Mind

[Luc Turpin]

13 minutes ago, iNow said:

How much is that?

 

This is remedially false. There are multiple lines of research showing the ways elderly folks losing memory compensate via other means and through use of mechanisms normally applied elsewhere. Emotion takes on a far greater role too, and reptilian portions of the brain regain much of the lost dominance they had shortly after birth.

 

Perhaps with YOUR current knowledge, but not with mine. Mine would say, details matter here. Incapacitated how, where, and when as obvious followup queries.

We would have to dig much deeper to get to the bottom of this. However, I, at least, and some others in the field find it particularly interesting that a man with such a deficiency is able to even function in the world.

i do not challenge that AD can adapt; i am only saying that in terminal lucidity where going from highly dysfunctional to almost fully functional in a matter of moments, appears to not involve adaptation.

i should have said with the prevailing theories of brain, functional specialization, theory of chemical transmission, neuronal connection, etc. 

1 minute ago, Luc Turpin said:

We would have to dig much deeper to get to the bottom of this. However, I, at least, and some others in the field find it particularly interesting that a man with such a deficiency is able to even function in the world.

i do not challenge that AD can adapt; i am only saying that in terminal lucidity where going from highly dysfunctional to almost fully functional in a matter of moments, appears to not involve adaptation.

i should have said with the prevailing theories of brain, functional specialization, theory of chemical transmission, neuronal connection, etc. 

I am having issues with my computer, who sent this reply without it being verified. Sorry!

[DrmDoc]

On 12/24/2023 at 8:37 AM, Luc Turpin said:

 

 

I admit to have read too much into the data. So much so that I forgot about the man having only a thin sheet of actual brain with a 75/100 IQ, a job, family and normal life, which concurs with your perspective that continued functionality is maintained in damaged brains. You also present hydrocephaly, leucotomy and other conditions as additional examples of maintained functionality.

 

Nonetheless, how does a man with a large part of his brain missing maintain almost full functionality and lucidity? Or how does an AD patient with significant brain atrophy, widespread damage, neuronal death and severed neuronal connections between various brain regions suddenly recover almost full functionality and lucidity? Other examples given raise similar issues. At play here is the role of brain size, specialized brain areas, neuronal count and neuronal connections on cognition. 
 

The brain may be trying to return to an homeostatic state through neuroplasticity in all of the stated examples, but it may be far from the full picture. Something else might also be at work. Findings like these call into question our conviction of knowing with quasi certainty how our brains work.

Happy holidays!

The crux of your inquiry here appears to question how a brain with severely degraded structure produces behaviors that suggest full functionality and lucidity.  The answer to that requires a cohesive and cogent understanding of brain function by way of its functional evolution.  My understanding of evolution informed me that the functionality of recent brain components is dependent on the function of earlier components and that the function of those early brain components was enhanced by those that emerged recently in brain development.

From my perspective of brain evolution, functionality developed along a clear contiguous path from components that appear to engage primitive functions to those that seem more evolved in their functionality.  To answer the question of functional plasticity in a severely degraded brain, let’s begin with the thalamus.

Most researchers regard the thalamus as a primitive brain structure relative to the neocortex. This suggests that the functionality of the neocortex likely developed after the functional development of the thalamus and that neocortical function is dependent on thalamic function for that reason—the neocortex can’t do what it does for our cognition without a fully functional thalamus as its base.

From my perspective of evolution, recent developments build upon and enhance the efficiency of earlier developments.  Evolution doesn’t necessarily discard primitive developments, but rather build upon and enhance those that are successful.  If that’s true, then our neocortex somehow builds upon and enhances the functionality of the thalamus—but how?

If we agree that the thalamus is our brain’s focal (hub) for sensory input (afference), integration, and output (efference) of our responses to sensory input, we should agree that neocortical function builds upon and enhances what our thalamus does for brain function—that’s if we accept the tenets of evolutional development as I’ve provided.

