Sunday, June 30, 2019

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


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

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

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

TIFU by explaining my synesthesia to my boyfriend

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

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

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

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

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






There's even a subreddit for people with aphantasia:



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





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

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


Footnotes

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

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

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

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


Further Reading

Aphantasia Index

The Eye's Mind

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

Imagine These Experiments in Aphantasia (my 2016 post).

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

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



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



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

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Sunday, June 16, 2019

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


Eve is plagued by a waking nightmare.

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


– from Pickering (2019).

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



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

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

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

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

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


When Westerners Attend Large Buddhist Retreats

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

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

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




Nameless Dread

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

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




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

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


Footnote

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


References

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

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

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

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

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


Further Reading

Derealization / Dying

Feeling Mighty Unreal: Derealization in Kleine-Levin Syndrome

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



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

- click table for a larger view -

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Sunday, May 19, 2019

The Secret Lives of Goats

Goats Galore (May 2019)


If you live in a drought-ridden, wildfire-prone area on the West Coast, you may see herds of goats chomping on dry grass and overgrown brush. This was initially surprising for many who live in urban areas, but it's become commonplace where I live. Announcements appear on local message boards, and families bring their children.


Goats Goats Goats (June 2017)


Goats are glamorous, and super popular on social media now (e.g. Instagram, more Instagram, and Twitter). Over 41 million people have watched Goats Yelling Like Humans - Super Cut Compilation on YouTube. We all know that goats have complex vocalizations, but very few of us know what they mean.





For the health and well-being of livestock, it's advantageous to understand the emotional states conveyed by vocalizations, postures, and other behaviors. A 2015 study measured the acoustic features of different goat calls, along with their associated behavioral and physiological responses. Twenty-two adult goats were put in four situations:
(1) control (neutral)
(2) anticipation of a food reward (positive)
(3) food-related frustration (negative)
(4) social isolation (negative)
Dr. Elodie Briefer and colleagues conducted the study at a goat sanctuary in Kent, UK (Buttercups Sanctuary for Goats). The caprine participants had lived at the sanctuary for at least two years and were fully habituated to humans. Heart rate and respiration were recorded as indicators of arousal, so this dimension of emotion could be considered separately from valence (positive/negative). For conditions #1-3, the goats were tested in pairs (adjacent pens) to avoid the stress of social isolation. They were habituated to the general set-up, to the Frustration and Isolation scenarios, and to the heart rate monitor before the actual experimental sessions, which were run on separate days. Additional details are presented in the first footnote.1





Audio A1. One call produced during a negative situation (food frustration), followed by a call produced during a positive situation (food reward) by the same goat (Briefer et al., 2015).


Behavioral responses during the scenarios were timed and scored; these included tail position, locomotion, rapid head movement, ear orientation, and number of calls. The investigators recorded the calls and produced spectograms that illustrated the frequencies of the vocal signals.



The call on the left (a) was emitted during food frustration (first call in Audio A1). The call on the right (b) was produced during food reward; it has a lower fundamental frequency (F0) and smaller frequency modulations. Modified from Fig. 2 (Briefer et al., 2015).


Both negative and positive food situations resulted in greater goat arousal (measured by heart rate) than the neutral control condition and the low arousal negative condition (social isolation). Behaviorally speaking, arousal and valence had different indicators:
During high arousal situations, goats displayed more head movements, moved more, had their ears pointed forwards more often and to the side less often, and produced more calls. ... In positive situations, as opposed to negative ones, goats had their ears oriented backwards less often and spent more time with the tail up.
Happy goats have their tails up, and do not point their ears backwards. I think I would need a lot more training to identify the range of goat emotions conveyed in my amateur video. At least I know not to stare at them, but next time I should read more about their reactions to human head and body postures.


Do goats show a left or right hemisphere advantage for vocal perception?

Now that the researchers have characterized the valence and arousal communicated by goat calls, another study asked whether goats show a left hemisphere or right hemisphere “preference” for the perception of different calls (Baciadonna et al., 2019). How is this measured, you ask?

Head-Turning in Goats and Babies

The head-turn preference paradigm is widely used in studies of speech perception in infants.

Figure from Prosody cues word order in 7-month-old bilingual infants (Gervain & Werker, 2013).




