Mystery… In The Right Temporal Lobe…
The area of “communication” certainly was a fascinating area of study. Perhaps one of the most fascinating of all aspects of communication, at least in my opinion, had to do with what I now referred to as “the mystery… in the right temporal lobe”.
The following was the “mystery in the right temporal lobe”:
Right temporal lobe damage was known to result in “incessant speech”. The “mystery” in this was that the right temporal lobe was not a part of the brain associated with “speech production”! As such, how could a part of the brain not normally associated with “speech production” – the actual verbalization of speech – result in “incessant speech” when this part of the brain was damaged?
Note that “incessant speech” appeared to imply “a lot of speech”. The medical community had well documented the fact that it appeared some functions could “relocate” themselves somewhat when there was brain damage. But, obviously, this could not be a case of “relocation” of the “speech production function” that normally resided in the frontal lobe. It was “temporal lobe” damage that resulted in “incessant speech”… not frontal lobe damage. As such, damage to the temporal lobe alone appeared to be enough to produce “incessant speech”. That certainly appeared to mean that “frontal lobe damage” and “relocation of the speech production function” to the temporal lobe was not the issue. Even if the relocation of speech production from the frontal lobe to the temporal lobe could be at play, how could it be that this relocation would result in “incessant speech”? Usually, when functions appeared to relocate, they did not do so to the point that you had “more of that function” than you originally had previously. When the brain “adapted” and appeared to relocate functions, they were only “reappearing” in very limited capacity. And again, “incessant speech” certainly appeared to imply – “a lot of speech” – not just “a little”.
Broca’s area, an area in the left frontal lobe, was usually considered the “language production area” in man. Wernicke’s area, in the left temporal lobe, was considered that part of the brain involved in the understanding of language. The left temporal lobe was also associated with memories for words, etc. The right temporal lobe, however, was not associated with “speech production functions”. Memories in the right temporal lobe also did not have to do with “words” but rather with memories as they related to faces, etc. Thus, again, how was it that an area of the brain, associated with neither the production of language nor the understanding of language – could result in “incessant speech” when damage occurred in the right temporal lobe? An interesting mystery indeed!
Note also the work of Dr. Ronald M. Lazar of Columbia University’s Department of Neurology and his paper entitled Neuropsychological Function And Brain Arteriovenous Malformations: Redefining Eloquence As A Risk For Treatment, published in Neurosurg Focus 11(5): Article 4, 2001.
Per his findings, When the frontal lobe of in some individuals who suffered from a specific type of brain injury known as arteriovenous malformations (AVMs) in the left frontal lobe, believed to occur while still in the womb, when the left frontal lobe was anesthetized, speech production was not impacted as it would be in normal persons and as such, science believed that “speech production functions” in these persons must have somehow “relocated” within the brain. In these same AVM individuals, if the left part of the brain dealing with the understanding of language – Wernicke’s area - was anesthetized, understanding of language was impacted, as it would be in a normal person. Interestingly, researchers found that, in these individuals, those areas activated during language production – as indicated via functional magnetic resonance imaging (fMRI) – were not in the left hemisphere (where language production usually occurred) - but in the right! – First Clue!
Thus, if anesthetized, in the frontal lobe area usually associated with “speech production” – Broca’s area – the speech of these individuals was not impacted! Hum. Very interesting!
Science has long known that there was tremendous “cross-over” in the brain. In other words, the left part of the brain controlled the right side and the right part of the brain controlled the left. – Second Clue!
What I saw as the “Third Clue” to this mystery involved anesthesia, secretin and children with - autism! I had started to “suspect” what I now believed to be perhaps part of the answer to the “mystery in the right temporal lobe” when I had written my second book, Breaking The Code To Remove The Shackles Of Autism: When The Parts Are Not Understood And The Whole Is Lost!
Below was a replication of a section written in my second book that in my opinion, clearly played into the “mystery of the right temporal lobe”. This was a rather long section, but it was well worth the read, because in my opinion, this had major implications for the production of language in children with autism and appeared to possibly hold the keys to unlocking the “mystery in the right temporal lobe”.
Start of Excerpt From Breaking The Code To Remove The Shackles Of Autism: When The Parts Are Not Understood And The Whole Is Lost! (taken from a book I had previously written - book 2)
“As I rested there a thought came into my mind. This thought had to do with the subject of anesthesia and the autistic child.
My sister-in-law had read a great many books on autism and spoken to many persons about her son’s issues over the many years she had dealt with this disorder. Her son Andrew was now 11 years old. Christine had long ago told me of the “secretin story”. She had heard someone else basically say that secretin, an enzyme occurring naturally in the body, had come to be viewed as a potential option for the autistic based upon something that had happened to a woman and her autistic son, who had surgery!
As Christine relayed this story to me, sketchy as it was, she basically said “this woman” had an autistic son who was nonverbal, that he went in for surgery and “came out talking”. She went on to explain that the mother, baffled by this had asked the doctors what they had done to her son – because he had “gone in” nonverbal yet “came out” talking. Christine then explained how the mother was told the son had been given an injection of secretin. And, here started the “secretin treatment option”.
From what I knew of secretin, pretty well everything indicated it was a very unproven therapy. As I wondered “why” results varied so much, my thoughts suddenly went to thoughts about anesthesia. I wondered why thoughts of “anesthesia” would enter my mind at this particular time… as I wondered about “secretin”. How could anesthesia and secretin be related, I wondered. I thought about that and within 15 minutes, I came to another theory in terms of this “nonverbal child becoming verbal”… perhaps the thing that had caused the child to speak was not the secretin, but the anesthesia!
Secretin, given that it was an enzyme occurring naturally within the body, may have helped address, not the issues of speech, but rather the natural opiate effect of casein and gluten in the autistic child… or simply helped with better digestion. This certainly could explain why secretin had such inconclusive results in terms of autistic children. Some autistic children were cfgf while others were not! This enzyme, secretin, was secreted at a very specific time during the digestive process to neutralize stomach acid. This enzyme was very much involved in digestion – that fact was certain - but how did that translate to a role in language production? I simply did not see that the two – secretin and language production - “went together”.
Zachary had been on digestive enzymes to break down foods and prevent the natural opiate effect of casein and gluten for over 6 months now. Yet, Zachary’s language production had not really been impacted by enzyme supplements. I suspected that secretin, also an enzyme, could have had some impact in autistic children in neutralizing the natural opiate effect of casein and gluten, but, again, I just did not see how it could have impacted language production. Secretin, from everything I had seen, was a rather expensive option in comparison to the enzymes I used with Zachary. Parents on message discussion boards seemed to indicate that the cost of secretin varied greatly… some saying it was as low as $45.00 per injection, others saying as high as several hundred dollars. If indeed, the effect of secretin was in that it was an enzyme and that its impact was really not one impacting speech development, but rather only one of addressing the natural opiate effect of children, then parents certainly had more affordable options.
In my opinion, the fact that secretin was an aid in digestive processes, certainly made sense in terms of my theory given that digestive functions were controlled within the brain stem – the only truly functioning area during the child’s procedure while under general anesthesia, and as such, secretin, a digestive enzyme, would have been allowed to “do its thing” even under anesthesia!
I wondered about whether or not the effect of secretin could have somehow been tied to a “more focused digestive process” during this child’s operation as a result of the numbing of the senses and thus, the fact that perhaps the body “reacted better” to the secretin and had somehow triggered the language. But, again, this could not have explained the generation of speech in this child – certainly not for any length of time. From what I knew of enzymes and how they worked, they were produced by the body and basically “used up” in digestion. They were not something that could be “stored” or used later. They acted on the foods at the specific time they were needed within the digestive process… and that was pretty well it. So, based on the functioning of enzymes, in general, there could be no long term effects based on secretin alone. Secretin could have only helped this child in matters relating to digestion (i.e., in eliminating the natural opiate effect of casein and gluten). Victoria Beck, the mother of this autistic child who had undergone an endoscopy, herself admitted that the changes in her child as a result of “secretin therapy” were over a two-year period. Although Zachary had not undergone secretin therapy, in the last two years, he too had made significant strides – strides I greatly attributed to his cfgf diet. Victoria Beck seemed to indicate that the initial secretin infusion for her son had been done by intravenous (IV). Secretin was known to stimulate the secretion of bile, the release of insulin, etc. But, again, these were digestive processes and, as such, yes simply in helping with digestive issues, the autistic child could do much better. But, I simply did not understand or see how secretin could be tied to language production – a function within the frontal lobe – where there clearly existed no functions tied to digestion.
