Astray Authorities #9

 Here is the latest in a series of videos I am making. 

We Cannot Trust Neuroscientists to Speak Accurately About What Brains Do and What Minds Experience

A cardiologist is a specialist in hearts and the human circulatory system. You can trust a cardiologist to speak accurately about how hearts work and what hearts do. For example, if a cardiologist tells you that hearts normally beat about 60 times a minute when people are resting, and often more than 100 times a minutes when people are running, you can trust that this statement is correct.  One of the reasons we can trust cardiologists to speak accurately about hearts is that cardiologists are not members of a belief community.  There is no set of dogmas that you are indoctrinated in if you train to become a cardiologist. 

But in regard to neuroscientists, we have a vastly different state of affairs. Neuroscientists are members of a belief community that we can call the NBC, the Neuroscientist Belief Community. Just as the members of some church share some particular articles of faith, neuroscientists share a set of dogmatic belief tenets that make up a creed.  The two main dogmas of this creed are:

(1) the belief that the human mind is merely the product of the human brain, or perhaps that the human mind merely consists of particular brain states;

(2) the belief that human memory is a product of the human brain -- that memory creation involves some act of storage going on in the brain, and that memory recall involves the retrieval of information stored in the brain. 

Because neuroscientists are members of a belief community that adheres to these dogmatic tenets, very much like church members clinging to some creed, we should not have a simple, uncomplicated trust in the accuracy of neuroscientists when they speak about brains and minds.  In particular:

(1) whenever neuroscientists talk about the cause of mental phenomena and attribute such phenomena to brains, we should be suspicious about whether their statements are accurate;

(2) we cannot even have high confidence when neuroscientists speak about how brains behave;

(3) we cannot have high confidence in the accuracy of neuroscientists when they generalize about the type of mental experiences that people have. 

The reasons why we should have such a lack of confidence include the following:

• In general, neuroscientists are very often not very thorough or deep students of human minds and human mental experiences, a topic of oceanic depth.  Part of the reason is that getting a neuroscience PhD does even require a deep study of the human mind and human mental experiences. You can look at the required courses needed to get a master's degree in neuroscience, and you will see that such courses involve very little study of the human mind and human mental experiences (often as little as one or two courses in psychology).
• The statements of neuroscientists are very strongly biased by their desire to propagate and bolster the belief tenets of the belief community they belong to. So when neuroscientists attempt to generalize about things such as memory and creativity, they will often be giving us little sermons that preach to us the central dogmas of the creed of their belief community. 

As Exhibit A backing up the title of this post, I refer you to a recent NPR article entitled "7 surprising facts about dreams — why we have them and what they mean." We have an interview with neuroscientist Rahul Jandial, who makes some statements that are inaccurate or poorly supported. 

First, we have this generalization that is incorrect:

"'Reports of nightmares and erotic dreams are nearly universal,' Jandial says, while people rarely report dreaming about math. Jandial says the lack of math makes sense because the part of your brain primarily responsible for logic — the prefrontal cortex — is typically not involved in dreaming."

There is no good basis for claiming that logic comes from the brain, or from any particular part of the brain. See my post "Reasons for Doubting Thought Comes from the Frontal Lobes or Prefrontal Cortex" for relevant facts and reasons. All regions of the brain are continually firing electrical signals, regardless of whether someone is awake or dreaming. So the idea that the prefrontal cortex is electrically inactive during dreaming is incorrect. The prefrontal cortex is just as active as any other region during dreaming. 

As for the idea that people don't dream about math or don't use logic in dreams, that is incorrect. I have for years recorded my dreams. I get numbers and number themes very frequently in my dreams. I have had many dreams involving complex math and philosophical topics. Several of my dreams dealt very explicitly with the extremely mathematical and philosophical topic of the fine-tuning of the universe's fundamental constants, and in some of these dreams I recalled and mentioned at least one specific mathematical fact relating to such a topic. In the dream accounts here (made from notes I took at night just after the dream), on the highly philosophical topic of whether very complex biological organization can be naturally explained, I recalled correctly the rough number of types of protein molecules in the human body (20,000), and also the rough number of types of cells in the human body (about 200), and used such facts as part of subtle complex logic. In another dream mentioned in that post, I used mathematical reasoning to back up claims I was making about the evidence for ESP. Just yesterday I had a dream involving people trying to compute the area of a rectangle with a big circular hole in its center, and I said in the dream "you'll probably end up using pi," and even recalled that pi is 3.14. My mathematical guess in the dream was correct; pi is used as part of the solution of such a problem (given in the Appendix of this post). My dreams very frequently refer to philosophical themes such as life after death. 

In Section 2 of the NPR post, we have the unbelievable claim that neuroscientist "Jandial learned something fundamental about dreams in the midst of performing brain surgery." We are told that during brain surgery done on a conscious patient "after one zap of electricity, Jandial’s patient experienced a nightmare that had recurred for him since childhood." The NPR story attempts to pass this off as some evidence that brains produce dreaming. It makes no sense, because the patient wasn't dreaming, but was awake. And you don't prove that X causes Y because of one case in which X and Y happen at the same time. Having open-brain surgery while awake (something like vivisection) and being zapped with electricity at the same time would for many people be a nightmarish experience. For someone to recall a recurrent nightmare he had during such a nightmarish brain surgery is something we might expect regardless of whether brains produce dreams. 

We then have a mixture of a false claim from the article writer, and a misleading claim by Jandial:

"Research has since confirmed that nightmares, and all dreams, arise from brain activity. 'Now we know from different measurements of electricity and metabolic usage, the sleeping-dreaming brain is burning hot. It's sparking with electricity. We might be asleep, but the brain is on fire,'  Jandial says."

No, brains don't get hotter during sleeping or dreaming, nor does neural electricity increase. Research has not confirmed that dreams are produced by brains. For related evidence, see my post "The Lack of Evidence That Brains Produce Dreaming, and Some Evidence Hinting They Don't." In a major study called the Dream Catcher study, discussed here, scientists looked at EEG readings taken just before sleeping patients woke up, and were asked about whether they were dreaming when awoken. Scientists tried to predict from the EEG readings whether subjects were or were not dreaming, based on the EEG readings. Their predictions were not better than chance. The study provided evidence clashing with the claim that your brain produces dreams. 

We then have an important-sounding statement by Jandial that is the exact opposite of the truth. He states this:

"Jandial says there’s evidence that death may come with one final dream. 'Once the heart stops, with the last gush of blood up the carotid [artery] to the brain, the brain's electricity explodes in the minute or two after cardiac death…Those patterns look like expansive electrical brainwave patterns of dreaming and memory recall,'  Jandial says."

What Jandial claims here is the exact opposite of the truth. When the heart stops, instead of "exploding" in the sense of greatly increasing, the  brain electrical activity very quickly dies away and flatlines, trailing off to a flat line usually within about 10 or 15 seconds. For a discussion of some neuroscience papers that deal with this subject, and show parallel graphs of heart activity and brain wave activity when the heart stops, see my post here. 

