When eyes move back and forth the fluid pressure inside changes ...

[Guest guest]

This is not as difficult to understand as it may sound...The pressure

of the fluid inside the eye increases and decreases as the eye moves

back and forth during involuntary rapid eye movement. The fact that

the eye is not perfectly round but somewhat oblong helps to

accentuate the pressure changes in the eye during involuntary RAPID

eye movement. The internal pressure change can be graphed as a

regular sine wave increasing and decreasing regularly as the eyes

change from moving left to right and back again. The pressure change

is greatest shortly after the eye reaches it's limitation of movement

in one direction and begins it's movement in the opposite direction.

This also the approximate point when the eye movement reaches it's

greatest accelleration or torque. If the movement was not rapid or

the eye was perfectly round inside, then the pressure variance would

be minimal. During normal night dreaming, the idea that the eyes are

trying to follow an object in a dream is very probably a

misconception. It is more likely that the movement of the eyes

during normal dreaming physically facilitates visual perception by a

physical mechanism which " triggers " the proven tuning ability of the

rhodopsin " trans " isomer to " clarify " the constant signal between the

eyes and the brain. This signal (tuned or untuned) is constant 24

hours a day in all humans even in complete darkness or while sleeping

but not dreaming. When the signal is " tuned " the person perceives a

sensation of vision (whether true vision or dream/hallucination). A

single photon of light is known (under specific threshold conditions)

to be able to trigger this " tuning " mechanism in the normal human

vision process. It is becoming understood that MOST vision experts

have the same basic misunderstandings about the visual receptors and

their functioning as well as how light interacts (on a quantum

defined level) within the eye. See the following weblink to

understand what early vision researchers learned (in part) but which

most eye experts today do not understand.

http://www.ghuth.com

> >

> > RESULTS: Seven (8.86%) of the 79 paroxetine-

> > treated patients developed mania.

> >

> >

> > Induction of mania in depression by paroxetine.

> >

> > Morishita S, Arita S.

> >

> > Department of Psychiatry, Kawasaki Medical School, Kurashiki,

> > Okayama, Japan. morisita@

> >

> > INTRODUCTION: An investigation of the proportion of patients who

> > have experienced mania with antidepressant treatment and their

> > characteristics would seem to be of clinical use. AIMS: The

purpose

> > of this clinical study was to examine the predictors of induction

of

> > mania in depression patients as a result of paroxetine treatment.

> > METHOD: A retrospective cohort analysis was carried out among

> > depression patients treated in the Department of Psychiatry,

> > Kawasaki Medical School Hospital, Kurashiki, Japan, in 2000 and

> > 2001. Some 79 patients were identified who were receiving

paroxetine

> > to treat depression. A variety of clinical factors including

gender,

> > the type of depression, frequency of episodes, family history, age

> > and daily dose were examined as possible predictors of induction

of

> > mania by paroxetine. RESULTS: Seven (8.86%) of the 79 paroxetine-

> > treated patients developed mania. A proportional hazards

> > analysis showed the type of depression and the history of family

> > psychiatric illness to be independent predictive factors of the

> > induction of mania by paroxetine treatment. CONCLUSIONS: The rate

of

> > mania induction of paroxetine is not substantially different from

> > that found for conventional antidepressants. The type of

depression

> > and the history of family psychiatric illness may be considered as

> > predictors of mania induction in depression patients taking

> > paroxetine treatment. Copyright 2003 Wiley & Sons, Ltd.

> >

> > PMID: 14533140 [PubMed - indexed for MEDLINE]

> >

> > ------------------------------------------------------------------

---

> > -----------

> >

>

[Guest guest]

This is not as difficult to understand as it may sound...The pressure

of the fluid inside the eye increases and decreases as the eye moves

back and forth during involuntary rapid eye movement. The fact that

the eye is not perfectly round but somewhat oblong helps to

accentuate the pressure changes in the eye during involuntary RAPID

eye movement. The internal pressure change can be graphed as a

regular sine wave increasing and decreasing regularly as the eyes

change from moving left to right and back again. The pressure change

is greatest shortly after the eye reaches it's limitation of movement

in one direction and begins it's movement in the opposite direction.

