Is sleep paralysis really an explanation?

[EyeOn]

Ichneumonwasp...it's easy to say...'that's impossible'...or 'it doesn't relate' or 'that's all it does', etc. and for the most part, such responses are influenced by what is known without taking into account things not yet known...or perhaps known, but yet to be applied to what is already known...and sometimes what we think we already know turns out to be very different. Like when scientists all thought it was impossible for brain cells to regenerate. Finally, there's credible enough evidence to support it. Somebody found it. In your position as a teacher, you are obligated to keep to what is already known and will communicate such. But in relaxed conversation as this is, keep an open mind, because what science does know can change if something is found to be relevant to change the definitions into what we do know.

As of the thoughts into the pineal gland and its possible relation to the thalami is direct, but without a direct physical attachment or even hormonal. I think information between the two are relative to communications between nerve cells…the synaptic gap…a space between where components like neurotransmitters do their jobs…and the pineal gland secretes its hormones according to the information it receives. We do know that the retina translates to the pineal, yes? I can see this being a translation of the light our eyes take in…light into retina…retina communicates this to the pineal. But, what about when the eyes are closed and there is no light coming in? This is where I think heat sensory takes over, when light to the retina is absent producing the same outputs through eyesight using heat sources.

Interestingly, hallucinations are common when our body temperature rises to a feverish degree.

About pinoline...

Pinoline gives suspicions into actual eyesight...the chemical component to eyesight. That's a hypothesis I have. I don't know if anyone else has the same suspicions. I'd like to meet them. The closest research I came across about pinoline found it in the retina and this is where cones and rods are. With pinoline in the immediate vicinity of cones and rods, gives a good possibility for interaction between these things...much more if pinoline weren't found in the retina. Eyesight itself is still a mysterious function. There are missing pieces of information about eyesight and how it works. We know the mechanics quite well and how they work, but as of how they are influenced, we only know a little. Scientists do know there are things still unknown about eyesight. It would be closed minded to say the pineal gland has nothing to do with eyesight and thus nothing to do with the hallucinations seen during sleep paralysis.

That studies about pinoline in the retina can be found here…http://www.ncbi.nlm.nih.gov/sites/entrez, but these studies are about something else. When I found these articles, they strengthened my suspicions about the pineal gland having any influence to vision.

We also know that hormones are rarely a single influence by themselves, but often work in conjunction with other substances. Biological systems work with very small individual systems working together and different sets reactions with these different substances will have different influences. It is very possible pinoline plays as an influence with melatonin in influence to the rate of metabolism where melatonin by itself may not.

I just find it too coincidental we get sleepy when our metabolism slows down and it always happens when melatonin secretions increase and when metabolism speeds up, we are more awake and on the go and it always happens when melatonin levels go down. Pinoline may be that tie.

I remember asking my grandmother’s sleep doctor what the medication he prescribed her was based on and I was specific in my question if Cylert was based on the pineal gland’s secretion of pinoline and he answered yes. This is what he prescribed to my grandmother to keep her awake and helped prevent cataplexy seizures. This is where I get the connection between being awake and pinoline from the pineal gland. Cylert was originally targeted to treat ADD and ADHD, but sleep experts found another use for it with narcoleptics. This was why there was such uproar from narcoleptics when the FDA stopped the production of Cylert, citing it put too much stress on the liver and there were other, less damaging sources to treat ADD and ADHD. Narcoleptics with cataplexy were also prescribed this drug and it worked. They were left out in the equation completely in the FDA’s decision.

About the cerebellum, quadregimena and the pineal gland...even pictures of real brains show these organs as though they were one system attached to the rest of the brain by nerves and the pineal gland reaches up to the thalami, which brings this post full circle with the thalami possibly influencing the pineal gland.

As of connections to sleep paralysis…there are different categories for different types of sleep paralysis. The sleep paralysis I get is the more rare type which includes going into REM sleep from wakefulness and coming out of REM sleep and includes extended paralysis…the paralysis extends beyond just skeletal muscles, but also involves non skeletal muscles. Visions are apparent in every incident. There is obviously a different influence here than what people know of the norm. This seems to be when the hallucinations are more profound…more than a sense of a shadow; more than the sense of an evil presence. I’ve spoken to people with mild forms of sleep paralysis and their paralysis is limited to their skeletal muscles. Their eyes are open and they can move their eyes to look around the room. They can also breathe freely without feeling heavy chested. They don’t get the shakiness that seems quite evident in most incidences of the more extreme cases. Their experiences also seem limited to coming out of REM sleep rather than it happening going into REM sleep. Timing of the incident may be everything. Who yet really knows? These milder forms of sleep paralysis may be taking place later in the process between sleep and wake, when inner type visual activity we know as dreams stop, while the more profound types may happen earlier in the process…allowing the visual activity to extend reactions with impulses as the individual begins to slip out of REM sleep…rather than when the process is almost complete.

These more extreme forms of sleep paralysis may involve the very things you claim do not involve the norm of sleep paralysis. They are different and very well may have different influences.

 

[EyeOn]

How about you answer the same thing? Your posts have been filled with "I feel" and "I think" statements. What qualifications do you possess that allow you to speculate about these biological processes and then get defensive (testy, even) when your speculation is called into question?

I've yet to get testy with anyone, but might throw in an attitude if I sense a little attitude in return...like when what I state is taken as a description of silly magic. Magic is a completely diffeent thing and the comments are fallacied.

