Hi, I Have A Complex, Unique Case Involving What I

Question: Hi,

I have a complex, unique case involving what I and other doctors. Including at least one Pharmacologist, believe may vert likely be a unique case of hepatic encephalopathy.

As is known about the condition, hepatic encephalopathy is not so much a liver disorder at the very root, but rather, is classified as a neuropsychiatric disorder, involving an imbalance between excessive GABAergic tone and deficient serotonergic tone, as the precipitating cause. I have made my case as to why I believe that this may be my disorder, which started after a pharmaceutical GABA drug poisoning.

If you are interested in examining the details more, i shall send attachments to yoy via the attachments email service. I am looking forward to hearing what you think!

Hi,

I have a complex, unique case involving what I and other doctors. Including at least one Pharmacologist, believe may vert likely be a unique case of hepatic encephalopathy.

As is known about the condition, hepatic encephalopathy is not so much a liver disorder at the very root, but rather, is classified as a neuropsychiatric disorder, involving an imbalance between excessive GABAergic tone and deficient serotonergic tone, as the precipitating cause. I have made my case as to why I believe that this may be my disorder, which started after a pharmaceutical GABA drug poisoning.

If you are interested in examining the details more, i shall send attachments to yoy via the attachments email service. I am looking forward to hearing what you think!

Hi, I have just sent seven documents to you via the attachments email service.

Please review carefully the details presented in the documents; they contain backstory, symptoms, and supporting evidence for my case as to why it is that I have been most highly likely suffering from what is, to at least me and a few others so far, extremely apparent case of Hepatic Encephalopathy. Also included is a favorable supporting opinion from one other doctor on this site, who is a pharmacologist.

At the conclusion of your review, please answer the following single question:

"Do you support Dr Vaishalee's conclusion for a diagnosis of Hepatic Encephalopathy to be made, based on all available evidence, information and context?"

Additionally, your profile says you have earned an MD in the XXXXXXX system, although you practice in Albania? Is this correct?

Thank you very much, Doctor!

Hi, I have just sent seven documents to you via the attachments email service.

Please review carefully the details presented in the documents; they contain backstory, symptoms, and supporting evidence for my case as to why it is that I have been most highly likely suffering from what is, to at least me and a few others so far, extremely apparent case of Hepatic Encephalopathy. Also included is a favorable supporting opinion from one other doctor on this site, who is a pharmacologist.

At the conclusion of your review, please answer the following single question:

"Do you support Dr Vaishalee's conclusion for a diagnosis of Hepatic Encephalopathy to be made, based on all available evidence, information and context?"

Additionally, your profile says you have earned an MD in the XXXXXXX system, although you practice in Albania? Is this correct?

Thank you very much, Doctor!

Doctor,

I have just re-sent the documents via the attachments email service. They ought to reach you successfully. Awaiting confirmation email from the attachments service to confirm that you have gotten the documents.

Unfortunately, the direct upload for pdfs never seems to work for me, as doctors are never able to view them properly when I upload these documents through here. This is why doctors have recommended for me to use the attachments email service.

Thank you for your time. Please read the documents 1 - 6 in order. Document number 7 is a symptoms list of what I have been dealing with as well.

Looking forward to your timely response and conclusion! P.S. I am very eager to provide a favorable opinion on my case from a specialist with a neurological background--such as yourself--to my gastrointestinal doctor when I see him this Monday. If you would be able to complete the review before the end of the weekend to provide your opinion, this would be greatly appreciated!

Thanks again

Doctor,

I have just re-sent the documents via the attachments email service. They ought to reach you successfully. Awaiting confirmation email from the attachments service to confirm that you have gotten the documents.

Unfortunately, the direct upload for pdfs never seems to work for me, as doctors are never able to view them properly when I upload these documents through here. This is why doctors have recommended for me to use the attachments email service.

Thank you for your time. Please read the documents 1 - 6 in order. Document number 7 is a symptoms list of what I have been dealing with as well.

