Saturday, August 24, 2019

Ivanka Trump to Head New Agency of Precrime


A Precog capable of predicting future crimes in the film version of Minority Report.


In a strange twist suitable for the dystopian reality show broadcast from the West Wing dining room, a charity formed to fight pancreatic cancer has morphed into project SAFE HOME — “Stopping Aberrant Fatal Events by Helping Overcome Mental Extremes”.



After three highly publicized mass shootings killed 34 people in the US, a variation on the “guns don't kill people...” trope was issued by President Trump: “mental illness and hatred pulls [sic] the trigger, not the gun.” He was right about hatred: two of the shooters espoused white supremacist views, the other was a misogynist. But rather than anger the NRA with tiny incremental changes to control access to firearms, a better approach is to develop a national plan to stigmatize people with mental illnesses, who are more likely to be the victims of violent crime than the perpetrators:
White House considers new project seeking links between mental health and violent behavior

Bob Wright, the former NBC chair and a Trump friend, is one of the proposal’s supporters.

The White House has been briefed on a proposal to develop a way to identify early signs of changes in people with mental illness that could lead to violent behavior.

Supporters see the plan as a way President Trump could move the ball forward on gun control following recent mass shootings as efforts seem to be flagging to impose harsher restrictions such as background checks on gun purchases.

The proposal is part of a larger initiative to establish a new agency called the Health Advanced Research Projects Agency or HARPA, which would sit inside the Health and Human Services Department. Its director would be appointed by the president, and the agency would have a separate budget, according to three people with knowledge of conversations around the plan.

The Suzanne Wright Foundation, started by Bob Wright to fight pancreatic cancer after his wife died from the disease, has advocated for the formation of a DARPA-like federal agency called HARPA. The original vision for HARPA was to “leverage federal research assets and private sector tools to develop capabilities for diseases, like pancreatic cancer, that have not benefited from the current system.”



91% of pancreatic cancer patients die within 5 years– often because the cancer is too advanced to treat by the time of diagnosis. An early detection test for pancreatic cancer would be the most effective weapon to save lives from this disease. ... CodePurple advocates for HARPA ... as the most promising vehicle to develop a pancreatic cancer detection test.



According to the Washington Post:
The HARPA proposal was initially pitched as a project to improve the mortality rate of pancreatic cancer through innovative research to better detect and cure diseases. Despite internal support over the past two years, the model ran into what was described as “institutional barriers to progress,” according to a person familiar with the conversations. 

So why not flip your game by seizing a tragic moment in time to transform yourself into legacy-making material?
“[Trump is] very achievement oriented and I think all presidents have difficulties with science,” Wright said in an interview. “I think their political advisers say, ‘No that’s not a game for you,’ so they sort of back off a bit.”

He added: “But the president has a real opportunity here to leave a legacy in health care.”

The newly-realized HARPA would use artificial intelligence, machine learning, commercial surveillance technology (e.g., Apple Watches, Fitbits, Amazon Echo, Google Home), and “powerful tools [NOT] collected by health-care provides like fMRIs, tractography and image analysis.”
HARPA would develop “breakthrough technologies with high specificity and sensitivity for early diagnosis of neuropsychiatric violence,” says a copy of the proposal. “A multi-modality solution, along with real-time data analytics, is needed to achieve such an accurate diagnosis.”

And because of her vast experience in these technologies and her theoretical contributions to the neuroethics of predicting violent behavior, Ivanka Trump is the best person to lead such an effort:
“It would be perfect for her to do it — we need someone with some horsepower — someone like her driving it. ... It could get done,” said one official familiar with the conversations.

Further Reading

Oh Good, White House Reportedly Considering Dystopian Plan to Try to Detect the Next Mass Shooter

The Minority Report, by Philip K. Dick


Further Watching

Person of Interest, created by Jonathan Nolan (Memento)

   ( How Person of Interest Became Essential Science Fiction Television )

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Sunday, August 11, 2019

Manipulating Visual Cortex to Induce Hallucinations




What is a hallucination? The question seems simple enough. “A hallucination is a perception in the absence of external stimulus that has qualities of real perception. Hallucinations are vivid, substantial, and are perceived to be located in external objective space.” When we think of visual hallucinations, we often think of trippy colorful images induced by psychedelic drugs (hallucinogens).