However, I don't know whether this paradigm is used to assess lateralization of speech perception in babies. In the animal literature, a similar head-orienting response is a standard experimental procedure. For now, we will have to accept the underlying assumption that orienting left or right may be an indicator of a contralateral hemispheric “preference” for that specific vocalization (i.e., orienting to the left side indicates a right hemisphere dominance, and vice versa).
The experimental procedure usually applied to test functional auditory asymmetries in response to vocalizations of conspecifics and heterospecifics is based on a major assumption (Teufel et al. 2007; Siniscalchi et al. 2008). It is assumed that when a sound is perceived simultaneously in both ears, the head orientation to either the left or right side is an indicator of the side of the hemisphere that is primarily involved in the response to the stimulus presented. There is strong evidence that this is the case in humans ... The assumption is also supported by the neuroanatomic evidence of the contralateral connection of the auditory pathways in the mammalian brain (Rogers and Andrew 2002; Ocklenburg et al. 2011).

The experimental set-up to test this in goats is shown below.



A feeding bowl (filled with a tasty mixture of dry pasta and hay) was fixed at the center of the arena opposite to the entrance. The speakers were positioned at a distance of 2 meters from the right and left side of the bowl and were aligned to it. 'X' indicates the position of the Experimenter. Modified from Fig. 2 (Baciadonna et al., 2019).


Four types of vocalizations were played over the speakers: food anticipation, food frustration, isolation, and dog bark (presumably a negative stimulus). Three examples of each vocalization were played, each from a different and unfamiliar goat (or dog).

The various theories of brain lateralization of emotion predicted different results. The right hemisphere model predicts right hemisphere dominance (head turn to the left) for high-arousal emotion regardless of valence (food anticipation, food frustration, dog barks). In contrast, the valence model predicts right hemisphere dominance for processing negative emotions (food frustration, isolation, dog barks), and left hemisphere dominance for positive emotions (food anticipation). The conspecific model predicts left hemisphere dominance for all goat calls (“familiar and non-threatening”) and right hemisphere dominance for dog barks. Finally, a general emotion model predicts right hemisphere dominance for all of the vocalizations, because they're all emotion-laden.

The results sort of supported the conspecific model (according to the authors), if we now accept that dog barks are actually “familiar and non-threatening” [if I understand correctly]. The head-orienting response did not differ significantly between the four vocalizations, and there was a slight bias for head orienting to the right (p=.046 vs. chance level), when collapsed across all stimulus types. 2

The time to resume feeding after hearing a vocalization (a measure of fear) didn't differ between goat calls and dog barks, so the authors concluded that “goats at our study site may have been habituated to dog barks and that they did not perceive dog barks as a serious threat.” However, if a Siberian Husky breaks free of its owner and runs around a fenced-in rent-a-goat herd, chaos may ensue.





Footnotes

1 Methodological details:
“(1) During the control situation, goats were left unmanipulated in a pen with hay (‘Control’). This situation did not elicit any calls, but allowed us to obtain baseline values for physiological and behavioural data. (2) The positive situation was the anticipation of an attractive food reward that the goats had been trained to receive during 3 days of habituation (‘Feeding’). (3) After goats had been tested with the Feeding situation, they were tested with a food frustration situation. This consisted of giving food to only one of the goats in the pair and not to the subject (‘Frustration’). (4) The second negative situation was brief isolation, out of sight from conspecifics behind a hedge. For this situation, goats were tested alone and not in a pair (‘Isolation’).”

2 The replication police will certainly go after such a marginal significance level, but I would like to see them organize a “Many Goats in Many Goat Sanctuaries” replication project.


References

Baciadonna L, Nawroth C, Briefer EF, McElligott AG. (2019). Perceptual lateralization of vocal stimuli in goats. Curr Zool. 65(1):67-74. [PDF]

Briefer EF, Tettamanti F, McElligott AG. (2015). Emotions in goats: mapping physiological, behavioural and vocal profiles. Animal Behaviour 99:131-43. [PDF]


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Saturday, April 27, 2019

The Paracetamol Papers


I have secretly obtained a large cache of files from Johnson & Johnson, makers of TYLENOL®, the ubiquitous pain relief medication (generic name: acetaminophen in North America, paracetamol elsewhere). The damaging information contained in these documents has been suppressed by the pharmaceutical giant, for reasons that will become obvious in a moment.1

After a massive upload of materials to Wikileaks, it can now be revealed that Tylenol not only...
...but along with the good comes the bad. Acetaminophen (paracetamol) also has ghastly negative effects that tear at the very fabric of society. These OTC tablets...