Looking forward to your timely response and conclusion! P.S. I am very eager to provide a favorable opinion on my case from a specialist with a neurological background--such as yourself--to my gastrointestinal doctor when I see him this Monday. If you would be able to complete the review before the end of the weekend to provide your opinion, this would be greatly appreciated!

Thanks again

Hi Doctor,

I am sending the response to you via pdf, as it is a bit more lengthy. Thank you for your time. Looking forward to your reply.

Hi Doctor,

I am sending the response to you via pdf, as it is a bit more lengthy. Thank you for your time. Looking forward to your reply.

Hi Doc,

Three attachments just sent. Thank you

Hi Doc,

Three attachments just sent. Thank you

Attached. Thank you

Attached. Thank you

Dr Spaho,

Thank you for a quality answer. I deeply appreciate this.

The most critical thing stated by you, is this statement: "Another MUST for the HE diagnosis is compromised consciousness and the tools to weight this are neuropsychological and other tests and exclusion of other possible neurological affecting conditions."

This is an accurate assessment of the nature of diagnosing the condition today.

Diagnosis of the condition is not perfect. The reason that this "Gold standard" test--this "must"-have criteria--is criticized by some of the world's leading experts of hepatic encephalopathy, is because there are flaws and shortcomings with it. Nevertheless, the medical establishment, to date, has not offered a more comprehensive nor reliable method of diagnosis.

Here is the issue, as best as I can explain it: it comes down to the difference between GABA-A agonism versus GABA-B agonism.

Why does hepatic encephalopathy exist? Largely because we notice it by its obvious, outwardly-observable symptoms--chief among them being a reduced level of consciousness as a result of excessive GABA-A neurologic tone caused specifically by the excessive build-up of toxic compounds that bear selective affinity for GABA-A receptors (usually ammonia, endogenous benzos, etc).

The observable symptom--reduced consciousness--usually seen is accepted as a symptom of CNS imbalance (excitatory/inhibitory, manifesting as excessive GABA with lowered serotonergic tone)...

...and it is this nervous system imbalance that is the common cause of both the reduced state of consciousness (along with the other outwardly observable signs such as reduced respiratory rate) and the inhibition of metabolic function (which is not outwardly observable, but can be suggested or confirmed by other signs such as lack of ammonia metabolization, among many others).

The "encephalopathy" part of hepatic encephalopathy does not, then, simply refer to the fact that reduced consciousness is the apparent issue--it is an assessment of the overall underlying state of the central nervous system, as it is taken for granted that if reduced consciousness is there, so is reduced metabolism! (This is why comatose patients are given hemoperfusion to detox from poisoning, while people who are awake are automatically--but often incorrectly--presumed by doctors to be able to metabolize toxins themselves naturally.)

Important, however, is this realization: it does not mean that someone who is NOT experiencing reduced cognition or reduced consciousness have absolutely no CNS excitatory/inhibitory imbalance, and no resultant inhibition of metabolism.

. . .

Doctor, it therefore appears to me that I am dealing with the following problem. I shall describe an allegorical example to use as an analogy.

. . .

Imagine that you and I are running a police precinct, filled with investigators who are trained to investigate and uncover crimes committed within the community.

There are many different kinds of crimes that take place.

For us, we have been recently focusing on robberies of jewelry stores that, for some reason, are located in snowy mountains. The normal type of thief operates in the following manner: He walks up the snowy mountain at night, where he leaves footprints in the snow. When he enters, he triggers the alarm, thus causing an activation of the alarm system. He, nevertheless, enters the store and cracks the safe and display cases, taking all the jewelry and money. He then leaves.

The police team, over the many years, have seen remarkable consistency in these crimes. They nearly always are conditioned to see two factors always correlating with the crime, that show that it happened: footprints in the snow at night, and a triggered alarm system.

Over time, new police officers trained in schooling are taught only these "symptoms," and learn to believe--simplistically--that "footprints in snow and triggered alarm mean crime has taken place. No footprints and no alarm, means no crime."

After a while, apparently, one case is reported to the police. They show up to a scene where a crime has, in fact, taken place. Money and jewelry were stolen.

However, this new, uncommon type of criminal has entered the premises using different tactics.