If our thalamus is a focal for processing (integration) afference and engaging efferently focused behaviors, what might the thalamus need to enhance that function? The answer is likely to be memory as it adds precision to our behaviors.  Next to comparing the relative nature and impact of our sensory experiences (integration), memory is perhaps most important because it allows us to mediate our behavioral responses according to our recall of past sensory experiences—Essentially, memory allows us to learn from our experiences.  This type of mediation would have been essential to the survival of ancestral animals because it would likely have allowed them to conserve their energetic responses to only that stimulus of survival significance.  Memory, among other things, allows us to mediate our behavioral responses to stimuli we’ve learned about and know not to be of significant impact on our experiences and that, at a minimum, is how neocortical function enhances thalamic function.

More precisely, neocortical function allows us to engage in precise behavioral responses relative to our current sensory experiences based on our prior experiences.  Our thalamus has adapted the neocortex as a kind of thinking cap or an extended workspace where the thalamus may attenuate its processing of sensory data.  Regarding plasticity with degraded neocortical structures, clearly a fully functional thalamus that has adapted to limited workspace doesn’t need as much neocortical structure to attenuate its processing as a healthy brain might require.  A functional thalamus in a healthy brain that has suffered severe degeneration requires time to adapt if it does at all within that compromised neural environment.  Resiliency and lucidity is likely dependent on our thalamus’ ability to adapt to its compromised neural environment.

[Luc Turpin]

On 12/25/2023 at 12:49 PM, DrmDoc said:

The crux of your inquiry here appears to question how a brain with severely degraded structure produces behaviors that suggest full functionality and lucidity.  The answer to that requires a cohesive and cogent understanding of brain function by way of its functional evolution.  My understanding of evolution informed me that the functionality of recent brain components is dependent on the function of earlier components and that the function of those early brain components was enhanced by those that emerged recently in brain development.

From my perspective of brain evolution, functionality developed along a clear contiguous path from components that appear to engage primitive functions to those that seem more evolved in their functionality.  To answer the question of functional plasticity in a severely degraded brain, let’s begin with the thalamus.

Most researchers regard the thalamus as a primitive brain structure relative to the neocortex. This suggests that the functionality of the neocortex likely developed after the functional development of the thalamus and that neocortical function is dependent on thalamic function for that reason—the neocortex can’t do what it does for our cognition without a fully functional thalamus as its base.

From my perspective of evolution, recent developments build upon and enhance the efficiency of earlier developments.  Evolution doesn’t necessarily discard primitive developments, but rather build upon and enhance those that are successful.  If that’s true, then our neocortex somehow builds upon and enhances the functionality of the thalamus—but how?

If we agree that the thalamus is our brain’s focal (hub) for sensory input (afference), integration, and output (efference) of our responses to sensory input, we should agree that neocortical function builds upon and enhances what our thalamus does for brain function—that’s if we accept the tenets of evolutional development as I’ve provided.

If our thalamus is a focal for processing (integration) afference and engaging efferently focused behaviors, what might the thalamus need to enhance that function? The answer is likely to be memory as it adds precision to our behaviors.  Next to comparing the relative nature and impact of our sensory experiences (integration), memory is perhaps most important because it allows us to mediate our behavioral responses according to our recall of past sensory experiences—Essentially, memory allows us to learn from our experiences.  This type of mediation would have been essential to the survival of ancestral animals because it would likely have allowed them to conserve their energetic responses to only that stimulus of survival significance.  Memory, among other things, allows us to mediate our behavioral responses to stimuli we’ve learned about and know not to be of significant impact on our experiences and that, at a minimum, is how neocortical function enhances thalamic function.

More precisely, neocortical function allows us to engage in precise behavioral responses relative to our current sensory experiences based on our prior experiences.  Our thalamus has adapted the neocortex as a kind of thinking cap or an extended workspace where the thalamus may attenuate its processing of sensory data.  Regarding plasticity with degraded neocortical structures, clearly a fully functional thalamus that has adapted to limited workspace doesn’t need as much neocortical structure to attenuate its processing as a healthy brain might require.  A functional thalamus in a healthy brain that has suffered severe degeneration requires time to adapt if it does at all within that compromised neural environment.  Resiliency and lucidity is likely dependent on our thalamus’ ability to adapt to its compromised neural environment.