This also the approximate point when the eye movement reaches it's

greatest accelleration or torque. If the movement was not rapid or

the eye was perfectly round inside, then the pressure variance would

be minimal. During normal night dreaming, the idea that the eyes are

trying to follow an object in a dream is very probably a

misconception. It is more likely that the movement of the eyes

during normal dreaming physically facilitates visual perception by a

physical mechanism which " triggers " the proven tuning ability of the

rhodopsin " trans " isomer to " clarify " the constant signal between the

eyes and the brain. This signal (tuned or untuned) is constant 24

hours a day in all humans even in complete darkness or while sleeping

but not dreaming. When the signal is " tuned " the person perceives a

sensation of vision (whether true vision or dream/hallucination). A

single photon of light is known (under specific threshold conditions)

to be able to trigger this " tuning " mechanism in the normal human

vision process. It is becoming understood that MOST vision experts

have the same basic misunderstandings about the visual receptors and

their functioning as well as how light interacts (on a quantum

defined level) within the eye. See the following weblink to

understand what early vision researchers learned (in part) but which

most eye experts today do not understand.

http://www.ghuth.com

> >

> > RESULTS: Seven (8.86%) of the 79 paroxetine-

> > treated patients developed mania.

> >

> >

> > Induction of mania in depression by paroxetine.

> >

> > Morishita S, Arita S.

> >

> > Department of Psychiatry, Kawasaki Medical School, Kurashiki,

> > Okayama, Japan. morisita@

> >

> > INTRODUCTION: An investigation of the proportion of patients who

> > have experienced mania with antidepressant treatment and their

> > characteristics would seem to be of clinical use. AIMS: The

purpose

> > of this clinical study was to examine the predictors of induction

of

> > mania in depression patients as a result of paroxetine treatment.

> > METHOD: A retrospective cohort analysis was carried out among

> > depression patients treated in the Department of Psychiatry,

> > Kawasaki Medical School Hospital, Kurashiki, Japan, in 2000 and

> > 2001. Some 79 patients were identified who were receiving

paroxetine

> > to treat depression. A variety of clinical factors including

gender,

> > the type of depression, frequency of episodes, family history, age

> > and daily dose were examined as possible predictors of induction

of

> > mania by paroxetine. RESULTS: Seven (8.86%) of the 79 paroxetine-

> > treated patients developed mania. A proportional hazards

> > analysis showed the type of depression and the history of family

> > psychiatric illness to be independent predictive factors of the

> > induction of mania by paroxetine treatment. CONCLUSIONS: The rate

of

> > mania induction of paroxetine is not substantially different from

> > that found for conventional antidepressants. The type of

depression

> > and the history of family psychiatric illness may be considered as

> > predictors of mania induction in depression patients taking

> > paroxetine treatment. Copyright 2003 Wiley & Sons, Ltd.

> >

> > PMID: 14533140 [PubMed - indexed for MEDLINE]

> >

> > ------------------------------------------------------------------

---

> > -----------

> >

>

[Guest guest]

This is not as difficult to understand as it may sound...The pressure

of the fluid inside the eye increases and decreases as the eye moves

back and forth during involuntary rapid eye movement. The fact that

the eye is not perfectly round but somewhat oblong helps to

accentuate the pressure changes in the eye during involuntary RAPID

eye movement. The internal pressure change can be graphed as a

regular sine wave increasing and decreasing regularly as the eyes

change from moving left to right and back again. The pressure change

is greatest shortly after the eye reaches it's limitation of movement

in one direction and begins it's movement in the opposite direction.

This also the approximate point when the eye movement reaches it's

greatest accelleration or torque. If the movement was not rapid or

the eye was perfectly round inside, then the pressure variance would

be minimal. During normal night dreaming, the idea that the eyes are

trying to follow an object in a dream is very probably a

misconception. It is more likely that the movement of the eyes

during normal dreaming physically facilitates visual perception by a

physical mechanism which " triggers " the proven tuning ability of the

rhodopsin " trans " isomer to " clarify " the constant signal between the

eyes and the brain. This signal (tuned or untuned) is constant 24

hours a day in all humans even in complete darkness or while sleeping

but not dreaming. When the signal is " tuned " the person perceives a

sensation of vision (whether true vision or dream/hallucination). A

single photon of light is known (under specific threshold conditions)

to be able to trigger this " tuning " mechanism in the normal human

vision process. It is becoming understood that MOST vision experts

have the same basic misunderstandings about the visual receptors and

their functioning as well as how light interacts (on a quantum

defined level) within the eye. See the following weblink to

understand what early vision researchers learned (in part) but which

most eye experts today do not understand.

http://www.ghuth.com

> >

> > RESULTS: Seven (8.86%) of the 79 paroxetine-

> > treated patients developed mania.