The term "isoelectric" or iso-electric in reference to brain waves means a flat-lining equivalent to no electrical activity in the brain, as measured by EEG readings. The paper here states, "Within 10 to 40 seconds after circulatory arrest the EEG becomes iso-electric." Figure 1 of the paper here says that such an isoelectric flat-lining occurred within 26 seconds after the start of ventricular fibrillation, the "V-fib" that is a common cause of sudden cardiac death, with "cortical activity absent." Also referring to a flat-lining of brain waves meaning a stopping of brain electrical activity, another scientific paper says, "several studies have shown that EEG becomes isoelectric within 15 s [seconds] after ischemia [heart stopping] without a significant decrease in ATP level (Naritomi et al., 1988; Alger et al., 1989)."  Another paper tells us this about brain waves and infarction (obstruction of blood flow), using CBF to mean cerebral blood flow:

"When normal CBF declines, the EEG first loses the higher frequencies (alpha and beta bands), while the lower frequencies (delta and theta bands) gradually increase. When the CBF decreases further towards an infarction threshold, the EEG becomes isoelectric." 

This is the exact opposite of what Jandial asserted. Similarly, another paper refers to blood pressure, and tells us, "When flow is below 20 mL/100 g/min (60% below normal), EEG becomes isoelectric." meaning that brain electrical activity flat-lines. The 85-page "Cerebral Protection" document here states, "During cardiac arrest, the EEG becomes isoelectric within 20-30 sec and this persists for several minutes after resuscitation." Another scientific paper states this: 

"Of importance, during cardiac arrest, chest compliance is not confounded by muscle activity. The EEG becomes isoelectric within 15 to 20 seconds, and the patient becomes flaccid (Clark, 1992; Bang, 2003)."

 Similarly, another paper A 2017 paper was "Electroencephalographic Recordings During Withdrawal of Life-Sustaining Therapy Until 30 Minutes After Declaration of Death." That 2017 paper studied the brain waves of four humans who died in Ontario, Canada after their hearts stopped. The paper stated, "We also did not observe any well-defined EEG states following the early cardiac arrest period as previously reported in rats." No "well-defined EEG states" means the same as no brain electrical activity.  Similarly, a recent paper referring to EEG readings of brain waves states this: "The trajectory of EEG activity following cardiac arrest is both well defined and simple. It consists of an almost immediate decline in EEG power, which culminates in a state of isoelectricity [flatlining] within 20 s [seconds]." 

Do a Google search for "EEG becomes isoelectric" or "EEG becomes iso-electric" and you can find quite a few other papers saying that brain waves (as measured by EEG) become isoelectric (in other words go flat or flat-line or die off) within about 20 seconds after a heart stops, or as soon as blood pressure falls below about 50% of normal. 

As for Jandial's claim about "expansive electrical brainwave patterns of dreaming and memory recall" there are no such brain wave patterns that tell when dreaming or memory recall is occurring. When people dream and recall, their brains do not have any kind of unusual or distinctive brain wave activity that allows you to distinguish such states. There is no distinctive neural correlate of either dreaming or recall. That's one reason the Dream Catcher study mentioned above produced only a null result, with scientists being unable to predict whether the subjects had been dreaming before they were awaken. For a discussion of the lack of any evidence that there is any such thing as distinctive brain patterns of memory recall, see my posts here, here and here. 

The glaring misstatement Jandial made about an explosion of electrical activity in the brain after the heart stops (totally contrary to the observed facts) is similar to misstatements made by another neuroscientist, misstatements I debunk in my post here.  A search for Jandial's scientific papers on Google Scholar shows very many intelligent-looking papers relating to the brain and neurosurgery, which make him sound like a good reliable doctor; but I can't find any paper by him about dreaming. A Google Scholar search for "Rahul Jandial+dreams" produces no relevant papers.  So I'm baffled by why NPR would be trying to present Jandial as some expert on dreaming. What we should remember is that in general most neuroscientists are not very careful scholars of human minds and human mental experiences, a topic of oceanic depth. The academic science involving the study of human minds and human mental experiences is not called neuroscience; it is called psychology. You don't have to study much psychology to become a neuroscientist or a neurosurgeon. 

In an article in the Guardian, Jandial gives us an account of dreaming that is not accurate:

"Dreams are the product of profound changes the brain automatically undergoes each night. The rational, executive network in the brain is switched off, and the imaginative, visual and emotional parts are dialed way up. As a result, the dreaming mind is given free rein in a way that has no parallel in our waking lives. We couldn’t think this way when we are awake even if we tried."

Not true. The brain does not undergo any profound change  when you are in bed.  I record my dreams at night, typically several times a night at different intervals during the night, and I experience normal rational mentality the instant I wake up, as I do while recording my dreams in darkness, and then thinking about what I have recorded, typically for quite a few minutes.  My rational mind ponders calmly and thoughtfully numerous times during the night. And people can think in imaginative dream-like ways when they are awake, as creative writers and daydreamers often do. 

In an interview Jandial offers a nonsensical-sounding account of why we dream. He states this:

"Why do we dream? The brain’s activity during dreams suggests it’s preserving or cultivating something essential. Some theories propose dreams as a form of threat rehearsal or a nocturnal therapist. I believe it’s more fundamental: similar to the ‘use it or lose it’ principle that applies to muscles, our brains engage in a nightly routine that stimulates thoughts and ideas not typically relied upon during the day. This built-in process keeps our thinking adaptive and nimble, fostering divergent thoughts and offering an evolutionary advantage. That’s the broader concept I’m exploring."

The explanation makes no sense at all. Dreams do not have any survival value, and cannot be explained as offering some "evolutionary advantage." Theories of why we dream are "a dime a dozen." As one scientist said in 2022, "I don’t think there’s a consensus on what dreaming is, why we dream, what we do, what the function of dreaming is, or even if there is a function."  Jandial has written a book entitled "This Is Why You Dream."  Such a title is a great example of the explanatory hubris of neuroscientists. Once again, we have a neuroscientist pretending to know something he does not know. No scientist understands why people dream, and Jandial does not sound at all like anyone with a credible theory of why dreams arise. Also, it is not true that "the brain’s activity during dreams suggests it’s preserving or cultivating something essential," because experimental studies trying to suggest this idea are in general poorly designed studies guilty of Questionable Research Practices such as way-too-small study group sizes. 

The idea advanced by Jandial that dreaming is a product of random brain activity is very much contrary to my own experience, which is several  consecutive years of dreams with meaningful content that is strongly thematic, being overwhelming centered upon a philosophical theme of life-after-death. You can read about such dreams in my post here. 

In a Salon interview, Jandial is asked why we dream, and he says, "The fundamental principle of neurons, neural tissue, is that either you use it or you lose it."  No, actually, totally contrary to such a claim I rode a bike very well when I tried to ride a bike after not riding a bike for ten years, and I could drive well after not driving for ten years. There is no strong evidence of mental inactivity being a big cause of neuron loss.  And people are often amazingly good at remembering things they learned or experienced decades ago and never thought about in the intervening years, contrary to such a "use it or you lose it" claim.  Jandial has no credible story to tell in the interview regarding why people dream.  In the same interview Jandial again makes the utterly untrue claim that an "explosion of brainwaves happens in the minute or two after the cessation of electrical activity on EKG," which is the opposite of the truth, as I show above (what actually happens is that brainwaves flatline -- become isoelectric -- within 20 seconds after " the cessation of electrical activity on EKG," the same as the heart stopping). 

In the same interview Jandial also makes the untrue claim that in the one or two minutes after the heart stops the brain "explodes with neurotransmitters." There is no good evidence that neurotransmitters appear more frequently after a heart stops, and the very strong evidence we have of the quick cessation of brain electrical activity upon a heart stopping is a strong reason for thinking no such increase in neurotransmitters occurs. The untruth of Jandial's claim here should be obvious when you consider that there is no device capable of measuring human neurotransmitter increases or decreases in the minutes after a heart stops. Neurotransmitters are measured by blood or urine tests, which are never done at the moment of death, and which require lab work.  