Are dreams hallucinations? How about visual imagery? Optical illusions of motion from viewing a non-moving pattern? No, no, and no (according to this narrow definition). Hallucinations are subjective and inaccessible to others, much as my recent posts discussed the presence or absence of visual imagery in individual humans. However, people can tell us what they're seeing (unlike animals).

Visual hallucinations can occur in psychotic disorders such as schizophrenia and schizoaffective disorder, although auditory hallucinations are more common in those conditions. Visual hallucinations are more often associated with neurodegenerative disorders. Among patients with Parkinson's Disease, 33% to 75% experience visual hallucinations, usually related to dopaminergic or anticholinergic drug therapy.

In contrast, hallucinations in dementia with Lewy Bodies (DLB) are diagnostic of the disease, and not related to pharmacological treatment. “Recurrent complex visual hallucinations ... are typically well-formed, often consisting of figures, such as people or animals.” The cause may be related to pathology in subcortical visual structures such as the superior colliculus and the pulvinar, rather than the visual cortex itself. A more specific hypothesis is that loss of α7 nicotinic receptors in the thalamic reticular nucleus could lead to hallucinations in DLB.


Charles Bonnet Syndrome (CBS)

Visual hallucinations are also caused by certain types of visual impairment, e.g. age-related macular degeneration, which leads to the loss of central vision. Damage to the macular portion of the retina can cause people to “see” simple patterns of colors or shapes that aren't there, or even images of people, animals, flowers, planets, and scary figures. Individuals with CBS know that the hallucinations aren't real, but they're distressing nonetheless.


image from the Macular Society 1


“Why are you discussing DLB and CBS here,” you might ask, “because these conditions don't involve abnormal stimulation of the visual cortex.” I brought them up because visual hallucinations in humans can occur for any number of reasons, not just from manipulation of highly specific cell types in primary visual cortex (which only occurs in optogenetic experiments with animals).



Electrical Stimulation Studies in Humans

A typical starting point here would be Wilder Penfield and the history of surgical epileptology, but I'll skip ahead to the modern day. Patients with intractable epilepsy present teams of neurosurgeons, neurologists, neurophysiologists, and neuroscience researchers with a unique opportunity to probe the inner workings of the human brain. Stimulating and recording from regions thought to be the seizure focus (or origin) guide neurosurgeons to the precise tissue to remove, and data acquired from neighboring brain bits is used to make inferences about neural function and electrophysiological mechanisms.




An exciting study by Dr. Joseph Parzivi and colleagues (2012) stimulated regions of the fusiform face area (FFA) in the inferior temporal cortex while a patient was undergoing surgical monitoring. Two FFA subregions were identified using both fMRI and electrocorticography (ECoG).



The location of the face-selective regions converged across ECoG and fMRI studies that presented various stimuli and recorded brain responses in the FFA and nearby regions (1 = posterior fusiform; 2 = medial fusiform). Then the investigators stimulated these two focal points while the patient viewed faces, objects, and photos of famous faces and places. Electrical brain stimulation (EBS) of the FFA produced visual distortions while the patient viewed real faces. Sham stimulation, and EBS of nearby regions, did not produce these perceptual distortions. The article included a video of the experiment, which is worth watching.




Another patient viewed pictures of faces during FFA stimulation and reported the persistence of facial images once they were gone, and the mixing of facial features, but no distortions (this is known as palinopsia). A third study induced the scary phenomenon of seeing yourself (self-face hallucination, or autoscopic hallucination), upon EBS of a non-FFA region (right medial occipitoparietal cortex). A video of this experiment is on YouTube.