> >

> >

> > Induction of mania in depression by paroxetine.

> >

> > Morishita S, Arita S.

> >

> > Department of Psychiatry, Kawasaki Medical School, Kurashiki,

> > Okayama, Japan. morisita@

> >

> > INTRODUCTION: An investigation of the proportion of patients who

> > have experienced mania with antidepressant treatment and their

> > characteristics would seem to be of clinical use. AIMS: The

purpose

> > of this clinical study was to examine the predictors of induction

of

> > mania in depression patients as a result of paroxetine treatment.

> > METHOD: A retrospective cohort analysis was carried out among

> > depression patients treated in the Department of Psychiatry,

> > Kawasaki Medical School Hospital, Kurashiki, Japan, in 2000 and

> > 2001. Some 79 patients were identified who were receiving

paroxetine

> > to treat depression. A variety of clinical factors including

gender,

> > the type of depression, frequency of episodes, family history, age

> > and daily dose were examined as possible predictors of induction

of

> > mania by paroxetine. RESULTS: Seven (8.86%) of the 79 paroxetine-

> > treated patients developed mania. A proportional hazards

> > analysis showed the type of depression and the history of family

> > psychiatric illness to be independent predictive factors of the

> > induction of mania by paroxetine treatment. CONCLUSIONS: The rate

of

> > mania induction of paroxetine is not substantially different from

> > that found for conventional antidepressants. The type of

depression

> > and the history of family psychiatric illness may be considered as

> > predictors of mania induction in depression patients taking

> > paroxetine treatment. Copyright 2003 Wiley & Sons, Ltd.

> >

> > PMID: 14533140 [PubMed - indexed for MEDLINE]

> >

> > ------------------------------------------------------------------

---

> > -----------

> >

>

[Guest guest]

This is not as difficult to understand as it may sound...The pressure

of the fluid inside the eye increases and decreases as the eye moves

back and forth during involuntary rapid eye movement. The fact that

the eye is not perfectly round but somewhat oblong helps to

accentuate the pressure changes in the eye during involuntary RAPID

eye movement. The internal pressure change can be graphed as a

regular sine wave increasing and decreasing regularly as the eyes

change from moving left to right and back again. The pressure change

is greatest shortly after the eye reaches it's limitation of movement

in one direction and begins it's movement in the opposite direction.

This also the approximate point when the eye movement reaches it's

greatest accelleration or torque. If the movement was not rapid or

the eye was perfectly round inside, then the pressure variance would

be minimal. During normal night dreaming, the idea that the eyes are

trying to follow an object in a dream is very probably a

misconception. It is more likely that the movement of the eyes

during normal dreaming physically facilitates visual perception by a

physical mechanism which " triggers " the proven tuning ability of the

rhodopsin " trans " isomer to " clarify " the constant signal between the

eyes and the brain. This signal (tuned or untuned) is constant 24

hours a day in all humans even in complete darkness or while sleeping

but not dreaming. When the signal is " tuned " the person perceives a

sensation of vision (whether true vision or dream/hallucination). A

single photon of light is known (under specific threshold conditions)

to be able to trigger this " tuning " mechanism in the normal human

vision process. It is becoming understood that MOST vision experts

have the same basic misunderstandings about the visual receptors and

their functioning as well as how light interacts (on a quantum

defined level) within the eye. See the following weblink to

understand what early vision researchers learned (in part) but which

most eye experts today do not understand.

http://www.ghuth.com

> >

> > RESULTS: Seven (8.86%) of the 79 paroxetine-

> > treated patients developed mania.

> >

> >

> > Induction of mania in depression by paroxetine.

> >

> > Morishita S, Arita S.

