Weekly Papers on Philosophy of Mind (40)

Abstract

Are corporations and other complex groups ever morally responsible in ways that do not reduce to the moral responsibility of their members? Christian List, Phillip Pettit, Kendy Hess, and David Copp have recently defended the idea that they can be. For them, complex groups (sometimes called collectives) can be irreducibly morally responsible because they satisfy the conditions for morally responsible agency; and this view is made more plausible by the claim (made by Theiner) that collectives can have minds. In this paper I give a new argument that they are wrong. Drawing on recent work in the philosophy of mind (what Uriah Kriegel calls “the phenomenal intentionality research program”) and moral theory (David Shoemaker’s tripartite theory of moral responsibility), I argue that for something to have a mind, it must be phenomenally conscious, and that the fact that collectives lack phenomenal consciousness implies that they are incapable of accountability, an important form of moral responsibility.

Abstract

Ambitious higher-order theories of consciousness aim to account for conscious states when these are understood in terms of what-it-is-like-ness. This paper considers two arguments concerning this aim, and concludes that ambitious theories fail. The misrepresentation argument against HO theories aims to show that the possibility of radical misrepresentation—there being a HO state about a state the subject is not in—leads to a contradiction. In contrast, the awareness argument aims to bolster HO theories by showing that subjects are aware of all their conscious states. Both arguments hinge on how we understand two related notions which are ubiquitous in discussions of consciousness: those of what-it-is-like-ness and there being something it is like for a subject to be in a mental state. This paper examines how HO theorists must understand the two crucial notions if they are to reject the misrepresentation argument but assert the awareness argument. It shows that HO theorists can and do adopt an understanding—the HO reading—which seems to give them what they want. But adopting the HO reading changes the two arguments. On this reading, the awareness argument tells us nothing about those states there is something it is like to be in, and so offers no support to ambitious HO theories. And to respond to the misrepresentation understood according to the HO reading is to simply ignore the argument presented, and so to give no response at all. As things stand, we should deny that HO theories can account for what-it-is-like-ness.

Abstract

I develop an interpretation of Maurice Merleau-Ponty's concept of motor intentionality, one that emerges out of a reading of his presentation of a now classic case study in neuropathology—patient Johann Schneider—inPhenomenology of Perception. I begin with Merleau-Ponty's prescriptions for how we should use the pathological as a guide to the normal, a method I call triangulation. I then turn to his presentation of Schneider's unusual case. I argue that we should treat all of Schneider's behaviors as pathological, not only his abstract movements (e.g., pointing), as is commonly acknowledged in the secondary literature, but also crucially his concrete movements (e.g., grasping). Using these facts of Schneider's illness, I reconstruct a ‘fundamental function’ of consciousness, as Merleau-Ponty called it, in which there are two kinds of bodily agency: the power of the body to be solicited by a situation and the power of the body to project a situation. I propose that these powers became dissociated in Schneider's case, as evidenced by his abstract and concrete movements, while in the normal case, these powers comprise a dynamic unity, enacted as motor intentionality. I also discuss how my interpretation complements Merleau-Ponty's assertion that motor intentions exist between mind and matter.

Abstract

Recently, it has been objected that naïve realism is inconsistent with an empirically well-supported claim that mental states of the same fundamental kind as ordinary conscious seeing can occur unconsciously (SFK). The main aim of this paper is to establish the following conditional claim: if SFK turns out to be true, the naïve realist can and should accommodate it into her theory. Regarding the antecedent of this conditional, I suggest that empirical evidence renders SFK plausible but not obvious. For it is possible that what is currently advocated as unconscious perception of the stimulus is in fact momentaneous perceptual awareness (or residual perceptual awareness) of the stimulus making the subject prone to judge in some way rather than another, or to act in some way rather than another. As to the apodosis, I show that neither the core of naïve realism nor any of its main motivations is undermined if SFK is assumed. On the contrary, certain incentives for endorsing naïve realism become more tempting on this assumption. Since the main motivations for naïve realism retain force under SFK, intentionalism is neither compulsory nor the best available explanation of unconscious perception.

Abstract

Recently, two apparent truisms about self-control have been questioned in both the philosophical and the psychological literature: the idea that exercising self-control involves an agent doing something, and the idea that self-control is a good thing. Both assumptions have come under threat because self-control is increasingly understood as a mental mechanism, and mechanisms cannot possibly be good or active in the required sense. However, I will argue that it is not evident that self-control should be understood as a mechanism, suggesting that we might also argue the other way around: if we have independent reason to hold onto the idea that self-control is inherently good and active, the conclusion might be that self-control cannot be a mechanism. I will show that Aristotle's original analysis of self-control actually offers grounds for both assumptions: he took there to be conceptual connections between self-control and goodness/activity. By examining these connections, I argue that an Aristotelian approach could offer promising leads for a contemporary non-mechanistic understanding of self-control as a normative capacity.

Abstract

There is an overriding orthodoxy amongst philosophers that attention is a unified phenomenon, subject to explanation by one monistic theory. In this paper, I examine whether this philosophical orthodoxy is reflected in the practice of psychology. I argue that the view of attention that best represents psychological work is a variety of conceptual pluralism. When it comes to the psychology of attention, monism should be rejected and pluralism should be embraced.

Abstract

The lore is that standard information theory provides an analysis of information quantity, but not of information content. I argue this lore is incorrect, and there is an adequate informational semantics latent in standard theory. The roots of this notion of content can be traced to the secret parallel development of an information theory equivalent to Shannons by Turing at Bletchley Park, and it has been suggested independently in recent work by Skyrms and Bullinaria and Levy. This paper explicitly articulates the semantics latent in information theory and defends it as an adequate theory of information content, or natural meaning. I argue that this theory suggests a new perspective on the classic misrepresentation worry for correlation-based semantics.

