Vision: Part III

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 What are we seeing here?  Disorders of visual recognition involve a higher order of abstraction than simple unprocessed vision. The visual image arrives at the primary occipital receiving station is processed here but then higher order processing and relationships are quickly handled by other areas of the brain, initially adjacent but ultimately far-removed from the calcarine cortex.  We know this in many ways.  You can follow a change in electrical activity evoked by simple and by complex visual stimuli over the surface of the brain. This is difficult because ordinarily such electrical potentials are small, only a small fraction of a microvolt in size and the electrodes used are far from the brain where such potentials arise, if they are ordinary electrodes placed over the surface of the skull.  But such evoked responses can be observed when the skull is open during neurosurgery at which time you can place electrodes directly over the surface of the brain.  This is rarely done except in epilepsy surgery where arrays of electrodes are placed in order to find the electrically active discharging focus of activity.  Also during surgery, you can put a probe over the brain surface and see what sort of experience the electrical probe evokes stimulating a specific anatomical spot over the brain.  This was originally done rather crudely many years ago by Wilder Penfield a Canadian neurosurgeon.  The patient needs to be awake and this is rarely done anymore.  T

 

     The PET (Positive Emission Tomography) scanner watches the utilization of glucose, in other words the metabolism or activity of brain regions. You can watch various brain regions metabolizing glucose as they become active using color-codes and use of various individual parts of the brain and charts the activity or glucose uptake over the brain’s surface. As a person looks at or scans an object you can see what parts of the brain become activated and the sequence of anatomical activation.  With that technique you see that even a simple visual object or scene, quickly activates a wide area of brain.  Over the years the most important information has been culled by examining patients with certain known cerebral lesions to give a picture of localization of function and the understanding of connections within the brain.  Neuroscientists have gradually evolved a picture of brain function that is modular.  Certain brain regions perform a specific given function.  There is primary visual, primary auditory, primary somateshtetic, olfactory, etc cortex and a language area of the brain.  Each of these areas has to perform a certain function and also be connected to the others.  Each are gray matter areas containing neurons.  They communicate using white matter tracts or bundles of axons. When a problem is detected there may be an anatomical defect in neurons or connecting axons.  For example, a person may be able to see and name letters, he may perform just perfectly on a Snellen eye chart with good visual acuity, and he may be able to write well, but may lose the ability to read.  This is alexia without agraphia inability to read with preserved ability to write.  The problem is that the visual image is received and processed well enough by the internal visual apparatus, but the signals aren’t sent well to the language area of the brain that lies around the Sylvian fissure in the left hemisphere.  You could say that the visual module, that large area of vision processing in the back of the brain, is disconnected from the language handling module further forward in on the left and you would be right.  So this modular picture of brain function has evolved.

 

     Lot’s of young children show up with specific language problems. Other cognitive functions may be intact or even superior yet they may not do well in school and have a learning disability.  A lot of kids who do poorly in school have specific problems.  If we can find what is wrong we may be able to get around the defect.  Other kids may have more pervasive problems that are more global or markedly multifocal.  These children are mentally retarded and as you may imagine trying to get past their difficulties and have them do well in school is impossible.  A child with a defect in higher order visual processing, say the jelling of individual letters into words or sentences may have an interruption of certain connections in the arcuate fasciculi running between the calcarine cortex and connections to the left temporal lobe.  He will present to his doctors just doing poorly in reading, math, spelling perhaps and all other subjects which is most of them that involve language function implicating visual to language connections.  At first it may be difficult to diagnose such a situation.  You might find that he speaks well and has a large vocabulary, yet can’t comprehend sentences that he reads very reliably. In that case once you make this specific diagnosis you may find an alternate strategy for teaching him to read, perhaps involving more rote memorization of whole words and try to teach him through his ears rather then through his eyes, with audiotapes and sounds.  As you can imagine, making such a diagnosis and coming up with a specific strategy is an art.  You must be able to separate kids out who can be treated, namely those with more focal and specific problems, from the ones with a poorer prognosis and more global dysfunctions, also recognizing and using intact abilities where you find them. This modular view of the brain is operationally very useful.