In a 2018 review of the literature, Ratner and colleagues warned:
“In many ways, the reviewed findings are alarming. Consumers assume that when they take an over-the-counter pain medication, it will relieve their physical symptoms, but they do not anticipate broader psychological effects.”

In the latest installment of this alarmist saga, we learn that acetaminophen blunts positive empathy, i.e. the capacity to appreciate and identify with the positive emotions of others (Mischkowski et al., 2019). I'll discuss those findings another time.

But now, let's evaluate the entire TYLENOL® oeuvre by taking a step back and examining the plausibility of the published claims. To summarize, one of the most common over-the-counter, non-narcotic, non-NSAID pain-relieving medications in existence supposedly alleviates the personal experience of hurt feelings and social pain and heartache (positive outcomes). At the same time, TYLENOL® blunts the phenomenological experiences of positive emotion and diminishes empathy for others' people's experiences, both good and bad (negative outcomes). Published articles have reported that many of these effects can be observed after ONE REGULAR DOSE of paracetamol. These findings are based on how undergraduates judge a series of hypothetical stories. One major problem (which is not specific to The Paracetamol Papers) concerns the ecological validity of laboratory tasks as measures of the cognitive and emotional constructs of interest. This issue is critical, but outside the main scope of our discussion today. More to the point, an experimental manipulation may cause a statistically significant shift in a variable of interest, but ultimately we have to decide whether a circumscribed finding in the lab has broader implications for society at large.


Why TYLENOL® ?

Another puzzling element is, why choose acetaminophen as the exclusive pain medication of interest? Its mechanisms of action for relieving fever, headache, and other pains are unclear. Thus, the authors don't have a specific, principled reason for choosing TYLENOL® over Advil (ibuprofen) or aspirin. Presumably, the effects should generalize, but that doesn't seem to be the case. For instance, ibuprofen actually Increases Social Pain in men.

The analgesic effects of acetaminophen are mediated by a complex series of cellular mechanisms (Mallet et al., 2017). One proposed mechanism involves descending serotonergic bulbospinal pathways from the brainstem to the spinal cord. This isn't exactly Prozac territory, so the analogy between Tylenol and SSRI antidepressants isn't apt. The capsaicin receptor TRPV1 and the Cav3.2 calcium channel might also be part of the action (Mallet et al., 2017). A recently recognized player is the CB1 cannabinoid receptor. AM404, a metabolite of acetaminophen, indirectly activates CB1 by inhibiting the breakdown and reuptake of anandamide, a naturally occurring cannabinoid in the brain (Mallet et al., 2017).



Speaking of cannabinoids, cannabidiol (CBD) the non-intoxicating cousin of THC has a high profile now because of its soaring popularity for many ailments. Ironically, CBD has a very low affinity for CBand CB2 receptors and may act instead via serotonergic 5-HT1A receptors {PDF}, as a modulator of μ- and δ-opioid receptors, and as an antagonist and inverse agonist at several G protein-coupled receptors. Most CBD use seems to be in the non-therapeutic (placebo) range, because the effective dose for, let's say, anxiety is 10-20 times higher than the average commercial product. You'd have to eat 3-6 bags of cranberry gummies for 285-570 mg of CBD (close to the 300-600 mg recommended dose). Unfortunately, you would also ingest 15-30 mg of THC, which would be quite intoxicating.



Words Have Meanings

If acetaminophen were so effective in “mending broken hearts”, “easing heartaches”, and providing a “cure for a broken heart”, we would be a society of perpetually happy automatons, wiping away the suffering of breakup and divorce with a mere OTC tablet. We'd have Tylenol epidemics and Advil epidemics to rival the scourge of the present Opioid Epidemic.

Meanwhile, social and political discourse in the US has reached a new low. Ironically, the paracetamol “blissed-out” population is enraged because they can't identify with the feelings or opinions of the masses who are 'different' than they are. Somehow, I don't think it's from taking too much Tylenol. A large-scale global survey could put that thought to rest for good.




Footnotes

1 This is not true, of course, I was only kidding. All of the information presented here is publicly available in peer-reviewed journal articles and published press reports.

2 except for when it doesn’t – “In contrast, effects on perceived positivity of the described experiences or perceived pleasure in scenario protagonists were not significant” (Mischkowski et al., 2019).

