskowitz, 1993; Theoharides et al., 2005). Also, infusion of histamine in migraineurs causes a severe pulsating headache compared to controls (Krabbe and Olesen, 1980). Although with some debate, anti-histamines have been effective in treating migraine in some clinical studies and their potential role in migraine is nicely summarized by Silberstein (Yuan and Silberstein, 2018). Histamine causes dilation of cranial arteries via activation of endothelial histamine receptor H1 and inducing formation of NO (Toda, 1990; Ottosson et al., 1991). Moreover, histamine disrupts endothelial barrier formation by altering vascular endothelial cadherin and inducing dilation of vessels (Ashina et al., 2015).

There is an overwhelming abundance of evidence that suggest inflammatory pain states can alter blood brain barrier (BBB) permeability. The BBB is a selective barrier that limits paracellular diffusion via tight junctions between endothelial cells (DosSantos et al., 2014). Given that migraine has increased release of pro-inflammatory peptides, it could involve BBB disruption, although this is still controversial. In a mouse model of cortical spreading depression, the detection of brain edema, plasma extravasation, and altered metalloprotease and matrix proteins were indicative of BBB dysfunction (Gursoy-Ozdemir et al., 2004). In addition to barrier dysfunction, alterations in gap junctions may play a role in migraine. Gap junctions are specialized regions of the plasma membrane that connect cytoplasms of adjacent cells. Tonabersat, a gap junction inhibitor that binds to connexin 43, has been shown to be effective in a subset of migraine patients with aura (Sarrouilhe et al., 2014). Of particular interest, connexin 43 is found on neuronal cells and is one of the connexin proteins associated with cells of the cardiovascular system (Figueroa and Duling, 2009). Given these data, the efficacy of tonabersat suggest a possible role for dysfunction of gap junctions in migraine.

Based on these observations, we propose a possible mechanism for how an altered trigeminovascular microenvironment may initiate vascular-neural cross talk (Figure 1). The meninges are densely vascularized and the layers are innervated by sensory fibers that relay information from the periphery to higher order neurons in the brain. Distention of intracranial blood vessels, possibly from the dura, mechanically activates trigeminal perivascular afferents (Davis and Dostrovsky, 1986; Buzzi et al., 1995). Those activated neurons can release molecules that cause mast cell activation and vasodilation of the nearby vessels in a feed-back loop (Figure 1). In this model, mast cell activation increases vascular permeability and/or causes neuronal activation and neuropeptide release, which causes subsequent release of inflammatory mediators from the vessels that modulate sensory input. Most studies focus on the effect of mast cells on neurons in migraine. Future studies that examine the effect of mast cells on vasculature in translational models of migraine could reveal a role for mast cells in vascular-neural coupling.

It is known that triptans are 5-HT1B/D/F serotonin receptor agonists that can inhibit the release of neuropeptides involved in migraine and act as vasoconstrictors (Jansen et al., 1992; Nozaki et al., 1992; Williamson et al., 1997; Knight et al., 2001; Wackenfors et al., 2005). Moreover, sumatriptan treatment reduced plasma levels of CGRP in humans (Goadsby and Edvinsson, 1993; Juhasz et al., 2003) and animal models (Buzzi and Moskowitz, 1990; Buzzi et al., 1991; Nozaki et al., 1992). Vascular studies of triptans in people have given insight into its mechanism of action and the roles vessels might play in migraine. In fact, a study using single-photon emission computed tomography combined with Doppler sonography showed that if sumatriptan is infused in people, only the abnormally dilated vessels were reversed back to normal (Asghar et al., 2010, 2011). This observation suggests that triptans only cause significant vasoconstriction on dilated vessels during a migraine. Furthermore, it is interesting to note that triptans work best if used within the first 2 h of the attack (Linde et al., 2006). This coincides with the vasodilatory period following CGRP administration (Lassen et al., 2002). In addition, sumatriptan does not appear to be effective for relieving pain in other disorders (Ahn and Basbaum, 2005), which may be due to the vascular events in migraine. These observations suggest that the vasoconstrictor activity of triptans should not be ignored.

CGRP receptors are found throughout the cranial vasculature. Olcegepant is a non-peptide CGRP antagonist that has high specificity for human CGRP receptors and reported to be efficacious in migraine (Edvinsson, 2008, 2015). Olcegepant blocks dilation of the middle meningeal and extracranial temporal arteries. Similarly, the CGRP receptor antagonist telcagepant has also been shown to inhibit vasodilation of cultured human cerebral and meningeal arteries (Edvinsson et al., 2010). These observations leave open the possibility that some of the CGRP receptor antagonist efficacy might involve the vasculature.

