Plasticity: why the brain is not like computer hardware

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Brain cells and their connections are not static. The brain grows new cells, these form ever-changing networks, which are to a large extent the physical basis of our psychological and emotional lives. Learning and memory take place because of dynamic alterations in the strength of the connections between cells, the grouping of cells into networks and the connections between networks.

In one sense, biologists and psychologists have known about these changes for a long time, and the label “neuroplasticity” is just a new name for old ideas.

However, there is a change in emphasis that the term points to. In particular, evidence that adult brains grow brand new nerve cells was very much in doubt just ten or twenty years ago.

This and other developments have forced the textbooks to be rewritten. Scientists are also learning more details about changes that take place in the brain in response to healthy and harmful stimuli. Together, these new findings give us an updated picture of the brain as made of dynamic, “self organizing” sets of networks that grow new components and which change in response to stress, damage, learning and novelty.

Are we wired, like microchips, or are we made of something more complex?

Growth of a neuron over time from Wikimedia Commons

Unlike fixed, rigid computer electronics, brains are dynamic, can recover in response to trauma, and show the ability to change structure without losing function (“plasticity”).

A single mote of dust can ruin manufacture of a microprocessor. Circuits in electronic devices eventually fail and do not regenerate; they are replaced if hardware is to function properly. Yet the human brain, presented with stress or damage, can display amazing powers of self-organization, dynamism, response to change at different scales and the ability to “re-wire” itself.

Except that the brain has no wires. It is vastly more complex than any computer ever designed, and is the most complex system known to exist in nature.

Nowadays, one may still encounter the idea that the brain is “hard wired” to engage in language, face recognition, memory and so forth. Psychologists, neuroscientists and cognitive scientists emphasize these functions are innate and instinctual. This is not so much wrong as slightly misleading. We do have instincts and we did evolve to be good at certain tasks, but our brains are not fixed and unchanging the way a microchip is.

Where did the idea that the brain is “hard wired” come from?

Around the time of World War II and it’s immediate aftermath, when brilliant early computer scientists coaxed their whirring vacuum-tube machinery to solve complex mathematical problems, the idea that the brain was a sort of computer took hold. The finding that neurons are electrical and generate all-or-nothing binary-like bursts of current made the brain seem like nature’s version of an electronic computing device.

Over the decades, a different emphasis on how the brain works has emerged, especially in recent years. One still reads about humans being “hard wired” by our genes to do this and that, but an increasing number of researchers use the term “neuroplasticity” to refer to the way the brain responds to change.

Dr. Jill Kays and colleagues explain the shift in thinking that has occurred among scientists and clinicians:

“Until fairly recently, the adult brain was considered largely fixed and stable. Although it was accepted that changes occurred in the context of learning and memory, the general consensus was that major processes essential to normal brain development (e.g., generation of new neurons, neuron migration, pruning) ceased once full development was reached.”

Defining neuroplasticity

The brain’s 100 billion neurons grow into each other like bushes sharing the same space. The branches of the neurons connect with each other to form networks. Cells reach out to each other via electrochemical “synapses”, which are microscopic, fluid-filled connective zones.

A family of hormones called nerve growth factors are periodically released and bind to specialized protein structures called receptors. Growth factors enable nerve cells to persist and to dynamically respond to the changing chemical environment in human physiology. These are only one of a series of hormones that are released in response to new situations, emotionally significant experiences, stressful contexts, brain damage and more. Nothing of the sort occurs with microprocessors.

Like making a new friend that you start hearing from more and more, synaptic connections can grow stronger. Yet they also may weaken, if not used enough. The strengthening and weakening of connections over time, which form the cellular basis of learning and memory, show the brain to be quite unlike a microchip, which is utterly rigid and has fixed circuits.

One of the difficulties with the term “plasticity” is finding a workable definition. Dr. Christopher Shaw and colleagues in Toward a Theory of Neuroplasticity define it as “induced change in some property of the nervous system that results in a corresponding change in function and/or behavior”.

