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Grey City Stroller

tmtnl — Sat, 07 Nov 2009 15:56:10 +0000

Just a quick update, before I forget the details.

On Thursday night I did something I haven’t done in a long time, I went somewhere on my own. Probably doesn’t sound like much, but for me it was a small victory. Since it was Guy Fawkes Night there were loads of Firework displays on all over the city, and the one with Les McKeown’s Legendary Bay City Rollers playing at it appealed to my love of incredibly cheesy retro entertainment – like the time I saw Right Said Fred play The Cathouse for £5 at the end of their career, they played Deeply Dippy 3 times in the set. I decided to miss out on The MacDonald Brothers, which I reckon was the right choice since I could hear them doing a cover of Mark Ronson’s cover of The Zutons Valerie. I just don’t “get” The Zutons, it seems like 90% of their songs are comprised of the singer repeating the same line over and over again. One day I’ll make a compilation of their most repetitive songs, with the repetition edited out, I’ll put it up on torrent sites under the name “The Zutons – Fixed” in tribute to the classic NIN remix album.

When I got near the park it was like being at a carnival, but a carnival where the dress code is ‘tracksuits tucked into your socks’. Normally I’d hate walking through a large group of people dressed like that, but they were all too busy being distracted by the bright lights and sparklers being sold by roadside traders. I now suggest carrying one of those necklaces with a blinking LED in your pocket at all times. Should a tracksuited oath threaten you then simply take it out and throw it as far away as you can, that should distract him for an hour or 2 while you make your escape. The band on stage when I arrived were S Club 3, who weren’t as abysmal as I’d expected them to be. I only caught their last 2 tracks, but I can’t remember what they were – not abysmal, but not memorable.

After S Club it was time for the fireworks display, which I was quite surprised by. The whole thing was done to music, and started with The Divine Comedy’s Light Of Day. After this it went through a whole load of songs themed around the sun and the moon, like The Beatles Here Comes The Sun. The fireworks were designed to compliment the music, and occasionally went right in time with the drums – all in all it was a well thought out display. What pleased the old indie kid in me the most was when they ended on Pulp’s Sunrise, all fireworks displays should be bookended by indie songs from the 90’s. I filmed the fireworks on my phone but missed the first few minutes, you can watch the 2 part video here and here. *videos uploading right now, so be patient*

With the fireworks out of the way it was time for Les McKeown’s Legendary Bay City Rollers, my main reason for being there in the first place. When they came on at first they had a few technical problems, so the first track was like a soundcheck. Turns out this was because Les McKeown had injured his foot on the way there, so he spent the whole set sitting on a bar stool – probably a strange scenario for a recovering alcoholic. Even though the band were massive in the 70’s it didn’t seem like many young people had a clue who they were. This worked out quite good for me as a lot of the crowd wandered off and I managed to get right up the front. THe keyboard player looked a bit like you’d imagine Bill Bailey to look if he’d never discovered drugs, the guitarist was like a slimmer Ian Lavender (Pike from Dad’s Army) and the bassist looked like a grumpy Richard Digance – perhaps because his monitors weren’t working throughout the entire set. They played a good set, but it wasn’t until the end when they really seemed to get their shit together. Just as I was getting a bit bored they started a great rendition of Shang-A-Lang which temporarily morphed into Deep Purple’s Black Knight. Fortunately I filmed this, and you can see it here.

So that’s the story of my first solo visit to the outside world in many moons, hopefully it won’t be too long until my next one.

*fingers crossed*

Drug use memories and relapse: Can medication provide addiction help?

Adi Jaffe — Sun, 01 Nov 2009 05:30:46 +0000

Originally posted on allaboutaddiction.com: About a year ago, while sitting in a lecture on learning

jacquelinekvz — Thu, 22 Oct 2009 20:32:03 +0000

It looks like the source of my dizzy spells may have been found. I had a referral to a neurologist about a month ago, and after checking my previous results and doing the usual tests said that it could be a form of migraine. Although this doesn’t really explain the earache, he said it would be worth trying anti-migraine medication and see what happens.

The medication he suggested was propranolol, an anti-hypertensive. After the first couple of weeks with only a very mild (positive) effect, I increased the dose. Since then, the dizziness has been significantly better – no nausea, no nearly falling and I can have more than a few beers and not feel like the world will never be still again! The anti-hypertensive effect has been noticable, particularly on a couple of occasions, but overall it’s fine and just a little low.

Not long after I started taking it, I was feeling a little light-headed so I went down to one of the clinics at my work to have my blood pressure taken. The nurse was quite obliging and it came out as low-normal. However, while she was taking and recording it, she was asking about what investigations I’ve had. As I’ve found with many people since this started, everybody seems to know what it could be.

Once people found out I was seeing an ENT last year, they would ask if he had checked for vertigo and Meniere’s disease. It was only with a lot of self-control that I didn’t give a sarcastic response about an ENT not knowing about any of that! Of course, these were the first things he investigated, being some of the most common causes of dizziness and earache.

Over the last 18 months or so that I’ve had this, I’d had that same response many times. People may have the right intention, but they need more common sense (and perhaps a little less ego).

The nurse took a different approach though, and asked what the problem was, what investigations I had had, and I’d already let her know I was on propranolol for suspected migraines. Being a nurse, I expected her to have a little more common sense than the others I’ve been referring to. However, she took a very strange approach and suggested that I needed to visit a cardiologist, as the low blood pressure could be causing dizziness!

I decided not to explain that I was actually just experiencing light-headedness due to the low blood pressure, caused by the anti-hypertensive. The dizziness was entirely separate and my blood pressure was fine before I started taking anti-hypertensives (surprisingly enough!) I decided to leave her with her delusions of medical knowledge and common sense and have since been taking my blood pressure at home. I only hope that she doesn’t try to give her patients advice.

Anyway, it seems that I might finally have found a cause for the dizziness, if not the earaches. Even after just a few weeks I’ve noticed a great improvement in my quality of life, fingers crossed that it continues to work!

Kill my memory, I am a soldier!

soulician — Fri, 25 Sep 2009 10:10:08 +0000

Propranolol … It is a drug that has been used for high blood pressure. It is also used in the treatment of irregular heart rhythms. It blocks the beta adrenalin receptor…Adrenaline functions through these receptors, blocking them will be helpful when too much adrenalin is not good for that part of the body.

I presented a review article published at a prestigious journal; Nature Neuroscience last January at a Neuroscience Journal Club where a staff member has to present an article that is relevant to psychiatry research. The paper’s title was: Targeting abnormal neural circuits in mood and anxiety disorders:from the laboratory to the clinic. It basically talks about the new treatment strategies to cure anxiety disorders. It was a very exciting and fulfilling article written by two great scientist; Helen Mayberg is one of them. She is an American scientist who works in Canada and one of the leaders of psychiatry research in Canada and in the world. If you’d like; you can access the full article free and read it. You can also see the power point presentation I presented at the Journal Club.

Among other new strategies such as deep stimulation of the brain (DBS) to treat anxiety disorders, the authors were also mentioning the use of propranolol in patients with anxiety disorders; such as in posttraumatic disorder (PTSD). PTSD comes after a traumatic event; such as being in a war and getting exposure to things that you really can not handle. Proporanolol can erase the memories right after the event occurs…So imagine the scene where a soldier is at emergency with a potential PTSD developing in the future. He gets his propranolol treatment and then he will forget what really happened…Actually as the authors state, he is going to forget the emotional part he observed during the traumatic event, but not what happened. This seems ok. We are curing a humanbeing. That is what doctors are for. Doctors simply fight against diseases. They do not support the concept of war, though. As phrased by the authors “ Although there are philosophical and ethical questions raised by a potential amnestic agent that would ‘erase’ a memory fully”; there must be questions to be asked to ourselves. Are not we going to justify the concept of “war” if we send back these soldiers back to war? Yes, a psychiatrist has to cure a PTSD patient; a woman who has been traumatized after raping, or a soldier after an explosion that occurred nearby. But this dilemma must be taken into account in favor of peace.