> >

> > Department of Psychiatry, Kawasaki Medical School, Kurashiki,

> > Okayama, Japan. morisita@

> >

> > INTRODUCTION: An investigation of the proportion of patients who

> > have experienced mania with antidepressant treatment and their

> > characteristics would seem to be of clinical use. AIMS: The

purpose

> > of this clinical study was to examine the predictors of induction

of

> > mania in depression patients as a result of paroxetine treatment.

> > METHOD: A retrospective cohort analysis was carried out among

> > depression patients treated in the Department of Psychiatry,

> > Kawasaki Medical School Hospital, Kurashiki, Japan, in 2000 and

> > 2001. Some 79 patients were identified who were receiving

paroxetine

> > to treat depression. A variety of clinical factors including

gender,

> > the type of depression, frequency of episodes, family history, age

> > and daily dose were examined as possible predictors of induction

of

> > mania by paroxetine. RESULTS: Seven (8.86%) of the 79 paroxetine-

> > treated patients developed mania. A proportional hazards

> > analysis showed the type of depression and the history of family

> > psychiatric illness to be independent predictive factors of the

> > induction of mania by paroxetine treatment. CONCLUSIONS: The rate

of

> > mania induction of paroxetine is not substantially different from

> > that found for conventional antidepressants. The type of

depression

> > and the history of family psychiatric illness may be considered as

> > predictors of mania induction in depression patients taking

> > paroxetine treatment. Copyright 2003 Wiley & Sons, Ltd.

> >

> > PMID: 14533140 [PubMed - indexed for MEDLINE]

> >

> > ------------------------------------------------------------------

---

> > -----------

> >

>

[Guest guest]

I think the issue here, and I think it's what you're saying, is that

people on SSRIs are suffering with sleep deprivation because, althouth

they may be getting the usual 8 or so hours/night, the amount of

recuperative REM sleep is being minimized (for supposed 'therapeutic'

reasons) to abnormal levels. The net result is people walking around

on SSRIs who are sleep deprived and suffering all the negative symptoms

from this ie. day dreaming, or altered conscious states. Of course

they themselves do not understand that they are sleep deprived given

that they 'sleep' the same hours as everyone else.

[Guest guest]

I think the issue here, and I think it's what you're saying, is that

people on SSRIs are suffering with sleep deprivation because, althouth

they may be getting the usual 8 or so hours/night, the amount of

recuperative REM sleep is being minimized (for supposed 'therapeutic'

reasons) to abnormal levels. The net result is people walking around

on SSRIs who are sleep deprived and suffering all the negative symptoms

from this ie. day dreaming, or altered conscious states. Of course

they themselves do not understand that they are sleep deprived given

that they 'sleep' the same hours as everyone else.

[Guest guest]

I think the issue here, and I think it's what you're saying, is that

people on SSRIs are suffering with sleep deprivation because, althouth

they may be getting the usual 8 or so hours/night, the amount of

recuperative REM sleep is being minimized (for supposed 'therapeutic'

reasons) to abnormal levels. The net result is people walking around

on SSRIs who are sleep deprived and suffering all the negative symptoms

from this ie. day dreaming, or altered conscious states. Of course

they themselves do not understand that they are sleep deprived given

that they 'sleep' the same hours as everyone else.

[Guest guest]

I think the issue here, and I think it's what you're saying, is that

people on SSRIs are suffering with sleep deprivation because, althouth

they may be getting the usual 8 or so hours/night, the amount of

recuperative REM sleep is being minimized (for supposed 'therapeutic'

reasons) to abnormal levels. The net result is people walking around

on SSRIs who are sleep deprived and suffering all the negative symptoms

from this ie. day dreaming, or altered conscious states. Of course

they themselves do not understand that they are sleep deprived given

that they 'sleep' the same hours as everyone else.

[Guest guest]

SSRIs cause nightmares, inside nightmares ,

and I found myself in many per night .

REM sleep , is deeper than the shallow

nightmare dream state of SSRI drugs .

There is no real rest on SSRI drugs .

Honestly, I woke up screaming out of nightmares

for years , in cold or hot sweats , soaking my bed.

Trying to get out of the nightmare world

on SSRIs is very dificult , because one is followed

by antoher and another , till finally its a great

struggle to wake out of them all.