“But wait,” you say, “you've been describing complex visual hallucinations and distortions of the face because the EBS was in higher-order visual areas that are specialized for faces. What happens when you stimulate primary visual cortex?” The answer is less exciting (but not unexpected): phosphenes, those non-specific images of light that appear when you close your eyes and press on your eyeballs (Winawer & Parvizi, 2016). These can be mapped retinotopically according to their location in the visual field. {also see this 1930 article by Foerster & Penfield: 2
"Stimulation of the occipital pole in area 17 produces an attack which is ushered in by an optic aura such as light, flames, stars, usually in the opposite visual field."}

But EBS of primary visual cortex is a coarse instrument. Here's where the latest refinements in optogenetics finally enter the picture (Marshel et al., 2019).



I won't attempt to cover the complex and novel techniques in Panel 1 and Panel 2 above. So I'll quote others who rave about what a breakthrough they are (and they are): amazing work, incredible breakthrough, Key advances in current paper include multiSLM to stimulate neurons based on function, and a red-shifted opsin allowing simultaneous 2p. And one day (hypothetically speaking), I'd like to present more than direct quotes and my cartoonish version of the optogenetic ensemble and behavioral training methods. But today isn't that day.
Using ChRmine [a fancy new opsin] together with custom holographic devices to create arbitrarily specified light patterns [horizontally or vertically drifting gratings], we were able to measure naturally occurring large-scale 3D ensemble activity patterns during visual experience and then replay these natural patterns at the level of many individually specified cells. We found that driving specific ensembles of cells on the basis of natural stimulus-selectivity resulted in recruitment of a broad network with dynamical patterns corresponding to those elicited by real visual stimuli and also gave rise to the correctly selective behaviors even in the absence of visual input.

Briefly, the investigators captured patterns of activity in V1 layer 2/3 neurons and layer 5 neurons that responded to horizontal or vertical gratings, and then played back the same patterns to those neurons in the absence of a visual stimulus. There goes the coarseness of EBS-induced phosphenes in humans... But obviously, the one great advantage of human studies is that your subjects can tell you what they see. Nonetheless, everyone wants to say that laser-activated nerve cells cause the mice to hallucinate vertical bars.

What really happened is that mice were trained to discriminate between horizontal and vertical gratings. The task required them to respond to the vertical, but not the horizontal. After training, visual stimulation with gratings was compared to optogenetic stimulation of classifier-identified neural ensembles in the absence of gratings. How well did the mice perform with optogenetic-only stimulation?

Modified from Fig. 5 (Marshel et al., 2019). (A) Discrimination performance during visual-only stimulation (black) and tuned-ensemble stimulation (red) over several weeks. (B) Discrimination performance for tuned-ensemble stimulation versus visual trials (P > 0.1 paired t test, two-tailed, n = 112 sessions across five mice).


Eventually the mice did just about as well on the discrimination task with optogenetic stimulation of the horizontally or vertically-tuned neurons, compared to when the horizontal or vertical stimuli were actually presented. Were these mice “hallucinating” vertical gratings?  Or did they merely learn to respond when a specific neural ensemble was activated? Isn't this somewhat like neurofeedback? During training, the mice were rewarded or punished based on their correct or incorrect response to the “vertical” ensemble stimulation. They can't tell us what, if anything, they saw under those conditions.

And the authors themselves noted the following limitation, that “mice initially required some training involving paired optogenetic and visual stimuli before optogenetic activation alone sufficed to drive behavioral discrimination.” Marshel et al. correctly invoked the “it takes a village” explanation that many other cortical and subcortical regions are required to generate a full natural visual percept.

My frustration with the press coverage stems from inaccurate language and overblown interpretations.3  [So what else is new?]  From the New York Times:

Why Are These Mice Hallucinating? Scientists Are in Their Heads
In a laboratory at the Stanford University School of Medicine, the mice are seeing things. And it’s not because they’ve been given drugs.

With new laser technology, scientists have triggered specific hallucinations in mice by switching on a few neurons with beams of light. The researchers reported the results on Thursday in the journal Science.