Instead of leaving footprints in the snow, he decided to use skis to carefully glide in without leaving the usual traces. In addition, he has also carries a portable EMP device that, upon activation, electronically prevents the alarm from being activated by destroying the functionality of the circuits.

He then goes in and does the same crime.

The investigators under you return--and state to you that, "We saw no footprints, and no alarm was activated. So we cannot diagnose the situation as being a robbery." They refused to investigate any further.

The owners hear about this. Frustratingly, they begin their own campaign to uncover evidence. They obtain video surveillance footage from a neighboring property of someone skiing in at night and then skiing away with large, filled bags. They manually lifted fingerprints from their place using their own materials, and found that fingerprints were obtained that match a person with a known criminal record of robbery. Other critical evidence is found too.

The owners come back. "There has been a jewelry store robbery," they say. We have all the evidence that one needs to reasonably see that this is what has happened. But the junior officers under you tell these people "--No means no. We are trained that, for a diagnosis of jewelry store robbery to be given, there MUST be footprints, and there MUST be an activated alarm. No alarm and no footprints means we cannot diagnose with jewelry store robbery. This is the pattern we have been trained to recognize by the actions of the historical robbers, and we therefore cannot be flexible enough to consider anything else."

You are the XXXXXXX officer in command of these idiot officers. You see that their approach is not practical or realistic in actually recognizing addressing the problem correctly. It is obvious to you. What do you do? Do you obviously open the investigation and treat this as the crime that it really is?

. . .

In this story, the traditional robbers of longstanding crimes are like the typical GABA-A type of neural tone seen in "confirmed" cases of HE. The missing money and jewelry is the missing metabolic capacity of the human body--robbed and taken away by the GABA-A molecular compound criminals.

The footprints in the snow and triggered alarm are the "symptoms" of GABA-A's presence: reduced neural tone and neural cognition, which clinicians are trained to rely on in order to assume presence of the suspected dysfunction.

The new type of stealthy robber is the GABA-B form of overwhelm. Just like the new type of robber is also successful at conducting the crime and taking the jewelry and money, GABA-B is also successful at causing the neural tone of the body to shut down to a point that microsomal function and metabolic pathways are stopped. However, even though GABA-B-related robbers leaves some of the same hints and cues as GABA-A-related robbers (an empty safe, broken jewelry cases, fingerprints, and evidence on some surrounding video cameras--just like regular forms of HE often show bradypnea and also Manny others of the 20+ signs I have listed), the GABA-B-related robber is different in that it does not show the signs of FOOTPRINTS and ALARM SYSTEM ENGAGEMENT, simply because he does not, by his very nature, show these particular symptoms while on his way to essentially conduct the same one form of crime and effect that the other GABA-A-related robbers have in the past.

The symptoms of footprints in the snow and the triggered alarm system, are like the symptoms of reduced cognition and consciousness and reduced neuropsychiatric test results and cognitive battery assessment that we are trained to see.

The absence of these symptoms in the new type of robbery is like the absence of severe neurocognitive issues with GABA-B. Just like we cannot blame the existence of skiis, EMP devices, and physics for the sad lack of proper investigative attention onto the crime, we cannot blame the fact that GABA-B is known to be a non-sedating inhibitor of the CNS, for the fact that modern medicine pretty much ignorantly views that we cannot have GABA-based/CNS-based inhibition of the liver function without coma and cognitive problems.

You, as the chief investigator, see the problem. Your junior officers are stuck to the old belief that they are brainwashed in, but cannot evolve the mind in order to see that if the new guy uses a different approach, he is able to cause the same damage and crime without showing the same symptoms. They have falsely mixed together "footprints = jewelry crime," and they cannot disassociate the two elements in their mind.

Similarly, the smart doctor may see the problem. Medicine has falsely mixed together decreased neurocognitive performance and status with neurally-sourced hepatic disablement, even though these two are not always found together. Medicine has not created any awareness of the exception, as it has no concept of the fact that ***NOT ALL GABA-BASED INHIBITION THAT DOES CAUSE LIVER FAILURE, ALSO CAUSES REDUCED COGNITIVE STATUS***

...