There have been few attempts to answer the twin challenges for alethic pluralists to maintain standard accounts of the logical operators and of logical consequence in a sufficiently systematic and precise way. In this paper, I propose an account of logic and semantics on behalf of pluralists that answers both challenges in a sufficiently systematic and precise way. Crucially, the account accommodates mixed atomics, and its first-order extension also accommodates quantified sentences. Accordingly, pluralists can answer all the distinctively logical challenges for their view.
Neuroscientist based at Yale in 1960s controlled bulls, monkeys and humans with brain implants and envisioned a “psychocivilized society”-- Read more on ScientificAmerican.com

Trying to focus but keep getting distracted? From mind-wandering to doodling, the simplest ways to stay on track are not what you expect

People with serious mental illness have a reduced life expectancy that is partly attributable to increased cardiovascular disease. One approach to address this is regular physical health monitoring. However, physical health monitoring is poorly implemented in everyday clinical practice and there is little evidence to suggest that it improves physical health. We argue that greater emphasis should be placed on primary prevention strategies such as assertive smoking cessation, dietary and exercise interventions and more judicious psychotropic prescribing.

The DSM and ICD have taken steps to introduce a grief disorder as a new diagnostic entity. Evidence justifies the inclusion of prolonged grief disorder, but not complicated grief, as a new mental disorder.

Late in his career, our Henry has established a glowing reputation on the international stage both as a riveting storyteller with Do No Harm and as an eloquent performer on YouTube and TV (Your Life in their Hands and The English Surgeon). Both Ian McEwan and The Economist ventured that neurosurgery had found its Boswell. In his new book Admissions, Henry is in reflective mode as he struggles with retirement, loss of professional identity, lost opportunities to put matters right and post-retirement blues. The book starts with his suicide kit and ends with his ambition not to wait for the end, but to be ready to leave, booted and spurred, when it comes. In between, there is a compelling mix of poignant patient vignettes interspersed with laments about his own clinical failings, the state of medicine at home and abroad, and fleeting observations on consciousness and the hereafter.
Abstract

Matthew Babb offers a strikingly elegant argument for, and explanation of, the essential indexicality of intentional argument. His two key thoughts are that intentional action always involves intentions, and intentions are essentially indexical. In particular, every intention is indexically about the agent whose intention it is, i.e. de se. In this paper, I set out two models on which at least some intentions are not de sethey are impersonaland I show that these models are compatible with the data Babb points to. I also set out some more data that an account of essential indexical cases ought to be responsive to. Its span suggests that the claim that all intentions are de se, even if true, cannot be what explains what is going on in essential indexical cases involving intention.

Abstract

In a series of papers, Jesper Kallestrup and Duncan Pritchard argue that the thesis that knowledge is a cognitive success because of cognitive ability (robust virtue epistemology) is incompatible with the idea that whether or not an agent’s true belief amounts to knowledge can significantly depend upon factors beyond her cognitive agency (epistemic dependence). In particular, certain purely modal facts seem to preclude knowledge, while the contribution of other agents’ cognitive abilities seems to enable it. Kallestrup and Pritchard’s arguments are targeted against views that hold that all it takes to manifest one’s cognitive agency is to properly exercise one’s belief-forming abilities. I offer an account of the notion of cognitive ability according to which our epistemic resources are not exhausted by abilities to produce true beliefs as outputs, but also include dispositions to stop belief-formation when actual or modal circumstances are not suitable for it (precautionary cognitive abilities). Knowledge, I argue, can be accordingly conceived as a cognitive success that is also due to the latter. The resulting version of robust virtue epistemology helps explain how purely modal facts as well as other agents’ cognitive abilities may have a bearing on the manifestation of one’s cognitive agency, which shows in turn that robust virtue epistemology and epistemic dependence are not incompatible after all.

Abstract

Descartes’ Rules for the direction of the mind presents us with a theory of knowledge in which imagination, considered as an “aid” for the intellect, plays a key role. This function of schematization, which strongly resembles key features of Proclus’ philosophy of mathematics, is in full accordance with Descartes’ mathematical practice in later works such as La Géométriefrom 1637. Although due to its reliance on a form of geometric intuition, it may sound obsolete, I would like to show that this has strong echoes in contemporary philosophy of mathematics, in particular in the trend of the so called “philosophy of mathematical practice”. Indeed Ken Manders’ study on the Euclidean practice, along with Reviel Netz’s historical studies on ancient Greek Geometry, indicate that mathematical imagination can play a central role in mathematical knowledge as bearing specific forms of inference. Moreover, this role can be formalized into sound logical systems. One question of general epistemology is thus to understand this mysterious role of the imagination in reasoning and to assess its relevance for other mathematical practices. Drawing from Edwin Hutchins’ study of “material anchors” in human reasoning, I would like to show that Descartes’ epistemology of mathematics may prove to be a helpful resource in the analysis of mathematical knowledge.

The algorithm can figure out when the word “moron” is used in good fun, and when a seemingly innocuous word like "animal" is being used to demonise people
We worry it’s going to steal our jobs – or even destroy humanity itself. But the real risks of AI are subtler and more tricky to handle
What pitfalls or rewards might await the Silicon Valley whiz kid apparently intent on creating a benign superintelligent digital deity, wonders Jamais Cascio

Sometimes a proposition is ‘opaque’ to an agent: (s)he doesn't know it, but (s)he does know something about how coming to know it should affect his or her credence function. It is tempting to assume that a rational agent's credence function coheres in a certain way with his or her knowledge of these opaque propositions, and I call this the ‘Opaque Proposition Principle’. The principle is compelling but demonstrably false. I explain this incongruity by showing that the principle is ambiguous: the term ‘know’ as it appears in the principle can be interpreted in two different ways, as either basic-know or super-know. I use this distinction to construct a plausible version of the principle, and then to similarly construct plausible versions of the Reflection Principle and the Sure-Thing Principle.

Abstract

Not only has the philosophical debate on causation been gaining ground in the last few decades, but it has also increasingly addressed the sciences. The biomedical sciences are among the most prominent fields that have been considered, with a number of works tackling the understanding of the notion of cause, the assessment of genuinely causal relations and the use of causal knowledge in applied contexts. Far from denying the merits of the debate on causation and the major theories it comprises, this paper is meant as a stimulus for theorists of causation in the philosophy of biomedicine, with a focus on clinical matters. Without aiming at putting forward an original theory of causation and starting from the narration of two actual but paradigmatic cases at the joints between biomedical research and clinical practice, we want to point out that some pathological situations addressed by molecular medicine actually prove resistant to (at least) some of our major epistemological accounts of causal explanation. Given this scenario, which is very frequent in our hospitals, our analysis aims to provide a stimulus for the debate among theorists of causation in biomedicine interested in real cases in science in practice. We believe that this might in turn encourage some more general rethinking of the complex intertwinement of science, philosophy of science and ethics, as well as of the role of philosophy of science for clinical medicine itself.

