A) The Utility of Empirical Findings
To continue from last time, we granted subjective experience as a given because attempts to the contrary appear to be self-refuting. However, subjective experience is often thought to reach out into the world and, at least attempts to, grasp external reality. In turn, relying on our senses in justifying the external world is the current methodology behind contemporary empirical science.
We pointed out the limits of such studies for cognition in the previous post, but within those limits science still has a useful role in disabusing people of unexamined presuppositions. One aspect that is highly lauded is neurological research that has located specific regions that control specific actions. By the methods of divide and conquer, empiricism claims to have isolated the pathway in the thalamus traveled by visual data as the lateral geniculate nucleus. Mutatis mutandis, the path for auditory data as the median geniculate nucleus, the path for somatosensory data as the ventral posterolateral nucleus, and the path for verbal memory as the left dorsal medial nucleus. Similarly, if a person has a lesion of the left angular gyrus, then that person can no longer perform basic mathematical tasks. And so on.
Sometimes it’s not just one area, but an interplay of neurons on a circuit that generates the process under investigation. For example, tinker with the mesolimbic system, and one experiences the positive symptoms of psychosis, while tinkering with the mesocortical system produces negative symptoms instead. So, for example, the process of memory has been associated with the hippocampal trisynaptic circuit shown here:
The practical payout for such findings is straightforward. Once we find a circuit for retrieving memory, we can start there when investigating abnormalities in memory. For example, confabulation, viz. lying without knowingly being deceptive, involves an intact hippocampus. This aligns with theories predicated on the hippocampus being a place to retrieve memories, ie. the problem is instead with encoding or storage but not retrieval.
And so scientific endeavors may appear to be continuing apace without any need to question the current methodology.
Read on for my reasons for skepticism.
B) Size Matters Not
A reasonable starting assumption would be that the complexity of human thought is due to simply the aggregation of a large amount of neural tissue that can hold many circuits. After all, the human brain has 100 billion neurons with 1000 trillion synapses. That number of neurons, in a brain of around 1.4 kg, makes the human brain roughly 1000 times larger than that of the mouse, which contains less than 100 million neurons, and still greater than the honeybee brain, which weighs only 1 mg and has only around 1 million neurons.
However, in absolute numbers, a whale’s brain weighs 9 kg and contains over 30 billion neurons. So it appears that absolute numerical advantage does not automatically explain our mind. Well then, how about altering the original assumption and look instead look for a ratio or number relative to weight and size? Still no good, as the African elephant brain weighs 2.5 kg and has over 250 billion neurons. So apparently neither absolute number nor relative number of neurons is the key ingredient.
Nevertheless, one may still think it is a safe assumption to grant larger areas a larger role in a larger realm of functionality. But, even in humans, some get by with less, such as this man who was living normally at 44 years old even though he had a 75% reduction in brain volume:
Furthermore, if we continue with comparative biology, we find that there are other curious examples demonstrating the limited role of brain size in an animal’s ethnological repertoire. The sea squirt needs its brain for a short time only and then devours its own brain. The slime mold Physarum polycephalum can solve mazes, choose foods, and make other apparent decisions – all while lacking a brain.
In short, size does not appear to be correlated with cognitive functioning. What was size supposed to show anyway? If you have larger area X why should that allow for higher computational capacity? Maybe the areas are larger simply because the animal is larger, viz. there are more neurons just because there are more muscles requiring neuronal input. As one scientist laments:
“In bigger brains we often don’t find more complexity, just an endless repetition of the same neural circuits over and over. This might add detail to remembered images or sounds, but not add any degree of complexity. To use a computer analogy, bigger brains might in many cases be bigger hard drives, not necessarily better processors.” – Lars Chittka
If we follow the computer analogy, if you took a larger computer like the Mark I, and compared to a smaller contemporary tablet, I think you’d pick the latter:
So size is probably not the overriding concern. Let us examine organization instead.
C) A Trebly Complex Thing
If not the size of the brain that matters, it could be the organization of structures relative to each other. So while the African elephant brain has 98% of the neurons in the cerebellum, in humans this is closer to 50%. This means there were only 5.6 billion neurons distributed in the African elephant cerebral cortex, compared to the usual 16 billion neurons in the human. Which seems to fit our intuitions about cognitive capacity, across those two species anyway. Turns out though, this trend continues across many species with humans consistently having higher cerebral capacity:
A simple way to look at the brain if we choose to focus on organization is by the triune brain. This theory postulates a triad of layers, ordered sequentially by evolution, with the following functions generated per organizational zone:
If this works out, then one can attribute functionality to certain areas of the brain and one can discover neurocorrelates for neurological and mental illnesses. For instance, schizophrenics have been found to have decreased medial temporal lobe mass as well as ventriculomegaly.