They are still working on this process. It is still not in use. But medical practice has be to used in favor of peace, as doctors in the world should work for world peace, not for war. Maybe, I am too naive?

How Much of Your Memory Is True?

pragmasynesi — Wed, 23 Sep 2009 16:14:33 +0000

As it turns out, you can’t always tell — just confirms how much you cannot trust your memories.

From the August 3, 2009 edition of Discover Magazine:

How Much of Your Memory Is True?

New research shows that memories are constantly being re-written by our minds.

by Kathleen McGowan

Rita Magil was driving down a Montreal boulevard one sunny morning in 2002 when a car came blasting through a red light straight toward her. “I slammed the brakes, but I knew it was too late,” she says. “I thought I was going to die.” The oncoming car smashed into hers, pushing her off the road and into a building with large cement pillars in front. A pillar tore through the car, stopping only about a foot from her face. She was trapped in the crumpled vehicle, but to her shock, she was still alive.

The accident left Magil with two broken ribs and a broken collarbone. It also left her with post-traumatic stress disorder (PTSD) and a desperate wish to forget. Long after her bones healed, Magil was plagued by the memory of the cement barriers looming toward her. “I would be doing regular things—cooking something, shopping, whatever—and the image would just come into my mind from nowhere,” she says. Her heart would pound; she would start to sweat and feel jumpy all over. It felt visceral and real, like something that was happening at that very moment.

Most people who survive accidents or attacks never develop PTSD. But for some, the event forges a memory that is pathologically potent, erupting into consciousness again and again. “PTSD really can be characterized as a disorder of memory,” says McGill University psychologist Alain Brunet, who studies and treats psychological trauma. “It’s about what you wish to forget and what you cannot forget.” This kind of memory is not misty and watercolored. It is relentless.

More than a year after her accident, Magil saw Brunet’s ad for an experimental treatment for PTSD, and she volunteered. She took a low dose of a common blood-pressure drug, propranolol, that reduces activity in the amygdala, a part of the brain that processes emotions. Then she listened to a taped re-creation of her car accident. She had relived that day in her mind a thousand times. The difference this time was that the drug broke the link between her factual memory and her emotional memory. Propranolol blocks the action of adrenaline, so it prevented her from tensing up and getting anxious. By having Magil think about the accident while the drug was in her body, Brunet hoped to permanently change how she remembered the crash. It worked. She did not forget the accident but was actively able to reshape her memory of the event, stripping away the terror while leaving the facts behind.

Brunet’s experiment emerges from one of the most exciting and controversial recent findings in neuroscience: that we alter our memories just by remembering them. Karim Nader of McGill—the scientist who made this discovery—hopes it means that people with PTSD can cure themselves by editing their memories. Altering remembered thoughts might also liberate people imprisoned by anxiety, obsessive-compulsive disorder, even addiction. “There is no such thing as a pharmacological cure in psychiatry,” Brunet says. “But we may be on the verge of changing that.”

These recent insights into memory are part of a larger about-face in neuroscience research. Until recently, long-term memories were thought to be physically etched into our brain, permanent and unchanging. Now it is becoming clear that memories are surprisingly vulnerable and highly dynamic. In the lab they can be flicked on or dimmed with a simple dose of drugs. “For a hundred years, people thought memory was wired into the brain,” Nader says. “Instead, we find it can be rewired—you can add false information to it, make it stronger, make it weaker, and possibly even make it disappear.” Nader and Brunet are not the only ones to make this observation. Other scientists probing different parts of the brain’s memory machinery are similarly finding that memory is inherently flexible.

Someday this new science of memory could cure PTSD and other mental traumas. Already it corrodes our trust in what we know and how we know it. It pokes holes in eyewitness testimony, in memoirs, in our most intimate records of truth. Every time we remember, it seems, we add new details, shade the facts, prune and tweak. Without realizing it, we continually rewrite the stories of our lives. Memory, it turns out, has a surprising amount in common with imagination, conjuring worlds that never existed until they were forged by our minds.

On the Trail of the Memory Meme
Neuroscientists have long viewed memory as a kind of neural architecture, a literal physical reshaping of the microstructure of the brain. In the 19th century, the pioneering neuroanatomist Santiago Ramón y Cajal theorized that information was processed in our heads each time an electrical impulse traveled across a synapse, the gap between one nerve cell and the next. Memories were made or altered, he proposed, when structures near the synapse changed.

More than a century later, the textbook description of episodic memory (conscious knowledge of an event) is a more sophisticated version of that same basic idea. Memory formation requires an elaborate chemical choreography of more than a hundred proteins, but the upshot is that sensory information, coded as electrical pulses, zips through neural networks of the brain. The impulses cause glutamate (one of the brain’s main neurotransmitters) to pop out of one nerve cell and travel across the synapse to activate the next by binding to its receptors, chemically active signaling stations on the cell surface. Ultimately the electrical and chemical signals reach the centers of memory, the almond-size amygdala and the banana-shaped hippocampus, adjacent structures buried on either side of the brain.

Neuroscientists believe that memory forms when neurons in these key brain structures are simultaneously activated by glutamate and an electrical pulse, a result of everyday sensory experience. The experience triggers a biochemical riot, causing a specialized glutamate receptor, called NMDA, to spring open and allow calcium ions to flood the cells. The ions stimulate dozens of enzymes that reshape the cells by opening up additional receptors and by prompting the formation of more synapses and new protrusions that contain still more receptors and synapses. In aggregate, these changes make neurons more sensitive to each other and put the anatomical scaffold of a memory in place.

Enacting all these changes takes time, and for up to a few hours the memory is like wet concrete—solidifying but not quite set, still open to interference. Once the process is over, though, the memory is said to be “consolidated.” In the textbook description, neuroscientists talk of memory the way geoscientists describe mountains—built through a dynamic process, but once established almost impossible to reshape quickly except by extraordinary means. By the late 1990s, this explanation of memory was so widely accepted by neuroscientists that its major author, Columbia University neuroscientist Eric Kandel, was awarded the Nobel Prize. It seemed that the most important questions about memory had been answered.

No wonder, then, that Nader—at the time a young postdoc studying the neurobiology of fear at New York University—was electrified when he attended one of Kandel’s lectures. “It was so beautiful and so convincing,” Nader says. But he began to wonder: What actually happens when we recall the past? Does the very act of remembering undo what happened? Does a memory have to go through the consolidation process again? Nader asked his adviser, the noted fear researcher Joseph LeDoux, if he could study these questions. LeDoux says his initial response was “Don’t waste our time and money,” but Nader talked him into it, little suspecting just how far this line of research would go.

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Meanwhile, doubts about the standard theory of memory were piling up in the world outside the neuroscience lab. In the early 1990s many people began reporting what seemed to be long-buried memories of childhood sexual abuse. These traumatic recollections frequently surfaced with the help of recovered-memory therapy techniques like hypnosis and guided imagery, in which patients are encouraged to visualize terrible experiences. Cognitive scientists suspected that some of these memories were bogus, the unwitting product of suggestion by the therapist. In support of this view, psychologist Elizabeth Loftus, then of the University of Washington, proved how easy it is to implant a false memory, especially one that is plausible. In a famous experiment, she gave volunteers a booklet narrating three true stories of events from their own childhood along with an invented tale that described their getting lost in the mall at age 5. When prompted later to write down all they could remember about the events, 25 percent were sure that all four events had actually happened to them.

