Brain evolution & Dreaming, continued

Maerd wrote:
Can you supply some scientific evidences to support your statement above (that evolution of brain structure followed the sequence from MYEL, MET … to TEL)?

Support for my perspective of brain evolution came from a critical analysis of evidence provided by multiple scientific disciplines. Those disciplines included anthropology, paleontology, neurophysiology, and comparative species analysis. My method of critical analysis required that I first establish the nature of evolution then assess whether that nature applies to brain structure and, if so, how it applies. We know Charles Darwin first postulated the theory of species evolution in 1872 through his work, The Origin of Species. The Digital Evolution Laboratory at Michigan State University has since provided more recent support for Darwin’s theory through the breeding of digital organisms that mimic DNA. A singular tenet of Darwin’s postulate suggests that simple organisms can become complex animals as they adapt to the demands of survival. Paleontological study of the fossil record has continuously provided evidence suggesting that modern humans evolved from less sophisticated (primitive) forms of life, which science has generally accepted. The fossil record of human evolution suggests that modern humans (homo sapiens) evolved from the apelike creature, Australopithecus ramidus. From Australopithecus, human ancestry can be traced to the shrewlike creatures of the subclass, Prototheria. Portotheria are considered the first mammalian-type animals and are also considered the direct descendents of the Cynodontia suborder of reptiles. The ancestor of Cynodontia and the first reptilian ancestors of mammalian animals alive today were a couple of synapsid lizard-sized reptiles named Hylonomus and Archaeothyris. Synapsid reptiles are linked to mammalian ancestry through a set of low openings behind each eye socket. The Illustrated Encyclopedia of the Prehistoric World by Douglas Palmer contains striking illustrations and much of the information I have shared to this point. As we follow the peleontological path of human evolution backwards in time, we arrive at the first cordate, Haikouella lanceolata about 540 million years ago. Haikouella is remarkable for providing the earliest fossil evidence of brain structure, which was barely more than a notochord punctuated by an anterior bump of neural ganglia. For a picture and further information about Haikouella, select the following link: http://www.palaeos.com/Vertebrates/Units/010Chordata/010.200.html#Haikouella

When we trace the likely path of human evolution through time, we find animals whose brains, through comparative species analysis, were likely less sophisticated than modern humans. Beyond Haikouella, species analysis suggests that the earliest form of neural structure was no more than a cluster of nerves. A critical analysis of the neuroanatomy of living animals comparable to human ancestry suggests that the human brain evolved from a simple structure to its current complexity as its ancestry evolved. Our next step is to determine whether any evidence of this evolution remains in brain structure and what may have been the compelling factors in that evolution. From functional study and comparative species analysis, we know modern brain structure contains recent and primitive components. Generally, cortical structure is considered recent and brainstem structure primitive. Elements of the brainstem are considered primitive because we have found these elements, minus cortical structure, in life forms of less complexity than humanity. We have found, for example, the most primitive element of brainstem structure in existing primitive life forms comparable to those that may have existed prior to Haikouella. The MYEL (spinal brain) and spinal cord are at the base of the brainstem and should be considered the most primitive components of brainstem structure because their structure and function is comparable to the simplistic nature of the notochord development and function we find in existing primitive life forms such as annelid worms. During the embryonic phase of vertebral growth, humans included, both brain and spinal cord development arise from a notochord stage reflective of precursory neural evolution. In the MYEL, as in notochord structure, we find afferent and efferent nerves associated with heart, lung, taste, and digestion. Relative to evolution, afferent neural adaptations suggest the stage in evolution when the neural system of primitive animals began to receive and process specialized sensory information. The afferent nerves of the MYEL are the Vagus and Glossopharyngeal. These nerves provide sensory from the heart, lungs, trachea, bronchi, larynx, pharynx, GI tract, posterior tongue (1/3), tonsil, external and middle ear (tactile only). When we compare MYEL sensory adaptations with those arising from MET afferents, we can perceive clearly this sequence of subsequent brain developments as enhancements to brain structure rather than replacements of prior structures—in accord with the evolutional process. The afferent nerves of the MET are the Vestibulocochlear, the Intermediate Facial, and the Trigeminal. The Vestibulocochlear nerve enhanced the tactile ear sensory of MYEL structure with the perception of sound sensory. The Intermediate Facial nerve enhanced the posterior taste distinctions of MYEL function with anterior tongue sensory (2/3) and soft palate distinctions. Finally, the Trigeminal provide sensory enhancements from the face, sinus, and teeth. These afferent nerves arise in MET structure separately and in the order given here. When we evaluate where and when these nerves appear in MET structure and the sensory capability they provide, we can track the evolutional direction of taste, sound, and facial perception from simplistic posterior developments to refined anterior developments. When we apply this kind of analysis to the rest of brain structure, I believe we find sufficient evidence of its evolutional path from MYEL to TEL--a path that suggests how more recent sensory developments enhanced the distinctions of prior developments. The Atlas of Human Anatomy, Third Edition by Dr. Frank H. Netter provides wonderful illustrations of brainstem neural development.

