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. 

Why Strokes, Alzheimer's Disease and Drunkenness Don't Prove the “Brains Make Minds” Dogma

A person believing that brains generate minds may refer us to cases of Alzheimer's disease, and say this proves this brains make minds and store memories. Or the person may make a similar argument when referring to strokes. Or the person may claim that drunkenness shows your brain makes your mind, because in that we see a physical liquid causing a judgment deterioration. In this post I will address these objections.

Alzheimer's disease could never prove that brains make minds, because we do not see in Alzheimer's disease an actual loss of the self or consciousness.  A mind with very poor memory is still a mind.

In regard to Alzheimer's disease or strokes, we cannot actually tell whether a person has suffered a loss of memories. For it might be that such patients merely experience a difficulty in retrieving memories.

Imagine you are used to visiting cnn.com to get the news each morning. But one day you turn on your computer and find you can no longer access any information at cnn.com. Does this prove that the information stored at cnn.com has been lost? It certainly does not. The problem could merely be an inability for you to retrieve information at cnn.com, perhaps because of a bad internet connection. Similarly, if I write the story of my life, and place it on my bookshelf, I may one day go blind and be unable to access that information. But the information is still there on my bookshelf.

In the same vein, the memories of people with Alzheimer's may be perfectly intact, but such persons may be merely experiencing some difficulty in retrieving their memories. There are, in fact, reports of incidents called terminal lucidity, in which people suffering from memory loss or dementia suddenly regained their memories shortly before dying. Such reports tend to support the idea that memory problems such as Alzheimer's involve difficulties in retrieving memories rather than the actual destruction of memories stored in the brain.

There is actually a way in Alzheimer's may argue against the idea that your memories are all stored in your brain. A doctor reports the following:

One of the big challenges we face with Alzheimer's is that brain cell destruction begins years or even decades before symptoms emerge. A person whose disease process starts at age 50 might have memory loss at 75, but by the time we see the signs, the patient has lost 40 to 50 percent of their brain cells.

If your brain cells were the place your memories were stored, why would you not notice memory loss until 40% or 50% of your brain cells were gone?

The evidence in regard to the cause of Alzheimer's diseases is actually pretty baffling. The most common explanation is that the disease is caused by something called amyloid plaques. But the Chicago Tribune tells us, “Scientists have learned that about a third of people who appear to have Alzheimer's disease do not have high levels of amyloid in their brains.”

A brain study was made of nine very old people who scored particularly high on a memory test. After these people died, their brains were examined. Three of the nine very old “super memory” people were found to have brains filled with the plaques often seen in Alzheimer's patients. These “super memory” people had brains in much worse shape than a large fraction of Alzheimer's patients with very poor memories.

In 2017 there was a news story entitled, "New Discovery Suggests Neuron Death Does Not Kickstart Dementia." The story reported this:

The leading theory in Alzheimer’s disease is that memory loss is the result of neuron death and nerve ending damage, which lead to memory loss, are caused by the formation of toxic protein clumps in the brain, called tau tangles and beta-amyloid plaques. But a new, small study challenges this theory, showing that the loss of neurons in brains of people with dementia is actually very small. What’s more, levels of neuron loss in patients did not indicate how far along the were in the disease, suggesting neuron death has little to do with the symptoms of dementia. 

The news story quotes a scientist saying the following:

Much to our surprise, in studying the fate of eight neuronal and synaptic markers in our subjects’ prefrontal cortices, we only observed very minor neuronal and synaptic losses. Our study therefore suggests that, contrary to what was believed, neuronal and synaptic loss is relatively limited in Alzheimer’s disease. 

A book on dementia says on page 34 that in the pioneering Blessed, Tomlinson and Roth study (1968) "there is only a rather low correlation between the brain plaque count and the test scores among the senile" -- not what we would expect if brain plaques were causing memory loss.  There were four cases with a high plaque count and low dementia. The book tells us that in a well-known study involving nuns and Alzheimer's disease, one of the nuns had high cognitive scores despite having "abundant neurofibrillary tangles and senile plaques." The book tells us that "predicting backwards from autopsy to clinical diagnosis appears unreliable and poorly predictive," which is not what we would expect if dementia was really caused by brain states. 