Zachary had been on TMG for close to two years. This was a supplement made by Kirkman Labs, a company that specialized in supplements for the autistic. Although I suspected this product had initially helped produce speech in Zachary, in our experience, once we removed the TMG, conversation in Zachary began to flourish. This had always puzzled me. Had this simply been a fluke? A coincidence? I had no way of knowing! I knew B12 and folate were both the in TMG. Science had shown that low levels of B12 or folate could actually increase one’s risk of losing hearing when older. Low B12 was also believed to lead to speech delays and permanent nerve damage if the B12 deficiencies were not corrected. Yet, enzymes, such as secretin, were not something you could “accumulate in the body”. Enzymes worked on the foods as they went through the digestive track. A person undergoing an endoscopy would most likely have very little food in the digestive system since substances to “clean out” the digestive track would most likely have been given prior to the procedure. Thus, again, I simply did not see how secretin and possibly “additional B12” [in the case of Zachary], could have been “the answer” as to what caused increased speech in this child.
As I thought about this situation, I realized that anyone undergoing an endoscopy would likely have had some kind of anesthesia or sedation procedure to alleviate pain. Although I had no way of knowing the type of sedation given to this child, I truly wondered if the anesthesia or sedation could have somehow played a role. In my totally non-medical opinion, anesthesia gases or the smell of sedatives could be a likely explanation for the actual production of speech.
Gases or sedation liquids had a smell to them – some rather strong - and the olfactory cortex was in the frontal lobe… the area responsible for speech production… and it was a known fact that the autistic were more difficult to sedate than “normal” children. I wondered if stronger sedatives were used with the autistic… or sedatives that somehow impacted the brain differently than most sedatives/anesthetics.
If you looked at the brain’s structure and function, it almost seemed to make no sense in certain cases. Why were specific functions not “grouped” into one area… and why was it that things like the sense of smell were grouped with motor functions and the production of speech, but visual and auditory processing were not? This was all very puzzling to me.
The structure and functions within the various lobes had to be somehow related… in other words, those things that went together, had to be there for a reason – even though, to me, initially, they appeared to make little sense in terms of “how things were scattered” in terms of structure and function. Thus, the olfactory cortex, I thought, simply had to be somehow “grouped with” speech production in the frontal lobe for a reason. If “things” within a specific area were together, and indeed, somehow related, then, if viewed that way, a lot of things did make sense!
The olfactory cortex, for example, was grouped in the frontal lobe, along with motor functions and language production. Anesthetic gas and other sedatives had a smell to them. If I ever tried to introduce new foods to Zachary, as soon as he smelled them, he ran off, literally! He did not simply, shy away or say, “no”, he literally RAN off – a motor response! Smell, I now believed, actually triggered motor activity to a large extent!
I knew that if I breathed in helium that somehow impacted my voice (i.e., talking funny)… the production of language – also in the frontal lobe! Helium, I believed, impacted the vibration – or motion - of the vocal cords. Interesting indeed!
Taking all these factors together, the sense of smell, motor activity, and language production, I wondered if the sense of smell actually did belong with motor activity and speech production in that it literally - triggered it!
If that was the case, could I assume that the location of the senses actually triggered the activity within each respective lobe? I now believed this to could indeed be the case!
If, indeed, this child who had undergone a medical procedure had come out talking, perhaps it had been due not to the secretin, but to the gas(es) or the smell of liquids used in anesthesia or prior to anesthesia. Pre-medication of patients (oral, nasal or rectal) was often done prior to actual intravenous conscious sedation or anesthesia. Given this child was autistic, I can only suspect the procedure had been done under general anesthesia, but I had absolutely no way of verifying that. A local anesthetic only may have been used. Usually, however, conscious sedation was done in order to allow the patient to respond to basic commands or instructions. I did not believe that an autistic child, especially an autistic child who was very limited verbally, would have necessarily benefited the doctors by remaining somewhat awake during the procedure. My guess was that this child had most likely undergone general anesthesia… although this was only a guess on my part. From what I could find on this matter on the Internet, the interview of Victoria Beck by Dateline NBC did show that she asked about everything that had been done to her son… including the dose of anesthesia, but that she felt perhaps the secretin had caused the change in her son – a little boy who had barely spoken in two years was now reading flashcards and using words he had not really used before.
If as I suspected this child had undergone anesthesia – as appeared to be the case given the mother’s comments – I truly believed that anesthesia, not secretin, could have been a much more likely and probably explanation for the production of speech in this child. As I thought of this particular boy, I then began to think of other autistic children whom I knew to have also undergone anesthesia.
My nephew, Andrew, had been born with a heart condition and as such, he had undergone heart surgery at a very, very young age. As such, Andrew, also had undergone anesthesia – and Andrew, at age 11, now spoke “incessantly”.
Persistent talking was an indication of damage to the right part of the temporal lobe!
As with everything in autism, it was always a matters of “degrees” – of “how much” one did something, at least in my eyes.
As I thought a little further about anesthesia and its possible role in autism, I could not help but remember another child, now a young man, approximately 30 years old, who, although not diagnosed as autistic when he was a child now also very much fit into this picture. This young man, although never diagnosed as autistic, had indeed exhibited, throughout his life, the uncanny ability to remember countless facts, had difficulty with social interaction and so on. Since this young man was very, very ill, in order to maintain his privacy, I would simply refer to him as Patrick, although this was not his name. I had always believed Patrick could certainly have been an undiagnosed case of autism – but there was much more about Patrick that now made me wonder about a lot of things – especially in relation to this issue of temporal lobe damage, incessant talking and the possible role of anesthesia!
Patrick had been born with serious kidney problems. He had been ill all of his life and had undergone several operations – including two failed kidney transplants! At approximately 30 years of age, Patrick could now no longer “take in” more than a cup or less of fluid per day. He was constantly exhausted and it took very little, physically, to drain him totally. He only had a very small part of one kidney working. Needless to say, he was a very, very ill young man and he was constantly undergoing dialysis. Indeed, the life of his parents had completely revolved around their son and his dialysis.
As I thought about these three children – my son Zachary, my nephew Andrew and this other child, Patrick - and their common characteristics, the possible role of anesthesia in their lives, troubled me!
Zachary, my own son, had undergone general anesthesia for a broken arm at the age of four. He had fallen off a table and had broken both bones in his left arm. Zachary had only been under the influence of general anesthesia for 15 minutes or so. Although I had wanted to go with local anesthesia only, the surgeon had insisted that for Zachary, he should be put “completely under” – that for young children like this, it “was best to put them under”. He felt this was moreso true given Zachary’s autism. I had always wondered about whether or not this was “accepted practice”, but, at the time, I had been so concerned about the fact that Zachary had broken his arm and the pain it had caused him (he cried incessantly), I just wanted it fixed with the least amount of stress and pain possible – but I certainly had raised my concerns and desire to have him only get a local anesthetic. In the end, however, I went with the “experts” and agreed to the general anesthesia. Since we had no health insurance, that simple broken arm ended up costing us over $5,500.00 – unbelievable! Zachary had only in the last two months started to show more conversation (the anesthesia had happened over a year ago).
Andrew, due to his heart operation, at approximately age 5, had also undergone general anesthesia – for a much longer period than had Zachary. Andrew spoke incessantly (a sign of right temporal lobe damage). He also had greater difficulty in remembering certain things than Zachary did. Andrew was now 11 years of age and other than being autistic, physically, he could now run, play, and live the life of a very active child. His mother could not recall exactly when speech “took off”, but she did state that she did not feel it was right away after the operation. She had been told that better cardiac capacity could result in improved speech.
Patrick had undergone the most anesthesia as a result of his two failed kidney transplant operations. He also exhibited the most “incessant talking”.
As I considered these three boys, their autistic characteristics, and their exposure to anesthesia, a few things became very troubling.
My sister-in-law had been told that “more talking” was the result of the heart working better. But, was it? I suspected, in my “non-medical” opinion, that it had less to do with heart functioning and more to do with temporal lobe damage.
