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

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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

1This 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 -

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

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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 whowerestunnedto 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. Onlinecommunities developed and grew, including resourcesfor 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.


Footnotes

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

2Somepeople 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...

Is there an objective test for Aphantasia?

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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.



Brain Awareness Video Contest 2019

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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...

The entire playlist is on YouTube.  


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Manipulating Visual Cortex to Induce Hallucinations

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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...






Ivanka Trump to Head New Agency of Precrime

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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 )

Are there evil people or only evil acts?

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“I can guarantee that someone in the world thinks you are evil. Do you eat meat? Do you work in banking? Do you have a child out of wedlock? You will find that things that seem normal to you don't seem normal to others, and might even be utterly reprehensible. Perhaps we are all evil. Or, perhaps none of us are.”

– Julia Shaw, Evil: The Science Behind Humanity's Dark Side

Earlier this month, Science magazine and Fondation Ipsen co-sponsored a webinar on Impulses, intent, and the science of evil. “Can research into humankind’s most destructive inclinations help us become better people?”

It's freely available on demand. Let the controversy commence...


Are There Evil People or Only Evil Acts?

Moderator (Sean Sanders, Ph.D. Science/AAAS):  “... How do we define evil? ... Are there evil people or only evil acts?”

In brief, Dr. Abigail Marsh said no, there are absolutely not evil people; Dr. David Brucato mostly agreed with that; and Dr. Michael Stone gave an elaborate example using an offensive term ("gay pedophile"– as if anyone would refer to a male pedophile who targets little girls as a "straight pedophile").



Dr. Marsh was not amused...

More detail below.


Michael Stone, M.D. Columbia University:  [I'm skipping his first response on etymology and religion.]

Abigail Marsh, Ph.D. Georgetown University:  “... I don't think it's ever appropriate to refer to a person as evil. Actions are certainly evil and some people are highly predisposed to keep committing evil actions, but evil does has this very supernatural connotation.


Um, and like so many supernatural ideas, I think the concept of evil is pulled in whenever we have trouble understanding why someone would do such a thing, right, we talk about evil spirits or forces because it's so difficult to understand, um, for most people why anybody would be driven to do something to cause people pain and suffering for no reason. Um... but there is an explanation, we may not know what it is yet, but there is an explanation for these behaviors, and so uh... but the use of the word 'evil' doesn't get us any closer to understanding that. It leaves us in this supernatural rut rather than thinking of these behaviors as things that do have unfortunately human motivations .. but that are not the totality of the person. Evil is a very essentialist term as well. It assumes this sort of homogeneity within the person which is not usually true.” [I'm biased in this direction.]

Gary Brucato, Ph.D. Columbia University:  [after the moderator has implied that Stone & Brucato's book suggests that although rare, there are truly evil people.]  “...... What we have to clarify is that rarely, even in the most egregious repeat offenders, do you see somebody that from dusk to dawn is committing acts that are considered evil.  ... [I'll note here that Dr. Marsh is subtly nodding her head.]

Dr. Stone:  “Therefore there are a very very small number of people ... who do evil things as it were from the minute they wake up in the morning until they go to sleep at night. The one who comes closest to mind is the one I interviewed for the Discovery channel program some years ago and that was uh David Paul Brown his real name, who then changed his name when he was in prison the first time to Benjamin Nathaniel Bar-Jonah [actually, it was Nathaniel Benjamin Levi Bar-Jonah] who was a gay pedophile [sic] who would seduce boys coming out of a theater and then try to capture them if he could and kill them and so on. Some of them escaped and managed to identify him.1 [He was imprisoned and then released] ... OK. So. Out in Montana, he dressed as a policeman with a fake badge... and would seduce little boys ... coming out of a school ... he would ... kill them, eat part of the boy ... [more details about cannibalism] ... He had thousands of pictures of boys and on the walls making up very bad comments and puns as if uh uh some young kid as if that were a Chinese menu item, on a menu, some young kid.” [other sources say girls were among the victims]. He could be counted on, one of the few people I know of, who was evil day in and day out. That's very rare...”



Dr. Stone seems amused...



Dr. Marsh looks dejected


Labels Don't Get Us Anywhere

Moderator:  “... I feel this disgust and you know repulsion uh thinking about this. And so I'm assuming that this is what drives people to label someone as evil. Um and I wonder if that label is useful. You know if we look at maybe the children that you Abby are doing your research with um if you see these inclinations is it helpful to put labels on them and where does that get us you know scientifically and and in terms of treatment?

Dr. Marsh:  “I don't think it gets us anywhere, it's one of the many reasons I wouldn't ever refer to that term uh to call a human being evil. Um... the children I work with didn't make a choice to have the personalities they do or to have the life experiences that have led them to the place that they are and instead we know that psychopathy— again this condition of having very low levels of remorse and caring and compassion for other people has all the hallmarks of a mental illness — has a strong heritability component, having negative life experiences causes the prognosis to get worse, there are very clear characteristic brain and cognitive changes. It looks like any other psychological disorder in these key ways and so calling people who are affected by this condition evil is not helping us to develop treatments to try to improve their prognosis and to try to improve the odds that they won't go on to do things that affect the rest of us negatively. Um because what I what it does is calling someone evil robs us of the ability to view someone compassionately.”


It's Nearly Impossible to Predict...

Moderator: Do we all have the propensity to do evil deeds?

Dr. Marsh:  “...[regarding] 'horrible and unpredicted' acts, shooting up dozens of innocent people ... I think that when acts like that are so unpredictable, it often leads us to draw the incorrect conclusion, I guess anybody is capable of an act of evil so serious because if we can't predict who it can be, I guess it can be anybody. Um it is true that it is very hard to predict accurately who will engage in acts of significant violence like that especially when dealing with young men in whom various psychological disorders may be emerging for the first time that contribute to those actions. But it's absolutely not the case that everybody is capable of actions like that...”


Prevention, Not Prediction

This brings us to my previous post on a proposal to predict mass shootings via Apple Watches, Fitbits, Amazon Echo, Google Home and AI, and how this effort would be futile (not to mention horribly intrusive and stigmatizing). But we wouldn't want to anger the NRA, now would we?

An FBI study on pre-attack behaviors of 63 active shooters in the US found that only 25% had ever been diagnosed with a mental illness (only three of whom were diagnosed with a psychotic disorder).

A Department of Defense report on Predicting Violent Behavior says:
There is no panacea for stopping all targeted violence. Attempting to balance risks, benefits, and costs, the Task Force found that prevention as opposed to prediction should be the Department's goal. Good options exist in the near term for mitigating violence by intervening in the progression of violent ideation to violent behavior.
It should seem obvious that...

Dr. Stone: “...it's much more easy to get rid of the weaponry that allows these things to happen than it is to do psychotherapy, particularly on people with psychopathic tendencies who are not very amenable to psychotherapy anyway...”

Most Americans favor stricter gun control, and many of us think that our lax gun control laws are the greatest insanity, as are the politicians who refuse to do anything about it.


Further Reading

Aggression Detectors: The Unproven, Invasive Surveillance Technology Schools Are Using to Monitor Students

Trump's claims and what experts say about mental illness and mass shootings

Ivanka Trump to Head New Agency of Precrime


Predicting Mass Shootings via Intrusive Surveillance and Scapegoating of the Mentally Ill

No news from the hypothetical HARPA organization (Health Advanced Research Projects Agency) or the Suzanne Wright Foundation since the initial Washington Post report on their joint proposal for project SAFE HOME— “Stopping Aberrant Fatal Events by Helping Overcome Mental Extremes.”


Footnote

1 I had initially included more of the gory details, then decided a truncated version was better.

Is Mourning Rewarding? (revisited)

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Can we reduce the persistent, unbearable pain of losing a loved one to 15-20 voxels of brain activity in the nucleus accumbens (O'Connor et al., 2008)? No? Then what if I told you that unrelenting grief — and associated feelings of sheer panic, fear, terminal aloneness, and existential crisis — isn't “suffering”. It's actually rewarding!

Well I'm here to tell you that it isn't.

Looking back on a post from 2011, you never realize it's going to be you.1


The top figure shows that activity in the nucleus accumbens was greater in response to grief-related words vs. neutral words in a group of 11 women with “Complicated” Grief (who lost a mother or sister to breast cancer in the last 5 years), compared to a group of 10 women with garden-variety Non-complicated Grief (O'Connor et al., 2008). Since the paper was published in 2008, and the standards for conducting fMRI studies have changed (larger sample sizes are necessary, no more “voodoo correlations”), I won't go on about that here.


When Grief Gets Complicated?

Grief is never simple, it's always complicated. The death of a cherished loved one can create a situation that seems totally intolerable. Almost everyone agrees that navigating such loss doesn't rely on one acceptable road map. Yet here it is. Normal people are supposed to move through a one year mourning period of “sorrow, numbness, and even guilt and anger. Gradually these feelings ease, and it's possible to accept loss and move forward.” If you don't, well then it's Complicated. This is a stigmatizing and limiting view of what it means to grieve the loss of a loved one.2

But is there really such there a thing as Complicated Grief? Simply put, it's “a chronic impairing form of grief brought about by interference with the healing process.” There are “maladaptive thoughts and dysfunctional behaviors” according to The Center for Complicated Grief. However, it's not named as an actual disorder in either of the major psychiatric manuals. In ICD-11, preoccupation with and longing for the deceased, accompanied by significant emotional distress and functional impairment beyond six months, is called Prolonged Grief Disorder. In DSM-5, Complicated Grief has morphed into Persistent Complex Bereavement Disorder, a not-exactly-reified condition subject to further study.


Dopamine Reward

Dopamine and its putative reward circuitry are way more complex than a simple one-to-one mapping. Studies in rodents have demonstrated that the nucleus accumbens (NA) can code for negative states, as well as positive ones, as shown by the existence of “hedonic coldspots” that generate aversive reactions, in addition to the usual hotspots (Berridge & Kringelbach, 2015). These studies involved microinjections of opioids into tiny regions of the NA.




If a chronically anguished state is portrayed as rewarding, it's time to recalibrate these terms. As I said in 2011:

If tremendous psychological suffering and loss are associated with activity in brain regions such as the ventral tegmental area and nucleus accumbens, isn't it time to abandon the simplistic notion of dopamine as the feel-good neurotransmitter? To quote the authors of Mesolimbic Dopamine in Desire and Dread (Faure et al., 2008):
It is important to understand how mesocorticolimbic mechanisms generate positive versus negative motivations. Dopamine (DA) in the nucleus accumbens is well known as a mechanism of appetitive motivation for reward. However, aversive motivations such as pain, stress, and fear also may involve dopamine in nucleus accumbens (at least tonic dopamine signals).