I do not contest the validity of any of the affirmation in your referenced text. Written with clarity and conciseness. We also agree that “the crux of my inquiry appears to question how a brain with severely degraded structure produces behaviors that suggest full functionality and lucidity”. Upon reading and re-reading carefully your text, I remain unconvinced that a brain evolution-plasticity perspective and current understanding of brain function can explain terminal lucidity in Alzheimer’s patients for example. In the context of imminent death, at the highest point of AD degradation, barely maintaining life, being unresponsive prior to lucidity, with numerous brain areas affected and dysfunctional repair systems, the brain is able to almost suddenly mount a late-minute surge to near normal functionality lasting for a few hours or more then suddenly extinguish itself as quickly as it came into being and, all this, just in time for death. I investigated what happens to an AD brain. Most if not all brain regions are irreversibly affected at the end-stage of the disease: neocortex, limbic system, hippocampus, thalamus, hypothalamus, corpus callosum, cerebellum, even the brain stem. Other hallmarks of AD are severe brain shrinkage, plaques and tangles blocking communication, severed neuronal connections, cell death, fibrous astrocytes, axonal swelling and transport disruptions, dysregulation of homeostatic firing and synaptic plasticity, disruption in brain wave pattern, rampant inflammation, major metabolic changes, etc. I reiterate, within the context described above, including the effects of multiple impacts of end-stage AD on the brain, how can it (the brain) even be able to temporarily mount a very-very fast broad-span adaptation and almost full reboot of itself, do so with severely damaged hardware and software, and then go completely off-line before dying? You believe that current knowledge explains terminal lucidity and I do not. To me, something is amiss. However, that we have divergent views on this matter is a suitable “état de fait”. Finally, I will be taking a respite from posting as I have other duties to attend.

[Luc Turpin]

13 hours ago, Luc Turpin said:

”. Finally, I will be taking a respite from posting as I have other duties to attend.

Correction: taking a respite from long posting only.

[DrmDoc]

On 12/27/2023 at 6:49 PM, Luc Turpin said:

I do not contest the validity of any of the affirmation in your referenced text. Written with clarity and conciseness. We also agree that “the crux of my inquiry appears to question how a brain with severely degraded structure produces behaviors that suggest full functionality and lucidity”. Upon reading and re-reading carefully your text, I remain unconvinced that a brain evolution-plasticity perspective and current understanding of brain function can explain terminal lucidity in Alzheimer’s patients for example. In the context of imminent death, at the highest point of AD degradation, barely maintaining life, being unresponsive prior to lucidity, with numerous brain areas affected and dysfunctional repair systems, the brain is able to almost suddenly mount a late-minute surge to near normal functionality lasting for a few hours or more then suddenly extinguish itself as quickly as it came into being and, all this, just in time for death. I investigated what happens to an AD brain. Most if not all brain regions are irreversibly affected at the end-stage of the disease: neocortex, limbic system, hippocampus, thalamus, hypothalamus, corpus callosum, cerebellum, even the brain stem. Other hallmarks of AD are severe brain shrinkage, plaques and tangles blocking communication, severed neuronal connections, cell death, fibrous astrocytes, axonal swelling and transport disruptions, dysregulation of homeostatic firing and synaptic plasticity, disruption in brain wave pattern, rampant inflammation, major metabolic changes, etc. I reiterate, within the context described above, including the effects of multiple impacts of end-stage AD on the brain, how can it (the brain) even be able to temporarily mount a very-very fast broad-span adaptation and almost full reboot of itself, do so with severely damaged hardware and software, and then go completely off-line before dying? You believe that current knowledge explains terminal lucidity and I do not. To me, something is amiss. However, that we have divergent views on this matter is a suitable “état de fait”. Finally, I will be taking a respite from posting as I have other duties to attend.