Patrick had undergone several operations. He was a fighter and I truly admired his determination and will to live. Over the years, however, Patrick had become weaker and weaker. An extended conversation was now enough to make him very tired. He was very, very pale (with almost transparent like skin) - to me, indicating a poor circulation - and as such, a badly functioning heart. Although dialysis was also tied to “the blood”, the simple fact was that dialysis did not change the color of the blood… the blood was red when it left the body and it was still red when it reentered the body. So dialysis alone, could not change Patrick’s overall skin color! Patrick’s “skin color”, in my “non-medical” opinion, was due more to his poor circulation than his kidney impairment. Given the fact that it now took very little to completely exhaust him, I could only suspect that his lungs were very, very weak also. Any physical activity totally exhausted him. Yet, Patrick, the boy who had undergone so much anesthesia and who had the weakest heart of all, did the most “incessant talking” of all three boys – again, a sign of right temporal lobe damage.
Zachary’s skin color, by far, was the best of all three boys! He had the best working heart, but still spoke the least of the three boys! Granted, there were age differences, but, again, this was truly a matter of “degrees”… and the simple fact was that the boy who appeared to have the weakest heart and lungs spoke the most – to me, indicating that “more speech” was not necessarily a function of better lung or heart capacity!
As I started to consider the possible role of anesthesia in the lives of these three boys, I really wondered just how it could be that “anesthesia” could cause “better speech development” from a better functioning heart, as parents had often been told, “was a side effect” of surgical procedures. In relation to the experiences of the three boys above, this could not be the case.
So, why was there “more conversation” in Andrew than in Zachary, and in Patrick than in Andrew? Even when in his early teen years, Patrick had also been much more talkative than had been Andrew. The boy with the best lungs and heart spoke the least and the boy I believed to have the weakest lungs and heart spoke the most! In my “non-medical” opinion, I truly suspected this had more to do with temporal lobe damage as a result of undergoing anesthesia!
Given my theory of the brain and how it worked, this too, in my “non-medical” opinion, would make sense.
If you thought about it, general anesthesia had the effect of making one “insensitive” in that “when under” your senses basically did not work – you could not hear, smell, see, touch – and I suspect, not taste either. At least, so I thought. Thus, sensory input to all lobes was impacted, as it simply “was not experienced”! Or was it? Hence, the age-old question… if a tree fell in the forest and no one was there to hear it fall…what impact did that have from a sensory perspective? Likewise, if a sound, or say, a smell was there during surgery, but the senses were somehow numbed, did those sounds and smells have an impact on the brain anyway? I now suspected that the sense of smell may actually still be active even while under general anesthesia. As I researched the topic of brain structure and function, I soon discovered that the thalamus, the part of the brain that acted as a gateway between the central nervous system and the peripheral nervous system, was involved in sensory relays for all senses, except the sense of smell. This was very interesting indeed, especially given the fact that I was convinced the thalamus was somehow involved in autism… as did I believe was the corpus callosum. As stated earlier, the corpus callosum was the area of the brain often “cut” to help alleviate epileptic seizures. Yet, for patients with epilepsy, the onset of an epileptic seizure was usually accompanied by a warning – an “aura” – a smell that indicated a seizure was coming. All this was truly very interesting! I could not help but wonder what happened with the sense of smell when one was under anesthesia. Was the sense of smell “still working” even though all other senses were “numbed” under anesthesia? I now believed that this, indeed, was a strong possibility!
Both auditory and olfactory processing occurred in the temporal lobe – the very lobe associated with “incessant talking”. The olfactory cortex was located in the frontal lobe… the very lobe associated with the production of speech! What happened to the senses while under anesthesia now became an intriguing question to say the least!
What happened in terms of the sense of touch, as surgeons worked? Although, clearly, one had no sensory input “felt” from touch while under anesthesia, did that mean the brain had not somehow “captured” that input anyway? These were all very interesting questions. Touch perception existed in the parietal lobe – the lobe responsible for sensory integration and somatosensory processing. It was a well known fact that anesthesia could result in issues with somatosensory processing. Many women who had been given local anesthetics during childbirth often loss control over bowel movement.
In this artificially induced sleep, only your brain stem activity, those things vital to life, continued, apparently, to work – so we thought! But, did the brain continue to “capture” the sensory information as well? I had absolutely - no idea! If it did however, what would happen to that information once a person “came out” of anesthesia-induced sleep?
In normal sleep, all sensory input was still very much working and still very much being integrated. The simple fact that I could heard a fire alarm or smelled smoke, and awoke as a result of sensory input, clearly showed that sensory input, integration and processing (relaying of information) as it related to vital functions and motor functions (making me open my eyes, get out of bed and out of the house), still worked while I slept. Yet, if a fire alarm went off or I smelled smoke while under anesthesia, I highly doubt I could awaken and leave the building on my own given sensory input, integration, processing and relaying were being blocked in terms of reaching my brain stem, so necessary to life functions and sight/sound reflexes. Interestingly, olfactory processing was in the temporal lobe (the lobe also associated with incessant speech) and in the frontal lobe (the lobe associated with speech production) – and the thalamus, the gateway for sensory information between the central and peripheral nervous systems, from what I could find, was not involved in the relay of olfactory information. Yet, sensory information as it related to the sense of smell also had to play some role in the parietal lobe (where sensory information was integrated), in the thalamus, and corpus callosum (the body’s two gateways) and possibly in the pons as well – that part of the brain that linked the medulla and the thalamus.
From what I could see, there were therefore, three gateways, the corpus callosum, the thalamus… and the pons – the pons being the critical gateway involved in sensory and motor functions to the brain stem – where all life functions resided! Interestingly, the thalamus was involved in all sensory processing EXCEPT for olfactory (smell) processing. The olfactory cortex was located in the frontal lobe and olfactory processing was believed to occur in the temporal lobe!
As such, anesthesia, by actually numbing sensory “perception” was a very different “sleep” in regards to “sensory input” than was normal sleep! But, did that mean that sensory input was not somehow “captured” anyway by the brain even while under anesthesia? I was beginning to think that olfactory input was indeed at play here and still somewhat active even under anesthesia.
Although this was simply my “non-medical” opinion, I had to believe that somehow, the corpus callosum , the thalamus, the pons and the temporal and parietal lobes – again – had to be “at play”. The corpus callosum, thalamus and pons seemed to all act as “gateways” in terms of sensory information, and the parietal lobe where integrated sensory information resided, but where also, somatosensory and touch processing seemed to reside and finally the temporal lobe, where auditory and olfactory processing resided – all had to play a role.
Visual processing – although not an issue with anesthesia, was located in the occipital lobe.
The “anesthesia-induced sleep” did impact overall functions as they related to life functions much in the same way they would be impacted in normal sleep, reducing the rate of vital functions to life. Its real impact, however was much more as it related to the flow of sensory information – either eliminating it completely (in the sense that input to the senses was not even “perceived” by the brain or numbing it completely (in the sense that even if captured by the brain, it was not being integrated and relayed)! Thus, it appeared the impact of anesthesia was only mild in terms of the brainstem life functions, but clearly impacted the functioning of the corpus callosum, thalamus and pons much more seriously.
I now also wondered, how longer exposure to anesthesia impacted both the parietal and temporal lobes in terms of sensory processing, integration and relaying of information.
Given what I knew to be true in these three boys, and the known structure and functioning of the brain, I now believed in my totally “non-medical” opinion, that, “incessant speech” possibly resulted from damage to the temporal lobe as a result of anesthesia gases inhaled – or smelled - during surgery. The case for incessant speech, indeed seemed stronger when viewed from a “sensory perspective” in terms of what was going on with the senses during anesthesia than it did from a purely life function enhancement perspective.
The fact was that with sensory input that had entered the four lobes via the central nervous system or with incoming sensory input from the peripheral nervous system, by the time either form of sensory input (from central nervous system or peripheral nervous system) had reached the pons, it had already been integrated by the corpus callosum or transferred to the thalamus to then be relayed to the pons in relation to life functions. Thus, this sensory information was no longer simply “raw sensory data”… it had already undergone extensive integration, processing and relaying functions. If “raw data” was not entering the brainstem via the pons, how could “raw data” leave the brainstem to flow “backwards”. I did not believe that occurred at all. There was no “raw data” from a sensory input perspective in the brainstem. As such, I wondered, how increased heart functioning possibly caused greater speech? In my “non-medical opinion” all that was happening in such things as heart surgery, was “something” related to life functions themselves… heart beat, breathing, digestion, swallowing, reflexes, regulation in body temperature, blood pressure, alertness, sleep and balance. I just could not see how any information could flow backwards to lead to “better speech” given these functions were isolated within the brain stem and the fact that no raw sensory input necessary to speech was present in the brain stem. Yes, you needed to breathe to speak… but there were plenty of speechless people who breathed too! As such, again, I simply did not believe that “life functions” were related to “speech functions” any more than they were related to any non-vital functions to life.