Grief-Related Words Are Rewarding

So what happens when you take a disputed diagnostic label and combine it with reverse inference in a neuroimaging study? (when you operate under the assumption that activity in a particular brain region must mean that a specific cognitive process or psychological state was present).

The NA activity was observed while the participants viewed grief words vs. neutral words that were superimposed over a photograph: a photo of the participant's deceased mother or a photo of someone else's mother. And it didn't matter whose mother was pictured, the difference was due to the words, not the images.3



Sample stimulus provides an [unintentional?] example of the emotional Stroop effect.


That's pretty hard to explain by saying that “the pangs of grief would continue to occur with NA activity, with reward activity in response to the cues motivating reunion with the deceased” if the effect is not specific to an image of the deceased.


Yearning and the Subgenual Cingulate

Why beat a dead horse, you ask? Because a recent study (McConnell et al., 2018) did not heed the advice above (sample size should be increased, beware reverse inference). The participants were 9 women with Complicated Grief (CG), 7 women with Non-complicated Grief (NG), and 9 Non-Bereaved (NB). The NA finding did not replicate, nor were there any differences between CG and NG and NB (over the entire brain). A post-hoc analysis then extracted a single question from a 19-item inventory and found that yearning for the dead spouse in all 16 Bereaved participants was correlated with activity in the subgenual cingulate (“depression-land” or perhaps “rumination-land”), for the comparison of an anticipation period vs. presentation of spouse photo. There were 5 spouse photos and 5 photos of strangers (note that it was not possible to predict which would be presented). The authors recognized the limitations of the study, yet pathologized yearning in Complicated and Non-complicated Grief alike.

I realize that the general motivation behind these experiments might be admirable, but you really can't come to any conclusions about how grief — a highly complex emotional response unique to each individual — might be represented in the brain.


Footnotes

1See There Is a Giant Hole Where My Heart Used To Be from October 2, 2018.

The posts on illness and death that I never wrote:
(yes, I was really serious about these)

2I was skeptical when someone sent me this book, It's OK That You're Not OK: Meeting Grief and Loss in a Culture That Doesn't Understand (by Megan Devine). I thought it was going to be overly 'self-helpy'. But it's actually been immensely helpful.

3 The idea of creating a self-relevant stimulus set was utterly horrifying to me.


References

Berridge KC, Kringelbach ML. (2015). Pleasure systems in the brain. Neuron 86(3):646-64.

Faure A, Reynolds SM, Richard JM, Berridge KC. (2008). Mesolimbic dopamine in desire and dread: enabling motivation to be generated by localized glutamate disruptions in nucleus accumbens. J Neurosci. 28:7184-92.

McConnell MH, Killgore WD, O'Connor MF. (2018). Yearning predicts subgenual anterior cingulate activity in bereaved individuals. Heliyon 4(10):e00852.

O'Connor MF, Wellisch DK, Stanton AL, Eisenberger NI, Irwin MR, Lieberman MD. (2008). Craving love? Enduring grief activates brain's reward center. Neuroimage 42:969-72.


The Neural Correlates of Channeling the Dead

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November 2nd is the Day of the Dead, a Mexican holiday to honor the memory of lost loved ones. If you subscribe to certain paranormal belief systems, the ability to communicate with the dearly departed is possible via séance, which is conducted by a Medium who channels the spirit of the dead.

Since I do not subscribe to a paranormal belief system, I do not think it's possible to communicate with my dead wife. Nor am I especially knowledgeable about the differences between mediumship vs. channeling:
Mediumship is mostly about receiving and interpreting messages from other worlds.

Mediums often deliver messages from loved ones and spirit guides during readings.
. . .

...channeling is often about receiving messages from other types of entities, such as nature spirits, spirit guides, or even angels.

In short, Channels can communicate with a broader class of non-corporeal entities, for instance Mahatma Ghandi or Cleopatra (not only the dead relatives of paying clients).

What seems to be uncontroversial, however, is that Channels who enter into a trance state to convey the wisdom of Gandhi may experience an altered or “expanded” state of consciousness (regardless of the veracity of their communications). This permuted state of arousal should be manifest in the electroencephalogram (EEG) as an alteration in spectral power across the range of frequency bands (e.g., theta, alpha, beta etc.) that have been associated with different states of consciousness.

A group of researchers at the Institute of Noetic Sciences adopted this view in a study of persons who claimed the ability to channel (Wahbeh et al., 2019). The participants (n=13; 11 ♀, 2 ) were on average 57 year old white women of upper middle class socioeconomic status, representative of the study site in Marin County, California. The authors screened 155 individuals to arrive at their final sample size.1 Among the stringent inclusion criteria was the designation of being a Channel who directly and actively conveys the communications of a discarnate entity or spirit (rather than being a passive relay).2The participants were free of major psychiatric disorders, including psychosis and dissociation (according to self-report). Oh, and they had the ability to remain still during the channeling episodes, which was advantageous for the physiological measurements.

The participants alternated between channeling and no-channeling in 5 minute blocks while EEG and peripheral physiological signals (skin conductance, heart rate, respiration, temperature) were recorded. At the end of each counterbalanced session (run on separate days), voice recordings were obtained while the participants read stories.




Contrary to the authors' predictions, they found no significant differences between the channeling and no-channeling conditions for any of the physiological measures, nor for the EEG analyzed in standard frequency bands (theta 3–7 Hz; alpha 8–12 Hz; beta 13–20 Hz and low gamma 21–40 Hz) across 64 electrodes. I'll note here that the data acquisition and analysis methods were top-notch. The senior author (Arnaud Delorme) developed the widely used EEGLAB toolbox for data analysis, which was described in one of the most highly cited articles in neuroscience.3

Modest differences in voice parameters were observed: the channeled readings were softer in volume and slower in pace. The authors acknowledged that the participants could have impersonated an alternate voice during the channeling segments, whether consciously or unconsciously.

So does this mean that channeling is a sham? The authors don't think so. Instead, they recommended further investigation: “future studies should include other measures such as EEG connectivity analyses, fMRI and biomarkers.”


Footnotes

1This is a rather esoteric population, so I won't fault the researchers for having a small sample size.

2“The channeler goes into a trance state at will (the depth of the trance may vary) and the disincarnate entity/spirit uses the channeler’s body with permission to communicate directly through the channeler's voice, body movements, etc. (rather than the channeler receiving information mentally or otherwise and then relaying what is being received).”

3 I was rather critical of a previous study by this research group, which was ultimately retracted from Frontiers in Neuroscience. See Scientific Study Shows Mediums Are Wrong 46.2% of the Time.


Reference

Wahbeh H, Cannard C, Okonsky J, Delorme A. (2019). A physiological examination of perceived incorporation during trance. F1000Research 8:67.



Bev Tull, the fake medium on Bad Girls.

Olfactory Attraction and Smell Dating

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Smell Dating, an interactive exhibit by Tega Brain and Sam Lavigne


A conceptual art installation, an extended olfactory performance piece, an elaborate participatory project, or an actual smell-based dating service? Smell Dating is all of these and more!




How it works
  1. We send you a t-shirt
  2. You wear the shirt for three days and three nights without deodorant.
  3. You return the shirt to us in a prepaid envelope.
  4. We send you swatches of t-shirts worn by a selection of other individuals.
  5. You smell the samples and tell us who you like.
  6. If someone whose smell you like likes the smell of you too, we'll facilitate an exchange of contact information.
  7. The rest is up to you.

My initial view of the project was based a recent showing of the interactive exhibit, where the participants could sniff small swatches of cloth, rate the unknown wearer's attractiveness (UNATTRACTIVE — NEUTRAL — ATTRACTIVE), learn how others voted, and see basic background information about the wearer (e.g., 30 year old female bisexual pescatarian). The first two I sniffed were odorless, but then there was #8...

The art installation is part of Useless Press, “a publishing collective that creates eclectic Internet things.” I assumed it was an elaborate joke, not an actual matchmaking service, but the artists must have had a grant to implement the idea in real life.





In Shanghai, people signed up over a two week period and paid ¥100 to become a “member.”
Smell Dating @ Shanghai [culminated] in the Sweat Lab, a participatory installation event... Visitors are invited to volunteer in the Smell Dating Sweat Lab and intimately experience the smells of strangers. During this event we will prepare the smell samples from our members t-shirts. Shirts will be meticulously cut up and batched to be sent back to Smell Dating members.

Smell Dating premiered in New York in March 2016 and received extensive press coverage, most of which took it seriously. Young female writers at The Guardian, Business Insider, Time, Racked, and a gay man at HuffPo tried out the service. The Buzzfeed reporter realized, “Yes, this is mostly a stunt-y gag” but also touched on the science behind smell and attraction. The health reporter at Time wrote about the underlying science in detail (e.g., major histocompatibility complex) and interviewed smell scientists, including Dr. Noam Sobel (founder of SmellSpace.com), Dr. Richard Doty (author of The Great Pheromone Myth), and Dr. Gary Beauchamp (Emeritus Director of the Monell Chemical Senses Center).

The creators of Smell Dating (Tega Brain and Sam Levine) consulted with olfactory scientists and provided an extensive reading list on the web site.

Most everyone agrees that odors evoke emotion, and the sense of smell has a unique relationship to autobiographical memory. But, as Richard Doty asks, do human pheromones exist?
While it is apparent that, like music and lighting, odors and fragrances can alter mood states and physiological arousal, is there evidence that unique agents exist, namely pheromones, which specifically alter such states?

It turns out that scientific opinion on this matter is decidedly mixed, even polarizing, as I'll discuss in the next post.


Reference

Doty RL. (2014). Human Pheromones: Do They Exist? In: Mucignat-Caretta C, editor. Neurobiology of Chemical Communication. Boca Raton (FL): CRC Press/Taylor & Francis; Chapter 19.




Smell Dating from Tega Brain.

Pheromone Friday

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Pheromones, emitted chemicals that elicit a social response in members of the same species, have been most widely studied in insects as a mode of communication. In the insect world, pheromones can signal alarm, mark trails, control worker bee behavior, and elicit sexual behavior.

Sex pheromones are the chemicals that come to mind in popular lore. Do human beings secrete substances that are likely to attract potential mates? Unscrupulous players in the fragrance industry would like you to believe that's the case. Unable to attract women (or men)? There's a difference between marketing an intoxicating and sensual fragrance that's pleasing to the nose and snake oil such as:




Amazon even cautions prospective customers about SexyLife.





{BTW, humans lack a functional vomeronasal organ, the part of the accessory olfactory system that detects pheromones / chemosignals / non-volatile molecules (Petrulis, 2013).}


Don't we already know that human pheromones are a crock?