[A] study that corroborates a role in migraine is a genome wide association meta-analysis in 2016 by Gormley et al. (2016) that identified 38 susceptibility loci that were enriched for genes associated with arterial tissue. Moreover, several of these genes are associated with smooth muscle dysfunction and cardiovascular disorders linked to migraine as a comorbidity.

The renin-angiotensin system (RAS), which is involved in hypertension, has been thought to be involved in migraine pathogenesis (Ba’albaki and Rapoport, 2008). Indeed, the efficacy of angiotensin converting enzyme inhibitors in migraine treatment is indicative of a link between migraine and hypertension (Tronvik et al., 2003). Additionally, blood pressure homeostasis is maintained by close communication between the RAS and natriuretic peptides. It has been reported that brain natriuretic peptide (BNP), which is produced by cardiac cells, is elevated in migraine (Uzar et al., 2011). However, BNP is reported to negatively regulate sensory neuron excitability (Vilotti et al., 2013). Further investigations are necessary to elucidate the role of BNP, RAS and hypertension in migraine.

The ability of vasoactive substances to induce migraine, effective drugs to have a vascular site of action, and the associated correlation of migraine and cardiovascular disease convey that vascular contributions should not be considered an epiphenomenon, but more so a causative component in migraine. Yet, clearly many lines of evidence establish that migraine is a neural disorder. We suggest that the vascular and neural theories can be linked by vascular activation of the nervous system (Figure 1). Understanding the communication between blood vessels, neurons and possibly mast cells will be integral in unraveling the pathophysiology of migraine and future studies should focus on dissecting this intersection of vascular and neural actions in migraine.

[jhavelikes]

Recent years have seen an evolving appreciation for the role of glial cells in the nervous system. As we move away from the typical neurocentric view of neuroscience, the complexity and variability of central nervous system glia is emerging, far beyond the three main subtypes: astrocytes, oligodendrocytes, and microglia. Yet the diversity of the glia found in the peripheral nervous system remains rarely discussed. In this review, we discuss the developmental origin, morphology, and function of the different populations of glia found in the peripheral nervous system, including: myelinating Schwann cells, Remak Schwann cells, repair Schwann cells, satellite glia, boundary cap-derived glia, perineurial glia, terminal Schwann cells, glia found in the skin, olfactory ensheathing cells, and enteric glia.

Peripheral glia diversity - PubMed

[drvikaskathuria]

[blogjavieralejo]

Markus Gabriel y la hipótesis del homúnculo: una aproximación

I.  Introducción: Neurocentrismo & Filosofía de la mente anti-naturalista

Markus Gabriel, el eminente filósofo alemán, famoso tras la publicación de su libro: Por qué el mundo no existe, discute algunos de los temas más peliagudos en filosofía de la mente en su libro: Yo no soy un cerebro. Una obra introductoria que a la vez ofrece argumentos en contra del neurocentrismo[1], al mismo tiempo que orienta al lector en el legado filosófico sobre el yo, la conciencia y la autoconciencia. En este ensayo se presenta, grosso modo, su filosofía de la mente y se problematiza en especial el tema de la conciencia en relación con la falacia del homúnculo.

Pero antes de entrar en dicho tema, vale destacar dos cosas. Primero: que ya en “Por qué el Mundo no Existe” (2013) había desarrollado algunas tesis que serán sostenidas también en “Yo no Soy un Cerebro” (2019). Una de ellas fue, interpretando la teoría de conjuntos, que no existe una imagen adecuada, total y perfecta del mundo[2], en el sentido de “el dominio de todos los dominios”, la totalidad irrestricta de toda cosa[3]; una más, co-orientada: fue que la visión científica no es sinónimo de racionalidad e ilustración inmaculada. Ahora, lo segundo sería describir en general cuál es el objetivo principal de la obra “Yo no soy un Cerebro”, que retrataré a continuación bajo el esquema de tres tesis.