Maerd wrote:
To my understanding, Dr. Hobson's activation-synthesis model was developed based on Dr. Jouvet's findings. But, Dr. Solms's article was a critique of activation-synthesis model. I suggest you to re-read Dr. Solms's paper titled "Dreaming and REM sleep are Contronlled by Different Brain Mechanisms", Behavioral and Brain Sciences, 2000; 23 (6):843-50.

I stand corrected. Solms, Siegel, Jouvet, and Hobson; I tend to lump them all together in my perspective. As I now recall of Solms’s assessment, his distinction of disassociation between REM and dreaming reside in lesioning and pharmacological studies focusing on prefrontal function. In his review, as I recall, whether or not dreaming occurred was dependent on a study participant’s ability to awake with memory of having dreamed. I believe we both agree on the importance of prefrontal function in the conversion of short-term to long-term memory. When we damage or interfere with prefrontal function, our ability to recall short-term experiences seems to disappear. In Solms’s view, REM and brain activity in sleep without any memory of dreaming upon waking is evidence that dreaming did not occur. To him, this is evidence of disassociation. Solms’s error, in my opinion, is his failure to consider the affect of prefrontal lesions and function inhibitors on a participant’s ability to remember dreaming. After all, reports of dreaming are memory dependent and any interference with those brain processes associated with memory could conceivably obliterate the memory experience of having dreamed as though it never occurred. In my view, the most reliable evidence of whether a person has dreamed is provided by functional analysis. To my knowledge, there is no reliable evidence that REM, in an intact brain, can occur without the brain activity we find in dream sleep. I encourage your further thoughts.

Maerd wrote:
I agree with you in general that brainstem is mainly primitive and cortical structure is mainly recent. However, not all cortical structures, in my view, are recent; and not all brainstem structures are primitive. For example, the reticular formation of the brainstem and the cortex probably started their evolution process at same period of time, as either destroying the reticular formation or severing cortex from the rest of brain will lead to a coma state.

This link, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7845593&dopt=Citation, provides an abstract of research that shows the resumption of paradoxical brain activity after the destruction of the medullary reticular formation. This suggests the independence of cortical activation from reticular function and belies the idea of their concurrent evolution. However, cortical dependency on subcortical afferents supports the contiguous and sequential nature of brain evolution. Clearly, reticular function does not depend on cortical activation. However, Jouvet’s experiments proved cortical function is non-existent in the absence of subcortical afferents. Like all other contiguous structures of our central nervous system, the functional dependency of a neural structure on another determines its place in the hierarchy of brain evolution. If agreed, then the cortex clearly evolved after the reticular formation.

Maerd wrote:
I don't think that prefrontal plays very important role in the conversion of short-term memory to long-term memory. With prefrontal leukotomy study as an example, damage along prefrontal system produces disorders characterized by reduced interest, reduced initiative, reduced imagination and reduced ability to plan ahead (where the patient does nothing unless instructed). Thus, some researchers describe prefrontal as the "seeking" or "wanting command system of the brain".