Spurred on by the controversy over recovered memory, other cognitive scientists found that false memory is a normal phenomenon. David Rubin, who studies autobiographical memory at Duke University, observed that adult twins often disagree over who experienced something in childhood. Each might believe, for example, that he was the one to get pushed off his bike by a neighbor at age 8. Apparently, even the most basic facts about a past event (such as who experienced it) could be lost.

Even harrowing memories—the so-called flashbulb memories that feel as if they have been permanently seared into the brain—are not as accurate as we think. Less than a year after a cargo plane crashed into an Amsterdam apartment building in 1992, 55 percent of the Dutch population said they had watched the plane hit the building on TV. Many of them recalled specifics of the crash, such as the angle of descent, and could report whether or not the plane was on fire before it hit. But the event had not been caught on video. The “memory” shared by the majority was a hallucination, a convincing fiction pieced together out of descriptions and pictures of the event.

By the late 1990s, hundreds of psychology experiments suggested that the description of memory as a neurally encoded recapitulation of the past was so oversimplified as to completely miss the point. Instead of being a perfect movie of the past, psychologists found, memory is more like a shifting collage, a narrative spun out of scraps and constructed anew whenever recollection takes place. The science of memory was conflicted, with the neurobiological and psychological versions at odds. If a memory is wired into brain cells—a literal engraving of information—then why is it so easy to alter many years after the fact? It took an outsider to connect the dots.

Rewriting the Past
In the hierarchy of memory science, Karim Nader hardly ranked—a lowly postdoc, only 33 years old, and not even a memory researcher. But in 1999, inspired by Kandel’s talk, he set out to satisfy his big questions about how we recall and forget through a simple experiment. Nader tweaked a standard method used in fear research, in which rats are trained to associate a tone with an electric shock to the foot. The animals quickly learn that the sound is bad news. If they hear it weeks later, they freeze in fear. It is an easy way for the experimenter to know that they remember what took place.

Nader trained some rats, then played the tone again 14 days later, prompting them to remember. He also simultaneously injected them with a protein-synthesis inhibitor, which prevents new memory from forming by prohibiting alteration at the synapses. According to the standard model of memory, the chemical should have no effect since the memory of the tone has already consolidated. In reality, the treated rats’ memory disappeared. When Nader sounded the tone again later, the animals did not freeze. LeDoux was won over by this simple but powerful demonstration. In 2000 Nader’s paper on reconsolidation sparked a commotion in the world of memory research. He showed that reactivating a memory destabilizes it, putting it back into a flexible, vulnerable state.

Immediately reconsolidation became a fighting word. The gossip Nader heard terrified him; some of the biggest bigwigs of memory research thought he had made a ludicrous mistake. “I had no idea how much of a backlash there was going to be,” he says. Even so, Nader kept at his experiments, and in the fall of 2001, he was scheduled to present his research at a huge Society for Neuroscience meeting. It would be his moment of truth, his one chance to persuade the field to take his finding seriously. “I knew the old guard was saying, ‘This sucks; it’s all crap,’?” he says. “I knew if I didn’t hit a grand slam, this thing was dead.” The talk drew an overflow crowd of more than a thousand, including the legend himself, Eric Kandel. (“I really wanted to die,” Nader says.)

That day, by addressing the major criticisms of his research, Nader managed to convince his colleagues that memory reconsolidation was at least worth a serious look. Various labs took on the challenge, soon repeating his findings and discovering that many types of memory in many different species reconsolidate. Other groups began teasing out the reconsolidation process molecule by molecule. Nader’s group found that the NMDA glutamate receptor—which solidifies memory—also is involved in destabilizing it. A group led by Sue-Hyun Lee at Seoul National University demonstrated that proteins must be actively dismantled to destabilize a memory, more evidence that the old memory is actually changed as it is recalled.

Brain researchers are still grappling with the implications of this idea, trying to figure out exactly how malleable memory really is. “People are willing to say we have to go back to the drawing board,” says LeDoux, whose group has also continued to study reconsolidation. At the 2008 Society for Neuroscience meeting in Washington, D.C., 43 presentations focused on reconsolidation, and Nader was besieged by students and young researchers eager to talk.

With this new understanding of memory has come the even more startling possibility of new ways to control it: The era of memory treatment has arrived. For Rita Magil, who got just two doses of propranolol over the course of a single day, the results were encouraging. Her heart rate and muscle tension eased while the drug was in her body. She sensed the difference too. “I felt more detached from it,” she says. “I felt that I was relating a narrative rather than describing something right in front of me right now.” After the study was over, the flashbacks returned, though with less intensity. For her, the only real cure was time.

Six-session treatments with a total of 12 doses of propranolol have shown better results. Collaborating with Harvard psychiatrist Roger Pitman, who was the first to try propranolol for post-traumatic stress, the McGill group has treated about 45 PTSD patients, ranging from soldiers to rape victims. Most had been suffering for years. But after the longer treatment, their symptoms declined by half and stayed that way even six months afterward. They still remember what happened, but it is less disturbing. “They say: ‘I’m not thinking about it as much. It just doesn’t bother me as much anymore,’?” Brunet says. As a group, they are considered to be in remission.

The researchers must still prove that the improvement will last. If it does, it could offer rare hope to millions of people with PTSD, a disorder from which only a third completely recover.

Brunet hopes that similar treatments can address other psychiatric problems, too. Anxiety, acquired phobias, and addiction are increasingly described as disorders of emotional memory. An overly powerful fear memory, for example, can crystallize into a phobia, in which a relatively safe experience like flying in a plane is inextricably linked to a feeling of extreme danger. No matter how the phobic person tries, his emotional memory refuses to update itself to incorporate reassuring information. A treatment that restores his emotional memory to a flexible state could help him cope.

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Addiction is another kind of pathological remembering, but in this case the memory is pleasurable. Just as adrenaline sears emotional memories into the brain with the help of the amygdala, drugs of abuse enlist the amygdala and the brain’s reward centers to forge unforgettable memories of pleasure. Anything connected to the bliss reawakens the memory, in the form of craving. “When you see someone with a beer and a smoke and you get a craving, you are suffering from reminiscence, from an emotional memory,” Brunet says. Adapting experimental methods of forgetting to addiction might make it easier to quit.

“For a hundred years, people thought memory was wired into the brain,” Nader says. “Instead, we find it can be rewired.”

The Reconsolidated Life
While neuroscientists were skeptical of Nader’s findings, cognitive scientists were immediately fascinated that memory might be constantly revamped. It certainly seemed to explain their observations: The home run you hit in Little League? Your first kiss? As you replay these memories, you reawaken and reconsolidate them hundreds of times. Each time, you replace the original with a slightly modified version. Eventually you are not really remembering what happened; you are remembering your story about it. “Reconsolidation suggests that when you use a memory, the one you had originally is no longer valid or maybe no longer accessible,” LeDoux says. “If you take it to the extreme, your memory is only as good as your last memory. The fewer times you use it, the more pristine it is. The more you use it, the more you change it.” We’ve all had the experience of repeating a dramatic story so many times that the events seem dead, as if they came from a novel rather than real life. This might be reconsolidation at work.