It depends on how you define pheromone, some would say.1“In mammals [rodents], few definitive cases have been identified in which single pheromone compounds evoke robust sexual behaviours, which might reflect an important contribution of signature mixtures in sexual communication” (Gomez-Diaz & Benton 2013, The joy of sex pheromones). In rodents, reproductive responses to “odor blends” or chemosignals are heavily modulated by experience, as opposed to the instinctive and fixed behaviors elicited by pheromones in insects. The evidence supporting the existence of mammalian pheromones is so weak that Richard Doty has called it The Great Pheromone Myth.

If rats don't have “pheromones” per se, why look for them in humans? Tristram Wyatt, who believes that human pheromones probably exist, wrote a paper called The search for human pheromones: the lost decades. He criticized the literature on four androgen-related steroids (androstenone, androstenol, androstadienone and estratetraenol), saying it suffers from publication bias, small sample sizes, lack of replication, and commercial conflicts of interest. There is no bioassay-based evidence that these molecules are human pheromones, yet “the attraction of studies on androstadienone (AND) and/or estratetraenol (EST) seems unstoppable” (Wyatt, 2015).

{Curiously, the SexyLife ad accurately lists the putative male pheromones, although their depicted functions are pure fantasy.}

Unstoppable it is. Supporters of human pheromones have recently published positive results on male sexual cognition, male dominance perception, cross-cultural chemosignaling of emotions, and sex differences in the main olfactory system.2


Olfactory Attraction

On the other hand, a null finding from 2017 drew a lot of attention from popularmediaoutlets and Science magazine, where the senior author stated: “I’ve convinced myself that AND and EST are not worth pursuing.” In that study, AND & EST had no effect on the participants' attractiveness ratings for photographs of opposite-sex faces (Hare et al., 2017).

The evolutionary basis of Smell Dating was given a cold shower by studies showing that the fresh (and odorless) armpit sweat of men and women, when incubated in vitro with bacteria that produce body odor, were rated identically on pleasantness and intensity (reviewed in Doty, 2014). Meanwhile, the day-old smelly armpit sweat of men was rated as equally unpleasant by men and women.3 Likewise, pleasantness and intensity ratings for female armpit sweat did not differ between men and women. This doesn't bode well for heterosexual dating...

Odors and fragrances are an important part of attraction, of course, but don't call them pheromones.


Footnotes

1 There is an accepted definition for "pheromone".

2 Since humans don't have an accessory olfactory system with its fun vomeronasal organ, the main olfactory system would have to do the pheromone-detecting work.

3 This could be due to larger apocrine glands, hairy armpits, and more carnivorous diets in men (Doty, 2014).


Further Reading

Scientific post in favor of human pheromones:
“Whether one chooses to believe in the existence of human pheromones or not, steroids clearly serve an essential olfactory signaling function that impacts broadly ranging aspects of the human condition from gender perception to social behavior to dietary choices.”

PET studies on AND, EST, and sexual orientation:

References

Doty RL. (2014). Human Pheromones: Do They Exist? In: Mucignat-Caretta C, editor. Neurobiology of Chemical Communication. Boca Raton (FL): CRC Press/Taylor & Francis; Chapter 19.

Gomez-Diaz C, Benton R. (2013). The joy of sex pheromones. EMBO Rep. 14(10): 874-83.

Hare RM, Schlatter S, Rhodes G, Simmons LW. (2017). Putative sex-specific humanpheromones do not affect gender perception, attractiveness ratings orunfaithfulness judgements of opposite sex faces. R Soc Open Sci. 4(3):160831.

Petrulis A. (2013). Chemosignals, hormones and mammalian reproduction. Horm Behav. 63(5): 723-41.

Wyatt TD. (2015). The search for human pheromones: the lost decades and the necessity of returning to first principles. Proc Biol Sci. 282(1804):20142994.


Computational Psychiatry, Self-Care, and The Mind-Body Problem

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Schematic example of how the “mind” (cerebral cortex) is connected to the “body” (adrenal gland) - modified from Fig. 1 (Dum et al., 2016):
“Modern medicine has generally viewed the concept of psychosomaticdisease with suspicion. This view arose partly because no neural networks were known for the mind, conceptually associated with the cerebral cortex, to influence autonomic and endocrine systems that control internal organs.”

Psychosomatic illnesses are typically seen in pejorative terms — it's all in your head so it must not be real! Would a known biological mechanism lessen the stigma? For over 40 years, Dr. Peter Strick and his colleagues have conducted careful neuroanatomical tracing studies of motor and subcortical systems in the primate brain. A crucial piece of this puzzle requires detailed maps of the anatomical connections, both direct and indirect. How do the frontal lobes, which direct our thoughts, emotions, and movements, influence the function of peripheral organs?

In their new paper, Dum, Levinthal, and Strick (2019) revisited their 2016 work. The adrenal medulla (within the adrenal gland) secretes the stress hormones adrenaline and noradrenaline. To trace the terminal projections back to their origins in the spinal cord and up to the brain, the rabies virus was injected in the target tissue. The virus is taken up at the injection site and travels backward (in the retrograde direction) to identify neurons that connect to the adrenal medulla with one synapse: sympathetic preganglionic neurons in the spinal cord. Longer survival times allow the virus to cross second-, third-, and fourth-order synapses. The experiments revealed that cortical influences on the adrenal originate from networks involved in movement, cognition, and affect.

Modified from Fig. 5 (Dum et al., 2016). Pathways for top-down cortical influence over the adrenal medulla. Motor areas are filled yellow, and medial prefrontal areas are filled blue. (A)lateral surface. (B)medial wall.

The mind–body problem: Circuits that link the cerebral cortex to the adrenal medulla

“The largest influence originates from a motor network that includes all seven motor areas in the frontal lobe. ... The motor areas provide a link between body movement and the modulation of stress. The cognitive and affective networks are located in regions of cingulate cortex. They provide a link between how we think and feel and the function of the adrenal medulla.”
Based on these anatomical results, the authors concluded with a series of speculative links to alternative medicine practices, including yoga and Pilates; smiling to make yourself feel better; and back massage for stress reduction.
Because of this arrangement, we speculate that there is a link between the cortical control of 'core' muscles and the regulation of sympathetic output. This association could provide a neural explanation for the use of core exercises, such as yoga and Pilates, to ameliorate stress.
  • The orofacial representation of M1 provides a small focus of output to the adrenal medulla.
This output may provide a link between the activation of facial muscles, as in a 'standard' or 'genuine' smile, and a reduction in the response to stress.
  • Another large motor output region is in postcentral cortex, corresponding to the sensory representation of the trunk and viscera in primary somatosensory cortex.
This output may provide a neural substrate for the reduction of anxiety and stress that follows passive stimulation of back muscles during a massage.
I was a bit surprised to see these suggestions in a high-impact journal. Which leads us to the next topic.




Self-Care and Its Discontents

What can be bad about trying to reduce daily stress and improve your own health?

A recent paper by Jonathan Kaplan (Self-Care as Self-Blame Redux: Stress as Personal and Political)1 is critical of the way the self-care movement shifts the burden of alleviating stress-related maladies from society to the individual. Economic disadvantage is disproportionately associated with poor health outcomes, to state the obvious. Kaplan argues that focusing on individual self-care blames the victim for their response to a chronically stressful environment, rather than focusing on ways to effect structural changes to improve living conditions. In his efforts to highlight social inequities as a cause of stress-related illnesses, Kaplan goes too far (in my view) to discount all self-help practices that aim to preserve health.

It can be empowering for patients to be active participants in their health care, whether at the doctor's office, in the hospital, or at home. One great example is CREST.BD: A Collaborative Research and Knowledge Exchange Network at the University of British Columbia. They've established the Bipolar Wellness Centre (online resource to support evidence-based bipolar disorder self-management) and developed a Quality of Life Tool (free web-based tool to help people with bipolar disorder and healthcare providers use CREST.BD’s bipolar-specific quality of life scale).2

Then we have the wellness industry. Depending on what pop health source you read, there are 5, 45, 25, 12, 10, 10, 20 (etc.) essential self-care practices that you can incorporate into your daily routine (if you have the time and money). Wellnesslifestyleinsta-brands of the rich and famous hold up an impossible standard for upper-middle class white women [mostly]3 to attain. Perhaps our friendly neuroanatomists want to work on their core strength — they can follow @sianmarshallpilates for Pilates inspiration!


Back to Kaplan's point about blame...




It's easy to urge your followers to “stay happy!” and “move on!” if you have a net worth of $250 million, and if you don't have a psychiatric diagnosis. These 'Six Things' occupy a place in the pantheon of victim-blaming. People with mental illnesses are not effortlessly able to “stay happy!” or “move on!” or stop repetitive hand-washing (OCD) or avoid reckless spending (manic episode). And this is NOT their fault. And it doesn't make them mentally weak.

Most psychiatric disorders, in essence, involve thoughts, emotions, and/or behaviors that spin out of control. Here, I'm using control in a colloquial (but not absolute) sense, meaning: it's frequently difficult to stop a downward spiral once it gets started. Although overly simplistic...
  • Major depression involves thoughts (ruminations) and feelings of worthlessness and utter bleakness that spin out of control.
  • Generalized anxiety disorder involves thoughts (worry) about an imagined awful future that spin out of control.
  • Panic disorder involves a thwarted escape or safety response to perceived danger that has spun out of control.
  • Mania involves elevated mood and intense motivation for reward that spin out of control.
  • Obsessive-compulsive disorder involves maladaptive repetitive behaviors (that spin out of control) meant to quell maladaptive worrisome thoughts that have spun out of control.
  • Borderline personality disorder involves overly intense negative emotions that spin out of control and lead to self-destructive behaviors.
If people were able to control all this (without external intervention), the condition wouldn't reach the level of “disorder” — causing functional impairment and (usually) significant distress (but not always; e.g., people in the midst of a full-blown manic episode lack insight). I know this cartoonish level of description can raise the specter of free will and responsibility, especially in the context of criminal behavior. Are people with antisocial personality disorder not accountable for their horrible deeds? This timeless debate is beyond the scope of this post.


Computational Psychiatry

Or you can get mathematically fancy and formalize every single mental illness as a result of “faulty Bayesian priors”. Meaning, the brain's own “prediction machine” has incorporated inaccurate assumptions about the self or others or how the world works. A disordered Bayesian brain also ignores empirical evidence that contradicts these assumptions. The process of active inference— the brain's way of minimizing “surprise” when reconciling a top-down internal model and bottom-up external input  — has gone awry (Prossner et al., 2018; Linson & Friston, 2019). Although a sense of agency (or control) is a critical part of the active inference framework, I don't think an impairment in active inference is a choice. Or that one has control over this impairment. In fact, there's a Bayesian formulation of behavioral control (or lack thereof) that considers depression in terms of pessimistic, overly generalized priors, i.e. the depressed person assumes a lack of control over their circumstances.

Learned Helplessness (Huys & Dayan, 2009).