Mind activity varies vastly, but brain activity (as measured by EEG and fMRI) is remarkably stable (unlike heart activity that varies by 200% or more). The lack of big changes in brain activity corresponding to changes in mental activity is one of many reasons for thinking that brains are not the source of minds. There is only one time when brain activity very sharply spikes: during the "electrical storm" events called seizures. If you're not talking about seizures or fevers and you're not talking about military destruction, you should not be using any language like that in the visual above. Brain imaging visuals typically involve misleading depictions of brain activity differences of less than 1%, differences so small they cannot be accurately described as some region of the brain "lighting up."  

Neuroscientists have an enormously bad speech habit regarding how they describe the activity of humans. The habit consists of senselessly claiming brains were the source of things that we only know came from people, things which cannot credibly be explained as brain-caused. So we have neuroscientists senselessly speaking like this:

• Instead of saying "people can recall things very quickly" a neuroscientist will say something like "brains can recall things very quickly."
• Instead of saying "people can solve hard math problems," a neuroscientist will say something like "brains can solve hard math problems."
• Instead of saying "people have strong beliefs about politics" a neuroscientist will say something like "brains can have strong beliefs about politics."
• Instead of saying "a person has a unified sense of the self," a neuroscientist will say something "the brain gives rise to a unified sense of the self." 
• Instead of saying "you use facts to guide your decisions," a neuroscientist will say something like "your brain uses facts to guide its decisions."
• Instead of saying "someone may recall an experience from long ago," a neuroscientist will say something like "a brain may recall an experience from long ago."

I could give endless similar examples. The fact is that neuroscientists have a bad habit of making unnecessary and dubious causal attributions to brains, rather than making simple and indisputable statements using words such as "people" or "someone" or "you." Neuroscientist have a dysfunctional speech habit of constantly saying "brains do..." when they should be saying "people do..." or saying "your brain does..." when they should be saying "you do..." This bad habit that they display over and over again is one major reason why you cannot trust a neuroscientist to speak accurately when talking about what brains do. You should treat with suspicion most claims a neuroscientist makes about what a brain does or can do. We can trust cardiologists to accurately describe what hearts do, but we cannot trust neuroscientists to accurately describe what brains do. 

Appendix:  It is an interesting brain teaser to ask someone how he would compute the area of a rectangle with a large hole in its center, one looking like the figure below. 

You can ask a person: "Suppose you know the radius of the circle, and the width and length of the rectangle. And suppose you have an internet connection. How would you compute as quickly as possible the area of the green shape?"

The answer is:

(1) First, you use the Internet to very quickly find the formula for computing the area of a circle, which is "area = pi times radius squared,"   and use that to compute the area of the circular hole.  

(2) Then you compute the area of the green rectangle, by multiplying its width by its length. 

(3) Then you subtract the first number from the second to get the area of the green figure. 

In my dream of yesterday, I was with people who were trying to solve this problem. In the dream I said to someone, "You'll probably end up using pi." That was correct. Pi (the ratio of the circumference of a circle to its diameter) is part of the correct solution of this problem. But how did I know this in my dream, having never previously pondered this problem, and certainly not knowing the formula for computing the area of a circle? The dream is one of many I have had that collectively bolster my belief (held mainly for other reasons) that dreams do not come from brains, and that dreams sometimes have a source beyond individual human minds.  

Cognitive Neuroscience Is Floundering, So the Kavli 2024 Neuroscience Prize Went to Low-Quality Research

If you look up the phrase "cognitive neuroscience" you will typically get a description that does not correspond to any scientifically established reality. You will typically get a description saying something like "the branch of science that investigates the neural causes of cognition," a description that presupposes the incorrect claim that cognition has a neural basis. Cognitive neuroscience is getting nowhere, mainly because it is based on the false assumption that the brain is the cause of the mind. Honest and properly designed studies will never produce evidence showing a neural basis for cognition. But there are 1001 ways to do poorly designed Questionable Research Practices studies that may fool someone into thinking that a little progress has been made in showing a neural basis of minds. 

The Kavli Foundation is a foundation founded by millions of dollars in grants from the late Fred Kavli. The foundation issues science prizes and science grants. One of its semi-annual prizes is in neuroscience. The 1 million dollar Kavli Prize in neuroscience was recently announced when a  false claim was made by the Kavli Foundation. The official citation appearing in the award announcement says that the 2024 prize was announced "for the discovery of a highly localized and specialized system for representation of faces in human and non-human primate neocortex." No such thing was ever discovered.  There are no representations of faces anywhere in the brain.  What we have in the 2024 Kavli neuroscience prize announcement is a bogus achievement legend, a claim that something big was done, when no such thing was ever done. 

Claims by neuroscientists that they have found "representations" in the brain (other than genetic representations) are examples of what very abundantly exists in biology: groundless achievement legends. There is no robust evidence for any such representations. 

Excluding the genetic information stored in DNA and its genes, there are simply no physical signs of learned information stored in a brain in any kind of organized format that resembles some kind of system of representation. If learned information were stored in a brain, it would tend to have an easily detected hallmark: the hallmark of token repetition.  There would be some system of tokens, each of which would represent something, perhaps a sound or a color pixel or a letter. There would be very many repetitions of different types of symbolic tokens.   Some examples of tokens are given below. Other examples of tokens include nucleotide base pairs (which in particular combinations of 3 base pairs represent particular amino acids), and also coins and bills (some particular combination of coins and bills can represent some particular amount of wealth). 

Other than the nucleotide base pair triple combinations that represent mere low-level chemical information such as amino acids, something found in neurons and many other types of cells outside of the brain, there is no sign at all of any repetition of symbolic tokens in the brain. Except for genetic information which is merely low-level chemical information, we can find none of the hallmarks of symbolic information (the repetition of symbolic tokens) inside the brain. No one has ever found anything that looks like traces or remnants of learned information by studying brain tissue. If you cut off some piece of brain tissue when someone dies, and place it under the most powerful electron microscope, you will never find any evidence that such tissue stored information learned during a lifetime, and you will never be able to figure out what a person learned from studying such tissue.  This is one reason why scientists and law enforcement officials never bother to preserve the brains of dead people in hopes of learning something about what such people experienced during their lives, or what they thought or believed, or what deeds they committed.    

But despite their complete failure to find any robust evidence of non-genetic representations in the brain, neuroscientists often make groundless boasts of having discovered representations. What is going on is pareidolia, people reporting seeing something that is not there, after wishfully analyzing large amounts of ambiguous and hazy data. It's like someone eagerly analyzing his toast every day for years, looking for something that looks like the face of Jesus, and eventually reporting he saw something that looked to him like the face of Jesus.  It's also like someone walking in many different forests, eagerly looking for faces on trees, and occasionally reporting a success. Read here for why claims of "place cells" in the hippocampus are unfounded claims based on low-quality research guilty of pareidolia. 

 The official citation page makes these claims:

"The present laureates used functional magnetic resonance imaging (fMRI) to localize different areas in neocortex specialized for face processing. Nancy Kanwisher pioneered the establishment of the functional region of interest (fROI) approach to localize the fusiform face area (FFA) in humans using fMRI. Kanwisher was the first to develop and employ a paradigm to identify a region sensitive to faces in each person. This finding strongly supported the idea of modular localization of cognitive function in the neocortex." 