Plasticity refers to the range of changes that brain cells can generate as their physiochemical environments shift. However, neurons cannot handle stress beyond a certain point. For instance, traumatic brain injury can shear the long cable-like axons of brain cells, producing serious neurological damage, coma or even death.

The clinical relevance of neuroplasticity

In previous eras of neurology, psychology and medicine more broadly, it was believed that adults did not develop new neurons. This may seem a technical point of interest primarily to anatomists or physiologists, but it was consistent with a certain emphasis on how development is constrained by genetics, inheritance, and the pre-determined “hard wiring” of the brain.

Overall, the emerging view is one in which the brain is understood to self-organize based on genetic instructions, to grow new cells, to adapt to new conditions, to respond to damage by a sort of re-routing, thereby compensating for damage in one area though other networks taking over that function. A computer must be programmed by someone external to itself, but brains have genetic instructions that allow it to “self-organize”, to grow and to make new connections.

Stress, trauma as well as learning and novelty can affect brain structure and function. Stress hormones such as cortisol are critical for the “fight or flight” response. However they can alter the way the brain’s cortex and hippocampus work together, and subvert the ability form new memories. This is a form of plasticity that clinicians would like to be able to prevent, and medications may in fact help with protecting these vital connections.

A stroke can deprive nerve cells of oxygen and kill them. Areas of “necrosis” (dead tissue) from a stroke or a blow to the head will tend to compromise mental functioning. Yet the plasticity of the brain can allow people to heal by recruiting other populations of cells to handle these processes. New networks can form to compensate for the loss of the old.

read the rest here

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Can drugs prevent dementia by altering it’s neurological correlates?

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Alzheimer’s disease will affect more and more people as the population ages. This disorder slowly robs the old and the not-so-old of their wits and memories, and there is no cure.

Evidence has accumulated that some people inherit genes that increase their risk for the condition. A project is underway to stop the dementia before it starts, by giving drugs to those with genes that are a risk factor for Alzheimer’s.

Despite decades of efforts, there is not a clear understanding of the neurological cause of Alzheimer’s. After many millions of dollars spent, countless studies and the efforts of some of the world’s best scientists, we can treat the symptoms and alleviate some of the suffering, but not heal the patient.

There has been great interest among scientists in preventing this disease. Now, a never-before attempted project is underway to use genetics to find those at risk for the disorder, and then to give them a drug called crenezumab.

It is possible crenezumab administered to normal people with family histories of the disease may prevent dementia symptoms from occurring.

Can crenezumab cure Alzheimer’s?

Scientists are particularly interested in individuals who aren’t yet showing symptoms of the disorder, but who have genes or family histories that predispose them to early-onset Alzhemier’s.

An extensive, multi-year, interdisciplinary initiative to measure the possible preventive benefits of crenezumab is being underaken by teams of researchers associated with the pharmaceutical firm Genentech, the Banner Alzheimer’s Institute and the National Institutes of Health.

The effort will administer crenezumab to 300 individuals who are members of families that have been identified as carrying genes connected to early onset Alzhemier’s. The goal is to find out, as stated in a Genentech news release, “if we intervene before cognitive function deteriorates, can we prevent the disease?”

If the answer is yes, it could be a game-changer for those who carry genes increasing risk for Alzheimer’s disease. Family histories and gene sequencing could give individuals crucial information about their risk status, and those who are at higher risk could take crenezumab or another beta amyloid-interacting drug.

Plaques, tangles and the biology of dementia

Scientists have examined the atrophied brains of the severely afflicted and found plaques and tangles. Researchers found these are associated with a complex, sticky material called beta amyloid that seems to be more present in the brains of those with the severest symptoms than in normal adults’ brains.

It’s not quite clear whether the plaques and tangles this material forms are the sole or primary cause of the memory problems and other mental deficits seen with Alzheimer’s patients. Alternatively, the material might be the result of nerve cells coping with the disease, and thus an effect, not a cause.

