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04-17-2007, 01:35 PM #3841
Aunty....I'm right there with you about the Virginia shooter. He probably either started or stopped an SSRI. I just heard that he was known to be a reserved person with no history of violence. They also said he was acting strange over the past few weeks. The lack of understanding and awareness about these drugs is so frustrating!
ElizabethMaria: I really feel for you. This withdrawal seems like it never ends! You get a better day or two and think your on the up and up and then you get pushed right back down again. At 6.5 months I def have seen improvement, but some of my symptoms just won't leave. It's so hard to not get discouraged. I sort of posted that Paxil story for you because that woman had constant seizures from withdrawal and she came out OK. You will, too!
04-17-2007, 02:04 PM #3842
Thank you for your support and advice. I thought I was doing it the right way! Silly me...
Since I cannot afford to go to doc, I will definitely try the supplements. Every day seems worse than the day before and it is really exhausting. The headaches have turned into migranes, and although I am constantly exhausted, I fear sleep because of the nightmares. It is soooooo depressing, but I have a teenage son that I am solely responsible for, so I must push on and do what I have to do. I know that I must do the outside-of-the-house things in the morning, because I feel worse and worse as the day goes on. I began taking Lex in order to feel "normal", and now I long for the pre-Lex days!
04-17-2007, 04:26 PM #3843
Hi guys. Get this my boyfriend said he will ween off! I don't believe it, but we will see. He has been cutting pills in half and for the last 2 days and says he feels fine....He said he doesn't anticipate any effects. Hum...... I find that hard to believe! Is that possible??? Cuz I know all you guys are def. having a difficult time. My heart goes out to all of you. Every time I go on here, my heart just sinks and feels so bad that you all have to go through this with these meds. (((((hugs))))))
I am wondering why the change???? I think maybe the gun thing, scared him? Thank the Lord I have it! I plan on taking it to the Police dept. tomorrow to just get rid of! Scary!!! I am a total believer that no one should have access to guns except the police!What ever happened to bow and arrow??
04-17-2007, 04:26 PM #3844
Need some good advice
Hi, I have been reading all the postings over several hours today and decided that I should share my story and see if someone can help me with some good advice.
I started taking Lexapro (10mg) almost 1 year ago, in December I noticed that the drug was losing it's effectiveness and had my dosage increased to 20mg. I was so naive in thinking that this wasn't doing some sort of harm to my body. Over the course of the last few months I have became very curious and concerned about what I put into my body. I have had several problems with my health and am so quick to make a doc appt. and receive yet more prescription meds. Well, I decided I wanted to quick taking my Lexapro and I discovered the hard way a few months ago that it's not an easy road. Of course my doctor never made me aware of that when she wrote the prescription. I ended up forgetting to take it and thought that I was losing my mind and went back on it. Well, now that I am more educated I decided that I would go "cold turkey". It's been 2 weeks today and I'm worse than ever. At first I thought it was going fine, but now I am agitated, irritable, tired and just feel miserable. Not to mention back pain and weird feelings in my head that I can only describe as dizziness, but not really. It's bizarre. Anyway I am getting concerned and was thinking maybe I should resume taking it and then taper off. Has anyone ever tried that after being off it for 2 weeks?
Please help! I'm afraid of what I am becoming. I can't believe that I have to deal with this...I can't believe that the FDA approves drugs like this.
04-17-2007, 08:41 PM #3845
Wow! It’s nice to see new “faces”. Sorry you all are having problems with our good friend (ha) Lexapro, but glad you found this forum. It has helped preserve my sanity.
Elizabethmarie Aw, bless your heart. this is unreal. But remember how you have had some better days-these are going to start getting more and more with the bad days becoming a rarity. It is just rough waiting for time to pass for your body to heal. It will heal though. Just keep thinking “One day closer”. You are going to get there. I pray for all you guys, but am adding extras up.
Angie R 65 I thought for a minute that I had developed another personality and was posting under a name! These are the bits that were me “However, I could no longer tolerate what Lexapro had turned me into: a fat, apathetic slug with no interest in sex or anything else, for that matter. My mental "edge" and sharpness were gone. I felt like I was perceiving and feeling everything through a thick blanket...everything felt very dulled. True, I no longer had anxiety, but that was because I simply didn't care about much of anything” and “not caring if my checkbook was overdrawn, having no ambition and not caring if my house was a mess and laundry piled up.” I was only on 10 mgs and have weaned off in the space of 21/2 months. This is really too fast and I may have side effects later on, but for now (2 weeks without) I am ok. PLEASE read the posts on this forum. I know not everyone will have issues, but enough do that you may want to resume at least part of your dose and taper down, especially if the effects get really bad. Oh, I am a new person. I felt the change with each increased taper. I know I am going to face some of the same issues but am going to try and deal with it naturally. Also want to warn you about what got me BACK on Lexapro after I stopped-rebound depression. It sneaks up on you several months AFTER you are off the Lexapro and is worse than any I have ever had-which says a lot.
sctschk Sorry to hear about your Excedrin experience. It is so tempting to do the no-no’s isn’t it? I drank soda last week and felt like h--- for two days afterwards. I have been naughty and taken Aleve but so far ok. I avoid my Excedrin because of the caffeine. I hate to say it, but not only are you going to have to let it get out of your system, you may feel a bit of the effects afterwards if it is anything like what soda did to me. I always did have to find out things for myself though. NOT a good trait sometimes, but I just can’t help it-ha.
spatzkey, Hey! That is good news. I have always believed that not everyone has problems with lexapro either while taking it or withdrawing from it. So maybe he is one of the fortunate ones. Just a warning, the withdrawal symptoms don’t kick in until about a week. So, to be cautious, remember all the things we’ve mentioned. I hope this is the end of your Lexapro experience, but please post and let us know how it turns out. I am interested if he will in fact not have any symptoms (ha-just so I can be jealous).
jesyka NOW you are on the right track. There is no reason to torture yourself through the “cold turkeys”. Go back on the dose you were taking before and do a SLOOOOOOW taper. There are several wonderful posts on here regarding how to convert the pill to liquid form and then what percentage to decrease each time you taper. It is a slow process but is best.
Sorry for the long post. Am trying to do better but keep writing a book.
04-17-2007, 10:45 PM #3846
You can reinstate and then start tapering off within six weeks of stopping lexapro..........after being off lexapro for six weeks reinstating will not fix the withdrawal symtoms.
Reinstate you dose and once you stabalize reduce by 5% of your dose and stay on that dose for about two to three weeks until you stabalize.
The Va gunman was on SSRI antidepressants.....not sure yet which one.
As all of you would have expected . . . it would not be long before we found
out what the shooter was taking. And it has just been released by the media
that he was taking antidepressants and having serious reactions to them that
we are used to seeing like starting a fire in his dorm, a long rambling
letter describing grievances - a particular dislike for the rich. We already had
several clues of antidepressant- induced automatic behaviors such as REM Sleep
Disorder: the time of day being early morning for this incident and the calm
demeanor of the shooter. We also have the antidepressant- induced manic
behaviors: fire starting, violent and aberrant behavior & rambling letters of
complaints. We have antidepressant- induced Autisic behaviors of not socializing,
being a loner. Stalking. False allegations of abuse. Too many things were
beginning to add up especially for all of us who are aware of these reactions
that I document in my book.
Mark Taylor and his mother Donna have been here visiting with me for the
past couple of weeks. So, we did local media interviews yesterday on the VA Tech
shootings. The possible antidepressant connection was mentioned in every
interview. I have included them for you below. Feel free to share them with your
local media. And we are certainly available for more interviews.
You will also find
Ann Blake Tracy, Ph.D.,
Executive Director, International Coalition For Drug Awareness
Website: _www.drugawareness. org_ (http://www.drugawar eness.org/)
Author: Prozac: Panacea or Pandora? - Our Serotonin Nightmare
& CD or audio tape on safe withdrawal: "Help! I Can't Get
Off My Antidepressant! "
Order Number: 800-280-0730
E-mail: _atracyphd1@ aol.com_ (mailto:atracyphd1@aol. com)
_http://www.woi- tv.com/global/ video/popup/ pop_player. asp?ClipID1= 1370419&h1= Co
lumbine%20Survivor% 20Remembers% 20Shooting& vt1=v&at1= News&d1=121100& LaunchPageA
dTag=Homepage& activePane= info&playerVersi on=1&hostPageUrl =http%3A/ /www.woi- tv.