 

     Now the interesting thing as I point out in the chapter on memory, is that a memory of an experience, perhaps a visual image, resides in the brain.  But should you try to expunge this memory by sticking specific little holes in various areas, say the image of your fifth birthday party or your mother’s face, the actual memory of an event or image is cannot be found to reside in a specific place in the brain or on the cortex of the brain.  Why?  This is because any image in fact any percept ramifies widely over the cortex and ends up in multiple modules. Some primary aspects of angle and color and movement are in the simple visual processing areas of the brain, but then is the memory includes sounds there is some information in the auditory cortex and if there are multimodal, or linguistic or emotional evocations, those areas will become involved as well, so that any memory especially a reasonably complex memory trace calls up the efforts of widely dispersed groups of neurons. In the primate brain there are over 30 such areas involved with vision alone which communicate and interdigitate, each contributing more or less abstract properties to the visual image in an hierarchical manner.  How do you recall a memory?  Something stimulates, tickles maybe a single mode that brings back the memory.  Maybe you  taste a piece of cake that resembled that chocolate cake at your fifth birthday party and all of a sudden you will recall your friends and family singing the birthday song, or perhaps the tables and chairs the smells or even your emotions at the time. 

 

     Or, if you’re a Vietnam Vet, someone will light a cigarette and blow smoke away and partly into your face, in just the same way your buddy did before his head was blown off suddenly and that will evoke the total emotion of the traumatic event that replays over and over again in your mind. This is the stuff of post-traumatic stress syndrome with multimodal emotional associations culled from widespread cortical and subcortical regions of the brain.  Each of these sensory mnemonic particles that calls up impulses from widespread brain regions, is like a handle attached to a weight that is the entire mental picture.  If you tug on it and it is connected strongly enough, you will be able to extract a whole scene on the basis of a single elemental memory engram. Other factors, may add additional weight blocking extraction of the entire memory such as lack of concentration and anxiety. The brain is a complex of individual interconnected (through white matter) gray matter modules.

 

IMAGERY RAMIFIES IN THE BRAIN:

     In visual imagery you call upon a characteristic of the image that is ordinarily more advanced rather than simple.  You tickle or stimulate a visual module that is higher up on an abstract hierarchy when you recall a full image.  Visual imagery or memory is thus a “top down affair” with modules in upper levels of abstraction stimulating lower level less abstract areas, the initial impetus coming from inside the brain.  In some ways this is the obverse of simple perception which calls upon a “bottom up”  paradigm involving first, an organ of perception and only later, abstract modules.[i]

 

     A stimulus is thus seen to excite a wider and wider area of cerebral cortex.  It is not just a matter of an image arriving intact on a surface as on a film in a camera. Various cortical areas further process this image and interpret it.  We have not even gotten to cross modal representations and comparisons yet which involve even wider areas of cerebral cortex. For every image, if is complex enough, there is a whole pattern of cortical activity that will eventually involve  a wide network of cells and it is this precise pattern of cell excitation that constitutes a total memory.  Emotions get evoked that recruit limbic areas, the frontal lobes, and deeper evolutionarily older brain regions.  Vision is not unique but is rather archtypical since it is a sensory modality that we happen to have a lot of information about.  Other sensory modalities are vastly similar in their topical organization, use of primary secondary and tertiary cortices involving higher degrees of abstraction and intermodal connection and arrival at language regions of brain also contact with regions of brain responsible for feeling tone and emotion. Once a plan works, the designer uses it over and over again. Its all hooked to  hooked together and then to the great descriptor which is the language module of the brain.  Each of the specializing regions of the brain may be more or less isolated from the others if the connecting fibers are somehow disconnected by affecting white matter.

 

 

 

 

 

 

	Figure 1: "Alice in Wonderland Syndrome. The distortion of visual image is associated with migraine.

 

 

 

 

     A funny thing happens when some of the primary visual cortex is destroyed  by a stroke one side.  The higher level visual processing regions of the brain receive information from both primary areas but let’s say the right calcarine cortex may have been destroyed.  The person will have a visual defect in the left visual field; he will not be able to see to his left and thus have a left hemianopsia. If an object appears to his right he may see it fine.  But then this secondary visual cortex receives and processes this image which may move into the blind left visual as far as the person in concerned seems to persist after the object is taken away or there may be an illusion of multiple objects even though just a single one appeared.  Stimulation of secondary visual regions while the primary region is knocked out is what is felt to be the problem in palinopsia the abnormal persistence of visual images that should have disappeared from vision. An even more remarkable phenomenon is that a person can be unaware that he is blind.  Let’s say blood clot affects both the left and right calcarine cortices.   Some secondary areas may come out unscathed as what seems to occur in migraine where blood vessel spasm seems to affect the blood supply to certain regions of the back of the brain. Then the person will hallucinate and see objects of various shapes including numerous visual distortions. Maybe there will be flashes of light, or wavy or ziz-zag wall like patterns, “fortification spectra” of bright colors are variously described that are migrainous visual phenomena.

 

     Louis Carroll who suffered from migraine, eloquently described many of these visual phenomena which probably occur when higher order visual processing areas secondary and tertiary visual cortical regions are deprived of input from primary visual areas.   Some migraneurs, typically children, experience marked distortions that they can’t easily explain, close objects appearing far away or vice versa macropsia micropsia etc so that this phenomenon has been called and Alice in Wonderland Syndrome.