Scientists have slowly been discovering certain compounds that interact with the plaques and tangles in potentially therapeutic ways. Laboratory science will have real world medical benefits if crenezumab prevents the formation of the plaques and tangles, and slows or prevents dementia symptoms.

Family history and genes offer clues to Alzhemier’s

Researchers have looked at different varieties of Alzheimer’s disease. Intriguingly, a minority of patients who are 30 to 60 years old have an early-onset variant. This subtype is more often inherited and called “familial Alzheimer’s disease.”

Overall, a series of genes on chromosomes connected to the disorder have been discovered, including for the more common common adult-onset Alzheimer’s type that generally afflicts those over 60. Family histories and DNA sequencing have added to what is still a very partial understanding of this condition, and researchers hope this will continue as more related genes are found.

Currently, genetic tests can detect genes that affect the likelihood of developing the memory loss and other cognitive problems characteristic of the disorder. However, the National Institutes of Health states, “It is unlikely that genetic testing will ever be able to predict the disease with 100 percent accuracy because too many other factors may influence its development and progression.”

Science may never have a completely accurate model of all such factors, but it will be very significant if crenezumab prevents or slows the onset of dementia symptoms for those that genetic tests reveal to be at risk. Those families in Columbia who show an unusual incidence of early-onset Alzheimer’s disease may be helping to push scientific knowledge into the new era of genetic medicine.

Are we near the turning point in the war against Alzhemier’s?

The current study will focus on those that family medical studies and genetic tests identify as likely to develop early-onset Alzhemier’s. Depending on the results, the much greater population whose symptoms appear in late middle-age or later may also benefit.

Although the researchers are hopeful about where this work will lead, there are no guarantees. Many medications that have interesting and novel properties in the lab turn out to have limited clinical benefits. Likewise, other drugs may work well therapeutically, but also cause serious and debilitating side effects.

The new initiative is still in its early stages. Crenezumab is not available to the public for combating Alzheimer’s yet. The MDs, Ph.Ds and others associated with Genentech, Banner Alzheimer’s Institute, and National Institutes of Health teams are being cautious about expectations for this initiative.

Read the rest here.

Neurophenomenology conference in the UK during September: call for papers

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 The Consciousness and Experiential Psychology Section of the British Psychological Society

Annual Conference
University of Bristol, 15th & 16th September 2012

Deadline for submissions: 1st May 2012

*** Conference Registration is Now Open – Early Registration Until June 30th ***

Neurophenomenology

Abstract
Standard approaches to understanding consciousness have found their progress interrupted by the explanatory gap purported to exist between the qualitative nature of experience and the quantitative nature of science. Whether it’s third-person scientific methods, which do not easily transfer from observation of the physical to the first-person nature of experience, or phenomenological study, which focuses on the analysis of experience whilst bracketing off theory, there would appear to be an insurmountable difficulty.

These problems are apparently avoided by the neurophenomenological method as first suggested by Francisco Varela (1996). Neurophenomenology operates by investigating the structural parallels between experience, as investigated by the phenomenological method, and the activity of biological systems, as investigated empirically with a particular emphasis on the insights of dynamical systems theory.

The conference will examine the aims and practices of neurophenomenology in an attempt to gauge its success at eradicating the explanatory gap. Our concerns include two core strands:

  • A consideration of neurophenomenology’s radical method, which requires subjects be trained in the practice of epoché and phenomenological reduction

In this strand, we aim to address: the possibility of performing a successful and complete suspension of theories and beliefs about experience; the ability of participants and experimenters to develop open questions which disclose stable experiential invariants; the construction of valid methods of intersubjective corroboration.

  • An evaluation of neurophenomenology’s approach to dynamical systems theory

Addressing questions such as: How should biological systems best be studied, in order to elucidate structural parallels with phenomenal experience?  What can dynamical systems theory contribute to such a study? How, and to what degree, can formal models ever capture experiential structure?