Sometimes a proposition is ‘opaque’ to an agent: (s)he doesn't know it, but (s)he does know something about how coming to know it should affect his or her credence function. It is tempting to assume that a rational agent's credence function coheres in a certain way with his or her knowledge of these opaque propositions, and I call this the ‘Opaque Proposition Principle’. The principle is compelling but demonstrably false. I explain this incongruity by showing that the principle is ambiguous: the term ‘know’ as it appears in the principle can be interpreted in two different ways, as either basic-know or super-know. I use this distinction to construct a plausible version of the principle, and then to similarly construct plausible versions of the Reflection Principle and the Sure-Thing Principle.

Abstract

Not only has the philosophical debate on causation been gaining ground in the last few decades, but it has also increasingly addressed the sciences. The biomedical sciences are among the most prominent fields that have been considered, with a number of works tackling the understanding of the notion of cause, the assessment of genuinely causal relations and the use of causal knowledge in applied contexts. Far from denying the merits of the debate on causation and the major theories it comprises, this paper is meant as a stimulus for theorists of causation in the philosophy of biomedicine, with a focus on clinical matters. Without aiming at putting forward an original theory of causation and starting from the narration of two actual but paradigmatic cases at the joints between biomedical research and clinical practice, we want to point out that some pathological situations addressed by molecular medicine actually prove resistant to (at least) some of our major epistemological accounts of causal explanation. Given this scenario, which is very frequent in our hospitals, our analysis aims to provide a stimulus for the debate among theorists of causation in biomedicine interested in real cases in science in practice. We believe that this might in turn encourage some more general rethinking of the complex intertwinement of science, philosophy of science and ethics, as well as of the role of philosophy of science for clinical medicine itself.

Abstract

Pre-natal genetic enhancement affords us unprecedented capacity to shape our skills, talents, appearance and perhaps subsequently the quality of our lives in terms of overall happiness, success and wellbeing. Despite its powerful appeal, some have raised important and equally persuasive concerns against genetic enhancement. Sandel has argued that compassion and humility, themselves grounded in the unpredictability of talents and skills, would be lost. Habermas has argued that genetically altered individuals will see their lives as dictated by their parents’ design and therefore will not acquire an appropriate self-understanding. How should we view enhancement efforts in light of these concerns? I propose that we begin by adopting a defeasibility stance. That is, I ask whether our belief that genetic enhancements serve in the best interests of the child is reason to genetically enhance, underscoring a sort of epistemic vulnerability. I utilize the epistemological notions of defeasible reasons, undercutting (also called undermining) and overriding (or rebutting) defeaters in order to better understand and systematically evaluate the force of such concerns. I argue that close examination of both objections using this framework shows that we have reason to enhance, a reason that is defeasible but as yet, undefeated.

Abstract

Judgment and Agency contains Sosa’s latest effort to explain how higher epistemic value of the sort missing from an unwitting clairvoyant’s beliefs might be a special case of performance normativity, with its superior value following from truisms about performance value. This paper argues that the new effort rests on mistaken assumptions about performance normativity. Once these mistaken assumptions are exposed, it becomes clear that higher epistemic value cannot be a mere special case of performance normativity, and its superiority cannot be guaranteed just by truisms about performance value. Sections 1 and 2 set the stage, clarifying the thesis and the relevant features of Sosa’s strategy, and explaining why the strategy requires the mistaken assumptions. Section 3 presents a dilemma for the new account of higher epistemic value. Section 4 deepens the case for one of the horns. Section 5 takes stock and draws some broader morals.

Abstract

Systematicity theory—developed and articulated by Paul Hoyningen-Huene—and scientific realism constitute separate encompassing and empirical accounts of the nature of science. Standard scientific realism asserts the axiological thesis that science seeks truth and the epistemological thesis that we can justifiably believe our successful theories at least approximate that aim. By contrast, questions pertaining to truth are left “outside” systematicity theory’s “intended scope” (21); the scientific realism debate is “simply not” its “focus” (173). However, given the continued centrality of that debate in the general philosophy of science literature, and given that scientific realists also endeavor to provide an encompassing empirical account of science, I suggest that these two contemporary accounts have much to offer one another. Overlap for launching a discussion of their relations can be found in Nicholas Rescher’s work. Following through on a hint from Rescher, I embrace a non-epistemic, purely axiological scientific realism—what I have called, Socratic scientific realism. And, bracketing the realist’s epistemological thesis, I put forward the axiological tenet of scientific realism as a needed supplement to systematicity theory. There are two broad components to doing this. First, I seek to make clear that axiological realism and systematicity theory accord with one another. Toward that end, after addressing Hoyningen-Huene’s concerns about axiological analysis, I articulate a refined axiological realist meta-hypothesis: it is, in short, that the end toward which scientific inquiry is directed is an increase in a specific subclass of true claims. I then identify a key feature of scientific inquiry, not generally flagged explicitly, that I take to stand as shared terrain for the two empirical meta-hypotheses. And I argue that this feature can be informatively accounted for by my axiological meta-hypothesis. The second broad component goes beyond mere compatibility between the two positions: I argue that, in want of a systematic account of science, we are prompted to find an end toward which scientific inquiry is directed that is deeper than what systematicity theory offers. Specifically, I argue that my refined axiological realist meta-hypothesis is required to both explain and justify key dimensions of systematicity in science. To the quick question, what is it that the scientific enterprise is systematically doing? My quick answer is that it is systematically seeking to increase a particular subclass of true claims.

Abstract

We may try to explain proofs as chains of valid inference, but the concept of validity needed in such an explanation cannot be the traditional one. For an inference to be legitimate in a proof it must have sufficient epistemic power, so that the proof really justifies its final conclusion. However, the epistemic concepts used to account for this power are in their turn usually explained in terms of the concept of proof. To get out of this circle we may consider an idea within intuitionism about what it is to justify the assertion of a proposition. It depends on Heyting’s view of the meaning of a proposition, but does not presuppose the concept of inference or of proof as chains of inferences. I discuss this idea and what is required in order to use it for an adequate notion of valid inference.