(http://www.woi- tv.com/global/ video/popup/ pop_player. asp?ClipID1= 1370419&h1= Columbine% 20Survivor% 20Remembers% 20Shooting& vt1=v&at1= News&d1
=121100&LaunchPageA dTag=Homepage& activePane= info&playerVersi on=1&hostPageUrl =h
ttp://www.woi- tv.com/&rnd= 53248238)
_http://www.kcci. com/news/ 12201556/ detail.html_
(http://www.kcci. com/news/ 12201556/ detail.html)
_http://www.whotv. com/Global/ category. asp?C=5533& nav=menu100_ 1_
(http://www.whotv. com/Global/ category. asp?C=5533& nav=menu100_ 1)
The suspected gunman in the Virginia Tech shooting rampage, Cho Seung-Hui,
was a troubled 23-year-old senior from South Korea who investigators believe
left an invective-filled note in his dorm room, sources say.
The note included a rambling list of grievances, according to sources. They
said Cho also died with the words "Ismail Ax" in red ink on the inside of one
of his arms.
Cho had shown recent signs of violent, aberrant behavior, according to an
investigative source, including setting a fire in a dorm room and allegedly
stalking some women.
A note believed to have been written by Cho was found in his dorm room that
railed against "rich kids," "debauchery" and "deceitful charlatans" on campus.
"Investigators believe Cho at some point had been taking medication for
depression. They are examining Cho's computer for more evidence."
_http://www.newsday. com/news/ nationworld/ nation/chi- 070417vtech- shootings, 0,48
(http://www.newsday. com/news/ nationworld/ nation/chi- 070417vtech- shootings, 0,4843160. story) BLACKSBURG, Va. -- The suspected gunman in the Virginia Tech
shooting rampage, Cho Seung-Hui, was a troubled 23-year-old senior from South
Korea who investigators believe left an invective-filled note in his dorm
room, sources say.
The note included a rambling list of grievances, according to sources. They
said Cho also died with the words "Ismail Ax" in red ink on the inside of one
of his arms.
Cho had shown recent signs of violent, aberrant behavior, according to an
investigative source, including setting a fire in a dorm room and allegedly
stalking some women.
A note believed to have been written by Cho was found in his dorm room that
railed against "rich kids," "debauchery" and "deceitful charlatans" on campus.
The English major from Centreville, Va., a rapidly growing suburb of
Washington, D.C., came to the United States in 1992, an investigative source said.
He was a legal permanent resident.
His family runs a dry cleaning business and he has a sister who graduated
from Princeton University, according to the source.
Investigators believe Cho at some point had been taking medication for
depression. They are examining Cho's computer for more evidence.
The gunman's family lived in an off-white, two-story town house in
"He was very quiet, always by himself," neighbor Abdul Shash said of the
gunman. Shash said the gunman spent a lot of his free time playing basketball,
and wouldn't respond if someone greeted him. He described the family as quiet.
Marshall Main, who lives across the street, said the family had lived in the
townhouse for several years.
According to court records, Virginia Tech Police issued a speeding ticket to
Cho on April 7 for going 44 mph in a 25 mph zone, and he had a court date
set for May 23.
Cho was found among the 31 dead found in an engineering hall. Police said
the victims laid over four classrooms and a stairwell.
"He was a loner," said Larry Hincker, a university spokesman, who added that
investigators are having some difficulty unearthing information about him.
A law enforcement official, speaking on condition of anonymity because the
information had not been announced, said Cho was carrying a backpack that
contained receipts for a March purchase of a Glock 9 mm pistol.
Ballistics tests by the federal Bureau of Alcohol, Tobacco and Firearms
showed that one gun was used in Monday's two separate campus attacks that were
two hours apart.
As a permanent legal resident of the United States, Cho was eligible to buy
a handgun unless he had been convicted of any felony criminal charges, a
federal immigration official said.
Police said Cho killed 30 people in a Virginia Tech engineering building
Monday morning and then killed himself.
Another two students were shot to death two hours earlier in a dorm room on
the opposite side of the university's sprawling 2,600-acre campus, bringing
the day's death toll to 33.
Students at Harper Hall, the campus dormitory where Cho lived, said they had
little interaction with him and no insight into what might have motivated
Timothy Johnson, a student from Annandale, Va., said people would say hello
to Cho in passing, but nobody knew him well.
************ ********* ********* ******** See what's free at http://www.aol. com.
04-17-2007, 10:45 PM #3847
Hi Jesyka, (that's a pretty name..)
Yes, taper is the only way, or you'll be in a place you never want to go again! -- I can't write much write now, but I think you are still in the time frame where you can go back on the Lex and slow taper, that is the BEST way to avoid the MOST Worst withdrawals... need to let your receptors rebuild and brain adjust, otherwise is too hard.. You can even end up in the hospital, and beyond by quitting cold turkey like that - your brain is in an altered state - meaning the receptors and nerve connections are changed, and they have to readjust to lowered dosages. Some people have trouble even walking, after going cold turkey.. so glad you found this here -- someone can help you plan the taper as well, I'm sorry I can't at this time... Sarita??? are you there? Aunty? what's best for her?? Hairyarmadillo?
take good care of yourself... this is a hard time for us all..
04-17-2007, 10:47 PM #3848
Aunty, did you read my last post with the seizure questions?? I think it's on the previous page... is that something common? haven't read any others with that...
thank you for more articles!
04-17-2007, 11:06 PM #3849
What I think you are experiecing is that you are not getting REM sleep and your body is going into a dream like state while awake. This is very common. Dr Anne Blake Tracy talks about it a lot in her book i great detail.
If your insurance will pay can you get a Sleep Study done.....................when one is in deep resorative REM sleep and one dreams the body is paralazed so that one cannot act out their dreams and get hurt. In the REM like wakesleep the body goes into a sleep pattern while awake and one can act out and sometimes have no recall of what actaually happened or have trouble telling whta is real and what is a dream. I think this may be what you are experiencing.
DO NOT COLD TURKEY off of 30 Mg of lexapro. You will have serious effects for years to come that may never go away. Your brain's neurotransmitters have been altered by the lexapro and only slow tapering will enable them to get back to functioning close to normal without the reuptake of the serotonin. You can reinstate the lexapro within six weeks of stopping. The depersonalization will be severe within the next several weeks from cold turkeying, nightmares, stomach cramps, flu like symptoms, brain zaps, crying, sweating...........it is not worth it.....................please reconsider. There are others that would give a million dollars to have the chance of reinstating the lexapro that cold turkeyed but too much time has passed.
04-17-2007, 11:11 PM #3850
When the Brain Disrupts the Night
By ERICA GOODE
The original title I chose for my book Prozac: Panacea or Pandora? was Our Serotonin Sleepwalk Nightmare. At the time of the first edition (1994) everyone argued that no one would know enough about serotonin to understand that the book was about antidepressants so we went ahead with the name of the most popular of the SSRIs - Prozac.
Now for those of you who have read my book or heard me lecture you are aware of the reason for the title I chose - my focus on the most serious of the side effects of SSRIs - the REM Sleep Behavior Disorder (RBD). The largest chapter of my book is devoted to this disorder which I consider the most dangerous of all the reactions to an SSRI. I firmly believe that RBD is the reason for much of the violence we see with the serotonergic antidepressants and the serotonergic antipsychotics as well as Fen-Phen and Redux which are also serotonergic.
To help those who have not read my book and are not familiar with RBD let me quote one statement from an article (below) that ran in the New York Times last month: “REM behavior disorder [RBD] is the only parasomnia routinely associated with violence. But sleepwalkers have also been known to stab their relatives, molest children or confidently stride out of third-story windows, in states varying from confused wakefulness to partial arousal to the deepest stages of non-REM or slow-wave sleep.”
Even though no one else has focused on this disorder as I have for so long and worked so hard to get the public to see that these drugs are causing the REM Sleep Behavior Disorder, the following information shocked even me! In fact I am still trying to catch my breath because the original medical article is even more shocking than this NY Times article.
Let me first give you a little background before you read the article. In 1991 I made a call to Dr. Carlos Schenk, the author of this study. I told him that I was concerned at how much evidence there was that Prozac (the only SSRI on the American market at the time) was causing the REM Sleep Behavior Disorder. I told him what patients on these drugs were reporting that would show they were experiencing this as a side effect.
He listened intently and then told me that there was not any research to back up my conclusion.
I told him that was okay, but that I had ABSOLUTELY NO DOUBT that Prozac was triggering this most dangerous sleepwalk state and that someone had better do the research because this was something that had the potential of affecting many people worldwide.
Dr. Schenk never called me back to let me know that he immediately began doing that research. He went back through the records at the Minnesota Regional Sleep Disorders Center in Minneapolis where he and his research partner Dr. Mark Mahowold are known as the leading researchers in America on this disorder. Amazingly he found in going through the records for the past 41 months that an astounding 48.8% of all those who had come through the clinic and been diagnosed as suffering from RBD were on Prozac!