The technique promises to provide clues to how the billions of neurons in the brain make sense of the environment. Eventually the research also may lead to new treatments for psychological disorders, including uncontrollable hallucinations.

The Stanford press release doesn't use “hallucination” in the title, but a few are sprinkled throughout the text for dramatic effect: “Hallucinations are spooky” and “Hallucinating mice.”

Should we classify the following as a spooky hallucination: Optical stimulation of 20 vertical bar neurons in behaviorally trained mice who then perform the task as if the drifting vertical gratings were present in their visual field. I would say no. To be fair, in the Science paper the authors used the word “hallucinations” only once, and it wasn't to describe mouse percepts.
Studying specific sensory experiences with ensemble stimulation under different conditions may help advance development of therapeutic strategies . . . for neuropsychiatric symptoms such as hallucinations or delusions. More broadly, the ability to track and control large cellular-resolution ensembles over time during learning, and to selectively link cells and ensembles together into behaviorally relevant circuitry, may have important implications for studying and leveraging plasticity underlying learning and memory in health and disease.

I'm focusing on only one small aspect of the study, albeit the one that grabs media attention. The results were highly informative in many other ways, and I do not want to detract from the monumental technical achievements of the research team.


Footnotes

1 This is a terrific resource, with loads of information, additional artistic renderings, an eBook, and a must-see video.

2 There's no escaping Penfield...

3 See Appendix for expert opinion, since I am not an expert...


References

Foerster O, Penfield W. (1930). The structural basis of traumatic epilepsy and results of radical operation. Brain 53:99-119.

Marshel JH, Kim YS, Machado TA, Quirin S, Benson B, Kadmon J, Raja C, Chibukhchyan A, Ramakrishnan C, Inoue M, Shane JC, McKnight DJ, Yoshizawa S, Kato HE, Ganguli S, Deisseroth K. (2019). Cortical layer-specific critical dynamics triggering perception. Science Jul 18.

Parvizi J, Jacques C, Foster BL, Witthoft N, Rangarajan V, Weiner KS, Grill-Spector K. (2012). Electrical stimulation of human fusiform face-selective regions distorts face perception. J Neurosci. 32(43):14915-20.

Winawer J, Parvizi J. (2016). Linking Electrical Stimulation of Human Primary Visual Cortex, Size of Affected Cortical Area, Neuronal Responses, and Subjective Experience. Neuron 92(6): 1213-1219.


Appendix

Before lodging this critique, I consulted select experts on Twitter...






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Monday, August 05, 2019

Brain Awareness Video Contest 2019



What Color is Monday? This video on synesthesia is one of the Top Ten videos in the Society for Neuroscience Brain Awareness Video Contest.  

Voting for the 2019 People's Choice Award closes 12 p.m. Eastern time on August 30, 2019.

However, it wasn't immediately apparent to me how you're supposed to cast your vote...


UPDATE (Aug 6 2019): vote for your favorite for the People's Choice award by liking it on YouTube.


The entire playlist is on YouTube.  


2


How Ketamine Treats Depression


3


Procrastination: I'll Think of a Title Later


4


Seeing Culture in Our Brain


5
6


How Neuroscience Informs Behavioural Economics


7


What Color is Monday


8


Why do adolescents go to sleep late?


9


An Inside Look: Alzheimer's Disease

10
 

Technology Makes Us Bigger

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Sunday, July 21, 2019

Is there an objective test for Aphantasia?




How well do we know our own inner lives? Self-report measures are a staple of psychiatry, neuroscience, and all branches of psychology (clinical, cognitive, perceptual, personality, social, etc.). Symptom scales, confidence ratings, performance monitoring, metacognitive efficiency (meta-d'/d'), vividness ratings, preference/likeability judgements, and affect ratings are all examples. Even monkeys have an introspective side! 1

In the last post we learned about a condition called aphantasia, the inability to generate visual images. Although the focus has been on visual imagery, many people with aphantasia cannot form “mental images” of any sensory experience. Earworms, those pesky songs that get stuck in your head, are not a nuisance for some individuals with aphantasia (but many others do get them). Touch, smell, and taste are even less studied mental imagery of these senses is generally more muted, if it occurs at all (even in the fully phantasic).