If the theory that increased speech was due to better functioning of say the heart and lungs were true, than, many more functions should also be better… but, clearly, that was not the case. A deaf person undergoing heart surgery remained deaf even after surgery. A blind person, undergoing heart surgery remained blind even after heart surgery. A paralyzed person undergoing heart surgery remained paralyzed even after heart surgery. A mute person undergoing heart surgery, it was believed, remained mute even after undergoing heart surgery. So, how had a nonverbal autistic boy gone into surgery without the ability to speak, yet two weeks later was very verbal? How long did anesthesia really impact the brain? To “come out” or awaken from anesthesia, the blood had to process the gas to make it leave the body via the lungs, but did all anesthetic gas molecules leave the brain? I truly wondered!
Given I now believed the sense of smell could possibly actually trigger motor function as it related to speech production, this could certainly explain why the autistic child who entered surgery mute, later became verbal. I suspected gases used in anesthesia or some other olfactory input in the form of a pre-medicating nasal or oral prep for sedation - an olfactory input to the frontal lobe - had been responsible for the production of language and played more of a role in this child’s recovery of speech than did the secretin injection – especially given the fact that I knew helium, also a gas, affected the vocal cords! I now suspected that although a patient did not “perceive” sensory input via the four lobes while under general anesthesia, that sensory input, somehow still was captured by the four lobes and triggered some sensory response – in this case, the sense of smell, could if my theory were true, surely have triggered the production of language given both the olfactory cortex and the production of language were located in the frontal lobe and the thalamus was not involved in the processing of sensory information as it related to the sense of smell!
The brain stem involved functions vital to life only – heart rate, breathing, digestion, swallowing, reflexes, regulation of body temperature via sweating, blood pressure, alertness level, sleep and balance (vestibular issues). Better life functions, in and of themselves did not result in better sensory processing… the blind remained blind… and the deaf remained deaf… those paralyzed as a result of spinal cord injury remained paralyzed…only the sense of smell could possibly have played a role in the recovery of this autistic child’s language!
In my opinion, the effect of sensory input was virtually non-existent in the brain stem with the exception of sight/sound reflexes! As such, damage to the senses, truly, as expected, would have very little impact on one’s life functions! One could be blind, deaf, paralyzed as a result of nerve damage or a spinal cord injury, etc., and still be quite alive!
I could only conclude, in my very “non-medical opinion” that “improved life functions” did not play a role in the generation of speech, although they certainly could play a role in the capacity of speech (i.e., better breathing leading to better enunciation). However, generation and capacity were two very separate issues!
In view of my theory, I looked at it in terms of how it related to these three boys and possible temporal lobe impact as a result of anesthesia! I use the word “impact” here, because, I do not necessarily know that all impacts could be “bad” or “negative”. In my view, some of these impacts were definitely bad, others, perhaps enhanced certain functioning. The temporal lobe was responsible for auditory and olfactory processing, memory acquisition, emotion, understanding language, categorization of objects, and some visual perception. Current research indicated that if the temporal lobe was damaged, one could experience selective attention in terms of sight and sound, difficulty understanding spoken words, issues with interest in sexual behavior, short term memory loss and interference with long-term memory loss, emotional issues (i.e., increased aggression), difficulty in face recognition, categorization issues and the persistent talking! Once again – how interesting!
In comparing Zachary and Andrew, my son and that of my sister-in-law, Zachary definitely did grasp math concepts much, much more easily than Andrew had. At age 11, Andrew could barely add numbers higher than the sum of 10 and he was very dependent on visual and motor input in doing math. By age 12, he could finally do basic math a little better. For Andrew, there appeared to be less ability to process an auditory input – a math question verbally asked. Yet, Zachary could often give me the answer to basic addition based on a question alone. Andrew was much, more aggressive than Zachary. Overall, Zachary was a very mild child. Although there could be simply age related factors there associated with the fact that Andrew had experienced so many more frustrations than had Zachary simply based on age alone, I could not help but wonder! Zachary had also been cfgf for over two years now. Andrew had never been placed on a cfgf diet. Zachary had been on digestive enzymes for just over 6 months now. Andrew only started to take digestive enzymes in September of 2002.
Andrew’s emotions, generally, I found were more difficult to control than Zachary’s… and there definitely was the fact that Andrew had more in terms of persistent or rapid speech, whereas Zachary was, overall, a much more quiet child – talking and answering some questions, but certainly not showing any signs, at least not yet, of rapid or incessant speech.
Patrick, as long as I had known him, and that was well over 10 years, had always been a very mild, non-aggressive person. He was very calm and easy going in spite of his overwhelming medical condition. Undoubtedly, the need for dialysis, from early on in life had taught him patience. All three boys had a fantastic ability to remember facts. From an auditory perspective, Patrick understood the most in terms of answering questions, then, I would say Zachary, followed by Andrew if those questions had to do with math. In terms of questions related to other activities, I believed Patrick would again be first, then Andrew, then Zachary… in terms of overall language comprehension. Given the great variance in age – 30, 11 and 5 - that alone, however, I felt could be the reason for this variation among the boys. This was as much information as I could really provide in comparing these three boys at this time in terms of functions within the temporal lobe.
My limited observations of these three boys, in relation to one another, certainly opened entirely new areas of interest. Yet, as limited as these observations had been, they certainly were completely in line with this theory that language in the autistic child who had entered surgery mute and become verbal could have been solely triggered by an olfactory sensory input, based on brain structure - this certainly seemed plausible.
Could the “smell” of anesthesia actually awaken us to new possibilities in terms of brain research and possible options while still keeping in mind the effects of temporal lobe damage? - effects that were very serious indeed! Yet, there were other issues too that now had to be considered! How many women who had autistic children had undergone anesthesia (C-section) when that child was born? What about epidurals? The simple fact that 10,000 people per year died from anesthesia alone should have awakened us to the fact that this was “no simple procedure without risk”. Perhaps many had lived through anesthesia only for us to discover later that they had possibly suffered temporal lobe damage. Again, the implications of this, for society, I knew were huge! All this was but a theory, but, from a “common sense” perspective, it certainly appeared that this could be quite probable – that anesthesia could play a role in temporal lobe damage and result in incessant speech.
Could anesthesia explain the 10% of cases known as “infantile autism”, those cases where autism was present from birth? I knew in my heart that Zachary had issues from very early on. I, myself, had never undergone anesthesia. I did, however, have a mouthful of silver fillings – mercury – and I suspected some of those could have “leaked” into my system and caused the damage – as could have the booster shot I received well before getting pregnant. From what I had read in the US Autism Ambassador’s book, Autism and Vaccines The Story A Closer Look, there seemed to be research indicating that vaccinations could trigger illnesses several years away. I had also discovered that many nursery lamps also contained mercury. Surely, as these lamps heated, there could be the possibility of mercury fumes being emitted above infants in maternity wards.
There were now so many issues potentially involved in autism – vaccinations, mercury fillings and now, possibly – anesthesia and nursery lamps! Given some of the research I had read, vaccinations and mercury fillings were definite possibilities. In speaking with the US Autism Ambassador, she mentioned that anesthesia, in her opinion, could definitely also be an issue based on research findings she had seen as they related to autistic children and the fact that many of them required oxygen at birth. My sister-in-law had undergone anesthesia. Andrew had been a very difficult birth, and after 30 hours of labor, the decision was made to go with a C-section. All these things now went through my mind!”
End of quote, book 2, Breaking The Code To Remove The Shackles Of Autism: When The Parts Are Not Understood And The Whole Is Lost!
As I thought about all these issues, I became more and more convinced that the sense of smell – found in both the frontal lobe (language production) and temporal lobe (comprehension of language) was indeed the key to actually triggering – language production!