In the first or second post I made, I did clarify that I am a student.

I deliberately use words such as "feel", "think", even "maybe" and "might", also "possible" when explaning something I've yet to come by any reliable means of information that either completely denies or confirms the thoughts.

I do know when something is completely absurd or completely accurate and when something is open for debate...for example...such as Intelligent Design is absurd, evolution is accurate and how DNA copy errors occur are open for debate.

 

[EyeOn]

That's usually a clear mark of woo.

Would you think the same about the person who tried to convince others the earth is actually round in a time when everyone swore the earth is flat?

 

[Lilith]

EyeOn - It appears to me that you are TRYING to use logical thinking, but you are basing your conclusions on false premises ... premises that you refuse to reconsider. It is clear that you have read a bit on the topic you address, and know some tough terminology, even a smattering of neuroanatomy (more than the average bloke, but not enough to argue convincingly). I would not be surprised if you have impressed others with your seeming knowledge, and received lots of good dopamine in consequence. Good for you, you are on the right track to making sense of the world and the brain ... but

I am curious to see if you will make the necessary steps to hone these (beginnings of) critical thinking skills. So many don't. I encourage you to learn to doubt whatever your source is for the claims you are making on this thread. Doubt it, and try to find where they got their information and what evidence contradicts it. You already express doubt at the responses here, so I know you can do it! And while you're at it, doubt your interpretations of your own experiences. To not do this is to have a closed mind, contrary to what others may tell you. The mind is a funny thing, and will try to make conclusions just so the world makes sense when things are fluky.

As for pinoline - I haven't read much about it - but I am curious why you put so much stock in a substance that has yet to be thoroughly studied. So far, it looks like it has been studied mostly for its protective effects against glutamate-induced lipid peroxidation in the retina.

 

[Ichneumonwasp]

it's easy to say...'that's impossible'...or 'it doesn't relate' or 'that's all it does', etc. and for the most part, such responses are influenced by what is known without taking into account things not yet known...or perhaps known, but yet to be applied to what is already known...and sometimes what we think we already know turns out to be very different.

Yes, it is very easy to say. That is why I do not say it lightly. I do not say that it is impossible, but that there is no evidence that the pineal gland has the effects you seem to think it does. I say this based on the fact that removal of it has limited affects on people -- which should be very clear evidence -- and because it lacks the connections with other structures to play the role that you seem to think it plays.

It has its role. It helps link the day-night cycle to sleep. But it is not the only system to do so.

And, yes, our knowledge is always changing. That is why all such statements are provisional.

Like when scientists all thought it was impossible for brain cells to regenerate. Finally, there's credible enough evidence to support it. Somebody found it. In your position as a teacher, you are obligated to keep to what is already known and will communicate such. But in relaxed conversation as this is, keep an open mind, because what science does know can change if something is found to be relevant to change the definitions into what we do know.

There is keeping an open mind and there is believing things that simply are not true. One needn't believe the untrue to say that one has an open mind.

As to the issue of neural stem cells -- the belief that neurons could not regenerate was based on fairly good evidence. People didn't just decide that neurons could not regenerate, they saw the effects of brain injury and looked at the limited functional recovery and thought the most likely possibility was the neurons could not regenerate. Keep in mind that this was felt to be true by analogy -- much like the limited regenerability of the heart and clearly different from the ability of the liver to regrow after injury or the constant turn-over of epithelial cells in the skin or mucous membranes. We have always been aware, however, that the nervous system could re-organize. For a long time it was simply felt that neurons re-connected in different ways to recover some function. Now we know that there is some limited ability to create new neurons. That is part of the beauty of science -- we do keep an open mind.

Part of my personal teaching method includes these concepts on a regular basis, so while I understand your concern, you really needn't tell me to keep an open mind.

As of the thoughts into the pineal gland and its possible relation to the thalami is direct, but without a direct physical attachment or even hormonal. I think information between the two are relative to communications between nerve cells…the synaptic gap…a space between where components like neurotransmitters do their jobs…and the pineal gland secretes its hormones according to the information it receives. We do know that the retina translates to the pineal, yes? I can see this being a translation of the light our eyes take in…light into retina…retina communicates this to the pineal. But, what about when the eyes are closed and there is no light coming in? This is where I think heat sensory takes over, when light to the retina is absent producing the same outputs through eyesight using heat sources.

Yes, there are direct retinal inputs into the pineal gland. That is how it is involved in setting sleep times in relation to the light-dark cycle. When the eyes are closed, we do not start to secrete melatonin. The system is a bit more complex than that. This system does not seem to use heat sensors. If the system were that simple, there would be a clear difference between closing your eyes in summer and winter. There is not.

Interestingly, hallucinations are common when our body temperature rises to a feverish degree.

Yes, that is true, but it appears to concern more the stochastic release of neurotransmitters and sodium channel function. Sodium channels work best within a fairly narrow range of temperatures -- they seem to have real problems when heat goes up. If you know anyone with multiple sclerosis there is an interesting phenomenon in which heat may cause worsening symptoms (it's called Uthoff's phenomenon). This happens because MS is caused by an autoimmune attack on the glia that create the myelin that surrounds the axons of nerve cells. When this myelin, which acts as insulation, is stripped away, neurons do not work as well -- it's much like insulation being stripped away from a wire. The electrical impulses are transmitted down an axon by the opening of sodium channels. Since these sodium channels are so sensitive to heat, and because the system is already stressed when the insulation is stripped away, someone with MS can have real problems just from taking a hot shower.

