Predicting Psychosis

"Prevention is better than cure", so they say. And in most branches of medicine, preventing diseases, or detecting early signs and treating them pre-emptively before the symptoms appear, is an important art.

Not in psychiatry. At least not yet. But the prospect of predicting the onset of psychotic illnesses like schizophrenia, and of "early intervention" to try to prevent them, is a hot topic at the moment.

Schizophrenia and similar illnesses usually begin with a period of months or years, generally during adolescence, during which subtle symptoms gradually appear. This is called the "prodrome" or "at risk mental state". The full-blown disorder then hits later. If we could detect the prodromal phase and successfully treat it, we could save people from developing the illness. That's the plan anyway.

But many kids have "prodromal symptoms" during adolescence and never go on to get ill, so treating everyone with mild symptoms of psychosis would mean unnecessarily treating a lot of people. There's also the question of whether we can successfully prevent progression to illness at all, and there have been only a few very small trials looking at whether treatments work for that - but that's another story.

Stephan Ruhrmann et al. claim to have found a good way of predicting who'll go on to develop psychosis in their paper Prediction of Psychosis in Adolescents and Young Adults at High Risk. This is based on the European Prediction of Psychosis Study (EPOS) which was run at a number of early detection clinics in Britain and Europe. People were referred to the clinics through various channels if someone was worried they seemed a bit, well, prodromal

Referral sources included psychiatrists, psychologists, general practitioners, outreach clinics, counseling services, and teachers; patients also initiated contact. Knowledge about early warning signs (e.g., concentration and attention disturbances, unexplained functional decline) and inclusion criteria was disseminated to mental health professionals as well as institutions and persons who might be contacted by at-risk persons seeking help.

245 people consented to take part in the study and met the inclusion criteria meaning they were at "high risk of psychosis" according to at least one of two different systems, the Ultra High Risk (UHR) or the COGDIS criteria. Both class you as being at risk if you show short lived or mild symptoms a bit like those seen in schizophrenia i.e.

COGDIS: inability to divide attention; thought interference, pressure, and blockage; and disturbances of receptive and expressive speech, disturbance of abstract thinking, unstable ideas of reference, and captivation of attention by details of the visual field...

UHR: unusual thought content/delusional ideas, suspiciousness/persecutory ideas, grandiosity, perceptual abnormalities/hallucinations, disorganized communication, and odd behavior/appearance... Brief limited intermittent psychotic symptoms (BLIPS) i.e. hallucinations, delusions, or formal thought disorders that resolved spontaneously within 1 week...

Then they followed up the 245 kids for 18 months and saw what happened to them.

What happened was that 37 of them developed full-blown psychosis: 23 suffered schizophrenia according to DSM-IV criteria, indicating severe and prolonged symptoms; 6 had mood disorders, i.e depression or bipolar disorder, with psychotic features, and the rest mostly had psychotic episodes too short to be classed as schizophrenia. 37 people is 19% of the 183 for whom full 18 month data was available; the others dropped out of the study, or went missing for some reason.

Is 19% high or low? Well, it's much higher than the rate you'd see in randomly selected people, because the risk of getting schizophrenia is less than 1% lifetime and this was only 18 months; the risk of a random person developing psychosis in any given year has been estimated at 0.035% in Britain. So the UHR and COGDIS criteria are a lot better than nothing.

On the other hand 19% is far from being "all": 4 out of 5 of the supposedly "high risk" kids in this study didn't in fact get ill, although some of them probably developed illness after the 18 month period was over.

The authors also came up with a fancy algorithm for predicting risk based on your score on various symptom rating scales, and they claim that this can predict psychosis much better, with 80% accuracy. As this graph shows, the rate of developing psychosis in those scoring highly on their Prognostic Index is really high. (In case you were wondering the Prognostic Index is [1.571 x SIPS-Positive score >16] + [0.865 x bizarre thinking score] + [0.793 x sleep disturbances score] + [1.037 x SPD score] + [0.033 x (highest GAF-M score in the past year – 34.64)] + [0.250 x (years of education – 12.52)]. Use it on your friends for hours of psychiatric fun!)

However they came up with the algorithm by putting all of their dozens of variables into a big mathematical model, crunching the numbers and picking the ones that were most highly correlated with later psychosis - so they've specifically selected the variables that best predict illness in their sample, but that doesn't mean they'll do so in any other case. This is basically the "voodoo" non-independence problem that has so troubled fMRI, although the authors, to their credit, recognize this and issue the appropriate cautions.

So overall, we can predict psychosis, sometimes, but far from perfectly. More research is needed. One of the proposed additions to the new DSM-V psychiatric classification system is "Psychosis Risk Syndrome" i.e. the prodrome; it's not currently a disorder in DSM-IV. This idea has been attacked as an invitation to push antipsychotic drugs on kids who aren't actually ill and don't need them. On the other hand though, we shouldn't forget that we're talking about terrible illnesses here: if we could successfully predict and prevent psychosis, we'd be doing a lot of good.

Ruhrmann, S., Schultze-Lutter, F., Salokangas, R., Heinimaa, M., Linszen, D., Dingemans, P., Birchwood, M., Patterson, P., Juckel, G., Heinz, A., Morrison, A., Lewis, S., Graf von Reventlow, H., & Klosterkotter, J. (2010). Prediction of Psychosis in Adolescents and Young Adults at High Risk: Results From the Prospective European Prediction of Psychosis Study Archives of General Psychiatry, 67 (3), 241-251 DOI: 10.1001/archgenpsychiatry.2009.206

Predicting Psychosis

"Prevention is better than cure", so they say. And in most branches of medicine, preventing diseases, or detecting early signs and treating them pre-emptively before the symptoms appear, is an important art.

Not in psychiatry. At least not yet. But the prospect of predicting the onset of psychotic illnesses like schizophrenia, and of "early intervention" to try to prevent them, is a hot topic at the moment.