Again, this would make complete sense if you considered the fact that a person had in the frontal lobes, a right and a left olfactory bulb. Given pretty well everything appeared to “cross over” in the brain that would mean that the left olfactory bulb (frontal lobe) would be tied to olfactory processing (temporal lobe) in the right temporal lobe – the very area tied to incessant speech when damaged! Thus, the sense of smell certainly could provide a link for “language production” between Broca’s area in the frontal lobe and the right temporal lobe – a part of the brain associated with “incessant speech” when damaged – a part of the brain not otherwise associated with “speech production”. The sense of smell appeared to be the one thing tying “speech production” in both parts of the brain – the left frontal lobe and the right temporal lobe!
This could mean that the actual “production” of speech was in the left frontal lobe – or Broca’s area – but that, possibly, the “control knob” involved in turning speech “on or off and the volume control in terms of how much speech” could actually be located in the right temporal lobe! This would also explain why speech production in Dr. Lazar’s AVM patients had not been impacted when the frontal lobe had been anesthetized! To impact speech production, you had to impact either the “control knob” or the actual muscles or physical structures involved in speech production (i.e., vocal cords, etc.).
The more I thought about all this, the more it made sense. Indeed, if you looked at “other functions” in the brain, they too were “scattered”. For example, in looking at “motor activity”, you had motor functions, the planning and execution of motor functions, activity in response to the environment (also motor), memory relating to motor activities and habits all located in the frontal lobe. Yet, the coordination of motor functions was located in the cerebellum – a completely different part of the brain.
Likewise, if you looked at vision, you saw much of the same type of thing. Although visual functions were primarily in the occipital lobe, you had visual attention in the parietal lobe, and visual perception as it related to faces, places and body parts in the temporal lobe. There were also functions related to vision in the cerebellum (i.e., reflex and motor responses tied to vision, etc.). Thus, again, you could have some aspects of vision in one part of the brain, and yet others in a completely different area.
Emotions were again very much the same. You had “control of emotions” and things like “translating judgments into appropriate feelings or responses” in the frontal lobe, perception of emotion in others in the amygdale (part of limbic system) – that structure that appeared to “integrate” much of the “emotional” info in our bodies, the basal ganglia (reward/punishment/ motivation, learned skills having to do with emotions, etc.), responses to emotions in the autonomic systems of the body (i.e., medulla and hormone systems) to allow you to “respond” to certain emotions (i.e., fear, stress, etc.), emotion as it relates to auditory and visual processing (i.e., tone and face or body language) in the right temporal lobe, emotion as it relates to words in the left temporal lobe, and some functions tied to emotions in the cerebellum. Interestingly, some research appeared to indicate that only by stimulating the amygdale could one generate the emotion of “fear” – something I had only very recently read.
Note that with emotions, the “control knob” was located in the frontal lobe and that emotions in children with autism tended to be in “extremes in terms of volume” – meaning that emotions were felt very, very intensely – or basically, not at all. This was also true of the perception of emotions in others. It seemed the “control knob” for perception of emotions was turned down very, very low in children with autism. That, made me wonder if the “control knob” for perception of emotion in others was located not in the temporal lobe, but in the amygdale. As such, it seemed each aspect to a specific function could very well have its own “control knob”. Note again, also, that emotions appeared to have their own “control knob” for the integration of emotion function too – the amygdale – the same area also responsible for the perception of emotions in others.
Clearly, the entire area of “emotions” was so complicated, involving sensory input, behavior, autonomic functions (i.e., hormones, reflexes), etc., that, in order to get an “appropriate” response, all of these inputs had to be properly integrated. Would this not be the same of basically all functions in the human brain? Was smell not also tied to motions, emotion, hormones, reflexes and so many other things in life?
Clearly, sensory input was integrated in the parietal lobe in order to allow for the understanding of a single concept. Likewise, the thalamus acted as a gateway between the information flowing between the cerebral cortex and the peripheral nervous system. The pons acted as a gateway between the thalamus and the medulla (where life functions were located). The corpus callosum acted as a regulator of information between the left and right hemisphere. Did that mean that these were “centers for integration” of information? Or were they only centers for relaying information that was already integrated somewhere else? Again, where were the “control knobs” and the “integration functions” for so many tasks accomplished in the human brain and/or body?
Interestingly, the sense of smell was the only sense that could bypass the thalamus. Why was that? What was it that made the sense of smell – so different? And, if it need not go through the thalamus for the “integration” function in terms of other senses, where was information as it related to the sense of smell “integrated” with information from other senses?
Clearly, if most critical functions in man appeared to be “scattered” in the brain not only in terms of the actual functions themselves but also in terms of the “control knobs” and “integrators” for those functions, why would we not assume the same to be true for language production – clearly a very key and very complicated function in humans. In my opinion, there simply had to be much, much more to language production than mainly “Broca’s area” and the coordination of muscles.
As I looked at the brain and its various tasks, it appeared that in so much, you could have perception in one area, production in another, control in yet another, integration of relevant information or sensory input for that task in yet another, understanding in yet another, planning in yet another, etc.
Indeed, language production seemed to require a great deal more than just the actual “production” of language. Did I not also have to “perceive” language production not only in others, but, in myself? Did I not have to “control” language production and know when to turn it on or off? Did I not have to “understand” language production (what I was actually verbalizing)? Did I not have to coordinate language production? Did I not have to somehow be “motivated” to produce language? Did I not have to integrate many factors (i.e., emotions, situations, sensory input, etc.) prior to language production? Did I not have to decide what “type” of language to use in the production of language? “Language production”, after all, could involve verbal/spoken language, written language, sign or motor language, body language (i.e., rolling eyes, body posture), etc. In a “normal” person, you would think the answers to these questions were “yes”, but was that really true?
Could I not “just produce language” with no understanding, perception or control of it? In my opinion, the answer to that was yes – the actual verbalization could be “just that” – “only verbalizations” or just the physical production of language – without any understanding of the language production itself. Note that I was not talking about the understanding of language here, but an “awareness” of sorts of actual language production – thus, an understanding of the language production itself. Although the function itself could be just a “physical production of language”, clearly, it could involve other parts of the brain that also played into “actual language production” – that made sense not only to others – but to myself as well – and that, could involve areas that would need to be responsible for a “yes” to the questions above relating to the “perception” of language production (i.e., an awareness that I was actually speaking), the “control” of language production (i.e., my ability to speak or not speak at will), the coordination of language production (i.e., putting words together in the proper order), the integration of all aspects necessary for the actual language production to occur (i.e., taking into consideration tone, pitch, body language in others, emotions, etc.), and so on. As such, language production involved a great deal more than just the actual “verbalization” of language. Broca’s area was perhaps involved in the actual production of language, but I suspected many other areas of the brain were perhaps involved in “other language production functions” too (i.e., perception, control, coordination, integration of language production functions, etc.).
As such, to assume that Broca’s language was basically “the key” area” for language production was a very bad assumption to make because clearly, most major functions in the brain had several key areas that needed to work together to accomplish a specific task – not just one! Given language was one of the primary things that set man apart from animals, I very much doubted this critical function was “that simple” when it came to the brain. Indeed, I now suspected that there were many, many, many areas tied to language production in the human brain – and that many of those areas could very well involve what had so long been seen as the most primitive sense of all, the sense I now believed to be among the most intricate and complicated of all – the sense of smell.
The fact that language production as we knew it today – Broca’s area , the sense of smell and motor functions were co-located in the frontal lobe only further solidified my suspicions. Only smell was found as a “sense” in this part of the brain – the frontal lobe. More and more, I wondered if the “sense” found in a specific region (i.e., the frontal lobe) did not actually somehow “trigger” other functions co-located in that area of the brain!
Interestingly, the sense of smell was he only sense to by-pass the thalamus – that part of the brain that controlled information flow to the cerebral cortex (the 4 lobes) and acted as a gateway between the central nervous system (brain and spinal cord only) and the peripheral nervous system (anything outside the brain and spinal cord). Note that it certainly appeared that “language production” itself was not dependent on the other senses. I could “produce language” without the ability to see, hear, touch, or taste. But, I certainly needed the sense of smell to produce language given that sense involved – respiration! In my opinion, it certainly was interesting that the only sense to by-pass the thalamus was also the only sense that appeared to be absolutely necessary for language production and the only sense actually co-located with the known language production area of the brain – Broca’s area – located in the frontal lobe.