If that information was not shocking enough as the information reached the doctors, who then began to watch for this connection, rather than having to go back through old records to see if there might be someone on Prozac who had this disorder, found that 80% of those with the signs of RBD were on Prozac!!! And on top of that the symptoms of this disorder continued in one patient for 19 months AFTER coming off only short term use of Prozac!! Severe sleep disturbance continued for months after coming off the drug. Which is why I mention the importance of using so many natural alternatives to rebuild after being on these drugs.
Of the significance of this information the author of the NY Times article states, “No one yet knows how common such side effect are, or their implications — if any.”
I would gladly tell them how common this side effect is and how far reaching the implications are!!!! That is what I have been trying to tell them for over a decade! Phil and Brynn Hartman would LOVE to explain to them the implications of SSRI induced RBD if they only could, as would thousands of others who have lost their lives to this side effect.
As I say in nearly every lecture I give, “What could be more terrible than to chemically induce first of all someone’s most horrifying nightmare and then sleepwalk? In this way the individual acts out the one thing that is the most terrifying thing to them.” This is clearly why we have cases of such loving and caring mothers, like Andrea Yates, killing their children - that was her worst nightmare. And no one loved Phil Hartman more than his wife Brynn who even went to a friend’s home after shooting him to the friend to come home with her to tell her if she had shot Phil or if she was having a nightmare because she could not tell which was real.
In my opinion the fact that SSRIs are producing the majority of RBD is possibly the most significant piece of research we have ever seen on SSRI antidepressants.
Dr. Ann Blake Tracy, Executive Director, International Coalition For Drug Awarenesswww.drugawareness.org & author of Prozac: Panacea or Pandora? - Our Serotonin Nightmare (800-280-0730)
Awake, Jim Smith was an amiable and popular man.
As the director of public works in the small town of Osseo, Minn., he could be counted on to make house calls day or night, attending to burst pipes or broken water mains.
In fall, he hunted deer with buddies, who affectionately called him Smitty. In summer, he took his family pan fishing for ********************pie.
It was only when Mr. Smith fell asleep that something changed.
Wrapped in slumber, he would shout obscenities, kick the walls, punch the pillows. Sometimes, he hit his wife, Dee, in the back or grabbed her by the hair. One night, dreaming that he was putting a wounded deer out of its misery, he came close to breaking his wife’s wrist.
“I just didn’t sleep real sound,” Mrs. Smith recalled. “Once he started talking or swearing, I would be afraid that the next thing, he would be swinging his fists.”
In an earlier century, Mr. Smith might have undergone exorcism to expel the demons that possessed him when his eyes closed. In the 1960’s, psychiatrists might have traced his problem to repressed aggression and prescribed a sojourn on the analytic couch.
But in the last two decades, researchers have begun to systematically investigate a variety of disorders — called parasomnias — involving odd or dangerous behavior during sleep. One is called REM behavior disorder, in which people act out their dreams.
This was the diagnosis Mr. Smith received in 1987 when he sought treatment at the Minnesota Regional Sleep Disorders Center in Minneapolis.
Parasomnias are more common than was once thought, researchers are finding. They can be successfully treated, and most have nothing to do with mental illness.
At the same time, research on such sleep problems is challenging basic assumptions about sleep and wakefulness, showing that the borders between the two states are far from clearly demarcated. And in the case of REM behavior disorder, one of the most studied parasomnias, investigators are finding surprising links to physical illness.
For example, at the annual meetings of the Associated Professional Sleep Societies in June, Dr. Carlos H. Schenck, a psychiatrist and senior scientist at the Minnesota sleep center, and Dr. Mark W. Mahowald, a neurologist and the director of the clinic, will present findings indicating that of 26 otherwise healthy patients in whom REM behavior disorder was diagnosed in the 1980’s, 17 went on to develop Parkinson’s disease.
Other studies, at the Mayo Clinic and elsewhere, have found associations between the sleep disorder and other neurodegenerative diseases related to Parkinson’s, including a form of dementia known as Lewy body disease and an illness called multiple system atrophy.
Mr. Smith, now 72 and retired, learned in May 2001 that he had Parkinson’s.
The connection between REM behavior disorder and Parkinson’s is the latest twist in a story that began 20 years ago, when a retired grocer named Donald Dorff came to Dr. Schenck complaining of what he called “violent moving nightmares.” In one such dream, Mr. Dorff, believing he was a quarterback heading for a touchdown, ran forcefully into his bedroom dresser.
Wiring his new patient up in the sleep laboratory, Dr. Schenck discovered that Mr. Dorff’s violent behavior occurred during periods of rapid eye movement, or REM, sleep, a stage that accounts for 20 to 25 percent of nighttime repose in humans and that shows up on electroencephalogram recordings as a pattern of electrical activity similar to that seen during waking. Most dreaming takes place in REM sleep.
During REM, the brain dispatches signals to the muscles, telling them to perform the movements that would be appropriate if the person were awake.
In most sleepers, however, another brain circuit also kicks into action during REM to prevent the dreamer from carrying out those instructions. Nerve cells transmit chemical messages that paralyze all muscles in the body except the diaphragm, one small muscle in the ear and the muscles that move the eyes.
04-17-2007, 11:13 PM #3851
Elazebeth Marie REMContinued
Mr. Dorff’s problem appeared to be that the normal paralysis of REM was missing. The same was true for four other elderly patients, described by Dr. Schenck and his colleagues in a 1986 report documenting the first human cases of the disorder. In fact, the researchers realized, the patients were acting a lot like a group of laboratory cats studied in the mid-1960’s by a French sleep expert, Dr. Michel Jouvet.
Trying to locate the regions of the brain responsible for REM sleep, Dr. Jouvet and his colleagues destroyed cells in an area of the brainstem called the pons. Even with this damage, the cats still entered REM sleep, the scientists found. But instead of lying still, they stood up, looked around and sometimes stalked imaginary prey.
Subsequent studies, by Dr. Adrian R. Morrison at the University of Pennsylvania School of Veterinary Medicine, showed that the extent of the behavior exhibited by the animals during REM depended on where in the pons the lesions were made. For example, when the cell damage encompassed nerve pathways extending from the amygdala, a brain structure involved with emotion, the cats would attack humans or other cats.
As with Mr. Dorff, who died in 1999, and Mr. Smith, studies show that more than 80 percent of patients who show up at sleep disorder clinics with REM behavior disorder are men, middle-aged or older, and most, Dr. Schenck said, are noticeably placid and good-natured in their waking life. Many display rhythmic movements of their legs even during non-REM or slow-wave sleep.
Most patients also report unusually vivid dreams (sometimes beginning long before they start acting them out) in which they are being threatened or attacked or engaging in active sports.
One man dreamed that his boss was chasing him with a hatchet; another that he was being pursued by a lion, said Dr. Bradley F. Boeve, a neurologist at the Mayo Clinic who studies REM behavior disorder and Parkinsonian illnesses.
Sometimes, Dr. Schenck said, a husband will awake from a dream in which he is protecting his wife from danger, only to find that in fact he has been pummeling her.
“She wants to know why he’s beating up on her and he says, `I’m not, I’m beating up this man,’ “ Dr. Schenck said.
In other cases, patients have no memory of what stirred them to action. On a hunting trip, for example, Mr. Smith leaped abruptly from bed and began singing “God Bless America,” to the amusement of his bunkmates. But he could not recall the dream that inspired this burst of patriotism.
An increasing number of studies link REM behavior disorder to neurological disease. The damage to the pons that in animals suspends paralysis during REM sleep is not regularly found in humans with the disorder. And it is not yet entirely clear how the sleep problem is connected to neurodegenerative illnesses later in life.
But recent work by Dr. Jerome Siegel at the University of California at Los Angeles offers another piece of the puzzle and may help explain a possible connection to Parkinsonian diseases.
Neurons in particular areas of the midbrain, just above the pons, have a potent effect in suppressing muscle tone, Dr. Siegel has found. In rats, damage to those areas produces muscle movements during REM similar to those seen in human patients with the sleep disorder. And the nerve cells in those regions are very close to, and interconnected with, neurons in a midbrain center known to suffer cell damage in Parkinson’s.
“Given the connection between REM behavior disorder and Parkinson’s,” Dr. Siegel said, “the hypothesis that we’re pursuing is that the degenerative process that causes Parkinson’s may spread to the region responsible for inhibiting muscle tone” or vice versa.
