When you hold in mind a sentence you have just read or a phone number you’re about to dial, you’re engaging a critical brain system known as working memory. For the past several decades, neuroscientists have believed that as information is held in working memory, brain cells associated with that information fire continuously. However, a new study from MIT has upended that theory, instead finding that as information is held in working memory, neurons fire in sporadic, coordinated bursts. These cyclical bursts could help the brain to hold multiple items in working memory at the same time, according to the
Development and Psychopathology – The theory of latent vulnerability: Reconceptualizing the link between childhood maltreatment and psychiatric disorder – Cambridge Journals Online
Letting structure emerge: connectionist and dynamical systems approaches to cognition – McCEtAl10TiCS_LettingStructureEmerge.pdf
Enhancing sleep after brain injury reduces brain damage, cognitive decline in rats — ScienceDaily
But logically, really, how can REC support a “replacement hypothesis”?
This the question that’s been pestering me for the past day or so.
Maybe I’m missing something here. That’s entirely possible. I’m no stranger to the concept of radical embodied cognition (REC). Although I’ve only recently come across this new approach to cognitive neuroscience, I’ve believed it for years. It’s how I’ve long understood much that I believe about the brain and its difficulties after concussion / mild TBI.
In short, I believe that a brain injury, no matter how initially mild, can unleash holy hell on the injured party — not due to the initial injury itself (though the axonal shearing / diffuse axonal injury and acute neurometabolic cascade don’t help matters any), but through the extended disruption of the overall “cognitive ecosystem” — a network which includes brain and body and external environment. Disruption to the external environment includes strained social connections, interruptions to interpersonal intimacies, as well as disruptions of the perceptual processes which enable cognitive contributions of brain and body.
So, REC really offers a fantastic scientific approach — with an emerging body of research (woot! woot!) to substantiate its claims.
So, I’ve been reading a bit about it. On Saturday, I read Andrew D. Wilson’s and Sabrina Golonka’s 2013 paper “Embodied cognition is not what you think it is” and I really enjoyed it – particularly the parts about REC discussing a replacement hypothesis of embodied cognition.
… if perception-action couplings and resources distributed over brain, body, and environment are substantial participants in cognition, then the need for the specific objects and processes of standard cognitive psychology (concepts, internally represented competence, and knowledge) goes away, to be replaced by very different objects and processes (most commonly perception-action couplings forming non-linear dynamical systems, e.g., van Gelder, 1995).
At first glance, it seemed to make sense. Standard cognitive explanations for behavior have never sufficed for me. They’ve always seemed to fall short — and I attributed that failing to their myopic avoidance of environmental interactions, including physiological ones.
But I’ve been puzzling for the past 24 hours about how REC can support a “replacement hypothesis”, where the representations and processes of the brain can be replaced by an embodied cognition approach.
If REC by definition involves the entire “cognitive ecosystem” of brain, body, and environment, how can we possibly get rid of the computational piece of neurological understanding? Seems to me, it’s part of it. And while I do believe we need to extend our understanding beyond the echo chamber of the representational view (which seems an echo chamber par excellence), I think that dismissing it outright and replacing it with something else actually costs us something valuable — something we can use.
The need to replace one theory with another strikes me as a bit too narrow. It’s territorial, and the either-or approach comes with a cost. It also provokes push-back from perfectly capable and skilled individuals, who could actually contribute their expertise and insights in a constructive way.
It makes no sense to me, to kick the cognitive psychology folks to the curb, when the areas they’re focusing on are actually part-and-parcel of the full cognitive ecosystem. Rather than excluding and narrowing, why not include and expand? There’s some seriously interesting work being done in a multitude of areas, and I believe if we follow them all to their logical conclusions, their findings can — and will — strengthen the whole, rather than limit it.
For my money, I think these theories can all strengthen and enrich each other. We don’t necessarily need to dismiss one to make room for the other. They can act like layers in a fine piece of laminated furniture — all the more beautiful for their contrasts. They can add much-needed dimensions to the discussion, covering similar territory in very different ways.
If our embodied cognition really consists of everything, how can we comfortably dismiss/replace anything?