As ever, we aim to hold a conference accessible to all with a broad interest in the academic study of conscious experience. We invite submissions from the full range of academic disciplines with an interest in neurophenomenology, including psychology, philosophy (both analytic and continental), biology, dynamical systems theory and neuroscience.

Keynote Speakers
Prof. Michel Bitbol – Director of Research, Centre National de la Recherche Scientifique (CNRS), at the Centre de Recherche en Epistémologie Appliquée (CREA), Ecole Polytechnique, Paris

Prof. Natalie Depraz – Professor, Department of Philosophy, University of Rouen; Associated researcher, CREA, Ecole Polytechnique/CNRS, Paris

Dr. Claire Petitmengin – Senior Lecturer, Department of Languages and Human Sciences, Institut Télécom, Evry, Essonne; Associated researcher, CREA, Ecole Polytechnique/CNRS, Paris

Dr. Elena Antonova – Lecturer, Institute of Psychiatry, King’s College, London

Location
Wills Hall, University of Bristol
(Accommodation and meals will be available at the conference venue on the 14th, 15th and 16th September, and can be booked via the conference website.)

Submission
Submission of work for presentation in paper or poster format (please specify if you have a preference for poster only) is now open. Non-keynote paper presentations will be 30-minute slots, approximately 20 minutes for the talk and 10 for questions.

Abstracts of up to 300 words should be sent to Dr. Michael Beaton (mjsbeaton@gmail.com) by the 1st May. Please include name and affiliation for all authors.

Key Dates
Submission deadline: 1st May 2012
Responses by: 31st May 2012
Early Registration Deadline: 30th June 2012
Conference: 15th & 16th September 2012

Website
For up-to-date conference information: http://cep.bps.org.uk/
Conference registration pages: http://cep.yolasite.com/

Looks like Autism and neurodevelopmental disorders are going to be re-classified in the new DSM-V

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Some of the work I did for my dissertation dealt with “nosology“, the categorization and classification of symptoms, signs, syndomes, and diseases. I took a class in neuropsychology with David Tucker, an excellent teacher and clinician who got my interest in this subject going. Clinical neuropsychologists confront the problem of how complex an individual’s experience is, and diagnostic criteria may not capture this very well.

A minor theme of my dissertation was the particular issue of knowledge representation for cardiac “body knowledge” or “body cognition” disorders compared to autism. Psychiatrists, neurologists, pediatricians, psychologists, and other clinicians wrestle with how different one autistic patient is compared to another. The new classifications for autistic spectrum disorder coming out in the 2013 DSM-V will re-work how autism is defined, hopefully leading to better diagnoses. I write about this issue for DailyRX:

“Much discussion has centered on exactly who should be considered autistic, based on which diagnostic rules doctors should use. Diaglogue among clinicians, scientists, and patient advocates has focused on the proposed reworked definitions to be published by the American Psychiatric Association’s Fifth Edition of the Diagnostic and Statistical Manual of Mental Disorders in mid-2013.

Currently, the 4th edition of the DSM categorizes autism, Asperger’s disorder, childhood disintegrative disorder, and “pervasive developmental disorder not otherwise specified” as separate conditions.

If the proposed changes are indeed ratified and published, the larger category of “autistic spectrum disorder” will be used to categorize individual experience and behavior, ranging from mild to severe impaired functionality.”

 

 

A study where the brain’s complexity is nested in a lovely, lucid, elegant layer of simplicity

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Most of the time when you study neuroscience you get the sense that every scale you look at, every system and subsystem you examine, every mechanism you investigate, is amazingly intricate and complicated. Turtles all the way down, so to speak. Just browse neurodynamics guru Walter Freeman’s free content if you don’t believe me.

I have on my table Eric Kandel and colleagues formidable Principles of Neural Science. You could actually get strong lifting this hefty tome. While over 1,000 pages it does not cover body cognition or mechanisms of interoception or neurophenomenology or body knowledge disorders or neurodynamics as I might prefer. There is just too much for one book to cover. Biology is like that. You could spend a year reading it and the field would have advanced…

And yet, and yet. Sometimes you find a study where all the complexity is nested in a lovely, lucid, elegant layer of simplicity. The baroque, spiraling layers of structure and process are folded into a rational, understandable, even beautiful, architecture:

A recent study by Van J. Wedeen of the Department of Radiology at Massachusetts General Hospital and colleagues reported surprising results from imaging brain fibers.