But there is no compelling reason to think those correlations are exhaustive. For instance, when investigating memory one can find many correlates with the hippocampus but also with other circuits in the brain. What is there to tell us that these are the only correlated locations?
If a person is in a strong fit of laughter, is she using her anterior prefrontal cortex to appreciate a joke? Or is she having a gelastic seizure, and is it from the cingulate gyrus or from the hypothalamus? Or did it originate from basically anywhere ie. from the frontal, parietal, temporal, or insular lobe? Also, let’s not forget to consider pseudobulbar affect.
We can also look to a patient who has all the hallmark symptoms of Klüver-Bucy syndrome. Is this after bilateral temporal lobectomy? Or is this after a generalized encephalitis? Or even after a more general immune response?
There is also no reason to presuppose that a process such as memory requires just the neurons in the brain. There is also the extracellular perineuronal net that restricts the formation of new synapses, viz. preserves memory. Looking farther out than the brain, what if the Egyptians were on to something and the heart is a major driver of the nervous system? It would explain the occurrences of psychosis and delirium after cardiotomy. It would also explain diseases such as Takotsubo cardiomyopathy and DaCosta’s syndrome that begin after emotional stress.
Or maybe the idea of “feeling it in your gut” is more valid than originally thought. The gut has its own nervous system and regulates itself, not just independently of the brain and spinal cord, but even after transplant. And from an armchair there is no real way to tell what further research into the gut-brain axis will tell us.
Or maybe its no one of these places because it is all of them:
“The mind and body communicate with each other through peptides; these are found in the brain, the stomach, and all of our major organs.” – Candace Pert
Due the interconnected nature of neurons, how do we know which is the causative area behind a certain aspect of functioning? Well, the cliché response is that we know by deprivation experiments, viz. make a lesion, see what’s missing in function, and declare that missing part to be the cause behind the aspect that is now lacking. By this logic, remove the brain and the person no longer feels sensation. Likewise, remove the heart and the person no longer feels sensation. Yet we attribute thought to the brain and not to the heart. Try as you might, I don’t see how Mill can logically parse your epistemic troubles.
The inevitable rebuttal is that to be a successful deprivation experiment one should only look at lesions that are small enough to continue the overall process but with a noticeable difference, which we can then attribute to the lesion. The most common example given is Phineas Gage. He was working on the railroad in 1848 when an accident drove a large iron rod through his head that destroyed most of his left frontal lobe. After the accident, Gage was reported to have a large change in personality and frequent emotional outbursts and the difference in mental state was attributed to the damage in the frontal lobe. However, there is also a more parsimonious explanation for his personality changes:
“[Phineas] Gage was suddenly disfigured, half blind, and suffered prolonged infections of the brain. He was only 25 years old and had no hope of recovery. Isn’t it possible that his outbursts of angry swearing meant just what they usually mean – that the man was enraged and suffering?” – Marilynne Robinson
Likewise, Urbach-Wiethe syndrome presents with skin abnormalities and is associated with mood disorders. Do we claim this is due to temporal lobe calcifications, or to the uncomfortable emotions one confronts when navigating social settings while being conscious of one’s aesthetic imperfections?
If this difference in interpretation was confined to ivory towers and academic debate, then it may not even be worth discussing. However, the scientific embrace that took the frontal lobe to be synonymous with regulation of thought meant that procedures such as frontal lobotomy became commonplace for mental illnesses such as schizophrenia.
Never mind that decreased prefrontal volume is connected to other conditions that would now be iatrogenically created, like OCD. Never mind that the initial findings in 1942 from Dr. Walter Freeman and his procedure showed that 23% had no improvement and 14% worsened. Never mind that the procedure became so widespread that it could even be weaponized. Never mind all that, give Egas Moniz his Nobel prize already, and do it proudly over the demands of surviving patients and their families that the prize be rescinded.
Alas, I digress. The point here is that using experiments of deprivation to inform us of the competent mind is allowing the deformed tail to wag the healthy dog. So instead it may behoove us to use a finer scalpel when analyzing things.
D) Different Levels of Analysis
If the generalizations found from neurocorrelates don’t spread as widely as previously thought, then maybe the approach should abandon nomothetic for idiopathic methodology. A unique interpretation to the individual’s brain might permit one to still locate structures, just not for all. After all, not every brain state is mental, not all brain activity manifests mentality.
So what distinguishes the two? A good explanation is found here:
“We use talk of disease and biology to distinguish between things we can expect to respond to Rational Choice or Social Incentives and the things that don’t…Some things happen that we can’t think about on human terms, like a seizure. We can’t explain in terms of desires or emotions or goals why an epileptic person is flailing their limbs, so we have to go down to the lower level brain chemical explanation.”