Not just a floating brain: Action and Cognition Lab studies human body’s impact on visual perception
Radical embodied cognition can speak to a whole host of sticky issues with TBI and long-term PCS. More on this, in the coming days, weeks, months…
This is an excellent article – and it really helps explain certain mysteries of post-concussion issues. I’m thinking and writing a fair amount about this, these days, tying in “embodied cognition” with the neurofunctional pieces.
Essentially, embodied cognition approaches our cognition as a result of a combination of influences — from inside and outside the brain. There are a number of different “definitions” and approaches, but the one that makes the most sense to me actually replaces the brain-only / mind-only definition of cognition.
I believe that our brain and biology both affects things, and so does our environment. We’re in constant interaction with the world around us, and that interaction is at the heart of our cognitive process. We’re more than brains floating around inside skulls, making up images and meanings and metaphors about our world and where we fit, then acting accordingly. The world around us, in…
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Another way of understanding the effects of TBI?
A few months back, I stumbled upon the relatively new field of Radical Embodied Cognition / Cognitive Neuroscience. I have to say, it seems like an elegant extension to what we know. And the principles it discusses seem to quite usefully explain some of the more puzzling effects that arise from TBI – especially PCS.
I’m still learning, still reading, and still considering. But there are a number of areas where its tenets really fill in the blanks about how and why PCS and TBI can be so disruptive for so many — even in the absence of measurable neurological damage.
It’s very exciting, and I look forward to exploring this more in the coming weeks, months, and years.
Preventing PCS – What are We Waiting For?
I’ve been really bothered, over the past several months, about how we actually know what can mitigate and prevent PCS symptoms. We’ve known this for 10+ years. And yet, the consistent, systematic application of this knowledge has not been achieved at a national level.
PCS, once developed, is difficult to treat . . . Kelly  observed that post-concussional symptom rates were higher when patients were given no explanation for their symptoms. Minderhoud et al.  gave patients a manual that contained information about the nature, causes and expected course of recovery, advising that any symptoms could be expected to attenuate and gradually remit after an initial period of rest followed by gradual resumption of work or school. They evaluated the effectiveness of this information retrospectively and found that, compared to a control group, the patients had fewer symptoms 6 months post-trauma. Gronwall  reported a similar effect when a booklet about the symptoms of concussion and how to cope with them was given to mild head injured patients. At a 3 month follow-up, control subjects were nine times more likely to be symptomatic than patients who had received this type of information. Alves et al.  randomly assigned patients to treatment or control conditions. In the treatment condition, information was given about the nature and prognosis of mild head injury symptoms, with reassurance that recovery would be uncomplicated and complete. In contrast, controls were discharged with instructions to return to the emergency department in the event of persistent problems occurring. The treatment condition was associated with a lowering of the relative risk for persistent post-concussional symptoms at 6 months follow-up. [WOOD RL1: Understanding the ‘miserable minority’: a diasthesis-stress paradigm for post-concussional syndrome. Brain Inj. Nov;18(11):1135-53, 2004].
So, we know what can help.
But we’re not doing it all across the board. Some places do, with some hospitals offering booklets and info pamphlets. But it’s routine. It’s not a standard of care, apparently.
Seriously, people, it makes no sense for 10-15% of the population to be embarking on extended convoluted “adventures” of disconnection, dis-ability, and suffering, when something as basic as a booklet and reassurance from a trusted source / authority, has been clinically shown in multiple instances to reduce the incidence of post-concussive symptoms.
It boggles the mind. Information is so freely available, these days, and so readily accessible. Putting it into a format that’s easy to read and “digest” is not hard. We have legions of technical writers and infographic designers who can — and do — translate complex scientific information into bits that are accessible to everyday people. The general population is not only more comfortable than ever before with scientific information, but our ability to convey sophisticated material in a straightforward manner has improved by leaps and bounds since the 1996 Ruff paper — even the 2004 Wood paper.
So, what are we waiting for? PCS is no joke. And apparently, it’s at least partly preventable. It was in 2004, anyway. What are the chances that’s changed in 10 years? Maybe new information has come to light? Or maybe not. Maybe we’ve been so caught up in our brain injury awareness campaigns that focus on how horrible and life-threatening it can be, that we’ve completely skipped over the interim step of helping those who have been injured — and need additional interventions to keep from descending into the hell that post-concussion symptoms can bring.
Concussion and brain injury can never be completely avoided. It’s a fact of life, no matter how advanced our helmets and automotive restraint systems may be. You walk around on the earth, and you run the risk of hitting your head – hard – on something. Or getting hit, yourself, only to see your entire life change.