The claims above are not accurate. No robust evidence has ever been provided that there are "different areas in neocortex specialized for face processing." One paper gets a result of only about 1% percent signal change when testing face recognition in different brain areas, getting only about a 1% signal difference for this FFA region.  Two other papers (this paper  and this paper) also find less than a 1% signal difference in this FFA region when testing facial recognition.  Another paper finds only a half of 1% signal change in the FFA during face recognition. Another paper using a larger sample size of 26 people reports a signal change of much less than 1% (only a small fraction of one percent) when testing this FFA region with face recognition. 

Such tiny percent signal changes do nothing to establish any reading of information from brains when visual recognition occurs. For one thing, since the sample sizes are mostly small (around 15 people per study), you could easily get a 1% or 2% signal variation by chance (just as you can easily get 55% of your coin flips being "heads" if you only flip 20 or 40 times).  If there is some tiny little signal change in one region of the brain when a face is recognized, that might be something that has nothing to do with reading memory information from brains. For example, it might be a little of an alert effect or an "aha" emotional boost effect caused by the mere fact of a successful recognition. 

The citation page of the 2024 Kavli neuroscience prize has a link to two papers by Nancy Kanwisher, neither one of which should create any confidence that she achieved what the citation page claims she did. The first paper is the 1997 paper by Kanwisher and others entitled "The Fusiform Face Area: A Module in Human Extrastriate Cortex Specialized for Face Perception." The paper is a bad example of a Questionable Research Practices study. A well-designed experimental neuroscience study will have all study group sizes being at least 15 subjects. That wasn't done in this study. The scientists started out with 15 subjects, and then started doing experiments on subsets of those subjects, those who performed in a way that the scientists found most encouraging. In the resulting study we have way-too-small study group sizes such as only five subjects per study group.  The study used no control subjects, and also completely failed to use any blinding protocol (a necessity for any study like this to be taken seriously). A sample size calculation would have revealed how inadequate the study group sizes were, but the authors failed to do any such calculation (or at least they do not have claim to have done such a calculation). The study was not a pre-registered study, and we get a strong feeling of the authors making up their methods as they gathered data, in violation of sound scientific procedure. 

It is amazing that a study this poorly designed is now being cited  on a prize page as an example of laudatory scientific work. The study would be more properly mentioned on some kind of "Hall of Lame"  page giving examples of poor-quality neuroscience research. Most ridiculously the citation page of the 2024 Kavli neuroscience prize includes a graph showing a 3% percent signal change in the brain of only a single subject. Citing this as evidence for a general effect in brains is as silly as claiming that male heartbeats increase when a male sees a picture of Taylor Swift, and using as your evidence a graph showing a very slight 3% heart rate increase in a single male. 

The only other paper by Nancy Kanwisher mentioned on the citation page of the 2024 Kavli neuroscience prize is her 2017 paper "The Quest for the FFA and Where It Led." That paper is a strange affair that diverges from the conventions of sound scientific research papers. It's a kind of "my glorious quest" paper that seemed to be telling us the wonderful story of how  Nancy Kanwisher progressed against her critics who complained about how weak her evidence was. The paper fails to provide any convincing evidence for Kanwisher's claim that she found a region of the brain specialized for recognizing faces. 

The paper has as its Figure 1 a groundless-looking "schematic map" depicting supposed brain regions specialized for particular tasks. No source is given for this map, which looks like one of those groundless phrenology maps that long appeared in scientific publications. No justification is given for any of the colors that appear in the map. Who made this map, and what data caused them to color the brain regions in these particular ways? The paper does not tell us. For all we know, it's just Nancy's wild guesses.  This extremely dubious Figure 1 is reproduced on the citation page of the 2024 Kavli neuroscience prize as if it was some kind of scientific data, which it is not. 

The citation page of the 2024 Kavli neuroscience prize discusses two other scientists who shared the prize money.  We read these incorrect triumphal claims on the page:

"Winrich Freiwald and Doris Tsao together used fMRI to localize similar face patches in macaque monkeys. Having localized these, they recorded from single neurons in each patch. They showed that the overwhelming majority of visually responsive neurons in the largest such region were face-selective. They proceeded to outline a system of multiple face patches, detailing their interconnections and functional specialization. Face recognition in the earliest patches was dependent on viewpoint, but later became viewpoint-independent through a series of processing stages. Winrich Freiwald in further work characterized populations of cells selectively responsive to faces familiar to the viewer. Doris Tsao identified different features of the face that make up a code enabling single cells to identify faces."

There are no literally "face-selective" neurons in any brain, and the very concept is obscure and implausible. There is no evidence that brains or any part of brains recognize faces. There is merely evidence that people and monkeys recognize faces. 

Let's look at the papers the  citation page of the 2024 Kavli neuroscience prize cite to try to back up the claims quoted above. The first is a 2008 paper by Winrich Freiwald, Doris Tsao and another researcher, one entitled "Comparing face patch systems in macaques and humans." This is a low-quality paper guilty of the same Questionable Research Practices so predominant in today's neuroscience, such as a total failure to follow any blinding protocol. The paper shows us brain scans of some monkeys, but only a too-small study group size of only 9 monkeys. The percent signal changes are shown in the paper's supplemental information document, and my guess is that they were buried there so that there would be a minimum chance of a reader discovering how unimpressive they were:  changes of only about 1% (Figure S8). Such changes are very unimpressive as evidence of monkey brain regions responding differently when they see faces. Given the too-small study group sizes, we have here no robust evidence to back up the paper's claim that there are "face-selective regions in monkeys." (A similar study also finds brain percent signal changes of only about 1% in the same type of monkeys when exposed to faces, and finds similar responses when the monkeys were exposed to faces and non-face objects.) 

The authors have used the typical misleading practice of showing a brain visual with some region colored in a bright color (such as yellow), to fool us into thinking that there was some big difference in some region, when the difference was only about 1%. Instead of giving us Figure S8 (which would let us know the difference was only about 1%), the   citation page of the 2024 Kavli neuroscience prize has reproduced one of those misleading diagrams. 

The other scientific paper of Winrich Freiwald and Doris Tsao referred to by the  citation page of the 2024 Kavli neuroscience prize is the 2009 paper "A face feature space in the macaque temporal lobe." That's a paper as low-quality as the 2008 paper I refer to above. In the 2009 paper the study group size used is a mere three subjects. Also, the paper failed to use any blinding protocol, something necessary for any paper of this type to be taken seriously.  The method described is a rather ridiculous one, in which the authors select particular cells for study, in an arbitrary manner, without any assurance that these were randomly selected cells, and not cells cherry-picked for some characteristic the authors were hoping to find. Based on arbitrary criteria chosen by the authors, the authors make the claim that an individual cell in the brain can be "face selective." What exactly was the criteria used to judge whether a cell was "face selective"?  The paper gives us no answer other than giving us a link to some external page that gives no answer. 

In another study by Tsao we seem to be given the idea that she regards a "face selective" cell as one that responds more when a monkey is shown a face, as opposed to some image that is not a face. A proper term for that would be "face responsive" not "face selective."  We can explain such a thing without any belief that brain cells are producing recognition. When shown a face (as opposed to a neutral sight such as a geometric shape), a monkey may become slightly more alert or attentive. Some cells may therefore "perk up" a bit. But that isn't evidence that cells in the brain are involved in face recognition. Similarly, your eyebrow may raise slightly when a pretty lady walks by, but that does nothing to show that your eyebrows produce recognition of pretty ladies. And a man's penis may start to slightly enlarge when a buxom lady walks by in a bikini, but the penis can't see anything and isn't recognizing anything.  It's the person who is recognizing something, not some part of his body. 