I checked my EEG results from 2 years ago. It was reported as normal. I distinctly remember this test being taken at a time where my respiratory rate was about 5 - 6 breaths per minute, and other GABA-B drug symptoms were present. And yet, "no abnormalities." This simply means that this test, and the evaluation of consciousness, is a poor-quality test to check for hepatic encephalopathy (aka, for GABA-induced liver failure, which is what hepatic encephalopathy REALLY is).

The police, in the situation conveyed, would be well-advised to take the common sense approach and investigate fully. This is the same as with our situation, in which the medical doctor in this case should take the case seriously, despite the old, trained rigid criteria, and use "presumptive diagnosis" to come to the conclusion of there being the specific dysfunction we suspect.

Presumptive diagnosis is the art of seeing what is really there, without conforming to a rigid, pre-described criteria and "confirmatory" test result. If the nature of the illness or condition is unusual, the route of presumptive diagnoses is often recommended, because if the doctors stick to rigid systems of definition, the disease will never fit into any pre-defined set of criteria perfectly enough in order to trigger a full classification into the diagnosis.

In those kinds of situations, as a result, no diagnosis is given. This leaves the patient with the implied conclusion by doctors that she is fine--but they know she is not, and she knows she is not.

. . .

Questions:

(1) In such a case, have doctors done their job well, by taking a woman they know with common sense has a certain disease, but choose not to diagnose because the old books falsely train them to worship specific symptoms and come to premature conclusions and restrict their ability in the absence of those symptoms?

(2) For yourself personally, would you SUPPORT the use of presumptive diagnosis for HE, LF, or related disorder, based on the evidence we see so far in my case?

And,

(3) I am seeing multiple doctors, including hematologists and neurologists next week. *HOW* can I most effectively get these doctors to understand that GABA-based inhibitory imbalance is taking place and is the root cause of hepatic disablement for the last three years (as shown by lack of drug breakdown, etc), despite the fact that I am not showing the signs of the GABA-A-based neuropsychiatric deficits?

. . .

I know what I am talking about. GABA-based inhibitory neural tone affecting liver workmate IS the practical definition of what I have, which is what HE is; yet these med school guys refuse to let go of their one almighty criteria of observable cognitive reduction, even though I am making the correct point and case that it is an ineffective and inappropriate expectation for GABA-B based syndromes and toxicities, as GABA-B potentiation can shut off the liver just as effectively as it can lower respiratory rate, but WITHOUT causing sedation of GABA-A.

Am I making perfect sense, or am I making perfect sense?

. . .

Thank you, Doctor

P.S. My pulmonologist just diagnosed me two days ago with metabolic alkalosis. I checked online, and this, too, is associated with HE and liver failure.

Dr Spaho,

Thank you for a quality answer. I deeply appreciate this.

The most critical thing stated by you, is this statement: "Another MUST for the HE diagnosis is compromised consciousness and the tools to weight this are neuropsychological and other tests and exclusion of other possible neurological affecting conditions."

This is an accurate assessment of the nature of diagnosing the condition today.

Diagnosis of the condition is not perfect. The reason that this "Gold standard" test--this "must"-have criteria--is criticized by some of the world's leading experts of hepatic encephalopathy, is because there are flaws and shortcomings with it. Nevertheless, the medical establishment, to date, has not offered a more comprehensive nor reliable method of diagnosis.

Here is the issue, as best as I can explain it: it comes down to the difference between GABA-A agonism versus GABA-B agonism.

Why does hepatic encephalopathy exist? Largely because we notice it by its obvious, outwardly-observable symptoms--chief among them being a reduced level of consciousness as a result of excessive GABA-A neurologic tone caused specifically by the excessive build-up of toxic compounds that bear selective affinity for GABA-A receptors (usually ammonia, endogenous benzos, etc).

The observable symptom--reduced consciousness--usually seen is accepted as a symptom of CNS imbalance (excitatory/inhibitory, manifesting as excessive GABA with lowered serotonergic tone)...