Using this mathematical model, you can confound the “stay happy!” crowd when you use all 24 equations to explain the concept of learned helplessness and its relevance to human depression.

Maybe one day, Bayesians will have a stable of Instagram influencers. Get to work on your branding ideas!


Footnotes

1 Thanks to Neuroskeptic for tweeting about this paper, along with the quote that individuals may "end up being seen (and seeing themselves) as responsible for their own failures to adequately ameliorate the stresses that they suffer."

2Full Disclosure: my late wife was a Peer Researcher with CREST.BD.

3While searching for health and wellness Instagram influencers, I was pleasantly surprised to find @hellolaurenash (a Chicago-based blogger, editor, and yoga and meditation teacher who founded a holistic wellness platform for marginalized communities) and @mynameisjessamyn (a body-positive yoga expert who wants to change the largely white and thin face of yoga and make the practice more accessible to all). I know absolutely nothing about the prevalence of diversity among health and wellness Instagram influencers, just like I know absolutely nothing about Computational Psychiatry.


References

Dum RP, Levinthal DJ, Strick PL. (2016). Motor, cognitive, and affective areas of the cerebral cortex influence the adrenal medulla. Proceedings of the National Academy of Sciences 113(35): 9922-9927.

Dum RP, Levinthal DJ, Strick PL. (2019). The mind–body problem: Circuits that link the cerebral cortex to the adrenal medulla. Proceedings of the National Academy of Sciences 116(52): 26321-26328.

Friston K, Schwartenbeck P, FitzGerald T, Moutoussis M, Behrens T, Dolan RJ. (2013). The anatomy of choice: active inference and agency. Frontiers in Human Neuroscience 7:598.

Huys QJ, Dayan P. (2009). A Bayesian formulation of behavioral control. Cognition 113(3):314-328.

Kaplan J. (2019). Self-Care as Self-Blame Redux: Stress as Personal and Political. Kennedy Inst Ethics J. 29(2):97-123.  PDF.

Linson A, Friston K. (2019). Reframing PTSD for computational psychiatry with the active inference framework. Cognitive Neuropsychiatry 24(5):347-368.

Prosser A, Friston KJ, Bakker N, Parr T. (2018). A Bayesian Account of Psychopathy: A Model of Lacks Remorse and Self-Aggrandizing. Computational Psychiatry 2:92-114.

Smash the wellness industry

... Wellness is a largely white, privileged enterprise catering to largely white, privileged, already thin and able-bodied women, promoting exercise only they have the time to do and Tuscan kale only they have the resources to buy.

Finally, wellness also contributes to the insulting cultural subtext that women cannot be trusted to make decisions when it comes to our own bodies, even when it comes to nourishing them. We must adhere to some sort of “program” or we will go off the rails.

People Neurology: Bennet versus Ann feud captured live!

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In a People Neurology exclusive, contentious footage of Dr. Ann McKee and Dr. Bennet Omalu was captured at the 5th Annual Chronic Traumatic Encephalopathy Conference. Dr. Omalu was not invited due to their long-standing animosity, but he crashed the party anyway during Dr. McKee's highly anticipated Keynote. While she was presenting quantitative proteomic analysis of the postmortem brain tissue of Aaron Hernandez, Dr. Omalu stood up and admonished the entire audience: “Remember, I discovered CTE! [NOTE: this is false.1] You will all answer for this on judgment day.”

The crowd gasped...
 
“Don't believe the blonde white woman who claimed she discovered CTE!”

“Ha. I never claimed I discovered CTE,” Dr. McKee snorted.
 
“His criteria don’t make sense to me! I don’t know what he’s doing.”

“The final decision is still with the doctor who is examining. Not every CTE case will have all those [NINDS] guidelines,” Dr. Omalu retorted.

“His criteria for diagnosing CTE are all over the map,” McKee said.

“This is the problem. People lump me with him, and they lump my work with him, and my work is nothing like this.”




The acrimonious exchange, the conference, and the ridiculous magazine cover are all fictitious, but the quotes are faithful renditions reported by the Washington Post in a scathing critique:
From scientist to salesman
How Bennet Omalu, doctor of ‘Concussion’ fame, built a career on distorted science

. . .
Nearly 15 years [after his first paper], Omalu has withdrawn from the CTE research community and remade himself as an evangelist, traveling the world selling his frightening version of what scientists know about CTE and contact sports. In paid speaking engagements, expert witness testimony and in several books he has authored, Omalu portrays CTE as an epidemic and himself as a crusader, fighting against not just the NFL but also the medical science community, which he claims is too corrupted to acknowledge clear-cut evidence that contact sports destroy lives.

. . .
But across the brain science community, there is wide consensus on one thing: Omalu, the man considered by many the public face of CTE research, routinely exaggerates his accomplishments and dramatically overstates the known risks of CTE and contact sports, fueling misconceptions about the disease, according to interviews with more than 50 experts in neurodegenerative disease and brain injuries, and a review of more than 100 papers from peer-reviewed medical journals.

Much of the reporting isn't new: it was widely known four years ago that Omalu exaggerated his contributions to the field (including the “discovery” of CTE), and that he blasted his critics:

“There is a good deal of jealousy and envy in my field. For me to come out and discover the paradigm shift, it upset some people. I am well aware of that.”

What was new is that respected experts publicly questioned Omalu's past work and his widely disseminated claims.

The biggest revelation was that the histology images in one influential paper did not show CTE, and did not appear to be from the brain of the subject in question.
McKee and other experts confirmed, in interviews, something that long has been an open secret in the CTE research community: Omalu’s paper on Mike Webster — the former Pittsburgh Steelers great who was the first NFL player discovered to have CTE — does not depict or describe the disease as the medical science community defines it.

On the more technical side, the WaPo article provided a basic overview of the CTE pathology and what it does to the brain, along with helpful graphics.

Our sister station, Netflix Neurology, will review Killer Inside: The Mind of Aaron Hernandez (the former NFL player and convicted murderer who died by suicide while incarcerated).



Ann McKee with the brain of Aaron Hernandez,
which showed extensive CTE findings


Footnote

1 In 1928, Harrison S. Martland published PUNCH DRUNK, a paper about boxers with brain damage. And the CTE syndrome was first named by Macdonald Critchley in 1949: Punch-drunk syndromes: The chronic traumatic encephalopathy of boxers.

Netflix Neurology: Inside the Brain of Aaron Hernandez (for a few seconds)

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from Dr. Ann McKee / Boston University


A recent addition to the Netflix “making a murderer” franchise is Killer Inside: The Mind of Aaron Hernandez. At the end of any such story, there is no single answer as to what “made” the murderer.

The story of Aaron Fernandez is still in the public eye because of his fame as a professional football player for the New England Patriots (2010-2012). He was so successful that he signed a 5 year, $40 million contract with the team in August 2012. His alleged involvement in a July 2012 double homicide came to light in 2014, after he had been charged with the June 2013 murder of his friend, Odin Lloyd. For the latter crime, he was found guilty and sentenced to life without parole. He was acquitted of the double homicide, but two days later he hanged himself with a bed sheet in his jail cell.

His brain was donated to the Boston University CTE Center. From extensive coverage in the New York Times and elsewhere, we already knew that the autopsy revealed extensive chronic traumatic encephalopathy (CTE).

If you hope to gain insight into repetitive head injury, brain pathology, and violent behavior from watching this documentary, you'll be disappointed. The 3-part series spent 5 minutes on CTE and 3 hours 15 minutes on everything else his childhood, violent father, hurtful mother, immense athletic talent, football career, ex-con friends, girlfriend and daughter, heavy drug use, street life, weapons collection, paranoia, alleged shootings, alleged same-sex relationships, arrests, murder trials, conviction, appeal, recorded jailhouse telephone conversations, outwardly professed homophobia, death by suicide, and numerous interviews with friends and former players.

Much of this material was pruient and unnecessary, especially the speculations about his hidden sexual orientation and how this might have fueled his anger.


Prosecution Considered a “Fear of Outing” Motive

This argument was preposterous and a rarity in the history of violence involving the LGBTQ community: Hernandez supposedly feared that his friend would reveal his secret life as a bisexual man, so he killed Lloyd to preserve his image as a hyper-masculine heterosexual man. This baffling obsession with sexuality is distracting and dangerous, as aptly explained by D. Watkins:
There's no evidence proving that Hernandez's sexuality made him a killer. So why is the newly resurfaced Hernandez conversation centered around his sex life? Probably because sex is juicy, forbidden and learning that Hernandez may have been gay provides the consumers with content for endless hours of gossip about what public figures do in their personal lives.
Fortunately, this argument was not allowed at trial.


The Potential Role of CTE Was an Afterthought

A Rolling Stone interview with director Geno McDermott revealed the project began as a 90 minute documentary initially presented at DOC NYC in 2018. Netflix was interested in expanding the doc into a multi-part series. The gay angle emerged when high school friend/lover Dennis SanSoucie agreed to an on-camera interview. Other additions included newly available recordings of prison phone calls, and a coda about CTE, the neurodegenerative disease that may be associated with repeated concussions in high-impact sports (in concert with other poorly delineated factors).

At the very end of Killer Inside, self-serving celebrity defense attorney Jose Baez spoke about the family's decision to donate Aaron's brain to the CTE Center at Boston University.



Dr. Ann McKee with the brain of Aaron Fernandez


Dr. McKee said Hernandez had very advanced disease for a 27 year old:
...and not only was it advanced microscopically, especially in the frontal lobes which are very important for decision-making, judgment and cognition, this would be the first case we've ever seen of that kind of damage in such a young individual.

I can say this is substantial damage that undoubtedly took years to develop. This is not something that is developed acutely or just in the last several years. I imagine these changes had been evolving over maybe even as long as a decade.



Then we see interviews with non-experts, who make causal connections between Aaron's CTE and his erratic, violent, tragic behavior. Worst of all is sleazy lawyer Jose Baez, who drummed up business for other players to sue the NFL under false pretenses (there is currently no way to accurately diagnose CTE in living persons).

Why didn't Aaron's brother, who grew up with the same abusive father and played football for many years, become a murderer? I'll let former NFL player Jermaine Wiggins have the last word:
My thoughts to people who think that CTE was somehow involved, I think that's an absolute cop out. There are thousands of former NFL players out there that might have dealt with concussions, I've dealt with them. So to use that as a cop out? I'm not... no, no. C'mon, we're smarter than that, people.”

Further Reading

Is CTE Detectable in Living NFL Players?
this 2013 post is still true today

Brief Guide to the CTE Brains in the News. Part 1: Aaron Hernandez

02202020

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New and exciting content will be available for you this weekend. Until then, please enjoy Lena Lovich and my four part series on money, religion, and numerology from 2008.