Brain scans of patients have added to the suspicion that the sleep disorder in some way signals the beginning of Parkinsonian disease. In 2000, Dr. Ilonka Eisensehr of the University of Munich reported finding a kind of “Parkinsonian fingerprint” — a reduction in the enzyme that transports the messenger chemical dopamine in the striatum, the region of the midbrain where Parkinson’s originates — in the brain scans of patients with REM behavior disorder who did not yet have any other signs of neurological disease.
In a development that experts call troubling, sleep clinics are also seeing a number of patients who develop some symptoms associated with REM sleep disorder while taking Prozac, Zoloft or others of the newer generation of antidepressant drugs called selective serotonin reuptake inhibitors or S.S.R.I.’s
A 1992 study by scientists at the Minnesota sleep clinic found that 20 of 41 patients taking Prozac for depression or obsessive-compulsive disorder exhibited “extensive, prominent eye movements” during light non-REM stages of sleep, a phenomenon the researchers have called “Prozac eyes.” In one patient, the eye movements were still present 19 months after the man stopped taking the antidepressant.
Other reports suggest that some people taking the drugs experience muscle jerks or other movements during sleep or waking.
Dr. John Winkelman, the medical director of the sleep health center at Brigham and Women’s Hospital in Boston, said he had seen a number of patients who developed REM behavior disorder while taking S.S.R.I.’s.
“A couple of people threw themselves out of bed,” Dr. Winkelman said.
No one yet knows how common such side effect are, or their implications — if any. And other drugs — barbiturates and stimulants, for example — can also contribute to REM behavior disorder. But the findings, the experts say, should encourage doctors to prescribe responsibly.
“The drugs are very effective,” Dr. Mahowald said. “But it’s the physician’s responsibility to make sure the patient’s condition is severe enough to warrant prescribing a neuroactive agent.”
On the other hand, some psychiatric drugs are effective in treating the sleep disorder. Dr. Boeve said he found the drug Seroquel helpful for some patients.
What eventually kept Mr. Smith from inflicting further damage on his wife was clonazepam, a tranquilizer that Dr. Schenck and other experts have shown almost always calms patients’ turbulent nights.
“It helped right away,” Mrs. Smith said.
REM behavior disorder is the only parasomnia routinely associated with violence. But sleepwalkers have also been known to stab their relatives, molest children or confidently stride out of third-story windows, in states varying from confused wakefulness to partial arousal to the deepest stages of non-REM or slow-wave sleep.
Other sleep disorder patients, who suffer from a condition called nocturnal dissociative disorder, awaken and leave their beds to re-enact scenes of physical or sexual abuse, sometimes cutting themselves with razors or banging their heads against the wall. Afterward, they remember nothing about their nighttime behavior.
Reports of violence during slumber date back to the ancient Greeks.
In Homer’s “Odyssey,” Elpenor, the youngest of Odysseus’ crew, wakes suddenly from a drunken nap and runs off the roof of a house, breaking his neck.
Simon Fraser, a 19th-century Scot who killed his 18-month-old son by dashing him against the wall, said he did so while dreaming that a wild beast had jumped on the bed and was attacking the boy. “I am guilty in my sleep, but not guilty in my senses,” he insisted.
More recently, the defendants in several murder cases have used sleep as a defense, in one instance successfully: a Canadian, Kenneth Parks, was acquitted after experts testified that he was in a somnambulistic state when, in May 1987, he drove 14 miles to the house of his in-laws, where he stabbed his mother-in-law to death and nearly killed his father-in-law.
Such cases, Dr. Mahowald said, make it clear that sleep and waking are hardly distinct states.
In many normal people, he said, detailed neurophysiological studies of the brain show that the signs of sleep persist for an hour after awakening, though an EEG indicates that the person is already fully awake.
“Most people’s concept is that the entire brain is in one state of being, and that’s just not true,” Dr. Mahowald said. “You can have parts of the brain that are awake while others are asleep.”
04-17-2007, 11:34 PM #3852
I think that may be what is happening.. I sleep well, and the body is rested, but I don't think there is REM sleep much at all as my mind is always exhausted - these episodes are so dramatic though, why I can't drive, go anywhere, as it can happen anytime and am paralyzed for a while, up to 6 more times a day... Is there anything to be done to help the REM come back? or is it only time at this point (4.75 months off)? We cannot thank you enough for all the help you give us here - my family is so greatful too as there are no answers from the doctors... hopefully the two day brainwave test will show what is happening there...
thank you a million times, and blessings to you and all your family, you are amazing...
04-17-2007, 11:35 PM #3853
Interesting explanation of How SSRI affect the body
Introduction: Neurons & Neurotransmitters
There are billions of working cells in our brain called Neurons and great variety in the kind of brain cells or neurons, with each group representing a specific cluster of functions. Neurons communicate with similar neurons by firing molecules from its nerve endings to the receiving nerve endings of the other neuron. The nerve endings of the firing part of the neuron are called axon terminals and the nerve endings of the receiving part of the neuron are called dendrites. The end of the axon terminals are called synapses. The synaptic cleft is the space where synapses and dendrites meet each other and where all the activity takes place. Each neuron is able to receive and fire molecules simultaneously. The molecules fired in the synaptic cleft are called neurotransmitters. Situated at the end of the axon terminals of the firing part of the neuron, the synapses work like "ball throwers." The dendrites of the receiving part of the other neuron, work like "catcher's mitts." They use receptor-molecules, or receptors, to capture the "thrown" neurotransmitters. (See Picture)
Once one neuron is firing neurotransmitters from it's synapse to the receiving dendrite of the other neuron, it is critically important that the "mis-fired" neurotransmitter left overs must be removed from the synaptic cleft. Any neurotransmitter which is not removed from the synaptic cleft, prevents further neurotransmitters from getting through. Re-uptake, the process of removing neurotransmitters after firing or release, allow these neurotransmitter left overs to be recycled for further use. Re-uptake is carried out by "transporter proteins" which bind to the mis-fired neurotransmitter and carry it across the plasma membrane back into the synapse of the firing neuron.
Medication classified "Re-Uptake Inhibitors" act on these transporter proteins and thereby inhibit the re-uptake of neurotransmitters back into the synapse of the firing neuron. SSRI-AntiDepressants or Selective Serotonin Re-uptake Inhibitors, belong to this class of medication. Each group of neurons fire specific neurotransmitter-molecules. The neurotransmitter Serotonin, also known as 5-Hydroxy-Tryptamine (5-HT) is such a molecule. SSRI-AntiDepressants inhibit the re-uptake of serotonin what means that more serotonin will be fired from synapse to dendrite in the synaptic cleft of every communicating serotonergic neuron in the brain.
2. The neurotransmitter "Serotonin"
In the brain, serotonin is synthesized from the amino acid precursor "Tryptophan". By enzymatic interaction, tryptophan converts into 5-HTP and eventually into serotonin. (see image) This neurotransmitter belongs to the group of serotonergic neurons which make the Serotonergic System in the brain. Levels of serotonin are highly concentrated in the Raphe Nuclei. Raphe Nuclei are present in the Medulla and Pons, 2 structures which are part of the Brainstem. From the Raphe Nuclei in the pons of the brainstem, also called "Rostral Raphe Nuclei", serotonin pathways project through parts of the Limbic System (like the Thalamus and Hypothalamus) into the Forebrain. (See Picture)
2.a. Serotonergic functioning
If you would believe the overwhelming advertisements of the pharmaceutical companies, you would think that serotonin primarily regulates mood. In fact, serotonin regulates a lot of other activities in the brain and body. In 1948, Maurice Rapport, a haematologist, found that serotonin tended to make blood form clots, and it tended to be a muscle- as well as a vasoconstrictor. Next to be a muscle- and vasoconstrictor, serotonin plays an important role in sleep, appetite, memory, aggression, sexual behaviour, cardiovascular activity, respiratory activity, motor output, sensory and neuroendocrine function, but most important, perception! Since 1988 the serotonin hype brought us several SSRI-AntiDepressants all stimulating this neurotransmitter. For about 11 years now, Dr. Ann Blake Tracy (Prozac: Panacea or Pandora?), persistently warns the public against raising serotonin levels. Doctor Tracy has taught us that an increase in serotonin produces rushes of insulin dropping sugar levels and chemically inducing hypoglycaemia (low blood sugar) in this way. Furthermore it has been established that too much serotonin damages blood vessels, particularly in the lungs, and may also harm heart valves. This would be due to the fact that serotonin is a powerful vasoconstrictor.
Affecting Mood or Mind?