3 Yes, I made this up too. It is entirely fictitious; no one has ever claimed this, to the best of my knowledge.


References

Mallet C, Eschalier A, Daulhac L. Paracetamol: update on its analgesic mechanism of action (2017). Pain relief–From analgesics to alternative therapies.

Mischkowski D, Crocker J, Way BM. (2019). A Social Analgesic? Acetaminophen(Paracetamol) Reduces Positive Empathy. Front Psychol. 10:538.

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Saturday, April 13, 2019

Does ketamine restore lost synapses? It may, but that doesn't explain its rapid clinical effects


Bravado SPRAVATO™ (esketamine)
© Janssen Pharmaceuticals, Inc. 2019.


Ketamine is the miracle drug that cures depression:
“Recent studies report what is arguably the most important discovery in half a century: the therapeutic agent ketamine that produces rapid (within hours) antidepressant actions in treatment-resistant depressed patients (4, 5). Notably, the rapid antidepressant actions of ketamine are associated with fast induction of synaptogenesis in rodents and reversal of the atrophy caused by chronic stress (6, 7).”

– Duman & Aghajanian (2012). Synaptic Dysfunction in Depression: Potential Therapeutic Targets. Science 338: 68-72.

Beware the risks of ketamine:
“While ketamine may be beneficial to some patients with mood disorders, it is important to consider the limitations of the available data and the potential risk associated with the drug when considering the treatment option.”

– Sanacora et al. (2017). A Consensus Statement on the Use of Ketamine in the Treatment of Mood Disorders. JAMA Psychiatry 74: 399-405.

Ketamine, dark and light:
Is ketamine a destructive club drug that damages the brain and bladder? With psychosis-like effects widely used as a model of schizophrenia? Or is ketamine an exciting new antidepressant, the “most important discovery in half a century”?

For years, I've been utterly fascinated by these separate strands of research that rarely (if ever) intersect. Why is that? Because there's no such thing as “one receptor, one behavior.” And because like most scientific endeavors, neuro-pharmacology/psychiatry research is highly specialized, with experts in one microfield ignoring the literature produced by another...

– The Neurocritic (2015). On the Long Way Down: The Neurophenomenology of Ketamine

Confused?? You're not alone.


FDA Approval

The animal tranquilizer and club drug ketamine now known as a “miraculous” cure for treatment resistant depression has been approved by the FDA in a nasal spray formulation. No more messy IV infusions at shady clinics.

Here's a key Twitter thread that marks the occasion:


How does it work?

A new paper in Science (Moda-Sava et al., 2019) touts the importance of spine formation and synaptogenesis basically, the remodeling of synapses in microcircuits  in prefrontal cortex, a region important for the top-down control of behavior. Specifically, ketamine and its downstream actions are involved in the creation of new spines on dendrites, and in the formation of new synapses. But it turns out this is NOT linked to the rapid improvement in 'depressive' symptoms observed in a mouse model.



So I think we're still in the dark about why some humans can show immediate (albeit short-lived) relief from their unrelenting depression symptoms after ketamine infusion. Moda-Sava et al. say:
Ketamine’s acute effects on depression-related behavior and circuit function occur rapidly and precede the onset of spine formation, which in turn suggests that spine remodeling may be an activity-dependent adaptation to changes in circuit function (83, 88) and is consistent with theoretical models implicating synaptic homeostasis mechanisms in depression and the stress response (89, 90). Although not required for inducing ketamine’s effects acutely, these newly formed spines are critical for sustaining the antidepressant effect over time.

But the problem is, depressed humans require constant treatment with ketamine to maintain any semblance of an effective clinical response, because the beneficial effect is fleeting. If we accept the possibility that ketamine acts through the mTOR signalling pathway, in the long run detrimental effects on the brain (and non-brain systems) may occur (e.g., bladder damage, various cancers, psychosis, etc).

But let's stay isolated in our silos, with our heads in the sand.


Thanks to @o_ceifero for alerting me to this study.

Further Reading

Ketamine for Depression: Yay or Neigh?