The citation page of the 2024 Kavli neuroscience prize also refers to a low-quality neuroscience paper by Doris Tsao and Le Chang entitled "The Code for Facial Identity in the Primate Brain." This is an example of what can be called parlor-trick neuroscience. They have  used  brain scan data from only two monkeys, and an arbitrary selection of particular cells from such monkeys. The authors have also used a database of 200 face images and some extremely elaborate statistical analysis and computer programming  they did on such images and their sparse brain data, with it all having a sound of "keep playing with the data until we get something publishable."  They claimed to have predicted something, but it's one of those deals where the predictive model (a product of abundant statistical and programmatic fiddling) is leveraging data outside of the brain scans, data found in the external database. We get no robust evidence of anything important, and the title is a misleading one. No evidence has been produced of any such thing as a code for facial identity in the primate brain.  We have mainly what sounds like scientists fiddling with data in arbitrary ways for a long time until they finally ended up with something that pleased them, after conjuring up a "spaghetti code" analysis pathway. Misleading studies like this are getting more and more common in the world of neuroscience. They involve combining data from external databases with data from brain scans or brain EEG readings, mixed with lots of arbitrary computer programming and extremely complex or convoluted make-things-up-as-you-go-along analytics, in some way that everything is so confusingly  entangled that the authors may get away with grand claims that are not justified. Typically what goes on is that the authors give you an impression "we got this from brain scans" when the reality is really "we got this from a very confusing mashup of brain scans, arbitrary computer programming and statistics fiddling,  and data pulled from outside of brain scans," with the mashup being so complex and entangled that you have no good evidence of something about brains alone. The paper critically depends on much computer programming, but the authors failed to follow good practice by publishing a link allowing anyone to inspect their code, and see whether it followed good practices. 

Because of an abundance of neural noise all over the place in brains (a strong reason for thinking brains cannot explain thought and memory recall that can occur with 100% accuracy), reliability of spike readings is a massive problem in some of the study types mentioned above, there being a huge problem of false positives in which cells are incorrectly identified as responding to some stimulus they did not actually respond to. A paper on the topic of single-unit neuron recording tells us this:

"Next, we examined a recording of 283,469 spikes recorded from mPFC [a brain region] in detail (Fig. 6b). Approximately 95% of the spikes recorded were considered noise as a result of low-amplitude spikes on several channels (Fig. 6b, left, gray points)."

Alas, the 2024 Kavli Neuroscience Prize has been awarded for low-quality research work which has not been well-replicated. The fact that this was done tells us something important about how cognitive neuroscience is getting nowhere these days. Cognitive neuroscience is based on false claims such as the claim that the brain is the source of the mind and the claim that the brain is the storage place of memories. It is no surprise that the scientists trying to back up these claims are floundering, running around in circles and getting nowhere. So when the committee of the Kavli Foundation searched for neuroscientists to be given a million dollar prize, all they could find is some low-quality research that was never well-replicated. 

For a scientific paper giving insight into the type of poor research that won the 2024 Kavli Neuroscience Prize, read the 2022 paper "The Failure of Blobology: fMRI Misinterpretation, Maleficience and Muddle" by brain imaging expert Stephen Jose Hanson.  The paper has this quote about the Fusiform Face Area (FFA) and the research of 2024 Kavli Neuroscience prize winner Nancy Kanwisher (I have underlined and boldfaced a few lines):

"Although the absurdity of the discovery of a 'face area' [an area of the fusiform gyrus that was somehow primarily responsible for face processing—fusiform face area (FFA) (Kanwisher et al., 1997)] wasn't sufficient reason to abandon the blobology program, subsequent years showed how bankrupt this phrenology (modularity) program had become. Because functional localization like the 'face area' has no actual anatomical anchors in the brain, but was based on a procedure, using another set or all the existing face stimuli in the experiment to, unfortunately, create circular kind of evidence for where the face area was to be found in the fusiform gyrus ('localizer logic', see Friston et al., 2010 who illustrates the dangers of localizers).... There is not sufficient space here to cover all the other FFA counter- evidence2. But suffice it to say, based on classifier evidence there is no '... fusiform face area, a blueberry-sized region on the bottom surface of the posterior right hemisphere that responds significantly more strongly when people look at faces than when they look at any other stimulus class.' (Kanwisher, 2006) Mathematically, this simply cannot be concluded from the GLM (unsupervised regression) or related tests."

The "Failure of Blobology" paper is an unflattering portrait of brain imaging neuroscientists gone astray, playing misleading games of "keep torturing the data until it confesses." 

Typical content from a cognitive neuroscientist

What goes on in the awarding of prizes such as the Kavli Neuroscience Prize is that there is a strong "help myself" element, in which judges may be doing themselves favors by awarding an award to a particular type of researcher. Researchers who have done a particular type of dubious research may be more inclined to award a prize to other researchers doing the same type of dubious research, because this makes people more likely to hold in high regard the type of dubious research such judges have done. Check the judge list awarding this year's Kavli Neuroscience Prize, and you will find one or two whose careers have been centered around the same type of dubious "blobology" that was awarded with this year's prize. 

Searching Hard for Evidence of Strokes Causing Loss of Episodic or Conceptual Memories, They Come Up Short

The word "amnesia" is what you can call a "loaded" word. When a person thinks of amnesia he may think of some movie or TV show in which a person asks "who am I" and seems not to be able to remember who he is. But the term "amnesia" is defined as "a total or partial loss of memory."  Total memory loss is virtually never reported in the literature.  Almost always when people use the word "amnesia" they are talking about some memory difficulty that is much smaller than total memory loss.  

One of the most common forms of amnesia is what is called transient global amnesia. During an episode of such amnesia, a person may not recognize how he got to his current location. The person may repeatedly ask the same question, as if his ability to learn is temporarily blocked. Symptoms typically last  less than 24 hours, with complete recovery. It is interesting that transient global amnesia is not usually associated with any kind of brain injury. The cause of transient global amnesia is unknown. 

The medical literature reports two more long-lasting types of amnesia: retrograde amnesia (involving a problem in accessing already-formed memories) and anterograde amnesia (involving a problem in forming new memories or learning or memorizing).  Although many people define "retrograde amnesia" as an inability to access old memories, all or almost all case reports of such a thing are something much less than a complete inability to access old memories. In fact, the term "retrograde amnesia" is loosely used to describe all kinds of cases in which someone is slow or imperfect in accessing old memories or previously acquired knowledge.  So when you hear a claim of "retrograde amnesia," it is typically something much, much less severe than the way such a term is commonly defined.  Similarly, the term "anterograde amnesia" is loosely or carelessly used for a wide variety of learning or memorization shortfalls. So typically when such a term is used, someone is talking about a problem much less severe than a complete inability to form new memories. 