A similar type problem can occur in association with a high fever, but there are other factors that also play into the delirium we see in that situation (since this usually occurs with infections and there are other immune factors released in an infection -- various cytokines).

Pinoline gives suspicions into actual eyesight...the chemical component to eyesight. That's a hypothesis I have. I don't know if anyone else has the same suspicions. I'd like to meet them. The closest research I came across about pinoline found it in the retina and this is where cones and rods are. With pinoline in the immediate vicinity of cones and rods, gives a good possibility for interaction between these things...much more if pinoline weren't found in the retina. Eyesight itself is still a mysterious function. There are missing pieces of information about eyesight and how it works. We know the mechanics quite well and how they work, but as of how they are influenced, we only know a little. Scientists do know there are things still unknown about eyesight. It would be closed minded to say the pineal gland has nothing to do with eyesight and thus nothing to do with the hallucinations seen during sleep paralysis.

That studies about pinoline in the retina can be found here…http://www.ncbi.nlm.nih.gov/sites/entrez, but these studies are about something else. When I found these articles, they strengthened my suspicions about the pineal gland having any influence to vision.

Um, OK. But the pineal gland has nothing to do with vision. The reciprocal interaction between the retina and pineal gland concerns the linking of the sleep-wake cycle to light-dark.

Once again, pineal glands are removed from time to time. These people can still see just fine. I've met a few of them.

We also know that hormones are rarely a single influence by themselves, but often work in conjunction with other substances. Biological systems work with very small individual systems working together and different sets reactions with these different substances will have different influences.

Most definitely.

It is very possible pinoline plays as an influence with melatonin in influence to the rate of metabolism where melatonin by itself may not.

Again, that is pure conjecture without any evidence to back it up. I don't know enough about pinoline to comment, however.

The pituitary is called the 'master gland' for a reason and the hypothalamus is the master of the master gland for a reason. If you want to look for metabolic control, look there.

I just find it too coincidental we get sleepy when our metabolism slows down and it always happens when melatonin secretions increase and when metabolism speeds up, we are more awake and on the go and it always happens when melatonin levels go down. Pinoline may be that tie.

Um, I don't follow. We get sleepy because of a variety of different factors that coincide with decreases in metabolism largely because of the circadian rhythms that are governed by the hypothalamus.

Once again, we take out people's pineal glands and they do fine. No one has survived removal of the hypothalamus. You can guess at things all you want, but there is clear evidence for what is important for metabolic control in our brains -- and it is largely housed in the hypothalamus and not the pineal gland.

I remember asking my grandmother’s sleep doctor what the medication he prescribed her was based on and I was specific in my question if Cylert was based on the pineal gland’s secretion of pinoline and he answered yes. This is what he prescribed to my grandmother to keep her awake and helped prevent cataplexy seizures. This is where I get the connection between being awake and pinoline from the pineal gland. Cylert was originally targeted to treat ADD and ADHD, but sleep experts found another use for it with narcoleptics. This was why there was such uproar from narcoleptics when the FDA stopped the production of Cylert, citing it put too much stress on the liver and there were other, less damaging sources to treat ADD and ADHD. Narcoleptics with cataplexy were also prescribed this drug and it worked. They were left out in the equation completely in the FDA’s decision.

I hate to tell you this, but there may have been a communication issue at play. No one knows how Cylert works precisely. It may have some effects through the dopaminergic system, but beyond that I don't think anyone really knows.

Cylert's generic name is pemoline, so he may not have actually understood what you were asking and just said 'yes' because he thought you were asking the generic name of the drug. I don't know for sure.

About the cerebellum, quadregimena and the pineal gland...even pictures of real brains show these organs as though they were one system attached to the rest of the brain by nerves and the pineal gland reaches up to the thalami, which brings this post full circle with the thalami possibly influencing the pineal gland.

Look, you don't know me from Adam, but I've done thirty autopsies by myself when I did a pre-doctoral fellowship in pathology and I've been involved in countless other brain cuttings. I have spent the last 25 odd years studying this stuff. I don't care what it looks like. Those connections simply don't exist. You are given a false sense of that type of connection because the sagittal pictures try to get a crucial bit of information across -- that there is an important structure that can cause real problems in the picture. It looks like there is a disconnect between the quadrigeminal plate and the rest of the midbrain because of the Aqueduct of Sylvius -- which is the connection between the third and fourth ventricle allowing the flow of CSF between those structures. One of the other big problems that can arise from pineal tumors that grow large enough is that this small channel -- the Aqueduct of Sylvius -- can be blocked and cause a build-up of cerebrospinal fluid (CSF) -- a condition known as hydrocephalus, which can be fatal. But there is no real disconnect, and those structures that can look like a pathway from an outside view do not form an important unit that works together in the brain. All of those structures are very important, mind you, but they are not an integrated system.

