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Lack of sleep, brain swelling?


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Hey guys! So I have a question. I work a retail job, and I work a lot of hours(I pulled off 78hours monday to friday this week[friday I only work 8am-2pm], and that's not the most I've done. so on avg mon-thurs is 18hours a day), and I don't get much sleep. I've worked a few 20hour days back to back before with maybe 45mins to an hour or so of sleep in between shifts if I was lucky. I've been doing this since September and I'm 20 years old.

 

 

Anyways, getting to the point, I recently had a work week week were nearing the end, my head felt like I had a tight hat on. Kind of like my head was swelling. Some friends have told me it has something to do with liquids to my brain or something like that and that it's dangerous. I wanted to know what you guys think of what may have happened. If it's truly dangerous I may stop these shifts. I've done my research and can't seem to find anything that explains what has happened.

 

Any feedback is greatly appreciated! Thanks!! (=

 

Edit** Also I forgot to mention, if this makes a difference, I don't eat as much as I should since I usually don't have time. But I do eat healthy.

 

Also, after I got some sleep, my head went back to normal. Though it happened again this week before I got sleep (though not as bad as the other time)

Edited by Davey101
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It's not likely that your brain actually swells, but a severe lack of sleep is going to affect a lot of things in your body... iNow already posted a good link in post #2. Read it.

 

You cannot go on like this forever, so you might as well try to solve it right now. Get some help, change the shifts, or change the opening hours.

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Self experience, lack of sleep kills the ability to concentrate and will put you in a bad mood, it will effect your health as well especially at the age of 20, it will have a lot of health problems result when you're older, try to get the sleep you deserve, or your situation is critical.

Edited by Nassar Jad
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Sleep deprivation is also going to change your blood pressure, both in the short and long term. I know I can feel my heard pounding pretty hard after nights of only a few hours of sleep. (Amusingly, I asked a physician friend of mine if this was normal once, he responded affirmatively, and I asked him about the mechanism. "We don't know why," he said. "It's sort of up there with not knowing why the hell we sleep to begin with.")

Edited by PhDwannabe
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I think you may be missing a deeper question, though. Why didn't we evolve in such a way that we conserve more energy and regenerate more efficiently while awake? It's clearly possible, but it didn't happen. Your argument amounts to, "we see this benefit while we sleep, and that's while we sleep," but that approach misses the real issue of, "why not those benefits while awake?"

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Below are comments I've posted in this and other forums regarding the nature of sleep:

 

"If some of us do not know why we sleep, it is because we haven't examined how sleep may have evolved among sleeping species. Nearly every species enters a state of rest that could be interpreted as sleep. This suggests a common evolutionary advantage to the sleep process among sleeping species; i.e., we would not have sleeping species if sleep did not offer some survival advantage to ancestral species.

 

When we examine the neurological components of sleep in most animals, we find that its various attributes arose at varying stages in neural evolution. Contemporary sleep processes in the human brain appear to be mediated by neurons in the lateral hypothalamus. Further down the brainstem, other components of the sleep process appear to suggest an earlier evolutionary incarnation of sleep.

 

During the earliy stages of sleep, the brain engages in diminishing activity until the onset of atonia, which is the lost of muscle elasticity. Interestingly, atonia can and does occur in animals without hypothalmic neural structure. This positions atonia as one of sleep's earliest incarnation because it appears to be mediated by neural structures earlier in the brain's evolution than that suggested by the hypothalamus.

 

If the brain evolved from some earlier form, we should be able to find some footprint of that form, which we can trace back to some earlier point. Most researchers agree that the brainstem is a primitive component of our central nervous system. Of the brainstems components, the spinal brain (myelencephalon) appears to be the most primitive segment because it most closely resemble the notochord development we find in existant species of primitive animal life.

 

When we examine the afferent neural systems of the spinal brain, we find those associated with feeding. This suggests that ancestral animals at this stage in brain evolution engaged behaviors requiring the intake of nutrients. Although the efferents neural paths of the spinal brain suggests movement at this stage in earlier ancestral animals, movement most likely evolved with the evolution of the metencephalon where we find more sophistocated afferent neural systems associated with sound detection. The ability to detect sound suggests ancestral animals at the stage where they were orienting themselves either away from or towards sensory stimuli.

 

Early spinal brained animals were probably not as mobile as later metencephlic animals. This suggested lack of mobility suggests that these animals had to adopt a stratergy that allowed for survival in the absences of readily available nutrients. In some archeological literature, it has been suggested that the earliest forms of complex life where a combination of plant and animal. During the prolonged absence of sunlight or nutrients in their primodial sea, immobile animals that could suspend their need for sustainance likely had a survival advantage over those that could not. During the atonic stage of sleep, we find a suspension of muscle readiness with energy devotion to organs more critical to our survival. Atonia appears to be mediated by the metencephalon/myelencephalon brainstem segments. In decerebration studies, test animals entered an atonic state while not being fed or otherwise stimulated for the duration of their survival. This suggests that the earliest components of sleep evolved likely as a means to sustain survival through periods of prolonged food privation.