Abstract

In a series of papers, Jesper Kallestrup and Duncan Pritchard argue that the thesis that knowledge is a cognitive success because of cognitive ability (robust virtue epistemology) is incompatible with the idea that whether or not an agent’s true belief amounts to knowledge can significantly depend upon factors beyond her cognitive agency (epistemic dependence). In particular, certain purely modal facts seem to preclude knowledge, while the contribution of other agents’ cognitive abilities seems to enable it. Kallestrup and Pritchard’s arguments are targeted against views that hold that all it takes to manifest one’s cognitive agency is to properly exercise one’s belief-forming abilities. I offer an account of the notion of cognitive ability according to which our epistemic resources are not exhausted by abilities to produce true beliefs as outputs, but also include dispositions to stop belief-formation when actual or modal circumstances are not suitable for it (precautionary cognitive abilities). Knowledge, I argue, can be accordingly conceived as a cognitive success that is also due to the latter. The resulting version of robust virtue epistemology helps explain how purely modal facts as well as other agents’ cognitive abilities may have a bearing on the manifestation of one’s cognitive agency, which shows in turn that robust virtue epistemology and epistemic dependence are not incompatible after all.

Abstract

Two different programmes are in the business of explicating accuracythe truthlikeness programme and the epistemic utility programme. Both assume that truth is the goal of inquiry, and that among inquiries that fall short of realizing the goal some get closer to it than others. TL theorists have been searching for an account of the accuracy of propositions. Epistemic utility theorists have been searching for an account of the accuracy of credal states. Both assume we can make cognitive progress in an inquiry even while falling short of the target. I show that the prospects for combining these two programmes are bleak. A core accuracy principle, Proximity, that is universally embraced within the Truthlikeness programme turns out to be incompatible with a central principle within the Epistemic Utility programme, namely propriety.

Abstract

Abstract. We consider how an epistemic network might self-assemble from the ritualization of the individual decisions of simple heterogeneous agents. In such evolved social networks, inquirers may be significantly more successful than they could be investigating nature on their own. The evolved network may also dramatically lower the epistemic risk faced by even the most talented inquirers. We consider networks that self-assemble in the context of both perfect and imperfect communication and compare the behaviour of inquirers in each. This provides a step in bringing together two new and developing research programs, the theory of self-assembling games and the theory of network epistemology.

Abstract

In this paper I will argue that the gender properties expressed by human voices are part of auditory phenomenology. I will support this claim by investigating auditory adaptational effects on such properties and contrasting auditory experiences, before and after the adaptational effects take place. In light of this investigation, I will conclude that auditory experience is not limited to low-level properties. Perception appears to be much more informative about the auditory landscape than is commonly thought.

Outcomes of 23- and 24-weeks gestation infants in Wellington, New Zealand: A single centre experience

Scientific Reports, Published online: 6 October 2017; doi:10.1038/s41598-017-12911-5

Abstract

Clinical diagnostic medicine is an experimental science based on observation, hypothesis making, and testing. It is an use dynamic process that involves observation and summary, diagnostic conjectures, testing, review, observation and summary, new or revised conjectures, i.e. it is an iterative process. It can then be said that diagnostic hypotheses are also ‘observation-laden’. My aim is to enlarge on the strategies of medical diagnosis as these are meshed in training and clinical experience—that is, to describe the patterns of reasoning used by experienced clinicians under different diagnostic circumstances and how these patterns of inquiry allow further insight into the evaluation and treatment of patients. I do not aim to present a theory and illustrate it with examples; I wish rather am to let a realistic example, similar to actual clinical scenarios, direct the exposition. To this end, I introduce an account of medical diagnosis—briefly comparing and contrasting it to other accounts—in order to focus on discussing the process of diagnosis through a detailed clinical case.

People have been found to experience stronger side effects when a treatment looks more expensive, according to a study of the nocebo effect

Abstract

This paper explicates and defends some of William James' more controversial claims in ‘The Will to Believe’. After showing some of the weaknesses in standard interpretations of James' position, I turn to James'Principles of Psychology and The Varieties of Religious Experience to spell out in more detail James' account of the nature of the attitudes of belief, doubt, and disbelief and link them to an account of the subject. In so doing, the moral force of the argument comes to the fore by casting the question ‘Can we believe at will?’ in a new light. Through a discussion of the conversion experiences of The Varieties of Religious Experience and the kinds of self-transformations in which beliefs that once appeared dead become live (or vice versa) that appear throughout James' psychology, the moral urgency of James' position in ‘The Will to Believe’ is clarified.

In a new study in Restorative Neurology and Neuroscience, investigators analyzed learning on two different types of video games – action and strategy – to determine if they were functionally different. They found that cognitive performance and white matter connectivity in the brain predicted how best we can learn to play the two types of games.

Researchers discovered unique results from each type of game. Specifically, they found that processing speed and white matter connectivity in a brain region related to memory were linked to learning to play the strategy game, while learning to play the action game was related to a brain region governing mood. Both genres of game lead to better performance on tasks having to do with working memory. They also found that improved performance on a speed task was unique to subjects playing the strategy game.

“When researchers use video games as a tool for cognitive enhancement, they assume that game performance relies on specific cognitive/brain function, yet there is a little evidence that establishes such a connection,” explained lead investigator Chandramallika Basak, PhD, Assistant Professor at The Center for Vital Longevity, University of Texas at Dallas. “Moreover, different researchers use different genres of video games, which makes this game-cognition-brain relationship even more complicated. Therefore, the aim of our study was not only to evaluate the three-way game-cognition-brain relationship, but also to assess this relationship for two different types of games.”

Adults of varying ages were recruited for the study, but all had little to no previous game playing experience. Subjects underwent an MRI scan and then were asked to play two different games, one action game (Tank Attack 3D) and one strategy game (Sushi-Go-Round). To measure white matter integrity, researchers used fractional anisotropy (FA), obtained by diffusion tensor imaging (DTI).