But most alarming is the serotonin and perception connection. Doctor Tracy as well as other sources described how the hallucinogenic drug LSD strongly acts on this neurotransmitter serotonin. The numerous examples of human LSD experiences have learned us that serotonin plays a major part in perception, our sense of reality, how we experience our in- and outside world! Other examples of drugs acting on the serotonergic system are PCP and MDMA (Ecstasy). Most of the readers will recognize also these serotonergic drugs for their capability to produce "an altered state of consciousness" in human beings. In the way that the serotonergic system responds to serotonergic drugs, we may conclude that this system is heavily involved in the determination of ones perception and therefore ones thought processes and emotions. The advertisements from the pharmaceutical companies, promoting elevated serotonin levels as were they purely mood lifting, therefore seem to be rather misleading then informative. SSRI-AntiDepressants are to be considered mind-altering drugs and not primarily mood-altering.
In all these years since 1988, scientists are still not sure why serotonin boosters seem to "alleviate" depression. They assume that low serotonin levels could be a possible cause of endogenous depression, but it's still just a theory and not a proven fact! New research present us a different view on serotonin, which may not even have that connection with mood as previously thought. By experimental research, scientists discovered that a new drug, code-named MK-869, blocked a neuropeptide called " Substance P." By blocking this neuropeptide, people became less depressed. An interesting fact was, that blocking substance P did not affect the function of serotonin! This raises new concerns about the involvement of serotonin in mood and/or depression.
"But why do I hear people talking about benefits from these SSRI-AntiDepressants?", you might want to ask in this stage. "They surely must work somehow don't they?" The answer is yes, they "work" somehow, but not in a very proper way. The mechanism of action on serotonergic neurons implies a lot of other neuro- endocrine responses. What actually happens when you increase serotonergic neuronal activity or elevate your serotonin levels is this: the stress hormones "Cortisol" & "Adrenaline" (Epinephrine) in the brain and body are triggered by increased serotonergic activity or elevated serotonin levels. It is a natural reaction from the body to combat the excessive serotonin levels. These released hormones, cortisol and adrenaline, are secreted from the "Adrenal Glands." They give the human personality a boost, producing a euphoric state, which can last for a prolonged period of time. In this manner SSRI-AntiDepressants initially produce the deceptive results the doctor and "patient" are both expecting. *
If a patient continues to ingest a particular SSRI-antidepressant over a prolonged period of time, eventually the bodies Adrenal Glands may lose their efficiency and "Adrenal Exhaustion Syndrome" will be the end result. Adrenal Exhaustion causes levels of adrenaline initially to fall and levels of cortisol to rise. Ultimately, also cortisol levels fall. When untreated, Adrenal Exhaustion will lead to seriously declining physical health. Many (former) SSRI-AntiDepressant users reported fatigue as a long term side-effect or were diagnosed with "Chronigue Fatigue Syndrome." People suffering from stress are generally diagnosed with this disorder. Symptoms range from simple exhaustion to much more complex problems that are secondary to excessive output of adrenal hormones in the bloodstream, leading to Adrenal Exhaustion. Unlike the other hormones, it takes a long time before the Adrenal Glands have their adrenaline levels restored. Could we say that the SSRI-AntiDepressant "works" by slowly excavating the body's Adrenal Glands?
04-17-2007, 11:37 PM #3854
Read to understand SSRI's
[ Actually, when a family doctor (GP) or psychiatrist is observing a patient in a "euphoric" state of being, this should ring warning bells immediately! The drug induced (iatrogenic) conditions Akathisia & Mania are well documented in the medical litarature. Drug induced Mania, an abnormally elated mental state, typically characterized by feelings of euphoria, racing thoughts and talkativeness, is a "forerunner" of Akathisia, a neurologically driven agitation ranging from mild leg tapping, feeling "caffeinated" to severe panic, an extreme manic state and hyper-sensitivity of the nervous system. Akathisia can lead to suicidal, aggressive and/or homicidal thoughts and behaviours. When a doctor or psychiatrist is observing symptoms of mania and/or akathisia in a patient, SSRI-AntiDepressant use should be discontinued immediately! The pharmaceutical companies are well informed regarding above mentioned conditions and the capacity of their antidepressant inducing these symptoms. Therefore it is strongly advised to medical professionals, physicians, to monitor a patient very closely after prescription of (SSRI) anti-depressant treatment. In the field of Bio-Psychiatry it was a conventional common thought that hypothalamic-pituitary-adrenal (HPA) system dysregulation/hyperactivity (and thus excessive secretion of cortisol) played an important role in the pathophysiology of depression and that normalization of HPA axis hyperactivity could be achieved by (SSRI) anti-depressant treatment, and thus relief of depression. However, a study and a case report involving the non-SSRI antidepressant Remeron (mirtazapine) and a review show us that nor amelioration of HPA system dysregulation, nor reduction of cortisol secretion in depressed patients is correlated with relief of symptoms of depression. See: (1), (2), (3). Furthermore, a study developed by D. Jezova & R. Duncko, Laboratory of Pharmacological Neuroendocrinology, demonstrated that repeated SSRI-antidepressant treatment in healthy men does not inhibit, but enhances stress-induced pituitary hormone release (neuroendocrine activation). Cortisol levels failed to be modified by antidepressants. A simple search through available PubMed articles uncovers clearly that SSRI-antidepressants not only fail to modify cortisol, but actually stimulate/increase cortisol release. See: (1), (2), (3), (4), (5), (6). Initially the rise in cortisol & adrenaline (secreted from the Adrenal Glands) may create the illusion of a patient making progress in his/her situation, but a potential tragedy may be surfacing very soon. It is very well known that (SSRI-AntiDepressant induced) increased cortisol secretion can lead to violent suicidal behaviour.
(I would like to encourage you to use your discernment when viewing antidepressant involved suicide/homicide/violence cases represented by the media. In the section casualties of this website, these cases are carefully stored up to be a "silent" witness for the future, in order to testify regarding the devastating & powerful destructive effects these "legal drugs" exercised on children, adolescents and adults, not discriminating between men and women). ]
The Serotonin-Cycle: beaconing of conscious awareness and dream sleep?
One of the first significant discoveries about the serotonergic system in the brain was that it's activity was dramatically altered across the sleep-wake cycle. Serotonergic activity gradually decreases as one becomes drowsy and enter slow-wave sleep. An overall slowing of serotonergic activity is observed during slow-wave sleep known as non-REM sleep. During REM sleep (Rapid Eye Movement-the original dream sleep), serotonergic activity falls completely silent. Serotonergic activity returns to it's basic level several seconds prior to the end of REM sleep. REM sleep occurs in roughly 90-100 minute cycles, alternating with non-REM sleep (around 4 to 5 times during sleep). During non-REM sleep, there is lots of movement, but during REM sleep, only the eye muscles move. REM-dreaming turns on neurons in the medulla of the brainstem that inhibit all other motor activity. In this way it prevents the dreamer from sleepwalking and to act out his/her dreams in real time.
Another significant discovery was that, when during REM sleep the serotonergic neurons in the brainstem were "off" (silent), cholinergic neurons in the brainstem were "on" (firing)! Cholinergic neurons fire the neurotransmitter "Acetylcholine." Acetylcholine not only plays an important role in dreaming, but also in long-term memory processes. In the brainstem, the cholinergic "REM-on" neurons can only trigger REM sleep (and thus dreaming) when the serotonergic "REM-off" neurons are inactive. This happens because, in the brainstem, the serotonergic neurons inhibit the cholinergic neurons whilst we are awake. When, in the brainstem, the serotonergic neurons release their inhibitory constraint, only then, the cholinergic brainstem neurons will be able to get active, triggering the REM-dream sleep. Both the REM-on and the REM-off cells are localized in the brainstem. These brainstem mechanisms work as an "oscillator", which controls the transitions from waking to sleeping and further controls the REM/non-REM cycle, which occurs 4 to 5 times during sleep.
Now at this moment you might ask yourself, how it is possible that so many individuals report bizarre vivid lifelike dreams whilst on serotonin boosters, when an active serotonergic system suppresses REM sleep, and thereby dreaming? Serotonergic suppression of REM sleep in humans by acute dosage of SSRI-AntiDepressants was indeed confirmed. (see article) This is what Dr. Tracy is also been telling us for many years in her book. The PubMed article discusses rebound of REM sleep after abrupt withdrawal from an SSRI-AntiDepressant, but it still doesn't answer the question how it is possible that individuals are experiencing disturbing dreams and nightmares whilst they are taking an SSRI-AntiDepressant over a prolonged period of time. When I delved deeper into this matter I discovered some interesting facts. Although there is an important link between REM sleep and dreaming, they are in fact doubly dissociable states. That is, REM can occur without dreaming and dreaming can occur without REM. Although REM is triggered from the brainstem, it alone will not result in dream states. Dreams require input from the forebrain and structures in the limbic system. The forebrain mechanisms are the final common path to dreaming. The brainstem is just one of the many arousal triggers that can activate these forebrain mechanisms. Although REM sleep is controlled by the brainstem, dreaming seems to be controlled by these forebrain mechanisms. It is now acknowledged that REM sleep is not necessary for dreaming, that dreaming can also occur during non-REM sleep, and that dream-like experiences can even be elicited during quiet wakefulness! The controversial human reports of very vivid lifelike dreams whilst taking an SSRI-AntiDepressant could therefore be explained as existing outside and independent of the REM (dream) sleep! But, -now that we know that the forebrain is the final common path to dreaming, and SSRI-AntiDepressants suppress the brainstem's REM arousal system (which normally activates forebrain dreaming)- what kind of arousal triggers are then responsible for the activation of forebrain dreams during use of SSRI-AntiDepressants?