Schizophrenia and similar illnesses usually begin with a period of months or years, generally during adolescence, during which subtle symptoms gradually appear. This is called the "prodrome" or "at risk mental state". The full-blown disorder then hits later. If we could detect the prodromal phase and successfully treat it, we could save people from developing the illness. That's the plan anyway.

But many kids have "prodromal symptoms" during adolescence and never go on to get ill, so treating everyone with mild symptoms of psychosis would mean unnecessarily treating a lot of people. There's also the question of whether we can successfully prevent progression to illness at all, and there have been only a few very small trials looking at whether treatments work for that - but that's another story.

Stephan Ruhrmann et al. claim to have found a good way of predicting who'll go on to develop psychosis in their paper Prediction of Psychosis in Adolescents and Young Adults at High Risk. This is based on the European Prediction of Psychosis Study (EPOS) which was run at a number of early detection clinics in Britain and Europe. People were referred to the clinics through various channels if someone was worried they seemed a bit, well, prodromal

Referral sources included psychiatrists, psychologists, general practitioners, outreach clinics, counseling services, and teachers; patients also initiated contact. Knowledge about early warning signs (e.g., concentration and attention disturbances, unexplained functional decline) and inclusion criteria was disseminated to mental health professionals as well as institutions and persons who might be contacted by at-risk persons seeking help.

245 people consented to take part in the study and met the inclusion criteria meaning they were at "high risk of psychosis" according to at least one of two different systems, the Ultra High Risk (UHR) or the COGDIS criteria. Both class you as being at risk if you show short lived or mild symptoms a bit like those seen in schizophrenia i.e.

COGDIS: inability to divide attention; thought interference, pressure, and blockage; and disturbances of receptive and expressive speech, disturbance of abstract thinking, unstable ideas of reference, and captivation of attention by details of the visual field...

UHR: unusual thought content/delusional ideas, suspiciousness/persecutory ideas, grandiosity, perceptual abnormalities/hallucinations, disorganized communication, and odd behavior/appearance... Brief limited intermittent psychotic symptoms (BLIPS) i.e. hallucinations, delusions, or formal thought disorders that resolved spontaneously within 1 week...

Then they followed up the 245 kids for 18 months and saw what happened to them.

What happened was that 37 of them developed full-blown psychosis: 23 suffered schizophrenia according to DSM-IV criteria, indicating severe and prolonged symptoms; 6 had mood disorders, i.e depression or bipolar disorder, with psychotic features, and the rest mostly had psychotic episodes too short to be classed as schizophrenia. 37 people is 19% of the 183 for whom full 18 month data was available; the others dropped out of the study, or went missing for some reason.

Is 19% high or low? Well, it's much higher than the rate you'd see in randomly selected people, because the risk of getting schizophrenia is less than 1% lifetime and this was only 18 months; the risk of a random person developing psychosis in any given year has been estimated at 0.035% in Britain. So the UHR and COGDIS criteria are a lot better than nothing.

On the other hand 19% is far from being "all": 4 out of 5 of the supposedly "high risk" kids in this study didn't in fact get ill, although some of them probably developed illness after the 18 month period was over.

The authors also came up with a fancy algorithm for predicting risk based on your score on various symptom rating scales, and they claim that this can predict psychosis much better, with 80% accuracy. As this graph shows, the rate of developing psychosis in those scoring highly on their Prognostic Index is really high. (In case you were wondering the Prognostic Index is [1.571 x SIPS-Positive score >16] + [0.865 x bizarre thinking score] + [0.793 x sleep disturbances score] + [1.037 x SPD score] + [0.033 x (highest GAF-M score in the past year – 34.64)] + [0.250 x (years of education – 12.52)]. Use it on your friends for hours of psychiatric fun!)

However they came up with the algorithm by putting all of their dozens of variables into a big mathematical model, crunching the numbers and picking the ones that were most highly correlated with later psychosis - so they've specifically selected the variables that best predict illness in their sample, but that doesn't mean they'll do so in any other case. This is basically the "voodoo" non-independence problem that has so troubled fMRI, although the authors, to their credit, recognize this and issue the appropriate cautions.

So overall, we can predict psychosis, sometimes, but far from perfectly. More research is needed. One of the proposed additions to the new DSM-V psychiatric classification system is "Psychosis Risk Syndrome" i.e. the prodrome; it's not currently a disorder in DSM-IV. This idea has been attacked as an invitation to push antipsychotic drugs on kids who aren't actually ill and don't need them. On the other hand though, we shouldn't forget that we're talking about terrible illnesses here: if we could successfully predict and prevent psychosis, we'd be doing a lot of good.

Ruhrmann, S., Schultze-Lutter, F., Salokangas, R., Heinimaa, M., Linszen, D., Dingemans, P., Birchwood, M., Patterson, P., Juckel, G., Heinz, A., Morrison, A., Lewis, S., Graf von Reventlow, H., & Klosterkotter, J. (2010). Prediction of Psychosis in Adolescents and Young Adults at High Risk: Results From the Prospective European Prediction of Psychosis Study Archives of General Psychiatry, 67 (3), 241-251 DOI: 10.1001/archgenpsychiatry.2009.206

Holy Week

This week is Holy Week. And our 2nd week off of school. Last week we were on Spring Break. This week we don't have school because it's Holy Week and I go to a Catholic School. But my Dad had to go back to work. He has to work until Wednesday.

We've been going to church almost every day during Lent. We go Tuesday, Thursday, and Friday nights. And on Sundays. I go every morning for school. My Dad and my Nana go on Wednesdays at lunch time too!