Reconsolidation research has helped foster a growing sense that the flexibility of memory might be functional—an advantage rather than a bug in the brain. Reconsolidation might be how we update our store of knowledge, by making old memories malleable in response to new information. “When you encounter a familiar experience, you are remembering the original memory at the same time, and ?the new experience somehow gets blended in,” says Jonathan Lee of the University of Birmingham in England, who recently found evidence for this effect in animals. “That is essentially what reconsolidation is.” The evident purpose of episodic memory, after all, is to store facts in the hope of anticipating what might happen next. From the perspective of survival, constructive memory is an asset. It allows you to pull together scraps of information to simulate the future on the fly.

“The brain knows there is a future,” says neuroscientist Yadin Dudai, head of the department of neurobiology at the Weizmann Institute of Science in Israel, who collaborates with Nader and LeDoux. Facing something new, we want to link the novel information with memories to better interpret the situation. If the side effect is a few mistakes, that is probably a small price to pay. “Having a memory that is too accurate is not always good,” he says.

Put another way, memory and imagination are two sides of the same coin. Like memory, imagination allows you to put yourself in a time and place other than the one we actually occupy. This isn’t just a clever analogy: In recent neuroimaging studies, Harvard psychologist Daniel Schacter has shown that remembering and imagining mobilize many of the same brain circuits. “When people are instructed to imagine events that might happen in their personal future and then to remember actual events in the past, we find extensive and very striking overlap in areas of brain activation,” he says. Other researchers have found that people with severe amnesia lose their ability to imagine. Without memory, they can barely picture the future at all.

The Spotless Mind
Reconsolidation modifies old memories, but other new research points the way toward erasing them wholesale. One technique for blanking out the past, developed by Joe Tsien at the Medical College of Georgia, flows from his studies of memory formation. When calcium floods a neuron as a memory is formed, it turns on an enzyme called CaMKII (calcium/calmodulin-dependent protein kinase). Among many other things, the enzyme responds to signals from NMDA receptors, leading to more receptor activity and stronger signaling throughout the network of cells.

You would think, therefore, that the more CaMKII, the more robust a memory would be. But in experiments with mice, Tsien has found there is a limit. If he drives CaMKII above the normal limit while the animal is actively remembering an experience, the memory simply vaporizes, as the connections between the cells suddenly weaken. The effect happens within minutes, and it is permanent and selective, affecting the recalled memory while leaving the others unchanged. Indeed, when Tsien trained a mouse to fear both an unfamiliar cage and a particular tone, then pumped up CaMKII while the mouse was in the cage, it forgot the cage-fear memory but not the tone-fear memory. “At the time the memory was retrieved, it disappeared,” he says. “It erases the memory being recalled. It is feasible that by manipulating specific molecules, we can selectively alter memories in the brain.”

Todd Sacktor, a professor of physiology, pharmacology, and neurology at the State University of New York Downstate Medical Center in Brooklyn, has found a blunter but more powerful technique that can eradicate whole categories of memory. He studies protein kinase M-zeta (PKMzeta), which is involved in memory maintenance. As calcium rushes into a memory neuron, PKMzeta is synthesized, linking up with spare glutamate receptors and dragging them to the synapse, where memory construction occurs. With more receptors at the synapse, signals are boosted and amplified and the memory persists.

When Sacktor deactivated PKMzeta with a compound called zeta-inhibitory peptide (ZIP), he got a spectacular response: total amnesia for one type of memory. Rats that had learned a day or a month before to avoid part of a platform that was rigged with electric shock forgot everything they knew about the location generating the jolt. “You inhibit the PKMzeta and those glutamate receptors float away very, very fast,” he says. “As a result, the memory is lost—very, very fast.”

Certain types of memory are encoded in different brain areas, and depending on where Sacktor injects the inhibitor in his animals, he can zap away different categories of memory. In the hippocampus, he erases memory for spatial locations like the platform; in the amygdala, fear memories; in the insular cortex, memories of nauseating taste. Very rarely, Sacktor says, neurosurgeons remove nerve clusters to help disturbed psychiatric patients who do not respond to any other treatment. His research may eventually provide a way to erase memory without causing damage.

The implications are staggering. If stored memories were inscribed in the brain, it is hard to imagine how flipping one chemical switch could erase them so quickly. “It really is a paradigm shift in how people think about long-term memories,” Sacktor says. In the old view, erasure should cause permanent brain damage as the synapses are ripped apart. Instead, Sacktor’s rats’ brains remain intact. Once the ZIP treatment wears off, the animals behave and even learn normally again. “It’s like wiping a hard disk,” he says.

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ZIP is nowhere near ready for human use. First, the compound would have to be made activity-dependent in order to target specific memories. You would also have to find a way to get it to the right spot in the brain without using a needle. People are clamoring to be test subjects anyway. When Sacktor’s study first came out in 2006, people, especially rape survivors, tracked him down, imploring him to eradicate their painful memories. “They were suffering,” he says. “They couldn’t work or have relationships. Some of them wanted everything erased.” They didn’t care that it would also vaporize all they had ever known.

Benevolent Forgetting
If you feel that you’ve heard this story before, there’s a reason. Moviemakers love the idea of erasing memory, and they work a consistent theme: If you try to undo the past, you pay the price. Nader’s research supposedly inspired the 2004 movie Eternal Sunshine of the Spotless Mind, in which Jim Carrey and Kate Winslet both pay to have memories of their painful love affair obliterated. Needless to say, it makes them both miserable. But not as miserable as Arnold Schwarzenegger’s character in Total Recall, from 1990, in which he learns that his real memories have been erased, that his life is a fake, and that his faux wife, played by Sharon Stone, is trying to kill him.

You don’t have to be a rape survivor or a soldier to have memories you would rather forget. For most people, though, unpleasant memories also serve as a guide. Indeed, some fear the consequences of undermining appropriately bad memories—say, allowing a murderer to forget what he did. Members of the President’s Council on Bioethics warn that altering the memory of a violent crime could unleash moral havoc by lifting the repercussions of malice. “Perhaps no one has a greater interest in blocking the painful memory of evil than the evildoer,” their report cautions.

Beyond all this, memory is the essence of who we are. Eternal Sunshine of the Spotless Mind is difficult to watch as Carrey’s character flails around in confusion and loss. His fear and desperation may be a realistic portrayal of what it would be like to erase your memory: basically, a waking nightmare. Memory is how you know who you are, how you point yourself toward a destination. We already know that people with Alzheimer’s disease do not feel liberated. They feel utterly lost.

Thankfully, Nader and Brunet’s studies suggest much more benevolent possibilities. If he had received reconsolidation therapy, Carrey’s character would not have forgotten Winslet’s. He simply wouldn’t care that much about her anymore. He would be able to look at his failed relationship as if through the wrong end of a telescope. What is on the other side is still visible, but it is tiny and far away.

That is basically what all these scientists hope to do. Nader, Brunet, and Pitman are now expanding their PTSD study with a new, $6.7 million grant from the U.S. Army, looking for drugs that go beyond propranolol. They are increasingly convinced that reconsolidation will prove to be a powerful and practical way to ease traumatic memories. Sacktor also believes that some version of the techniques they apply in the lab will eventually be used to help people. Most recently, LeDoux’s lab has figured out a way to trigger reconsolidation without drugs to weaken memory, simply by carefully timing the sessions of remembering. “The protocol is ridiculously simple,” LeDoux says.

None of these researchers are looking to create brain-zapped, amoral zombies—or even amnesiacs. They are just trying to take control of the messy, fragile biological process of remembering and rewriting and give it a nudge in the right direction. Brunet’s patients remember everything that happened, but they feel a little less tortured by their own pathological powers of recollection. “We’re turning traumatic memories into regular bad memories,” Brunet says. “That’s all we want to do.”