Forebrain Nightmares and Forebrain Seizures
An even more exciting discovery was that dreaming can also be induced by focal forebrain stimulation and by complex partial forebrain seizures during non-REM sleep, without the involvement of the brainstem's REM mechanism! There is a causal link between epileptic activity and recurring nightmares during non-REM sleep. This was demonstrated by neurosurgeon and researcher Wilder Penfield, who was able to reproduce these anxious experiences artificially in the form of waking "dreamy state" seizures. The causal link between forebrain seizures and recurring nightmares was confirmed by the fact that both the underlying seizure disorder and the nightmares responded to anticonvulsant therapy.
Here is an example of a recurring nightmare, caused by epileptic activity in the forebrain:
The patient [35 year old woman with idiopathic complex-partial seizures] reported a recurrent dream about her [dead] brother ... which has reappeared several times. The dream is as follows: "I am walking down the street. I meet him. He is with a group of people whom I know now. I feel that I will be so happy to see him. I say to him, `I'm glad you're alive,' but he'll deny that he is my brother and he'll say so, and I'll wake up crying and trying to convince him."' Electroencephalography revealed a poorly defined right anterior temporal / right temporal spike focus which appeared with the onset of drowsiness and light sleep (Epstein & Ervin 1957, p. 45).
Could it be that the bizarre vivid lifelike dreams, reported by SSRI-AntiDepressant users are epileptiform of nature? Notice the "poorly defined spike focus." Could it be that this is epileptic activity which remains undiscovered because it is barely detectable? Standard tests for epilepsy included?
3. The Pineal Gland
04-17-2007, 11:38 PM #3855
Continued from above
3. The Pineal Gland
The Pineal Gland -also called the epiphysis- looks like a miniature pine cone and is situated in the middle of the brain beneath the two brain halves, surrounded by the ventricles, under the roof of the corpus callosum (cross-beam connecting the 2 brain halves). (see picture) This active organ has, together with the Pituitary Gland (see picture), the next highest blood circulation after the kidneys. It is not protected by the blood-brain barrier and therefore makes this gland fragile to any substance entering the bloodstream. It is, for instance, very sensitive to fluoride.
Another factor involved in affecting the Pineal Gland can be excessive high or even toxic levels of an SSRI-AntiDepressant in the bloodstream. Certain individuals have a metabolic deficiency in the metabolism of anti-depressant medication. In the liver, a group of enzymes named " cytochrome P-450" enzymes, particularly the "CYP2D6 enzymes" of this group of enzymes, metabolise SSRI-AntiDepressants. When not properly metabolised, because one has a metabolic deficiency, a daily therapeutic dose can build up to excessive high or even toxic levels in the bloodstream. Hence, the Pineal Gland would be an easy target, since it is not very well protected by the blood-brain barrier. It is it's connection to serotonin what makes this organ so very interesting.
3.a. The Pineal Gland-Serotonin connection
Nicholas Giarmin, a professor of pharmacology and Daniel Freedman, a professor of psychiatry, confirmed that the human brain manufactures serotonin at various sites in the brain. For example, in the Thalamus, they discovered 61 nanograms of serotonin per gram of tissue; in the Hippocampus, 56 ng.; in the Central Gray Section of the Midbrain, they found 482 ng. But in the Pineal Gland, they found 3140 ng. of serotonin per gram of tissue. The Pineal Gland was unmistakably the richest site of serotonin in the brain! This discovery implicates the Pineal Gland as an important site of serotonergic activity.
The neurohormone Melatonin & the Endocrine System
One of the neurotransmitters secreted by the Pineal Gland is Melatonin, also known as N-Acetyl-5-Methoxy-Tryptamine (NA-5-MT). In the Pineal Gland, serotonin converts into melatonin by enzymatic interaction. Melatonin is also an important hormone to the body, that's why it is called a neurohormone. It is necessary to regulate the function of all organs of the Endocrine System in the body. The organs or glands of the endocrine system are: the Pituitary Gland, situated in the brain; the Thyroid + Parathyroid Glands; the Thymus; the Pancreas; the Ovaries/Testes (see image). All of these endocrine organs/glands secrete their hormones to the blood. The Pituitary Gland stimulates the secretion of these hormones, while the Pineal Gland apply the brakes on them through it's neurohormone melatonin. If the endocrine organs/glands release too much of their hormones, for instance when we are stressed, then the Pineal Gland releases melatonin to counteract these hormones. Also serotonin gets released when stress is involved. The increased serotonin triggers the release of adrenaline, which allows the body to work through the stress.
The Pineal Gland is a magneto sensitive organ, what means that it is sensitive to electromagnetic fields (EMF). It is sensitive to electromagnetic waves from computer monitors, cellular phones, microwave ovens, high voltage lines, etc.. Electromagnetic fields suppress the activity of the Pineal Gland and reduce melatonin production. EMF also affect serotonin.
The neurohormone Melatonin & the Eye-SCN-Pineal Gland Axis
The Pineal Gland is also a photosensitive organ, what means that it is sensitive to light. It normally releases melatonin when it no longer receives light impulses. Just like serotonin, also melatonin has it's own day & night cycle (circadian rhythm) which begins where the cycle of serotonin normally ends. When serotonin reaches it's lowest level at night (in the dark) during slow wave sleep, the Pineal Gland starts to convert it's store of serotonin into melatonin to be released prior to REM sleep. Melatonin has it's peak around 02:00 AM. During daytime, the daylight inhibits the release of melatonin. This works as follows: when, during daytime, light reaches the eyes, then it's presence gets translated into nerve impulses, which travel through the optic nerve between the eyes and a region of the Hypothalamus called the "Suprachiasmatic Nucleus" (SCN). (see picture) The SCN in it's turn sends it's nerve impulses to the Pineal Gland. These impulses inhibit the Pineal Gland's production of melatonin until it gets dark, when it's to be released again.
Melatonin is not only present in the brain and body but also in the eye! One has speculated whether or not high melatonin levels in the eyes during daylight exposure, may bring damage to them over time. Visual/eye problems (light sensitivity, spots, blurred vision) are other symptoms, frequently reported by (former) SSRI-AntiDepressant users. I questioned myself if these problems could be related to elevated melatonin levels in the eye. When serotonin accumulates in the Pineal Gland, on account of an SSRI-AntiDepressant, then it would come under pressure to produce more melatonin out of the excessive amounts of serotonin. Hence, during daytime, melatonin levels in the eyes would be significantly higher then normally would occur... But, I had to revise this hypothesis. In a PubMed study, SSRI-AntiDepressants were found not to elevate melatonin levels in humans. Although "Luvox" and "Paxil" increases melatonin to a more or lesser amount, apparently this seemed not to be the case for the other SSRI-AntiDepressants. However, since the Pineal Gland does contain a complete map of the visual field of the eyes, could there be a correlation between visual/eye problems and a dysfunctional Pineal Gland?
A case, noted by Dr. Berman, could give us some more insight into this matter:
A child was brought to a German clinic suffering from eye trouble and headaches. He was five years old and very mature, and apparently had reached the age of adolescence. He was abnormally bright mentally, discussing metaphysical and spiritual subjects. He was strongly group-conscious and only happy when sharing what he had with others. After his arrival at the clinic, he rapidly grew worse and died in a month. An autopsy showed a tumour of the pineal gland. - Berman, Louis, M.D., The Glands Regulating Personality, p. 89.
Could it be that the visual/eye problems (light sensitivity, spots, blurred vision), frequently reported by (former) SSRI-AntiDepressant users, are caused by some element of Pineal Gland dysfunction?
Continue... Serotonin & the Pineal Gland -Part 2
04-17-2007, 11:41 PM #3856
Last edited by auntybiotic; 04-17-2007 at 11:45 PM.