En primer lugar, ofrece una tesis anti-reduccionista. La cual indica que no somos "meramente nuestro cerebro". La complejidad de la mente humana (en el sentido de Geist, como a continuación describiré) no es reducible a una interacción de ciertos flujos eléctricos y químicos. Además, cuestiona la idea de que el experto de la mente o del cerebro tiene que ser exclusiva y necesariamente el neurocientífico.  Markus Gabriel realiza la quizá arriesgada distinción, por una parte, entre filosofía de la conciencia, lo que equivaldría a la filosofía mainstream de la mente, y, por otra, la filosofía del Geist, una filosofía que investigaría la mentalidad humana (o human mindedness), como una capacidad compleja de y para producir auto-concepciones y diferenciaciones conceptuales (Gabriel, 2019, p. 31). El concepto de Geist es preciso y no posee una traducción literal ni al inglés ni al español. Markus Gabriel lo resume y define así: lo que es ser un animal con mente (geistig) es concebirse a sí mismo de una manera amplia (Gabriel, 2019, p. 3). Esta “manera amplia” supone que hay una pluralidad de visiones y campos de sentido que fungen analógicamente y que no son subsumidos en una teoría o sistema específico.

En segundo lugar, ofrece una tesis anti-naturalista (anclada a su sesgo anti-reduccionista, mucho más rampante). Porque piensa que no todo lo que existe puede ser explicado en términos meramente químico-biológicos. A la pregunta por lo que hay no se le contesta en meros términos naturales, sostiene nuestro filósofo. Así, pues, hay otra especie de explicaciones. La amistad, por ejemplo, no es un elemento químico que es detonado en el cerebro, no es una cosa material. Así como la idea de materia que nos hacemos en la mente no es lo mismo que lo matérico de dicha idea[4].

En tercer lugar, ofrece otra tesis que podríamos denominar crítica del determinismo en pos de la libertad y la responsabilidad. Lo que intenta defender en este último apartado de su texto es que, más allá de las elecciones ejecutadas previamente a su reconocimiento, no deberíamos defender un cinismo del automatismo; ese cinismo autocomplaciente que afirma que la responsabilidad y libertad humana se subordinan a mecanismos cerebrales ambiguos, en cierto sentido contingentes y aleatorios. Esta huida la califica de complacencia moral, exculpatoria. Aunque no se tiene el espacio y el tiempo para enunciar los principales argumentos, dejo constancia que la defensa de la libertad va ligada a otra postura que igualmente defiende, lo que denomina un neo-existencialismo que a su vez es preponderantemente anti-naturalista[5] y se define como una perspectiva que sostiene que no hay un fenómeno o realidad singular que corresponda al concepto de la “mente” (Gabriel, 2018, p. 9)[6].

 Así, de fondo a estas tres tesis, la filosofía de Gabriel es la de un pluralismo ontológico. Que se enfrenta a lo que denomina “materialismo en bruto” e “idealismo en bruto”; el primero sosteniendo que el universo es idéntico a materia y energía y el segundo negando la existencia de objetos no-mentales (Gabriel, 2018, pp. 12-13). Dicha esta presentación sintética del libro, pasaré al tema principal.

 I.                   Homúnculo y Conciencia

El tema de la conciencia ha sido estudiado desde tiempos inmemoriales, pero quizá uno de sus puntos más álgidos fue durante el idealismo alemán, en especial desde Joseph Friedrich Schelling[1], quien ofreció la transparente metáfora de que en el ser del ser humano la naturaleza abre sus ojos y vuelve a sí misma. La espectacular imagen del cosmos volviéndose consciente de sí mismo. La cual ha sido encuadrada en un cierto enigma. Así, este misterio de la conciencia es un asunto que ha provocado que distintos filósofos, como Thomas Nagel, proclamen que ella no puede ser explicada en términos meramente materialistas, en buena medida por aquella naturaleza de la conciencia que Chalmers denominó su problema difícil, el cual, no obstante, ya había sido anticipado, aunque prematuramente, por Leibniz, cuando se preguntaba cómo es posible que las cosas materiales tengan una vida interior (Gabriel, 2015, p. 48).

El mismo Chalmers abogaba por cierta irreductibilidad de la conciencia con su experimento metafísico y lógico de los Zombies. A saber, que él mismo podía ser totalmente operativo pese a que no tuviera conciencia de sí, pese a ser un autómata. El problemático experimento de Chalmers, siendo inclusive lógica y especulativamente consistente, es irrelevante. Puesto que el zombie es biológica y naturalmente imposible y puesto que la ciencia y la filosofía no se ocupan ni les importa (salvo quizá secundariamente) los mundos infinitos posibles, a saber, el mundo en donde los Zombies se manifiestan, la realidad en la que Chalmers es un zombie, sino que su interés se enfoca en este mundo físico, ecológico-biológico y cultural, en el que estamos inmersos y del que somos parte. Los zombies filosóficos son, en términos de inmanencia planetaria, un flatus vocis. Chalmers, sin embargo, hizo énfasis en lo cualitativo y en la unicidad de una experiencia arraigada en lo que es ser una entidad viviente específica.