After telling us on page 35 that "there are many reports of people carefully diagnosed...as clearly having the clinical symptoms of dementia and yet showing no evidence of brain pathology,"  the book gives this quote from a neuroscientist named Robert Terry:

Over the years, investigators have sought assiduously for lesions or tissue alterations in the Alzheimer's brain which...might at least correlate with clinical determinants of the disease severity....Despite 30 years of such efforts, clinico-pathologic correlations have been so weak or entirely lacking that determination of the proximate, let alone the ultimate, cause of Alzheimer's disease (AD) has not been possible. 

The scientific paper here made an examination of 14 brains of recently deceased people who had donated their brains to medical science. Four were controls, five were people with Alzheimer's disease but no dementia, and five were people with Alzheimer's and dementia. The paper made detailed comparisons of the number of neurons in the brains and the total number of cells in the brains as a whole. The "bottom line" of the study is in Figure 6, which is below. The white bars are the controls; the gray bars are those with asymptomatic Alzheimer's; the black bars are those with Alzheimer's and dementia. 

We see here nothing to back up common claims that Alzheimer's is some disease that robs people of large number of neurons. The number of neurons is about the same for all three groups, and the total number of cells is greater for those with Alzheimer's.  Such a study shows that a common visual (showing a normal brain side- by- side with a shrunken Alzheimer's brain) is misleading, and that the idea of very large neuron loss as a hallmark of Alzheimer's is incorrect. 

The 2009 study "Comparison of Different MRI Brain Atrophy Rate Measures with Clinical Disease Progression in AD" compared brain shrinkage in 55 normal people and 64 people with Alzheimer's disease.  In Table 2 we see that 40 of the normal people had whole brain shrinkage of 0.4 % per year, and 15 of the normal people had whole brain shrinkage of 0.8 % per year.  For those with Alzheimer's disease, 32 had whole brain shrinkage of 0.6 % per year (less than 1% per year), and that 33 had whole brain shrinkage of 1.4% per year.  In short, there was hardly any difference between the brain shrinkage rates for those with Alzheimer's and the normal people.  The 2019 paper "Lifespan Changes of the Human Brain In Alzheimer’s Disease" presents a model based on brain scans of hundreds of healthy controls and hundreds of people with Alzheimer's disease. Figure 1 of the paper depicts the lifespan changes of white matter and gray matter of those with Alzheimer's disease and normal healthy people. The lines look almost identical. 

Given these conflicting findings, it seems that the evidence is not telling us any clear tale in regard to what causes Alzheimer's. Very many of the people with Alzheimer's have amyloid plaques in the brains, but one third do not. And apparently lots of people with very good memories have amyloid plaques, and many do not. There is also no strong correlation between neuron loss and dementia. Such evidence gives us no clear signal as to whether our memories are stored in our brains.

As for strokes, they can damage an ability to move, speak or understand language. Understanding language is partially based on auditory processing, and speaking language is based on muscular finesse in the vicinity of the tongue and vocal chords. We know that the brain helps the senses do their work, and is involved in muscular control. But an article in US News and World Report says, "It’s important to recognize that strokes do not cause a drop in overall intelligence.” On quora.com, someone states, "My speech therapist was pretty adamant that having a stroke does NOT, in any way, affect your intelligence." That's something we would not expect under the theory that the brain generates the mind. Under that theory, we might expect that people would lose half or more of their intelligence after a stroke.

If our memories were stored in our brains, what we would expect is that people would often get amnesia after a stroke. But such a thing seems to happen only very rarely.  A scientific paper says, "Reports of amnesic syndrome due to unilateral stroke have appeared infrequently." The paper lists some new cases which it claims are new examples, but when we read the examples we find typically only mild things like an inability to recall a daughter's phone number. Speaking of strokes, the paper says, "There have been two reported cases of persistent amnesia following unlitateral infarctions in which there were no other neurological deficits," indicating the rarity of such a thing. The paper also says that of a group of 68 patients who had brain infarctions, there were no cases of amnesia.  Talking about strokes, this paper says, "Amnesia as the main symptom of acute ischemic cerebral events is rare, mostly transient, and easily mistaken for TGA [ transient global amnesia]." 

What about drunkenness? Does drinking alcohol really cause you to “lose your mind”? Not really.

Consider the case of the drunk asked to walk a straight or to touch his finger to his nose. If such a person really had his mind dulled by the alcohol, he would be unable to interpret the police officer's language. But instead such a drunk will normally understand the command just fine, and attempt to follow it.