The data shows the brain fibers are aligned into an unexpectedly simple grid-like structure, rather similar to intersecting streets.

Can conscious experience affect neural states via “downward causation”?

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My students have been asking questions about how the chemical processes in the brain are related to emotions.

This is forcing me to really think about how neurophenomenology should relate to dualism, monism, panpsychism, reductionism, elimitivism, and other stances regarding conscious states and neural states.

In a broad sense I favor Merleau-Ponty’s notion of la corporeal, which conceives of that physiological body that is observed by science as in some fundamental sense the same as my body, my flesh, embodied me, the foundation of my experience.

What about the specific, in principle falsifiable question of whether conscious experience can affect neural states via “downward causation”? I found a few resources to address this question.

I first encountered this idea in an Omni interview with the eminent neuroscientist Roger Sperry:

“In wrestling with the split-brain problem, I realized that this kind of interaction with objects requires that consciousness have a causal impact on brain activity. Consciousness can be viewed as a higher emergent entity that supercedes the sum of it’s right and left brain awareness”

Once you have an interesting idea like that to ponder, you are primed for more! For what’s it worth, Dave Demaris, coming from a neurodynamics, computational neuroscience and systems engineering background, tells me he finds nothing controversial about downward causation from mind to brain. I suspect Francisco Varela was ahead of all of us on this, I am still very slowly working my way through his massive output. Someone needs to get Walter Freeman to get his views on this documented (for what’s it worth, Walter told me in 2001 his general views on mind and brain are closer to Varela’s than people seem to think).

I found thoughtful, provocative writing from the clinical psychologist Brian Kohler at http://www.isps-us.org/koehler/neurophenomenology.htm:

“Neurophenomenology relies on two key concepts: emergence and embodiment. Emergence extends and enriches the notion of natural causation, without violating the supposed causal closure of physics. Emergence entails both upwards and downwards causation. Embodiment provides the tools for criss-crossing the ‘explanatory gap’ between first-person phenomenology and third-person neuroscience. This is not closing the gap via reductionism, rather it is a way of moving productively from the one domain to the other by way of a third mediating domain, ie, dynamical systems.Varela and Thompson (2003) noted:“Given that the coupled dynamics of brain, body, and environment exhibit self-organization and emergent properties at multiple levels, and that emergence involves both upwards and downwards causation, it seems legitimate to infer that downwards causation may occur at multiple levels in these systems, including that of…cognitive acts in relation to local neural activity” (p.276).

These authors cited the idea of J. A. S. Kelso who wrote: “Mind itself is a spatiotemporal pattern that molds the metastable dynamic patterns of the brain.” Walter Freeman described consciousness as an order parameter and state-variable operator in the brain that mediates relations among various neurons. According to Freeman, mind is not epiphenomena, rather, it plays a crucial role in intentional behavior-it is the task of the neurodynamicist to define and measure what that role is. Another good example, and clinically useful, of ‘downward causation,’ is recent research on human epileptic activity. There is evidence that subjects can voluntarily affect the conditions leading to the initiation and course of seizure activity ( see Francisco Varela & Evan Thompson’s “Neural synchrony and the unity of mind: a neurophenomenological perspective” in Axel Cleermans’ edited volume “The Unity of Consciousness: Binding, Integration, and Dissociation” published in 2003 by Oxford University Press).