           Con este punto solo quiero evidenciar que hay múltiples aproximaciones e intereses en el tema de la conciencia e ir anticipando algunos presupuestos sobre el homúnculo. La conciencia se despliega y exhibe como el último misterio que probablemente no pueda resolverse. A pesar de esa familiaridad que los individuos establecen con la conciencia, al despertar en la mañana y a través de la vigilia en las rutinas diarias, hasta el recuerdo unitario de algo que fueron o que fue.

Ahora bien, 2 cosas quiero mencionar al respecto: hay un tipo de perspectiva interna en primera persona de la conciencia, por la que se puede hablar de “mi conciencia” o “tú conciencia”. Digamos que es una condición de posesión: la experiencia de la conciencia como algo que está en alguien o es de alguien (Gabriel, 2019, pp. 48-49). Por lo que, bajo este criterio, se afirma que hay estados privativos de la conciencia y estados privativos mentales. Que decir entonces que un individuo consciente solo tiene un acceso indirecto a la conciencia de otro, mientras que está directamente presente en sí mismo en su conciencia (Gabriel, 2019, p.50)[2]. En lo que sigue se ahondará en esta condición y se vinculará con el problema del homúnculo.

 II.                Crítica a la Falacia del homúnculo

Recapitulando, Markus Gabriel describe el vínculo íntimo que sostiene el individuo con su propia conciencia. Porque la conciencia es naturalmente entendida como la conciencia de X o de Y. Esta condición de posesión, resalta que cada quien está particularmente familiarizado con su conciencia, más de lo que estaría con la de otro[3].

No trataré del homúnculo desde el punto de vista ni de la alquimia, ni de los homúnculos sensoriales o motores, ni como mapa de la sensibilidad. Ahora bien, la antigua falacia del homúnculo, básicamente, establece la existencia de un pequeño individuo que reside detrás de nuestros pensamientos, como si fuese un testigo permanente de todas las cosas que ocurren en el teatro de las percepciones. Literalmente significa en su raíz latina: hombrecillo. Ahora, en lo que resta de este escrito, plantearé tres críticas a dicha hipótesis falaz.

Primero. Esta idea propone que en nuestra mente hay, un alma o alguien, que decide y elige. Dicha falacia deductiva tiene su origen en la metafísica mecanicista de Descartes (o al menos en ciertos de sus intérpretes). La mente es considerada el centro operativo de la subjetividad y de la corporalidad. Desde donde se ejecutan una suerte de comandos y direcciones que sus distintas partes deben ejecutar o cumplir. Dennett (1995) denominó a este panel de control como el teatro cartesiano, donde habita una entidad que toma las decisiones. El problema de partida con esta explicación de la conciencia, entendida como aquella facultad necesaria por la que es posible pensarse como una cosa de ciertas características en un mundo, es que postula a un fantasmita, –a una pequeña persona– o, lo que es lo mismo, a otra más minúscula mente que finalmente solo desplaza el problema ad infinitum.

Markus Gabriel (2019, p. 55) ilustra este problema con el caso de la serie de tv Doctor Who?, cuando aparecen unas criaturas ciborgs, voraces y egoístas, que operan como autómatas, para devorar a toda especie viva que no forme parte de la suya; lo que ocurre en el episodio que trae a colación Gabriel es que el personaje principal transformado en un nano-doctor, logra introducirse en la cabeza de estas criaturas y observa que hay dos imágenes, una que proviene del exterior y una que capta un ojo, en donde parece haber otro receptáculo: otro cerebro con otro homúnculo que vuelve a re-proyectar las imágenes. Como es evidente, esta descripción solo complica la explicación. Denomino a este lío: el problema de la regresión.

Segundo. Esta idea transmigraría a otros pensadores. Así, mientras que para John Locke el yo –la identidad personal de la conciencia– permitía que en particular hubiera cierta continuidad y homogeneidad de la experiencia a través del tiempo, Hume dudó y negó haber encontrado, sumido en sus profundas reflexiones psicológicas, el elemento constante, fijo o suficiente de este yo. En Hume, entonces, encontramos un rechazo consistente sobre la teoría del homúnculo, aunque desde Aristóteles (en su De Anima) ya se rechaza dicha hipótesis.