What we mainly see in drunkenness is a kind of overconfidence and loss of inhibition, along with mood changes and a deterioration of muscle skills. You don't really see people losing their minds or memories while they are drunk. If they did, they would probably forget how to start up their cars (or do something like putting their combs or their fingers in the ignition slot rather than their keys).

A CBS New story says that people who consumed alcohol were actually better at certain creative problems.

In fact, there is no such thing as a “temporary stupid potion” that will cause an intelligent person to regress to the intelligence level of a small child, nor is there any such thing as a “temporary amnesia potion” that will cause you to forget where you grew up or where you live or what your mother's name is. Wikipedia.org has an article on “drug induced amnesia,” but gives us no examples of any such drug other than benzodiazepines (which do not produce retrograde amnesia, the inability to recall old memories) but only help produce antograde amnesia (the inability to make new memories).

But if your memories do actually come from your brain, and your intelligence comes from your brain, we would think that such potions should have been invented already. If your memories do actually come from your brain, and your intelligence comes from your brain, it should have been easy for scientists to create some potion that would temporarily disrupt the chemistry supposedly needed for memory recall and thinking. The nonexistence of any such potion is actually further evidence against the claim that your brain is the source of your thoughts and the storage place of your memories.

Postscript: A recent study (which found no correlation between the number of neurons in the brains of 50 subjects and their IQs) refers to the fact "that highly demented female Alzheimer’s disease patients have normal neocortical neuron numbers (Regeur et al. 1994, Pelvig et al. 2003)`"

Against the objections of its advisory Peripheral and Central Nervous System Drugs Advisory Committee, the FDA approved not long ago a drug for Alzheimer's, the first such drug to be approved since 2003. The drug is fantastically expensive, costing more than $50,000 per year, and there is no compelling evidence that it works. People are arguing that it "provides hope for families," but so would a placebo pill, which would be very inexpensive.  In early 2024 we heard that Biogen is abandoning the drug, apparently because of its low effectiveness. 

Some studies (mostly with small study group sizes such as about 25) have claimed to find smaller volumes in the hippocampus of those with Alzheimer's, with such people having perhaps 15% smaller hippocampus volume. Such studies are problematic partially because of the small number of subjects and also because of the small volume of the hippocampus, which is only about 1/400 (one four-hundredth) the size of the brain. A 2016 study has the title "

No Association of Lower Hippocampal Volume With Alzheimer’s Disease Pathology in Late-Life Depression." It involved more than 50 patients and 50 controls. In a section entitled "Associations between clinical factors, hippocampal volume, and amyloid binding in patients," we read that "No main effects were detected for measures of episodic memory, including total learning, delayed recall, and delayed recognition." The largest study of hippocampal volume is the study here, involving 19,000 people, and showing a decline from about 8000 cubic millimeters at age 50 to about 7200 cubic millimeters at age 75. 

A 2023 press release on a study  tells us that "a University of California, Irvine-led team of researchers have discovered that the oldest-old, those who live to be 90+ and have superior cognitive skills, have similar levels of brain pathology as Alzheimer’s patients." The study is  the paper here entitled "A Population-Based Clinicopathological Study in the Oldest-Old: The 90+ Study." We read this:

"Half of all non-demented participants (49%) and just over half of demented participants (57%) met pathological criteria for AD [Alzheimer's Disease], ... The pathologies examined to date failed to explain all dementia in this cohort, as almost one quarter (22%) of all demented participants did not have significant AD or any other pathology to explain their cognitive loss."

The visual below has a graph from the paper:

Another recent study tells us the number of people with Alzheimer's Disease and the typical brain pathology claimed to cause that disease is even less than the 57% depicted in the graph above, and also tells us that some things described as causes of dementia are found in almost all who died without ever having dementia.. In the study  we read this:

"Pure AD [Alzheimer's Disease] neuropathology is observed in less than half of patients diagnosed with probable AD dementia in life... Some level of AD pathology has also been observed in nearly 40% of dementia patients, who were considered to have non-AD diagnoses during life. Moreover, many elderly individuals considered cognitively normal proximate to the time of death have been demonstrated to have AD pathology at autopsy.....Boyle et al. [90] reported that among 467 individuals who had been studied longitudinally and remained non-demented till autopsy, the vast majority had beta-amyloid, all had tangles, about a quarter had macroscopic infarcts, another quarter had microinfarcts, and between 5 and 10% had neocortical Lewy bodies."