This was all very interesting when you looked at all other functions in the brain as they related to the sense of smell, their relationship to other brain functions and whether or not they were “needed” to perform something else. For example, although the production of language itself did not appear to be dependent on “other senses”, clearly, the understanding of language was. The understanding of language produced by others involved either the sense of hearing, sight, or touch. Each of these went through the thalamus. As such, it certainly appeared that the thalamus could play some role in the understanding of language. Likewise, face and voice recognition were dependent on senses that went through the thalamus. The more I looked at the sense of smell, the more I became fascinated by it.
In looking at the sense of smell, there could be no doubt that those structures in the nose were a direct link to the frontal lobe. Indeed, smell appeared to provide the quickest route or access to the brain when it came to body chemistry, as clearly evidenced by the fact that so many drugs were “inhaled”. The sense of smell was discussed in much greater detail in both my second and third books, Breaking The Code To Remove The Shackles Of Autism: When The Parts Are Not Understood And The Whole Is Lost! and Breaking The Code: Putting Pieces In Place! In my opinion, the sense of smell was the most fascinating of all in view of what it appeared to be tied to in the human body and/or brain (i.e., motions, emotions, memories, higher thought processes (i.e., imagination, etc.), sexuality, identification of the self and others, and yes, it appeared – at least in my opinion – even language production).
Our “most primitive sense” appeared to be anything but “primitive” – especially when one considered that “breathing” played an extremely important role in riding the body of toxins (i.e., carbon dioxide, etc.) and as such, clearly, the sense of smell also very much played into the immune system and other functions so necessary to life as well, such as sleep, digestion, alertness, arousal, heart rate (i.e., smell of smoke), and on and on and on. What was it about “breathing in gas” that was so very different? Clearly, there were other ways to rid the body of toxins. That could be done via the liver, the kidneys, the urine, the feces, etc. Why was it that some functions required “gas exchange” and others did not? What was it about the “gas itself” and the sense of smell that was “so special” – especially as it related to the production of speech?
There could be no denying that the production of speech required gases moving in and out of the lungs. One could not hold his breath and still be able to speak nor could one continue speaking once gas had exited the lungs – one had to stop and take - another breath! I could not help but think that the actual production of speech was tied to “gases” we inhaled much more intricately than we may have ever imagined. The fact that helium was known to impact the vocal cords, and hence, production of speech, and the fact that at least 4 boys with autism (1 appearing to be an undiagnosed case of autism) who underwent anesthesia appeared to have language production functions somehow impacted, only made me more convinced that this was indeed the case – that gases somehow impacted the area of language production in the brain – both Broca’s area and what I now considered the “speech production control knob” – the right temporal lobe – both areas linked directly to the sense of smell!
As there was no denying that the lungs were necessary for speech, so was it true of the vocal cords. I had found a website that discussed the issue of “grunting” and how it was related to proper breathing and the vocal cords and that grunting could be a sign of respiratory distress. I quote:
“Five common presenting physical signs relay indirect information regarding pulmonary function. These are respiratory rate, retractions, nasal flaring, grunting, and cyanosis… nasal flaring is another sign of respiratory distress frequently observed in infants… grunting… with normal breathing the vocal cords abduct during inspiration and adduct (without any sound) during expiration. When respiratory function is disrupted, the work of breathing is greatly increased, and neonates attempt to compensate by closing their vocal cords during expiration. Expiration through partially closed vocal cords produces the grunting sound. Grunting may either be intermittent or continuous depending on the severity of the lung disease. During the initial phase of expiration, the infant closes the glottis, holds air in the lungs, and produces an elevated transpulmonary pressure in the absence of airflow. During the last part of the expiratory phase, gas is expelled from the lungs against partially closed vocal cords, causing an audible grunt. It is not actually the grunt, then, that produces the elevated transpulmonary pressure, but the ability of the infant to partially close the vocal cords after end inspiration. During the expiratory phase, when the vocal cords are partially or completely closed, there is an improved ventilation/perfusion ratio because of increased airway pressure and increased lung volume. The end result of this airway closure may be an impairment in gas exchange”. [end of quote, emphasis added, Pulmonary Function In Newborn, Division of Neonatology, Cedars-Sinai Medical Center, Los Angeles, CA, http://www.neonatology.org/syllabus/pulmonary.html].
Thus, this appeared to indicate that children who experienced respiratory distress had the ability to actually “close off” the vocal cords in order to facilitate breathing. Again, needless to say that was very, very interesting given 50% of children with autism were considered “non-verbal”. It certainly would be interesting to study how many “non-verbal” children with autism showed signs of “grunting” – an indication of respiratory distress. I knew Zachary had definitely exhibited “grunting” and “nasal flaring” – another sign of problems with proper breathing!
In my third book, I had also mentioned how insulin appeared to be tied to fetal lung development. Indeed, in mothers with gestational diabetes, not only was the “switch” to alpha-beta blood delayed in the unborn child, but there now appeared to be research indicating that the lungs of a full term baby may not be mature at birth in mothers with insulin problems. Throughout my entire journey with autism, the fact that Zachary had been given that “little glucose bottle” at birth because his glucose levels were low had always been in the back of my mind. I had not been specifically diagnosed with gestational diabetes during pregnancy, but I certainly suspected that I indeed did have problems with insulin metabolism. These issues, insulin, lung development and much, much more were discussed in my third book, a book I very strongly encouraged all families to read as the information in this book had certainly put many, many pieces of my puzzle in place when it came to understanding not only Zachary, but autism in general. This third book I had written was entitled, Breaking The Code: Putting Pieces In Place! It was available in full on my website.
Certainly, when one thought of “speech production”, one did not think of the sense of smell as it related to the actual production of language. We all knew inhaling and exhaling was necessary for speech production, but, I suspected very few of us ever thought that the sense of smell could be involved in perhaps triggering actual language production. Broca’s area - that part of the brain associated with speech production - obviously had to have blood flowing to it. Thus, if oxygen alone was needed for language production, it certainly could be obtained via the blood. Yet it did not appear that oxygen via the blood was involved in language production but rather, perhaps it was oxygen in the form of a gas – via the nose – a structure with a direct links to the brain and hence to Broca’s area and the right temporal lobe, as well as to the amygdale – a part of the brain associated with the perception of emotion in others and as such a part of the brain very closely linked to language production – a part of the brain that was known to synapse directly with the frontal lobes – the location of the olfactory cortex – a part of the brain also very much tied to the temporal lobes… where we found functions relating to the “understanding of language” and where we, perhaps, also found the “control knob” for language production – the right temporal lobe.
Crying was a newborn’s first “production of language” – and that, clearly, involved the exchange of gases as the lungs began to work shortly after birth. Although scientists were not sure as to what actually caused that “first breath” to be taken in an infant it certainly appeared to be the case that “gasping for that first breath” was pretty well always associated with crying – or “language production” in a newborn.
All infants appeared to cry at birth. Why was that? Why could they not simply start to breathe without crying? Was it simply because of the “shock” involved in leaving the womb - a nice, warm environment that had now been exchanged for a cold one? Was it the lights or sounds that caused an infant to cry? Was it gravity? Was it the “small slap on the bottom”? Or, could it perhaps be the fact that the lungs, as they began to function and bring oxygen to those parts of the brain involved in language production actually did just that – result in the production of language – in the form of – crying!
Clearly, while in the womb, the lungs functioned very, very differently and were not involved in respiration or breathing. Yet they were without a doubt very much involved in breathing and the exchange of gas and the actual production of language from the very first breath!
When Zachary was born, I remembered thinking it was odd that the obstetrician had not slapped his little bottom to activate the lungs but had simply touched the soles of Zachary’s feet. There had to have been basically no pain involved in that for Zachary – as there could perhaps have been with a slap on the bottom – and as such, as I now looked back, I wondered, why did all babies cry at birth! Why did the lungs not just “start to work” without crying? Why did the child simply not start to breathe in a nice, relaxed way? And why did all newborns appear to have this thing known as the “startle/Moro reflex" – a motion during which the lungs were flung wide open and then retracted. As stated in a quote in my third book, that indeed did appear to be a seemingly perfect motion to help expand the lungs at birth.
Another “reflex” that newborns appeared to have was the “gasping reflex” that seemed to occur due to the need for oxygen. In animals, the umbilical cord was pretty well automatically cut during the birthing process and this resulted in a “gasping reflex”. This “automatic severing of the umbilical” was obviously not the case in humans. In humans, the umbilical cord was much thicker and more difficult to cut, undoubtedly, providing additional protection for the child during delivery and shortly after birth. The umbilical cord provided a means for obtaining oxygen prior to the activation of the lungs. There were now concerns being raised over the fact that perhaps, modern practices were now resulting in the premature clamping of the umbilical cord. It was believed that this could lead to oxidative stress in the newborn.