But the fact that education and information is prophylactic against PCS seems to have gotten lost in the narrative of How Horrible Traumatic Brain Injury Is. I hate to be cynical, but I can’t help but think it’s mighty hard to drum up legislation and financial support for an injury that can be mitigated by something as “simple” as a well-designed booklet, some honest professional reassurance, and a few weeks’ rest & recuperation. Stories of successful avoidance of PCS — and recovery from symptoms — don’t do much to fuel critical new developments in helmet design and rule changes. And it doesn’t encourage a change in behavior that steers us clear of risky choices and self-destructive actions. The Concussion Prevention Machine grinds on and on.
On the other hand, those who do get brain injured exist as evidence of our collective “failure” to protect each and every human being from concussion / brain injury. So that’s uncomfortable, and people would rather not think about it, frankly. They don’t want to talk about it — address it head-on, so to speak — because it implies a surrender to a condition that so much time and energy and re$ources are going into preventing.
And yet, our cynicism and fear and marketing campaigns obscure an serious interim neglect of acute issues. It’s a significant failing of our healthcare system and our society in general. Right in front of us are indications of a potential PCS solution we’ve been needing for years. And this approach may actually do some good. But what are we doing about it?
Not much constructive.
Here and there, yes. But not all across the board.
And that needs to change.
I believe it can. But we need to redirect the conversation away from the horror and towards constructive steps that actually do some good. The steps may not be dramatic and earth-shattering enough to make the front page or the evening news — or even everyone’s Facebook feed — but they can save lives, and save a whole lot of suffering in the meantime.
And I think that’s a goal worth pursuing.
Finding Opportunity – Using the legacy of Ruff’s 1996 “Miserable Minority” paper to stop PCS suffering
Several months back, I dove into literature around the so-called “Miserable Minority” (hereafter “MM”) of post-concussion syndrome sufferers whose symptoms resist treatment and drag on for months and years beyond the typical ~1-3 month window for concussion recovery. [LEVIN, H. S., MATTIS, S., RUFF, R. M. et al.: Neurobehavioral outcome following minor head injury: three-center study. Journal of Neurosurgery, 66, 234± 243, 1987.]
The 1996 paper [RUFF, CAMENZULI, MUELLER: Miserable minority: emotional risk factors that influence the outcome of a mild traumatic brain injury.
Brain Inj. Aug;10(8):551-65, 1996] which first introduced that catchy, alliterative MM moniker was written by a leading specialist in brain injury assessment who’s designed a number of neuropsychological tests. (I believe I’ve taken at least one of his tests — maybe more.)
It puzzled over the persistence of lingering, disruptive symptoms among some, while so many others recover and get on with their lives. It discussed how lingering issues “can represent one or more of the following factors: (1) neurogenic; (2) psychogenic; (3) co-morbid medical complications (i.e. neck injury, vestibular problems); or (4) financial gain.” [Ruff et. al.]
Further explanation focused on emotional risk factors, including:
- narcissistic features
- grandiosity and
- borderline personality traits
The MM term caught on, and it’s been frequently used in the press and clinical community for many years. It’s also infuriated a number of folks, as well as prompted professional calls for a reconsideration of its use.
I have a number of issues with this particular approach, and since the paper dates back some 20 years — predating all our current imaging techniques and technology which were once all but unthinkable — some have suggested it can be basically ignored.
The only problem is, the MM designation persists — not only in the press, but also in the minds of clinicians and experiences of concussed folks. And that’s maddening. No matter how updated our neuro knowledge may be, the media lags — and it’s always hungry for “bleeding” headlines which will tug at the heartstrings of potential readers/buyers of their various advertised goods. And references to the Miserable Minority have persisted.
I’d love to dismiss that whole conceptualization outright. Ruff et al’s pronouncements strike me as dismissive and condescending, not to mention a clear product of their times that lacked so much of the insight we’ve gained over the past two decades. Can’t we just flush it all, and get rid of that MM concept entirely?
But PCS is an enduring issue, and something really needs to be done — even if it’s only understanding the condition for what it is. And while I was exploring the associated literature further, another thread emerged from a 2004 paper [WOOD RL1: Understanding the ‘miserable minority’: a diasthesis-stress paradigm for post-concussional syndrome. Brain Inj. Nov;18(11):1135-53, 2004]. And this thread provides a glint of gold among the proverbial gravel that I’ve been panning.