The paper also tells us the following, which doesn't sound like what we would find if the cause of dementia was mainly physical: "Among a cohort of over 1000 elderly individuals without dementia at baseline, followed for an average of 12 years, the rate of global cognitive decline in five domains of cognitive function was reduced by an average of 70% in persons who were at the 90th percentile of social activity, compared to persons who were at the 10th percentile." 

An excellent paper on this topic is the paper "Exploring why 'memory loss' is a misleading descriptor of people living with dementia and can lead to dysfunctional care" by Steven R. Sabat and Alison Warren. The paper points out that there are many types of memory and aspects of memory, and that it is misleading to be using the term "memory loss" for someone who has difficulty with one aspect of memory but who may still have other aspects of memory. We read this:

"Explicit episodic memory is the type of memory most affected by the disease process of AD [Alzheimer's disease], but implicit memory types are relatively spared and can contribute to familiarity that informs recognition (Deason et al., 2019). Explicit and implicit memory are only two of many types of memory. Not only are there several types of memory systems (i.e., short-term; working; long-term; declarative/explicit; nondeclarative/implicit; autobiographical; episodic; emotional, etc.), but also different ways in which they interact in the daily milieu of human existence (Poldrack et al., 2001). ... Remarkably, there have been observations of significant lucidity despite an advanced stage of disease (Griffin et al., 2022; Mashour et al., 2019; Ramirez et al., 2023). The salient concept is that the severity of memory problems, or likewise, the ability to retrieve information from memory, fluctuates greatly. Indeed, persons with dementia have memory difficulties, but to say they have memory loss is clinically inaccurate. Furthermore, the memory difficulties that manifest can vary by dementia type. For example, a person with AD may have difficulty with episodic memory of events and personal experiences, but maintain procedural memory (learned skills, habits) (Kudlicka et al., 2019), while other forms of dementia,...affect memory quite sparingly and instead result in visual deficits (Crutch et al., 2012; DeTure & Dickson, 2019). Regardless of the type of dementia, it has long been known, but rarely discussed, that persons with dementia retain considerable cognitive capacities and are capable of new learning (Kudlicka et al., 2019). For example, studies examining cognitive plasticity and learning potential in persons with MCI and AD have demonstrated improved performance in visual memory, verbal learning, and executive function in all participants (Backman, 1992; Fernandez-Ballesteros et al., 2006), challenging the enduring notion that persons with dementia lose their memory but are also incapable of creating new memories. In addition to the preservation of implicit memory in general, persons with dementia maintain other components under this classification, including emotional memory, emotional communications, a variety of skills, and ability to learn....Furthermore, research supports that even during cognitive decline, persons with cognitive impairments can continue to learn new skills and thus create new memories (Sabat, 2018). Considering the evidence, dementia is a syndrome of memory retrieval difficulties rather than loss and characterizing it as such can have far reaching consequences for persons with dementia, especially how they are treated and the fate of their quality of life."

A paper states this:

"Patients with the same neurological disease and comparable brain damage often display different functional outcomes. For example, more than 25% of elderly individuals with no sign of cognitive impairment met post-mortem pathological criteria of Alzheimer’s disease (AD).1 By the same token, 10–40% of individuals with mild to moderate brain pathology showed no clinical symptoms of dementia."

The 2024 paper "More Similar than Different: Memory, Executive Functions, Cortical Thickness,and Glucose Metabolism in Biomarker-Positive Alzheimer’s Disease and Behavioral Variant Frontotemporal Dementia"  has a Table 5 that lists cortical thickness numbers for 11 regions of the brain. We have these numbers for both 79 people with Alzheimer's disease, and 39 healthy controls. The differences are very small. The 79 subjects with Alzheimer's disease had an average cortical thickness  2.47 millimeters, and the 39 healthy controls had an average cortical thickness of 2.6 millimeters. We have no mention of a blinding protocol in the analysis, and the slight difference could easily be due purely to a tendency to measure the healthy controls as having a greater cortical thickness. The 2008 paper "Frequent Amyloid Deposition Without Significant Cognitive Impairment Among the Elderly" stated this: "Similar to the results of several recent neuropathological studies, we did not find significantly worse cognitive performance among amyloid-positive subjects." It was a claim contradicting the idea that amyloid deposits in the brain cause Alzheimer's, a claim that has soaked up very many millions in research dollars without any effective treatment emerging. 