But we all enjoy going to church. This week, we are going every day. I wish my Nana was going to be here for Easter. But she is going to visit her family. We're going to miss her. I'm going to miss her a lot. Because I don't have school this week. Last week, she came over a few times. We cooked and baked. And she helped me with my sewing. We had a lot of fun! :) C

Practicals

Uh oh. Science education in British schools is in trouble, say the BBC:

'Too few' practical experiments in science lessons

For according to an online poll conducted by the Science Learning Center,

A combination of curriculum pressure and over-assessment is strait-jacketing science teachers and limiting the amount of time spent on vital classroom practicals, according to a survey...96% of the 1,339 science teachers and technicians surveyed said they were in some way hindered from undertaking science practical work.

How, well, scientific this poll was we are not told, and as a poll it only tells us what people think, not whether practicals are actually getting harder to do or less common. But still, let's suppose it's true. Does it matter? Practicals are widely seen as an important part of science education. But what good they really do?

One answer is that practicals teach you experimental skills that you'll need if you want to do research. That would be good if it were true, but it's not. I went to a good school and we had many practicals, but as far as I can remember not one of them was useful to me when studying science at university or as a researcher. In physics we did stuff with springs and pendulums. None of the physicists I know have touched one since school. In biology, I looked at plenty of yeast down a microscope, and counted a bunch of shells on a beach, but not once did I run a Western blot or do some PCR, basic techniques that almost all biologists actually use in real life.

Maybe practicals serve to "help students to develop skills such as observation", as 82% of the polled science teachers think? If so, they are not very good at it: what usually happened at my school anyway was that most people's experiments wouldn't work for whatever reason, so instead of observing and recording the actual results, people looked up what the answer was meant to be and fudged their data to fit. Even when everything did work this didn't teach us to observe, because we already knew what to expect, so it simply confirmed that we'd done it right.

Perhaps they're there to help us "develop an understanding of scientific enquiry" (80%)? I hope not, because doing real science is almost exactly the opposite of doing a practical. You don't get told what to do, you have to decide what to do in order to answer a question; you don't get told what methods to use; you don't know what the answer should be; and you don't know that your experiment will even work, because no-one has done it before.

In my experience practicals succeed at doing one thing: they make science lessons less boring. They're essentially entertainment. This is not a criticism - anything that keeps kids interested in science is a good thing, and a well-run practical is a lot more interesting than a textbook will ever be. So they're important. But we shouldn't pretend that practicals actually show people how to do science.

For that matter, though, neither does anything else: university practicals ("labs") don't either, although they're more likely to involve useful experimental techniques. Doing science is a skilled activity, like swimming: you can't be taught it in the abstract. A good teacher might help by holding your hand and making sure you don't sink, but ultimately you learn by diving in and actually doing it.

Practicals

Uh oh. Science education in British schools is in trouble, say the BBC:

'Too few' practical experiments in science lessons

For according to an online poll conducted by the Science Learning Center,

A combination of curriculum pressure and over-assessment is strait-jacketing science teachers and limiting the amount of time spent on vital classroom practicals, according to a survey...96% of the 1,339 science teachers and technicians surveyed said they were in some way hindered from undertaking science practical work.

How, well, scientific this poll was we are not told, and as a poll it only tells us what people think, not whether practicals are actually getting harder to do or less common. But still, let's suppose it's true. Does it matter? Practicals are widely seen as an important part of science education. But what good they really do?

One answer is that practicals teach you experimental skills that you'll need if you want to do research. That would be good if it were true, but it's not. I went to a good school and we had many practicals, but as far as I can remember not one of them was useful to me when studying science at university or as a researcher. In physics we did stuff with springs and pendulums. None of the physicists I know have touched one since school. In biology, I looked at plenty of yeast down a microscope, and counted a bunch of shells on a beach, but not once did I run a Western blot or do some PCR, basic techniques that almost all biologists actually use in real life.

Maybe practicals serve to "help students to develop skills such as observation", as 82% of the polled science teachers think? If so, they are not very good at it: what usually happened at my school anyway was that most people's experiments wouldn't work for whatever reason, so instead of observing and recording the actual results, people looked up what the answer was meant to be and fudged their data to fit. Even when everything did work this didn't teach us to observe, because we already knew what to expect, so it simply confirmed that we'd done it right.

Perhaps they're there to help us "develop an understanding of scientific enquiry" (80%)? I hope not, because doing real science is almost exactly the opposite of doing a practical. You don't get told what to do, you have to decide what to do in order to answer a question; you don't get told what methods to use; you don't know what the answer should be; and you don't know that your experiment will even work, because no-one has done it before.

In my experience practicals succeed at doing one thing: they make science lessons less boring. They're essentially entertainment. This is not a criticism - anything that keeps kids interested in science is a good thing, and a well-run practical is a lot more interesting than a textbook will ever be. So they're important. But we shouldn't pretend that practicals actually show people how to do science.

For that matter, though, neither does anything else: university practicals ("labs") don't either, although they're more likely to involve useful experimental techniques. Doing science is a skilled activity, like swimming: you can't be taught it in the abstract. A good teacher might help by holding your hand and making sure you don't sink, but ultimately you learn by diving in and actually doing it.

BOM DIA, MEUS LINDOS AMIGOS!!!

Quero aproveitar e agradecer a todos os meus amigos.
Dizer que estou um pouco ausente em função do trabalho.. Estou com aulas de reforço em casa, para ajudar as crianças com dificuldades de aprendizagem..Está muito corrido. mas sempre estarei te visitando.
Só peço um poquinho de carinho e compreensão. Esta muito puxado.
Mas vou manter contato com você.
És um SER muito Especial na minha VIDA!!!

A VOTAÇÃO CONTINUA ATÉ A MANHÃ.
CONTAREI COM O SEU VOTO.

Vote no Melhor Texto AQUI! 8. Sandra Andrade: Onde cresceu o meu Pai: Bela e pequena, Ituporanga

Poetas-Um Voo Livre-

Sinal de Liberdade-uma expressão de sentimento-

Blog Coletivo-Uma Interação de Amigos-

Meus Mimos-E SEUS PRESENTES-

SANDRA

Where To Buy Converse High Heels

On Thursday April 1 all go to the Plaza de los Dos Congress!!