As of connections to sleep paralysis…there are different categories for different types of sleep paralysis. The sleep paralysis I get is the more rare type which includes going into REM sleep from wakefulness and coming out of REM sleep and includes extended paralysis…the paralysis extends beyond just skeletal muscles, but also involves non skeletal muscles. Visions are apparent in every incident. There is obviously a different influence here than what people know of the norm. This seems to be when the hallucinations are more profound…more than a sense of a shadow; more than the sense of an evil presence. I’ve spoken to people with mild forms of sleep paralysis and their paralysis is limited to their skeletal muscles. Their eyes are open and they can move their eyes to look around the room. They can also breathe freely without feeling heavy chested. They don’t get the shakiness that seems quite evident in most incidences of the more extreme cases. Their experiences also seem limited to coming out of REM sleep rather than it happening going into REM sleep. Timing of the incident may be everything. Who yet really knows? These milder forms of sleep paralysis may be taking place later in the process between sleep and wake, when inner type visual activity we know as dreams stop, while the more profound types may happen earlier in the process…allowing the visual activity to extend reactions with impulses as the individual begins to slip out of REM sleep…rather than when the process is almost complete.

These more extreme forms of sleep paralysis may involve the very things you claim do not involve the norm of sleep paralysis. They are different and very well may have different influences.

OK, but the pineal still isn't involved in this.

 

[EyeOn]

And while you're at it, doubt your interpretations of your own experiences. To not do this is to have a closed mind, contrary to what others may tell you. The mind is a funny thing, and will try to make conclusions just so the world makes sense when things are fluky.

As for pinoline - I haven't read much about it - but I am curious why you put so much stock in a substance that has yet to be thoroughly studied. So far, it looks like it has been studied mostly for its protective effects against glutamate-induced lipid peroxidation in the retina.

I'm always crossing doubts into the ESP activities I am less than 100% certain, but keep them in mind for observation reasons for comparisons between those I am 100% certain on. Those I am completely convinced are those that show in true form. It'd be nice to establish proof between these visions and their actual events.

I'm being coached as a student on how to track down reliable sources of information...like staying away from .com sources and the associated press and look at info. on .net, .org, .gov and .edu sources when dealing with the Internet. Medical and life science sources are always good given they are provided by experts in that field of medicine and I've always known better to stick with a biological base already well established. It makes for a better skeleton to build a hypothesis on. I look forward to learning more as I go along, adding and subtracting information.

As of investing into a substance like pinoline, because it is so vaguely known about, it's a wide open area for study. Little competition at the moment and less clutter of scrutiny to 'swim' through...lol. Also, for studying and researching the unknown, wouldn't it be a good place to start at something that is also largely unknown? Especially when there are indications of a possible connection such as pinoline having hallucinogenic properties and being found in the retina and it just so happens to come from the pineal gland, which does bear an influence to the timing of sleep and wake when these visual perceptions take place. I know the argument is inductive, but has some strength to it.

I appreciate the inspiration. Thank you.

 

[EyeOn]

Cylert's generic name is pemoline, so he may not have actually understood what you were asking and just said 'yes' because he thought you were asking the generic name of the drug. I don't know for sure.

I have thought of that, but I was specific to include "pineal gland secretion" in my question...and asked again...even spelled it out for him. Maybe Pemoline is a name derrived from what it's synthesizing and the pineal gland is an influence. I don't know.

One of the other big problems that can arise from pineal tumors that grow large enough is that this small channel -- the Aqueduct of Sylvius -- can be blocked and cause a build-up of cerebrospinal fluid (CSF) -- a condition known as hydrocephalus, which can be fatal.

I'm really interested to know about this, but specific to meningitis.

A little off topic from sleep paralysis, but...

One of the more outstanding deaths my grandmother experienced was when she was a few months old and was legally pronounced clinically dead from meninigitis. I would love to find these medical records. Someone, I presume a doctor, gave her a heart message and a dose of whiskey and it revived her.

I am aware of alcohol fermentation and its influence in producing ATP in an oxygen starved environment. I would like to know your thoughts to this scenario and if you think this could relate in any way to narcolepsy and cataplexy...which sleep paralysis is a common complaint among these patients, but sleep paralysis is irrelevant to what I am asking you.

I want to understand more about what happened to her at this moment in time, which was back in 1924.

Thanks

 

[Ichneumonwasp]

I have thought of that, but I was specific to include "pineal gland secretion" in my question...and asked again...even spelled it out for him. Maybe Pemoline is a name derrived from what it's synthesizing and the pineal gland is an influence. I don't know.

I don't know precisely how pemoline's name was derived, but I kind of doubt it has anything to do with penoline. I could probably find out with a little asking around though.

I'm really interested to know about this, but specific to meningitis.

A little off topic from sleep paralysis, but...

One of the more outstanding deaths my grandmother experienced was when she was a few months old and was legally pronounded clinically dead from meninigitis. I would love to find these medical records. Someone, I presume a doctor, gave her a heart message and a dose of whiskey and it revived her.

I am aware of alcohol fermentation and its influence in producing ATP in an oxygen starved environment. I would like to know your thoughts to this scenario and if you think this could relate in any way to narcolepsy and cataplexy...which sleep paralysis is a common complaint among these patients, but sleep paralysis is irrelevant to what I am asking you.

I want to understand more about what happened to her at this moment in time, which was back in 1924.

Thanks

Regarding your grandmother, I don't know. I would assume that what happened is that she stopped breathing, not too uncommon in infants especially when sick, since respiratory control is not completely set -- that is part of the reason why sudden infant death can occur.

