The brain is not dead when the cortex is dead.

[Max_B]

Thought this was a topical letter from 2014, considering the recent discussions on here between myself and Tim, which might be of interest...? I stumbled across it when I was researching something else.

I've also quoted from paper [3]... which shows stark differences in how thalamus neurons respond to oxygen and glucose deprivation, in comparison to deeper brain neurons within the hypothalamus.

[3] Ischemic vulnerability of the brain decreases rostrocaudally

Magnetic Resonance imaging of patients who survive global ischemia but remain in a persistent vegetative state (PVS), show relatively normal brainstem function but dysfunctional higher brain activity [5] [6] [30] [7], a finding supported by numerous studies measuring regional metabolism [8]. There is also evidence from animal studies that anoxic depolorisation (AD) which is acutely damaging in higher brain [31] is comparatively weak in brainstem. Specifically, AD arising from respiratory arrest in intact rat brain measured using K + -sensitive electrodes [17] showed that the profile of elevated [K + ] o (representing AD strength) is delayed, is slower to rise, and peaks at lower levels in hypothalamus and brainstem compared to cortex and striatum. As well, global ischemia in dogs for 20 minutes [11] evoked a gradient of neuronal injury assessed 7 days later as follows: neocortex, hippocampus, cerebellum > basal ganglia> thalamus > brainstem. In fact, they detected no injury in midbrain, pons or medulla despite all regions being deprived of blood over the same period. The adult hypothalamus and brainstem do not naturally undergo spreading depression [12] so it is not surprising that they are also less supportive of AD.

Neurons in higher brain undergo strong AD (see Introduction) while hypothalamic and brainstem neurons show weak or no AD [15] [16][32]. This also holds for the less metabolically stressed version of AD, spreading depression (ibid) and in slices is obviously independent of regional variation in blood flow. Specifically, using whole-cell patch and 2-photon microscopy, we have previously reported a clear difference in neuronal responses to Oxygen/glucose deprivation between susceptible neocortical pyramidal neurons and more resilient Magnocellular Neuroendocrine Cells in the hypothalamic supraoptic nucleus [15]. Here we examined if and where a demarcation in susceptibility to anoxic depolorisation and spreading depression generation can be identified. We show that the transition from vulnerable to more resilient is at the thalamus-hypothalamus interface. Following 10 minutes of Oxygen/glucose deprivation in rodent slices, the thalamus is essentially dead. No new thalamic neurons can be obtained post-Oxygen/glucose deprivation, even following up to 1 hour recovery in control artificial cerebral spinal fluid. Thalamic neurons, like those of neocortex [33], CA1 hippocampus [34] [35] [36] and striatum [2] undergo strong and irreversible AD that kills the neurons in brain slices.

In contrast, tens of microns away in hypothalamus we recorded three neuronal types in the paraventricular nucleus (PVN) and suprachiasmatic nucleus (SCN) showing comparative resilience to 10 or 15 minutes of Oxygen/glucose deprivation. These neurons recover their membrane potential, input resistance and action potential amplitude. Moreover, newly acquired neurons are readily obtained in the hypothalamus following Oxygen/glucose deprivation, a feat not possible in adjacent thalamus, even following up to an hour of recovery in control artificial cerebral spinal fluid. Their resting membrane potential, input resistance and action potential amplitude are similar to their neuron counterparts not previously exposed to Oxygen/glucose deprivation, further indicating good recovery from Oxygen/glucose deprivation. This resilience is similar to that reported in a fourth hypothalamic region, the supraoptic nucleus [15]. That study sampled only one type of `higher` (neocortical) neuron and one type of `lower` hypothalamic Magnocellular Neuroendocrine neuron but there was no way to generalize that hypothalamic neurons resist ischemic resistance. By sampling 3 additional hypothalamic neuronal types and comparing them to nearby thalamic neurons, this study can make that conclusion.​

 

[tim]

That's so easy to deal with, Max

I've never said that absence of a functioning cortex means that a patient can't be brought back. I'm not qualified to make statements like this doctor above... but it doesn't matter what is wrong with the cortex, if the brain stem is down. Without a brain stem (cardiac arrest) everything stops after 10-20 seconds. You don't seem to get this but it is a fact.