Working memory and inhibition predicted learning of both games, but better performance on the perceptual speed task was related only to the strategy game. The DTI results revealed key differences between the two genres of game: white matter FA in the right fornix/stria terminalis correlated with the action game learning and white matter FA in the left cingulum/hippocampus was related to the strategy game learning, even after controlling for age in both cases.

“Although cognition, to a large extent, was a common predictor of both types of game learning, regional white matter FA could separately predict action and strategy game learning,” said Dr. Basak. “Given the neural and cognitive correlates of strategy game learning, strategy games may provide a more beneficial training tool for adults suffering from memory-related disorders or declines in processing speed.”

While researchers found that playing strategy games better engaged memory and cognitive control brain regions, making them better suited for improving memory tasks, they hypothesize that action games that stimulate the limbic area and elicit more emotional arousal might be beneficial for other clinical populations like patients with mood disorders.

 

White matter integrity of different brain regions uniquely predicts action (in orange) vs strategy game (in green) learning (credit: Chandramallika Basak and Nicholas Ray).

 

Video games will continue to be the subject of scrutiny, both scientifically and societally, but investigators hope that this study opens the door to thinking about the nuances of different types of games. “Not all games are created equal, yet people generalize results from one video game to other video games,” concluded Dr. Basak. “Such oversimplification has serious consequences on research on video game training. I believe that we need to investigate the specific brain-cognition associations for different genres of video games before theorizing about the potential impact of a training on a particular genre of video game.”

###

NOTES FOR EDITORS
Full study: “Evaluating the relationship between white matter integrity, cognition, and varieties of video game learning,” by Nicholas R. Ray, Margaret A. O’Connell, Kaoru Nashiro, Evan T. Smith, Shuo Qin, and Chandramallika Basak. Published online in advance of Restorative Neurology and Neuroscience, Volume 35, Issue 5 (October 2017), DOI 10.3233/RNN-160716, by IOS Press.

This project was supported in part by funding provided to Dr. Chandramallika Basak by the Darrell K Royal Research Fund for Alzheimer’s Disease. We thank W. Christian Martin, Xi Chen, M. Irene Cunha, Melissa Druskis and Juan Mijares for assistance with data collection.

Contacts:
Full text of the article is available to credentialed journalists upon request. Contact Diana Murray, IOS Press at +1 718-640-5678 ord.murray@iospress.com.
Journalists wishing to interview the authors should contact Chandramallika Basak at cbasak@utdallas.edu.

ABOUT RESTORATIVE NEUROLOGY AND NEUROSCIENCE
An interdisciplinary journal under the editorial leadership of Bernhard Sabel, PhD, Restorative Neurology and Neuroscience publishes papers relating the plasticity and response of the nervous system to accidental or experimental injuries and their interventions, transplantation, neurodegenerative disorders and experimental strategies to improve regeneration or functional recovery and rehabilitation. Experimental and clinical research papers adopting fresh conceptual approaches are encouraged. The overriding criteria for publication are novelty, significant experimental or clinical relevance and interest to a multidisciplinary audience. www.iospress.nl/journal/restorative-neurology- and-neuroscience

RNN Editorial Office:
Prof. Dr. Bernhard Sabel
Institut für Medizinische Psychologie
Medizinische Fakultät
Otto-v.- Guericke Universität Magdeburg
39120 Magdeburg
Germany
T: +49 391 672 1800
E: rnn@med.ovgu.de

ABOUT IOS PRESS
Celebrating its 30th anniversary in 2017, IOS Press (www.iospress.com) is headquartered in Amsterdam with satellite offices in the USA, Germany, India and China and serves the information needs of scientific and medical communities worldwide. IOS Press now publishes over 100 international journals and about 75 book titles each year on subjects ranging from computer sciences and mathematics to medicine and the natural sciences.

Background

Altered autobiographical memory (ABM) functioning has been implicated in the pathogenesis of depression and post-traumatic stress disorder and may represent one mechanism by which childhood maltreatment elevates psychiatric risk.

Aims

To investigate the impact of childhood maltreatment on ABM functioning.

Method

Thirty-four children with documented maltreatment and 33 matched controls recalled specific ABMs in response to emotionally valenced cue words during functional magnetic resonance imaging.

Results

Children with maltreatment experience showed reduced hippocampal and increased middle temporal and parahippocampal activation during positive ABM recall compared with peers. During negative ABM recall they exhibited increased amygdala activation, and greater amygdala connectivity with the salience network.

Conclusions

Childhood maltreatment is associated with altered ABM functioning, specifically reduced activation in areas encoding specification of positive memories, and greater activation of the salience network for negative memories. This pattern may confer latent vulnerability to future depression and post-traumatic stress disorder.

Like fingerprints and facial recognition, the shape and beat of your heart can be used to verify your identity. Christopher Intagliata reports.-- Read more on ScientificAmerican.com

An obscure drug, oxiracetam, seems to boost the brain's blood supply and reduce cognitive deficits caused by altitude, according to a study at 4000 metres
 

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 Human Brain Mapping

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COVER ILLUSTRATION: Brain connectivity in pre and post sleep onset conditions at sigma band.

Drive and Reinforcement Circuitry in the Brain: Origins, Neurotransmitters, and Projection Fields

Neuropsychopharmacology, Published online: 6 October 2017;doi:10.1038/npp.2017.228

Cell division and differentiation depend on massive and rapid organelle remodeling. The mitotic oscillator, centered on the Cdk1-APC/C axis, spatiotemporally coordinates this reorganization in dividing cells. Here, we discovered that non-dividing cells could also implement this mitotic clock-like regulatory circuit to orchestrate subcellular reorganization associated with differentiation. We probed centriole amplification in differentiating mouse brain multiciliated cells. These post-mitotic progenitors fine-tuned mitotic oscillator activity to drive the orderly progression of centriole production, maturation and motile ciliation while avoiding the mitosis commitment threshold. Insufficient Cdk1 activity hindered differentiation, whereas excessive activity accelerated differentiation yet drove post-mitotic progenitors into mitosis. Thus, post-mitotic cells can redeploy and calibrate the mitotic oscillator to uncouple cytoplasmic from nuclear dynamics for organelle remodeling associated with differentiation.