04-17-2007, 11:44 PM #3857
I think you are having partial forebrain seizures as explained in article above. Sleep study will confirm this and most are paid by insurance
04-18-2007, 09:08 AM #3858
Thank you all so much for the help and all the information. I feel lucky to have found a community to help guide me. I have absolutely NO trust in doctors and think it's a money scam at best and genocide at worst! I have struggled with depression since the age of 15 and have been on and off meds (which now looking back is probably why I've struggled). I've been on prozac, paxil, zoloft and now lexapro, before I knew better I almost shifted to effexor! Thank the Lord above I found some common sense.
I am currently considering seeing a Natropathic doctor to help get my system cleansed and maybe help some of these issues. I hate the idea of getting back on the lex just to start tappering, but I can't live like this. I have 2 small children and I am a stay at home mom, and honestly I can't deal with them right now and am scared about how bad I could get. Yesterday I cried most of the day and I just flip into a rage and it's impossible to control. I'm sure I don't have to explain this to anyone here.
I am also wondering about interactions with supplements. I have been taking a supplement that affects your adrenal glands (I am going to stop until this is over), but I also have an antioxidant that I would like stay on. It's called OPC_3 and it's mostly grape seed extract, billberry and pinebark. I take it everymorning. Does anyone know if this will mess with me while I'm under the influence of the lex poison?
I plan on following your advice and going back on my 20 mg. Then do I taper by 25% each week...or is it less. My doctor wanted me to taper from 20 to 10 for 1 week and then from 10 to 5 for another week and then 5 every other day for another week and then done. Does that sound reasonable?
Thank you, thank you, thank you!!!!
04-18-2007, 10:02 AM #3859
I am very new to this site, and to Lex withdrawl, but I DO know that your dr. is way off! I was on 20mg. for 7 months I thought I did the right thing by cutting them in half (down to 10mg) and taking that amount for about 3 weeks. I then cut those in half (5mg) and took those for about 10 days. I could not have been more wrong. Or more sorry! I have a constant and crushing headache, brain zaps that never seem to end, and I am afraid to go anywhere because my brain just seems to stop working every once in a while. (For instance, yesterday I forgot how to exit my shower! Couldn't remember if the shower door opens in or out, or on the right or the left!). I have many more symptoms, but you can read everyone else's posts for full descriptions. Suffice to say, DO NOT taper that fast or you will be very very sorry. As I am. Someone has posted a liquid Lex taper that I am certain would be wonderful, as you would have very strict control over te dosages. I would defintely ask your doc for the liquid, and again SLOOOOOOOOW is the way to go!
Good luck, and remember that we're all in this together.
Ladies: Check out this article from Psychology Today regardng SSRI's and relationships
Last edited by deanna.a; 04-18-2007 at 10:35 AM.
Reason: New Article link
04-18-2007, 01:31 PM #3860
I have just purchased Phosphatidyl Serine from a health food store. It was recommended to me by a woman working there. She said that it does wonders for getting the brain synapses to work well. Has anyone tried this? I also purchased Noni juice (as some of the posters here have recommended), as well as a natural Liver Detox supplement. Anyone have experiences with these?
04-18-2007, 02:09 PM #3861
Shakey hands/tired arms??
Hi guys. Ok - new symptom for me. UGH! Something new all the time. I'm happy to report that after about a month and a half, the muscle jerking and twitching have really decreased. That's good, since that was really worrisome. Now, I know better than to say it's gone (because it's not) and could possibly return, but for now, it's leaving me alone. Head bobbing is still there intermittently, mostly when I'm concentrating on something (computer screen, book, TV, etc).
The new symptom that has taken it's place now is that my hands are shaking! It goes off and on with my legs and voice, but the most obvious are the hands. I feel like I have Parkinson's or something. Mentally, I'm doing fine with the anxiety, but my hands will shake when I hold them up. I'm also waking up with my arms really weak and it takes longer in the mornings to wake them up and function. They feel pretty heavy and clumsy for the first hour of the day, then off/on as the day goes on, but the shaking is the most freaky. I'm just hoping this will go away in it's own time, as did the other stuff. Am I alone with the shakey hands? (Of course, I'm just looking for reassurance that I'm not the only one and don't have to go back to the doc to check to see if I developed Parkinsons!!)
Had a GREAT massage yesterday - fixed my neck that has been so cramped up from all this body workout! That was awesome!
Saying hi and good afternoon to all my fell Lex w/d friends!
04-18-2007, 02:24 PM #3862
I'm also a mother of three I just became a member of this site once I seen so many stories simular to mine. I also took lexapro a very low dose. My doctor suggested I take lexapro because I was feeling depressed. I didn't know at the time I was pregnant.When I found out I had been taking lexapro for a little under a month.The doctor told me to stop taking the drug.The next month I started getting dizzy it lasted a 1 1\2 weeks 24/7. I didn't Know what was going on . The the next time 6months later it happened again this time it lasted 3weeks 24/7 when I experience this dizziness I get really sick the first 24 hours and I can't barely walk without holding on to something .The next time 4months after that it lasted for a little over 3 weeks 24/7.I still feel some dizziness and the doctor still can't tell me what's the problem.First they thought it was my pregnancy ,then it was my ears but they don't know. I was fine before I took lexapro.I suggest if you're concerned about your health get test ran and make your doctor find out what's going on.I'm going to three different doctors and more if I have to until I find out what's going on.Stay positive and don't forget to pray they will be answered.
Last edited by KYMA; 04-18-2007 at 02:44 PM.
04-18-2007, 03:10 PM #3863
Originally Posted by momma2threebabes
I'm kyma I post my story today #129 on the list it's a kind of simular to yours. Please read it and respond.
Last edited by KYMA; 04-18-2007 at 03:13 PM.
04-18-2007, 03:30 PM #3864
My suggestion may be to reistate at the full dose until all of your symptoms are gone, possibly that may take two to three weeks. Once atble you may want to taper by 10% since your dose is so high. That would be a dose of 18 Mg of lexapro.
You can crush the pill and mix with cranberry juice and taper as described in a post on the previous page on how to convert lexapro tablet to liquid for a taper or else you can ask your physician to prescribe the lexapro liquid.............the pharmacy will give you BP syringes for measuring) you will need a 10 Ml syringe amd a 1Ml syringe for later).
Start at 18 Mg of Lexapro daily for about two to three weeks and once you are stable reduce to 16 Mg/ml. of lexapro. When you get down to about 10 Mg of lexapro you may want to decrease your tapers to 5%. If you continue to have severe withdrawal at 10 % you may actually only be able to reduce by 5% from the beginning which would be from 20 Mg to 19MG.....only you can tell what you are able to withstand but you may want to attempt a 10% taper to begin with and see how you do. I will take about a week before you notice the withdrawals and the first will be flu type symptoms, runny nose, agitation, nightmares but hopefully you may not have these with a slow taper.
04-18-2007, 03:35 PM #3865
Originally Posted by momma2threebabes
I'm Kyma Iposted my story on this site #129 on the list it's simular to yours kind of.Please read and respond. Thankyou
04-18-2007, 04:16 PM #3866
Nervous about Withdrawal
I've been reading everyone's notes about withdrawal and I am so nervous. I don't trust my psychopharmacologist, and would rather wean off on my own.
I have been taking 10mg for about 4 months and have gained about 12 lbs. The weight gain and slight decrease in my anxiety is not enough to keep me on this. I want out!
Here is what I think I can do to wean off (but please advise if I am going about this wrong)
I plan on taking 5 mg for the next two weeks, until my RX runs out. I had to stop taking lexapro for a few days about a month ago and all I felt was dizzy - but so happy to be alive and off of these ******************** drugs. Am I going about this correctly? THANK YOU SO MUCH!!!!!!
04-18-2007, 11:49 PM #3867
This could exlain your seizure activity:
4. Side-Effects: withdrawal or brain-damage?
SSRI-AntiDepressants certainly don't raise your serotonin levels in a gentle manner. They prevent serotonin from being removed from the synaptic cleft. As a result, a lot of excess firing takes place and therefore more serotonin remains in the synaptic cleft. In this manner, the (receiving) post-synaptic receptors get bombarded with serotonin. According to Gary Null, Ph.D., all this over stimulation causes a decrease in the number of post-synaptic receptors. Depending on the intensity and duration of blocking re-uptake, around 30% to 40% of the post-synaptic receptors will be eliminated (Eli Lilly, the manufacturer of Prozac, would knew about the disappearance of receptors from their laboratory experiments). It is not established whether or not receptors ever come back after discontinuing an SSRI-AntiDepressant. The damage may be permanent or not.