...and it is this nervous system imbalance that is the common cause of both the reduced state of consciousness (along with the other outwardly observable signs such as reduced respiratory rate) and the inhibition of metabolic function (which is not outwardly observable, but can be suggested or confirmed by other signs such as lack of ammonia metabolization, among many others).

The "encephalopathy" part of hepatic encephalopathy does not, then, simply refer to the fact that reduced consciousness is the apparent issue--it is an assessment of the overall underlying state of the central nervous system, as it is taken for granted that if reduced consciousness is there, so is reduced metabolism! (This is why comatose patients are given hemoperfusion to detox from poisoning, while people who are awake are automatically--but often incorrectly--presumed by doctors to be able to metabolize toxins themselves naturally.)

Important, however, is this realization: it does not mean that someone who is NOT experiencing reduced cognition or reduced consciousness have absolutely no CNS excitatory/inhibitory imbalance, and no resultant inhibition of metabolism.

. . .

Doctor, it therefore appears to me that I am dealing with the following problem. I shall describe an allegorical example to use as an analogy.

. . .

Imagine that you and I are running a police precinct, filled with investigators who are trained to investigate and uncover crimes committed within the community.

There are many different kinds of crimes that take place.

For us, we have been recently focusing on robberies of jewelry stores that, for some reason, are located in snowy mountains. The normal type of thief operates in the following manner: He walks up the snowy mountain at night, where he leaves footprints in the snow. When he enters, he triggers the alarm, thus causing an activation of the alarm system. He, nevertheless, enters the store and cracks the safe and display cases, taking all the jewelry and money. He then leaves.

The police team, over the many years, have seen remarkable consistency in these crimes. They nearly always are conditioned to see two factors always correlating with the crime, that show that it happened: footprints in the snow at night, and a triggered alarm system.

Over time, new police officers trained in schooling are taught only these "symptoms," and learn to believe--simplistically--that "footprints in snow and triggered alarm mean crime has taken place. No footprints and no alarm, means no crime."

After a while, apparently, one case is reported to the police. They show up to a scene where a crime has, in fact, taken place. Money and jewelry were stolen.

However, this new, uncommon type of criminal has entered the premises using different tactics.

Instead of leaving footprints in the snow, he decided to use skis to carefully glide in without leaving the usual traces. In addition, he has also carries a portable EMP device that, upon activation, electronically prevents the alarm from being activated by destroying the functionality of the circuits.

He then goes in and does the same crime.

The investigators under you return--and state to you that, "We saw no footprints, and no alarm was activated. So we cannot diagnose the situation as being a robbery." They refused to investigate any further.

The owners hear about this. Frustratingly, they begin their own campaign to uncover evidence. They obtain video surveillance footage from a neighboring property of someone skiing in at night and then skiing away with large, filled bags. They manually lifted fingerprints from their place using their own materials, and found that fingerprints were obtained that match a person with a known criminal record of robbery. Other critical evidence is found too.

The owners come back. "There has been a jewelry store robbery," they say. We have all the evidence that one needs to reasonably see that this is what has happened. But the junior officers under you tell these people "--No means no. We are trained that, for a diagnosis of jewelry store robbery to be given, there MUST be footprints, and there MUST be an activated alarm. No alarm and no footprints means we cannot diagnose with jewelry store robbery. This is the pattern we have been trained to recognize by the actions of the historical robbers, and we therefore cannot be flexible enough to consider anything else."

You are the XXXXXXX officer in command of these idiot officers. You see that their approach is not practical or realistic in actually recognizing addressing the problem correctly. It is obvious to you. What do you do? Do you obviously open the investigation and treat this as the crime that it really is?

. . .

In this story, the traditional robbers of longstanding crimes are like the typical GABA-A type of neural tone seen in "confirmed" cases of HE. The missing money and jewelry is the missing metabolic capacity of the human body--robbed and taken away by the GABA-A molecular compound criminals.

The footprints in the snow and triggered alarm are the "symptoms" of GABA-A's presence: reduced neural tone and neural cognition, which clinicians are trained to rely on in order to assume presence of the suspected dysfunction.