I may have been a bit wordy in explaining my position.  To simplify, lucid behavioral expression is largely dependent on the connection and exchanges between the neocortex and the thalamus.  Between these two components the thalamus is more vital to our survival and brain function than the neocortex.  The thalamus importance is suggested by how little cortical structure is required for behavioral expression and how nothing happens in the brain without thalamic function.  Lucidity can occur with a severely degrade cortex because it is not as essential to that state as the thalamus' ability to rewire and adapt its function to limited cortical function.

Behavioral efference (output) is coordinated through thalamic function; therefore, lucid behaviors are an output of thalamic function.  To attenuate, refine, and focus its behavioral output, the thalamus relies on a healthy cortex throughout the life of a healthy individual.  When there's degradation in the brain, this doesn't necessarily infer degradation of thalamic function. When we see moments of lucidity in AD patients this suggests that their thalamus has adapted new cortical connection to express that lucidity.  Those connections may become tenuous as the AD cortex continues to degrade.  Sporadic periods of lucidity suggest the tenuous nature of the neural connectivity between the cortex and thalamus in a deteriorating neural environment--like a damaged wire connecting a lamp to its power source.    

[Luc Turpin]

On 12/28/2023 at 8:54 PM, DrmDoc said:

To simplify, lucid behavioral expression is largely dependent on the connection and exchanges between the neocortex and the thalamus. 

AD dysregulates the connection and exchanges between the neocortex and the thalamus

"We present here several lines of evidence that suggest that dysregulation of the corticothalamic network may be a common denominator that contributes to the diverse cognitive and behavioral alterations in AD."

" However, alterations in the corticothalamic network are most likely responsible for a number of other deficits that accompany AD such as sleep fragmentation, attention deficits, cognitive processing deficits, and non-convulsive seizures. Notably, many of these other symptoms become evident even prior to memory deficits."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5854522/

On 12/28/2023 at 8:54 PM, DrmDoc said:

 Lucidity can occur with a severely degrade cortex because it is not as essential to that state as the thalamus' ability to rewire and adapt its function to limited cortical function.

 

AD degrades the thalamus’ ability to rewire and adapt its function to limited cortical function

"Impaired functional connextivity of the thalamus in Alzheimer's disease and mild cognitive impairement: a resting-state fMRI study"

https://pubmed.ncbi.nlm.nih.gov/23905993/

Our DTI analyses indicate that the integrity of thalamic connectivity is progressively disrupted following cognitive decline in AD and that DTI parameters in the column and body of the fornix show promise as potential markers for the early diagnosis of AD and for monitoring disease progression.

https://pubmed.ncbi.nlm.nih.gov/26141074/

On 12/28/2023 at 8:54 PM, DrmDoc said:

 When there's degradation in the brain, this doesn't necessarily infer degradation of thalamic function. 

AD and dementia degrades thalamic function

"Thalamus pathology is an important contributor to cognitive and functional decline, and it might be argued that the thalamus has been somewhat overlooked as an important player in dementia. In this review, we provide a comprehensive overview of thalamus anatomy and function, with an emphasis on human cognition and behavior, and discuss emerging insights on the role of thalamus pathology in dementia."

When the central integrator disintegrates: A review of the role of the thalamus in cognition and dementia - Biesbroek - Alzheimer's & Dementia - Wiley Online Library

"Increasing evidence points to the thalamus as an important hub in the clinical symptomatology of the disease, with the ‘limbic thalamus’ been described as especially vulnerable."

"The results showed widespread thalamic nuclei atrophy in EOAD and LOAD compared to their respective healthy control groups, with EOAD showing additional atrophy in the centromedian and ventral lateral posterior nuclei compared to YHC."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10313877/

 

On 12/28/2023 at 8:54 PM, DrmDoc said:

When we see moments of lucidity in AD patients this suggests that their thalamus has adapted new cortical connection to express that lucidity.   

I have not found any evidence corroborating this suggestion. It may be a valid hypothesis, but remains unsubstantiated.