Apparently this is not the only neuro damage caused by SSRI-AntiDepressants. In a recent study, researchers saw marked changes in the axon terminals (nerve endings) of serotonergic neurons in rats, treated with SSRI-AntiDepressants. The terminals shrivelled or took on corkscrew shapes. These changes were similar to those observed with the serotonin booster drug "Ecstasy" (MDMA). In studies with baboons who were treated with Ecstasy, researchers used Positron Emission Tomography (PET) to take brain scans of them. The researchers found that Ecstasy was toxic to the brain and damaged the axon terminals (nerve endings) of serotonergic neurons. This damage was still present in the baboons 7 years after discontinuing the drug. Later studies in humans who had used Ecstasy, documented the same damage at serotonergic neurons as observed with the baboons. Likewise, the SSRI-AntiDepressant induced brain damage observed in the rats, could be present in humans as well.
Previously we discussed that an SSRI-AntiDepressant induced hyper-active serotonergic system, could lead to disruption of the circadian (daily) serotonin cycle and excessive amounts of serotonin in the Pineal Gland. Another dangerous situation occurs when a hyperactive serotonergic system causes a condition called the "Serotonin Syndrome." This is a serious life threatening condition which needs immediate and adequate treatment.
An under-active serotonergic system will be a result of (1)the damaged axon terminals at the firing part of the serotonergic neuron and/or (2)the eliminated receptors at the dendrites of the receiving part of the serotonergic neuron. When discontinuing an SSRI-AntiDepressant, serotonergic activity dramatically decreases because the neurons aren't able to communicate properly with each other anymore. As a result of this decreased serotonergic activity, side-effects occur, which are falsely defined as "withdrawal side-effects."
Some of these side-effects are the frequently reported electrical shocks, zaps or shivers through the head (brain) and/or body, light flickering in the head, "falling into walls" along with "pins and needles" in the skin. Sometimes these phenomena are so severe that the individual who's experiencing them, feels very confused or like being on the verge of blacking out, losing consciousness.
It's striking how consciousness seem to be involved in these "sensory disturbances." I was thinking about an indirect neuronal mechanism, responsible for these phenomena. Serotonin is an inhibitory neurotransmitter. An under active serotonergic system would not inhibit other neurotransmitters anymore, like dopamine, or acetylcholine released by the cholinergic neurons in the brainstem (which are responsible for the extreme rebound of REM dreams when discontinuing an SSRI-AntiDepressant). Hence, these neurons would start to fire excessively, causing the side-effects as described above.
Another explanation could be that the serotonergic neurons are excessively firing their impulses through the axon to the axon terminals and synapses, as a compensatory mechanism for the loss of electrochemical activity in the synaptic cleft. In this manner, serotonergic electrochemical bursts of discharges would take place in the brain. Both examples of excessive electrochemical activity in the brain could be defined as epileptic activity. (see chapter 2.a. (3)Forebrain Nightmares and Forebrain Seizures)
One reason why these "sensory disturbances" side-effects are not recognized as epileptic activity, could be because they are not the full blown epileptic seizures that we know of and which are visible to others. As a matter of fact, epileptic activity can occur as petit mal seizures called "absences." Absences are blanks in the short-term memory that remain invisible to the observer. Researchers Hutt and Gilbert of the University of Keele in England, performed tests on children with epilepsy, in which they were using stroboscope flashlights. It occurred that 18 flashlights per second induced these absences in epileptic children.
This reminded me of the problems which some former SSRI-AntiDepressant users reported that they had with flashing sunrays through the trees when passing them in a car, or that they were forgotten that they were doing something in the midst of the process of doing it. Could these problems, as well as the other side-effects, be related to epileptic activity, possibly in the forebrain? Some SSRI-Antidepressant users were even more less fortunate, they developed full blown epileptic seizures whilst taking the drug, which remained after discontinuation.
Another factor in epileptic activity could be a malfunctioning Pineal Gland. In 3 PubMed articles the Pineal Gland, as well as it's neurohormone melatonin are discussed in relation to epileptic seizures. Significant changes were found in "day-night melatonin levels during convulsions, consistent with the hypothesis that melatonin has an inhibitory function on central nervous system activity." (1) Patients with epileptic seizures had "a significantly lower urinary secretion of melatonin, which may indicate that melatonin has a protective effect on seizures" (2) and the Pineal Gland and melatonin "exert a major influence in the control of brain electrical activity and have been shown to be involved in seizure and sleep mechanisms." (3)
My particular attention got attracted by the Pineal Gland as a magneto sensitive organ. Former SSRI-AntiDepressant users reported that the electrical shocks, zaps or shivers through the head (brain) and/or body, as well as the light flickering in the head, increased in severity when working behind a computer monitor. Computer monitors are known to radiate low frequency electromagnetic waves. Knowing that electromagnetic fields (EMF) affect serotonin, melatonin and the Pineal Gland, these electromagnetic waves could therefore trigger epileptic activity by altering the functions of the Pineal Gland. Here is a field of research to establish if these post-SSRI-Antidepressant side-effects are indeed epileptiform of nature and if forebrain seizures -whether serotonergic, dopaminergic or cholinergic- as well as the Pineal Gland are involved.
Hypoglycaemia (Low Blood Sugar)
04-19-2007, 12:10 AM #3868
Hypoglycaemia (Low Blood Sugar)
Ramo Kabbani, the Director of the Prozac Survivors Support Group (PSSG) in England, developed seizures within a month of going on Prozac. She had four EEGs, three of which proved abnormal but inconclusive. This means that there was some minor abnormality there, but they did not know what was causing it and they didn't bother investigating it further. Remember the case of Epstein and Ervin (see chapter 2.a. (3)Forebrain Nightmares and Forebrain Seizures) in which EEG also revealed a poorly defined spike focus in a woman who was experiencing seizures.
An interesting fact that Ramo discovered was, that every time when she had a seizure or a zap, her sugar levels plummeted to extremely low levels. Other (former) Prozac users that have been having seizures and zaps, who contacted the help line of the PSSG in England, have all found that they have low blood sugar levels. Low blood sugar, or low blood glucose, occurs when blood levels of glucose drop too low to fuel the body's activity. This condition is called "Hypoglycaemia," when the body isn't able anymore to maintain normal levels of glucose in the bloodstream. Glucose levels are determined by how fast glucose enters and leaves the bloodstream. When glucose leaves the bloodstream it enters the brain, which needs a constant supply of it to function properly.
In other PubMed articles the involvement of the Pineal Gland was discussed in the regulation of glucose metabolism in the brain (1; 2). In animal studies the Pineal Gland's neurohormone melatonin was found to significantly increase both brain and blood levels of glucose i.e. by enhancing carbohydrate metabolism into glucose (1; 2). Previously I mentioned that Doctor Tracy has taught us that an increase in serotonin, produces rushes of insulin, dropping sugar levels and chemically inducing hypoglycaemia (low blood glucose) in this way. In another animal study published at PubMed it was found that insulin-induced hypoglycaemia also affected the Adrenal Glands and caused a dramatic decrease of serotonin in the Pineal Gland. (1) This could lead to disturbances in melatonin secretion after which blood glucose levels can fall even lower.
Whether or not the function of the Pineal Gland gets affected by SSRI-AntiDepressants, either owing to a metabolic deficiency, or damaged serotonergic nerve terminals and receptors, or as a result of a hyperactive serotonergic system, needs to be established. A malfunctioning Pineal Gland could lead to disturbances in the natural circadian rhythm of melatonin secretion, as well as disturbances in glucose metabolism in the brain and an overall decrease of brain and blood levels of glucose. Hence, the natural defence to epileptic activity in the brain will fall off, as well as the natural defence to a hyperactive Endocrine System.
Going from 10 Mg of lexapro to 5 Mg would be a 50% reduction...................10% is the most people should do without causing problems with severe withdrawal. Please read the articles on this page that I posted to explain why you get the withdrawals and how the SSRI's affect the neurotransmitters and the pineal gland...........you will then understand the importance of a SLOW TAPER of 5 to 10% so the body regulation system in the brain and pineal gland has a chance to get use to not having the serotonin reuptake taking place.
A 10 % taper would be approx. 8 Mg for two to three weeks or until stable. Next taper would be to to 7.1 Mg for two to three weeks, next 10% taper would be to to 6.4 Mg for two to three weeks and so on until you are off of the lexapro. These are only suggestions. I am not a doctor and you may run this by your doctor and ask that he prescribe liquid lexapro to help with the tapering.
04-19-2007, 01:39 AM #3869
Thanks Hairy! z:)
04-19-2007, 07:08 AM #3870
I was not able to edit the previous post, not sure why but could not.
The correct calculations for a 10% taper are as follows.
10 Mg of lexapro to 9 Mg
9 Mg of lexapro to 8.1 Mg
8.1 Mg of lexaro to 7.3 Mg
7.3 Mg of lexapro to 6.9 mg and so on till off.
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