About the alcohol fermentation issue -- there is a difference between the fermentation process and what happens in the body when we consume alcohol. The fermentation process is anaerobic, yes.

But that has nothing to do with the way that alcohol affects our bodies. For the most part, alcohol is a CNS depressant. The reason it is given is to relax people, much like Morphine in heart patients -- both to kill the pain and because it has venodilating effects. Alcohol has its primary effects at a certain subset of glutamate receptors (NMDA receptors), inhibiting them, and by potentiating the effect of GABA a receptors in the brain.

It has effects on the circulatory system as well since it is a bit of a venodilator too. I'm guessing that is why it was given. There weren't very many treatments back then -- that was even pre-penicillin days. I doubt it was used for any reason other than as a relaxant.

Are you really sure that she had meningitis? That was generally fatal in the 20s before we had good antibiotics. Sulfa drugs were available, so she could have survived because of that.

ETA:

I forgot to add that, yes, alcohol makes all sleep disorders worse. So, yes, there is a connection, in a way, between alcohol and sleep paralysis. I never asked any narcoleptics if they had more problem when they drank alcohol. People with sleep apnea clearly get worse when they drink, though.

 

[Hokulele]

Thanks for the neuro book recommendations. I'm reading one now by Ramachandran called Phantoms in the Brain - really interesting.

I second aggle-rithm's comments on this book. If you haven't read it yet, the Oliver Sacks' book The Man Who Mistook His Wife for a Hat that Ichneumonwasp mentioned is also excellent.

 

[Ichneumonwasp]

EyeOn,

Thinking about it, here is a scenario that might explain what happened with your grandmother.

You might not like it, though, because it is not a sexy as a doctor striding in and saving her life with heart massage and a shot of whiskey.

Febrile seizures are not that uncommon during infancy -- about 5% of the population are predisposed to them. Febrile seizures are seizures that occur in children usually under the age of five. They usually only occur with what we consider fairly high fevers -- like 102 F -- but which are not that uncommon in kids. When someone has a seizure, especially along with a fever, they are often thought to have meningitis. It could be that she had a febrile seizure from some type of infection from which she could recover.

Surviving meningitis, especially for infants, in the pre-antibiotic days (at least the pre-penicillin days) was pretty rare.

It is probably more likely that the doc over-reacted a bit to a febrile seizure and did what he could -- rub her chest and give her alcohol.

This could also play into some of the other events that you described if she simply had a seizure disorder exacerbated by fever -- very common in a particular type of temporal lobe epilepsy that is very difficult to treat with anti-epileptic medications and known as mesial temporal sclerosis. Folks with this condition will often have their first seizures associated with fever, but as opposed to the benign febrile seizure they continue to have a kind of seizure throughout life -- complex partial seizures.

 

[Miss Whiplash]

Would you think the same about the person who tried to convince others the earth is actually round in a time when everyone swore the earth is flat?

Eyeon, that set off logical fallacy alarms. Like Lilith, I believe you are trying to use logic. You may want to review the 42 Logical Fallacies and Shermer's 25. Heresy does not equal correctness.

 

[EyeOn]

EyeOn,

Thinking about it, here is a scenario that might explain what happened with your grandmother.

You might not like it, though, because it is not a sexy as a doctor striding in and saving her life with heart massage and a shot of whiskey.

Febrile seizures are not that uncommon during infancy -- about 5% of the population are predisposed to them. Febrile seizures are seizures that occur in children usually under the age of five. They usually only occur with what we consider fairly high fevers -- like 102 F -- but which are not that uncommon in kids. When someone has a seizure, especially along with a fever, they are often thought to have meningitis. It could be that she had a febrile seizure from some type of infection from which she could recover.

Surviving meningitis, especially for infants, in the pre-antibiotic days (at least the pre-penicillin days) was pretty rare.

It is probably more likely that the doc over-reacted a bit to a febrile seizure and did what he could -- rub her chest and give her alcohol.

This could also play into some of the other events that you described if she simply had a seizure disorder exacerbated by fever -- very common in a particular type of temporal lobe epilepsy that is very difficult to treat with anti-epileptic medications and known as mesial temporal sclerosis. Folks with this condition will often have their first seizures associated with fever, but as opposed to the benign febrile seizure they continue to have a kind of seizure throughout life -- complex partial seizures.

Either way...without doing the chest rub and the shot of whiskey, me and five other members of my family probably wouldn't be here today.

What the family has always questioned and no one's really been able to answer is if she could have gotten the narcolepsy from that scenario...be it from meningitis or a febrile seizure or what most of the family thinks...being given whiskey. I think it's from whatever they were treating. No one else in the family has ever had narcolepsy and the most of any sleep disorder known in my family before her was insomnia. After her...both my mother and her twin sister are diabetic, have sleep apnea...though obstructive, not central and both have complained of vivid sleep disturbances. My uncle was always skinny, though he also use to be a drug addict, so any indications of sleep disorders would be masked from that abuse. I have heard about his daughter talk about dreams coming true. I get the sleep paralysis with hallucinations that come true. My son just informed me of his first experiences with sleep paralysis...and they've happened both ways...into REM sleep and out of REM sleep, which apparently, falling into REM sleep from wakefulness is a remote sign of narcolepsy...a possibility. He has also mentioned about hallucinations. From my grandmother down to my son...the youngest (with the exception of my uncle due to circumstance)...we all have sleep disturbances and a bit more than what's considered normal. I have every reason to believe this is genetic and though not a valid means of certainty, I've always had an odd feeling that what happened to her then holds a clue to narcolepsy, cataplexy and sleep paralysis. Sleep paralysis can manifest without narcolepsy, unlike what is known where cataplexy is always associated with narcolepsy, but I think the type of sleep paralysis is the same as those with narcolepsy...somehow a marker for the genetic mutation that could lead to narcoleptic behavior.