Progress, Chaos, and Bathtime Fun

mejan — Wed, 18 Mar 2009 01:08:03 +0000

So. I’m sure some of you have been wondering if Lila had any SVT episodes, since we took her off the propranolol yesterday at noon. The answer is….NOPE! Not yet, anyway. She will still be closely monitored by Cardiology for a while longer, even after we leave the hospital, but we are VERY cautiously taking this as a positive sign. Her heartrate is still a little on the low end, but higher than before (low 100s to 120s), and we may need to give the medicine more time to leave her system before saying for sure.

Another positive result of taking Lila off the beta blocker is that she was awake a lot today. She is SO much more alert when she is awake too, Jon and I are obsessed. She did take a giant nap today, from 11-3, of course when Auntie Lyndsay was visiting, silly girl. We’ll have to work on her sleep schedule more once she’s home.

Staring intently at her goofy dad

Lila also had another follow up echo this morning. We don’t have the final report back on it yet, but the initial report looks like nothing has changed much since her echo on Friday (I think they referred to it as “unremarkable change”), and still shows a slight depression, which we’ve known about. We will likely have another echo before she is discharged, to be sure nothing new pops up. As a result from the echo, Lila was taken off of the lasix today as well. Cardiology wanted to keep her on it initially, but are happy with the echo results, so will be seeing how she does without it. Hopefully she will be unaffected by coming off of it, and her respiratory rate will stay in the normal range (it was high before going on the lasix). We already know the lasix did its job of flushing the excess fluid from Lila’s system, so we just need to see how her heart functions without it.

We will be having another meeting with Lila’s neonatologist and the Cardiology group tomorrow afternoon. This will mainly be to go over where we are on everything at this point, as well as to discuss the final results of the echo. The main items we have left, it seems, are to continue to monitor Lila as she comes off of the propranolol and lasix, and work on her feeding. I’m hesitant to even speak of an ideal situation for us at this point, so I won’t. Let’s just say that if all goes well with all of this, we could potentially be seeing the light at the end of the tunnel. Not that we have been given ANY timeframe for a discharge date, but it’s nice to know that we are slowly crossing things off of our list.

Lila did well with feeding again today. I know I say this a lot, but we do still have a lot of work to do with it. She will get there, with our help. She is probably nursing “well” about every other feeding, and is getting about 1/2 of what she needs when she does this. There are SO many factors that could be the cause of all of the less successful feedings–from her being sleepy, or over hungry, to being distracted by the alarms, people, and constant noise in the NICU. As I mentioned last night, this is something we will be working on with her doctors. So we will just stick with it, as frustrating as it can be, for all of us (not that SHE is frustrating us, the whole situation is–how many newborns do you know that stick to a strict feeding schedule, and mandatory amount of milk, per feeding? Yet we must make her do this, in order to get her home). Ugh. Anyway.

Another new baby came into our bay today too, so we have a full house in there. Talk about chaos. This of course also happened right at Lila’s 3pm feeding, so I was surprised that she even nursed at all. Thank goodness we have the window, and can hide back there.

The last big news we have for today, is that Lila got her first bath from her dad! The nurses have been giving her baths when we aren’t there, so it was nice to be able to do this with her. They both did SO awesome. Lila didn’t even cry, we think she kind of liked it! I know you’re probably wondering why I didn’t help–and trust me, by not participating, I was helping. I kept my comments to a minimum, and let dad do his thing. I’m sure he appreciated it.

Bathtime with dad

Snuggled up in a towel to get warm after her bath

I hope after tomorrow’s meeting, we have a more defined idea of where things stand with us…and how much farther we have to come, in order to get our little girl home. Jon and I were talking tonight about how it feels like we babysit all day, or “rent” her for the day. It’s weird how she feels so much like our daughter at some times, and at others, like we’re going through the biggest exam of our lives, to see if we are qualified to take her home or not. As amazing as everyone at Children’s has been to us, and to Lila, we can’t wait until this is over. I want my daughter home.

I swear, we didn't put her hands like that. She's just that cute.

Sleep well, sweet girl, we love you.

Keep the Courage

mejan — Tue, 17 Mar 2009 00:52:25 +0000

That’s what one of Lila’s doctors said to me today. She is the neurologist heading up the Hypothermia Protocol Therapy (and one of our favorite doctors), and stopped by tonight as I was leaving, just to say hi and check on Lila. She told me that Lila has shown amazing courage, and that we need to do the same. She also said that crying is not only okay, it is expected (I was a little teary, typical of every night, when I have to leave Lila). Neurology is going to be signing off on Lila’s case, and will do a follow-up appointment with us 6 months after she is discharged, but we are, for the most part, done with that side of things.

The cuteness just kills me.

Now we need to work on the cardiac side, and her eating. I met with Cardiology this afternoon, and they are recommending we take Lila off of the propranolol, to see if the SVT returns. The dose we have her on now (half of the original dose) is still keeping her heart rate just a touch low. In taking her off, we are looking to see if the SVT comes back, or if her heartrate will move into a more normal range. We would also see if Lila will be less sleepy once off of the beta blocker (and could possibly improve her feeding). We will eventually want to try to wean her from it anyway, and Jon and I decided we’d be more comfortable trying this in the current controlled setting, where Lila is being monitored 24/7, than trying to do so at home, in 6 months or a year. If the SVT returns, we will put her back on the beta blocker, possibly at an even lower dose. However, if we cut the current dose in half, it would be considered to have a “low theraputic effect”, so may or may not be effective. Alternately, there are other medications we can try, but carry more side effects than the beta blocker, and require more constant testing, so we are trying to avoid this if possible.

So Lila is off of the propranolol as of now–please pray that the SVT doesn’t come back. That would be the ideal outcome…and we could really use a break.

I also spoke with Lila’s neonatologist about trying other options with her feeding. She seems to be at a standstill with this, and I want to see if we can do anything to help move this along. We decided to keep an eye on her adjustment from going off the beta blocker first, and after a day or two, depending on how she does, we will work on other feeding options. We are going to try moving us to a room for her feedings, so there aren’t so many distractions, and so she doesn’t feel so stressed. I’m hoping the quiet helps. We may also work to feed her “on demand”, instead of on her current schedule of every 3 hours. This could backfire, and result in her snacking all day, but we have to try. I would also like to try to stop using the feeding tube for a period of time, and see if she will “give in” and eat once she is hungry. It’s a tricky situation, which I’m sure all of you parents can understand. I don’t want to stress her out, or have her associate feeding time with being a negative thing, but we need to get her eating orally, instead of depending on the feeding tube to provide her with a full belly. So we will be working with some of these options once we have more answers about her beta blocker. Who knows, coming off of that may make her more alert, and she may just pick up nursing on her own. Only time will tell.

Aunt Caitlin came to spend some time with us today, it was great having company this afternoon. Cait was able to listen to Lila cry for a bit, she was a little fussy when she first got there. But once she settled down, she slept most of the afternoon (Lila, not Cait). Lila loved hanging with her aunt, and heard lots of stories about her cousin Gracie, who is SO excited to meet her.

Hanging out with Aunt Cait, wide awake

There is another new baby in our bay today too, so we’re almost full over there (3 of 4 beds are full now). The weekend reprieve of having the bay to ourselves has ended, and it’s much more busy and crowded now. Sigh.

Jon’s first day back in the office went as well as could be expected. It was tough for him to be away from Lila, but I sent him pictures all day, and he will be seeing her tomorrow. It will be good for all of us to start getting used to Jon working again, especially since the money machine I keep in the basement is out of ink. It will just be easier once Lila is home with us, because he can go peek in on her sleeping when he gets home from work.