Tomorrow I'll stick up some information from the doctor that first utilised EEG, Dr Ernst Rodin (who is not a proponent). He told me that it is the most reliable method of indicating whether or not brain death has occurred in patients that are in coma after severe brain damage for whatever reason.

 

[Max_B]

That's so easy to deal with, Max

I've never said that absence of a functioning cortex means that a patient can't be brought back. I'm not qualified to make statements like this doctor above... but it doesn't matter what is wrong with the cortex, if the brain stem is down. Without a brain stem (cardiac arrest) everything stops after 10-20 seconds. You don't seem to get this but it is a fact.

Tomorrow I'll stick up some information from the doctor that first utilised EEG, Dr Ernst Rodin (who is not a proponent). He told me that it is the most reliable method of indicating whether or not brain death has occurred in patients that are in coma after severe brain damage for whatever reason.

Did you even read what I wrote?

The letter's authors are very clear that they believe isoelectric measurements from scalp EEG are insufficient to say when all brain function has ceased following complete circulatory arrest. They say isoelectric scalp EEG measurements are insufficient for up to 5 minutes after complete circulatory arrest, because deeper neurons (that cannot be measured using scalp EEG) have been shown to remain functional for up to 5 minutes after complete circulatory arrest (from this paper).

This paper demonstrates clearly and unambiguously that deeper brain neurons (the brainstem being the deepest structure) may continue to function for some 5 minutes after complete Oxygen and Glucose deprivation, in comparison to higher neurons which die (and cannot recover), and this study is really really detailed, using patch clamp techniques on individual neurons themselves.

You understand that EEG is so crude, it can only measure slower synchronized post synaptic cellular currents (not the actual 'fast' firing) from hundreds of thousands of neurons.

 

[tim]

The letter's authors are very clear that they believe isoelectric measurements from scalp EEG are insufficient to say when all brain function has ceased following complete circulatory arrest.

Are you pulling my leg ? I know you are wedded to this ludicrous theory of yours but I really thought you were kind of smart.
I already said that a flat EEG doesn't rule out a return to consciousness. However, when the brainstem is not functioning, there is nothing going on in the brain that could have any relevance to what you are trying to sell us ! No brain stem functioning = zilch.

 

[Baccarat]

lol

 

[Max_B]

I already said that a flat EEG doesn't rule out a return to consciousness.

Yes indeed, all you now need to accept is that an isoelectric scalp EEG within seconds of cardiac arrest, does not mean that there is no neuronal activity deeper within the brain for as long as 5 minutes - as the paper clearly demonstrates is possible within the hypothalamus. I mean, there is nobody who doesn't get that but you it seems?

 

[tim]

Yes indeed, all you now need to accept is that an isoelectric scalp EEG within seconds of cardiac arrest, does not mean that there is no neuronal activity deeper within the brain for as long as 5 minutes - as the paper clearly demonstrates is possible within the hypothalamus. I mean, there is nobody who doesn't get that but you it seems?

Max, I've just tried to explain to you the facts about how the brain works. As I've told you before, if you, Max, want to re-write the textbooks (of how the brain works) then please go and address the Royal College of Surgeons. As I've said above, I will address your points in detail as soon as I can tomorrow (today)

 

[malf]

Max, I've just tried to explain to you the facts about how the brain works. As I've told you before, if you, Max, want to re-write the textbooks (of how the brain works) then please go and address the Royal College of Surgeons. As I've said above, I will address your points in detail as soon as I can tomorrow (today)

Hmmm. The 'textbooks' are re-written all the time by new studies, that is a weak argument. There's nothing very controversial here.

Now, I'm not sure whether 'an experience' is occurring after 2-3 minutes post cardiac arrest but that point appears moot anyhow as the experience could have formed in the 1st 10-20s, or after the heart was restarted.