The Vividness of Visual Imagery Questionnaire (VVIQ, Marks 1973)2 is the instrument used to identify people with poor to non-existent visual imagery (i.e., aphantasia). For each item on the VVIQ, the subject is asked to “try to form a visual image, and consider your experience carefully. For any image that you do experience, rate how vivid it is using the five-point scale described below. If you do not have a visual image, rate vividness as ‘1’. Only use ‘5’ for images that are truly as lively and vivid as real seeing.” By its very nature, it's a subjective measure that relies on introspection.

But how well do we really know the quality of our private visual imagery? Eric Schwitzgebel has argued that it's really quite poor:3
“...it is observed that although people give widely variable reports about their own experiences of visual imagery, differences in report do not systematically correlate with differences on tests of skills that [presumably] require visual imagery, such as mental rotation, visual creativity, and visual memory.”

And it turns out that many of these cognitive skills do not require visual imagery. A recent study found that participants with aphantasia were slower to perform a mental rotation task (relative to controls), but they were more accurate (Pounder et al., 2018). The test asked participants to determine whether a pair of objects is identical, or mirror images of each other. Response times generally increase as a function of the angular difference in the orientations of the two objects. The overall slowing and accuracy advantage in those with aphantasia held across all levels of difficulty, so these participants must be using a different strategy than those without aphantasia.




Another study found that people with aphantasia were surprisingly good at reproducing the details of a complex visual scene from memory (Bainbridge et al., 2019).4

What test does require visual imagery? The phenomenon of binocular rivalry involves the presentation of two different images to each eye using specialized methods or simple 3D glasses. Instead of forming a unified percept, the images presented to the left and right eye seem to alternate. Thus, binocular rivalry involves perceptual switching. The figure below was taken from the informative video of Carmel and colleagues (2010) in JoVE. I highly recommend the video, which I've embedded at the end of this post.


A recent study examined binocular rivalry in aphantasia using the setup shown in Fig 1 (Keogh & Pearson, 2018). The key trick is that participants were cued to imagine one of two images for 6 seconds. Then they performed a vividness rating, followed by a brief presentation of the binocular rivalry display. Finally, the subjects had to report which color they saw.

- click for larger view -



The study population included 15 self-identified aphantasics recruited via Facebook, direct contact with the investigators, or referral from Professor Adam Zeman, and 209 control participants recruited from the general population. The VVIQ verified poor or non-existent visual imagery in the aphantasia group.

For the binocular rivalry test, the general population showed a priming effect from the imagined stimulus they were more likely to report that the subsequent test display matched the color of the imagined stimulus (green or red) at a greater than chance level (better than guessing). As a group, the individuals with aphantasia did not show priming that was greater than chance. However, as can be seen in Fig. 2E, results from this test were not completely diagnostic. Some with aphantasia showed better-than-chance priming, while a significant percentage of the controls did not show the binocular rivalry priming effect.


Fig. 2E (Keogh & Pearson, 2018). Frequency histogram for imagery priming scores for aphantasic participants (yellow bars and orange line) and general population (grey bars and black dashed line). The green dashed line shows chance performance (50% priming).


Furthermore, scores on the VVIQ in the participants with aphantasia did not correlate with their priming scores (although n=15 would make this hard to detect). Earlier work by these investigators suggested that the VVIQ does correlate with overall priming scores in controls, and binocular rivalry priming on an individual trial is related to self-reported vividness on that trial. Correlations for the n=209 controls in the present paper were not reported, however. This would be quite informative, since the earlier study had a much lower number of participants (n=20).

What does this mean? I would say that binocular rivalry priming can be a useful “objective” measure of aphantasia, but it's not necessarily diagnostic at an individual level.