Hello friends!.
On Thursday April 1 will be an event in the Plaza de los Dos Congresos TGD-Parent organized by Argentina in commemoration of International Day of Autism Awareness.
As you know, here in Argentina, on Friday, April 2 in addition to being a holiday for Easter is celebrated Veterans Day and Memorial Falklands. Whereupon, organize something for this day is impossible. That's why we decided to move the event to this day.
To give more detail about it, I then publish the information which I received by mail through the mail TGD-PADRES:

"Friends

as you guys know on April 2, is the global day of awareness about autism, Resolution No. ° 62/139, adopted by the United Nations on December 18, 2007.

Just like that, last year, PDD PARENTS, your contribution will make the next day Thursday 1 April at the Plaza the two conferences, Callao and Rivadavia Avenue . Since the April 2 meet several things (holidays, long weekend, day Falklands, Good Friday, the anniversary of the death of dr. Alfonsin, etc)

Our proposal is from 12 pm, until 16 pm.

We will make our contribution to society to raise awareness about the disorder suffered by our children, who lead the fight so they can have access to treatments, education and a full social life. We will make a great flyer that contains a brief summary of PDD concept, its main symptoms of alarm and our demands. At 15.30 there will be a release of balloons, and then will say a few words of closure.

also be a good opportunity to gather signatures for our bill, as well as a new opportunity to meet and exchange experiences.

call on all parents, professionals, friends, media, family and neighbors in the city to participate, especially with the presence, albeit 30 minutes or 4 hours, and can cooperate in qeu, flyers, collect signatures, encouraging. also ask the diffusion of the banner attached to acquaintances, relatives, dae media communication, facebook chains, to anyone you know. diffusion that everyone can do will be valuable for everyone.

invite you to take flags or signs that identify us, they can download from the following link

http://www.tgd- padres.com. ar / diffusion. Htm

invite and ask for this via our referring to the same April 1 may be made manifest of this kind in each of the provinces.

remember, and particularly the new sucriptos from the list of all the country you can contact our references for each province in the following link

http://www.tgd- padres.com. ar / contact. Htm

although an awareness day, is also a holiday!

expect them.

SUSPEND OR NO RAIN, NO NOTHING. "


also attached the press release they sent for distribution in any field, especially those who have access to media.
Personally, I took some copies to take to the garden of my son to be distributed, as well as neighboring businesses. Here it is:

Press Release April 1, 2010

So April 1 Plaza de los Dos Congresos: GOING BEYOND!

I'll be there, taking advantage of Valencia's grandparents do not work that day. In this way everyone wins, because I'm going quiet and he has blast with her grandparents, who aware of everything ... best, no?
So to all those mothers of Argentina that could go would be nice if we can find there on this special day. Hopefully we can organize ourselves so that you can give!. My email is posted on my blogger profiled, as well as contact the little sign in the right column Facebook blog. Anything write me and see how we can arrange to meet.

are waiting!

Birthday Party

Yesterday we had a big birthday party at our house. It was for Maribel, Lauren, my Nana, and me. All of our birthdays are close together. And Lauren and Maribel's moms just had babies. Their birthday parties were supposed to be last weekend. But my Nana and my Tio Berto asked us if we could make them all at the same time. Since that is when the babies started to come. I was really excited! And my Dad said it was OK to have all the parties together.

Maribel and Lauren turned 3. I turned 12. I'm not sure how old my Nana is. But she is 20 something. Tio Berto asked me to keep the secret. We surprised my Nana. She thought the party was just for us 3 girls. But Tio Berto bought my Nana a big birthday cake, her own pinata, and lots of presents. :)

Our birthday parties are always Matanzas too. That's when you kill a pig and cook it. Early yesterday morning, all my tios and my Dad killed 3 pigs. And then they started to cook. They're really good at it. 2 of the pigs had been at my Tio Berto's house. And 1 had been here. We fatten them up until the day they kill them. My favorite part, are the chicharrones. It's pretty much fried pork fat. But it tastes good in fresh tortillas. :)

Everyone had a lot of fun! My tios played too! They're mariachis. And my Nana sang with them. They even got Maribel to sing a song. She's getting really good! There was a lot of dancing and eating. And we got to see both sets of twins. They came for a little while on their way home.

This was my best birthday ever! I got to spend it with a lot of people I love. And I got to share my birthday party with my 2 friends and my Nana! :) C

BOM DIA MEUS LINDOS AMIGOS VIRTUAIS....

TEM VOTAÇÃO NA ALDEIA DE MINHA VIDA..LÁ EM PORTUGAL..
ABAIXO DESSA IMAGEM LÁ NA ALDEIA TEM A BARRA PARA VOTAR.
CONTO COM O SEU CARINHO.

A VOTAÇÃO VAI DE HOJE DIA 28 ATÉ DIA 31.
NÃO ESQUEÇA. CONTO COM VOCÊ.

BLOGAGEM DE MARÇO

Vote no Melhor Texto AQUI! 8. Sandra Andrade: Onde cresceu o meu Pai: Bela e pequena, Itupiranga

NÃO ESQUEÇA É NO Nº 8.
CARINHOSAMENTE, AGRADEÇO SEU VOTO, MEU QUERIDO AMIGO(A)VIRTUAL...

PARA REVER O TEXTO CLIQUE AQUI
http://aldeiadaminhavida.blogspot.com/2010/03/onde-cresceu-meu-pai-bela-e-pequena.html

Blog Coletivo-Uma Interação de Amigos- TEM UM CAFEZINHO PARA VOCÊ..VOU TE ESPERAR...

Meus Mimos-E SEUS PRESENTES-

SANDRA

How Long Will Mayonnaise Packets Last

visit with your neurologist and news in your treatment ...