Warning about Ketamine in the American Journal of Psychiatry

Chronic Ketamine for Depression: An Unethical Case Study?

still more on ketamine for depression

Update on Ketamine in Palliative Care Settings

Ketamine - Magic Antidepressant, or Expensive Illusion? - by Neuroskeptic

Fighting Depression with Special K - by Scicurious

On the Long Way Down: The Neurophenomenology of Ketamine


Reference

Moda-Sava RN, Murdock MH, Parekh PK, Fetcho RN, Huang BS, Huynh TN, Witztum J, Shaver DC, Rosenthal DL, Alway EJ, Lopez K, Meng Y, Nellissen L, Grosenick L, Milner TA, Deisseroth K, Bito H, Kasai H, Liston C. (2019). Sustained rescue of prefrontal circuit dysfunction by antidepressant-induced spine formation. Science 364(6436). pii: eaat8078.

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Sunday, March 31, 2019

An Amicable Discussion About Psychology and Neuroscience


People like conflict (the interpersonal kind, not BLUE).1 Or at least, they like scientific debate at conferences. Panel discussions that are too harmonious seem to be divisive. Some people will say, “well, now THAT wasn't very controversial.” But as I mentioned last time, one highlight of the 2019 Cognitive Neuroscience Society Annual Meeting was a Symposium organized by Dr. David Poeppel.2

Special Session - The Relation Between Psychology and Neuroscience, David Poeppel, Organizer, Grand Ballroom
Whether we study single cells, measure populations of neurons, characterize anatomical structure, or quantify BOLD, whether we collect reaction times or construct computational models, it is a presupposition of our field that we strive to bridge the neurosciences and the psychological/cognitive sciences. Our tools provide us with ever-greater spatial resolution and ideal temporal resolution. But do we have the right conceptual resolution? This conversation focuses on how we are doing with this challenge, whether we have examples of successful linking hypotheses between psychological and neurobiological accounts, whether we are missing important ideas or tools, and where we might go or should go, if all goes well. The conversation, in other words, examines the very core of cognitive neuroscience.

Conversation. Not debate. So first, let me summarize the conversation. Then I'll get back to the merits (demerits) of debate. In brief, many of the BIG IDEAS motifs of 2017 were revisited...
  • David Marr and the importance of work at all levels of analysis 
  • What are the “laws” that bridge these levels of analysis?
  • Emergent properties” – a unique higher-level entity (e.g., consciousness, a flock of birds) emerges from the activity of lower-level activity (e.g., patterns of neuronal firing, the flight of individual birds)... the sum is greater than its parts
  • Generative Models – formal models that make computational predictions
...with interspersed meta-commentary on replication, publishing, and Advice to Young Neuroscientists. Without further ado:

Dr. David Poeppel – Introductory Remarks that examined the very core of cognitive neuroscience (i.e., “we have to face the music”).
  • the conceptual basis of cognitive neuroscience shouldn't be correlation 
For example, fronto-parietal network connectivity (as determined by resting state fMRI) is associated with some cognitive function, but that doesn't mean it causes or explains the behavior (or internal thought). We all know this, and we all know that “we must want more!” But we haven't the vaguest idea of how to relate complex psychological constructs such as attention, volition, and emotion to ongoing biological processes involving calcium channels, dendrites, and glutamatergic synapses.
  • but what if the psychological and the biological are categorically dissimilar??
In their 2003 book, Philosophical Foundations of Neuroscience, Bennett and Hacker warned that cognitive neuroscientists make the cardinal error of “...commit[ting] the mereological fallacy, the tendency to ascribe to the brain psychological concepts that only make sense when ascribed to whole animals.”
For the characteristic form of explanation in contemporary cognitive neuroscience consists in ascribing psychological attributes to the brain and its parts in order to explain the possession of psychological attributes and the exercise (and deficiencies in the exercise) of cognitive powers by human beings.” (p. 3)

On that optimistic note, the four panelists gave their introductory remarks.

(1) Dr. Lila Davachi asked, “what is the value of the work we do?” Uh, well, that's a difficult question. Are we improving society in some way? Adding to a collective body of knowledge that may (or may not) be the key to explaining behavior and curing disease? Although still difficult, Dr. Davachi posed an easier question, “what are your goals?” To describe behavior, predict behavior (correlation), explain behavior (causation), change behavior (manipulation)? But “what counts as an explanation?” I don't think anyone really answered that question. Instead she mentioned the recurring themes of levels of analysis (without invoking Marr by name), emergent properties (the flock of birds analogy), and bridging laws (that link levels of analysis). The correct level of analysis is/are the one(s) that advance your goals. But what to do about “level chauvinism” in contemporary neuroscience? This question was raised again and again.