 

     Some patients are stone blind but the language module that communicates with the outside world is disconnected with the visual area so they may maintain they are not blind, even though they are perfectly incapable of describing an object in their environment, the famous Anton syndrome. They are blind but they don’t  “know” it or at least as far as the language area of the brain is concerned, they can see. Something of an opposite situation holds in the phenomenon of “blindsight”. The interesting thing is that someone may functionally see but yet be unaware that he sees.  In a sense the subject is unaware of something right, as the converse of not knowing that something is wrong.   Here a person will report that he is blind but when he’s tested it is found he can respond to certain characteristics of a visual stimulus yet have no awareness that he’s actually seen it. This is not mysterious in light of descriptions given above regarding vision.  Some of the connections are intact but the language sector of brain may be not be receiving visual information that can be described.  So depending on what connectors are disconnected, you can easily be fooled into believing that you can see when you can’t, that you can’t see at all when in fact you are still able to respond to some visual aspects of an object, and you can distort and even hallucinatef . 

 

     In the same vein it has even been found that some subjects whose eyes are so blind that they can’t distinguish darkness and light nevertheless can tell the difference between night and day[ii].  Not that they can do this verbally.   The retina also connects with the hypothalamus which lies just above the optic chiasm in the brain and is in charge of lot of basic functions such as appetite, thirst, temperature control, endocrine glands and sleep wake cycles.  The hypothalamus through the suprachiasmatic nucleus that connects with the eye, is tied with the pineal gland which makes Melatonin, a pineal gland hormone mostly secreted in the dark.  In blind persons whose melatonin secretion does not cycle properly, there may be a sleep wake disorder.   Others where melatonin secretion is intact can sleep normally.  Somehow these messages can reach the hypothalamus even through blind eyes.  All of us have intrinsic sleep wake cycles that really are part of an internal bodily rhythm.  In experimental subjects who are isolated these natural intrinsic days or circadian rhythms are slightly longer than our 24 hour day.  But in a normal person exposed to ordinary cues such as light and darkness, this rhythm is entrained to be approximately 24 hours which is why some of us will arouse at exactly a certain time without an alarm clock.

 

     Despite what common sense tells us, that a person really ought to know whether he can see or not we know of blind persons who think that they can see, and all kinds of visual distortions and partially sighted persons who report that they can not see,  and that function to tell the brain about light or darkness for which  the functionally blind person has no awareness.   You just can’t trust a person when he tells you he can or cannot see even if he thinks he is telling you the truth.   Some of the very same processes must occur with all other sensory modalities, audition, smell, touch but are not as well described.

 

 

Figure 2: A person with a lesion in the right occipital lobe will not be able to see to his left and have a left hemianopsia.

     A sensory stimulus arriving at the brain will eventually spread to other cortical regions.  What if it stimulates an area again and again like tying your shoelace or driving the same route to work everyday?  Then these cortical connections and the whole pattern of stimulation will be strengthened.  One mechanism for this might be so-called long term potentiatation (see “Beginnings”) but there are likely to be many others.  As you use a connection over and over it strengthens.  Or there may be an extreme stimulus say one that evokes high emotions or causes pain. In that case the pattern of connections might be strong right from the beginning.

 

     All of this becomes especially applicable to the modern understanding of pain.  When a person is injured there is a whole pattern of reaction in the brain just as there is when he is scanning a visual scene.  What if he continues to have pain for a while and this pain is extreme?  These connections and a whole pattern of connections including his emotional reactions to pain will be frequently evoked and will strengthen.  What if he has a second or third injury?  These patterns will be strengthened again and his reactions to pain will become extreme.  Perhaps he has strained his neck in a whiplash incident and the pain is bad for a while until the stretch injury heals.  Then he is injured again in a second collision.  The pain and its response is well-learned inside the brain, connections and patterns are strong and much easier to recall.  This time the reaction is severe and the person is miserable and disabled with pain. This is a syndrome that I call exuberant pain and doctors see this frequently though it is a concept they fail to understand.  Repeated headaches can beat a path of patterns of response throughout the brain, repeated injuries can make former pains and their response easier to recall and the response will be vigorous and extreme, worse than it has a right to be given the limited amount of actual injury.  The pain response is anamnestic (see “Beginnings”). This is one of the most difficult situations to manage in medicine.  There is little to be done in the periphery where a relatively minor injury has already healed. Even if you could cut off the offending limb (many patients literally beg you to do just that) the strength of association will be so extreme that the person will think the limb to be still there (the phantom-limb phenomenon).  The only thing you might be able to do is to strengthen pleasant non-painful associations with manipulations of that limb - a difficult task and not immediately rewarding. What about techniques used by a lot of physicians, further surgeries injections and focusing on the painful area.  This will make the pain worse in the long run by further strengthening these associations.  Moreover in many patients pain spreads to involve other areas or even spreads out to involve the whole body. The more the doctors intervene especially if they do so invasively the worse the pain gets.  If you leave them alone and don’t intervene much over a long space of time, associations may weaken in the same way that you forget what you have learned last year or two years ago.  Am I saying that a pain response is learned?  Absolutely!