Epileptogenic zones are embedded in a complex network of other neural regions that actively participate in mental life. These networks are multiple and distributed over a large scale. The global level of integration ( the result of ‘upwards causation’ ) may produce ‘downwards’ effects, acting eventually upon the local level of the epileptogenic zones. Recent studies by Varela and colleagues have demonstrated that there are deterministic temporal patterns within the apparent random fluctuations of human epileptic activity, and that these patterns can be modified during cognitive tasks (Le Van Quyen et al 1997). Varela and Thompson (2003) concluded: “ …the act of perception on the part of the patient contributes in a highly specific manner, via the phase synchrony of its associated neural assembly…to pulling the epileptic activities towards particular unstable periodic orbits. Thus downwards causation need be no metaphysical will-o’-the wisp, but can be an empirically tangible issue” (p. 277). “

I successfully defended my dissertation and am getting my Ph.D

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I can’t tell you how much work this whole thing has been!

Note to anyone hiring postdocs or profs: I identify as a cognitive scientist, not a psychologist. The University of Texas is notating transcripts to reflect their approval of my completion of a program of work via the Ad-Hoc Interdisciplinary PhD, and labeling it as Medical Cognitive Science.

The title is “”Modeling the clinical predictivity of palpitation symptom reports: mapping body cognition onto cardiac and neurophysiological measurements.”

This dissertation models the relationship between symptoms of heart rhythm fluctuations and cardiac measurements in order to better identify the probabilities of either a primarily organic or psychosomatic cause, and to better understand cognition of the internal body. The medical system needs to distinguish patients with actual cardiac problems from those who are misperceiving benign heart rhythms due to psychosomatic conditions. Cognitive neuroscience needs models showing how the brain processes sensations of palpitations. Psychologists and philosophers want data and analyses that address longstanding controversies about the validity of introspective methods. I therefore undertake a series of measurements to model how well patient descriptions of heartbeat fluctuations correspond to cardiac arrhythmias.

First, I employ a formula for Bayesian inference and an initial probability for disease. The presence of particular phrases in symptom reports is shown to modify the probability that a patient has a clinically significant heart rhythm disorder. A second measure of body knowledge accuracy uses a corpus of one hundred symptom reports to estimate the positive predictive value for arrhythmias contained in language about palpitations. This produces a metric representing average predictivity for cardiac arrhythmias in a population. A third effort investigates the percentage of patients with palpitations report actually diagnosed with arrhythmias by examining data from a series of studies.

The major finding suggests that phenomenological reports about heartbeats are as or are more predictive of clinically significant arrhythmias than non-introspection-based data sources. This calculation can help clinicians who must diagnose an organic or psychosomatic etiology. Secondly, examining a corpus of reports for how well they predict the presence of cardiac rhythm disorders yielded a mean positive predictive value of 0.491. Thirdly, I reviewed studies of palpitations reporters, half of which showed between 15% and 26% of patients had significant or serious arrhythmias. In addition, evidence is presented that psychosomatic-based palpitation reports are likely due to cognitive filtering and processing of cardiac afferents by brainstem, thalamic, and cortical neurons. A framework is proposed to model these results, integrating neurophysiological, cognitive, and clinical levels of explanation. Strategies for developing therapies for patients suffering from identifiably psychosomatic-based palpitations are outlined.

The challenge of building a clinical neurophenomenology of palpitations and cardiodyamics

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from spiritualnetworks.com

Heart disease is a leading threat to health, and people worry when they feel changes

in their heartbeat. Should clinicians trust descriptions of these palpitations? How should

clinicians and scientists model personal, phenomenological statements about what is

happening inside the body of a subject or patient? In an increasingly standardized,

scientific, and objective world of medicine, what role is there for a doctor’s intuitions and

instincts about a patient’s bodily sensations?

These are not simple questions, as they attempt to straddle a fundamental duality

between patients understood as embodied persons in an existential context of health and

disease, and humans understood as systems, as bio-machines modeled by science.