The new type of stealthy robber is the GABA-B form of overwhelm. Just like the new type of robber is also successful at conducting the crime and taking the jewelry and money, GABA-B is also successful at causing the neural tone of the body to shut down to a point that microsomal function and metabolic pathways are stopped. However, even though GABA-B-related robbers leaves some of the same hints and cues as GABA-A-related robbers (an empty safe, broken jewelry cases, fingerprints, and evidence on some surrounding video cameras--just like regular forms of HE often show bradypnea and also Manny others of the 20+ signs I have listed), the GABA-B-related robber is different in that it does not show the signs of FOOTPRINTS and ALARM SYSTEM ENGAGEMENT, simply because he does not, by his very nature, show these particular symptoms while on his way to essentially conduct the same one form of crime and effect that the other GABA-A-related robbers have in the past.

The symptoms of footprints in the snow and the triggered alarm system, are like the symptoms of reduced cognition and consciousness and reduced neuropsychiatric test results and cognitive battery assessment that we are trained to see.

The absence of these symptoms in the new type of robbery is like the absence of severe neurocognitive issues with GABA-B. Just like we cannot blame the existence of skiis, EMP devices, and physics for the sad lack of proper investigative attention onto the crime, we cannot blame the fact that GABA-B is known to be a non-sedating inhibitor of the CNS, for the fact that modern medicine pretty much ignorantly views that we cannot have GABA-based/CNS-based inhibition of the liver function without coma and cognitive problems.

You, as the chief investigator, see the problem. Your junior officers are stuck to the old belief that they are brainwashed in, but cannot evolve the mind in order to see that if the new guy uses a different approach, he is able to cause the same damage and crime without showing the same symptoms. They have falsely mixed together "footprints = jewelry crime," and they cannot disassociate the two elements in their mind.

Similarly, the smart doctor may see the problem. Medicine has falsely mixed together decreased neurocognitive performance and status with neurally-sourced hepatic disablement, even though these two are not always found together. Medicine has not created any awareness of the exception, as it has no concept of the fact that ***NOT ALL GABA-BASED INHIBITION THAT DOES CAUSE LIVER FAILURE, ALSO CAUSES REDUCED COGNITIVE STATUS***

...

I checked my EEG results from 2 years ago. It was reported as normal. I distinctly remember this test being taken at a time where my respiratory rate was about 5 - 6 breaths per minute, and other GABA-B drug symptoms were present. And yet, "no abnormalities." This simply means that this test, and the evaluation of consciousness, is a poor-quality test to check for hepatic encephalopathy (aka, for GABA-induced liver failure, which is what hepatic encephalopathy REALLY is).

The police, in the situation conveyed, would be well-advised to take the common sense approach and investigate fully. This is the same as with our situation, in which the medical doctor in this case should take the case seriously, despite the old, trained rigid criteria, and use "presumptive diagnosis" to come to the conclusion of there being the specific dysfunction we suspect.

Presumptive diagnosis is the art of seeing what is really there, without conforming to a rigid, pre-described criteria and "confirmatory" test result. If the nature of the illness or condition is unusual, the route of presumptive diagnoses is often recommended, because if the doctors stick to rigid systems of definition, the disease will never fit into any pre-defined set of criteria perfectly enough in order to trigger a full classification into the diagnosis.

In those kinds of situations, as a result, no diagnosis is given. This leaves the patient with the implied conclusion by doctors that she is fine--but they know she is not, and she knows she is not.

. . .

Questions:

(1) In such a case, have doctors done their job well, by taking a woman they know with common sense has a certain disease, but choose not to diagnose because the old books falsely train them to worship specific symptoms and come to premature conclusions and restrict their ability in the absence of those symptoms?

(2) For yourself personally, would you SUPPORT the use of presumptive diagnosis for HE, LF, or related disorder, based on the evidence we see so far in my case?

And,

(3) I am seeing multiple doctors, including hematologists and neurologists next week. *HOW* can I most effectively get these doctors to understand that GABA-based inhibitory imbalance is taking place and is the root cause of hepatic disablement for the last three years (as shown by lack of drug breakdown, etc), despite the fact that I am not showing the signs of the GABA-A-based neuropsychiatric deficits?