(2) Dr. Jennifer Groh jumped right out of the gate with this motif. There are competing narratives in neuroscience we can call the electrode level (recording from neurons) vs. the neuroimaging level (recording large-scale brain activations or “network” interactions based on an indirect measure of neural activity). They make different assumptions about what is significant or worth studying. I found this interesting, since her lab is the only one that records from actual neurons. But there are ever more reductionist scientists who always throw stones at those above them. Neurobiologists (at the electrode level and below) are operating at ever more granular levels of detail, walking away from cognitive neuroscience entirely (who wants to be a dualist, anyway?). I knew exactly where she was going with this: the field is being driven by techniques, doing experiments merely because you can (cough — OPTOGENETICS — cough). Speaking for myself, however, the fact that neurobiologists can control mouse behavior by manipulating highly specific populations of cells raises the specter of insecurity... certain areas of research might not be considered “neuroscience” any more by a bulk of practitioners in the field (just attend the Society for Neuroscience annual meeting).

(3) Dr. Catherine Hartley continued with the recurring theme that we need both prediction and explanation to reach our ultimate goal of understanding behavior. Is a prediction system enough? No, we must know how the black box functions by studying “latent processes” such as representation and computation. But what if we're wrong about representations, I thought? The view of @PsychScientists immediately came to mind. Sorry to interrupt Dr. Hartley, but here's Golonka and Wilson in Ecological Representations:
Mainstream cognitive science and neuroscience both rely heavily on the notion of representation in order to explain the full range of our behavioral repertoire. The relevant feature of representation is its ability to designate (stand in for) spatially or temporally distant properties ... While representational theories are a potentially a powerful foundation for a good cognitive theory, problems such as grounding and system-detectable error remain unsolved. For these and other reasons, ecological explanations reject the need for representations and do not treat the nervous system as doing any mediating work. However, this has left us without a straight-forward vocabulary to engage with so-called 'representation-hungry' problems or the role of the nervous system in cognition.

They go on to invoke James J Gibson's ecological information functions. But I can already hear Dr. Poeppel's colleague @GregoryHickok and others on Twitter debating with @PsychScientists. Oh. Wait. Debate.

Returning to The Conversation that I so rudely interrupted, Dr. Hartley gave some excellent examples of theories that link psychology and neuroscience. The trichromatic theory of color vision — the finding that three independent channels convey color information — was based on psychophysics in the early-mid 1800s (Young–Helmholtz theory). This was over a century before the discovery of cones in the retina, which are sensitive to three different wavelengths. She also mentioned the more frequently used examples of Tolman's cognitive maps (which predated The Hippocampus as a Cognitive Map by 30 years) and error-driven reinforcement learning (Bush–Mosteller [23, 24] and Rescorla–Wagner, both of which predate knowledge of dopamine neurons). To generate good linking hypotheses in the present, we need to construct formal models that make quantitative predictions (generative models).

(4) Dr. Sharon Thompson-Schill gave a brief introduction with no slides, which is good because this post has gotten very long. For this reason, I won't cover the panel discussion and the Q&A period, which continued the same themes outlined above and expanded on “predictivism” (predictive chauvinism and data-driven neuroscience) and raised new points like the value (or not) of introspection in science. When the Cognitive Neuroscience Society updates their YouTube channel, I'll let you know. Another source is the excellent live tweeting of @VukovicNikola. But to wrap up, Dr. Thompson-Schill asked members of the audience whether they consider themselves psychologists or neuroscientists. Most identified as neuroscientists (which is a relative term, I think). Although more people will talk to you on a plane if you say you're a psychologist, “neuroscience is easy, psychology is hard,” a surprising take-home message.


Debating Debates

I've actually wanted to see more debating at the CNS meeting. For instance, the Society for the Neurobiology of Language (SNL) often features a lively debate at their conferences.3 Several examples are listed below.

2016:
Debate: The Consequences of Bilingualism for Cognitive and Neural Function
Ellen Bialystok & Manuel Carreiras

2014:
What counts as neurobiology of language – a debate
Steve Small, Angela Friederici

2013: Panel Discussions
The role of semantic information in reading aloud
Max Coltheart vs Mark Seidenberg

2012: Panel Discussions
What is the role of the insula in speech and language?
Nina F. Dronkers vs Julius Fridriksson


This one-on-one format has been very rare at CNS. Last year we saw a panel of four prominent neuroscientist address/debate...
Big Theory versus Big Data: What Will Solve the Big Problems in Cognitive Neuroscience?