Clinicians collect measurements and interpret data about that category of object known as

a human body, and must compare this externalized, ostensibly objective, techno-scientific

knowledge to their patients’ description of what their bodies feel like. Like the Roman

god Janus, the healer faces two worlds. As modern medicine becomes more involved

with science, integrating these two domains requires ever-more flexibility,

thoughtfulness, and careful techniques for acquiring and modeling data. As complex as

these practical necessities are, science peers even deeper, into the meaning of the often

enigmatic gap that can exist between patient descriptions of the heart speeding up or

missing beats, and the lack of corresponding measurement of heart electrical output as

measured through electrocardiograms (ECG). Medicine needs good approaches for

distinguishing palpitations of psychosomatic origin from those with cardiac etiology, as

well as general guidelines for the trustworthiness of patient-reported data about their

bodily sensations. Science needs to understand what mechanisms in the brain, body, and

mind explain both accurate and inaccurate palpitations reports.

Knowledge of, and theories about, fluid dynamics, hematology, processing of cardiac

state by the peripheral nervous system, receptor activation, hormone binding, protein

signaling, up-regulation and down-regulation of genes, and models of perfusion support

sophisticated models of cardiodynamics. Yet the heart can be thought of in rather more

intuitive terms, as a pump made of muscle that moves oxygen-poor blood to the lungs,

and newly oxygenated blood to the rest of the body. Electrocardiograms show the

rhythms of this pumping as sometimes more regular and periodic and other times less so.

But how much personal knowledge do patients have about what the heart is doing?

Personal knowledge of the body is a problem for mechanistic science. While cardiac

periodicity is an object of scientific measurement, and therefore clinically and

epistemologically privileged for scientists constructing explanations, the personal

experience and phenomenological knowledge of the body may be considered merely

subjective opinion or anecdotal.

People introspecting about their interior sensations sometimes report to their doctor

that their heart is racing, pounding, or skipping beats. In some instances, such data are

compared to that from publically available sources such as ECG, and a diagnosis of

cardiac etiology is made, but in other cases doctors believe the patient is  psychosomatically

cognizing benign heart rhythms as dangerous. When measurements of cardiodynamics do

not correspond well to unwelcome sensations of altered heartbeats, how should medicine

and science understand the discrepancy? This work addresses this problem directly,

by modeling the probabilities that a patient’s experience corresponds to

a medically important heart rhythm disorder. For the patient, feeling a change in

the rhythm or intensity of this fundamental aspect of ongoing embodied existence can

be very worrisome. When the cause is psychosomatic, medicine categorizes it as unexplained,

and cognitive neuroscience faces an explanatory challenge. Somewhere between the cardiac nerves,

brainstem, thalamus,and cortical regions, normal heart rhythms are processed as abnormal and

threatening, but why?

A true understanding of such a gap between personal bodily feelings and cardiac

measurement requires an implicit or explicit mapping of cardiographic, radiological, and

other data onto a description from the patient about what is going on inside their body, or

vice versa. This is not the sort of problem that cognitive science has heretofore usually

focused on, but the field of medical cognitive science can apply ideas from neuroscience

to come up with an explanation. Current evidence (Damasio, 2010) suggests a role for

multiple areas in the peripheral and central nervous systems that process cardiac rhythm

signals, which are cognized into feelings of skipping beats and other abnormal rhythms

(Barsky, 2000).

Such theoretical problems aside, clinicians must apply complex psychological,

anatomical, neurophysiological, and etiological concepts to interpret their patients’

symptom reports. What patients have to say about what is happening in their bodies must

be taken seriously, but not necessarily believed. Traditionally, a doctor might have had

some intuition about the reliability of a patient’s description of their heart fluttering or

racing and would consider the possibility that emotions, stress, and existential or

psychological issues partially or mostly explain the diagnosis. Yet the demands placed on

modern clinicians increasingly constrict the time they may spend listening to the patient,

making it harder for them to get a rich description of the proper existential context

framing the presenting complaint. As such, the need for quickly ascertaining the

probability that palpitation symptoms have a cardiac or psychosomatic etiology becomes

paramount.

What good is patient phenomenology in this new world of evidence-based medicine?