080808 (god is a number part 1)

01 1 01 1 01 (god is a number part 2)

3.14159265 (god is a number part 3)

7 (god is a number part 4)





You certainly do have a strange effect on me
I never thought that I could feel the way I feel
There's something in your eyes gives me a wild idea
I never want to be apart from you my dear
I guess it must be true
My lucky number's two

--Lena Lovich, Lucky Number

The City of Lost Engrams

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I was travelling back in time to an unreal place when The City appeared again after a long absence. It had been 16 months since we’d been together, and The City was not pleased. A vivid image of the security lines at the airport ushered me out of town to continue my journey to The Place That Doesn’t Exist.

A diabolical entanglement known as time has stolen memories from their homes in the dentate gyrus, lateral amygdala, precuneus, and elsewhere. These engrams hold the key to the past and the future. Without them – and their mysteriously stored representations – “we are condemned to an eternal present.”

Dwelling in the present is the path to enlightenment – “…the only moment to be alive is the present moment.”1  There is no past and no future. The amnesiac icon H.M. was the perfect being.

And yet, avoiding the past makes everything seem unreal. So does avoidance of an unlivable present. Perhaps I am preoccupied with a future of Other Deaths. That, I am not ready for.

The dead are neglected and forgotten by other people because their windows of tolerance are closed to further mourning. Their lack of reinforcement negates my grief. The opportunities for systems consolidation2 are waning.

Time. Avoidance. Neglect. They all silence my memories of The City.

I've had hundreds of involuntary visual images appear in my mind's eye like photographs, and I've documented all of them.




The images visit me rarely these days. They must be forcefully shaken from their torpor.

My passport expired 6 months ago. I finally noticed this recently.



I used to be able to cry, but now I can’t cry even though I want to.


Engram Cells

This meditation on memory, loss, and memory loss was inspired by a recent review article on memory engrams (Josselyn & Tonegawa, 2020). An “engram” is the neural substrate for storing and recalling memories. Futuristic “Inception-like” experiments in mice have shown that conditioned fear memories (tone-shock or context-shock associations) can be deleted or “inserted” by manipulating a functionally-defined class of neurons known as engram cells.



A pink engram cell alongside a white nonengram cell (modified from Josselyn & Tonegawa, 2020). Within the hippocampus, dentate gyrus cells were filled with a tracer to examine cellular anatomy (white). Engram cells active during fear conditioning were engineered to express the red fluorescent protein mCherry, which appears pink (because of overlap with the white tracer).


A primary truism of neuroscience is that memory storage is mediated by structural and synaptic plasticity. If engram cells are dedicated to preserving specific memories, the next question is: how do you define “a memory”? Most rodent studies search for engram cells associated with memories like “this location = bad”. But what about engrams formed after learning a list of words? Memories of Tomato, Attic, PliersMotorcycle, etc. are presumably represented by overlapping/distinctive groups of engrams distributed across multiple brain regions. What about complex autobiographical memories, like what you did on your 21st birthday? The full day (and night) of festivities consisted of many different events tied together by their temporal proximity and autobiographical significance. Studies of event perception and segmentation (Zacks, 2020) are informative in this regard:
What is the relationship between event structure in perception and that in memory? There is strong evidence that the segments that are identified during event perception correspond to the representational units in subsequent memory. First, the boundaries themselves are remembered exceptionally well. ... Second, event boundaries tended to occur at points in time when many features were changing, and the participants remembered those points better.

Life Beyond Engrams

The development of an appropriate animal model to allow selective manipulation of the whole-brain engram associated with one “birthday event” (but not the others) seems remote. Likewise, the often-involuntary nature of autobiographical memory retrieval (Bernsten, 2010) — in my case, the spontaneous appearance of visual images associated with loss and grief — is not illuminated by current engram research. Nor is the feeling of self-alienation that occurs when those memories start to fade.


Footnotes

1“Dwelling in the present moment
    I know this is a wonderful moment.”

   –Thich Nhat Hanh, Being Peace [PDF]

But the Present Moment usually isn't all that great,” I say.

2 Or contextual binding, depending on your degree of hippocampal dependence.


References

Berntsen D. (2010). The unbidden past: Involuntary autobiographical memories as a basic mode of remembering. Current Directions in Psychological Science 19(3):138-42.

Josselyn SA, Tonegawa S. (2020). Memory engrams: Recalling the past and imagining the future. Science 367(6473).

Zacks JM. (2020). Event Perception and Memory. Annu Rev Psychol. 71:165-191.


The Place that Doesn't Exist







I can’t remember the last time I was there. It seems like I was just there. I am always here.




All my lovers were there with me
All my past and futures
And we all went to heaven in a little row boat
There was nothing to fear and nothing to doubt

--Radiohead, Pyramid Song

(I can cry now)

Coping with COVID-19: Resources for Managing Mental Health

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  • Don't shake hands. 
  • Maintain a distance of 6 feet. 
  • Don't touch surfaces that could contain respiratory droplets. 
  • Don't touch your face. [It's very hard to not touch your face.]

When your leaders fail to follow the most basic guidelines for preventing the spread of COVID-19, trust and confidence are eroded.





The coronavirus pandemic has raised (nearly) everyone's level of anxiety and stress. Rampant panic buying, superstore shelves emptied of toilet paper, selfish people hoarding hand sanitizer. Worries about elderly relatives, jobs, money, health care costs.

If you already have a serious anxiety disorder, how can you possibly cope in the current climate of fear and uncertainty? What if one of the core recommendations to help prevent disease transmission is the very pathology you've worked so hard to overcome?


Obsessive-Compulsive Disorder

Contamination fears cause many individuals with OCD to compulsively wash their hands. Meanwhile, the directive to frequently wash your hands with soap & water for 20 seconds could be quite triggering for some. The International OCD Foundation has provided helpful resources:

Resources for the OCD and related disorders community during the COVID-19 outbreak
In times like these, what the experts are recommending temporarily becomes our new normal. This may mean that you need to make some changes to your treatment, including which exposures you do, when you do them, how frequently, etc. What might normally be considered a “baseline” for people with OCD to aspire to should shift to match the recommended guidelines for as long as those guidelines are in place. A good suggestion would be to talk about the guidelines with your treatment team at your next session and go over how, if at all, your plan might change for the near future.

It is important for all of us in the OCD and related disorders community to remember that this is temporary, and understand that it may feel uncomfortable. You are not going backwards in your recovery journey because the baseline changes. These troubled times will end, and you will keep doing your best in the meantime.
They also provide recommendations for what you should and should NOT do.

Examples of What to do:
  • set a time limit of 5 minutes per day for reading news and updates from trusted sources
  • take breaks and allow yourself to do things you enjoy
  • consult your treatment team
Examples of What NOT to do:
  • avoid the temptation to learn “everything” about COVID-19
  • do not excessively wash your hands
  • don’t let “social distancing” rob you of your support networks seek online connections

Generalized Anxiety Disorder

Tips from Health Canada:

What to do if you’re anxious or worried about coronavirus (COVID-19)
  • Be self-compassionate
  • Limit the news & unplug from social media
  • Stop talking about coronavirus
  • Protect yourself
...and more


Health Anxiety
The constant new barrage of developments regarding the current outbreak of COVID-19 can cause particular challenges for people living with anxiety, stress and/or anxiety-based depression especially those that have health anxiety and/or OCD.
Suggestions from Anxiety UK:

Health and other forms of anxiety and coronavirus
  • Firstly, try to limit your exposure to news sources which are covering the coronavirus issue as this only serves to feed fear.
[an ongoing theme]


COVID-19 and anxiety – part 2
  • For those that have anxiety disorders such as claustrophobia, agoraphobia and panic disorder, some of the potential management strategies that are being discussed in relation to COVID-19 might give rise to specific challenges and thoughts of ‘feeling trapped’.
  • Fearing being ‘out of control’ and ‘being unable to tolerate uncertainty’ are actually common characteristics of many anxiety disorders and therefore it stands to reason why so many individuals with pre-existing anxiety may now be seemingly experiencing an exacerbation of their anxiety as a result of COVID-19.
[see Intolerance of uncertainty, appraisals, coping, and anxiety: The case of the 2009 H1N1 pandemic]


Post-Traumatic Stress Disorder

Suggestions from the National Center for PTSD:

Managing Stress Associated with the COVID-19 Virus Outbreak
  • Increase Sense of Safety 
  • Stay Connected
  • Cultivate Ways to be More Calm
  • Improve Your Sense of Control and Ability to Endure
Those who have been faced with life-threatening situations recommended the following strategies:
  • Quickly recognize, acknowledge, and accept the reality of the situation.
  • Make a plan for dealing with feelings of being overwhelmed or overly distressed.
  • Combat unhelpful emotions by using distraction or staying busy—both mentally and physically.
  • Avoid impulsive behavior.
  • Increase positive coping behaviors that have worked in the past.
  • Shift negative self-statements to statements that allow you to function with less distress.
...and more


Managing Healthcare Workers' Stress Associated with the COVID-19 Virus Outbreak
A strong service-orientation, a lack of time, difficulties in acknowledging or recognizing their own needs, stigma, and fear of being removed from their duties during a crisis may prevent staff from requesting support if they are experiencing stress reactions. Given this, employers should be proactive in encouraging supportive care in an atmosphere free of stigma, coercion, and fear of negative consequences.
[...this link has guidelines for a crucial segment of the population Heath Care Workers  — who may neglect their own self-care.]


Of Interest to Mental Health Professionals

Mental Health Concerns Arise Amid COVID-19 Epidemic
Experts studying the spread of novel coronavirus disease (COVID-19) are increasingly concerned about the psychological ramifications of the epidemic, particularly for older adults and medical staff working on the ground. The issue has been raised in several correspondence pieces published in Lancet Psychiatry.

Coronavirus on the inpatient unit: A new challenge for psychiatry

by Dr. Dinah Miller (contributor to the iconic and now-retired Shrink Rap blog)
. . .

COVID-19 represents a new challenge for the inpatient psychiatry unit. Some patients on an acute psychiatric unit may be agitated, uncooperative, or even violent, and it’s not hard to imagine the distress of anyone who has a patient spit on them as we’re all trying to remember not to shake hands. Inevitably, there will be patients who present for psychiatric admission with no respiratory symptoms, who are admitted and then become ill and are diagnosed with COVID-19. In the meantime, the potential is there for contagion to other patients on the unit, the hospital staff, and visitors to the unit.

Readers if you have any suggestions for helpful resources or personal coping strategies, feel free to comment here or on Twitter.

The "Six Feet Away" Rule is Woefully Inadequate

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“...the rapid international spread of COVID-19 suggests that using arbitrary droplet size cutoffs may not accurately reflect what actually occurs with respiratory emissions, possibly contributing to the ineffectiveness of some procedures used to limit the spread of respiratory disease” (Bourouiba, 2020).