On Tuesday we visited with Dr. Comas, your family doctor, excellent professional and human being. As I said in other entries, we will always see him every three months to evaluate you and see how they follow from then on treatment. Evaluate whether you need to take another course or if this road we are doing well ... It is super container with us, and very sweet to you.

He was happy, because before entering to his office I told you you had to greet and kiss. So when you came in you said: "Hi Dotor Cobas!, And TAS?." Hahaha!, And he with a huge smile to hear you say those words I returned the greeting with a kiss and a "Hey Valentine!, How you doing?"
This return, in addition to carrying some material with images to see how little by little you improve your language, I decided to take your beloved whiteboard with your bookmarks, because it seemed a good idea to observe how to draw, and as you write single words, being aware of what you write and not doing it "by heart."
His mouth fell open when you took the marker and started write your name, so prolijito, so clear. He said: "how awful!", "For his age is amazing, because even in children without this diagnosis is very difficult to see these achievements."
was laughing when I answered what you asked and until you tell (your way) moments before the reception, we had skidded on the floor and you had fallen flower giving blow in the mouth: "I fell!, flat wrong!, here mouth! "
put us happy to see him so happy with the little steps that you are giving ... and realize that we are on track, or at least I tried. He told us he could see that your language and your connection had improved markedly and the mischief in your eyes was incredible.
Your hyperactivity, often beyond us, but improved a lot, sometimes you have days when you do not stop a second and everything gets boring and any good reason for a tantrum. Your dad let her know your concerns about whether it would be necessary to evaluate the possibility of medicate, to what He said no.
He explained that there are two types of hyperactivity, both of which went hand in hand or were the result of a neurological problem: that which is revealed when the children were making up things or steps in its maturation, which become very restless, bored quickly of all, put anxious and looking to explore and look around all the time and did not stop a second, we said it was inevitable and which had to be filled with patience and set limits. The other is one in which children have an activity "nonsense" walking disconnected from side to side, climbing all over, without showing any interest in any business or any person. That this type of hyperactivity of you had noticed during the first consultation, which did not stay still for a second, I went up to the table, you climb the scale, to the chair, you lowered your, walked from one side to another, try to open the closet doors, the office, at which point should get you so you will not escape. That today this is not the case, he watching you now, to have a dialogue with you, see how you cope, and understand everything, they respond to the slogans and others, sees no reason to think medicate. That relieved me a lot.

also asked me to remind you that room were ... I told him, as did stay in room two in 2009, now with 4 years you were making room 3. He told me to see you wondered why you were cognitively thought for a 4-room quietly. I commented that your bosom Silvi had also discussed the same day of the meeting of parents in the garden. But both were agree that while this is true, there are several aeras where you're still out of date for your age and in my opinion, you feel lost in a room 4. To be in room 3 was going to allow you time to mature and on the other hand, it was good, in a way, you're a little ahead of the rest of your peers in terms of content that works with you Silvi in the room, because this way we avoid frustration on your part.

talked also the theme of this year, I wanted to give it another path to your treatment and stop traveling across both collective and forth every day of the week. It was exhausting for both, but especially for you. So for this and other reasons I decided to leave to the psychologist with whom we work from 2008 until late 2009, certainly on good terms and super grateful for the work they had done with Valen and how much he had been with him. We decided to find a psychologist who could work with you at home.
Your neurolonguista and a couple of moms friends recommended us a psychologist who makes home therapy (CBT) to take into account. We contacted her, and truth, we loved it!. We felt super professional, very sweet and very organized. We really liked the plan of treatment that you want to help implement. So after having a meeting with it and consult with the social work we decided to go this way.
I think this type of therapy is going to come in handy to achieve more.

in brackets, said he never did this type of therapy Valen, because at first I was not quite agree, I thought it would be too. On the other hand Dr Comas we suggested that we start with the professionals that he recommended to us and see how Valencia responded that according to that from then on we would see that course would take.
you are booted to Rachel, you neurolinguist and Silvia, your psychologist, both in clinic, which then add TO and music therapy ... Responded so well to treatment with each of them and although at first it was slow and cost hooked, you did and the progress is going to see over the course of months. Thus decided to continue on this path.
I think with this new professional can achieve many things, and that, obviously, is what we aim for.

The idea is to come (after social work aprube me because until that happens will come less) twice a week two hours each time. Have meetings to guide and control us and also have meetings once a month in the garden with your womb and the principal. Dr Comas
strongly agreed and believes that going barbarian come to polish certain aspect of your behavior with that deal more difficult for us. So we will make a note to introduce social work so we cover all the hours of treatment. Hopefully with this is enough and what they approve.

So this year started with everything. With this therapy Agustina and called the new psychologist who is super sweet with you and goes beyond patience, lol!, And the rest of the therapies that keep doing: neurolinguistics (still with Rachel), TO (with Leo ), music therapy (with Flavia) and spa on Saturday (with Ceci and Flower)., most obviously, integration into your garden with Lucia who hit her with a wave that is very beautiful and tender with you. So

bold mine, we will follow, struggling to see small step for step, loving you as always ... back at you every smile, every kiss, every hug, every look.
Here we will keep fighting melee with autism, to give battle, as every day of our lives. Here we
, celebrating a new word every mischief, each charade, everything that makes us realize that you were more connected with us, with your loved ones in your environment.
for us is to touch the sky with my hands and feel renewed hope and faith is enlarged with every achievement yours, however small, because for some will be small steps, but we are leaps and bounds.

We love you!

H1N1-- A GRANDE POLÊMICA!!!

FAZER OU NÃO FAZER A VACINA???
EIS A QUESTÃO!!!!

RECEBI POR EMAIL, VÁRIOS TEMAS SOBRE A H1N1

8 Motivos para Não tomar a vacina da H1N1

A vacina H1N1 contém mercúrio - a segunda substância mais perigosa do planeta depois do urânio!