So, overall, a decent day. Tomorrow Lila will be having a follow-up echo, to just check on her heart again–hopefully there won’t be any new surprises (Cardiology doesn’t think there will be). We will be hoping and praying for no SVT episodes tonight (or ever) also.

The sweetest face ever, asleep in Aunt Cait's arms

Good night, little one, sleep well. We will see you tomorrow, we love you!

Drug to help people erase bad memories?

maryhealth — Sat, 14 Mar 2009 04:12:22 +0000

I was just listening to NPR, and found out to my surprise that researchers are seeking to launch a drug that will help people block out bad memories. The team at the forefront of this investigation is Dr Merel Kindt from Amsterdam. This drug is technically a “beta-blocker” called propranolol. Beta blockers are something that doctors commonly prescribe for people with heart disease.

These researchers in Amsterdam showed scary photos of spiders to people and then gave one group a placebo and one group this beta-blocker drug. People who took the drug apparently had very few residual symptoms of fear from their recent exposure to these scary spider pictures. So, of course, these days there is a drug to treat everything under the sun. But bad memories… really?

If you have been reading my blog, you likely already know I am NOT a big fan of medicine. In fact, for nearly everything I try to think about natural health alternatives. However, Kindt’s drug got me thinking.

Hmmm… what are the applications for this? Would this help me forget about all those deeply buried childhood events that haunt me? It might help me out to erase my disastrous relationship with my ex-boyfriend from my mind. Yes, that would indeed be rather nice. However, I am sure there are some rather uncool applications of this drug. Is it really right to control people’s emotions to this extent?

Here is a link to the article on Aol news- already with 237 comments. This is a hot topic indeed.

What do you think? Is a drug to block bad memories simpy a bad idea?

Pulmonary Fibrosis

sarahketurah — Thu, 26 Feb 2009 20:58:38 +0000

Scarring of the Lungs

First, what is Pulmonary Fibrosis? “Pulmonary Fibrosis literally means lung (pulmonary) scarring (fibrosis). The lung scarring occurs in the tissue of the lung called the interstitium, which supports the structures of the lung (air sacs/alveoli). There are an estimated 130-200 related diseases called Interstitial Lung Disease that are similar in characteristics and can result in scarring. Pulmonary Fibrosis causes the lung tissue to thicken and become stiff. Scarring inhibits oxygen from entering the blood stream.”

Symptoms include “shortness of breath (dyspnea), especially during or after physical activity, and a dry cough.” -Mayo Clinic

What damages your lungs? There are quite a few possible causes, including environmental factors, gerd, radiation, and various medical conditions, but don’t be surprised that it could be your medication. “Many drugs can damage your lungs, especially chemotherapy drugs (methotrexate, cyclophosphamide); medications used to treat heart arrhythmias and other cardiovascular problems (amiodarone, propranolol); certain psychiatric medications; and some antibiotics (nitrofurantoin, sulfasalazine).”-Mayo Clinic

If you are in the advanced stages of Pulmonary Fibrosis, your doctor may give you little hope. “No cure exists for pulmonary fibrosis, and current treatments often fail to slow the progress of the disease or relieve symptoms.”-Mayo Clinic

Before you give up, alternative medications may be your best option. Why Enzymes work: “Enzymes eat scar tissue and fibrosis. Fibrosis is scar tissue and most doctors learn in anatomy that it is fibrosis that eventually kills us all. Let me explain. As we age, which starts at 27, we have a diminishing of the body’s output of enzymes. This is because we make a finite amount of enzymes in a lifetime and we use up a good deal of them by the time we reach our 40’s (Cystic Fibrosis patients who have virtually no enzyme production to speak of, even as children usually don’t make it past their 20’s before they die of the restriction and shrinkage in the lungs from the formation of fibrosis or scar tissue).

So our body begins to dole out our enzymes with an eyedropper instead of with a tablespoon. Result: the repair mechanism of the body goes off balance and has nothing to reduce the over abundance of fibrin it deposits in nearly everything from simple cuts, to the inside of our internal organs and blood vessels. It is then when most women begin to develop things like fibrocystic breast disease, uterine fibroids, and endometriosis. We all grow arterial sclerotic (meaning scar tissue) plaque, and have fibrin begin to spider web its way inside of our internal organs, reducing their size and function over time. This is why as we age our wounds heal with thicker, less pliable, weaker and very visible scars.

If we replace the lost enzymes, we can control and reduce the amount of scar tissue and fibrosis our bodies have. As physicians in the US are now discovering, even old scar tissue can be “eaten away” from surgical wounds, pulmonary fibrosis, and kidney fibrosis even colloid years after their formation. Medical doctors in Europe and Asia have known this and used orally administered enzymes for such for over 40 years! “

Sounds too good to be true? If you have no options, why wouldn’t you try alternative medications. According to Biomediclabs, “Within 4 weeks, patients should notice improvement of their symptoms including shortness of breath and coughing with phlegm. After a 3-6 month treatment, patients should have significant improvement in their lung structure. We recommend that patients take a chest x-ray before and after the treatment and compare the diagnostic results to monitor their progress.”

Before I tried alternative medications, I didn’t truly believe in miracles. Serracor-NK was created for Pulmonary Fibrosis. I know it has changed my life, and I have Rheumatoid Arthritis. I believe in this product because of what it has done for me.

Small study indicates propranolol may stop previously frightening experiences, images from causing anxiety.

abrandemihl — Wed, 18 Feb 2009 00:24:25 +0000

Bloomberg News (2/16, Waters) reported that, according to a study published in the Feb. 15 advance online issue of Nature Neuroscience, the “widely used heart drug” propranolol “may be able to stop frightening images or experiences from lodging in the memory and repeatedly resurfacing to cause fear and anxiety.” For the study, researchers from the University of Amsterdam in the Netherlands “gave the medication” to 60 “test subjects in a complex experiment that measured how people reacted when they were shown pictures of spiders they’d been taught to fear.” The team “first conditioned their test subjects to fear a particular kind of spider by showing them pictures of the spider, followed by an electrical shock to the wrist.” By the following day, “the experience had been consolidated and stored in their memory.”
Participants were then “split into two groups — one was given the beta blocker propranolol and the other a dummy drug before both were shown the same pictures again,” BBC News (2/16) explained on its website. The investigators “assessed how fearful of the pictures the volunteers were by playing sudden noises and measuring how strongly they blinked, something called the ’startle response.’” The team found that “the group that had taken beta blockers showed less fear than the group that had taken the placebo pill.”
HealthDay (2/15, Perkel) added that “on the third day,” when the participants “were tested again,” the investigators found that the “physiological response to the fear-inducing cue — pictures of spiders — was eliminated in the propranolol group, but not in the placebo group.” The authors concluded that the study’s findings “are consistent with those of a recent preliminary study of patients with post-traumatic stress disorder in which post-retrieval propranolol seemed to reduce subsequent physiological responding to traumatic memory.” The Boston Globe (2/16) also covered the story.

Pill Could Erase Bad Memories

heidilore — Tue, 17 Feb 2009 19:24:29 +0000

*Thanks, Silky…disturbing*

Scientists have discovered a drug that could erase fearful memories in humans.

The method, using existing blood pressure pills, could be useful for weakening or erasing bad memories in people with post-traumatic stress disorder, the researchers say.

Unfortunately, other research has shown, bad memories stick better than good ones.