Just a thought.

 

[EyeOn]

Eyeon, that set off logical fallacy alarms. Like Lilith, I believe you are trying to use logic.

I know...did it deliberately to show a relative response to the poster. Just a way to show that, although I may not know them all, I do know some and can throw them right back. I'll be honest and admit, it was meant to be sarcastic.

 

[EyeOn]

Are you really sure that she had meningitis? That was generally fatal in the 20s before we had good antibiotics. Sulfa drugs were available, so she could have survived because of that.

ETA:

I forgot to add that, yes, alcohol makes all sleep disorders worse. So, yes, there is a connection, in a way, between alcohol and sleep paralysis. I never asked any narcoleptics if they had more problem when they drank alcohol. People with sleep apnea clearly get worse when they drink, though.

Over looked this reply...

As far as I know from family, it was meningitis. Recently I spotted something mentioning an ATP behavior with the illness, but haven't really dug into that yet for any details.

An idea that had crossed my mind at one point was maybe there's an ATP behavior in connection to states of 'suspended animation' like what is seen with cataplexy and catalepsy as well as coma. Maybe there's a sudden drop in ATP or a sudden drop in available oxygen in the body to make the brain shut the body down for oxygen conservation.

That's what I originally thought of when I first read about alcohol fermentation and remembered the situation with my grandmother when she was an infant and the fact she was a narcoleptic with cataplexy, catalepsy and sleep paralysis.

You said alcohol does make sleep disorders worse, but can alcohol cause a sleep disorder such as narcolepsy? And...as far as I know, my grandmother didn't drink alcohol except maybe a little eggnog around the holidays...lol.

 

[chillzero]

I think the turn of this discussion relates more to the Science and Medicine section, so I am moving it there.

Replying to this modbox in thread will be off topic  Posted By: chillzero

 

[Ichneumonwasp]

An idea that had crossed my mind at one point was maybe there's an ATP behavior in connection to states of 'suspended animation' like what is seen with cataplexy and catalepsy as well as coma. Maybe there's a sudden drop in ATP or a sudden drop in available oxygen in the body to make the brain shut the body down for oxygen conservation.

Well, you wouldn't want a drop in ATP to be the cause of any behavior in any system. A serious drop in ATP would mean that you are dying.

Look into how muscle works and you will see that this is not possible anyway. If muscle lacks ATP it does one thing -- it becomes rigid. This is what happens with rigor mortis. The energy using step in muscle ratcheting is not contraction but relaxation interestingly enough. Myosin ratchets on actin naturally when they are brought together (depends on the presence of calcium and a conformational change involving troponin). ATP is necessary for muscle to relax. No ATP and muscle becomes rigid; it cannot relax.

What happens with cataplexy has nothing to do with ATP (except that everything involves ATP) -- at least not drops in ATP. It is due to a particular set of neurons becoming active -- neurons that inhibit and cause the drop in tone. We need this during REM sleep because without it we would act out our dreams -- this actually occurs in some people and is called REM behavior disorder.

You said alcohol does make sleep disorders worse, but can alcohol cause a sleep disorder such as narcolepsy? And...as far as I know, my grandmother didn't drink alcohol except maybe a little eggnog around the holidays...lol.

No. The sleep disorder has another cause. Alcohol can worsen sleep disorders because it is a CNS depressant, and because it disrupts the normal sleep-wake cycle. It can cause insomnia with long term use and worsen sleep apnea, but it does not cause narcolepsy or cataplexy.

 

[Ichneumonwasp]

Either way...without doing the chest rub and the shot of whiskey, me and five other members of my family probably wouldn't be here today.

Possibly so.

What the family has always questioned and no one's really been able to answer is if she could have gotten the narcolepsy from that scenario...be it from meningitis or a febrile seizure or what most of the family thinks...being given whiskey.

Meningitis causing narcolepsy -- theoretically possible -- but, again, I doubt that is what she had, since the chances of survival were so low at that time. From a febrile seizure? No, no association there. From alcohol? No, not likely.

I think it's from whatever they were treating.

I think you are probably right about that. Anything that can affect the brainstem -- stroke, tumor, MS, infection with cell damage -- can cause apnea (stopping breathing) and can result in narcolepsy if the right area is damaged. MS is well recognized as one of the secondary causes of narcolepsy. All of those entities can cause seizures too. Secondary causes of narcolepsy are generally much more difficult to treat.

Sleep paralysis can manifest without narcolepsy, unlike what is known where cataplexy is always associated with narcolepsy, but I think the type of sleep paralysis is the same as those with narcolepsy...somehow a marker for the genetic mutation that could lead to narcoleptic behavior.

Yes, sleep paralysis may occur without narcolepsy. Cataplexy's association with narcolepsy is a bit more complex largely because narcolepsy clinically is defined as sleep fits in association with cataplexy in many countries. In the U.S. there is a different definition of narcolepsy that depends critically on sleep study findings. All of these definitions are probably going to change since orexin/hypocretin has been identified.