Dr. Lydia Bourouiba has published an important paper that updates 1930s-era models of respiratory infectious disease transmission based on the size of droplets emitted when a person breathes or talks or coughs or sneezes. Large droplets were thought to contaminate the area immediately surrounding an infected individual, because they settle before evaporating. In contrast, small droplets evaporate quickly and form residual particulates, or aerosols. However, the classification of droplet size (and therefore the mode of transmission) is not based on modern science. Yet this scheme still informs public health policy to this day.

The figure above shows a Multiphase Turbulent Gas Cloud From a Human Sneeze (Bourouiba, 2020). The puff trapped droplets of many sizes and carried them quite a long distance (23-26 feet!) while evading evaporation. Droplets that settle can contaminate surfaces. Aerosols may persist in the air for hours, depending on ambient temperature and humidity, as well as prevailing winds or airflow of indoor ventilation systems.1

Watch the educational video showing Respiratory Pathogen Emission Dynamics and you will be truly horrified!!

This newer understanding of respiratory emission dynamics has implications for mask and respiratory design, social distancing recommendations, and other public health interventions during and after the COVID-19 pandemic.”


Speaking of masks, droplets are visible after sneezing into a surgical mask (Granville-Chapman & Dunn, 2007). Although the paper was a light-hearted study appearing in the Christmas issue of BMJ, the spread of respiratory droplets is no longer a joke.




Footnote

1 A recent report by investigators in Singapore suggested the possibility of significant environmental contamination (including air vents) in the hospital rooms of SARS-CoV-2 patients (Sean Wei Xiang Ong et al., 2020). The air samples themselves were negative, however. And standard cleaning  procedures effectively decontaminated surfaces.


References

Bourouiba L (2020). Turbulent Gas Clouds and Respiratory Pathogen Emissions: Potential Implications for Reducing Transmission of COVID-19. JAMA March 26.

Granville-Chapman J, Dunn RL. (2007). Excuse me!BMJ 335:1293.

Ong SW, Tan YK, Chia PY, Lee TH, Ng OT, Wong MS, Marimuthu K. (2020). Air, surface environmental, and personal protective equipment contamination by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) from a symptomatic patient. JAMA March 4.


Thanks to @midendian and @perrymetzger for alerting me to this article.

The Noble Prize for a Life Well-Lived

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In honor of a beautiful and affectionate cat.



RIP, beloved Max
April 19, 2003 April 24, 2020


So much acrimony and confusion and death...


In the true meaning of the word, Max lived a noble life.

“But he was just a cat,” you say. Yes, that's true. But he was loving and kind and selfless until the very end. He was a wonderful companion, and a great source of comfort to me (especially after my partner died in October 2018).



Max and Sandra
Feb. 2, 2017


He was cherished by previous caretakers and human friends, who showered him with gifts.



Christmas Eve, 2017




Christmas Day, 2018


But now he's gone and life continues, filled with acrimony and confusion and death.


The Very Real Threat of Trump’s Deepfake by David Frum

While reading this article in The Atlantic, I was immediately struck by how a cat could hold human values and respect human life to a greater extent than the President of the United States. Sounds absurd, doesn't it? But not really. Not any more. Here's David Frum:
April 26, 2020, was an especially manic day in the presidency of Donald Trump.  ...  something was gnawing at him. Perhaps his business troubles were weighing on him.  ...  Or perhaps Trump was still seething at the widespread ridicule of his press conference of April 23, when he suggested using disinfectant “by injection.” Or perhaps something else had shifted his mood from its usual setting of seething aggrievement to frothing fury.

Whatever the cause, between early afternoon and near 9 o’clock eastern time, Trump fired off a sequence of crazy-even-for-him tweets and retweets. He demanded that reporters be stripped of the “Noble prizes” they had supposedly been awarded for their reporting on Trump scandals, apparently conflating them with the Pulitzers—and then pretended that his misspelling of Nobel had been intentional.  ...  He retweeted an increasingly wild and weird range of supporters’ Twitter accounts.

Trump shows no compassion for the suffering around him, no sympathy for the families devastated by the loss of their loved ones, and only hollow praise for the health care workers, the bus drivers, the home delivery drivers, the grocery store clerks, and the sanitation workers who put their lives on the line every day.

Eternal optimists say “we're all in this together” while sitting at home on Zoom meetings, placing endless orders on Amazon, and fretting about their sourdough starter. I'm only marginally better, but I realize I'm privileged. {I've tried to help financially contributing to homeless organizations, a fund for unemployed hourly workers, bookstores, museums, etc.}

And obviously I'm way more pessimistic.

How does this rant honor my cat??


Case History

Max was diagnosed with intestinal lymphoma in August 2019 at the age of 16. He also had a murky ailment that made it difficult for him to eat (“his tongue is inflamed” or later, “he has a mass at the base of his tongue”), but the true cause was never confirmed. He was prescribed oral chemotherapy pills three times a week and an oral steroid (prednisolone syrup) twice daily. I declined the chemo pills, opting for quality of life for both of us. Max's oral steroid became unworkable after four doses.

This was not fair, especially after my wife suffered through Stage 4 cancer for a year.

Another vet started bimonthly / monthly injections of Depo-Medrol (methyl prednisolone) to reduce the inflammation in his mouth, and as a partial treatment for his lymphoma. It worked wonders (for a while). He ran up and down stairs, played with his toys, and jumped over the red chair!

He started getting worse in January. His weight was down to 9.5 lbs (4.3 kg), a 2 lb loss in two months. He was prescribed buprenorphine as needed for pain and transdermal mirtazapine as an appetite stimulant. My quest for palatable foods became more and more challenging. I spent hours walking the aisles of pet superstores.




His last regular appointment was March 9. And then the shelter-in-place orders were issued.


Pet Care During the COVID-19 Pandemic

Max's condition was getting worse. Depo-Medrol was less and less effective, and he needed injections every two weeks. The veterinary practice enacted stringent measures to protect its essential workers. In-person appointments were reserved for animals showing signs of extreme pain and suffering. Virtual Vet was used for consults and for recommending treatment plans. We had an appointment on March 27. Max was prescribed his usual meds. I picked them up curbside (calling upon arrival) and paid via contactless transaction. I watched a helpful YouTube video and then administered his subcutaneous injection of Depo-Medrol.

By April 16, I had grown desperate. The poor fellow was having a severe bout of diarrhea that lasted for days. I tried scheduling a Virtual Vet appointment and called for a refill of buprenorphine. Finally I got through and picked up more meds the next day. These included oral metronidazole, a hideously bitter and distressing medication that made his mouth foam.

He improved slightly. I was up for hours in the middle of the night, trying to coax him to eat. Some "meaty morsels" and "flaked' varieties were palatable for their gravy. I got out the food processor and whirled them into a very soft format, which he mostly rejected. “But you were just licking the gravy off these meaty morsels!” I told him. Finally I came up with a winning concoction. But this was only a palliative interlude before the inevitable.

Then I realized I'd established a Palliative Care Unit for my cat.

On April 23, I could no longer care for him myself. I brought him to the ER for severe dehydration. He had blood work and an "incidental" ultrasound, neither of which he'd had since his initial diagnosis. The results were devastating. Anemia due to suspected blood loss from his GI tract. Elevated white blood cell count (no surprise). Emerging diabetes mellitus (e.g., glucose in his urine), a known side-effect of steroid treatment. He weighed only 3.8 kg (8.4 lbs).

Most concerning was “free fluid in the abdomen and what looks like masses, possibly lymph nodes and fluid distended bowel loops.”  /  “If he does not improve in the next few days to a week, humane euthanasia should be considered given what we know.”

I picked him up and brought him home. He hated car rides much more than actual visits to the vet or treatments of any sort. Veterinary staff all loved him. The report from his ER doc even said, “Max is a very good cat.”

He was withdrawn for several hours. Then he got over it and sat on my lap in the red chair, purring. Here he is, as beautiful as ever.




The change in Max from that day to the next was astounding. He couldn't hold his head up any more. He tried to drink some water but couldn't manage to do it. I don't think any additional intervention would have improved his condition. I didn't want to wait any longer and had to act quickly.

I was fortunate to find a caring and compassionate vet who made house calls, and wasn't ridiculously overboard on COVID-19 restrictions. Some said they wouldn't enter the main living area — it had to take place outside or in the garage or in their mobile van. But Max was in a comfortable and familiar environment, at least. And then he didn't have to suffer any longer.


Max was such a sweet, loving, affectionate cat. He sought me out until the end, until his very last day when he was too weak to do so.




This is another story of love, and of loss. How we care for the most helpless among us is an enduring sign of our humanity.



MORE CAT PHOTOS below.



Max loved to bask in the sun.




He was very well-read.






And excellent at camouflage.



On rare occasions, he pretended to be fierce.



And in his youth, he was a proud hunter.




But mostly, he was a non-dominant scaredy cat...





...who loved to play with catnip toys...



...and snuggle up in the laps of his companions.


Max and Sandra
June 27, 2015


Tragically, I'm forced to go on without them, during an unprecedented time of anxiety and social isolation.


I love you and miss you both.
💔 😭 🐈

The COVID Stress Scales

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Danger. Deprivation. Xenophobia. Contamination. These are some of the fears related to COVID-19. Scores of COVID questionnaires have popped up recently to assess fear, anxiety, stress, and depression related to the novel coronavirus and its massive disruption to daily life. Most are freely available for use as research tools, but few have been validated and peer reviewed.

The COVID Stress Scales (CSS) developed by Taylor and colleagues (2020) were recently published in the Journal of Anxiety Disorders. The authors propose a new COVID Stress Syndrome, and present evidence that the CSS subscales are intercorrelated (which is suggestive of a “coherent” condition).

To develop the CSS, representative samples of people in Canada (n=3,479) and the US (n=3,375) completed a 58-item survey on Qualtrics. Factor analysis identified five subscales...
  1. COVID danger and contamination fears
  2. COVID fears about economic consequences
  3. COVID xenophobia
  4. COVID compulsive checking and reassurance seeking
  5. COVID traumatic stress symptoms

...and limited the questionnaire to 36 items. I'll note that “fears about economic consequences” were restricted to a lack of supplies at grocery stores and pharmacies, rather than fears of crushing debt, eviction, hunger, and homelessness because of unemployment.

One can view this new syndrome as a context-related extension of OCD contamination fears, compulsive checking, and health anxiety (preoccupation with the possibility of serious illness). Indeed, convergent validity was confirmed by showing correlations with established measures of those conditions. Unique aspects of COVID Stress Syndrome not seen in other diagnoses include fears that grocery stores would run out of toilet paper,1 and especially a fear of foreigners (xenophobia). Xenophobia is promulgated by politicians and amplified by bad actors on social media and IRL. I don't think xenophobia (specifically, anti-Asian sentiment) is on the list of symptoms for any DSM diagnosis.