Added-value entertainment was provided by Dr. Gary Marcus, which speaks to the issue of combative personalities dominating the scene.4


Gary Marcus talking over Jack Gallant. Eve Marder is out of the frame.
image by @CogNeuroNews


I'm old enough to remember the most volatile debate in CNS history, which was held (sadly) at the New York Marriott World Trade Center Hotel in 2001. Dr. Nancy Kanwisher and Dr. Isabel Gauthier debated whether face recognition (and activation of the fusiform face area) is a 'special' example of domain specificity (and perhaps an innate ability), or a manifestation of plasticity due to our exceptional expertise at recognizing faces:
A Face-Off on Brain Studies / How we recognize people and objects is a matter of debate
. . .

At the Cognitive Neuroscience Society meeting in Manhattan last week, a panel of scientists on both sides of the debate presented their arguments. On one side is Nancy Kanwisher of MIT, who first proposed that the fusiform gyrus was specifically designed to recognize faces–and faces alone–based on her findings using a magnetic resonance imaging device. Then, Isabel Gauthier, a neuroscientist at Vanderbilt, talked about her research, showing that the fusiform gyrus lights up when looking at many different kinds of objects people are skilled at recognizing.
Kudos to Newsday for keeping this article on their site after all these years.


Footnotes

1 This is the color-word Stroop task: name the font color, rather than read the word. BLUE elicits conflict between the overlearned response ("read the word blue") and the task requirment (say "red").

2 aka the the now-obligatory David Poeppel session on BIG STUFF. See these posts:
3 Let me now get on my soapbox to exhort the conference organizers to keep better online archives  — with stable urls — so I don't have to hunt through archive.org to find links to past meetings.

4 Although this is really tangential, I'm reminded of the Democratic Party presidential contenders in the US. Who deserves more coverage, Beto O'Rourke or Elizabeth Warren? Bernie Sanders or Kamala Harris?

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Friday, March 22, 2019

#CNS2019



It's March, an odd-numbered year, must mean.... it's time for the Cognitive Neuroscience Society Annual Meeting to be in San Francisco!

I only started looking at the schedule yesterday and noticed the now-obligatory David Poeppel session on BIG stuff 1 on Saturday (March 23, 2019):

Special Session - The Relation Between Psychology and Neuroscience, David Poeppel, Organizer,  Grand Ballroom

Then I clicked on the link and saw a rare occurrence: an all-female slate of speakers!



Whether we study single cells, measure populations of neurons, characterize anatomical structure, or quantify BOLD, whether we collect reaction times or construct computational models, it is a presupposition of our field that we strive to bridge the neurosciences and the psychological/cognitive sciences. Our tools provide us with ever-greater spatial resolution and ideal temporal resolution. But do we have the right conceptual resolution? This conversation focuses on how we are doing with this challenge, whether we have examples of successful linking hypotheses between psychological and neurobiological accounts, whether we are missing important ideas or tools, and where we might go or should go, if all goes well. The conversation, in other words, examines the very core of cognitive neuroscience.

Also on the schedule tomorrow is the public lecture and keynote address by Matt Walker Why Sleep?
Can you recall the last time you woke up without an alarm clock feeling refreshed, not needing caffeine? If the answer is “no,” you are not alone. Two-thirds of adults fail to obtain the recommended 8 hours of nightly sleep. I doubt you are surprised by the answer to this question, but you may be surprised by the consequences. This talk will describe not only the good things that happen when you get sleep, but the alarmingly bad things that happen when you don’t get enough. The presentation will focus on the brain (learning, memory aging, Alzheimer’s disease, education), but further highlight disease-related consequences in the body (cancer, diabetes, cardiovascular disease). The take-home: sleep is the single most effective thing we can do to reset the health of our brains and bodies.

Why sleep, indeed.

Meanwhile, Foals are playing tonight at The Fox Theater in Oakland. Tickets are still available.




view video on YouTube.


ADDENDUM: The sequel was finally posted on March 31: An Amicable Discussion About Psychology and Neuroscience.


Footnote

1 See these posts:

The Big Ideas in Cognitive Neuroscience, Explained #CNS2017

Big Theory, Big Data, and Big Worries in Cognitive Neuroscience #CNS2018

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