Más contemporáneamente, la neurociencia ha desbancado la idea de un ego prístino, ya que, por un lado, no ha podido identificar un área del cerebro que sea el correlato de la conciencia, y por otro, cómo la conciencia y su área de activación tendría que ver con el homúnculo, esto es, el observador de los escenarios. Kant ya combatía esta falacia cuando analogaba al hombrecillo de la caverna de nuestros pensamientos con el alma: la araña que se trepa en su telaraña equivale al ego en las conexiones neurales. Dicha comparación es reproducida en diversos campos en la actualidad cuando se le asocia con la conciencia y ésta última con una parte específica del cerebro. Esta falacia también colabora con la idea de que no podemos acceder o reconocer un mundo externo, puesto que toda imagen es un constructo mental originado en nuestra mente, esto, no obstante, se retomará en el tercer y último punto.

En resumen, no podemos encontrar el área cerebral en la que residiría exclusivamente tal homúnculo, como una especie de supraconciencia, que supuestamente se encargaría de ordenar todas las facultades mentales y, en segundo lugar, lo que sea que corresponda a la conciencia en el cerebro, la actividad cerebral que sintetiza imágenes y conceptos, no puede simplemente tener forma de homúnculo o de “alma” (si es que tiene sentido decir que ella tenga forma). Además, no hay experiencia que tenga el ser humano que le permita verificar que su ego se encuentra en una pequeña parte de su cerebro (Gabriel, 2019, p. 52) y no puede enclaustrarlo en una sola área.

Tercero. Según Gabriel (2019), asocia el homúnculo con un neuro-constructivismo ontológico por la idea de que el homúnculo, estando en el comando neural, constituye con su operatividad lo real. Pero no se ha demostrado que haya unidad singular en el cerebro que construya lo real[4]. Al postular que la conciencia es un estadio interno y exclusivo del yo, y que opera bajo la naturaleza del homúnculo, que es a su vez diseñador e ingeniero de lo real, la conciencia parece deslindarse de la pregunta o reflexión sobre la realidad exterior. ¿Cómo explicar la realidad percibida por X, Y y Z? ¿Cómo saber en primer lugar que hay algo ahí cuyas coordenadas son trazadas por los tres observadores? Solo percibimos imágenes mentales, creaciones del ego solipsista u ocluido en sí. A la pregunta por lo que hay, el neuroconstructivista, contesta: electrones y campos electromagnéticos que la conciencia pone como ahí fuera. Esto nos conduce a una especie de contradicción, puesto que se parte de una ya determinada imagen de lo real. Esta teoría perdería “contacto con la realidad” para luego supuestamente hablarnos de qué es esa realidad.  

Por otro lado, cuando estoy en un salón de clases es mucho más plausible pensar que un termo o un vaso de agua existen en un lugar localizable en vez de que existan ahí en el momento en que vuelvo mi rostro hacia el espacio en donde aparecen, escurridos o derramados. Es absurdo creer que mi conciencia cargue con una serie de objetos y que los va plasmando cuando tiene esa intención (Gabriel, 2019, pp. 60-61). Los mesabancos y las ventanas y los zapatos no son cosas que cargue mi conciencia y que se reflejen en un cierto instante contingente.

Aparte, si la conciencia se redujera finalmente al homúnculo y su show representado en su escenario, la ciencia no podría describir nada más allá de los estados particulares, privativos e interiores. ¿Pero de dónde procedería entonces la experiencia si aquello que observa el homúnculo es su propio teatro? ¿De dónde fabricaría sus ilusiones? No faltaría más que afirmar que ha sido él quien ha estado engañando a las individualidades con respecto a las interacciones que establece con un mundo exterior e independiente a su yo. Dicho de otro modo, constituye una consecuencia perniciosa para la ciencia, porque ella no podría describir nada más allá de nuestros estados privativos interiores. Habría más graves problemas para identificar un objeto que está siendo percibido por varias individualidades. Si tal fuese el caso, solo podríamos conformar o formular teorías especulativas relativamente arriesgadas y salvajes acerca de lo que hay, si fuese cierto que nuestra experiencia fuese un constructo dependiente únicamente a un estadio interno a nuestro cráneo (Gabriel, 2019, p. 62).

Bibliografía y cibergrafía:

Dennett, D (1995). La conciencia explicada. Trad. Sergio Balari Ravera. Paidos: Barcelona.

Gabriel, M. (2019). I am not a Brain. Translated by Christopher Turner. Polity: Great Britain.

Gabriel, M. (2018). Neo-existencialism. Polity: Great Britain.

Gabriel, M. (2015). Why the World does not exist. Polity.

Cavanna, A. & Nani, A. (2014). Consciousness. Theories in Neuroscience and Philosophy of Mind. Springer: New York.

Chalmers, D. (1996). The Conscious Mind: in Search of a Fundamental Theory. Oxford University Press: New York.