The following links provide evidence of research associating prefrontal function with memory: http://www.nature.com/nature/journal/v386/n6625/abs/386604a0.html http://www.csbmb.princeton.edu/ncc/PDFs/Atten-Ctl-WM%20&%20PFC-DA/Neuroimaging/Braver%20et%20al%20(NeuroImage%2097).pdf http://jocn.mitpress.org/cgi/content/abstract/16/6/908 http://www.pnas.org/cgi/content/abstract/95/3/906

Maerd wrote:
In my view, dream recalls are not dependent of long-term memory. Although we all dream every day when we sleep, we can seldom recollect more than a few minutes worth of our dreams after waking. Our experience told us that unless being recalled immediately after waking, dreams cannot be remembered.

Prefrontal function has been associated with short-term memory (working memory). I believe dreaming only involves working memory, which is one reason why we forget them so quickly when we awake. Although most of our dreams are forgotten when we awake, we still have memory of having experienced something in our sleep. That memory residue is likely a product of working memory. As I have proposed, when we lesion the brain or interfere with those brain processes associated with forming dream memory, we can conceivable awake with no recollection of having dreamed. This, I believe, is essentially what Solms did not consider in his review.

Maerd wrote:
I don't know if you are familiar with a widely studied case of memory impairment, a patient named as "H.M." or "Henry M". After removal of large sections of the medial temporal lobes (includes the hippocampus) of the brain to relieve epilepsy in 1953, Henry could only remember recent events for a few minutes. Isn't this in some way mirror the same problem that we face for dream recall?

Although I am not familiar with Henry M’s case, I am familiar with the work of Dr. Brenda Milner who used a similar surgical procedure for treatment of intractable epilepsy. She experienced similar memory results. My perspective of prefrontal structure and working memory is that its function plays an important role in the memory formation process. Any interference with that process could affect our ability to remember our experiences and, especially, those experiences that do not appear to involve true physical reality—such as dreams.

I perceive the experience of dreaming as a process entirely comprised of working memory. I believe prefrontal function plays a significant role in the lasting memories we retain from our working memory. From my perspective of working memory and dreaming, lasting or long-term memory is the recollection of having experienced something amid sleep; i.e., I perceive those fading sensations we experience when waking from sleep as our dreaming brain’s equivalent of long-term memory. Although we may ultimately forget our dream experiences when we awake, our fading residual memories of them are the working memories I believe our brain has tried to convert to long-term. I welcome your continued thoughts.

Maerd wrote:
http://brain.oxfordjournals.org/cgi/content/full/126/7/1524 : http://download.videohelp.com/vitualis/med/reticular_formation.htm http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=284730&dopt=Abstract

I selected the links you provided to get some sense of the basis for your perspective on brain evolution. Your second link did not appear to access actual research and your third link provided merely a title; however, your first link did have content from which I have provided this excerpt:

"In the beginning of the 20th century, Bremer (1935 ) showed that in lightly anaesthetized cats, the transection of the brainstem at the pontomesencephalic level caused coma, whereas a transection at the level of the spinomedullary junction did not. In another experiment, Moruzzi and Magoun (1949 ) showed that stimulation within the brainstem reticular formation of lightly anaesthetized cats resulted in high frequency/low amplitude (so-called desynchronized) EEG, an electrophysiological correlate of the conscious state, whereas lesions of the same region of the reticular formation caused coma with low frequency/high amplitude (so-called synchronized) EEG. These results led to the suggestion that the upper brainstem reticular formation is the origin of a system involved in activating the cerebral cortex, namely the ARAS, and that the process of cortical activation is indispensable for the maintenance of consciousness (Fig. 1A). Subsequent clinical observations showed that lesions in the upper brainstem reticular formation are a major cause of coma (Loeb, 1958 ; Loeb and Stirling Meyer, 1965 ; Chase et al., 1968 ). Eventually, Plum and Posner (1980 ) used a series of clinical and pathological observations to establish the now classical notion that coma in humans is caused by lesions occurring in the reticular formation territory extending from the upper third of the pons to the upper limits of the midbrain."