So, what is that magical piece of the puzzle?
In the 2004 paper, Wood elaborates: (bold emphasis is mine),
PCS, once developed, is difficult to treat . . . Kelly  observed that post-concussional symptom rates were higher when patients were given no explanation for their symptoms. Minderhoud et al.  gave patients a manual that contained information about the nature, causes and expected course of recovery, advising that any symptoms could be expected to attenuate and gradually remit after an initial period of rest followed by gradual resumption of work or school. They evaluated the effectiveness of this information retrospectively and found that, compared to a control group, the patients had fewer symptoms 6 months post-trauma. Gronwall  reported a similar effect when a booklet about the symptoms of concussion and how to cope with them was given to mild head injured patients. At a 3 month follow-up, control subjects were nine times more likely to be symptomatic than patients who had received this type of information. Alves et al.  randomly assigned patients to treatment or control conditions. In the treatment condition, information was given about the nature and prognosis of mild head injury symptoms, with reassurance that recovery would be uncomplicated and complete. In contrast, controls were discharged with instructions to return to the emergency department in the event of persistent problems occurring. The treatment condition was associated with a lowering of the relative risk for persistent post-concussional symptoms at 6 months follow-up.
So, in a very real way, “the risks of vulnerable people developing a condition may be reduced if they are protected from certain stressors and helped to feel secure.” [Wood, 2004]
What a remarkable dichotomy — hidden within plain view, eclipsed by discussions on the debilitating long-term effects of concussion along with the psychological / emotional explanations, are indications of what actually prevents PCS. There are verified, official, documented references to what’s been clinically proven to alleviate symptoms and has correlated with improved outcomes after a mild traumatic brain injury.
And this begs the question:
Why THE HELL are we not using this information and putting it uniformly into practice to prevent – or at least mitigate – post-concussive issues?
It boggles the mind.
More on this later, but for now, let me just say that
- We have documented evidence that PCS is preventable – or can at least be mitigated. It’s been substantiated in at least three published papers – maybe more.
- We’ve had this information for years. 10 years, in fact.
- Unfortunately, the signposts to success have been overgrown by the conceptual jungle of emotional and psychological attributions that make PCS sufferers look like narcissistic, grandiose, attention-seeking malingerers just looking for a payout of some kind.
- The suffering continues. Needlessly
None of these are insurmountable, however. They’re problematic, but they can be overcome — with the right information and willingness to do what’s needed.
Just like PCS.
Modeling of Large-Scale Functional Brain Networks Based on Structural Connectivity from DTI: Comparison with EEG Derived Phase Coupling Networks and Evaluation of Alternative Methods along the Modeling Path
Here we use computational modeling of fast neural dynamics to explore the relationship between structural and functional coupling in a population of healthy subjects. We use DTI data to estimate structural connectivity and subsequently model phase couplings from band-limited oscillatory signals derived from multichannel EEG data. Our results show that about 23.4% of the variance in empirical networks of resting-state fast oscillations is explained by the underlying white matter architecture. By simulating functional connectivity using a simple reference model, the match between simulated and empirical functional connectivity further increases to 45.4%. In a second step, we use our modeling framework to explore several technical alternatives along the modeling path. First, we find that an augmentation of homotopic connections in the structural connectivity matrix improves the link to functional connectivity while a correction for fiber distance slightly decreases the performance of the model. Second, a more complex computational model based on Kuramoto oscillators leads to a slight improvement of the model fit. Third, we show that the comparison of modeled and empirical functional connectivity at source level is much more specific for the underlying structural connectivity. However, different source reconstruction algorithms gave comparable results. Of note, as the fourth finding, the model fit was much better if zero-phase lag components were preserved in the empirical functional connectome, indicating a considerable amount of functionally relevant synchrony taking place with near zero or zero-phase lag. The combination of the best performing alternatives at each stage in the pipeline results in a model that explains 54.4% of the variance in the empirical EEG functional connectivity. Our study shows that large-scale brain circuits of fast neural network synchrony strongly rely upon the structural connectome and simple computational models of neural activity can explain missing links in the structure-function relationship.