Given insulin was known to impact lung development, and Zachary had been given that “little glucose bottle” at birth, I now very much suspected that Zachary’s lung were not mature at birth. Looking back, I did think his cord had been clamped rather quickly. Both my husband and daughter had witnessed Zachary’s birth and also thought the clamping had occurred almost immediately. Of course, “cord-clamping time” was not something hospitals recorded, and as such, I had no way of knowing exactly how long the doctor had waited prior to clamping the umbilical cord. Those studying this issue argued for at least a “two-minute waiting period” prior to the clamping of the cord. If indeed Zachary had immature lungs at birth, then early cord clamping certainly would have only made any already existing oxidative or respiratory stress - worse! It was a well-known fact that the brain could go approximately 4 minutes without oxygen before brain damage occurred. As such, one could perhaps argue that early cord clamping was not an issue given the child could start breathing on his own. However, again, the key words here were “normal child” – and, in the first few minutes of birth, truly no doctor could determine “how normal” a child was in terms of “how mature” the lungs really were! As such, in a child such as Zachary, early cord clamping certainly could be a contributory factor in oxidative stress or respiratory distress. I very much suspected that in humans, perhaps there also existed this “gasping reflex” once oxygen from the cord was no longer an option for the child as the cord was either clamped or cut.
As I thought about this issue - respiration in the newborn - and of “crying” and how it related to speech production in infants at birth, I could not help but remember the first two hours of Zachary’s life. Below were words I had written in my first book, Saving Zachary: The Death And Rebirth Of A Family Coping With Autism!
“My nap of two hours after Zachary’s birth was brought to a rather unusual end. I awoke to a nurse tapping on my arm and saying, “you’re going to have to take your son now, he’s been screaming for two hours straight and we can not take it anymore”. My first thought was, “you idiot, why did you let him cry that long, you should have come and woke me right away”, but I did not say anything, not wanting to upset the person who cared for my son while he was in the nursery. As soon as I took Zachary into my dark room, he fell asleep within a couple of minutes. I kept him with me pretty well until I was discharged the next day. He slept almost the entire time, although looking back, I can recall that after feedings, he had a hard time actually falling asleep and I had to walk around with him to calm him down.
Perhaps the first indication we should have had that something was not right was the fact that for the first two hours after his birth, Zachary cried non-stop. Looking back, I guess that should have been a sign to any parent or healthcare professional that something was wrong. Did not the fact that a newborn cried for two hours non-stop in itself seem very abnormal? Almost every newborn I had ever seen just slept in the first few hours after birth.” [end of quote, emphasis added, book 1, Saving Zachary: The Death And Rebirth Of A Family Coping With Autism!].
When I had first written these words, they were written in a section having to do with “nursery lamps”. I wondered if Zachary was somehow oversensitive to the heat lamps under which all newborns were placed. I did not doubt that this indeed was the case. But, now, I wondered how much of Zachary’s initial crying at birth could have been an indication of other problems – such as respiratory distress. I did not think that crying actually helped with breathing – actually, I believed just the opposite – that crying interfered with proper breathing.
Persons who were grief stricken and/or cried deeply always seemed to be gasping for air. Each time I had been so filled with sorrow and cried so deeply, I had always felt more difficulty in breathing. As such, I could not help but wonder about the role of crying and gas exchange in newborn infants as a means of activating “language production functions”.
Crying, obviously, was a means of communication in infants. Had this been Zachary’s way of trying to tell all of us that something was horribly wrong? Although I now very much suspected that had been the case, I simply had no way of knowing for sure why Zachary had cried almost nonstop the first two hours after his birth. The fact that I had once read nursery lamps could have mercury in them obviously did not add to my “comfort” regarding this issue. As nursery lamps heated up, could that possibly result in mercury fumes over my newborn son? Again, I wondered what had really happened to make Zachary cry so when he was first born.
It was now appearing to me that, as had so often been the case in this journey with autism, what I had once known to be true was perhaps not the way things were after all.
Society tended to look at “crying” as pretty well simply an expression of emotion – a function with implications for the frontal lobe, temporal lobe and amygdale. Coincidently, these were also very much parts of the brain associated with the sense of smell!
The sense of smell and the sense of taste were closely associated. Of that, I had no doubt. Yet, the critical difference between the two was that taste had to do with a “sample” on the mouth, whereas smell involved only gases – something that could actually be some distance away from the body. It was estimated that the average person could perceive approximately 200 different tastes. Yet, the sense of smell – what was considered our “most primitive” sense – was much, much more sensitive – able to distinguish, by some estimates, about 2000 various odors.
Note also that the sense of smell was the only sense that could actually by-pass the thalamus. This, again, was all very interesting given the thalamus was a major “gateway” between the central nervous system (brain plus spinal cord only) and the peripheral nervous system (everything outside the brain and spinal cord). Why was the sense of smell allowed to do this? Had the fact that the smell by-passed the thalamus played into our belief that the sense of smell was a “primitive sense”, less relied on by other senses when it came to integrating our world? If that were true, then we may have made a serious error in judgment in evaluating the value of the sense of smell. Perhaps the reason the sense of smell by-passed the thalamus was due to the fact that it was so important that it needed “special processing” in terms of the relaying and integration of information from this system as it related to so much in human activity.
It was interesting to note that those senses that did go through the thalamus – taste, touch, hearing and sight, were not really critical to the function of “language production”. I could have impaired taste buds and still be able to “produce language” or verbalize sounds. Likewise, I could be blind, deaf or paralyzed and still be able to “produce language” or verbalizations. Only the sense of smell – the one sense that bypassed the thalamus – was absolutely critical to actual speech production – the one sense that was found in both the frontal (olfactory cortex) and temporal lobes (olfactory processing) – both areas associated with language. The sense of smell was the only sense that could truly link language functions between the frontal and temporal lobes given this was the only sense that appeared to be found – in both – and as such, my reason for believing that the sense of smell was the key to the mystery of the right temporal lobe!
As I considered the sense of smell, I wondered why it was that this sense did not have “its own cortex” in the brain. Vision had its own lobe… why not smell, too? Perhaps the answer to that was in the fact that vision was perhaps a much more primitive sense than smell. One could be blind and still function very, very well. Although one could have an impaired sense of smell, the fact was that without the functions associated with the sense of smell – functions such as breathing – there could be – no life! Breathing – or the gaseous exchange that occurred as a result of inhalation – a function involving the nose - was absolutely critical to life. We usually only thought of “breathing” as a “life function” located in the brainstem. But, clearly – breathing - involved something else that was very critical – the nose – and that involved both the frontal and temporal lobes! As such, although we usually did not think of the sense of smell as involved in anything other than “smelling” – clearly – in actuality – the sense of smell – what we had so long seen as perhaps the most primitive of senses – was truly the most critical of all when it came to life itself!
There could be no denying that “smell” was tied to so many critical functions in human life. It was associated with motor functions, activity in response to the environment, imagination, the concept of self, memories, and emotions and I now suspected, perhaps very much also associated with language functions. Indeed, it appeared to me that the sense of smell played more of a role in the human brain than any other sense and as such, I simply did not understand how we could have come to view this as our most “primitive sense”. I now had a whole new appreciation for what I believed was not the most primitive sense of all – but, rather – perhaps the most misunderstood sense of all - the sense of smell.
Note that the sense of smell and the sense of taste were considered the “chemical senses”. Also note that the sense of hearing was also very much impacted by the sense of smell. When the sinuses were filled with mucous, hearing was clearly impacted. Everyone knew that a plugged nose impacted hearing, but we really did not give much thought to what an infection in the ears could do in terms of impacting the proper functioning of the sense of smell.
If the nose was filled with mucous, obviously that impacted airflow. Certainly, that appeared to be something that could contribute to “oxidative stress” in infants. Obviously, gases flowing in were impacted by congestion in the nasal system. But what about gases and the impact of obstruction for gases flowing out? Was more carbon dioxide left in the body when there was congestion in the nasal passages? If so, what impact did this additional toxin have on the brain? And, what about the ear canals? If the ears were infected, what effect did that have on proper airflow within the body? Given so many children with autism had suffered from chronic earaches, I could not help but wonder how “earaches” impacted the sense of smell and its proper functioning given these systems were so very closely related and how “earaches” may contribute to “oxidative stress” in these children.