If I understand correctly, this article provides research supporting a conclusion that damage to the “upper third” of the reticular formation causes coma, whereas, damage to the lower two-thirds does not. If I also understand correctly, you have provided this article as evidence of some concurrent cortical and brainstem evolution. To prove concurrency, the research should show an interdependency of function between the cortex and reticular formation. Also, the research should suggests some exclusivity of cortical and reticular function. Clearly, your first reference provides research that does not show mutual dependency between the cortex and reticular; it shows that cortical activation is dependent on reticular function and not the other way around. If brain structure follows a path prescribed by evolution, then primitive elements of brain structure should provide a foundation for recent elements. Again, your first reference supports the idea of the cortex evolving after the reticular of the brainstem because its research provides brainstem (reticular) function as a foundation for cortical activation. A further analysis of this research also belies exclusivity of function. As your reference clearly provides, two-thirds of reticular structure did not evolve exclusively to stimulate cortical activity and evidence of fatal hyperthermia suggests that the upper third did not initially evolve that purpose as well. The occurrence of fatal hyperthermia after destruction of the upper reticular suggests a connection between the reticular and hypothalamic thermoregulation. Contiguously, the hypothalamus arises in brain structure before the cortex and after the reticular.

Maerd wrote:
Since consciousness can be eliminated by either destroying the reticular formation in the brainstem (the headquarters of consciousness, in my view) or the whole cortex (its supporting systems, in my view), this indicates that it is a necessary condition for both reticular formation and, at least, one subsystem of cortex to be functional to have consciousness. Thus, I don't think the whole cortex evolved after the reticular formation (although I agree that most part of cortex evolved after).

I disagree. The behaviors of decorticate animals and congenitally decorticate children suggests the cortex may not be necessary for consciousness and likewise for reticular activity. Here are a couple of references: Oakely, D.A. “Performance of Decorticated Rats in a Two-Choice Visual Discrimination Apparatus.” Behav Brain Res. (1981): 3(1): 55-69 Shewmon, D.A. etal, “Consciousness in Congenitally Decorticate Children: Developmental Vegetative State As Self-Fulfilling Prophecy.” Dev Med Child Neurol. (1999): 41(6): 364-74 You should also consider a search of Google Scholar for further “Decorticate” research.

Maerd wrote:
Although its concept (by Baddeley, 1974) was initially developed from short-term memory, working memory refers to the structures and processes used for temporarily storing and manipulating information. In the theoretical framework of working memory, short-term memory is only a very small portion of it…The links that you referred above are studies of working memory (mainly about human information processing and manipulating). It is true that results of scientific studies have strongly suggested that prefrontal played a very important role in working memory processing and manipulating. But, not in memory saving, as Solms and other researchers described prefrontal function as the "seeking" or "wanting command system of the brain".

If you recall, I disagreed with Solms assessment because he and others did not consider how brain lesioning and function inhibitors might affect a sleeper’s capacity to remember the experience of dreaming. He and others perceive no memory of dreaming as evidence of non-dreaming occurrence. I said that any interference with the brain processes that produce memory could conceivably affect a sleeper’s ability to awake with memories of having dreamed. I perceive no distinction between short-term and working memory. However, our general perception of working memory as you have described is how I perceive the experience of dreaming. If you agree that prefrontal function plays “a very important role in working memory processing and manipulating,” and “dreaming indicates that working memory is working during sleep,” isn’t it possible that damage of the prefrontal and interference with its function could affect a sleeper’s ability to recall dreaming after waking from sleep?

Maerd wrote:
Actually, Dr. Milner was the first to study H.M. case. She co-authored the paper "Loss of Recent Memory after Bilateral Hippocampal Lesions" with Dr. Scoville (who did the surgery) in 1957 about H.M. case. Based on the patterns of Henry's memory loss, researchers formed the following hypotheses about memory formation: 1.) Short-term memories are biologically different from long-term memories because they do not require the hippocampus for formation. 2.) Long-term memories are stored throughout the brain, but the hippocampus is necessary for the information to reach long-term storage. Once the memory is permanently stored, however, the hippocampus is no longer required. Said another way: the hippocampus is important for long-term memory formation, but not for memory maintenance or retrieval.