The stereotyped spatial architecture of the brain is both beautiful and fundamentally related to its function, extending from gross morphology to individual neuron types, where soma position, dendritic architecture, and axonal projections determine their roles in functional circuitry. Our understanding of the cell types that make up the brain is rapidly accelerating, driven in particular by recent advances in single-cell transcriptomics. However, understanding brain function, development, and disease will require linking molecular cell types to morphological, physiological, and behavioral correlates. Emerging spatially resolved transcriptomic methods promise to fill this gap by localizing molecularly defined cell types in tissues, with simultaneous detection of morphology, activity, or connectivity. Here, we review the requirements for spatial transcriptomic methods toward these goals, consider the challenges ahead, and describe promising applications.

Value information about a drug, such as the price tag, can strongly affect its therapeutic effect. We discovered that value information influences adverse treatment outcomes in humans even in the absence of an active substance. Labeling an inert treatment as expensive medication led to stronger nocebo hyperalgesia than labeling it as cheap medication. This effect was mediated by neural interactions between cortex, brainstem, and spinal cord. In particular, activity in the prefrontal cortex mediated the effect of value on nocebo hyperalgesia. Value furthermore modulated coupling between prefrontal areas, brainstem, and spinal cord, which might represent a flexible mechanism through which higher-cognitive representations, such as value, can modulate early pain processing.

Abstract

Advances in neuroimaging have enabled the mapping of white matter connections across the entire brain, allowing for a more thorough examination of the extent of white matter disconnection after stroke. To assess how cortical disconnection contributes to motor impairments, we examined the relationship between structural brain connectivity and upper and lower extremity motor function in individuals with chronic stroke. Forty-three participants [mean age: 59.7 (±11.2) years; time poststroke: 64.4 (±58.8) months] underwent clinical motor assessments and MRI scanning. Nonparametric correlation analyses were performed to examine the relationship between structural connectivity amid a subsection of the motor network and upper/lower extremity motor function. Standard multiple linear regression analyses were performed to examine the relationship between cortical necrosis and disconnection of three main cortical areas of motor control [primary motor cortex (M1), premotor cortex (PMC), and supplementary motor area (SMA)] and motor function. Anatomical connectivity between ipsilesional M1/SMA and the (1) cerebral peduncle, (2) thalamus, and (3) red nucleus were significantly correlated with upper and lower extremity motor performance (P ≤ 0.003). M1–M1 interhemispheric connectivity was also significantly correlated with gross manual dexterity of the affected upper extremity (P = 0.001). Regression models with M1 lesion load and M1 disconnection (adjusted for time poststroke) explained a significant amount of variance in upper extremity motor performance (R2 = 0.36–0.46) and gait speed (R2 = 0.46), with M1 disconnection an independent predictor of motor performance. Cortical disconnection, especially of ipsilesional M1, could significantly contribute to variability seen in locomotor and upper extremity motor function and recovery in chronic stroke. Hum Brain Mapp, 2017. © 2017 Wiley Periodicals, Inc.

Abstract

Parkinsons disease is a neurodegenerative disorder characterized by nigrostriatal dopamine depletion. Previous studies measuring spontaneous brain activity using resting state functional magnetic resonance imaging have reported abnormal changes in broadly distributed whole-brain networks. Although resting state functional connectivity, estimating temporal correlations between brain regions, is measured with the assumption that intrinsic fluctuations throughout the scan are stable, dynamic changes of functional connectivity have recently been suggested to reflect aspects of functional capacity of neural systems, and thus may serve as biomarkers of disease. The present work is the first study to investigate the dynamic functional connectivity in patients with Parkinsons disease, with a focus on the temporal properties of functional connectivity states as well as the variability of network topological organization using resting state functional magnetic resonance imaging. Thirty-one Parkinsons disease patients and 23 healthy controls were studied using group spatial independent component analysis, a sliding windows approach, and graph-theory methods. The dynamic functional connectivity analyses suggested two discrete connectivity configurations: a more frequent, sparsely connected within-network state (State I) and a less frequent, more strongly interconnected between-network state (State II). In patients with Parkinsons disease, the occurrence of the sparsely connected State I dropped by 12.62%, while the expression of the more strongly interconnected State II increased by the same amount. This was consistent with the altered temporal properties of the dynamic functional connectivity characterized by a shortening of the dwell time of State I and by a proportional increase of the dwell time pattern in State II. These changes are suggestive of a reduction in functional segregation among networks and are correlated with the clinical severity of Parkinsons disease symptoms. Additionally, there was a higher variability in the network global efficiency, suggesting an abnormal global integration of the brain networks. The altered functional segregation and abnormal global integration in brain networks confirmed the vulnerability of functional connectivity networks in Parkinsons disease.

Just like physical exercise, the kind of improvements you get with meditation depend on exactly how you train
We don’t know much about the genetic evolution of the human brain. Now experiments suggest genes involved in cell stickiness may have given our brain its folds
For the first time, scans of sleeping people have shown how memories are moved in the brain, and suggest that the first hours of shut-eye are key for memory

FKBP5 Moderates the Association between Antenatal Maternal Depressive Symptoms and Neonatal Brain Morphology

Neuropsychopharmacology, Published online: 3 October 2017;doi:10.1038/npp.2017.232

Abstract

Glioblastoma are highly aggressive brain tumours that are associated with an extremely poor prognosis. Within these tumours exists a subpopulation of highly plastic self-renewing cancer cells that retain the ability to expand ex vivo as tumourspheres, induce tumour growth in mice, and have been implicated in radio- and chemo-resistance. Although their identity and fate are regulated by external cues emanating from endothelial cells, the nature of such signals remains unknown. Here, we used a mass spectrometry proteomic approach to characterize the factors released by brain endothelial cells. We report the identification of the vasoactive peptide apelin as a central regulator for endothelial-mediated maintenance of glioblastoma patient-derived cells with stem-like properties. Genetic and pharmacological targeting of apelin cognate receptor abrogates apelin- and endothelial-mediated expansion of glioblastoma patient-derived cells with stem-like properties in vitro and suppresses tumour growth in vivo. Functionally, selective competitive antagonists of apelin receptor were shown to be safe and effective in reducing tumour expansion and lengthening the survival of intracranially xenografted mice. Therefore, the apelin/apelin receptor signalling nexus may operate as a paracrine signal that sustains tumour cell expansion and progression, suggesting that apelin is a druggable factor in glioblastoma.