Studies in animal models have shown that fearful memories sometimes change when recalled, a process known as reconsolidation, and that this reconsolidation stage is vulnerable to the blood pressure drugs, called beta-adrenergic receptor blockers.

In the new study on humans, by Merel Kindt and colleagues at University of Amsterdam in The Netherlands, 60 subjects were taught to associate pictures of spiders with a mild shock, creating a fearful memory. Later, they were given either a beta-blocker called propranolol or a placebo.

The group given propranolol had a greatly decreased fear response to the spider pictures 24 hours later, according to a synopsis of the work from the journal Nature Neuroscience. And the fear response did not return, suggesting that their fear memory was completely erased.

Some ethicists see problems, question whether such treatments begin to alter what it means to be human.

“An interesting complexity is the possibility that victims, say of violence, might wish to erase the painful memory and with it their ability to give evidence against assailants,” said professor John Harris, an expert in biological ethics at the University of Manchester, in an article in the Daily Mail. “Similarly criminals and witnesses to crime may, under the guise of erasing a painful memory, render themselves unable to give evidence.”

Meantime, scientists are zeroing in on how fear grips the mind.

In 2005, researchers found a fear-factor gene that helps distinguish between people who have no fear and those who are afraid of everything. And last fall, scientists discovered the glue that keeps fearful memories stuck in the brain, a protein called beta-catenin that helps long-term memories solidify.

There’s apparently a natural way to rid yourself of bad memories, too. A 2007 study involving brain scans found that test subjects had the ability to suppress specific memories at a particular moment in time through repeated practice.

http://www.livescience.com/health/090216-bad-memories.html

hmmmm

Sun, 15 Feb 2009 18:13:03 +0000

More on the ethical questions Dr Daniel Sokol, a lecturer in medical ethics at St George’s, Un

PANCREAS

headnecksurgery — Fri, 23 Jan 2009 11:23:52 +0000

Physiology

Pancreatic islet cells produce insulin, glucagon, human pancreatic polypeptide, and somatostatin. Insulin, derived from proinsulin, consists of an alpha and beta chain connected by a C peptide. The basal secretion level is raised in a biphasic response to stimulation. The rapid phase may release stored preformed insulin in response to glucose, amino acids, glucagon, and some gastrointestinal hormones. With continuous glucose administration, both preformed and new insulin is released in the delayed phase. Release is stimulated by the vagal nerve and b-adrenergic receptors and inhibited by b-adrenergic blockers, sympathomimetic amines (e.g., epinephrine, norepinephrine), and somatostatin, which also inhibits glucagon. Stress triggers the release of glucagon, glucocorticoids, GH, and catecholamines, which are antagonists to insulin, resulting in glycogenolysis, gluconeogenesis, ketogenesis, lipolysis, and nitrogen wasting. Stress also affects wound healing, electrolyte and fluid balance, and susceptibility to infection.

Dysfunction

There are two types of diabetes mellitus with seemingly different causes, but they are both associated with similar complications. Type I (i.e., juvenile onset) usually appears in patients younger than 25 years who are insulin deficient, ketosis prone, and usually not obese. The cause is thought to be an autoimmune response to beta cells triggered by infection. The insulin levels of these patients are generally difficult to control. Type II (i.e., adult onset) has a more gradual onset. Patients are generally obese, over 40 years old, ketosis resistant, and more stable and easier to control. It is thought to be the more inheritable form of diabetes. Obesity reduces the number of insulin receptors on insulin-responsive cells, altering glucose tolerance. With fasting and weight loss, the number of receptors increases to normal levels.

In addition to random fasting blood sugar levels, screening for diabetes is accomplished with the 2-hour postprandial glucose tolerance test, using a fixed amount of glucose after a 3-day period of carbohydrate loading. Serum glucose determinations are 10% to 15% higher than whole blood determinations; therefore, it is important to know which test is performed.

Surgical diabetic patients under stress or anesthesia are thought to undergo hormone imbalances, causing glucose intolerance. They are also at greater perioperative risk due to disease-impaired cardiovascular, renal, and neurologic systems. Before surgery, careful assessment of these systems is important, as is assessing glucose control and modifying the patient’s regimen if necessary.

Symptoms of angina, which must be sought, may be absent. Autonomic dysfunction presents with orthostatic hypotension, nocturnal diarrhea, early satiety, or difficulties with erections and ejaculations in the male patient. Nocturia, dry mouth, blurred vision, weakness, palpitations, hunger, and nightmares are symptoms related to poor glucose control. The effects associated with hypoglycemia may be masked by neuropathies or b-adrenergic blockers (e.g., propranolol).

A thorough examination of the heart and peripheral pulses is necessary with an examination for bruits and orthostasis. An electrocardiogram should be obtained preoperatively and postoperatively to detect a silent myocardial infarction. Laboratory data should include preoperative fasting glucose, electrolytes, blood urea nitrogen, creatinine, chest radiograph, and clean-catch urinalysis. Long-term control can be assessed with the hemoglobin A1C determination, which is elevated with high glucose levels due to incorporation of glucose into the hemoglobin molecule. Levels remain elevated for 4 to 6 weeks, the lifespan of an erythrocyte. Before surgery, the patient in ketoacidosis should be stabilized as much as possible or surgery should be delayed to establish better glucose control or clear up bacteria in the urine. Diabetics are at increased risks for diseases with a predilection for immunocompromised patients, such as invasive fungal and bacterial infections. In addition, they suffer from poor wound healing, as may be evident after surgical procedures.

PREVENCIÓN Y TRATAMIENTO DE CUADROS DE ESTRÉS POR TERRORISMO

drabrito — Thu, 06 Nov 2008 15:05:01 +0000

El autor revisa los estudios que están siendo realizados en los últimos años con la globalización de

Causes and types of tremor 3 of 4

Thixia — Tue, 21 Oct 2008 13:41:34 +0000

What support and treatments are there? A summary of the types of treatments available for tremor.

my god is that time of the month AGAIN???

faketastic — Wed, 27 Aug 2008 04:56:54 +0000

i dont think it is but it sure as shit feels like it. Am i the only chick ready stick a knife in her throat the day before the urine runs red? for your sake, i hope so. i hate to brag, but my period lasts 8-12 days. you’re jealous, i know. More likely you wish you were my boyfriend who asks himself every16 days: “How did i get saddled with this bloodbag of a girlfriend?”

The question i really want to ask is: why is Propranonal the leading referrer to my blog? are there that many people out there desperate for propranonol info? i’ve let you people down. forgive me.

ok, so i cant spell the word (proprananol?) but heres

What i know about Propranolol

1. It’s hard to say, easy to swallow.

2. It’s a beta blocker. People take it for migraines, heart attacks and hypertension (and other things. im not a doctor. surprised?). i take it because i have a nervous breakdown when i have to speak in front of more than 3 people. Otherwise known as Anxiety. This beta-blocker works for anxiety because its magic! and it blocks the adrenaline/epinephrine that is released in your body so you can do that whole fight or flight thing [flight or flight in my case]. i know what you are thinking: “What a pussy she is,” right? Who doesn’t get nervous when they address a crowd of 3+ people? I’m totally with you. Hear me out: when i went back to school 3 years ago my “nervous” was turning into something my doctor calls “Anxiety” – whole body flushing, chills, sweating, shaking hands, knotted stomach, searing back pain, dry mouth, blank mind, hours of dread before the event, panic attack minutes before, during and after the event, obsession with the event before, during and after, coupled with suicidal thoughts. In sum, I was really starting to lose it. I didnt know about the magic! pill and i was embarassed to tell my doctor what a complete idiot i was (thus confirming what a complete idiot i was). Naturally, i counseled myself and came up with 3 possible solutions: a) quit school, b) commit suicide, c) get drunk. “C” was obviously the correct choice, right? So things started to get better: i came to school every day an hour early, secured a nice cozy parking spot on campus and then drank in my parked car until i could muster the courage to go in to class. As illustrated in paragraph 1, I’m a catch. I know.