Basically, it seems that a coherent condition called COVID Stress Syndrome would require racist beliefs and a fear of people who are Chinese, Chinese-American, or Chinese-Canadian.2The prevalence of COVID Stress Syndrome in their Canadian and American samples was not specified, nor was the cut-off point for such a diagnosis. Plenty of Americans are xenophobic, but they don't have bad dreams about coronavirus.

In an editorial, Taylor and Asmundson (2020) said:
It appears that people who develop COVID Stress Syndrome have pre-existing psychopathology, particularly pre-existing high levels of health anxiety and obsessive-compulsive checking and contamination symptoms. It remains to be seen whether the COVID Stress Syndrome is simply an adjustment disorder, abating once the pandemic is over, or whether it will become chronic for some individuals.

So much about COVID-19 “remains to be seen”, and this level of uncertainly is a major source of anxiety on its own.


Footnotes

1The toilet paper question just missed the cut...included were worries about water, cleaning supplies, medications, etc. The original version also included “worry about looting & rioting.”

2 One could really say East Asian people more broadly. Or actually, anyone considered “Other”.


References

Taylor S, Asmundson GJG. (2020). Life in a post-pandemic world: What to expect of anxiety-related conditions and their treatment. J Anxiety Disord. 2020; 72:102231.

Taylor S, Landry CA, Paluszek MM, Fergus TA, McKay D, Asmundson GJG. Development and initial validation of the COVID Stress Scales. J Anxiety Disord. 2020; 72:102232.


Additional Scales (from a compendium of COVID questionnaires on Google docs)

Epidemic-Pandemic Impacts Inventory Racial/Ethic Discrimination Addendum (15 items).

COVID-19 Stressful events (13 items)

COVID-19 Concerns (9 items)

Coronavirus Stressor Survey (9 items)

CRISIS (The CoRonavIruS Health Impact Survey V0.3) - more here

Covid-19 Staff Needs and Concerns Survey (18 items)

COVID-19 Family Stress Screener (10 items)


ADDENDUM (June 1, 2020): MORE!

UCLA Brief COVID-19 Screen for Child/Adolescent PTSD

Fear of COVID-19 Scale (10 items)
Ahorsu DK, Lin CY, Imani V, Saffari M, Griffiths MD, Pakpour AH. The Fear of COVID-19 Scale: Development and Initial Validation. International Journal of Mental Health and Addiction. 2020 Mar 27:1-9.
Coronavirus Anxiety Scale (5 items)
Lee SA. Coronavirus Anxiety Scale: A brief mental health screener for COVID-19 related anxiety. Death Studies. 2020 Apr 16:1-9.




Traces of Fear in Aphantasia

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When reading a vivid story that describes a shark attack, do you imagine yourself in the ocean, seeing the dorsal fin approach you?
“...sun glints off the waves / suddenly a dark flash / in the distant waves / maybe it was a shadow / you turn to the beach / more people are pointing / they look anxious / looking back out to sea / a large fin / slices the surface / moving closer...”



Or is your “mind's eye” — your visual mental imagery of the evocative scene ⁠— essentially a blank?



early warning: picture of snake below

One's subjective internal life of thinking, perceiving, imagining, and remembering belongs to oneself and nobody else. [Brain scanning is still not a mind reader.] An increasing number of media reports (and scientific studies) have shined a light on this fact: the mental life of one person differs from that of another, sometimes in startling ways. It's always been that way, but now it's out in the open.

The cat is out of the bag.



When reading that sentence, did you have a fleeting mental picture in your mind's eye? Maybe it was clear, maybe it was hazy. Or maybe you saw no visual image at all... if that was the case, you might have a condition known as Aphantasia, the inability to voluntarily generate mental imagery. This is a normal variant of human experience, albeit an uncommon one.

What are the “consequences” of having Aphantasia? You may be more likely to choose a scientific or mathematical occupation, although artists and photographers with Aphantasia certainly exist. Aphantasia is often associated with poor autobiographical memory (diminished ability to recall the past episodes of your life).

Does Aphantasia affect your emotional reactions to ordinary experiences like looking at pictures or reading a story? If visual imagery is important for having an affective response to the shark story, would people with Aphantasia show physiological (bodily) signs of emotion while reading? Wicken and colleagues (2019) asked this question by comparing the skin conductance response (sweaty palms) evoked by reading vs. looking at pictures. This was a pilot study reported in a preprint (not yet peer reviewed).

If visual imagery is necessary for an affective response to evocative stories, then A-Phantasics should have diminished (or absent) skin conductance responses (SCRs) compared to Typical-Phantasics. In contrast, SCRs to unpleasant pictures should not differ between the two groups, because the picture-viewing experience doesn't require imagery. However, it's still possible that imagery-based elaboration (or verbal elaboration, for that matter) could amplify the SCR, especially since each picture was presented for 5 seconds.




For the reading condition, stories were presented as sequential short phrases (to match reading speed across subjects). The control conditions weren't well-matched, unfortunately. This was especially true for Stories, where reading the task instructions served as the neutral comparison condition (instead of reading a neutral story).


Participants

The participants were 24 individuals with intact imagery (based on the Vividness of Visual Imagery Questionnaire and binocular rivalry priming1 scores within the typical range) and 22 self-identified Aphantasics (who were older, on average, than the control participants).2 For the Aphantasia group, seven (out of the original 29) were excluded because their VVIQ or priming scores exceeded the cut-off.


Results

For the Pictures (Perception) condition, the physiological response to Unpleasant vs. Neutral stimuli was not significantly different for the two groups. Incidentally speaking, the skin conductance level (SCL = SCR) was quite variable, as shown in the shaded portion of the graph below.



Adapted from Fig. 1D (Wicken et al., 2019).  Left: Aggregated progressions of baseline-corrected SCL across the duration of the frightening photos sequence (sampled as average across 5 sec time bins). Right: Mean and standard error across time bins.


The Stories were another story... For the Stories (Imagery) condition, the Aphantasic group did not show an elevated SCL for the scary stories, unlike the controls.



Adapted from Fig. 1B (Wicken et al., 2019).


Or as the authors suggested, “[Aphantasia] is associated with a flat-line physiological response to frightening written, but not perceptual scenarios, supporting imagery’s critical role in emotion.”

I'd say “flat-line” is a little judgy, with the semantic implication that the Aphantasics were dead or something.

I'd like to see subjective ratings of emotion (affect and arousal) for the Pictures and Stories, especially since the primary means of identifying people with Aphantasia is based on subjective report. Nonetheless, this is an intriguing finding, with additional evidence forthcoming (or so I imagine)...


Footnotes

1 See: Is there an objective test for Aphantasia? Binocular rivalry priming can be a useful “objective” measure of aphantasia (Keogh & Pearson, 2018), but it's not necessarily diagnostic at an individual level.

2 Mean age = 33.7 yrs for Aphantasia, mean = 23.0 for controls. I don't know why they didn't recruit age-matched controls from the community, other than the convenience of recruiting university students.


Reference

Wicken M, Keogh R, Pearson J. (2019). The critical role of mental imagery in human emotion: insights from Aphantasia. bioRxiv. 2019 Jan 1:726844.




What Color is Your Mental Parachute?

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Aphantasia and Occupational Choice


NOTE: This isn't a real test of visual imagery. Click HERE for the Simple Aphantasia Test, which assesses whether (and how well) you can imagine pictures in your mind's eye.


Do you prefer to learn by studying material that is visual, auditory, verbal (reading/writing), or kinesthetic (“by doing”) in nature? A massive educational industry has promoted the idea of distinct “learning styles” based on preference for one of these four modalities (take the VARK!). This neuromythhas beenthoroughlydebunked (see this FAQ).

But we humans clearly vary in our cognitive strengths, and this in turn influences our choice of career. This should come as no surprise.

A recent study queried the occupational choices of self-selected populations of people at the extremes of visual imagery abilities: those with Aphantasia (n=993 male/981 female) or Hyperphantasia (n=65 male/132 female). This was assessed by their scores on the Vividness of Visual Imagery Questionnaire (VVIQ). There was also a control group with average scores on the VVIQ, but they were poorly matched on age and education.


Fig. 4 (Zeman et al., 2020). Percentage of participants with aphantasia and hyperphantasia reporting their occupation as being:
1 = Management, 2 = Business and financial; 3 = Computer and mathematical/Life, physical, social science; 4 = Education, training, and library; 5 = Arts, design, entertainment, sports and media; 6 = Healthcare, practitioners and technical.


As expected, people with fantastic visual imagery were more likely to be in arts, design, entertainment, and media, as well as sports (an excellent ability to imagine a pole vault or swing a bat would be very helpful). People with poor to no visual imagery were more likely to choose a scientific or mathematical occupation. These categories are rather broad, however. For instance, “media” includes print media. And artists and photographers with Aphantasia certainly do exist.

The study had a number of limitations, e.g. washing out individual differences and relying on introspection for rating visual imagery ability (as noted by the authors). There are more objective ways to test for imagery, but these involve in-person visits. Although the authors were circumspect in the Discussion, they were a bit splashy in the title of their paper (Phantasia–The Psychological Significance Of Lifelong Visual Imagery Vivdness Extremes). And the condition of “Aphantasia” existed long before it was named and popularized. But these researchers have caught the imagination of the general public, so to speak:
The delineation of these forms of extreme imagery also clarifies a vital distinction between imagery and imagination: people with aphantasia–who include the geneticist Craig Venter, the neurologist Oliver Sacks and the creator of Firefox, Blake Ross–can be richly imaginative, as visualisation is only one element of this more complex capacity to represent, reshape and reconceive things in their absence.

Reference

Zeman A, Milton F, Della Sala S, Dewar M, Frayling T, Gaddum J, Hattersley A, Heuerman-Williamson B, Jones K, MacKisack M, Winlove C. (2020). Phantasia–The Psychological Significance Of Lifelong Visual Imagery Vivdness Extremes. Cortex. 2020 May 4; S0010-9452(20)30140-4.

The Mundane Spectacle of the Three Little Pigs

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“This Neuralink is implanted in the region of the brain that uh where where the snout the snout is located which is actually quite a large part of the pig's brain.”1

Elon Musk held a press event (product demo) to make grandiose claims about the Neuralink 1024-channel brain implant currently under development by his start-up.

Three pigs were unveiled, all healthy and happy: Joyce (the one without an implant), Dorothy (who formerly had an implant), and Gertrude, the star of the day with her snout boops. The crowd applauded, impressed at this monumental accomplishment. However, recording spike trains from the brains of animals is as old as time. And actually, wirelessImplantable Neuroprosthetics in Pigs is so2011...2


The title of this post in TNW said it best:

I was excited for Neuralink. Then I watched Elon Musk’s stupid demo
“Here’s the one fact you need to know: Neuralink's actual device is less capable than similar medical BCIs already on the market. The big claim to fame here is that Neuralink hopes one day to bring this technology to the masses.”