The MMSE test seems to be the main test used for dementia or cognitive impairment. You can get a score between 0 and 30 on the test, and any score of 25 or higher is considered "normal." It must be remembered that every single time a person answers one of the questions on the test correctly, that is a demonstration of some memory ability -- because any ability to recognize or use language requires some memory skill, skills such as recognition (of words heard) or recall of the correct words you need to use to state a correct answer.   

The scientific paper "Word retrieval in connected speech in Alzheimer’s disease: a review with meta-analyses" has a Table 1 that shows the MMSE scores for more than 1000  Alzheimer’s disease patients. Page 10 of the paper tells us that the average MMSE score for those with Alzheimer's disease (AD) was 19.07, and that the median was also about 19 (18.95). 

Although definitely an indication that Alzheimer's involves some memory difficulty, this data shows what a glaring error it is to speak about such people by saying that they "lack memory" or "have no memory." To the contrary, every single score above 0 on the MMSE is an indication that some memory ability still exists;  and data showing that Alzheimer's patients score an average of about 20 on this test (which has a maximum score of 30) suggests that on average those with Alzheimer's have most of the memory skill that they had in their prime. 

Similar data is found in Table 1 of the paper here, entitled "Brain-age predicts subsequent dementia in memory clinic patients."  We have cognitive performance data on 664 patients classified as "non-dementia," and 476 patients classified with "dementia."  The average MMSE score for those with dementia (about 22 out of 30) is almost as high as the average MMSE score for those classified as "non-dementia," a score of about 24. It would be very wrong to say those classified with dementia were "lacking memory," as you need quite a lot of memory skills to score 22 out of 30 on the MMSE test. The table also gives us figures for brain volume for both groups, and the brain volume for those classified with "dementia" is only slightly less than those classified as "non-dementia." Figure 3 of the paper is the scatter plot below, which tells us no clear tale about any clear relation between "brain age" (largely how much of your brain was loss to atrophy) and whether or not you will have dementia.  The plot is consistent with the idea that your brain is not the source of your mind. 

See my post "Men Have Faster-Shrinking Brains, But Women Get an Alzheimer's Diagnosis About Twice as Often as Men" for a discussion of a new study presenting finding inconsistent with claims of a causal relation between brain shrinkage and Alzheimer's.

More Evidence of High Mental Function Despite Large Brain Damage

In another post on this site, I presented many cases showing that people can have very high mental function despite massive brain damage. In this post I will look some additional cases showing such a thing.

First let's look at some results concerning strokes. This article in US News and World Report says, "It’s important to recognize that strokes do not cause a drop in overall intelligence.” This paper refers to “the generally minor effect of stroke on IQ” in children. 

A paper here noted a case of retrograde amnesia (failure to remember previous memories) that went across many domains of knowledge. But the paper noted, "Across all domains tested, LSJ showed losses of knowledge at a level of breadth and depth never before documented in retrograde amnesia."  Note the "never before documented."  If brains are storing our memories, you would think that many such cases would have been previously documented, because of all the people suffering brain jury from disease, cancer, or car accidents. 

The recently published scientific paper here is entitled “A Lesion-Proof Brain? Multidimensional Sensorimotor, Cognitive, and Socio-Affective Preservation Despite Extensive Damage in a Stroke Patient.” Here is an astonishing report from the paper's abstract, describing a patient who seems mentally undamaged despite massive brain injury:

At age 43, patient CG sustained a cerebral hemorrhage and a few months later, she suffered a second (ischemic) stroke. As a result, she exhibited extensive damage of the right hemisphere (including frontal, temporal, parietal, and occipital regions), left Sylvian and striatal areas, bilateral portions of the insula and the amygdala, and the splenium. However, against all probability, she was unimpaired across a host of cognitive domains, including executive functions, attention, memory, language, sensory perception (e.g., taste recognition and intensity discrimination), emotional processing (e.g., experiencing of positive and negative emotions), and social cognition skills (prosody recognition, theory of mind, facial emotion recognition, and emotional evaluation).

Below is the paper's startling discussion of the very well-preserved memory in this patient who had suffered heavy brain damage from two strokes:

Even more striking are her mnemonic skills: her procedural and semantic knowledge is fully preserved, as shown in her smooth execution of various action routines (e.g., handling her cell phone, tying her shoe laces) and her intact naming and classification skills (e.g., she could flawlessly denominate all the objects she had thematically organized in different sections of her purse); furthermore, her declarative memory is extremely detailed for events which happened weeks, months, and even years ago. She could describe scenes from her childhood and adolescence, she meticulously narrated episodes occurring immediately before and after her strokes, she remembered the names, specialties, and suggestions of all her doctors, and she could recount details of dozens of books she had read throughout her life.