Consultado por última vez el día 10 de noviembre del 2019: https://www.patheos.com/blogs/driventoabstraction/2018/09/markus-gabriel-neurocentrism-brain-freedom-science/

Consultado por última vez el día 10 de noviembre del 2019: https://elsemanario.com/colaboradores/jose-luis-diaz-gomez/311941/el-yo-la-autoconciencia-el-animal-humano/

Consultado por última vez el día 20 de noviembre del 2019: http://pespmc1.vub.ac.be/HOMUNCUL.html

Consultado por última vez el día 27 de noviembre del 2019: https://definicion.de/homunculo/

[1] El tema del yo obtuvo un desarrollo bastante riguroso en la obra de Fichte.

[2] Debe quedar claro que la postura de Gabriel no niega ni que nuestra mente tenga como precondición biológica al cerebro, pero tampoco dice que todas las ideas, y todo el contenido genuinamente inmaterial, se reduzca a químicos. En otras palabras, sostiene un grado de emergentismo neurobiológico, aunque rechaza el reduccionismo fisicalista.

[3] Desde la perspectiva de Daniel Dennett, no hay nada sorprendente en poseer una especie de experiencia y perspectiva de primera persona. Todo lo que vive subjetiva y experiencialmente una persona, puede ser compartido, y por tanto mostrado cómo es ser tal subjetividad, a través de lo que él denomina la heterophenomenología, que quiere decir, la fenomenología, el aparecer de..., el otro. Creer que realmente hay algo especial en la persona que somos, como un yo ´que no puede reflejarse o mostrarse cómo es ser como tal X, es apostar por el homúnculo, es decir, privilegiar ese sitio, ese espacio dentro del cerebro, en donde ese misterioso expectador visualiza todo lo que aparece en el escenario (Cavana & Nani, 2014, p. 26-28).

[4] En relación con Kant, en ocasiones se le vincula erróneamente con el neuroconstructivismo. De hecho, Kant se percató de la contradicción en la que se enmarañaba éste. En la Crítica de la Razón Pura se encargó “en demostrar, entre otras cosas, que la identificación con lo que sostiene nuestros procesos de pensamiento con cualquier tipo de cosa (siendo una inmaterial o el cerebro) es una falacia que se impone así misma en nosotros en el dominio de la auto-conciencia y el auto-conocimiento (…)” (Gabriel, 2019, p. 59). Se trata de un paralogismo que se basa en la creencia en que aquello que sostiene el pensamiento es una cosa que encontramos en el mundo, como un trozo de corteza cerebral o un alma inmaterial. “El paralelismo identifica al sujeto pensante con un objeto del mundo externo” (ibid).

[1] Lo que dictamina el neurocentrismo es que el pensamiento, la racionalidad y la intelectualidad se encuentra exclusivamente en el cerebro. Pareciera conformar una postura que resulta epistemológicamente totalizada o cerrada ante otras posibilidades. Es más: el neurocentrismo argumenta que el yo es el cerebro; algo parecido a decir que el ser es la mente o que nuestra identidad es nuestro organismo.

[2] Markus Gabriel distingue, sin embargo, mundo de universo: “Whereas the former refers to the domain of objects studiedd by our best natural sciences (maybe ideally by futuristic unified physics or, depending on the status of the unity/disunity of science, by any relevant ensemble of establishedd present and future disciplines), the latter is the hypothetical all-encompassing domain of objects” (Gabriel, 2018, p.10).

[3] En cuanto a esta crítica a los pensamientos de una totalidad de cosas existentes como formando parte de una teoría específica que los explica definitiva y absolutamente, le parecen espejismos, ilusiones metafísicas que deben ser superadas. A esta superación la nombra nihilismo meta-metafísico. Lo que viene a afirmar es simplemente que deberíamos rechazar o por lo menos siempre sospechar de cualquier teoría que pretenda dar cuenta de la definición y razón de todo lo que hay.

[4] En cuanto a la teoría de la verdad, escribe que la verdad no se limita a la ciencia natural; se hallan en las ciencias sociales y humanas, en el arte, y otros campos del saber, incluso en las circunstancias más sencillas y comunes, cómo reconocer que alguien está furioso, que no implica indagar científica y profundamente en s estado cerebral (Gabriel, 2019).