To determine this, I shall focus in particular on comparing the predictive utility of patient

palpitation reports for cardiac arrhythmias to other clinically predictive measures that do

not depend on introspective data from the patient. This predictivity will support the

differential diagnosis of cardiac-based palpitations against psychosomatic etiology, but

modeling how well symptoms correspond to physiological measurements can also serve

to operationalize what I will term “body cognition” and “body knowledge.” Palpitations

are usually defined as unwelcome awareness of cardiac activity (Barsky, 2000), such as

skipping, racing, or thumping heartbeats. Do people with such presenting complaints

have heart rhythm abnormalities requiring medical attention, benign heart rhythm

fluctuations, or normal heartbeats somehow sensed as strange, unpleasant, and abnormal?

Evidence suggests that patients reporting palpitations who have an anxiety disorder are

less likely to have arrhythmias (Abbott, 2005), but the reasons people with normal heart

rhythms report palpitations must be considered a mystery for science, and a challenge

(Barsky, 2000).

Five MD’s respond to my questions about the believability of symptom-report phenomenology

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Q-As a doctor, when a patient tells you they are experiencing “palpitations” or “racing heart” or “skipped beats”, what affects whether or how much you believe them? What else would they have to say for you to think they are accurately reporting on their physiological state?

1: “Regarding patients reporting palpitations. I almost always believe them about that. It’s pretty easy to tell when you have palpitations, and when they are significant they scare the shit out of people, so they notice, remember, and report. If I see a patient in atrial fibrillation, and they say they’ve noticed palpitations for 3 months, I will take that as fairly strong evidence that they have had atrial fib with a rapid ventricular rate for approximately 3 months. It’s not a commonly misperceived experience, I don’t think. There’s not many things that masquerade as ‘palpitations’ that aren’t. Maybe gastroesophageal reflux could make people feel that like they are having palpations when in fact they are refluxing, in which case taking a careful medical history would clear this up.
so what effects how much I believe them…
-the patient’s medical history: does the patient have a history of cardiac arrhythmias? Do they know what tachycardia feels like? If yes, then it makes the subjective report very reliable. for example, if a patient is having chest pain and says “this feels just like my last heart attack” then I would take the complaint very seriously.
-the history of present illness: the details of the patient’s chief complaint can be very useful in the interpretation of their “palpitations”. for example, what was the onset? if suddenly the patient noticed (felt) their heart racing, that would be more consistent with an ectopic cardiac foci suddenly misbehaving than if the patient described a gradual increase in awareness of a racing heart (maybe they were getting stressed out, and developed a gradual sinus tachycardia, or maybe they were exercising and developed a physiological tachycardia).
-patient’s mental status: this prolly goes without saying, but is the patient alert and oriented to person, place, time? do they understand why they are in the hospital? do they make sense? can you believe anything they say? are they rational and coherent in they’re descriptions of other physiological processes?”

2 “Even though they are generally synonymous…I take “palpitations” and “racing heart” more seriously because both connote speed and a rhythm problem; whereas, “skipped beats” can mean a normal rate but with an arrhythmia. As for accuracy and belief, I tend to find patterns or repetition of symptoms more believable (which is not accuracy but precision). If it happens once, it is easier to shrug it off.”

3. “I think I generally believe that complaint since there’s no reason to lie about that sensation- not like they’re looking for narcotics. Things that would make me more concerned would be light headedness, loss of consciousness, chest pain, family history of arrhythmia or sudden cardiac death. “

4 “I tend to believe the patient. Whether there is real disease or not it’s a concern and it’s real to them- I rather not assume the patient is just histrionic or borderline. Then I check their vitals, evaluate their risk factors (age, gender, etc.) for the different etiologies. Then based on the possibilities I order studies if necessary (TSH, EKG, Holter, etc.). If work up is negative then reassure, reassure, reassure. “

5 “I would rank my reliance on phrases as: 1) racing heart, 2) palpitations, 3) skipped beats. Mainly because palpitations is such a low-frequency word in general usage. Although I do interpret them all as palpitations per history with equal reliance on patient accuracy. “