Related Posts

The Shock of the Unknown in Aphantasia: Learning that Visual Imagery Exists

Imagine These Experiments in Aphantasia


Footnotes

1 see Mnemonic introspection in macaques is dependent on superior dorsolateral prefrontal cortex but not orbitofrontal cortex.

2 The VVIQ is not without its detractors...

3 Thanks to Rolf Degan for bringing this paper to my attention.

4 Also see this reddit thread on Sketching from memory.


References

Bainbridge WA, Pounder Z, Eardley A, Baker CI (2019). Characterizing aphantasia through memory drawings of real-world images. Cognitive Neuroscience Society Annual Meeting.

Keogh R, Pearson J. (2018). The blind mind: No sensory visual imagery in aphantasia. Cortex 105:53-60.

Marks DF. (1973). Visual imagery differences in the recall of pictures. British journal of Psychology 64(1): 17-24.

Pounder Z, Jacob J, Jacobs C, Loveday C, Towell T, Silvanto J. (2018). Mental rotation performance in aphantasia. Vision Sciences Society Annual Meeting.

Schwitzgebel E. (2002). How well do we know our own conscious experience? The case of visual imagery. Journal of Consciousness Studies 9(5-6):35-53.  {PDF}

Shepard RN, Metzler J. Mental rotation of three-dimensional objects. (1971) Science 171(3972): 701-3.



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Sunday, June 30, 2019

The Shock of the Unknown in Aphantasia: Learning that Visual Imagery Exists


Qualia are private. We don’t know how another person perceives the outside world: the color of the ocean, the sound of the waves, the smell of the seaside, the exact temperature of the water. Even more obscure is how someone else imagines the world in the absence of external stimuli. Most people are able to generate an internal “representation1 of a beach — to deploy imagery — when asked, “picture yourself at a relaxing beach.” We can “see” the beach in our mind’s eye even when we’re not really there. But no one else has access to these private images, thoughts, narratives. So we must rely on subjective report.

The hidden nature of imagery (and qualia more generally)2 explains why a significant minority of humans are shocked and dismayed when they learn that other people are capable of generating visual images, and the request to “picture a beach” isn’t metaphorical. This lack of imagery often extends to other sensory modalities (and to other cognitive abilities, such as spatial navigation and autobiographical memories), which will be discussed another time. For now, the focus is on vision.

Redditors and their massive online sphere of influence were chattering the other day about this post in r/TIFU: A woman was explaining her synesthesia to her boyfriend when he discovered that he has aphantasia, the inability to generate visual images.

TIFU by explaining my synesthesia to my boyfriend

“I have grapheme-color synesthesia. Basically I see letters and numbers in colors. The letter 'E' being green for example. A couple months ago I was explaining it to my boyfriend who's a bit of a skeptic. He asked me what colour certain letters and numbers were and had me write them down.  ...

Tonight we were laying in bed and my boyfriend quized me again. I tried explaining to him I just see the colors automatically when I visualize the letters in my head. I asked him what colour are the letters in his head. He looked at me weirdly like what do you mean in "my head, that's not a thing"

My boyfriend didnt understand what I meant by visualizing the letters. He didn't believe me that I can visualize letters or even visualize anything in my head.

Turns out my boyfriend has aphantasia. When he tries to visualize stuff he just sees blackness. He can't picture anything in his mind and thought that everyone else had it the same way. He thought it was just an expression to say "picture this" or etc...

There are currently 8652 comments on this post, many from individuals who were stunned to learn that the majority of people do have imagery. Other comments were from knowledgeable folks with aphantasia who described what the world is like for them, the differences in how they navigate through life, and how they compensate for what is thought of as "a lack" by the tyranny of the phantasiacs.






There's even a subreddit for people with aphantasia:



How did I find out about this? 3  It was because my 2016 post was suddenly popular again!