We know that Alzheimer’s disease can cause an inability to recall memories, although whether the memories are actually lost is debatable. What is remarkable is the fact that a large fraction of the brain can be ruined by Alzheimer’s disease before a patient can become noticeably poor at remembering things. Here is a quote from an expert on the disease:

One of the big challenges we face with Alzheimer's is that brain cell destruction begins years or even decades before symptoms emerge. A person whose disease process starts at age 50 might have memory loss at 75, but by the time we see the signs, the patient has lost 40 to 50 percent of their brain cells.

The same very astonishing thing is said in this article, which quotes an expert saying the following:

In Alzheimer’s, brain cells start to die 10, 15, or 20 years before symptoms appear. By the time we observe memory lapses, 40 percent to 50 percent of brain cells are gone, and it’s too late to make a difference.

These statements are astonishing. If our memories are all stored in our brains, why would you have to lose 40 to 50 percent of your brain cells before people started noticing your memory loss? Again, this suggests merely a low correlation between brain health and mental function.

On this page we have the amazing story of an MIT student who helped doctors find a baseball-sized tumor in his brain. Doctors performed surgery and removed the tumor. Later, the student gave a presentation to cancer researchers. A video of the presentation is included on that page. Amazingly, the young man seems to show no sign whatsoever of a damaged mind. He walks and talks normally, and seems to have slick presentation skills sufficient to land him a job as a host on a morning TV show. The page tells us that this young man is now pursuing a PhD in mechanical engineering. In the presentation, the young man tells us that the doctors removed about 12 billion neurons in his brain.

The paper here studied memory effects in 63 patients who had undergone surgery for brain cancer, in addition to other patients who had undergone both brain surgery and radiotherapy. 91% of these 63 patients experienced “no deterioration” in immediate recall; 80% experienced “no deterioration” in delayed recall; and 77% experienced “no deterioration” in recognition. This is a relatively low correlation between brain damage and memory, particularly considering that about half of the patients had 2 or more brain metastases (areas in which the cancer was growing).

Figure 8 of this paper gives us a graph that compares verbal IQ with brain tumor size in a variety of brain cancer patients. Under materialist assumptions, we would expect that there should be a strong inverse correlation between something like verbal IQ and the size of a brain tumor; the bigger the brain tumor, the lower your verbal intelligence should be. But what we see is only a low correlation – a correlation of only .28. High correlations have values like .75 or .85. Astonishingly, the person with the highest verbal intelligence had the biggest brain tumor, and the person with the second highest intelligence also has a very large brain tumor. We can easily account for the slightly-below-average IQ scores of brain tumor patients by simply assuming that in these brain tumor patients there would often be visual perception problems, muscular coordination problems, psychological distress, and head pain problems, which would tend to slightly decrease scores in pencil-and-paper IQ tests, without there actually being a decrease in intelligence.

It is part of the dubious folklore of neuroscientists that the prefrontal cortex is some center of higher reasoning. But the scientific paper here tells us that patients with prefrontal damage "often have a remarkable absence of intellectual impairment, as measured by conventional IQ tests." The authors of the scientific tried an alternate approach, using a test of so-called "fluid" intelligence on 80 patients with prefrontal damage.  They concluded "our findings do not support a connection between fluid intelligence and the frontal lobes." Table 7 of this study reveals that the average intelligence of the 80 patients with prefrontal brain damage was 99.5 – only a tiny bit lower than the average IQ of 100. Two of the brain-damage patients had genius IQs of higher than 140. This is not a result consistent with the claim that brains make minds. 

In a similar vein, the paper here tested IQ for 156 Vietnam veterans who had undergone frontal lobe brain injury during combat. If you do the math using Figure 5 in this paper, you get an average IQ of 98 for these 156 brain-damaged veterans, only two points lower than average. You could plausibly explain that 2 point difference purely by assuming that those who got injured had a very slightly lower average intelligence before they were injured. 