. . .

I know what I am talking about. GABA-based inhibitory neural tone affecting liver workmate IS the practical definition of what I have, which is what HE is; yet these med school guys refuse to let go of their one almighty criteria of observable cognitive reduction, even though I am making the correct point and case that it is an ineffective and inappropriate expectation for GABA-B based syndromes and toxicities, as GABA-B potentiation can shut off the liver just as effectively as it can lower respiratory rate, but WITHOUT causing sedation of GABA-A.

Am I making perfect sense, or am I making perfect sense?

. . .

Thank you, Doctor

P.S. My pulmonologist just diagnosed me two days ago with metabolic alkalosis. I checked online, and this, too, is associated with HE and liver failure.

Thanks for your response Doc--I will write back very shortly

Thanks for your response Doc--I will write back very shortly

Doctor,

You are correct that, from a neurological standpoint, it is the case that, "Since the term encephalopathy is involved, we need evidence to confirm it and are the symptoms and features that define it."

--This is because medicine highly values its ability to observe the relevant features, symptoms and signs--and test results--in order to confirm a thing.

. . .

Here is my analysis of the diagnostic situation for HE, as it stands, from a neurological perspective. Please tell me whether you agree with the following.

(1) We know that H.E. is a form of liver failure (manifesting as an neuronally-rooted inability to metabolize the toxins of the body into byproducts) that is distinguished or differentiated by (a) lowered CNS activity, usually caused by (b) excessive GABAergic tone.

(2) In order to be sure that the given form of liver failure observed is of the type associated with low CNS activity/high GABAergic tone (which is the type we call H.E.)--and is not of any other type--we must have medical clues to support the fact that low CNS activity is present in the system.

(3) Because the state of the CNS system is not easily observable or testable, medicine make a set of assumptions about people with low CNS activity, and their outwardly observable sypmtoms--and then creates a diagnostic standard based around this (which is a neuropsychiatric battery of tests to determine cognitive and consciousness status).

(4) However, we know that, for my unique case of GABA overwhelm, which is GABA-B-based, there may not be lowering of cognitive status How, then, can medicine evaluate of confirm the presence of lowered neurological status, lowered CNS activity, or high GABAergic tone, in a way that could provide the confirmation of altered neurological status that the neurologist needs in order to render a diagnosis of hepatic encephalopathy?

(5) I believe I have the best answer for this! For my own personal case:

--I was officially just diagnosed with bradypnea, or low respiratory rate, by a specialist, several days ago!

Such a diagnosis of bradypnea is known to be (1) an indication of lowered CNS activity and tone! The bradypnea that was diagnosed is furthermore reported by the patient (myself) as being nearly chronic for over 3 years ,starting exactly after the day of the poisoning.

QUESTION:

We know, and can reasonably believe, that the same root CNS alteration that causes lowered respiratory rate may also be causing (or at least be associated with) the simultaneous lowering of liver metabolic function. Can the official diagnosis of bradypnea reasonably be used, in the absence of availability of confirmatory neuropsychiatric test results, to indicate to the neurologist the presence of diminished CNS activity that is consistent with HE--therefore allowing the presumptive diagnosis of HE to be made?

SUCH A PRECEDENT OF, or encouragement of, using the observation of bradypnea as a suitable diagnostic replacement and suitable symptom of relevant indication, would be fantastic in my case. If such a tactic were to be encouraged by you, I can gladly show your support of such a reasonable position to my own neurologist (who is just starting to learn about my case now), to encourage her to consider that:

- Demonstrations of lower performance of neurocognitive battery of tests is not needed to determine lower CNS activity consistent with HE, as the mere observation and diagnosis of bradypna may be enough to show such a relevant alteration. (Once again, the diagnosis of bradypnea is official, and is now within my medical record).

Please let me know what you think, doctor! Thank you so much

Doctor,

You are correct that, from a neurological standpoint, it is the case that, "Since the term encephalopathy is involved, we need evidence to confirm it and are the symptoms and features that define it."