That piece was spurred by an eloquent essay on what's it's like to discover that all your friends aren't speaking metaphorically when they say, “I see a beach with waves and sand.” Research on this condition blossomed once more and more people realized they had it. Online communities developed and grew, including resources for researchers. This trajectory is akin to the formation of chat groups for individuals with synesthesia and developmental prosopagnosia (many years ago). Persons with these neuro-variants have always existed,4 but they were much harder to locate pre-internet. Studies of these neuro-unique individuals have been going on for a while, but widespread popular dissemination of their existence alerts others – “I am one, too.”

The Vividness of Visual Imagery Questionnaire (VVIQ) “is a proven psychometric measurement often used to identify whether someone is aphantasic or not, albeit not definitive.” But it's still a subjective measure that relies on self-report. Are there more “objective” methods for determining your visual imagery abilities? I'm glad you asked. An upcoming post will discuss a couple of cool new experiments.

ADDENDUM (July 21 2019): the follow-up post is finally here!
Is there an objective test for Aphantasia?


Footnotes

1 This is a loaded term that I won’t explain – or debate – right now.

2 Some people don’t believe that qualia exist (as such), but I won’t elaborate on that, either.

3 I don’t hang out on Reddit, and my Twitter usage has declined.

4 Or at least, they've existed for quite some time.


Further Reading

Aphantasia Index

The Eye's Mind

Bonus Episode: What It's Like to Have no Mind's Eye, a recent entry of BPS Research Digest. There's an excellent collection of links, as well as a 30 minute podcast (download here).

Imagine These Experiments in Aphantasia (my 2016 post).

Involuntary Visual Imagery (if you're curious about what has been haunting me).

In fact, while I was writing this post, intrusive imagery of the Tsawwassen Ferry Terminal in Delta BC (the ferry from Vancouver to Victoria Island) appeared in my head. I searched Google Images and can show you the approximate view.



I was actually standing a little further back, closer to where the cars are parked. But I couldn't quite capture that view. Here is the line of cars waiting to get on the ferry.



During this trip two years ago (with my late wife), this sign had caught my eye so I ran across the street for coffee...

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Sunday, June 16, 2019

'I Do Not Exist' - Pathological Loss of Self after a Buddhist Retreat


Eve is plagued by a waking nightmare.

‘I do not exist. All you see is a shell with no being inside, a mask covering nothingness. I am no one and no thing. I am the unborn, the non-existent.’


– from Pickering (2019).

Dr. Judith Pickering is a psychotherapist and Jungian Analyst in Sydney, Australia. Her patient ‘Eve’ is an “anonymous, fictionalised amalgam of patients suffering disorders of self.”   Eve had a psychotic episode while attending a Tibetan Buddhist retreat.
“She felt that she was no more than an amoeba-like semblance of pre-life with no form, no substance, no past, no future, no sense of on-going being.”



Eve's fractured sense of self preceded the retreat. In fact, she was drawn to Buddhist philosophy precisely because of its negation of self. In the doctrine of non-being (anātman), “there is no unchanging, permanent self, soul, or essence in living beings.” The tenet of emptiness (śūnyatā) that “all things are empty [or void] of intrinsic existence” was problematic as well. When applied and interpreted incorrectly, śūnyatā and anātman can resemble or precipitate disorders of the self.

Dr. Pickering noted:
‘Eve’ is representative of a number of patients suffering both derealisation and depersonalisation. They doubt the existence of the outer world (derealisation) and fear that they do not exist. In place of a sense of self, they have but an empty core inside (depersonalisation).

How do you find your way back to your self after that? Will the psychotic episode respond to neuroleptics or mood stabilizers?

The current article takes a decidedly different approach from this blog's usual themes of neuroimaging, cognitive neuroscience, and psychopharmacology. Spirituality, dreams, and the unconscious play an important role in Jungian psychology. Pickering mentions the Object Relations School, Attachment Theory, Field Theory, The Relational School, the Conversational Model, Intersubjectivity Theory and Infant Research. She cites Winnicott, Bowlby, and Bion (not Blanke & Arzy 2005, Kas et al. 2014, or Seth et al. 2012).