[5] Según Donald Davidson, el dominio de lo físico se distingue del dominio de lo mental en que el segundo es impredecible, abierto y relacionado con un todo, mientras que el primero es determinístico y cerrado. Esto se puede explicar, por ejemplo, si alguien quiere chocolate, a la vez se relaciona con la creencia de que hay una caja de chocolates en la cocina, y luego quizá que la cocina se halla en el primer piso, y así sucesivamente. Sobre lo mental se predican un conjunto de aspectos involucrados en los denominados eventos mentales (Cavanna y Nani, p.22, 2014). Este planteamiento de Davidson se conecta también con el de Markus Gabriel de combatir el cinismo neurocéntrico y defender cierta autonomía de la libertad y autonomía humana frente a una realidad en constante cambio. Aunque su visión además permite adecuar un campo con otro. Es decir, si bien hay determinismo en uno, en otro hay posibilidad de sustraerse mínimamente a él.

[6] Escribe: “the view that there is no single phenomenon or reality corresponding to the ultimately very messy umbrella term the mind” (p. 9).

[wellandable]

Neurocentric Approach to Manual Therapy for Massage Therapists and other manual therapists - 2-day course 14PE credits with the CMTBC: CDI campus, South Surrey 9am-430pm

Learn how and when to treat your patients painful complaints

Put the nervous system first and start changing your patients painful conditions. Specifically, I’m looking at pain that originates from a mechanical deformation of nerve tissue and that can change with position or movement. It is important here to look at the origin of the painful experience as opposed to cause. What do I mean by that? By origin, I mean it as the point or place where something begins, arises, or is derived. With pain there are only four origins where pain may arise from. Cause, on the other hand, is something that brings about an effect or a result. To look for the cause of someone's pain can result in thousands of reasons each reason giving little illumination on how to proceed with treatments. Alternatively, the origins of pain give us a clearer path to resolution.

From Barrett Dorko the originator of Simple Contact:

“Almost without exception therapists interviewing a patient in pain begin to try and figure out how this patient came to be the way that they are. They work to create a story that explains this and then search for evidence. This is called looking for the cause, and I think it’s a tremendous waste of time. It’s a great black hole, and I suggest you stop doing this as soon as you possibly can.”

I find that if you understand the four origins of pain you will have the best chance of success with your patients. Specifically, I would like to look at pain that originates in the mechanical deformation of nervous tissue. This type of pain is an abnormal neurodynamic and can be changed with position or movement. If the mechanical stress on the nerve is not corrected it can result in neuritis or even a neuroma.

What I hope to achieve with this course is to provide my students with a way to better understand how painful conditions arise and how we can successfully treat these conditions with passive movements that target peripheral nerves and active movements that empower the patient to help themselves achieve a resolution of their pain. This active treatment is based on Barrett Dorko’s Simple Contact. An approach and method of treatment that attempts to remove the barriers of self-correction. With simple hand placements, we let the patient guide the movement towards unloading mechanically deformed nerve tissues in the body. This is achieved by allowing ideomotion to express itself. This may resemble other treatments such as fascial unwinding or Cranial Sacral Therapy but is based on a stronger base of plausibility and has greater outcome predictability.

The second part of the course looks at passive treatments that are based on Neurodynamics. Neurodynamics is a method popularized by David Buttler and Michael Shacklock who are two prominent Physios from Australia. Concurrently, here in BC, a very similar method called End Range Loading was developed by David DeCamimilis DC. These methods are well researched as Manual Therapies go.Learning Outcomes for Neurocentric Approach to Persistent Pain.

• Identify the difference between pain causes and origins

• Learn how the four origins of pain help us understand pain physiology

• Introduction to what ideomotion is in a pain resolution context

• Be able to better assess people in pain and use that assessment in a manual therapy interaction

• Be able to perform a neurodynamic test and use it in decision-making process

• Learn how the small skills of nonspecific effects, culture and context affect the experience of pain

SEPTEMBER 15-16 2022, 9AM-430PM

LOCATION:

14928 56 Ave, Surrey, BC V3S 2N5

[boxrite]

View this post on Instagram

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[ngeorgeault]

#machinelearning with @GoogleCanada @desjardinslab #IntelligenceArtificielle Let see how #Neurocentric will be this speech... #NeuralNetwork (at Complexe Desjardins)

[theoldcurator]