On 12/28/2023 at 8:54 PM, DrmDoc said:

Those connections may become tenuous as the AD cortex continues to degrade.  Sporadic periods of lucidity suggest the tenuous nature of the neural connectivity between the cortex and thalamus in a deteriorating neural environment--like a damaged wire connecting a lamp to its power source.    

I have not found either any evidence on these statements either. 

On 12/28/2023 at 8:54 PM, DrmDoc said:

I may have been a bit wordy in explaining my position.  To simplify, lucid behavioral expression is largely dependent on the connection and exchanges between the neocortex and the thalamus.  Between these two components the thalamus is more vital to our survival and brain function than the neocortex.  The thalamus importance is suggested by how little cortical structure is required for behavioral expression and how nothing happens in the brain without thalamic function.  Lucidity can occur with a severely degrade cortex because it is not as essential to that state as the thalamus' ability to rewire and adapt its function to limited cortical function.

Behavioral efference (output) is coordinated through thalamic function; therefore, lucid behaviors are an output of thalamic function.  To attenuate, refine, and focus its behavioral output, the thalamus relies on a healthy cortex throughout the life of a healthy individual.  When there's degradation in the brain, this doesn't necessarily infer degradation of thalamic function. When we see moments of lucidity in AD patients this suggests that their thalamus has adapted new cortical connection to express that lucidity.  Those connections may become tenuous as the AD cortex continues to degrade.  Sporadic periods of lucidity suggest the tenuous nature of the neural connectivity between the cortex and thalamus in a deteriorating neural environment--like a damaged wire connecting a lamp to its power source.    

The following link summarizes many of the diverse effects of alzheimer on the thalamus, its function and connectivity to other brain areas.

Here is one excerpt of The effect of alzheimer's disease of the thalamus

"The thalamus is one of the earliest brain regions to be affected by amyloid deposition in AD (Ryan et al., 2013). Our review shows that AD impacts both the thalamus itself (e.g., decrease in volume and cell loss), as well as thalamus’s connections to other brain regions, including hippocampus, Papez circuit, the retrosplenial cortex, and other cortical areas."

https://www.researchgate.net/profile/Rasu-Karki/publication/354341403_The_effect_of_Alzheimer's_disease_on_the_thalamus/links/6419001b92cfd54f84186534/The-effect-of-Alzheimers-disease-on-the-thalamus.pdf

I reiterate, within a severe disease context, how can the brain even be able to temporarily mount a very fast broad-span adaptation and almost full reboot of itself, do so with severely damaged hardware and software, and then go completely off-line before dying? You believe that current knowledge explains terminal lucidity and I do not. To me, something is amiss.

Respectfully! 

[DrmDoc]

2 hours ago, Luc Turpin said:

AD dysregulates the connection and exchanges between the neocortex and the thalamus

"We present here several lines of evidence that suggest that dysregulation of the corticothalamic network may be a common denominator that contributes to the diverse cognitive and behavioral alterations in AD."

" However, alterations in the corticothalamic network are most likely responsible for a number of other deficits that accompany AD such as sleep fragmentation, attention deficits, cognitive processing deficits, and non-convulsive seizures. Notably, many of these other symptoms become evident even prior to memory deficits."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5854522/

AD degrades the thalamus’ ability to rewire and adapt its function to limited cortical function

"Impaired functional connextivity of the thalamus in Alzheimer's disease and mild cognitive impairement: a resting-state fMRI study"

https://pubmed.ncbi.nlm.nih.gov/23905993/

Our DTI analyses indicate that the integrity of thalamic connectivity is progressively disrupted following cognitive decline in AD and that DTI parameters in the column and body of the fornix show promise as potential markers for the early diagnosis of AD and for monitoring disease progression.

https://pubmed.ncbi.nlm.nih.gov/26141074/

AD and dementia degrades thalamic function

"Thalamus pathology is an important contributor to cognitive and functional decline, and it might be argued that the thalamus has been somewhat overlooked as an important player in dementia. In this review, we provide a comprehensive overview of thalamus anatomy and function, with an emphasis on human cognition and behavior, and discuss emerging insights on the role of thalamus pathology in dementia."