A group of scientists tried hard to get evidence that strokes can cause amnesia or memory loss. We read about the technique they used:

"The Medline database was searched through 2017 by combining the search terms 'stroke,' or 'cerebrovascular,' or 'ischemia,' or 'hemorrhage,' with the terms 'amnesia,' or 'memory'. The criteria not 'subarachnoid,' not 'dementia,' not 'cardiac arrest,' not 'transient global amnesia' were also added and search returns were limited to human studies. This search returned 4855 possible matches. These returns were limited to English language articles, and the titles of 1000 papers most related to the search criteria were reviewed, identifying the most relevant 500 papers. These abstracts were reviewed, identifying the most relevant English language papers. Abstract review looked for articles on human studies, primarily about a patient with memory loss, memory loss acquired by a lesion, and the etiology was not transient global amnesia, not Alzheimer’s disease-related, and not a brain tumor or other non-acquired lesions. From this set, we reviewed 250 full-text articles and included reports that fit the following criteria: (1) Case report format or individual case description; (2) Adult population; (3) Clinically relevant episodic memory deficits by bedside or neuropsychological tests attributed by the authors to an acute brain lesion; (4) Availability of a CT or MRI image depicting the lesion location(s) of sufficient quality that the lesion could be transcribed onto a standard brain template (Supplementary Fig. 1). Fifty-three cases of amnesia were found with identifiable causative brain lesions (mean age 57.5 ± 13 years, range 27–72, 66% male). '

To get a list of the 53 papers, you must consult Table 1 of the Supplemental Information part of the paper, which can be read here.  At the end of the table listing the papers, we read this:

"References for the 53 case studies meeting inclusion criteria for our analysis, taken from 50 unique journal articles. All 53 lesion cases were classified as “severe” amnesia (the memory deficit was clinically apparent even without formal neuropsychological testing), involved anterograde memory loss, and included documented impairment in verbal memory. 30/53 cases reported a formal measure of amnesia severity, but the metrics varied. The most common metric was the Weschler Memory Scale general score (13 cases) followed by Cambridge Cognitive Examination memory score (five cases). Only nine cases provided both a Wechsler Memory Scale  general score and IQ score to allow for the calculation of a WMS discrepancy score. 19/53 cases reported whether there was some element of retrograde amnesia: 18/53 reported impairment while one reported that retrograde memory was intact. Only one case reported a score for retrograde amnesia via neuropsychological testing. 20/53 cases reported whether visual memory was impaired, all 20 of which reported impairment. Seven cases reported formal scores for visual memory impairment using the Benton Visual Memory Task. Finally, other characteristics of amnesia were rarely reported such as impairment in semantic memory (four cases), autobiographical memory (two cases), or temporal order memory (one case)."

The confession at the end is interesting. The authors confess that they found almost no evidence of semantic memory being disturbed by strokes, and almost no evidence of autobiographical memory being disturbed by strokes. That is not something we would expect under the hypothesis that memories are stored in brains. Under such a hypothesis you might expect to very often hear of someone whose autobiographical memories were damaged after he had a stroke. 

Below is a table I made discussing some of the cases listed in Table 1 of the paper, as many as I can find.  I may note that many of the titles and quotes use inappropriate adjectives and nouns.  A neuroscientist wishing to maximize his chance of getting a paper published may tend to use the word "amnesia" for something that is a mere performance shortcoming, and may also use the word "severe" to describe something that is not very severe at all.  The more dramatic the report sounds, the higher the chance will be that the paper will be published, to the benefit of such a neuroscientist.  We must remember that scientists live in a "publish or perish" culture in which it is as if the key goal of their lives is to get as many papers published, with as many citations as possible.  In such a culture exaggeration is to be expected. In fact, in today's world of neuroscience it is massively common for papers to have titles that do not accurately describe the research findings made, and it is also massively common for papers to have claims in their abstracts that are not justified by any findings reported. 

In quite a few of the cases I will discuss below,  amnesia or "amnesic syndrome" is claimed, but inadequate evidence is given for such a claim. You can only reliably verify a claim of long-lasting amnesia by careful tests done on multiple days. There are any number of short-term reasons why a person might perform poorly on some quick memory test on a particular day. The person might be distracted or indifferent or in pain or not paying attention or in a foggy state of mind.  So, for example, the fact that a patient is asked to repeat words he was told to remember (after a gap of five minutes) is no strong evidence of "anterograde amnesia."  There are any number of reasons why someone might say "I don't remember" when asked to remember something like words he was told to remember five minutes ago, or asked for the names of the presidents before the current president. Explanations such as lack of effort or indifference or distraction (extremely common effects) are the most plausible explanation for such failures rather than the exotic explanation of stroke-produced amnesia. The visual below illustrates the point:

Here is the table showing the papers from Table 1 of the paper mentioned above. I omit almost all papers that were behind paywalls, making it too difficult to find the relevant details. 