 

THE BRAIN HARBORS AN IMAGE OF THE WORLD:

     One of the most obvious changes in learning is an alteration of the representation of reality inside the brain.  One true to life situations that brings this to the fore is the phenomenon of phantom limb pain.  Many amputees continue to feel excruciating pain in a limb years after it has been amputated. This is even truer in cases where the limb was painful or painful and immobilized at the time of the amputation. Even in the situation where no pain is felt in an amputation, various sensations, touch and movement may be experienced in the phantom limb.

 

     Every part of the body has a specific area of representation over the cortex.  This is true both for motor and sensory parts of the brain.  Motor functions are taken care of mostly by the frontal lobe, anterior to the central sulcus of the brain, sensory function is posterior in the parietal lobe which is behind the central sulcus.  Information from the hand goes to one part of the parietal cortex, sensory data from the face goes to another part etc.  if you take an electric probe during surgery as Penfield had done,  sensations in specific areas will be felt by the awake subject who is undergoing the surgery,  just as if a stimulus had occurred on the body part represented at the probe.  In this way the cortical representation of peripheral body sensations is mapped.  If the area that represents the hand is somehow destroyed, say for example by a stroke, then there will be numbness, the lack of sensation perceived in that body part.  This is called the sensory homunculus  (little man) of the brain (Figure 3).  It is just as if a distorted little elf is draped over the cerebral cortex, except as you will notice from the picture, the head is inverted and certain much more strategic body parts, especially the face, hands and lips, are over-represented while others such as the trunk and buttock, warrant less cortical surface and devotion of nerve cells.

 

      When you cut off a limb, say an arm and hand, the cortical area that will of course, stop receiving sensory data from that limb.  The cortical brain region stays intact, stands ready to receive data, but receives nothing.  It may go on as usual as if it the limb was still present, and confabulate, make up information, as time goes on.  One of the easiest things to do probably is to continue to assume things as just as they were before the limb was amputated, before it stopped getting data from the limb.  That would explain why so many patients who had been in pain, perhaps unable to move the limb before their amputation, still felt pain, sometimes years after the limb had been removed.  The responsible area of cortex stood ready to get data represented somatotopically over its surface. The area of brain after amputation of the limb ceased to have afferent sensory input, was de-afferented.  So as we see as de-afferented group of cortical cells may simply make up the missed stimuli, in other words it may confabulate.

 

Figure 3: Rendering of Sensory homunculus.

 

     After an amputation other interesting phenomena occur. A series of elegant experiments on amputees by V.S. Ramachandran, showed that this classical pattern as is taught in all basic neuroscience courses could be changed.  The area of cortex devoted to the arm and hand amputated is no longer used.  Adjacent areas of representation, the face, lips and shoulder start to invade the "unused” portion of cortex!  It is as if actively feeling areas of the body compete, according to the level of activity for central cortical representation.  Over a variable time period, the area devoted to the amputated arm functions both as the sensory area for the arm and the facial areas that invaded it. In Ramachandran's experiments, a touch over specific parts of an amputee's face will also be felt on a specific portion of the amputee's phantom limb.  Touch one part of the cheek and he will feel something in his forefinger.    That is because the same cortical region is now taking care of both body regions.  Learning has taken place in the nervous system.

 

     Now, as mentioned, many amputees continue to feel severe phantom pain after their amputation.  Some who were paralyzed an had a limb locked in a specific position,  may continue to experience this long after the limb is gone.  Using a simple box and mirror, Ramachandran trained a subject to alter uncomfortable sensations in his phantom limb, alter his percept of this body, simply by using the intact arm and having the subject "see" movement in the perceived amputated limb.  For some persons this could conceivably bring great relief from their painful sensation[iii].

 

     The cortical representation of sensory perception is subject to change even in adults.  This has been shown elegantly by Ramachandran and others and also undoubtedly occurs in the setting of brain injury and recovery.  Central processing of peripheral painful stimuli must also be altered over time by patterned experience.  Painful events such as peripheral injury alter painful responses.  Clinically it is common to see patients with injuries whose pain not only magnifies over time long after an injury or after suffering severe migraine headaches, but begins to affect adjacent body areas as pain persists.  Chronic pain tends to spread over the body and to become less specifically characterized.  The descriptions of pain given by a chronic pain sufferer tend to be less specific or if descriptors are specific they tend to describe multiple types of pain, and to be more generalized. 