O veneno de uma cascavel é menos perigoso que o mercúrio!

O Mercúrio em outras vacinas está ligado à epidemia de autismo entre crianças!

. Ela contém esqualeno, uma substância que quando injetada no corpo pode fazer o sistema imunológico humano voltar-se contra si mesmo!

. Ela contém células de câncer de animal que pode provocar câncer nas pessoas!

. Até o governo federal não está confiante quanto à segurança da vacina H1N1, é por isso que foi dada às indústrias farmacêuticas imunidade contra ações judiciais.

Isto significa que se seu filho ou esposa ficar inválido ou morrer por causa da vacina H1N1, você não poderá processar a indústria farmacêutica que fez a vacina!!!

. A entrada no mercado da vacina foi acelerada, o que significa que todos os efeitos colaterais a médio e longo-prazo não são conhecidos!

. Em 1976 o instituto médico afirmou que havia uma situação crítica relativa à gripe suína, quando de fato somente 5 pessoas em todo o país adoeceram com ela.

A situação crítica foi uma fraude na época tal como é uma fraude agora.

As pessoas começaram a morrer ou ficarem inválidas após tomarem a vacina contra a gripe suína!

. As estatísticas e os fatos estão sendo manipulados para provocar pânico!

O número de pessoas que supostamente estão com o H1N1 são somente estimativas, não números reais.

Os testes usados para o H1N1 NÃO são aprovados pela FDA (Agência de Drogas e Alimentos dos EUA), e esses testes NÃO são confiáveis!

Os poucos que supostamente morreram por causa do H1N1 também estavam com pneumonia ou outras doenças, entretanto, o instituto médico quer que você acredite que o H1N1 foi a única causa dessas mortes.

VÁRIOS ENDEREÇOS PARA VC SE INFORMAR SOBRE ESTA VACINA E DECIDIR SE VAI TOMAR OU NÃO.

http://realidadeoculta-novo.blogspot.com/2009/08/patente-da-vacina-h1n1-foi-registada-em.html

http://www.prisonplanet.com/canadian-doctor-h1n1-vaccination-a-eugenics-weapon-for-mass-extermination.html

Vacina H1N1 - Cientististas que ajudaram a desenvolver a vacina da varíola recusam
receber a vacina H1N1.

Alguns membros da comunidade médica não consideram a vacina segura.

VÁRIOS BLOGS DE PESSOAS SE MANIFESTANDO E CONTANDO CASOS.

http://so-me-apetece-cobrir.blogspot.com/2009/11/vacina-h1n1-portugal-polonia-e-suecia.html

VACINA H1N1 - NAO TOME, PESQUISE ANTES!
http://www.youtube.com/watch?v=qigXGlCEFo8

Tá chegando a hora da vacina Quem viver verá

1 - http://www.youtube.com/watch?v=PCJnBrPsuKk

2 - http://www.youtube.com/watch?v=erbo2vlIWSM

Cientistas e Enfermeiras recusam a tomar a Vacina para a Gripe A (proposta de Quarentena)
http://www.youtube.com/watch?v=vSyTwEP-cc4

Gripe Suína - A Tragédia da Vacina que Pode se Repetir
http://www.youtube.com/watch?v=4LCaEm5gvPQ

PARA VC SABER O QUE É O VIRUS

TUDO SOBRE O VÍRUS DA GRIPE SUÍNA H1N1 INFLUENZA
MINISTÉRIO DA SAÚDE BRASIL

http://www.youtube.com/watch?v=-dALUQcY-s4

VENHA FAZER PARTE E CONVERSAR UM POUQUINHO POR AQUI:

Poetas-Um Voo Livre-

Sinal de Liberdade-uma expressão de sentimento-

Blog Coletivo-Uma Interação de Amigos- TEM UM CAFEZINHO PARA VOCÊ..VOU TE ESPERAR...

Meus Mimos-E SEUS PRESENTES-

SANDRA

Going Home

We're on our way home. We had such a fun time at Nono's house! My Nono and I are already planning our summer trip. My Dad said that we will get to come for at least 2 weeks in the summer.

We couldn't stay longer because the big birthday party and Matanza is tomorrow. Maribel and Lauren are going to share my birthday party too! I'm so excited. Because I think we'll have a really good time. My Tio Berto and my Nana have been working hard on it all week. :)

My Dad also has to go back to work next week. But only for 3 days. He didn't get off for Holy Week like I did. I think my Nana is off too! She told me that she will come over and spend time with me. Probably on Monday or Tuesday. Because she is going out of town for the rest of the week.

But we had fun. And I bought lots of presents. I got some special ones for all the birthday girls too! And for the new babies. :) C

DESTAQUES!!!!

VEJA ONDE FUI DESTAQUE:

Obrigada amiga.Adorei o destaque.

obrigada amiga..

Obrigada JOANA


OBRIGADA MARCIA

OBRIGADA JOANA.




















OBRIGADA MENINAS.
FICO MUITO FELIZ COM O PRESENTE.
SANDRA

BOM DIA MEUS LINDOS AMIGOS VIRTUAIS....

HOJE EU QUERO SIMPLESMENTE AGRADECER...
ESTOU VISITANDO VOCÊ..NA MEDIDA DO POSSÍVEL.
SÃO MUITO OS AMIGOS...E ESTOU MUITO FELIZ COM A SUA PRESENÇA.
MUITO OBRIGADA!!!!O TEMPO ESTE MUITO CURTO..MAS ESTOU RETRIBUINDO..
UM FORTE ABRAÇO..SANDRA

Poetas-Um Voo Livre-

Sinal de Liberdade-uma expressão de sentimento-

Blog Coletivo-Uma Interação de Amigos- DEIXE O SEU CARINHO

Meus Mimos-E SEUS PRESENTES-

SANDRA

How Blind is Double-Blind?

There's a rather timely article in the current American Journal of Psychiatry: Assuring That Double-Blind Is Blind.