Paper	Description	Comment
Amnesia after a discrete basal forebrain lesion	A man had surgery for a 5 mm. aneurysm in his brain. "Immediately after the surgery, he developed disorientation and agitation."	Although the man's state is  described in the paper as amnesia, nothing very serious-seeming is described.  We hear vague mentions of "difficulties" without much in the way of specifics.
Teaching NeuroImages: amnesia due to fornix infarction	We hear vaguely of "acute confusion and short-term memory difficulties, including significant retrograde and anterograde amnesia," but get no specifics.	The abstract fails to convincingly link this case to any brain problem. We hear a claim that "small vessel disease" was "the most likely cause," but no evidence to support that claim.
Clinical Reasoning: A puzzling case of amnesia	A woman "could not recall events that occurred in a 2-week period surrounding neurosurgery."  Since that sentence does not use "any events," we do not know how serious a memory difficulty was involved.	We get no specifics documenting that any real amnesia occurred.   The report is too vague to conclude that amnesia really occurred to any large degree.
Fractionation of memory in medial temporal lobe amnesia	We hear of a patient RH with mild memory difficulties and a patient JC with poor visual and verbal recall,  Regarding Patient RH, we read, "the volume of her right hippocampus was 58.6% smaller than her left hippocampus." Patient RH "with selective right hippocampal damage, performed well on several verbal memory tests and her estimates of recollection and familiarity for words were normal." But "RH’s performance on standard tests of prose recall and a test of delayed recall for names was poor."  We read, "RH performed normally on tests employing human faces."  But "the bilateral hippocampal amnesic, JC, showed a profound verbal memory impairment."	Neither of the cases is  amnesia according to common understanding of the word.  We seem to have learning difficulties related to speech, visual perception or language processing.  Although we are given evidence Patient RH had brain damage, we are given no convincing evidence that Patient JC had any brain damage.  The paper claims that JC had "bilateral hippocampal damage" but provides no compelling evidence to back up such a claim, and we are told his  "neurological examination was unremarkable," contradicting such a claim..
Pure amnesia after unilateral left polar thalamic infarct: topographic and sequential neuropsychological and metabolic (PET) correlations	15 days after experiencing severe turbulence on a flight, a woman admitted to a hospital was "unable to recall her profession." "During the first few days, she was slow, easily tired, and disoriented in time, but she always knew that she was in a hospital and found her way around easily. Her behaviour and contact with the examiners was always adequate. Spoken and written language, praxias, visuocognitive functions, and spatial orientation were largely preserved.... with the exception of difficulties in naming objects and people." "Memory testing ... revealed sparing of short term memory and preserved learning of new skills, but major deficits in episodic memory and in acquisition of new material. The latter deficit was always more severe for verbal than non-verbal material." "The patient read fluently and, 4 months after the onset of the illness, was able to recall a read story."	Despite the "pure amnesia" in the title, the evidence prevented for memory dysfunction is spotty.  We read of a small one-centimeter lesion found in the patient's brain, but we don't knew whether this was the cause of her problem.  Some of the trouble might be related to psychological trauma from the flight turbulence.
"Frontal Verbal Amnesia"	A man "noted the sudden onset of difficulty in speaking and weakness of the right side of his body."  "The patient performed normally on a wide range of language tasks and exhibited a normal verbal IQ. In spite of his at least relatively normal language skills, however, he has a marked verbal memory deficit with sparing of nonverbal memory."	It seems misleading for the authors to have called this case "amnesia." The dysfunction documented is very limited.
"Cognitive disconnective syndrome by single strategic strokes in vascular dementia."		Six cases are described in too sketchy a manner for one to draw any conclusion about memory effects of a stroke.
"Amnesia following thalamic hemorrhage. Another stroke syndrome"	"Results of standard psychometric tests indicated above-average intellectual ability. On the Weschler Adult Intel1igence Test his verbal IQ was 111, performance IQ 108, and full-scale IQ 110. No obvious verbal performance discrepancy was present, but administration of the Weschler Memory Scale yielded a memory quotient below normal and impaired ability for new verbal learning." The patient soon died.	Another case of the inappropriate use of the word "amnesia" for mere sub-normal test performance.  No evidence for amnesia is documented.
"Memory loss from a subcortical white matter infarct."	"He was able to repeat four numbers forward, could not recall any of three objects after 3 minutes, but was able to remember recent presidents. Spontaneous speech was grammatically correct with mild hesitancy on initiation of sentences and a tendency towards echolalia. Repetition, naming, reading and writing were all preserved. Verbal comprehension was mildly impaired only when dependent upon understanding complex syntactic relationships. Finger naming, right/left orientation and calculations were normal. Visual-spatial testing of spontaneously drawn and copied figures was normal. ... Neuropsychological assessment included Form I of the Wechsler Memory Scale. Despite scoring nearly flawlessly on the personal information (6/6) and orientation (4/5) subtests, the patient only recalled 4/24 and 2/22 memories from the logical memory subtest (about 2 SD below that expected for his intelligence and age).... In contrast, nonverbal memory function was less affected, as shown by his visual reproduction subtest score (4/14), only 1 SD below mean."	Another misleading paper title. After an apparent stroke, the subject seemed to have only a minor performance defect in memory tests.
"Bilateral hippocampal infarction and amnesia:A case report"	"The mild confusion was present in the form of constant repetition of the same questions as well as the temporal and spatial disorientation." But the patient scored 23 and three months later scored 25 on the MMSE test, the second score requiring fairly good memory (a score of 26 being normal). And the patient scored normally on a Digits Span Forward memory test and  Digit Span Backward memory test.	The paper claims "Severe anterograde amnesic syndrome, related to the domain of episodic memory, dominated," and claims that "the patient was unable to recall any of the previously presented information."  The claims are not backed up by robust evidence, and are contradicted by the MMSE scores given and the Digit Span scores given.
"Acute bilateral thalamic infarction as a cause of acute dementia and hypophonia after occlusion of the artery of Percheron."	No claim of amnesia is made, and no proof is given that the patient suffered from dementia. We merely read the hesitant claim that "after all these tests and the total clinical assessment of the patient, thalamic dementia was under a reasonable consideration."	No evidence is given for amnesia, and the only evidence given for dementia is a single MMSE test with a score below 18.
"Where am I?’ –An unusual stroke presentation"	We read of a man who had a stroke, and we hear the claim that he "he had no recollection of events of the past decade." Since this statement does not contain the word "any" we have no idea of how bad the memory problem was.	The paper is a very short one, and we have no specifics of memory tests. So it is unclear how bad this person's memory problem was. It is also not clear that stroke caused any memory problem the man had.
"Retrosplenial amnesia without topographicdisorientation caused by a lesion in the nondominanthemisphere"	An old man had "normal remote memory," and the claim is made he had trouble navigating in the hospital because of "amnesia."  We have the claim that "he could not learn the disease name, patient room number, and the primary physician's name, suggesting mainly anterograde amnesia." But no proof is provided for such a claim.	There could be details supporting the claim of anterograde amnesia, but none are found outside of a paywall. We don't know whether other issues might have caused the patient to fail to learn the items mentioned.
"The paramedian diencephalic syndrome: a dynamic phenomenon"	We read of an attorney who had a variety of problems after a heart operation. We hear of a downward gaze, lack of attention to doctors and confabulation. and we get a vague reference to "amnesic syndrome."	We don't get specific details about memory loss. We read that the patient did well on "repetition" and "naming," and that on reading and writing his performance varied from normal to grossly deficient.
"Migrainous stroke causing thalamic infarction and amnesia during treatment with propranolol"	We hear a claim that a patient  "had significant confusion and amnesia."  But we get no details backing up that claim, and no mention is made of a chronic memory problem.
"Amnesia due to fornix infarction"	We hear that a 71-year-old with brain lesions had " anterograde amnesia for verbal and visual information,"  although we don't hear of much to support that claim.  We read, "Her immediate memory for the Rey-Osterreith Complex Figure... was at the first percentile, and after a delay, it was nonexistent. Her performance was average on the Boston Naming Test and Wisconsin Card Sorting Test."  We read, "On the follow-up visit 1 month later, she showed significant improvement in her short-term memory. She was able to recall 3 objects after 5 minutes and displayed marked progress in her ability to register verbal and visual information. However, she had no recall of the events of her hospitalization."	No evidence has been given here of serious amnesia, other than forgetting events of a hospitalization.
"Amnestic Syndrome of the Subcallosal Artery: A Novel Infarct Syndrome"	The paper is half-way behind a paywall. The part we can read makes no mention of loss of episodic or conceptual memories, but merely claims "severely impaired recall of both verbal and visual information," and mentions an inability to recall three words after three minutes.
Unilateral Amnesic Stroke	The paper confesses "reports of amnesic syndromes due to unilateral stroke have appeared infrequently and unsystematically." It presents six cases it claims are examples of "amnesic stroke." No evidence is presented of any serious long-lasting amnesia in any of the six patients.  We merely hear spotty reports of imperfect performance on some memory tests (such as remembering 3 words after 3 minutes, but not after 5 minutes), and a few anecdotal reports of scattered failures such as a failure to name past presidents.	The authors are using the term "amnesic stroke" without adequate warrant.  The old people described have memory shortcomings common in old people. I may note that failing to name three words you were asked to remember after five minutes is never convincing evidence of memory impairment, unless verified in multiple tests on different days. There are any number of reasons (pain, distraction, indifference, etc.) why a person might not answer such a question at a particular time.
"Bilateral posterior cerebral artery infarction"	Other than mention of confusion upon being admitted to the hospital, we hear mention only of a short-term memory problem, but no specifics.	We have here an example of writers making unjustified use of the term "amnesic syndrome." We read: "There was evidence of a profound amnesic syndrome with impaired delayed recall (0/3 on Mini-Mental State Examination recall). He could not remember why he had been brought to the hospital." The MMSE mention is a mere mention of failing to recall three words you were asked to remember.  There are any number of reasons why a person might fail such a request other than amnesia (distraction, indifference, etc.).  Failing to remember why you were brought to hospital is no strong evidence of amnesia.
Hippocampal Lesion Patterns in Acute Posterior Cerebral Artery Stroke	We have some memory tests on patients who had damage to the hippocampus because of a stroke infarct, who are referred to below as HI patients (hippocampal infarct patients).  We read, "In the MMSE, the patients reached a score of 24.30±3.91 (lying in the mildly impaired range), with no difference between groups, t(18)=1.33, P=0.202. In the Clock Drawing Test, the patients reached a score of 2.84±1.26 (at the border of the normal range), with no difference between groups, t(17)=0.51, P=0.618."  In regard to results of a RBMT test of long-term verbal memory, we read this: "Compared to normative samples, the scores of patients with left HI were within the mildly impaired range, whereas the scores of patients with right HI were only slightly below the mean of the normative sample."	The results defy common claims that the hippocampus is crucial for memory. We have hippocampus- damaged patients who have performed fairly well on memory tests.
"Diaschisis after thalamic stroke: a comparison of metabolic and structural changes in a patient with amnesic syndrome"	The paper wrongly claims it has a patient with "classic amnesic syndrome," but it provides no data backing up that claim. The patient's MMSE score (largely a memory test) was above-average for a patient of her age, and we merely read of a "mild semantic memory disorder."
"Amnestic Syndrome and Vertical Gaze Palsy: Early Detection of Bilateral Thalamic Infarction by CT and NMR."	We read of a 27-year-old acting in a strange and sleepy manner. Her memory performance is spotty. "Long term memory was affected in an uneven fashion. Previous addresses, jobs, and acquaintances were recited accurately, but she was unable to give her phone number, and could not name present or past California governors or U.S. presidents. Digit span, however, was excellent — seven digits forward and five in reverse. Affect was characterized by indifference, facetiousness, and paucity of spontaneous speech."  We are told, "At three months she was felt by friends and family to have entirely recovered, and on neurologic exam was normal."	The case was too short-lived and spotty to be called a serious case of amnesia.
"A case of amnestic syndrome due to right thalamic infarction"	A 66-year-old is described with only minor mental symptoms, and she seems to have near-normal memory performance.  No justification is given for a claim of "amnesic syndrome."
"Preserved complex emotion-based learning in amnesia"	We have a report of an 85-year-old man with some bad memory performance, and we hear that he had a stroke. But there is no evidence given that his bad memory was a sudden result of his stroke. Strangely the same person performed above-average on some memory tasks.	It is well-known that very many very old people have memory problems. The paper does not make clear whether this person's memory problems came on gradually, or resulted suddenly from a stroke.
"Retrospinal amnesia"	We read of a 39-year-old man who was hospitalized with a severe headache. He apparently had some kind of stroke or infarction, and had a brain operation while hospitalized. We read, "All language and language-related functions were intact, as was performance on tasks associated with frontal-subcortical functions (i.e., Verbal Fluency (Benton, 1968; Lezak, 1976), Proverb Interpretations, Stroop, Visual-Verbal Test (Siegel, 1957))." We hear a claim that he had "profound amnesia," but that is followed by a claim that "His remote memory, however, appeared intact, as assessed by the Albert Remote Memory Battery (Albert el al., 1979)."  We hear of poor performance on verbal memory tests asking a subject to remember words and stories, but we are told "he performed much better on nonverbal recent memory tasks."  We are told, "T.R.'s memory deficit was to some extent material-specific. Verbal tasks showed a consistent deficit; while tests of nonverbal memory, except for the Rey-Osterreith Complex Figure Test, were performed normally."  We are told he "he had remarkably intact general intellectual functions.'	The patient seems to have had some brain problem causing some kind of  deterioration in verbal processing.  No very strong evidence has been given of a loss of old  episodic or conceptual memories, other than some scattered anecdotes.
"THE SEPTO-HIPPOCAMPAL PATHWAYS AND THEIR RELEVANCE TO HUMAN MEMORY: A CASE REPORT."	We hear of a young man who went to the hospital with a bad headache, and who then had a brain operation. We read, "Autobiographical memory revealed an almost complete loss of information from the two months prior surgery. Otherwise, major personal events were preserved, although some details, particularly events of the preceding year, were no longer available. His domain-specific (professional) knowledge was by and large spared."  We hear about a low performance in memory tests, but also are cautioned that the patient had low motivation, which might have produced scores lower than could have been produced if he were motivated.
"Diencephalic amnesia and apraxia after left thalamic infarction"	We read of a 78-year-old woman speaking only Hungarian hospitalized in Australia because of strange behavior.  The evidence value of the report is limited by the lack of any test scores, and by the fact that the woman was questioned not directly by the doctor, but through an interpreter, because she spoke a language the doctor did not speak.  We have no idea of how accurate the translation was (presumably those who speak Hungarian are rare in Australia). We read this: " She acknowledged she was in a hospital, but maintained it was in Budapest and the year was 1947. Although her recollections regarding her early life and wartime Hungary seemed accurate, she confabulated when asked for details of recent events." But how long did this strange state last? We are not told. We are merely told that 3 months later the woman still had some kind of memory problem.	The lack of a detailed follow-up report on this strange case is suspicious. We may reasonably suspect that the strange described condition was a short-term thing, and we may wonder whether some glitch in language translation was largely responsible for the strange report. We have no clear evidence of a stroke, but merely read of an fMRI showing something "consistent with a stroke."
"Acute Korsakoff Syndrome Following Mammillothalamic Tract Infarction"	We have this claim about a 56-year-old man: "In addition to anterograde amnesia, he also had retrograde amnesia and could not recall events of the previous 4 years."  The lack of the word "any" in such a sentence leaves it unclear how bad the man's recall of events of the past four years was. The only specifics we are given is the claim that the man did not believe that his father had died, which has occurred two years earlier.  We are told, "The level of general intelligence, previously learned skills, immediate recall, and ability to calculate in short formulae were retained."  We read a claim that the man's memory had not improved 4 weeks later and 8 weeks, although no evidence is given for such claims, except for the claim that the man still did not believe his father had died.	We have no test scores and no specifics to back up the claim of either antegrade or retrograde amnesia, other than a vague statement that the patient "could not recall events of the previous 4 years" without making it clear whether the author meant "any events," and the claim that the patient did not acknowledge his father's death (which might have occurred for any number of reasons not related to memory).  The patient could have had amnesia, but the paper fails to document such a condition in any convincing way.