 

[EyeOn]

but, again, I doubt that is what she had,

Not to be rude and it doesn't mean I don't appreciate the information you are sharing, but who are you to doubt another doctor without examination? Take it as if it was meningitis, because that is what is known and recorded. Just because survivng meningitis was really low, maybe she was one of those lucky ones...and just may be she was really dead...and just may be because of that...dead...because of meningitis...set in the narcolepsy when she was revived and the whiskey would make sense of alcohol fermentation, because of the absence of ATP due to an absence of oxygen...who knows how long she was actually dead, but we all know damage occurs for every moment the brain is without oxygen.

Interestingly, Catalepsy behaves like rigor mortis. Muscle tone is rigid. Though Cataplexy was the main player in her seizures, it was noted to me and have noted in another post, she also had Catalepsy. As far as I know, the difference between the two is muscle tone and the duration the seizures play out. Catalepsy can play out for seconds up to days or weeks...even longer is suspected, whereas cataplexy plays out generally for a few seconds up to an X number of hours. Though both conditions can place their patients in the morgue due to misdiagnosis, Catalepsy is the noted famed cause of "premature burials", because it mimicks rigor mortis.

This would fit the description mentioned when ATP levels drop.

If a drop in ATP generally means you're dying, then the brain would sense the body is in danger and possibly react to shut the body down in an effort to preserve life by means of suspended animation. When sensory impulses are restricted like that...ESP activity, in the way I hypothesize it to work, would be in full swing, because that person is incapable of protecting themselves due to the extreme physical loss. This could account for the hallucinations that occur in these states.

Even more interesting...

Narcolepsy, cataplexy, sleep paralysis and catalepsy...when expressed together may be a step down toward suspended animation, but on an automatic basis rather than a consciously or temperature controlled means such as seen with deep meditation and hibernation. You have the sudden urge to go to sleep...narcolepsy...then the collapse of muscle tone...cataplexy....the brain recognizes a drop in oxygen, sending alarm signals to prepare a descend into suspended animation...sleep paralysis occurs between the transition of wakefulness and sleep during this step down, skipping all the other stages of sleep, because suspended animation is the target action. If oxygen availability continues to be low or decrease further, a drop in ATP production would follow...catalepsy.

Respiratory distress is an immediate threat to life. Respiratory arrest can soon follow and cause the heart to stop, prevent blood to flow and cause the brain to die. One of the most terrifying experiences of sleep paralysis I had clued in to a possible cause to the respiratory distress I was experiencing at the time. Don't know for sure, but it nags my thoughts. All the while I saw myself as I was on the bed, there was a shadow that came in, wrapped his hands around my throat and choked me. As I was being choked, I noticed the heater was on and the light that shined in from the moon dimmed. When the shadow stopped choking me, the heater turned off and the light that shined in from the moon brightened. The shadow started choking me again and the heater kicked on and the moonlight dimmed. Shadow stopped choking me...etc., etc. Other things during the sleep paralysis was shown. Kind of weird...but I saw myself crawl out of bed, still being choked, I was on the floor trying to pound at the walls around me to make noise to wake my husband up in another room. The room as it was seen in the halluciantion was how I had the room a few months before that. I had chinese water dragons and had their cage somewhere else than where they were located in the halluciantion. Maybe I was seeing a reverse reflection, but everything else in the room was at where they were really at...all the doors and windows were at where they were really at. And while I was seeing all of this, I also saw I was on the bed laying down as I really was.

I've always wondered if there was an increasing level of CO2 coming in from the heater. I never ran the heater after that without cracking the window open a little. I know...kind of defeats the purpose, but it still heated the room up a little more than it would have without.

This, to me, would express ESP activity. The body is in danger and because of being in a vulnerable state...paralyzed. The effects are seen through sensory processing, because channels are open under both tenses of being awake and being asleep, thus impulses meant for elsewhere in the brain or body to protect itself against the rising CO2, are diverted to the thalami for this sensory processing.

This, along with other hallucinations during sleep paralysis...whether shown in true form or metaphor, may well be the brain's way of bringing an awareness of caution or danger, present or future to your conscious attention. If breathing is hampered at the time, there's an extra sense of danger. One curious behavior I've noticed...the harder it is to breathe, the darker the hallucinations appear as if oxygen is needed to react with something in order to see light...and hey...pinoline as well as melatonin are known to be oxidative substances and pinoline does oxidate at least one substance known to date in the retina and the retina does communicate to the pineal gland.

Even though there's yet to be any solid conclusive evidence, who else is actually out there looking for it?...IMO, there's enough to suspect a connection that may be escaping our current knowledge.

The pineal gland has long been suspected as an optical capable organ. It's stimilated by light, at least one of the substances it produces, pinoline, has hallucinogenic properties and is found in the retina where cones and rods 'reside'. There's even ancient biological evidence alive today that suggests the pineal gland, even before dinosaurs, is an optical capable organ. Look into the tuatara and its visible third eye on the top of its head, which can also be found in present day species of lizards like iguanas, chinese water dragons and Australian frilled dragons. The third eye on the tuatara is connected to a pineal body.