Challenging Neurocentrism: Exploring the Limits of Neuroscience

Neurocentrism, the belief that all mental processes can be reduced to brain functions, has become a dominant paradigm in recent years. However, this reductionist approach to understanding human cognition and behavior has limitations that must be acknowledged. In this article, we explore the challenges of neurocentrism and discuss alternative approaches to studying the mind. One major limitation of neurocentrism is its focus on individual brains rather than social and cultural contexts. Human behavior is shaped by many factors beyond biology, including social norms, cultural traditions, and historical events. To fully understand human cognition and behavior, we must examine these broader contexts. Another challenge of neurocentrism is its reliance on reductionism. By breaking down complex phenomena into their constituent parts, reductionist approaches can overlook emergent properties that arise from interactions between those parts. For example, studies of brain activity may not capture the full complexity of human emotions or social interactions. Finally, neurocentrism can reinforce a deterministic view of human nature that undermines some ethical principles. If all mental processes are reducible to brain functions, then individuals may have less agency over their behavior than we typically assume. This could have implications for how we think about responsibility and accountability in legal contexts. In summary, while neuroscience has made significant contributions to our understanding of the mind and brain, it is important not to overstate its capabilities or overlook the limitations of a neurocentric approach. By taking into account broader social and cultural contexts and avoiding reductionist assumptions about complex phenomena, we can develop more nuanced and comprehensive models of human cognition and behavior. https://theoldcurator.beehiiv.com/subscribe Read the full article

[mostlysignssomeportents]

#6yrsago Brainwashed: Neuroscience vs neurobollocks

Brainwashed: The Seductive Appeal of Mindless Neuroscience is a smart and sometimes devastating critique of "neurobollocks" -- the propensity for using brain-science (and, particularly, brain imaging) to reductively explain human motivation. The authors, Sally Satel and Scott O. Lilienfeld, are a psychiatrist and a psychologist (respectively) and so it's hard not to suspect that there's a little professional rivalry at play here, but they present a compelling argument nonetheless -- a picture of promising science oversold in the name of winning grants, winning court cases, and, at the worst, duping the gullible.

Brainwashed is broken into five brisk sections that each address a different critique of "neurocentrism," or the belief that there is something special about the brain (and especially the brain scan) that trumps virtually every other account of human behavior. The authors open up with a scathing indictment of "neuromarketing," whose practitioners distort and manipulate the literature on brain imaging, getting rich off of gullible clients who are seduced by the idea of a scientific method for "pushing the brain's Buy Now button." This is complemented by a later chapter on the use of neurological imaging for lie-detection, another extremely profitable field based on shaky science. This later chapter is also interesting in the questions it raises about the nuance of falsehood, by way of illustrating the difference between successfully identifying the "induced falsehood" of a lab subject and determining whether an accused adulterer or murderer is spinning lies.

Also immediate and practical are the chapters on addiction and criminal culpability. On addiction, the authors show how neurocentric views of addiction ("I'm not a crack addict, my brain is") rests on a nonsense theory of addiction as a chronic, relapsing brain disease that has become War on Drugs dogma, and which, therefore, produces proscriptions that add little to the practical business of helping people who struggle with painful drug problems. On the subject of neuroscience and guilt, the authors introduce the nuanced and chewy idea of human agency and free will, and the larger social purpose of a justice system. This discussion is accompanied by a philosophical argument about the need for "retributive justice" (punishment) as a means of creating legitimacy in the justice system, presented as an argument against the idea of treating crime as a neurological disease. This was, for me, the book's weakest argument, and reflective of the political agenda of the American Enterprise Institute, a libertarian thinktank where Sally Satel is Resident Scholar.  

The book ends with a wider philosophical inquiry into what neuroscience can tell us about free will -- not much, in the authors' view, especially not much that hasn't already been captured by centuries of philosophical debate. But this closing chapter is also a good summary of the overall message of the book: that we are irrationally swayed by brain imaging, imputing to it a precision and informative value that far exceeds the present state of the science -- a science that is extremely promising and fascinating, but which is routinely oversold.

At 150 pages (with 50 pages of dense end-notes), this book is a brisk read, but a good one -- and, I would argue, an important one.

Brainwashed: The Seductive Appeal of Mindless Neuroscience

https://boingboing.net/2013/11/28/brainwashed-neuroscience-vs-n.html

[jhavelikes]

Recent years have seen an evolving appreciation for the role of glial cells in the nervous system. As we move away from the typical neurocentric view of neuroscience, the complexity and variability of central nervous system glia is emerging, far beyond the three main subtypes: astrocytes, oligodendrocytes, and microglia. Yet the diversity of the glia found in the peripheral nervous system remains rarely discussed. In this review, we discuss the developmental origin, morphology, and function of the different populations of glia found in the peripheral nervous system, including: myelinating Schwann cells, Remak Schwann cells, repair Schwann cells, satellite glia, boundary cap-derived glia, perineurial glia, terminal Schwann cells, glia found in the skin, olfactory ensheathing cells, and enteric glia.

Peripheral glia diversity - PubMed