Generally, when the list of the authors' conflicts of interest (550 words) is nearly as long as the text of the paper (740 words), it's not a good sign, but this one isn't bad. Perlis et al remind us that if you do a double-blind placebo controlled trial:

The blind may be compromised in a variety of ways, however, beginning with differences in medication taste or smell. Of particular concern may be the emergence of adverse effects, particularly when those adverse effects are known to be associated with a specific medication ... Indeed, when the degree of unblinding is assessed in antidepressant trials, multiple reports suggest that it is extensive: at least three-quarters of patients are typically able to correctly guess at their treatment assignment.

The point of a placebo-controlled trial is that neither the patients nor their doctors know whether they're getting the placebo or the real drug. Hence the strength of the placebo effect should be the same in each group, allowing the "real" drug effect to be measured.

But if the drug causes side effects, as pretty much all do, then people could work out which group they're in by noticing whether they're feeling side effects or not. This might enhance the placebo effect in the drug group, and make the drug seem to work better than it really does. Or it might not. But the possibility that it might is worrying.

This is called the active placebo effect. It's why I'm skeptical of claims that scopolamine and ketamine have rapid-acting but short lived antidepressant effects. I may be wrong, but while both of these drugs have been shown to work better than placebo, both have very pronounced subjective effects, so there's no chance the blind will have been intact.

Whether the active placebo effect also underlies the efficacy of established antidepressants like Prozac is very controversial. There have been 9 trials comparing antidepressants to active placebos, i.e. drugs that have similar side effects to antidepressants and that should therefore help to preserve the blind. (The active placebos were all atropine which is basically the same as scopolamine.)

The trials were reviewed by antidepressant critic Joanna Moncrieff et al who found that the overall effect size of antidepressants vs. active placebos was d = 0.39. That's not very high, although it's not too bad, and ironically it's actually higher than the effect that Moncrieff's friend and fellow Prozac-baiter Irving Kirsch found in his famous 2008 antidepressant vs. sugar pill placebo meta-analysis, d=0.32. So if you take that seriously, the active placebo effect plays no part in antidepressant efficacy. However the active placebo trials are mostly small and old, so to be honest, we don't really know.

*

A point that's often overlooked is that a drug could have an active placebo effect via having a "real" psychoactive treatment effect. Diazepam (Valium), for example, has basically no peripheral side effects at all: unlike scopolamine it doesn't cause dry mouth, nausea, etc. But it is a tranquillizer; it causes calmness and, at higher doses, sleep. They're pretty noticeable. So if you were to give a depressed person Valium and tell them that it's not only a tranquillizer, it's an antidepressant, then the active placebo problem would arise.

In fact, any active drug will also produce active placebo effects - almost by definition, if you think about it. These may be hard to disentangle from the "real" effects. Say you're anxious about giving a speech so you take some diazepam hoping to feel calmer. A short while later you feel the lovely warm tranquillizing feeling setting in. Phew, you're calm now, anxiety's gone, the speech will be no worry. That thought might well be tranquillizing in itself. In other words the anti-anxiety effects of diazepam are partially driven by active placebo responses due to... the anti-anxiety effects of diazepam.

*

This leads onto another point. Suppose a drug has a genuine effect which improves some of the symptoms of a disease. Does that drug "treat" that disease? In a weak sense, yes, and it might be a helpful drug, but it's not a specific treatment. Morphine's very helpful in cancer, because it treats pain, but it doesn't cure cancer. Likewise insomnia is a symptom of depression, but we feel that in order to qualify as an antidepressant a drug has to treat the core symptoms: mood, anxiety, etc. rather than just being a sleeping pill.

But suppose someone suffered from low mood and you gave them a treatment which stopped them feeling any moods or emotions. That solves their low mood problem: no mood, no problem. But is that a specific treatment for depression? It's a bit of a grey area, but many would say no.

Many people say that this is exactly what SSRI antidepressants do: they blunt your emotions. That doesn't mean they're not helpful in depression: a lot of people find them very useful. I did. But then are they really "antidepressants", or just anti-mood? SSRIs are the drugs of choice not just for depression but also most anxiety disorders, and obsessive-compulsive disorder, etc. In fact they work better in OCD than they do in depression, relative to placebo. So are SSRIs actually antiobsessives that happen to be helpful in some cases of depression? Good question.

Here's Chris Rock on the issue of non-specific effects...

*

Perhaps an ideal clinical trial of a drug for a psychiatric condition should have 4 groups: the drug you're studying, another psychotropic with non-specific effects (e.g. Valium, or caffeine if you want a stimulant), an active placebo with purely peripheral side effects, and sugar pills. But even then, if the active drug performed better than the other 3 groups, a die-hard skeptic could say that maybe it's just more effectively causing non-specific sedation, or blunting, or whatever, than the Valium. Ultimately, a randomized controlled trial can never prove that a psychotropic drug has a specific as opposed to a non-specific effect.

So where do we stand? Does that mean we don't know what drugs do? No - unless we're some cloistered soul who only reads papers as opposed to talking to people, reading subjective reports, or taking drugs themselves. I know what alcohol does, not because I've read papers about it, but because I've drunk it. I've also been depressed and taken antidepressants, and for what it's worth, in my experience, some of the drugs currently marketed as antidepressants do have a specific anti-depression effect, although others don't. Overall, though, my view is that we know surprisingly little about what antidepressants actually do.

Perlis RH, Ostacher M, Fava M, Nierenberg AA, Sachs GS, & Rosenbaum JF (2010). Assuring that double-blind is blind. The American journal of psychiatry, 167 (3), 250-2 PMID: 20194487

Moncrieff J, Wessely S, & Hardy R (2004). Active placebos versus antidepressants for depression. Cochrane database of systematic reviews (Online) (1) PMID: 14974002

How Blind is Double-Blind?