It also should be remembered that brain-damaged patients taking standard IQ tests may have higher intelligence than the test score suggests.  A standard IQ test requires visual perception skill (to read the test book) and finger coordination (to fill in the right answers using a pencil). Brain damage might cause reduced finger coordination and reduced visual perception unrelated to intelligence; and such things might cause a subject to do below-average on a standard IQ test even if his intelligence is normal.  And if you're a patient with a terminal brain tumor, you may have psychological distress and head pain that may cause a reduced score in your paper-and-pencil IQ test. 

There is a type of surgery called a hemispherectomy, and is sometimes performed on children experiencing severe seizures. The operation involves surgically removing half of the brain. The surgery is described in a Scientific American article entitled Strange but True: When Half a Brain Is Better than a Whole One. The article states: “Unbelievably, the surgery has no apparent effect on personality or memory.”

According to this link, 70% of the children who had half of their brains removed were able to speak well, and 42% older than 6 were able to read well. Given that only about 60% of the American population can read well, this 42% figure is amazingly high.  A paper here tracks the before and after IQ scores of 12 children who had a hemispherectomy operation to remove half of their brain (usually to treat severe seizures). Half of the children had higher IQ scores when tested two years after half of their brains were removed, compared to their scores before the operation. 

When we consider sudden traumatic injury to the brain, we also find some cases where the correlation between brain health and mental function seems to be merely a low correlation. One astonishing case is that of Gabby Giffords, a US congress representative who was shot at point-blank range in the back of the head. Not only did she live, but she has recovered to a remarkable degree, to the point of being able to bike, and speak clearly (although in shorter sentences). A similar case was the famous case of Phineas Gage, a nineteenth century railroad worker who had a thick iron railroad spike accidentally drive through his skull, piercing his frontal lobes. A physician reported after examining Gage that he was “quite recovered in his faculties of body and mind.” Gage seems to have had some personality changes later, which may or may not have been related to his injury. But such changes are trivial compared to what we would have expected from such an injury under materialistic assumptions about the brain. An expert on Gage has stated that the personality change “did not last much longer than about two to three years,” but Gage lived for 12 years after the accident.

A Lancet study involving nearly three million people found only a small relation between traumatic brain injury and the risk of dementia. Those with severe traumatic brain injury were only 35 percent more likely to develop dementia. Since the lifetime risk of dementia is less than 20 percent, this means that 70 percent or more of people who suffer traumatic brain injury do not get dementia.  With a correlation this small, we can't even be sure whether there is a causal relation. By comparison, you are 2300% more likely to develop lung cancer if you smoke. 

It has been estimated that the cerebellum contains between 50 percent and 80 percent of the neurons in the brain.  In China a woman was discovered to have no cerebellum at all. But her defects were relatively minor, such as slurred speech, a need to use something like a cane to walk, and a lack of athletic ability. The woman could understand speech well enough. According to a scientific paper describing her, she had merely "mild mental impairment." This is yet another case showing only a small correlation between brain health and intellectual ability. 

In the paper "Subtotal agenesis of the cerebellum in an adult," we read this: 

"We describe a 58-year-old asymptomatic woman with subtotal developmental absence of the cerebellum. MRI evaluation showed minute remnants of cerebellar tissue corresponding to the anterior quadrangular lobules."

Note the word "asymptomatic." This is a case of a woman who suffered no symptoms despite not having a cerebellum, the part of the brain where most neurons exist. Similarly, in the 1950 link here, on the far right, we read of a man who "was born without a cerebellum and seemed to suffer no noticeable disadvantage from the fact."

These cases all tell us the same thing: that there is merely a low correlation between brain health and mental function, and that people can often have very high mental function even when their brains are greatly damaged. As a scientific paper says, “There does not appear to be a direct relationship between the degree of brain pathology or brain damage and the clinical manifestation of that damage.”

Such cases are not at all compatible with the conventional thinking of neuroscientists that the human mind is merely the product of the brain. But such cases are compatible with the assumption that the human mind is mainly the product of some mysterious reality beyond our understanding: a soul or some cosmic consciousness infrastructure much greater than a human body.

But a mainstream might argue that we should believe our memories are all stored in our brains, on the grounds that brains are active when we are remembering, and very heavy brain damage may be associated with memory loss. The visual below illustrates why such

reasoning is not convincing.

Below is a very notable case of the almost complete destruction of a brain by a brain tumor, but with a high preservation of mental function. It comes from page 71 of the document here (and the newspaper story here repeats the same details).