Unfortunately, I did not recall her patient’s name having not referenced her work for some time now. It was my recollection that she performed the surgery but had to take second chair on the credits because of her female status. So much for long-term memory.

Maerd wrote:
So, it is the hippocampus that plays an important role in the memory formation process (from short-term to long-term). I don't know why you believe the prefrontal structure "plays an important role in the memory formation process".

In explanation, I provide this excerpt from our prior discussion:

"The evidence in evolution suggests that the cortex evolved as an enhancement to the memory function initiated by limbic development (hippocampus included). Although elements of the limbic system have been associated with emotions, the research evidence clearly provides its strongest association with memory functions. As an enhancement to memory, the cortex allows us to create a mental environment in which we can modify or construct behavioral responses to obtain our subcortical objectives. In studies of prefrontal damage and lobotomy, the primary lost in brain function appears to be associated with an inability to assess consequence or a lack of interest in the consequences of one's actions. In animals ancestral to humans, the only influences of consequence were those of physical impact on their survival. During D-sleep (dreaming), prefrontal function is depressed while other brain areas increase in activity. This function remains depressed because physical sensory does not enter the cortex during D-sleep as it does when we are consciously awake. Physical sensory is encoded by our physical senses. Dream imagery is produced by resonant influences from the brainstem that are not encoded by our physical senses. Therefore, the prefrontal remains inactive during dream sleep. Because our prefrontal makes us care about [the consequences of] our physical experiences, the experiences we encounter while awake are easier to remember. Because dreams do not contain the physical markers of conscious physical experience, our prefrontal does not attach significance to dreams and we forget them easily as a consequence. When we remember our dreams, that memory is a product of our awaking sensory systems that begin to integrate their physical/material information with the information swirling in our heads, from our dream experiences, as we wake. This integration from our physical sensory arouses our prefrontal function, which attaches the significance to our dream experiences that makes them memorable."

Maerd wrote:
I would say that, yes, dreaming indicates that working memory is working during sleep. However, the fact that we don't remember our dreams suggests that dreams have not been converted into long-term memory during sleep. As a result, we can only recall dreams saved in the short-term memory if we recall them immediately after arousal.

If we are recalling dreams immediately after arousal, I believe what we are recalling is working memory. In my view, our effort to retrieve dream memories when we awake is an effort to convert working memories into long-term memories. Dreaming, in my view, is a mental experience comprised entirely of working memory. Working memory, in my perspective, is like an echo; it reverberates strongly in the beginning but fades unless renewed. As I perceive, dreaming is an experience of the mental reverberations from our conscious life that persist into sleep. I welcome your further thoughts.

Maerd wrote:
My purpose of referring these references was to point out that reticular formation function is necessary for consciousness.

If you recall these comments, which began this direction in our discussion:

Maerd wrote:
However, not all cortical structures, in my view, are recent; and not all brainstem structures are primitive. For example, the reticular formation of the brainstem and the cortex probably started their evolution process at same period of time, as either destroying the reticular formation or severing cortex from the rest of brain will lead to a coma state.

As I have said, the references you provided does not appear to support your conclusion of mutual brainstem and cortex evolution. Clearly, reticular function is a foundation for cortical activation and the reticular’s contribution to thermoregulation suggests that cortical activation is not its only evolutionary function. This all appears to support the idea that the reticular evolved before and independent of cortical structure.

Maerd wrote:
Your first reference stated: "Normal rats and rats with 98.8% (S.D. ± 1.4) of neocortex surgically removed…” I only found an abstract of the article, I don't know if they have any example of total decortication in this study. Your second reference gave four cases of congenitally decorticate children…However, none of the cases…can be claimed as total decortication (absolutely devoid of cortical tissue).