Recovery time in the morning is , sometimes an hour .

The user has to put the alphabet , and at least

a hundred numbers back in their thoughts.

This is in case psychiatry questions them on these

matters to see if they can count backwards from

100 subtracting 9 each time.

Same with alphabet questions.

Psych knows all about this , they know exactly

what SSRIs do, and they push different drugs for

different answers given for their questions .

If we are harassed , during this period of time

our ability to use the alphabet, or numbers is

diminished to make us look retarded .

Its part of the SSRI maiming and labeling

process mark , used to identify the users .

I can see a user of SSRI drugs a mile off .

Its a slight vibration shake , for those who

use small amounts , and a totally un natural

movement from the ones using heavy amounts .

I can also tell the difference between an

SSRI user and a nuroleptic user .

The vocal patterns are also different .

These drug users are in all walks of common life .

The police discount witness, from

the users

of psych meds . A user of SSRI drugs can exempt themselves

from jury duty on grounds of SSRI use .

Supposed mental labels also can be used to exempt .

The same for hospital workers .

We are discounted/exempt ,

and our information is always questioned????

When withdrawing from psych meds , at the start,

the dox changed my 25 year diagnosis of assorted

schizophrenia , to manic , to push zoloft , and

resperidone .

These drugs caused a different nightmare .

I had been taking other SSRIs but not like these .

These are the homicidal pattern SSRIs .

I knew during this time I had to stop them at all costs .

or be engulfed in the nightmares themselves .

I dont care what a doctor says, sometimes , a

risk must be taken , or

something worse than the risk

will occur.

Its better to be made sick from W/D than to self destruct

or harm others .

Time is of the essence using SSRIs .

Eventually , violence or self destruction will erupt .

Its just a matter of time .

>

>

>

>

> I think the issue here, and I think it's what you're saying, is

that

> people on SSRIs are suffering with sleep deprivation because,

althouth

> they may be getting the usual 8 or so hours/night, the amount of

> recuperative REM sleep is being minimized (for

supposed 'therapeutic'

> reasons) to abnormal levels. The net result is people walking

around

> on SSRIs who are sleep deprived and suffering all the negative

symptoms

> from this ie. day dreaming, or altered conscious states. Of

course

> they themselves do not understand that they are sleep deprived

given

> that they 'sleep' the same hours as everyone else.

>

[Guest guest]

No wonder I was blind with blupherospazm and ocular

rigidity for four years .

The psychs lied about the nuroleptic being

the cause , so that is why they withdrew it

and doubled the SSRI drugs .

They knew all about it .

3 types of SSRIs at the same time.

Blinding me even worse .

Those sones of bits .........

I had what the dox called shombergers disease

on my lower legs , which

was really diabetic shingles all along .

Dam what mal practice Psychiatry is .

Totally and completely criminal

diabolical , delusional ,

and insane .

>

>

>

>

> I think the issue here, and I think it's what you're saying, is

that

> people on SSRIs are suffering with sleep deprivation because,

althouth

> they may be getting the usual 8 or so hours/night, the amount of

> recuperative REM sleep is being minimized (for

supposed 'therapeutic'

> reasons) to abnormal levels. The net result is people walking

around

> on SSRIs who are sleep deprived and suffering all the negative

symptoms

> from this ie. day dreaming, or altered conscious states. Of

course

> they themselves do not understand that they are sleep deprived

given

> that they 'sleep' the same hours as everyone else.

>

[Guest guest]

yes that's basically it but we should try to always make a distinction

between saying " sleep deprived " and " REM deprived " to limit confusion

in those who don't have our mutual understanding of the problem.

>

>

>

>

> I think the issue here, and I think it's what you're saying, is that

> people on SSRIs are suffering with sleep deprivation because,

althouth

> they may be getting the usual 8 or so hours/night, the amount of

> recuperative REM sleep is being minimized (for supposed 'therapeutic'

> reasons) to abnormal levels. The net result is people walking around

> on SSRIs who are sleep deprived and suffering all the negative

symptoms

> from this ie. day dreaming, or altered conscious states. Of course

> they themselves do not understand that they are sleep deprived given

> that they 'sleep' the same hours as everyone else.

>