So we have a way to discuss behavior, ie. the neuronal level, if the common attribution of mentality fails to provide sufficient causal reasoning. So pure motor phenomena such as Nodding Syndrome or tremors explain the motor actions of an individual when the individual denies voluntarily committing those actions.
With other conditions, an idiopathic interpretation becomes a possibility. In the case of temporal psychomotor epilepsy, behavioral changes can be noted in the post-ictal period. But maybe this can be better explained at the individual, rather than neuronal, level. Maybe the individual is simply learning to enjoy the post-ictal sensations and thus presents with a “clouded” sensorium. Similar to Howard Becker‘s analysis that the pleasurable aspects of marijuana intoxication need to be taught to users, maybe this “experience” is learned. But if it is learned, then the level of analysis need not be neuronal. Those of intellectual means, such as writers, certainly could discover this on their own:
“For several instants I experience a happiness that is impossible in an ordinary state, and of which other people have no conception. I feel full harmony in myself and in the whole world, and the feeling is so strong and sweet that for a few seconds of such bliss one could give up ten years of life, perhaps all of life…All of you healthy people don’t even suspect what happiness is, that happiness that we epileptics experience for a second before an attack.” – Fyodor Dostoyevsky, on his seizures
This should alter how one thinks about mood disorders associated with temporal lobe epilepsy. Is the interictal dysphoria a side-product of lacking that “bliss” that one has previously experienced? Do we attribute the behavioral characteristics of hypergraphia and circumstantial thought to seizure activity or to the personality of a writer? One should look to the individual before reaching a conclusion.
There are also cases where an individual interpretation is necessary in order to differentiate causes since brain findings alone will not cut it. If we find hippocampal atrophy, are we to lean towards OCD or PTSD? If a person has a reduced splenium of the corpus callosum, is that individual suffering from alexia or do we see it as a marker to monitor treatment for ADHD? In such cases, there isn’t a way to achieve a diagnosis without asking about patient phenomenology and understanding the first-person subjective experience.
And as we dig deeper with our analysis, we still haven’t hit bedrock.
E) Commiserating after a Commisurotomy
The problem is that even at an idiopathic level of analysis, ambiguity persists. Something that should be solved by considering analysis at the level of the individual, such as lateralization of language to the left or right hemisphere (often correlated with handedness and motor function) is not really resolved. To see this one looks to split-brain patients, ie. those who had surgery cutting the corpus callosum that connects signals across the cerebral hemispheres.
Here is Thomas Nagel on this unique presentation:
“The two severed sides could be taught conflicting discriminations simultaneously, by giving the two eyes opposite stimuli during a single course of reinforcement…[Experiments show] what is flashed to the right half of the visual field, or felt unseen in the right hand, can be reported verbally. What is flashed to the left half field or felt by the left hand cannot be reported, though if the word ‘hat’ is flashed on the left, the left hand will retrieve a hat from a group of concealed objects if the person is told to pick out what he has seen. At the same time he will insist verbally that he saw nothing.”
What does this really tell us? Well, sometimes the agenesis of a structure doesn’t contribute much to our understanding. And removal of the structure after development under normal circumstances still does not tell us much:
“Even though a number of patients had had their cerebral commissures surgically severed in operations for the treatment of epilepsy…no significant behavioral or mental effects on these patients could be observed, and it was conjectured that the corpus callosum had no function whatever, except perhaps to keep the hemispheres from sagging.”
What it does confirm is the role of person as something other than an automaton. This, again, works against eliminativism:
“What the right hemisphere can do on its own is too elaborate, too intentionally directed and too psychologically intelligible to be regarded merely as a collection of unconscious automatic responses.”
It also works against theses suggesting a dominant hemisphere, usually presumed to be the left. The prototype of bicameralism is that the right hemisphere sends messages to the left hemisphere which then acts as the executive in charge. However:
“The data present us not merely with slivers of purposive behavior, but with a system capable of learning, reacting emotionally, following instructions, and carrying out tasks which require the integration of diverse psychological determinants. It seems clear that the right hemisphere’s activities are not unconscious, and that they belong to something having a characteristically mental structure: a subject of experience and action.”
Such experiments also work against theses suggesting that the individual has two minds corresponding to the two hemispheres:
“When they are not in the experimental situation, their startling behavioral dissociation disappears, and they function normally. There is little doubt that information from the two sides of their brains can be pooled to yield integrated behavioral control.”
So the only possibility remaining is that there is one mind separated by experiment. This is also opposed however by Nagel because:
“In these patients there appear to be things happening simultaneously which cannot fit into a single mind: simultaneous attention to two incompatible tasks without interaction between the purposes of the left and right hands.”
So again I ask, whether after split-brain surgery or a spike through the orbit, are we really locating the areas of function?