 

     The classic example is reflex sympathetic dystrophy (RSD).  In this mysterious disorder, there is an injury or injuries to a body part.  Over time the hapless subject starts to feel what is described as a burning or aching pain.  Untreated this problem persists.  He immobilizes the painful limb, possibly in an attempt to splint a painful part. The pain is persistent but slowly spreads to affect adjacent areas of the body. As time goes on the pain becomes more severe and less localized.  Some physicians feel that this occurs in the periphery and postulate abnormal activity in the sympathetic nervous system because it is very often the case that pain diminishes when sympathetic nerves are blocked.  Also there are abnormalities in the appearance of the limb, sweating and hair growth, so-called “trophic” changes that may have to do with function of the sympathetic nervous system, hence the name reflex sympathetic dystrophy (dystrophy a type of atrophy or shrinkage, change of appearance of the affected limb which often occurs).  However, we do not know what actually happens in RSD, nor do we have a good explanation for why pain tends to spread to involve a larger part of the limb and to become poorly localized.  It is just as likely, perhaps more likely that such change occurs in the brain, perhaps induced by changes in the homunculus map that occur as a result of learning.   The central cortical representation of peripheral stimuli over the cortex may well be competitive.  Those areas of the body surface that speak the loudest,  i.e. painful limbs may well take over adjacent areas of cerebral cortex, invade adjacent regions on the homunculus  causing a spread or metastasis and a worsening of pain,  exuberant pain. 

 

     This may bear on how such persons should be treated.  One needs to mobilize the affected limb, to break the association between pain, to intervene early as the pain response is being set up and the central response is possibly altered.  Invasive techniques ought to be eschewed in favor of simple mobilization and early aggressive therapies aimed at breaking the pain cycle.  More importantly it points to the critical role of learning in the pain response.  Something learned can ordinarily be unlearned.  Conditioning is more than likely a part of the pathogenesis of exuberant pain as well as part of its cure or solution.

 

     What is the converse of repetitive or strong sensory input is lack of input. I’ve mentioned what takes place in two visual circuits deprived of input.  In one, language part of the brain gets no visual input.  The patient, instead of being aware that he is blind when visual cortex is destroyed may instead report verbally that he can see.  He does not appear to know he cannot see.  An analogous situation occurs with a lesion in the right parietal lobe that receives sensory input from the left side of the body.  A lesion there will cause a disconnection of the primary sensory cortex from the language module on the left.  The person will report that there is no problem with sensation on the left part of the body.  This is anosognosiay , lack of awareness of a disease or deficit. The language area, disconnected from the sensory cortex, does not report out a deficit, at least it doesn’t learn of a problem through a direct brain connection which is interrupted in this instance. This is a transient problem and it is likely the person learns about his problem through other means perhaps observing with his eyes that he does not feel when something touches his left body.  In the meantime he will not complain that he is blind when the occipital lobe is destroyed or that he cannot feel on the left side of his body.  Not only that, in order to make sense of his predicament, thinking that he can see or feel, he will confabulate.  He will make up an answer to a visual or tactile question.  Confabulation, neurological faking, seems to require anosognosia, unwareness of a deficit. Patients with Korsakov’s syndrome have severe amnesia but they don't know there is a problem, that they are unable to register memories. They also confabulate, make up a response if questioned.  Sometimes their made up responses can get very detailed.  One lie can lead to another.  The end organ, deprived of its nerve supply is denervated.  But the end-organ here the language module or language area of the brain on the borders of left Sylvian fissure, may respond, sometimes quite robustly, sometimes overly robustly as if to “make up” for its lack of input.

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Weird things happen, as mentioned, when secondary higher order visual cortex is deprived of input from primary visual cortex in other words if something temporarily or permanently interrupts input from the calcarine or primary visual cortex.  Again, the secondary areas seem to react robustly and a person may see flashes of stars or bright lights or fortification spectra or rarely, a persistence of imagery, as mentioned above.  This is what happens in migraine, which causes arteries to spasm in the occipital or visual area of the brain, and then we have fireworks that are, in effect a visual confabulation, also often an accompaniment of blindness in some visual area or black or neutral spots called scotomata.