There's a rather timely article in the current American Journal of Psychiatry: Assuring That Double-Blind Is Blind.

Generally, when the list of the authors' conflicts of interest (550 words) is nearly as long as the text of the paper (740 words), it's not a good sign, but this one isn't bad. Perlis et al remind us that if you do a double-blind placebo controlled trial:

The blind may be compromised in a variety of ways, however, beginning with differences in medication taste or smell. Of particular concern may be the emergence of adverse effects, particularly when those adverse effects are known to be associated with a specific medication ... Indeed, when the degree of unblinding is assessed in antidepressant trials, multiple reports suggest that it is extensive: at least three-quarters of patients are typically able to correctly guess at their treatment assignment.

The point of a placebo-controlled trial is that neither the patients nor their doctors know whether they're getting the placebo or the real drug. Hence the strength of the placebo effect should be the same in each group, allowing the "real" drug effect to be measured.

But if the drug causes side effects, as pretty much all do, then people could work out which group they're in by noticing whether they're feeling side effects or not. This might enhance the placebo effect in the drug group, and make the drug seem to work better than it really does. Or it might not. But the possibility that it might is worrying.

This is called the active placebo effect. It's why I'm skeptical of claims that scopolamine and ketamine have rapid-acting but short lived antidepressant effects. I may be wrong, but while both of these drugs have been shown to work better than placebo, both have very pronounced subjective effects, so there's no chance the blind will have been intact.

Whether the active placebo effect also underlies the efficacy of established antidepressants like Prozac is very controversial. There have been 9 trials comparing antidepressants to active placebos, i.e. drugs that have similar side effects to antidepressants and that should therefore help to preserve the blind. (The active placebos were all atropine which is basically the same as scopolamine.)

The trials were reviewed by antidepressant critic Joanna Moncrieff et al who found that the overall effect size of antidepressants vs. active placebos was d = 0.39. That's not very high, although it's not too bad, and ironically it's actually higher than the effect that Moncrieff's friend and fellow Prozac-baiter Irving Kirsch found in his famous 2008 antidepressant vs. sugar pill placebo meta-analysis, d=0.32. So if you take that seriously, the active placebo effect plays no part in antidepressant efficacy. However the active placebo trials are mostly small and old, so to be honest, we don't really know.

*

A point that's often overlooked is that a drug could have an active placebo effect via having a "real" psychoactive treatment effect. Diazepam (Valium), for example, has basically no peripheral side effects at all: unlike scopolamine it doesn't cause dry mouth, nausea, etc. But it is a tranquillizer; it causes calmness and, at higher doses, sleep. They're pretty noticeable. So if you were to give a depressed person Valium and tell them that it's not only a tranquillizer, it's an antidepressant, then the active placebo problem would arise.

In fact, any active drug will also produce active placebo effects - almost by definition, if you think about it. These may be hard to disentangle from the "real" effects. Say you're anxious about giving a speech so you take some diazepam hoping to feel calmer. A short while later you feel the lovely warm tranquillizing feeling setting in. Phew, you're calm now, anxiety's gone, the speech will be no worry. That thought might well be tranquillizing in itself. In other words the anti-anxiety effects of diazepam are partially driven by active placebo responses due to... the anti-anxiety effects of diazepam.

*

This leads onto another point. Suppose a drug has a genuine effect which improves some of the symptoms of a disease. Does that drug "treat" that disease? In a weak sense, yes, and it might be a helpful drug, but it's not a specific treatment. Morphine's very helpful in cancer, because it treats pain, but it doesn't cure cancer. Likewise insomnia is a symptom of depression, but we feel that in order to qualify as an antidepressant a drug has to treat the core symptoms: mood, anxiety, etc. rather than just being a sleeping pill.

But suppose someone suffered from low mood and you gave them a treatment which stopped them feeling any moods or emotions. That solves their low mood problem: no mood, no problem. But is that a specific treatment for depression? It's a bit of a grey area, but many would say no.

Many people say that this is exactly what SSRI antidepressants do: they blunt your emotions. That doesn't mean they're not helpful in depression: a lot of people find them very useful. I did. But then are they really "antidepressants", or just anti-mood? SSRIs are the drugs of choice not just for depression but also most anxiety disorders, and obsessive-compulsive disorder, etc. In fact they work better in OCD than they do in depression, relative to placebo. So are SSRIs actually antiobsessives that happen to be helpful in some cases of depression? Good question.

Here's Chris Rock on the issue of non-specific effects...

*

Perhaps an ideal clinical trial of a drug for a psychiatric condition should have 4 groups: the drug you're studying, another psychotropic with non-specific effects (e.g. Valium, or caffeine if you want a stimulant), an active placebo with purely peripheral side effects, and sugar pills. But even then, if the active drug performed better than the other 3 groups, a die-hard skeptic could say that maybe it's just more effectively causing non-specific sedation, or blunting, or whatever, than the Valium. Ultimately, a randomized controlled trial can never prove that a psychotropic drug has a specific as opposed to a non-specific effect.

So where do we stand? Does that mean we don't know what drugs do? No - unless we're some cloistered soul who only reads papers as opposed to talking to people, reading subjective reports, or taking drugs themselves. I know what alcohol does, not because I've read papers about it, but because I've drunk it. I've also been depressed and taken antidepressants, and for what it's worth, in my experience, some of the drugs currently marketed as antidepressants do have a specific anti-depression effect, although others don't. Overall, though, my view is that we know surprisingly little about what antidepressants actually do.

Perlis RH, Ostacher M, Fava M, Nierenberg AA, Sachs GS, & Rosenbaum JF (2010). Assuring that double-blind is blind. The American journal of psychiatry, 167 (3), 250-2 PMID: 20194487

Moncrieff J, Wessely S, & Hardy R (2004). Active placebos versus antidepressants for depression. Cochrane database of systematic reviews (Online) (1) PMID: 14974002