F) Mirror, Mirror
We’ve gone from ambiguity in nomothetic analysis, to ambiguity in idiopathic analysis, to ignorance in split brain patients. Similarly, while the empirical divide and conquer approach works well for referred pain, it goes beyond ignorance into error in explaining phantom limb pain.
A good overview of the work of V.S. Ramachandran on phantom limb phenomena can be found here by Katia Guenther. The explanation behind the phantom limb is given as:
“If we wanted to flex our arm, a signal would be sent from the motor cortices to the biceps muscle. At the same time, a copy of the signal (efferent copy) would be sent to parietal cortices for forward prediction of the imminent sensory state of the biceps, termed ‘re-afference’. The predicted re-afferent signal would contribute to what Ramachandran called a ‘dynamic body image’, an internal impression of the moving arm and its sensory consequences…It provided an ordering expectation of the subsequent sensory impressions.”
So in phantom limb, or phantom eye, or phantom genitals, et cetera, we have instead a situation where:
“The internal ‘imagined’ expectation was lent greater credibility than the external ‘real’ movement.”
This is a good explanation for a myriad of disorders from pseudocyesis to psychogenic dwarfism and others. It also explains social mental phenomena in other animals as well, such as mice tested in dyads with identical noxious stimuli experience increased pain when observing their neighbor in pain.
Not only is it a good explanation, it looks likely to be the only game in town since this cannot be reduced to a purely physical phenomena because:
“If the phantom limb depends upon physiological conditions and is thereby the effect of a third person causality, then it is inconceivable how it can also result from the personal history of the patient, from his memories, his emotions, or his desires.” – Maurice Merleau-Ponty
One should also consider what happens after the treatment of a phantom limb by the Krukenberg procedure, which consists of a surgeon splitting an amputated stump to allow pincer movements. Instead of removing the phantom limb, this can instead leave the patient with the feeling of a divided phantom limb:
This sensation of splitting shouldn’t be the case as no physically causal material was divided. But as the stump was split, so is the patient’s mental representation. So what does work as a treatment is changing a patient’s representation of events by mirror neurons.
Mirror neurons are a set of neurons found in macaques in the inferior premotor cortex that respond both when the monkey is going to pick up an object and also when the monkey is watching the same action in others. It is unsurprising that the same neurons would carry the same information from the same perceptual consequences, ie. picking up an object. However, this is not merely a case of seeing another entity act since most mirror neurons are activated not by mirroring but by anticipated motor responses. This shows both that the presence of mental activity and rules out the action as a visual reflex because:
“If it is the same neuron that fires [for both seeing and doing] then why doesn’t it always end in mimicry?” – Hubert Dreyfus
Mirror neurons can be activated by the act of watching another so treatment based on a mirror box was created that allows mental feedback to inform the physiology. Thus, mirroring by mirror neurons acting through a mirror box works in these patients. And so:
“The ability to produce a faithful image [and] the ability to dissociate the image from what it reflected – [shows] an outline of a fairly traditional theory of mind: a realm of representations which may or may not correspond to the real world.” – Katia Guenther
Thus, in “locating” the mental, we sometimes reach outside our body through our mind’s representations. That won’t be found on any homunculus that we currently have.
G) Contemporary Outlook for Phrenology
The development of phantom limbs points to plasticity:
‘Phantom maps’ could develop rapidly in newly amputated patients, sometimes over the course of weeks, which demonstrated the plasticity of map building.” – Katia Guenther
The treatment with a mirror box, whether phantom limb or fibromyalgia or anything else, also points to plasticity:
“The disappearance of [a patient’s] phantom arm…after practice with the mirror box was the result of the ‘long term cortical reorganization of brain maps’…With the appropriate visual input, the body image was malleable.” – Katia Guenther
Surely there are structures in the brain that are resistant to remodeling. It is thought that most of the linear growth and arborization of dendrites of cortical neurons and the formation of over 80% of cortical synpases takes place in the first postnatal year. Within the critical period, areas can be rewired instead of completely lacking function. For the congenitally blind, language processing can occur in the occipital cortex. The congenitally blind on LSD can experience visual hallucinations and there can be auditory hallucinations in deaf patients, as if the processing remains available but rewired when not used.
But even outside of the critical period, and even within a clearly defined area, like Broca’s area, there are cases of children recovering linguistic function after the entire left hemisphere has been removed. So to rethink what was discussed above, the perineuronal net that acts as a “physical brake” for further synaptic growth can also be the source of re-opening a window for growth after injury or illness if removed.
With variability as prevalent as it is, why persist in searching for correlates that in the end may lack generalizability? Especially if areas are plastic, why bother with finding extensive connections when those same connections change with time?
Finding the mental in spatial coordinates such as amount or organization appears to have firm limits. Perhaps a better avenue of exploration will be in temporal coordinates, ie. activity that commences throughout a system. That’s what we’ll look at next.