 

CUTTING INPUT:

     In tardive dyskinesia a drug such as Thorazine used to treat psychosis may be needed for many years.  This effectively blocks the effect of Dopamine an important neurotransmitter. A lack of Dopamine or dopamine blockade causes a person to look as if they have Parkinson’s disease.  But if Dopamine is blocked for a long time, neurons that usually receive Dopamine start to respond to abnormally small amounts of the stuff; they crave it and a very little bit will have a dramatic effect.  Abnormal twisting and dancing movements result which is the what happens if neurons secrete an excess of Dopamine.  The neurons that respond to it are hypersensitive; too much Dopamine and oversensitivity to it have the same effect, perpetual uncontrolled movement about the mouth and in the arms and legs, choreiform dancing movement or tardive dyskinesia. A basic principal in the nervous system is that a neuron craves and overresponds to input that it formally lacked.  This is denervation hypersensitivity. If a motor nerve is interrupted the nerve gets little of the transmitter acetylcholine normally secreted by the nerve that tells the muscle to contract, A muscle with a good nerve supply is happy and silent when not asked to move.  But cut its nerve supply and after days to weeks of being deprived, it will crave acetylcholine and start to respond to even the tiny amounts that it is exposed to in the blood. It will start to wiggle around under the skin or fasciculate which can be felt and seen under the skin or fibrillate which has to be looked for electrically.  Here is denervation hypersensitivity in a different form.  An end organ that lacks nerve input, craves it and begins to respond abnormally to the chemical secreted by the interrupted nerve.

 

 

Figure 4: Denervation hypersensitivity: Prolonged Dopamine blockade makes the post-synaptic neuron hypersensitive to any Dopamine in the synapse. The same holds for a neuromuscular junction. If the neuron is damaged the muscle cell becomes oversensitive.

 

 

     A neuron lacking input craves it. This is true on the macroscopically on the level of the intact organism.   The basic neural mechanisms are reflected grossly.  A person who gets no sensory stimulation craves it, so much that he starts to invent his own. That is what happens to your imagination in the dark or when you’re sleeping.  Lacking external stimuli, it simply becomes hyperactive.  It’s the stuff dreams and hallucinations are made of.  Also as we have seen it occurs when there is impaired sensory input. It’s why we see witches, alien flying machines and have religious experiences at night.  We go to see a movie in the dark, not only because we can see it better, that there is nothing else to distract us, but our imaginations are far more active in the dark and our disbelief is suspended when we lack the light of day.  A universal in sensory deprivation experiments is that imagination becomes much more active, in isolation and with prisoners of war.  A lot of people testify to the fact that either they keep their minds active in a discipline that connects with physical reality, or they literally go crazy, by which is meant that they sink into the world of fantasy and hallucination.   Consequently the most successful prisoners of war are the ones who incorporate reality-testing regimes into a sort of daily routine. If deprived of sensation many persons will begin to hallucinate, which is just like the confabulation described above.

 

     How does imagination relate to sensory deprivation?  The celebrated case of Helen Keller is instructive.  Books on Helen Keller’s life are mostly written for children because she bested extreme adversity.  She was born hearing and seeing, a highly intelligent child who acquired some language function by the age of about 19 months when she suffered from a meningoencephalitis which left her blind and deaf.  In one fell swoop she lost her two most important sensory modalities and effectively the ability to communicate since she could no longer get feedback from her hearing.  Think for a moment what it is like to exist in a silent black world, the extreme frustration involved in being imprisoned in such a body.  As a child Helen was unruly and violent at times. Yet, while young she’d also learned to sign and had enough memory from when she could see, to imitate certain things, her father reading his paper in his favorite chair with spectacles on,  her aunt’s bonnet strings tied under her chin, and even locked her mother in a pantry and folded clothes. She was described as a loving and lovable child, clearly mentally alive.  One wonders if her native intelligence would ever have had a chance to develop under other circumstances, had she been born deaf and blind or into poorer surroundings.  Her parents knew little of how to reach her but sought out and found at when Helen was 7 years old, Anne Sullivan, herself nearly blind but head of her class at The Perkins School for the Blind in Boston. There had been at least on predecessor to Helen at the School one Laura Bridgeman who was stricken with scarlet fever at an early age and was deaf, blind, and mute with an impaired sense of smell.  With only a sense of touch that could be relied upon, Ms. Bridgeman proved educable. There’s a picture of her threading a needle with her tongue as Helen later learnt to do.   The rest of the story is common knowledge and remembered somewhat idealistically in THE MIRACLE WORKER.  Helen Keller had lost her two most important sensory modalities and with it most of her ability to communicate.  Her most precious sensory asset was touch that would become her bridge to the outside world.  Through a system of tactile communication she was meticulously taught to express herself, read and write with others’ help, and write she did, very eloquently. 