I must reiterate some important points here:

• Scientists and many doctors live in a "publish or perish" culture in which they are largely judged on the basis on how many scientific papers they have produced, and how many citations such papers have got. In such a situation we should expect for there often to occur exaggerated claims in scientific papers, and that does occur massively. So we should be suspicious of all uses of the word "amnesia" or claims of "severe amnesia" or "acute amnesia," and wonder whether such language has been chosen to maximize the chance of paper publication and paper citation. 
• Extraordinary claims of amnesia require very strong evidence, which is typically lacking in the reports above. 
• It is fallacious to cite a single case of low performance on a memory test as proof of amnesia, as there are any number of reasons other than amnesia why a person might perform poorly on a memory test (reasons such as distraction or indifference or failing to understand the speaker).  Patients often don't understand English well, and doctors often speak English in a thick accent, a factor that by itself can explain poor performance on a verbally-given memory test. 
• You have given no clear evidence of amnesia by a claim such as "the patient could not remember events of the past year," because such a statement (lacking the word "any") leaves it unclear whether the patient could not remember any events or merely could not remember some events. 
• It is usually impossible to tell when a stroke occurred and often impossible to tell if a stroke occurred, so claims of a stroke cause in the cases above are typically questionable, and often involve guesswork.  A paper claiming that brain scan results are "consistent" with a stroke has typically not shown that a stroke occurred, and has not shown that stroke caused the observed memory performance shortfall. 

The end result here is that none of these papers convincingly demonstrate a permanent loss of episodic memories or conceptual memories from a stroke event.  Overall, the results are consistent with the claim that memories are not stored in the human brain.