Why did I read this paper? Sometimes it's useful to consider the value of alternate perspectives. Now we can examine the potential hazards of teaching overly Westernized conceptions of Buddhist philosophy.1 


When Westerners Attend Large Buddhist Retreats

Eve’s existential predicament exemplifies a more general area of concern found in situations involving Western practitioners of Buddhism, whether in traditional settings in Asia, or Western settings ostensibly adapted to the Western mind. Have there been problems of translation in regard to Buddhist teachings on anātman (non-self) as implying the self is completely non-existent, and interpretations of śūnyatā (emptiness) as meaning all reality is non-existent, or void?
. . .

This relates to another issue concerning situations where Westerners attend large Buddhist retreats in which personalised psycho-spiritual care may be lacking. Traditionally, a Buddhist master would know the student well and carefully select appropriate teachings and practices according to a disciple’s psychological, physical and spiritual predispositions, proficiency and maturity. For example, teaching emptiness or śūnyatā to someone who is not ready can be extremely harmful. As well as being detrimental for the student, it puts the teacher at risk of a major ethical infringement...

I found Dr. Pickering's discussion of Nameless Dread to be especially compelling.




Nameless Dread

I open the door to a white, frozen mask. I know immediately that Eve has disappeared again into what she calls ‘the void’. She sits down like an automaton, stares in stony silence at the wall as if staring into space. I do not exist for her, she is totally isolated in her own realm of non-existence.

The sense of deadly despair pervades the room. I feel myself fading into nothingness, this realm of absence, unmitigated, bleakness and blankness.We sit in silence, sometimes for session after session. I wonder what on earth do I have to offer her? Nothing, it seems.




ADDENDUM (June 18 2019): A reader alerted me to a tragic story two years ago in Pennsylvania, where a young woman ultimately died by suicide after experiencing a psychotic episode during an intensive 10-day meditation retreat. The article noted:
"One of the documented but rare adverse side effects from intense meditation retreats can be depersonalization disorder. People need to have an especially strong ego, or sense of self, to be able to withstand the strictness and severity of the retreats."

Case reports of extreme adverse events are rare, but a 2017 study documented "meditation-related challenges" in Western Buddhists. The authors conducted detailed qualitative interviews in 60 people who engaged in a variety of Buddhist meditation practices (Lindahl et al., 2017). Thematic analysis revealed a taxonomy of 59 experiences across seven domains (I've appended a table at the end of the post). The authors found a wide range of responses: "The associated valence ranged from very positive to very negative, and the associated level of distress and functional impairment ranged from minimal and transient to severe and enduring." The paper is open access, and Brown University issued an excellent press release.


Footnote

1 This is especially important given the appropriation of semi-spiritual versions of yoga and mindfulness, culminating in inanities such as tech bro eating disorders.


References

Blanke O, Arzy S. (2005). The out-of-body experience: disturbed self-processing at the temporo-parietal junction. Neuroscientist 11:16-24.

Kas A, Lavault S, Habert MO, Arnulf I. (2014) Feeling unreal: a functional imaging study in patients with Kleine-Levin syndrome. Brain 137: 2077-2087.

Lindahl JR, Fisher NE, Cooper DJ, Rosen RK, Britton WB. (2017). The varieties of contemplative experience: A mixed-methods study of meditation-related challenges  in Western Buddhists. PLoS One 12(5):e0176239.

Pickering J. (2019). 'I Do Not Exist': Pathologies of Self Among Western Buddhists. J Relig Health 58(3):748-769.

Seth AK, Suzuki K, Critchley HD. (2012). An interoceptive predictive coding model of conscious presence. Front Psychol. 2:395.


Further Reading

Derealization / Dying

Feeling Mighty Unreal: Derealization in Kleine-Levin Syndrome

A Detached Sense of Self Associated with Altered Neural Responses to Mirror Touch



Phenomenology coding structure (Table 4, Lindahl et al., 2017).

- click table for a larger view -

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