Note...thanks chillzero

 

[calebprime]

but, again, I doubt that is what she had,

Not to be rude and it doesn't mean I don't appreciate the information you are sharing, but who are you to doubt another doctor without examination? Take it as if it was meningitis, because that is what is known and recorded. Just because survivng meningitis was really low, maybe she was one of those lucky ones...and just may be she was really dead...and just may be because of that...dead...because of meningitis...set in the narcolepsy when she was revived and the whiskey would make sense of alcohol fermentation, because of the absence of ATP due to an absence of oxygen...who knows how long she was actually dead, but we all know damage occurs for every moment the brain is without oxygen.

I'd suggest re-wording rather than saying "not to be rude...but who are you to doubt..." Just a thought.

Doubting is what we do, and you're actually talking to an expert.

The stats on meningitis are remarkable--sulfa drugs completely turned things around:

quote:

1) The history of community-acquired bacterial meningitis arguably represents the best example of the salutary effect of the introduction of antimicrobial agents. Before the use of specific antiserums, the outlook for patients with bacterial meningitis was dismal. In the 1920s, 77 of 78 children at Boston Children's Hospital who had Haemophilus influenzae meningitis died. The prognosis for untreated pneumococcal meningitis was equally bleak: of 300 patients, all died. In the first decade of the 20th century, untreated meningococcal meningitis was associated with a mortality rate of 75 to 80 percent.

2) In 1913, Simon Flexner (1863-1946) was the first to report some success in treating bacterial meningitis with intrathecal equine meningococcal antiserum: among 1300 patients with epidemic meningitis, mortality was reduced to 31 percent.[1] Among 169 children with meningococcal meningitis treated with intrathecal antiserum at Bellevue Hospital, New York, between 1928 and 1936, the outcome was even more favorable, with mortality of about 20 percent. Fothergill reported in 1937 that treatment of H. influenzae meningitis with combined intravenous and intrathecal antiserums reduced mortality among 201 children to 85 percent. The prognosis for patients with pneumococcal meningitis remained extremely grave even after the introduction of specific antiserums. There were only anecdotal reports of recovery after treatment with systemic and intrathecal antipneumococcal serum.

3) In the 1930s, with the introduction of sulfonamides, the mortality associated with meningococcal meningitis decreased to 5 to 15 percent. By 1944, Alexander had reported that treatment with both a sulfonamide and intravenous rabbit antiserum in 87 children with H. influenzae type b meningitis had reduced mortality to 22 percent. In the early 1950s, chloramphenicol treatment (with sulfadiazine) reduced the fatality rate of H. influenzae meningitis to 5 to 10 percent and made the use of antiserum unnecessary. The results of sulfonamide treatment of pneumococcal meningitis were less favorable, with mortality ranging from 45 to 95 percent.


http://scienceweek.com/2005/sc050211-3.htm

 

[Ichneumonwasp]

Not to be rude and it doesn't mean I don't appreciate the information you are sharing, but who are you to doubt another doctor without examination? Take it as if it was meningitis, because that is what is known and recorded. Just because survivng meningitis was really low, maybe she was one of those lucky ones...and just may be she was really dead...and just may be because of that...dead...because of meningitis...set in the narcolepsy when she was revived and the whiskey would make sense of alcohol fermentation, because of the absence of ATP due to an absence of oxygen...who knows how long she was actually dead, but we all know damage occurs for every moment the brain is without oxygen.

Not to be rude, but I told you exactly why I doubt the diagnosis. People are misdiagnosed all the time. A huge part of my job consists in looking at actual evidence and the way stories fit together -- and if you're not up for the real shocker, here it comes anyway: doctors get stuff wrong all the time.

Interestingly, Catalepsy behaves like rigor mortis. Muscle tone is rigid.

Why is that interesting? The mechanism for catalepsy has nothing to do with ATP (aside from the fact that nothing happens without it).

Though Cataplexy was the main player in her seizures, it was noted to me and have noted in another post, she also had Catalepsy. As far as I know, the difference between the two is muscle tone and the duration the seizures play out. Catalepsy can play out for seconds up to days or weeks...even longer is suspected, whereas cataplexy plays out generally for a few seconds up to an X number of hours. Though both conditions can place their patients in the morgue due to misdiagnosis, Catalepsy is the noted famed cause of "premature burials", because it mimicks rigor mortis.

Look, I'm sorry, but your claims are becoming increasingly bizarre. Do you honestly expect me to believe that your grandmother had meningitis (I'm assuming you mean bacterial meningitis) at 2 months of age in an era before the discovery of penicillin to the point of actual death and yet magically survived it because someone rubbed her chest and gave her a shot of alcohol? And you want me to believe that she had not only narcolepsy but all other sleep disorders? And she had epilepsy, but not just epilepsy -- some special kind that no one has ever heard of before that was set off by cataplexy? And catalepsy -- which in epilepsy is extraordinarily rare (I've seen a total of one case) but is not all that uncommon in folks with mental illness?

And that this all ties into ATP metabolism -- because alcohol is created by, but does not affect the body by an anaerobic process -- and the pineal gland?

I was hoping that you were learning something from this exercise, but I'm afraid I've had enough now.

Good luck to you.




If anyone is reading this, no one has ever, to my knowledge, ever been accused of being dead as a result of catalepsy or cataplexy. That is just complete and utter bunk. Generally the presence of a heart beat and blood pressure keep most people out of the morgue, but who am I to question?