 

Although food privation is not a severe concern for some of us, our modern brain rest upon a primitive foundation that was dependent on the periodic suspension of activity to conserve energy for more vital physiological systems. In our brain develpment, evolution built upon its successful systems rather than replace those systems. Sleep evolved from a vestigial need that has become integral to how our contemporary brain functions."

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interesting post drmdoc.. in response to that and regarding the article phdwannabe posted;

 

the brown bats only wake to feed, we sleep at night when light and prey arent available.

 

marine life might not follow circadian rhythms due to lack of light, allowing dolphins to feed at all hours resulting in their lack of prolonged inactivity.

 

is it possible that we only sacrifice efficient hours of rest to gain more energy in the end? if our window of time to do so was slimmer, would we sleep more hours?

 

maybe a better question isnt why do we sleep, but rather, why are we ever awake?

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interesting post drmdoc.. in response to that and regarding the article phdwannabe posted;

 

the brown bats only wake to feed, we sleep at night when light and prey arent available.

 

marine life might not follow circadian rhythms due to lack of light, allowing dolphins to feed at all hours resulting in their lack of prolonged inactivity.

 

is it possible that we only sacrifice efficient hours of rest to gain more energy in the end? if our window of time to do so was slimmer, would we sleep more hours?

 

maybe a better question isnt why do we sleep, but rather, why are we ever awake?

 

All forms of life require the intake of nutrients to survive. Maintaining the ability to actively seek and procure nutrients requires the expenditure of energy. Although prolonged dormancy may conserve energy through periods of privation, energy renewal and uptake remains essential to sustaining life. When animals adapt the ability to absorb a stable and steady supply of nutrients amid a inactive, dormant state, then the need for sleep could become unnecessary. However, I am not aware of any nutrient source or catalyst that is stable or steady. Even the sun is not such a source or catalyst because of the earths rotation.

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  • 3 weeks later...

Huh, I guess I'm more out of loop with the science community than I thought because I was sure that scientists had settled to agree that energy restoration and regeneration were but a small part to the reason behind sleep. Leaving the major reason to be that it is when our brain "teaches" our body or even itself what it learned since its last time of sleep. Hence the whole REM cycle to prevent us from moving and how a soccer player will typically dream of a soccer ball or my own unofficial theory of how those dreams where it feels like we are moving in slow motion is more of "systems check" than a odd dream where we're trying to escape a jack-a-lope...

But to get back to the topic of the OP, reiteration of get more sleep somehow (power-naps or even 12sec-5min states of serene breathing can do well to replace any lost hours of sleep (they just require extreme mental discipline)), do something about the swelling (neck rolls/rotations work supremely, even stretching down to the fingertips helps alleviate head pressure at times), and if it persists a physicians insight is always recommended. However, if meds and paying for common sense aren't ideal, remembering that head pressures are some irritation of either swelling or fluid build up in the meninges or interstitial spaces: you might wanna consider diet and exercise modifications (more running/jogs; less salts; half an extra helping of greens; and water through out the day).

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Huh, I guess I'm more out of loop with the science community than I thought because I was sure that scientists had settled to agree that energy restoration and regeneration were but a small part to the reason behind sleep. Leaving the major reason to be that it is when our brain "teaches" our body or even itself what it learned since its last time of sleep. Hence the whole REM cycle to prevent us from moving and how a soccer player will typically dream of a soccer ball or my own unofficial theory of how those dreams where it feels like we are moving in slow motion is more of "systems check" than a odd dream where we're trying to escape a jack-a-lope...

But to get back to the topic of the OP, reiteration of get more sleep somehow (power-naps or even 12sec-5min states of serene breathing can do well to replace any lost hours of sleep (they just require extreme mental discipline)), do something about the swelling (neck rolls/rotations work supremely, even stretching down to the fingertips helps alleviate head pressure at times), and if it persists a physicians insight is always recommended. However, if meds and paying for common sense aren't ideal, remembering that head pressures are some irritation of either swelling or fluid build up in the meninges or interstitial spaces: you might wanna consider diet and exercise modifications (more running/jogs; less salts; half an extra helping of greens; and water through out the day).

Actually, REM didn't evolve as a means to solidify memory (muscle or mental) or to prevent movement amid sleep. Although REM appears to benefit our mental acuity, atonia (essentially the loss of muscle readiness) likely evolved as means to sustain physical and neural systems more vital to survival among ancestral animals than muscle readiness amid their periods of inactivity or rest. Atonia isn't muscle paralysis amid REM as some seem to believe. We don't move amid REM or dream sleep because dreams are not true physical material experiences; i.e., they do not involve the actual physical experiences of true reality. The sleeping brain, for the most part, is able to distinguish that difference. Dreams don't generally generate the sensory experiences that activate our gross motor response systems. It is likely that the benefits of REM sleep arise from the cessation of muscle readiness, which allows for the production of Orixen-A a neuotransmitter shown to restore mental acuity amid REM deprivation studies.