 

[tim]

Yes indeed, all you now need to accept is that an isoelectric scalp EEG within seconds of cardiac arrest, does not mean that there is no neuronal activity deeper within the brain for as long as 5 minutes - as the paper clearly demonstrates is possible within the hypothalamus.

I'm getting bored with your neuron fetish, Max. Are you so desperate to keep your theory alive that you are willing to make up your own neuroscience ?

You've presented one poorly written letter and an ambiguous set of charts on one (of 4) patients ? (No, one of 4 rats !!!! ) showing some kind of activity from a part of the (rat) brain that is responsible for processing nerve impulses etc. I'm supposed to take this seriously ? Are you trying to postulate that this tiny effect is responsible for hyper lucid veridical OBE's ?

ONE ambiguous experiment on a rat brain ? :) And we have to abandon everything that we know about how the brain works ? It might be enough to convince Malf, Max but that's about it's limit.


This is what happens to brain cells during fainting which is nowhere near as damaging as cardiac arrest


http://neuropathology-web.org/chapter2/chapter2aHIE.html

With this background, let us examine what happens with different grades of HIE. Suppose that someone has a brief episode of global ischemia, say from fainting. Within seconds, energy failure causes electrical activity in neurons to cease and the patient loses consciousness. Neurons and glial cells are viable and, if circulation is promptly restored, the patient returns to normal. If, however, ischemia lasts longer, first the integrity of cell membranes will be compromised and then cellular metabolism will cease and neurons will die. Ischemia lasting 4-5 minutes can damage irreversibly hippocampal and neocortical pyramidal cells, striatal neurons, and Purkinje cells. More protracted ischemia can damage thalamic and brainstem neurons.

Dr Ernst Rodin on the effectiveness of EEG monitoring (He pioneered it's use)

The electroencephalogram is the single most reliable laboratory test for assessment of the physiological capabilities of the brain. In as much as this is my professional specialty and it is routine practice to obtain EEGs when a patient has seizures, or is comatose. CT scans provide evidence for structural changes, but tell us nothing about residual function. The EEG on the other hand provides objective facts on current brain activity down to the millisecond range.


Apparently Dr Rodin died last month which I did not know.

Floating off onto the next adventure, Dr. Ernst Rodin, MD, b. Vienna, Austria Aug. 30, 1925 passed away suddenly on Feb. 5th at home. Dr. Rodin was the former President of the American Clinical Neurophysiology Society and had received the association’s Jasper Lifetime Achievement Award in 2015 for his extensive contributions to the field. He was Adjunct Emeritus in the Department of Neurology at the University of Utah and had earlier been a faculty member at the University of Michigan and Wayne State University. Following his residency at Mayo Clinic in Neurology and Electroencephalography he became the long-standing director of the Epilepsy Program at Lafayette Clinic in Detroit, in addition to holding hospital appointments at Children's Hospital and Harper Hospital. He became internationally known for his work in epilepsy and published extensively in the field. He was actively publishing and submitting new research papers until his passing.

 

[tim]

Hmmm. The 'textbooks' are re-written all the time by new studies, that is a weak argument. There's nothing very controversial here.

Now, I'm not sure whether 'an experience' is occurring after 2-3 minutes post cardiac arrest but that point appears moot anyhow as the experience could have formed in the 1st 10-20s, or after the heart was restarted.

There is no point in responding to you, Malf other than to say this. You're a good comedian and I don't dislike you but posts like this above demonstrate that for some reason (best known to yourself) you prefer to be "stuck on stupid."

 

[Max_B]

Ischemia lasting 4-5 minutes can damage irreversibly hippocampal and neocortical pyramidal cells, striatal neurons, and Purkinje cells. More protracted ischemia can damage thalamic and brainstem neurons.

Yes, that is in agreement with this paper.

 

[tim]

Yes, that is in agreement with this paper.