Abstract

An underlying assumption in computational approaches in cognitive and brain sciences is that the nervous system is an input–output model of the world: Its input–output functions mirror certain relations in the target domains. I argue that the input–output modelling assumption plays distinct methodological and explanatory roles. Methodologically, input–output modelling serves to discover the computed function from environmental cues. Explanatorily, input–output modelling serves to account for the appropriateness of the computed function to the explanandum information-processing task. I compare very briefly the modelling explanation to mechanistic and optimality explanations, noting that in both cases the explanations can be seen as complementary rather than contrastive or competing.

A graphic from the Scientific American archive provides a look into the brain’s molecular clock—research that contributed to this year’s Nobel Prize in Physiology or Medicine-- Read more on ScientificAmerican.com

      

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In a new study in Restorative Neurology and Neuroscience, investigators analyzed learning on two different types of video games – action and strategy – to determine if they were functionally different. They found that cognitive performance and white matter connectivity in the brain predicted how best we can learn to play the two types of games.

Researchers discovered unique results from each type of game. Specifically, they found that processing speed and white matter connectivity in a brain region related to memory were linked to learning to play the strategy game, while learning to play the action game was related to a brain region governing mood. Both genres of game lead to better performance on tasks having to do with working memory. They also found that improved performance on a speed task was unique to subjects playing the strategy game.

“When researchers use video games as a tool for cognitive enhancement, they assume that game performance relies on specific cognitive/brain function, yet there is a little evidence that establishes such a connection,” explained lead investigator Chandramallika Basak, PhD, Assistant Professor at The Center for Vital Longevity, University of Texas at Dallas. “Moreover, different researchers use different genres of video games, which makes this game-cognition-brain relationship even more complicated. Therefore, the aim of our study was not only to evaluate the three-way game-cognition-brain relationship, but also to assess this relationship for two different types of games.”

Adults of varying ages were recruited for the study, but all had little to no previous game playing experience. Subjects underwent an MRI scan and then were asked to play two different games, one action game (Tank Attack 3D) and one strategy game (Sushi-Go-Round). To measure white matter integrity, researchers used fractional anisotropy (FA), obtained by diffusion tensor imaging (DTI).

Working memory and inhibition predicted learning of both games, but better performance on the perceptual speed task was related only to the strategy game. The DTI results revealed key differences between the two genres of game: white matter FA in the right fornix/stria terminalis correlated with the action game learning and white matter FA in the left cingulum/hippocampus was related to the strategy game learning, even after controlling for age in both cases.

“Although cognition, to a large extent, was a common predictor of both types of game learning, regional white matter FA could separately predict action and strategy game learning,” said Dr. Basak. “Given the neural and cognitive correlates of strategy game learning, strategy games may provide a more beneficial training tool for adults suffering from memory-related disorders or declines in processing speed.”

While researchers found that playing strategy games better engaged memory and cognitive control brain regions, making them better suited for improving memory tasks, they hypothesize that action games that stimulate the limbic area and elicit more emotional arousal might be beneficial for other clinical populations like patients with mood disorders.

 

White matter integrity of different brain regions uniquely predicts action (in orange) vs strategy game (in green) learning (credit: Chandramallika Basak and Nicholas Ray).

 

Video games will continue to be the subject of scrutiny, both scientifically and societally, but investigators hope that this study opens the door to thinking about the nuances of different types of games. “Not all games are created equal, yet people generalize results from one video game to other video games,” concluded Dr. Basak. “Such oversimplification has serious consequences on research on video game training. I believe that we need to investigate the specific brain-cognition associations for different genres of video games before theorizing about the potential impact of a training on a particular genre of video game.”

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NOTES FOR EDITORS
Full study: “Evaluating the relationship between white matter integrity, cognition, and varieties of video game learning,” by Nicholas R. Ray, Margaret A. O’Connell, Kaoru Nashiro, Evan T. Smith, Shuo Qin, and Chandramallika Basak. Published online in advance of Restorative Neurology and Neuroscience, Volume 35, Issue 5 (October 2017), DOI 10.3233/RNN-160716, by IOS Press.

This project was supported in part by funding provided to Dr. Chandramallika Basak by the Darrell K Royal Research Fund for Alzheimer’s Disease. We thank W. Christian Martin, Xi Chen, M. Irene Cunha, Melissa Druskis and Juan Mijares for assistance with data collection.

Contacts:
Full text of the article is available to credentialed journalists upon request. Contact Diana Murray, IOS Press at +1 718-640-5678 ord.murray@iospress.com.
Journalists wishing to interview the authors should contact Chandramallika Basak at cbasak@utdallas.edu.

ABOUT RESTORATIVE NEUROLOGY AND NEUROSCIENCE
An interdisciplinary journal under the editorial leadership of Bernhard Sabel, PhD, Restorative Neurology and Neuroscience publishes papers relating the plasticity and response of the nervous system to accidental or experimental injuries and their interventions, transplantation, neurodegenerative disorders and experimental strategies to improve regeneration or functional recovery and rehabilitation. Experimental and clinical research papers adopting fresh conceptual approaches are encouraged. The overriding criteria for publication are novelty, significant experimental or clinical relevance and interest to a multidisciplinary audience. www.iospress.nl/journal/restorative-neurology- and-neuroscience

RNN Editorial Office:
Prof. Dr. Bernhard Sabel
Institut für Medizinische Psychologie
Medizinische Fakultät
Otto-v.- Guericke Universität Magdeburg
39120 Magdeburg
Germany
T: +49 391 672 1800
E: rnn@med.ovgu.de

ABOUT IOS PRESS
Celebrating its 30th anniversary in 2017, IOS Press (www.iospress.com) is headquartered in Amsterdam with satellite offices in the USA, Germany, India and China and serves the information needs of scientific and medical communities worldwide. IOS Press now publishes over 100 international journals and about 75 book titles each year on subjects ranging from computer sciences and mathematics to medicine and the natural sciences.