 

     Helen Keller was nearly deafferented.  She very nearly lost sensory (afferent) contact with her environmentY ,  but is not quite comparable  because in such situations many persons theorize at least that the unaffected sensations, touch, smell, awareness of one’s own body become even more acute.  One might think that some persons who are not of a strong constitution perhaps older folks, might begin to hallucinate or at least retreat into their own world.  Helen Keller became an eloquent spokesperson for the disabled, but more than that she could appreciate the tenuous relationship we have with our physical environment.  Her religious faith is interesting in this regard.  Her religion like that of the father of William and Henry James was developed out of the voluminous writings of one Emanuel Swedenborg who wrote of material sensations in face of an inner intuitive faith and a gentler, less deterministic, brand of Christianity.  The conflict between sensation of the material world and faith is incorporated into the following in which she comments that an inner faculty:

 

 “that brings distant objects within the cognizance of the blind so that even the stars seem to be at our very door.  This sense relates me to the spiritual world.  It  surveys the limited experience I gain from an imperfect touch world, and presents it to my mind for spiritualization.  This sense reveals the Divine to the human in me, it forms a bond between the earth and the great beyond, between now and eternity, between God and man.  It is speculative, intuitive, reminiscent. There is not only an objective physical world, but also an objective spiritual world.”[iv] 

 

 

     With real world sensation impaired you are less bound to matter.  The process is liberating in a sense.  As their connection with physical reality becomes more tenuous, imagination takes hold. It’s the same when we close our eyes to become less bound to the material world and entering a fabricated alternate existence, the mental world of dreams and freedom of expression.  Many artists and writers maintain that they do their best work in seclusion. They are more inventive when shielded from reality.  Edgar Degas was blind and isolated in his later years.  We all know of the example of Beethoven, practically deaf in his later life. Music is composed abstractly in the pure mental sphere analogous to pure mathematical thought.  The relationship of music and math as pure isolated systems that may be disconnected from experience has been frequently noted. Edward Rothstein in his recent book Emblems of the Mind makes this point:

 

“These moments of illumination -- finding relationships and hearing links where none existed before--are known to all who have been students of mathematics and  music, but it would be hard to say just what is learned or how.  That illumination also seems to have little relationship to life experience.  In both disciplines the extent of one’s understanding seems strongly determined by ‘gifts’--gifts of temperament ad insight, ability to coordinate concepts (and in music, to coordinate finger and breath with concepts).  The “prodigy” is a figure almost native to music, mathematics, and other activities like chess--dependent less upon experience with the world than with insight into a seemingly closed, abstract universe.  For example, Felix Mendelssohn had, u the age of seventeen, composed a dozen symphonies and the famous Midsummer Night’s Dream overture.  Mozart’s abilities at an even earlier age caused him to be paraded around Europe by his ambitious father.  Despite early abilities, of course, musicians may require experience to mature into great artists;  but mathematicians do not require even that.  The mathematician Carl Friedreich Gauss corrected his father’s calculations before he was three years old and jested that he knew arithmetic before he could speak.  Mathematics is a “young man’s game” as the mathematician G.H. Hardy put it (and few enough women have gone into it)).  Hardy pointed out that Galois died at twenty-one, Abel at twenty-seven, Ramanujan at thirty-three, Riemann at forty--all having achieved near immortal Stature in the history of mathematics.” [v]

 

ISOLATION:

     Music, mathematics and chess are in their own ways pure isolated systems where real life practical experience makes very little impact.  These systems of thought are pristine and isolated from the real world hence embracable by a child’s mind.  The brain of a prodigy likely does have anatomic connections, synapses that prepare it, yield aptitudes for certain specific endeavors.  No where is this more apparent than in fields of thought, music, math, chess, that do not require much contact with the real world,  These are pure systems unto themselves. It is as if the brain is structurally the link between experience and invention is broken.  The sphere of pure thought is sometimes better unhinged from ordinary material reality.  In his book SEARCHING FOR BOBBY FISCHER Fred Waitzkin which is really about his own son, a child chess prodigy gives rare insight into how a young child with a natural aptitude  is drawn magnetically into a field of endeavor almost as a key into a lock or a hand in a glove.  In chess and in mathematics it is not unusual at all for a child to manifest his talent, spontaneously outstripping adults.  Child prodigies typically are drawn to their field of genius despite any attempts on the part of their adult parents to discourage them. The father was also drawn to chess at an early age but his son was beating him regularly before the age of seven[vi].  Sensory experience is sometimes necessary for invention but sensory deprivation may also be an asset as it was at times for Beethoven. Skilled composers don’t usually use auditory feedback that  ordinary persons would  depend on if they were to set down music.  To those with such musical skill an inner voice gains precedence.   Beethoven, at the height of his powers became deaf and withdrawn, retreating into an inner world of intense abstraction so that some of his greatest works were produced in the torment of his later life, the last quartets and his Ninth Symphony.+  Of Beethoven’s later years David Ewen writes:

 

“When the spirit seized him, and he had to put down on paper the visions that tortured him, Beethoven was seized by what he once described as “raptus.”  This happened to him when he wrote Missa Solemnis.  “In the living room, behind a locked door, “ described his friend Schindler,  “we heard the master singing, howling, stamping.  After we had been listening a long time to this almost awful scene, and were about to go away, the door opened and Beethoven stood before us with distorted features, calculated to excite fears...Never, it may be said, did so great an art work see its creation under more adverse circumstances.”