One neuron is not conscious. Neither are two neurons or twenty two thousand and two. So why should billions of neurons be conscious ?There is no experiment that has ever been conducted that has demonstrated how consciousness, our sense of self, arises out of the passing of a bit of electricity and some chemicals between neurons, which are not much different from other cells in the body.

 

[Max_B]

One neuron is not conscious. Neither are two neurons or twenty two thousand and two. So why should billions of neurons be conscious ?There is no experiment that has ever been conducted that has demonstrated how consciousness, our sense of self, arises out of the passing of a bit of electricity and some chemicals between neurons, which are not much different from other cells in the body.

I dunno what your comment has to do with the paper, which shows neuronal activity is possible within deeper brain structures (in comparison to the cortex) for as long as 5 minutes after complete Oxygen/glucose deprivation.

Hence an isoelectric scalp EEG within seconds of cardiac arrest, does not mean that there is no neuronal activity deeper within the brain for as long as 5 minutes - as the paper clearly demonstrates is possible within the hypothalamus.

 

[tim]

as the paper clearly demonstrates is possible within the hypothalamus.

That paper is worthless as regards NDE research. One tiny effect in one rat is not sufficient to overturn all the stacks of previous research in other animals (sadly) which shows that after cardiac arrest, (10-15 seconds) global electrical activity is lost. It doesn't matter if there are some neurons wobbling about a bit in the thalamus, hypothalamus ....that's not going to produce a birds eye, crystal clear real time vision of the operating room, that's not going to allow you to see what your mother and father are doing in the hospital canteen.

And it certainly is not going to be capable of receiving some kind of ultra real "transmission" from other people's brains and storing it.

 

[Max_B]

That paper is worthless... ...after cardiac arrest, (10-15 seconds) global electrical activity is lost.

The paper is a nice piece of evidence that shows why you're wrong about there being a *global* loss of electrical activity with 10-15 seconds of cardiac arrest. Neurons within deeper structures may continue functioning for up to 5 minutes following total oxygen and glucose deprivation, unlike neurons in higher structures like the cortex (where activity is commonly measured with scalp EEG).

 

[tim]

The paper is a nice piece of evidence that shows why you're wrong about there being a *global* loss of electrical activity with 10-15 seconds of cardiac arrest.

And I've just pointed out to you, Max that one tiny effect in a rodent doesn't constitute evidence. It may not even be electrical activity anyway, could be calcium surge/build up or something else. There is no way of correlating such miniscule activity (especially as it's a rat) with anything to do with consciousness.

 

[Max_B]

And I've just pointed out to you, Max that one tiny effect in a rodent doesn't constitute evidence.

On the contrary, the paper is good evidence that neurons in deeper brain structures (that we can't measure with scalp EEG) can continue to function for longer, and have greater resilience to damage when totally deprived of oxygen and glucose, in comparison to higher structures that we do measure with EEG.

 

[tim]

On the contrary, the paper is good evidence that neurons in deeper brain structures (that we can't measure with scalp EEG) can continue to function for longer, and have greater resilience to damage when totally deprived of oxygen and glucose, in comparison to higher structures that we do measure with EEG.

As I pointed out, there is no way to correlate anything meaningful relating to consciousness from a tiny area in the brain of a rat. Unless you were a bit desperate, that is.

 

[Max_B]

As I pointed out, there is no way to correlate anything meaningful relating to consciousness from a tiny area in the brain of a rat. Unless you were a bit desperate, that is.

Well I don't know if that is true or not, but it has little to do with the paper... or why I posted it.

As scalp EEG can only measure activity in the cortex, and not the deeper brain structures. This paper seems important, as it demonstrates that neurons from these deeper structures can continue to function for longer than their cortex cousins, when completely deprived of oxygen and glucose. For upto 5 minutes.

 

[tim]

No, it doesn't demonstrate that conclusively, at all. You are simply interpreting one irrelevant anomaly in a rat brain, in support of your completely unsupported (by any evidence) theory.

You've been given until 2020 (you will know what I mean) to carry on selling us this nonsense, Max. Shame, what a waste of your time and abilities.