In this issue, Falkenberg et al explore the practicability of magnetic resonance imaging (MRI) as part of the initial clinical assessment in patients with first-episode psychosis and the prevalence, nature and clinical significance of radiological abnormalities in these patients. They provide evidence for the use of MRI data to detect gross brain abnormalities. In addition, improvements in quantitative analyses makes MRI an indispensable tool to elucidate the neurobiological substrates that might underlie primary (or idiopathic) psychotic illness.

Neuroscientist based at Yale in 1960s controlled bulls, monkeys and humans with brain implants and envisioned a “psychocivilized society”-- Read more on ScientificAmerican.com

      

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Abstract

Repeated practice of a specific task can improve visual performance, but the neural mechanisms underlying this improvement in performance are not yet well understood. Here we trained healthy participants on a visual motion task daily for 5 days in one visual hemifield. Before and after training, we used functional magnetic resonance imaging (fMRI) to measure the change in neural activity. We also imaged a control group of participants on two occasions who did not receive any task training. While in the MRI scanner, all participants completed the motion task in the trained and untrained visual hemifields separately. Following training, participants improved their ability to discriminate motion direction in the trained hemifield and, to a lesser extent, in the untrained hemifield. The amount of task learning correlated positively with the change in activity in the medial superior temporal (MST) area. MST is the anterior portion of the human motion complex (hMT+). MST changes were localized to the hemisphere contralateral to the region of the visual field, where perceptual training was delivered. Visual areas V2 and V3a showed an increase in activity between the first and second scan in the training group, but this was not correlated with performance. The contralateral anterior hippocampus and bilateral dorsolateral prefrontal cortex (DLPFC) and frontal pole showed changes in neural activity that also correlated with the amount of task learning. These findings emphasize the importance of MST in perceptual learning of a visual motion task. Hum Brain Mapp, 2017. © 2017 The Authors Human Brain Mapping Published by Wiley Periodicals, Inc.

Abstract

Partial visual deprivation from early monocular enucleation (the surgical removal of one eye within the first few years of life) results in a number of long-term morphological adaptations in adult cortical and subcortical visual, auditory, and multisensory brain regions. In this study, we investigated whether early monocular enucleation also results in the altered development of white matter structure. Diffusion tensor imaging and probabilistic tractography were performed to assess potential differences in visual system white matter in adult participants who had undergone early monocular enucleation compared to binocularly intact controls. To examine the microstructural properties of these tracts, mean diffusion parameters including fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD) were extracted bilaterally. Asymmetries opposite to those observed in controls were found for FA, MD, and RD in the optic radiations, the projections from primary visual cortex (V1) to the lateral geniculate nucleus (LGN), and the interhemispheric V1 projections of early monocular enucleation participants. Early monocular enucleation was also associated with significantly lower FA bidirectionally in the interhemispheric V1 projections. These differences were consistently greater for the tracts contralateral to the enucleated eye, and are consistent with the asymmetric LGN volumes and optic tract diameters previously demonstrated in this group of participants. Overall, these results indicate that early monocular enucleation has long-term effects on white matter structure in the visual pathway that results in reduced fiber organization in tracts contralateral to the enucleated eye. Hum Brain Mapp, 2017. © 2017 Wiley Periodicals, Inc.

Abstract

Mirror movements (MM) might be observed in congenital and acquired neurodegenerative conditions but their anatomic-functional underpinnings are still largely elusive.

This study investigated the spectral changes of resting-state functional connectivity in Kallmann Syndrome (hypogonadotropic hypogonadism with hypo/anosmia with or without congenital MM) searching for insights into the phenomenon of MM.

Forty-four Kallmann syndrome patients (21 with MM) and 24 healthy control subjects underwent task (finger tapping) and resting-state functional MRI. The spatial pattern of task-related activations was used to mask regions and select putative motor networks in a spatially independent component analysis of resting-state signals. For each resting-state independent component time-course power spectrum, we extracted the relative contribution of four separate bands: slow-5 (0.01–0.027 Hz), slow-4 (0.027–0.073 Hz), slow-3 (0.073–0.198 Hz), slow-2 (0.198–0.25 Hz), and analyzed the variance between groups.

For the sensorimotor network, the analysis revealed a significant group by frequency interaction (P = 0.002) pointing to a frequency shift in the spectral content among subgroups with lower slow-5 band and higher slow-3 band contribution in Kallmann patients with MM versus controls (P = 0.028) and with lower slow-5 band contribution between patients with and without MM (P = 0.057). In specific regions, as obtained from hand motor activation task analysis, spectral analyses demonstrated a lower slow-5 band contribution in Kallmann patients with MM versus both controls and patients without MM (P < 0.05).

In Kallmann syndrome, the peculiar phenomenon of bimanual synkinesis is associated at rest with regionally and spectrally selective functional connectivity changes pointing to a distinctive cortical and subcortical functional reorganization. Hum Brain Mapp, 2017. © 2017 Wiley Periodicals, Inc.

Retrograde semaphorin–plexin signalling drives homeostatic synaptic plasticity

Nature 550, 7674 (2017). doi:10.1038/nature24017

Authors: Brian O. Orr, Richard D. Fetter & Graeme W. Davis

Homeostatic signalling systems ensure stable but flexible neural activity and animal behaviour. Presynaptic homeostatic plasticity is a conserved form of neuronal homeostatic signalling that is observed in organisms ranging from Drosophila to human. Defining the underlying molecular mechanisms of neuronal homeostatic signalling will be essential in order to establish clear connections to the causes and progression of neurological disease. During neural development, semaphorin–plexin signalling instructs axon guidance and neuronal morphogenesis. However, semaphorins and plexins are also expressed in the adult brain. Here we show that semaphorin 2b (Sema2b) is a target-derived signal that acts upon presynaptic plexin B (PlexB) receptors to mediate the retrograde, homeostatic control of presynaptic neurotransmitter release at the neuromuscular junction in Drosophila. Further, we show that Sema2b–PlexB signalling regulates presynaptic homeostatic plasticity through the cytoplasmic protein Mical and the oxoreductase-dependent control of presynaptic actin. We propose that semaphorin–plexin signalling is an essential platform for the stabilization of synaptic transmission throughout the developing and mature nervous system. These findings may be relevant to the aetiology and treatment of diverse neurological and psychiatric diseases that are characterized by altered or inappropriate neural function and behaviour.

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