Certainly, it was well known that antibiotics used to treat earaches destroyed the healthy bacteria in the intestinal wall and as such, contributed to problems in digestion in these children. But, could antibiotics also be doing something that impaired the sense of hearing or smell in these children too? Of course, I had no way of knowing either way – although I truly wondered!
When it came to the sense of smell and children with autism, there was no denying that these children appeared to have a very, very sensitive sense of smell. Interestingly, the sense of smell was one of the only areas in the brain (the other being the hippocampus – tied to memories and also to the sense of smell) known for a fact to continue to generate new cells throughout life according to work done by Dr. Fred Gage. Note that the amygdale, associated with memories tied to emotions, also synapsed directly with the sense of smell.
This sense of smell was intriguing indeed. Man had always wondered why the brain did not produce “new cells” throughout the brain over the course of life. So far, only two areas had been identified as “producing new cells” in the brain – the olfactory cortex and the hippocampus. Why was that? Could it be because via the production of new cells in the olfactory system, we simply did not need new cells in other regions? Could it be that new “smell cells” rejuvenated other functions too somehow? Could, via the sense of smell, other major functions not be finding “new life” also? Smell functions seemed to be found in so, so many parts of the brain. Although not technically found in the parietal lobe, could one not argue that the skin provided “air” too – and as such, indirectly, would that not involve “air exchange processes” that could then be tied to the parietal lobe given the parietal lobe involved the sense of touch, or, – the skin. Like the nose, did the skin not also – breathe? Could this somehow play into the fact that studies were finding persons who were more active physically also seemed to function longer mentally as well? There was no doubt that physical exercise was good for the body overall, but what was the role of “smell” or “gas exchange” in mental activity or functioning?
Could one have an impaired sense of smell and yet, still have great mental capability due simply to the gas exchanges going on? Clearly I could have an impaired sense of smell and be unable to actually smell something properly but yet still have that “gas exchange” going on in terms of oxygen going to my brain. Olfactory dysfunction had been well documented in autism, schizophrenia and Alzheimer’s. Zachary, for example, had a very, very sensitive sense of smell. Yet, I suspected that as he got older, this sensitivity would decrease as I very much believed his sense of smell would become not “overly sensitive” but very much less sensitive – in other words, I suspected he would begin to lose functioning in this area. Recently, I certainly had noticed that Zachary rubbed his nose a great deal and he very much showed “olfactory distress” if I could use that term. He seemed to be constantly sniffing or rubbing his nose, and this certainly was of concern to me given I now suspected the sense of smell could be tied to much more than we may ever have imagined.
Perhaps that helped to explain why so many children with autism – children who were very, very picky eaters - came to more easily accept more foods as time went on.
The reason I suspected Zachary might lose his sense of smell was because mercury appeared to target developing cells or at least, had a much greater impact on immature cells. Those cells that were the most immature of all appeared to be most targeted by mercury. In early life, that would be the cerebellum – a part of the brain that took close to twenty (20) years to mature – the very part of the brain that appeared to be most impacted in young children with autism. Yet, as time went by and most of the brain was formed, if only the olfactory cortex and the hippocampus continued to develop new cells, then, I suspected these would be the very areas targeted by mercury later in life.
Indeed, in Alzheimer’s, olfactory dysfunction was clearly documented as was the fact that the hippocampus was perhaps the area “hardest hit” by this disorder. I also suspected that for children with autism, that changes in olfactory processing and impairment in the sense of “less smell” would be triggered with the onset of puberty – a time when the brain was known to prune and reorganize itself – a time that should normally involve gray matter thickening (new cells being formed) but that, in actuality, involved gray matter loss in persons with schizophrenia – as clearly explained in my third book, Breaking The Code: Putting Pieces In Place! If indeed mercury targeted immature cells, this certainly would make sense!
In my third book, I had provided over one hundred and forty (140) parallels between autism and schizophrenia and over one hundred and sixty (160) parallels between autism and Alzheimer’s. In my opinion, these were nothing more than the same disorder over the life spectrum – disorders that also all shared a very, very common history! Note that autism used to be called “childhood schizophrenia” and schizophrenia used to be called “dementia praecox” – as was also the case for Alzheimer’s. In fact, Alois Alzheimer was the protégé of Emil Kraepelin – the man who discovered schizophrenia - and they appeared to have agreed that based on age of onset – these disorders would be viewed as “different”!
Age of onset was also one of the primary considerations in distinguishing between autism and schizophrenia, completely irrelevant criteria, in my opinion, given that the brain was not a constant over time. As such, how could you possibly compare a disorder involving the brain across generations when the brain underwent such tremendous change over time – and this, clearly had to play a role in what we saw in autism, verses schizophrenia, verses Alzheimer’s.
There was a great deal more provided on this issue in my third book, and I strongly encouraged all families impacted by these disorders to read this book, posted in full on my website. Truly enlightening information!
I had looked for two days on the Internet for a “neurologist’s explanation” of “the mystery in the right temporal lobe” and how an area of the brain not associated with language production could result in incessant speech when damage to this area occurred. Many sites acknowledged the issue – stating that indeed, damage to the right temporal lobe resulted in incessant speech – but, I could find nothing that really explained why this was so. Thus, “the statement was made”, but, from what I could find, no explanation for this was provided.
Experiments dealing with subjects that had impaired speech production in terms of damage to Broca’s area seemed to simply assume that the function of speech production had simply “relocated itself” within the brain. I suspected that this indeed was not the case and that the issue was more one having to do with the actual “control knob” – the “on/off and volume” switch for language production that appeared to exist in the right temporal lobe and appeared to be very much associated with the sense of smell. As such, the function of language production had not “relocated itself”, but rather, we had simply perhaps stumbled upon another part of the brain associated with a particular function – in this case, the “control knob” for speech production!
If indeed the sense of smell was associated somehow with the production of language, then, speech functions perhaps were not “relocating” themselves in brain damaged patients, so much as they were perhaps simply activating “speech production reserves” already there given functions of “smell” already resided in the temporal lobes.
Much as many different aspects relating to specific functions in the human brain were located in various parts of the brain, so too, did it appear to me that there were various “control knobs” to be found throughout the brain for these functions – and often, it appeared to me – these “control knobs” were located in an area separate from the actual “production” of the function itself or functions relating to the “integration” of critical inputs for the “production” of that function.
As I thought about everything I had learned over the past three years, and thought again about these boys with autism who had all undergone anesthesia and looked for “other explanations” to the productions of speech and/or rapid speech in these children, I could not help but wonder about “temporal lobe damage” in and of itself – somehow occurring in these boys – outside of anesthesia.
Certainly, that could be a possibility. It was a known fact that children with autism often developed seizures at puberty onset. Yet, at least in three of the four boys, Victoria Beck’s son, my nephew Andrew, and my son, Zachary, puberty had not yet been reached when these issues with speech had surfaced. I did not know enough about the fourth boy, Patrick, to comment on his situation in terms of when issues of rapid speech had surfaced. Could these boys have experienced seizures or some other type of temporal lobe damage prior to puberty – of course – that was a possibility, but that little voice inside of me still made me lean toward anesthesia as part of the answer to this particular puzzle.
Neither Zachary nor Andrew had undergone an MRI. I did not know if either Patrick or Victoria Beck’s son had undergone this procedure. It certainly would be interesting, in my opinion, if Victoria Beck’s son had undergone an MRI prior to his anesthesia – and one after this procedure requiring anesthesia – in order to compare the scans for right temporal lobe damage – something very much associated with “incessant speech”. Whether or not my theories about anesthesia would prove true or false – I supposed perhaps time would tell.
I had simply provided “my theory” – a possible clue or explanation for this mystery – in the right temporal lobe. How damage to a part of the brain not associated with speech production could result in “incessant speech” was a rather fascinating mystery indeed!
Of course, this was just “my theory” as to what we were seeing in terms of “the mystery in the right temporal lobe” and other things we were seeing in terms of brain structure and function. I suspected that as we learned more about the sense of smell, how it changed over time and, how it played into so much, that we could come to better understand perhaps not only the mystery of the right temporal lobe – but many other mysteries relating to not only specific disorders but brain structure and function in and of itself!