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Actually, REM didn't evolve as a means to solidify memory (muscle or mental) or to prevent movement amid sleep. Although REM appears to benefit our mental acuity, atonia (essentially the loss of muscle readiness) likely evolved as means to sustain physical and neural systems more vital to survival among ancestral animals than muscle readiness amid their periods of inactivity or rest. Atonia isn't muscle paralysis amid REM as some seem to believe. We don't move amid REM or dream sleep because dreams are not true physical material experiences; i.e., they do not involve the actual physical experiences of true reality. The sleeping brain, for the most part, is able to distinguish that difference. Dreams don't generally generate the sensory experiences that activate our gross motor response systems. It is likely that the benefits of REM sleep arise from the cessation of muscle readiness, which allows for the production of Orixen-A a neuotransmitter shown to restore mental acuity amid REM deprivation studies.

 

Out of curiosity, might I ask for a link to your references? I think we're a few pages off from being homeostatic with eachother as Atonia is symptom commonly called full body paralysis and is an effect of the body transitioning into a REM state ( http://www.medterms.com/script/main/art.asp?articlekey=9811 ). A state that as I said before was an essential factor of dreaming the dreams that restore and reiterate us and our experiences ( http://sleep.health.am/sleep/REM-sleep/ ). Orixen-A itself is dually a sleep cycle control hormone or an energy booster of sorts when in lack there of ( http://www.sciencedaily.com/releases/2008/01/080102093936.htm ).

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Out of curiosity, might I ask for a link to your references? I think we're a few pages off from being homeostatic with eachother as Atonia is symptom commonly called full body paralysis and is an effect of the body transitioning into a REM state ( http://www.medterms....articlekey=9811 ). A state that as I said before was an essential factor of dreaming the dreams that restore and reiterate us and our experiences ( http://sleep.health....leep/REM-sleep/ ). Orixen-A itself is dually a sleep cycle control hormone or an energy booster of sorts when in lack there of ( http://www.scienceda...80102093936.htm ).

I've made a personal study of dreams and the dreaming brain for over three decades and have written a couple of books on the subject. In that time, I've notice how little some researchers understand about their own research. Focusing on a specific idea or area of study without a proper foundation has likely limited their ability to fully comprehend what their findings actually suggests. The proper foundation for understanding the components of sleep or any component of brain function begins with brain evolution and where in that evolution did those components first likely appear. If we can prove that atonia evolved independent of REM and that REM can arise independent of atonia, then it is highly likely that atonia did not evolve to serve the REM state.

 

First, atonia defines the loss or lack of muscle tone or elasticity rather than muscle paralysis, as is the standard medical definition, which is indeed a condition opposite the ready and responsive state of muscle tonal posture. Therefore, atonia also describes a loss or lack of muscle readiness. Atonia is mediated by the peri-locus ceruleus, which is located in that part of our central nervous system that does not generate the low-amplitude, high-frequency EEG waves associated with REM (http://sleep.health....leep/REM-sleep/). The locus ceruleus is situated in the metencephalic segment of brainstem, which envelopes neural functions considered less recent in our contemporary brain development than those brain structures (neocortex) where dream generation is thought to occur. Therefore, the neural components of sleep that generate atonia likely developed or evolved in what would become our neurostructure before that structure was capable of generating dreams. This suggest that atonia evolved for some reason other than the inhibition of movement amid dreaming. Animal studies have shown that "...subceruleus lesions created REM sleep without atonia." Therefore, atonia is not essential to the production of REM. The position of the structure believed to mediate atonia in the pimitive segment of brainstem coupled with the creation of REM sleep without atonia suggest that atonia likely did not evolve to serve the REM state.

 

Regarding http://www.scienceda...80102093936.htm, if you'll read the article, orexin-A is indeed described as a peptide that is produced by a "small mumber of neurons".The article goes on to say that orexin-A effectiveness is cognitive related rather than energy boosting. The article states that this peptide "has no effect on performance if the animals where not sleep deprived." Rather than fueling or boosting the energy level of test animals, this article suggest that the orexin peptide merely establishes normal acuity or cognitive efficiency in brain function, which is unlike the boosting effects of energizers such as glucose or anphetimines.

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...the neural components of sleep that generate atonia likely developed or evolved in what would become our neurostructure before that structure was capable of generating dreams. This suggest that atonia evolved for some reason other than the inhibition of movement amid dreaming. Animal studies have shown that "...subceruleus lesions created REM sleep without atonia." Therefore, atonia is not essential to the production of REM. The position...

In my haste, I did not include these reference, http://www.ncbi.nlm..../pubmed/1611494 and Absence of shivering in the cat during paradoxical sleep without atonia, for that quote. Please pardon my oversight. Also, low-decerebrate studies have shown that test animals experience atonia when not being fed or otherwise stimulated for the duration of their survival period (Proposed model of postural atonia in a decerebrate cat). This suggests the evolutionary root and association of atonia, which is mediated by neurons in one of the most primitive segments of our central nervous system, with metabolic mediation amid periods of privation and inactivity.

Edited by DrmDoc
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