 

     Here we see the other side of exuberant pain in which intense and prolonged input beats a learning pathway in the brain. The opposite, also a potent force physiologically, is lack of input, denervation hypersensitivity, which increases activity in susceptible neurons. The Associative areas of the cortex react to a lack of sensory input. Some deaf persons are observed to crave auditory input, so much that they create it.  In the case of Beethoven, his latter compositions are the culmination of his art in the third or greatest period of composition.  But inadequacies in other areas of his life, namely his lack of a stable relationship with a woman and other human relationships,  clearly drove his art.  Artists such as Dostoyevsky and Solzhenitsen and even people imprisoned over long periods often find isolation and sensory deprivation, the lack of distractions and dependence on one’s own imagination, advantageous for creation.  Terry Waite the emissary of the Archbishop of Canterbury held for 1763 days in Lebanon, passed the time in captivity much of it in solitary confinement writing his autobiography which perhaps might never have been written under more pleasant circumstances[vii].

 

     Denervation hypersensitivity is a neurophysiologic mechanism for such creativity in isolation from the mundane or real world. Which can actually interfere with the creative abilities.  At  times  productivity increases in direct proportion of to disconnection from the reality, when associative areas of the brain are allowed to function without interference from sensory input.  The deepest areas of human speculation are advantaged by the disconnection from reality.  How closely is creativity tied to perception?  This is how Einstein puts it quite eloquently:

 

“There exists a passion for comprehension, just a there exists a passion for music.  That passion is rather common in children, but gets lost in most people later on.   Without this passion, there would be neither mathematics nor natural science.  Time and again the passion for understanding has led to the illusion that man is able to comprehend the objective world rationally, by pure thought, without any empirical foundations - in short , by metaphysics. I believe that every true theorist is a kind of tamed metaphysicist, no matter how pure a “positivist” he may fancy himself. The metaphysicist believes that the logically simple is also the real. The tamed metaphysicist believes that not all that is logically simple is embodied in experienced reality, but that the totality of all sensory experience can be “comprehended” on the basis of  a conceptual system built on premises of great simplicity.  The skeptic will say that this is a “miracle creed.”  Admittedly so,  but it is a miracle creed which has been borne out to an amazing extent by the development of science.”[viii]

 

     This “passion” which Einstein rightly mentions is more obvious in youth, is natural and has to do with brain anatomy and physiology (for “passion” read “nature”). In certain remote regions of human endeavor Pure logic and reason are very likely built in to the structure of the associative areas of the brain.  One way of rephrasing the above is that associative regions of cortex may continue to function connected to or disconnected from the sensory areas and that at times associative processes work to advantage in isolation from sensory (“empirical”  or “positivist” ) regions.

 

     Lastly, here’s an observation I have made as a non-musician. Beethoven was obsessed I think, taken over by relatively simple themes and melodies which would consume him and this one can see in his music.   These it would appear, went round and round in his head,  creating an explosion of emotion.  Everyone’s familiar with the rather simple theme in the “Ode to Joy” and how it builds through repetition in the finale of the Ninth Symphony.  A similar theme had been in Beethoven’s brain for years before that expressed in his Fantasia written considerably earlier. Most of us mortals may hum or whistle a tune and then leave it alone.   We can let go of a simple melody after a while. There’s the wonderful “Sanctus” of his Missa Solemnis too, led by the violin and soloists that develops into a thing of beauty. And this violin theme is very similar to the main theme of the first movement of his violin concerto.  His music is full of such examples.  Beethoven was easily obsessed and consumed by simple themes in much of his music, some of which  almost seem never ending. Indeed it seems to me that once a good idea came into his mind, he had a problem getting it out.   Less interference or distraction from outside sounds and noises might contribute but such obsession, it would appear is a necessary but not sufficient condition for creativity, a pretext for high concentration of effort.   You can say the same about other music.  Just a couple of examples: Janacek’s iterations of two or three notes and of course,  Tchaikovsky’s emotional crescendos built on simple “answering” or repetition of themes by one part of the orchestra,   then another until an emotional apotheosis is attained.  Given that creation is in many cases an obsession, it is reasonable to ask whether the rest of us too easily give up on a theme without seeing its true intrinsic beauty or without being able to develop it fully.

To Part IV

 

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