--This is because medicine highly values its ability to observe the relevant features, symptoms and signs--and test results--in order to confirm a thing.

. . .

Here is my analysis of the diagnostic situation for HE, as it stands, from a neurological perspective. Please tell me whether you agree with the following.

(1) We know that H.E. is a form of liver failure (manifesting as an neuronally-rooted inability to metabolize the toxins of the body into byproducts) that is distinguished or differentiated by (a) lowered CNS activity, usually caused by (b) excessive GABAergic tone.

(2) In order to be sure that the given form of liver failure observed is of the type associated with low CNS activity/high GABAergic tone (which is the type we call H.E.)--and is not of any other type--we must have medical clues to support the fact that low CNS activity is present in the system.

(3) Because the state of the CNS system is not easily observable or testable, medicine make a set of assumptions about people with low CNS activity, and their outwardly observable sypmtoms--and then creates a diagnostic standard based around this (which is a neuropsychiatric battery of tests to determine cognitive and consciousness status).

(4) However, we know that, for my unique case of GABA overwhelm, which is GABA-B-based, there may not be lowering of cognitive status How, then, can medicine evaluate of confirm the presence of lowered neurological status, lowered CNS activity, or high GABAergic tone, in a way that could provide the confirmation of altered neurological status that the neurologist needs in order to render a diagnosis of hepatic encephalopathy?

(5) I believe I have the best answer for this! For my own personal case:

--I was officially just diagnosed with bradypnea, or low respiratory rate, by a specialist, several days ago!

Such a diagnosis of bradypnea is known to be (1) an indication of lowered CNS activity and tone! The bradypnea that was diagnosed is furthermore reported by the patient (myself) as being nearly chronic for over 3 years ,starting exactly after the day of the poisoning.

QUESTION:

We know, and can reasonably believe, that the same root CNS alteration that causes lowered respiratory rate may also be causing (or at least be associated with) the simultaneous lowering of liver metabolic function. Can the official diagnosis of bradypnea reasonably be used, in the absence of availability of confirmatory neuropsychiatric test results, to indicate to the neurologist the presence of diminished CNS activity that is consistent with HE--therefore allowing the presumptive diagnosis of HE to be made?

SUCH A PRECEDENT OF, or encouragement of, using the observation of bradypnea as a suitable diagnostic replacement and suitable symptom of relevant indication, would be fantastic in my case. If such a tactic were to be encouraged by you, I can gladly show your support of such a reasonable position to my own neurologist (who is just starting to learn about my case now), to encourage her to consider that:

- Demonstrations of lower performance of neurocognitive battery of tests is not needed to determine lower CNS activity consistent with HE, as the mere observation and diagnosis of bradypna may be enough to show such a relevant alteration. (Once again, the diagnosis of bradypnea is official, and is now within my medical record).

Please let me know what you think, doctor! Thank you so much

Thank you for your helpful reply!

Yes, fortunately my pulmonary doc was able to also rule out hypothyroidism, and there is no opioid or other drug issue (other than the long-term poisoning of Pheninut/Fasoracetam, which at least one other doctor and I both consider to be the *true* cause of both bradypnea and HE in my oen specific case).

Can the presence of bradypnea by itself--if believed to be rooted in HE--be enough by itself to give sufficient cause for a neurologist to diagnose with HE?

Thank you for your helpful reply!

Yes, fortunately my pulmonary doc was able to also rule out hypothyroidism, and there is no opioid or other drug issue (other than the long-term poisoning of Pheninut/Fasoracetam, which at least one other doctor and I both consider to be the *true* cause of both bradypnea and HE in my oen specific case).

Can the presence of bradypnea by itself--if believed to be rooted in HE--be enough by itself to give sufficient cause for a neurologist to diagnose with HE?

Thank you. You have been of tremendous help.

I may have additional questions regarding other symptoms, at some point in time soon as well. I may contact you about these questions soon.

Thank you. You have been of tremendous help.

I may have additional questions regarding other symptoms, at some point in time soon as well. I may contact you about these questions soon.