And really, invasive intracranial technology is likely to obsolete by the time the requisite advances in neural decoding would occur (if ever). As Kording Lab member Ari Benjamin told BBC News:
“Once they have the recordings, Neuralink will need to decode them and will someday hit the barrier that is our lack of basic understanding of how the brain works, no matter how many neurons they record from.

Decoding goals and movement plans is hard when you don't understand the neural code in which those things are communicated.”

Another winner in the snark department was MIT Technology Review, with:

Elon Musk’s Neuralink is neuroscience theater
“...Neuralink has provided no evidence that it can (or has even tried to) treat depression, insomnia, or a dozen other diseases that Musk mentioned in a slide. One difficulty ahead of the company is perfecting microwires that can survive the ‘corrosive’ context of a living brain for a decade. That problem alone could take years to solve.

The primary objective of the streamed demo, instead, was to stir excitement, recruit engineers to the company (which already employs about 100 people), and build the kind of fan base that has cheered on Musk’s other ventures...”

The cult of Musk is indeed cheering, in a rather credulous fashion (e.g., Why Neuralink Will Change Humanity Forever).


Footnotes

1 It's actually correct that the representation of the snout in pig somatosensory cortex occupies a disproportionately large portion of the cortex.

2Borton et al. (2011) reported on their “complete neural prosthetic developmental system using a wireless sensor as the implant, a pig as the animal model, and a novel data acquisition paradigm for actuator control.” At that time, the system had 'only' 16 channels, but the field as a whole has evolved since then.


ADDENDUM (Sept 1, 2020):
from Neuralink Progress Update, Summer 2020



An implantable device will solve all these problems by correcting aberrant electrical signals. And drive summon your Tesla telepathically too!

  • Save and replay memories!
  • Super-Vision! (ultraviolet or infrared)
  • Use a computer by thought alone!

Neuralink in a Dozen Pigs

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In a far-ranging chat with Kara Swisher, Elon Musk talked about sustainable energy, brain implants, the stupidity of the press, and more. He gave a casual update on the “Three Little Pigs” demo of Neuralink's 1024-channel chip, finally admitting that his lofty goals are in a “very, very primitive stage”:

Elon Musk: You can make people walk again. You could solve extreme depression or anxiety or schizophrenia or seizures. You could give a mother back her memory so she could remember who her kids are, you know. Basically, if you live long enough, you’re going to get dementia of some kind. And you’ll want to have something to help you. [NOTE: here, he didn't acknowledge the potential for advancements in biological treatments for dementia.]

Kara Swisher:  Could it program in empathy? Or other things? Do you imagine that being part of this? [LAUGHTER] Or hey you could—

EM: You could technically program anything. So empathy is probably a good one.

KS: So where are we in doing this?

EM: So where we are right now is we’re still in a very, very primitive stage. Where thus far we’ve had a lot of successful implants in pigs. And we now have a pig that has had an implant that’s working well and it’s been there for over three months. And we now have implanted about a dozen pigs. And the sensors are working well. A large part of a pig brain is about its snout. So you can literally rub the pig on its snout and we can detect exactly where you touch the snout. [NOTE: “Yeah, that's called somatotopic mapping,” said John Hughlings Jackson in 1886.]


Listen to the podcast: Elon Musk: ‘A.I. Doesn’t Need to Hate Us to Destroy Us’ 

In a conversation with Kara Swisher, the billionaire entrepreneur talks space-faring civilization, battery-powered everything and computer chips in your skull.


Bonus!! Musk on Trump:

Kara Swisher: Do you like him? Are you voting for him?

Elon Musk: [SIGHING] I mean, I’m — to be totally frank I’m not — I mean, I think — let’s just see how the debates go. You know?

KS: That’s going to be your thing, the debates?

EM: Well, I think that is probably the thing that will decide things for America.

KS: Why is that?

EM: I think people just want to see if Biden’s got it together.

KS: Mm-hmm. And if he does?

EM: If he does, he probably wins.

 

He hasn't yet tweeted about the disgraceful dumpster fire... 

 




Previous Article Next Article

COVID-19, Predictive Coding, and Terror Management

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Pandemics have a way of bringing death into sharper focus in our everyday lives. As of this writing, 1,188,259 people around the world have died from COVID-19, including 234,218 in the United States. In the dark days of April, the death rate was over 20%. Although this has declined dramatically (to 3%), it’s utterly reckless to minimize the risks of coronavirus and flaunt every mitigation strategy endorsed by infectious disease specialists.


He's like an evil Oprah. You're getting COVID. And you're getting COVID!

One might think that contracting and recovering from COVID-19 would be a sobering experience for most people, but not for the Übermensch (Nietzschean 'Superman'... but really, 'Last Man' is more appropriate) who had access to the latest experimental treatments.1 Trump's boastful reaction is exactly how the 'Coronavirus Episode' of the (scripted) White House reality show was written: “I feel better than I did 20 years ago!” and “I'm a perfect physical specimen.”

This dismissive display reinforces the partisan divide on perceptions of the pandemic and the federal response to it. A recent study by Pew Research Center found major differences in how Democrats and Republicans view the severity of COVID-19. Results from the survey (conducted Aug. 31-Sept. 7, 2020) were no surprise. 

 

 

And as we know, Democrats and Republicans exist in alternate universes constructed by non-overlapping media sources (CNN vs. Fox, to oversimplify), which in turn correlates with whether they wear masks, practice social distancing, and avoid crowds. A new paper in Science (Finkel et al., 2020) integrated data from multiple disciplines to examine the partisan political environment in the US. They found that Democratic and Republican voters have become:

“...POLITICALLY SECTARIAN -- fervently committed to a political identity characterized by three properties: (1) othering (opposing partisans are alien to us), (2) aversion (they are dislikable & untrustworthy), and (3) moralization (they are iniquitous).”

The authors concluded that the combination of all three core ingredients is especially toxic. Furthermore:



Perfect! Dread and existential threat to a fervent political identity during a pandemic that reminds us of our own mortality. The Science paper has a sidebar about motivated (or biased) cognition and whether Democrats and Republicans are equally susceptible (many studies), or whether Republicans are more susceptible than Democrats (other studies).2 

 


We seek out information that confirms our views and push away evidence that contradicts our pre-existing beliefs about “the other”.


Death Denial to Avert Existential Crisis

We also push away thoughts of our own demise: death is something that happens to other people, not to me. Awareness of death or mortality salience— pondering the inevitability of your own death, a time when you will no longer exist — triggers anxiety, according the Terror Management Theory (TMT). In response to this threat, humans react in ways to boost their self-esteem and reinforce their own values (and punish outsiders). These cognitive processes are conceptualized as nebulous “defenses” [nebulous to me, at least] that are deployed to minimize terror. Notably, however, experimental manipulation of mortality salience did not affect “worldview defense” in the large-scale Many Labs 4 replication project, which throws cold water on this aspect of TMT.


Predictive Coding and Perceived Risk of COVID-19

An alternative view of how we disassociate ourselves from death awareness is provided by predictive coding theory. This influential framework hypothesizes that the brain is constantly generating and updating its models of the world based on top-down “biases” and bottom-up sensory input (Clark, 2013):

Brains ... are essentially prediction machines. They are bundles of cells that support perception and action by constantly attempting to match incoming sensory inputs with top-down expectations or predictions. This is achieved using a hierarchical generative model that aims to minimize prediction error within a bidirectional cascade of cortical processing. 

Prediction errors are minimized by perceptual inference (updating predictions to better match the input) or active inference (sampling the input in a biased fashion to better fit the predictions). A recent paper considered this framework with regard to beliefs generated during the pandemic, and how they're related to health precautions adopted by individuals to mitigate spread of the virus (Bottemanne et al, 2020). This paper was conceptual (not computational), and it was written in French (meaning I had to read it using Google translate). 

In brief, pandemics are massive sources of uncertainty. There was a delay in the perception of risk, followed by unrealistic optimism (“certainly I do not run the risk of becoming infected”) despite the growing accumulation of evidence to the contrary. The reduced perception of risk leads people to flaunt precautionary mandates, even in France (which is currently showing a greater spike in cases than the US). Subsequently, overwhelming media saturation on the daily death toll and the dangers of COVID-19 updates predictions of risk and triggers mortality salience (Bottemanne et al, 2020). 

And in support of TMT,Framing COVID-19 as an Existential Threat Predicts Anxious Arousal and Prejudice towards Chinese People. Every day in the US, the president and his minions call the novel coronavirus “the China virus and other disparaging terms. Is it any wonder that discrimination and violence against Asian-Americans has increased?


If you're American, PLEASE VOTE if you haven't already.


Further Reading

Covid-19 makes us think about our mortality. Our brains aren’t designed for that.

Existential Neuroscience: a field in search of meaning

Neuroexistentialism: A Brain in Search of Meaning

Existential Dread of Absurd Social Psychology Studies

Terror Management Theory

Footnotes

1The Last Man is the antithesis of the Superman:

An overman [superman] as described by Zarathustra, the main character in Thus Spoke Zarathustra, is the one who is willing to risk all for the sake of enhancement of humanity. In contrary [is] the 'last man' whose sole desire is his own comfort and is incapable of creating anything beyond oneself in any form.

Trump's declaration: “...All I know is I took something, whatever the hell it was. I felt good very quickly . . . I felt like Superman.” Whether his kitchen-sink treatment regimen was a good idea has firmly challenged.

2 There's a large literature on potential cognitive and neural differences between liberals and conservatives, but I won't cover that here. I wrote about many of these studies in the days of yore.


References

Bottemanne H, Morlaàs O, Schmidt L, Fossati P. (2020). Coronavirus: cerveau prédictif et gestion de la terreur [Coronavirus: Predictive brain and terror management]. Encephale 46(3S):S107-S113.

Clark A. (2013). Whatever next? Predictive brains, situated agents, and the future of cognitive science. Behavioral and Brain Sciences 36(3):181-204.

Finkel EJ et al. (2020). Political sectarianism in America. Science 370:533-536.


“What's going on with this guy?”

 


 

What is the truth underneath the tweet?

  AP Photo


President Trump showed labored breathing during his first appearance on the White House balcony


Regarding his joyride in the black SUV while he was still hospitalized at Walter Reed:

He did not look tough; he looked trapped.

He looked desperate. He looked pathetic. He looked weak — not because he was ill or because he was finally wearing a mask but because instead of doing the hard work of accepting his own vulnerabilities in the face of sickness, he’d propped himself up on the strength and professionalism of Secret Service agents. Instead of focusing on the humbling task of getting better, he was consumed by the desire to simply look good.

 the end.