When the central integrator disintegrates: A review of the role of the thalamus in cognition and dementia - Biesbroek - Alzheimer's & Dementia - Wiley Online Library

"Increasing evidence points to the thalamus as an important hub in the clinical symptomatology of the disease, with the ‘limbic thalamus’ been described as especially vulnerable."

"The results showed widespread thalamic nuclei atrophy in EOAD and LOAD compared to their respective healthy control groups, with EOAD showing additional atrophy in the centromedian and ventral lateral posterior nuclei compared to YHC."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10313877/

 

I have not found any evidence corroborating this suggestion. It may be a valid hypothesis, but remains unsubstantiated.

I have not found either any evidence on these statements either. 

The following link summarizes many of the diverse effects of alzheimer on the thalamus, its function and connectivity to other brain areas.

Here is one excerpt of The effect of alzheimer's disease of the thalamus

"The thalamus is one of the earliest brain regions to be affected by amyloid deposition in AD (Ryan et al., 2013). Our review shows that AD impacts both the thalamus itself (e.g., decrease in volume and cell loss), as well as thalamus’s connections to other brain regions, including hippocampus, Papez circuit, the retrosplenial cortex, and other cortical areas."

https://www.researchgate.net/profile/Rasu-Karki/publication/354341403_The_effect_of_Alzheimer's_disease_on_the_thalamus/links/6419001b92cfd54f84186534/The-effect-of-Alzheimers-disease-on-the-thalamus.pdf

I reiterate, within a severe disease context, how can the brain even be able to temporarily mount a very fast broad-span adaptation and almost full reboot of itself, do so with severely damaged hardware and software, and then go completely off-line before dying? You believe that current knowledge explains terminal lucidity and I do not. To me, something is amiss.

Respectfully! 

Citations aside for the moment, consider the objective evidence which is that no expression of lucidity exists without some connection between the cortex and thalamus. Consider the distinction between a mildly impaired and severely impaired thalamus in that mild impairment is likely not sufficient to obstruct periods of lucidity.  None of the citations you've provided suggested impairments that would prevent occassional expression of lucid behaviors with sufficient function and connectivity with the brain--succinctly, there's no behavioral expressions without sufficient brain function and connectivity.

Although AD progression can severely damage the connectivity between the thalamus and cortex, periods of lucidity can persist with sufficient function and connection between the thalamus and cortex. This sufficient function and connection is proved by your observance of lucidity expression within a severely compromised AD neural environment.  The observance that lucidity can persist with a severely damaged brain isn't evidence of anything particularly miraculous, it is merely a testament to the plasticity of our central nervous system amid periods of severe distress.

[Luc Turpin]

1 hour ago, DrmDoc said:

Citations aside for the moment, consider the objective evidence which is that no expression of lucidity exists without some connection between the cortex and thalamus. Consider the distinction between a mildly impaired and severely impaired thalamus in that mild impairment is likely not sufficient to obstruct periods of lucidity.  None of the citations you've provided suggested impairments that would prevent occassional expression of lucid behaviors with sufficient function and connectivity with the brain--succinctly, there's no behavioral expressions without sufficient brain function and connectivity.

Although AD progression can severely damage the connectivity between the thalamus and cortex, periods of lucidity can persist with sufficient function and connection between the thalamus and cortex. This sufficient function and connection is proved by your observance of lucidity expression within a severely compromised AD neural environment.  The observance that lucidity can persist with a severely damaged brain isn't evidence of anything particularly miraculous, it is merely a testament to the plasticity of our central nervous system amid periods of severe distress.