Agreed. It may be that 1.2% of cortical structure in rodents and minor remnants of cortical tissue in children are all that is necessary to manifest the behaviors researchers have observed. However, there are better examples of normal or near normal behaviors in animals devoid of cortical structure, such as: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=630411&dopt=Citation From the extract:

“The thalamic preparation [all structures excised above the thalamus in rats] exhibited a wider range of intact neurological responses than the decerebrate. Cage climbing, resistance to gravity, suspension and muscle tone reactions, rhythmic vibrissae movements and examination of objects with snout and mandible were difficult to distinguish from controls.”

http://www.springerlink.com/content/j371x40818hm7t01/ From the summary:

“Bilateral removal of the cerebral cortex was made in cats neonatally. Spontaneous and imposed behaviour was studied while they were growing up and after they had become adult. Special emphasis was put on the utilization of visual cues and on learning. The cats ate, drank and groomed themselves adequately. Adequate maternal and female sexual behaviour was observed.”

Although the results obtained through animal research cannot be obtained ethically through human research, their implication in lower life forms at the very least suggest that much of the behaviors we associate with consciousness either exist or remain in brain structure in the absence or near absence of the cortex. Such results suggest how some aspects of consciousness may not have evolved with cortical structure.

Maerd wrote:
Also, consider this question: if cerebral cortical function is not necessary for conscious, why should consciousness not occur in all decorticated situation?

Perhaps the following excerpt from Shewmon’s article provides an answer: http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1469-8749.1999.tb00621.x?cookieSet=1
Shewmon wrote:
"If these children had been kept in institutions (as subject 2 was for the first 1.5 years) or treated at home as ‘vegetables’ (the prognosis being accepted uncritically by parents), there can be little doubt that they would have turned out exactly as predicted. What surely made all the difference was that their parents ignored the prognoses and advice, and instead followed their instinct to shower the children with loving stimulation and affection. Such children and their families have much to teach about not only the neurophysiology of consciousness."

Maerd quotes:
DrmDoc wrote: If you agree that prefrontal function plays “a very important role in working memory processing and manipulating,” and “dreaming indicates that working memory is working during sleep,” isn’t it possible that damage of the prefrontal and interference with its function could affect a sleeper’s ability to recall dreaming after waking from sleep?

Maerd response: Interference with working memory function does not necessarily affect short-term memory. Working memory and short-term memory are two distinct concepts.

From your perspective, I agree that the concepts of working memory and short-term memory seem different; however, that was not my question. My question, more succinctly, was whether interference with working memory in the prefrontal could affect the working memory associated with dreaming? If so, couldn’t this affect a sleeper’s recall of dreaming?

Maerd wrote:
In my view, dream recall is to use our working memory to retrieve whatever we have in our short-term memory store…The reason that we have to retrieve them immediately after arousal is because short-term memory has a very limited capacity, decays rapidly and will be replaced by new incoming information once we turn our attention to a new task…While awake, anything that processed by working memory will be saved into long-term memory, including dream recall…In my view, working memory is like the computer processors plus supporting RAM. Dreaming is a result of our brain (working memory) interpreting and processing (mainly) internally generated inputs. Long-term memory is the main source for these internally generated inputs.

As I now understand, your perspective of memory is based on a standard model consisting of working memory, short-term, and long-term. My perspective is non-standard consisting of just working and long-term memory. From your perspective, dreaming involves the retrieval of long-term memories into working memory and dream recall is an effort to retrieve the short-term memories resulting from the working memories associated with dreaming. In my view, dreaming is caused by the resonant mental effects of life experience that linger into sleep. Dream recall, in my view, is an effort to identify those resonant mental effects that persist after sleep. As I perceive, the mental effects that linger into sleep and persist after sleep are effects of working memories. In my view, dreaming is a mental effect of working memory and working memory a mental process effected by life experience. When we awake and try to remember our dreams, our effort to remember is an effort to reinforce the mental effects we experience in sleep with physical/material references. This effort, I believe, causes the memories of dreaming we keep long-term. In my view, long-term describes any memory experience that we do not immediately forget. I welcome your further thoughts.

To be continued...