I think that your last post speaks to the crux of the matter. I agree that there should not be any behavioral expressions without sufficient brain function and connectivity. But the data may be (not definitive, but may be) telling us that at a critical junction (between life and death), something else or something more is at play. Let's make the following postulates for end-stage AD: cortico-thalamic link sufficiently maintained; thalamus sufficiently functional; brain still benefiting from plasticity and still seeking homeostasis. Why then do we not see progressively diminishing periods of behavioral expressions followed by progressively increasing periods of non-behavioral expression? Not linear, but average regression! What we usually see in late-stage AD is a long period (months, year) of almost complete non-behavioral expression (typical of significant brain degradation) followed by a brief (hours, day), robust (near full functional) and very-late (close to death (hours, days)) spontaneous burst of behavioral expression. Near death appears to be, but not always, a determining factor here. I am sure that you can find counter points to my points. But isn’t it strange that these things called terminal (hours) or paradoxical (days) lucidity happen mostly near death, when the body is maximally degraded by AD! Also, I am not looking for a miracle to explain what is going on, but a mechanism.  Maybe electro-magnetic wave bursts; very speculative. Maybe sheer willingness to survive; also, very speculative. Finaly, I do not think that we can settle this matter as we would need data that is currently unavailable to do so.

[DrmDoc]

2 hours ago, Luc Turpin said:

I think that your last post speaks to the crux of the matter. I agree that there should not be any behavioral expressions without sufficient brain function and connectivity. But the data may be (not definitive, but may be) telling us that at a critical junction (between life and death), something else or something more is at play. Let's make the following postulates for end-stage AD: cortico-thalamic link sufficiently maintained; thalamus sufficiently functional; brain still benefiting from plasticity and still seeking homeostasis. Why then do we not see progressively diminishing periods of behavioral expressions followed by progressively increasing periods of non-behavioral expression? Not linear, but average regression! What we usually see in late-stage AD is a long period (months, year) of almost complete non-behavioral expression (typical of significant brain degradation) followed by a brief (hours, day), robust (near full functional) and very-late (close to death (hours, days)) spontaneous burst of behavioral expression. Near death appears to be, but not always, a determining factor here. I am sure that you can find counter points to my points. But isn’t it strange that these things called terminal (hours) or paradoxical (days) lucidity happen mostly near death, when the body is maximally degraded by AD! Also, I am not looking for a miracle to explain what is going on, but a mechanism.  Maybe electro-magnetic wave bursts; very speculative. Maybe sheer willingness to survive; also, very speculative. Finaly, I do not think that we can settle this matter as we would need data that is currently unavailable to do so.

A burst of energetic behavioral expressions near death after a pregressively degenerative brain condition isn't miraculous especially if the neural apparatus for such expression remains sufficiently functional--which it must be for such expressions to occur.  What's left is for us to investigate what neural apparatus remains in place that has allowed for near normal behavior expression amid a severely degradated brain state. 

The observation that these burst of enegetic expressions occurs near death suggest a power-up in a system where the power supplied by limited resources have been redirected from less functional pathways to those that remain sufficiently functional to produce those expressions.  Again, this isn't particularly miraculous given what we aready understand about the nature of plasticity in brain function. 

Edited December 31, 2023 by DrmDoc
grammar

[Luc Turpin]

14 hours ago, DrmDoc said:

A burst of energetic behavioral expressions near death after a pregressively degenerative brain condition isn't miraculous especially if the neural apparatus for such expression remains sufficiently functional--which it must be for such expressions to occur.  

  Again, this isn't particularly miraculous given what we aready understand about the nature of plasticity in brain function. 

I am not looking for a miracle, but a more satisfactory understanding of terminal lucidity and possible ramifications in the on-going debate on mind-brain connection.

[DrmDoc]

2 minutes ago, Luc Turpin said:

I am not looking for a miracle, but a more satisfactory understanding of terminal lucidity and possible ramifications in the on-going debate on mind-brain connection.

Yes, but it appears only extraordinary findings will satisfy your quest for understanding rather than findings that are clearly ordinary. The ordinary answer to your inquiry resides in the resiliency of our physiology, which itself is truly extraordinary--imho.

[Luc Turpin]

1 hour ago, DrmDoc said:

Yes, but it appears only extraordinary findings will satisfy your quest for understanding rather than findings that are clearly ordinary. The ordinary answer to your inquiry resides in the resiliency of our physiology, which itself is truly extraordinary--imho.

We both agree to disagree on terminal lucidity and both agree on the extraordinary nature of our physiology.