3. Now that im on Propranowhatever, things are really really drastically insanely much better. I don’t have to self-medicate with alcohol. I take between 2-4 pills only one time, an hour or so before the anxiety producing event. This stuff starts to work pretty fast. It makes me stray dog thirsty, so I have water with me on the days i take it. Propranolol doesn’t get rid of the anxiety (like vicodin or valium does), but it gets rid of the physical symptoms. So, i’m still nervous on the inside but im confident knowing that it is not showing on the outside. for some reason, this brings comfort, and all the obsession goes away. I know nervousness is normal, and that i can handle it. Its the whole fashioning-my-sweater-into-a-noose-and- hanging-myself-in-the- broom-closet stuff that i have trouble dealing with.

4. Weird side effects include profuse sweating and heat on the small of my back. Its like all that fear and energy is cut off (or blocked! get it?) from climbing up to my overactive brain. it can only reach the middle of my back –and it goes wild in there apparently.

5. The doctor won’t admit it, but it will keep you up. I can pretty much set my watch to it- about 8 hours after i’ve taken 2, 3 or 4 pills i have this burst of I’M AWAKE energy and i cannot sleep. Usually I stay up all night or get to sleep around 5:30 am. Totally sucks but i’m not suicidal from the anxiety anymore so its a small price to pay. The End.

Yes, i want to punch people who say “im nervous when i make speeches, i should get on that.” Are you really that nervous that it requires drugs? Is the nervousness affecting your ability to function normally in everyday life? Is it something that goes away minutes after the speech? I hate having to take prescribed drugs, i wish i could flush them all down the toilet. i dont understand why someone would WANT to be on uneccessary drugs (that dont get them high. being high- THAT i can understand). Its not cool to be depressed, anxious and suicidal, or a prescription drug idiot, okay??

now its 12:58 AM, i have to get up at 5:30 for work and (thanks to magic! propranolol) i can’t sleep. I took some vicodin (PDI!)* to make me sleep but so far, nothing. now im wondering if mixing those 2 drugs can be fatal? i guess we’ll know for sure in the morning…

*prescription drug idiot

Sad Day for the Shooting Sports at the Olympics

rhutch — Fri, 15 Aug 2008 18:23:27 +0000

Today the IOC announced that North Korean shooter KIM Jong Su tested positive for propranolol , a prohibited substance. Propranolol is a beta-blocker which has many legitimate use, but is banned both in and out of competition for shooters and no Theraputic Use Exemtions (TUE) are even allowed. Even the most inexperienced competitve shooter knows that beta blockers are banned, so ignorance is no excuse. Of course his excuse is that he took a ancient remedy, Kusimhwan, for which he enquired if it contained any banned substance. Here is a transcript of the IOC decision.

This is the third high profile doping violation in shooting in the recent past, two other athletes Andrija Zlatic, of Serbia and Ann Potter of New Zealand were stripped of their quota spots for the Beijing Olympics for doping violations prior to the games.

You really have to ask yourself “what were they thinking”, I don’t condone drug use but I can see the draw in other sports, namely that being the money. I can also see that in other sports the users feel they can get away with it because the drugs aren’t required to perform, but to increase the volume and level of training so that performance gains can be realized. As they aren’t using them at the time of competition they feel their chances of getting caught are slim, even with random drug testing. A shooter has to be actually using the drugs during competition to gain any benefit. Maybe they thought that there friends in communist China would fake the results.

Of course it comes from a country where their image is more important than anything, sport is used to show their superiority over the rest of the world. The downside is little as the likelihood of the people of North Korea finding out the truth is relatively remote and even if they did it really doesn’t matter they will just blame it on the rest of the world picking on them.

I hope the ISSF comes own on these cheats short bans are not the answer in shooting where careers can be long. I think the message needs to be sent for blatant performance drug violations, that being life time bans. Maybe even bans for the countries from where the athlete comes from, this way it will ensure their participation in removing drugs from this sport. I’m not talking about inadvertent violations of taking substances that have no know performance enhancing effects, for which the list is large with regards to shooting sports. I think the punitive measures have to be commensurate with the offense. An athlete that accidentally takes something on the list, such as a masking agent for steroids, should not be punished the same as an athlete that takes a known performance enhancing substance. Both should have consequences but for the later the consequences should be swift and severe.

The sad part is that these incidents bring the whole sport into question, and all performances are then looked at with suspicion, for there really is no way of proving any performance is free of performance enhancing drugs no matter how good the testing is.

Drug memories and relapse: A light at the end of the tunnel?

Adi Jaffe — Wed, 13 Aug 2008 18:57:45 +0000

From All About Addiction: About a year ago, while sitting in a lecture on learning and memory, the i

Rozmowa o "Pigułce zapomnienia" w "TP"

Paweł Bakalarz — Thu, 29 May 2008 00:44:04 +0000

W nr. 20 (3071) z 18 maja 2008, “Tygodnik Powszechny” opublikował rozmowę z dr. Jackiem

Jeg lægger mit hjerte i deres hænder

80imin — Wed, 12 Mar 2008 07:58:59 +0000

Dagen før ablationen skulle være, havde man gjort forundersøgelsen på mig – tidligere beskrevet hér: Forundersøgelse på Rigshospitalet. Nu var jeg så klar til ablationen, som jeg blev nødt til at være. Jeg havde overnattet på Riget og lægerne havde heldigvis ladet mig tage mine betablogger – det ville ikke påvirke ablationen at jeg indtog pillerne, for jeg havde næsten konstant takykardi. Hvorfor kunne jeg så ikke bare lade være med at indtage pillerne? Sagen var den, at jeg troede på, at det var pillerne, der holdt mig i live.

Dagen før havde jeg snakket med en fyr, der havde været igennem ablation. Han havde siddet i sit hospitalstøj og set så sølle ud.

- Jeg var over 8 timer på bordet!

- Gud, tog det så længe? Men er du ok nu så?

- Det håber jeg. For et par måneder siden fik jeg foretaget ablation. Og efter et par uger kom takykardien igen. Nu må vi se..

Jeg var selvfølgelig rystet. Også fordi han fortalte, at man ikke kunne stoppe blødningerne ved indsstikstedet. Han var stor-ryger. Måske var det derfor der havde været komplikationer? Efter den skrækhistorie var det godt, at jeg havde mit stakit omkring mig – mine to dejlige veninder og min peptalende mor.

Alligevel sagde jeg ikke meget den formiddag, hvor jeg ventede på at komme til ablation. Damerne gjorde snakken. Når de henvendte sig til mig svarede jeg bare ved hovedrysten eller små smil. Hjertet var i sit værste lune – som om det ville give mig den sidste svada af takykardi. Udenfor Rigets vinduer skinnede marts-solen. Bilerne kørte intetanende rundt og København var slet ikke klar over, at det var i dag, jeg skulle dø.

Da sygeplejersken kom op med en beroligende pille og sagde, at nu kom portøren snart, kunne jeg ha besvimet af skræk. Men jeg blev ved bevidsthed – sådan en slags bevidsthed, der opfangede lyde men ikke gjorde mig i stand til at forstå så meget andet end ord som ‘ablation’, ‘takykardi’ og ‘ nu er det din tur’! Det kan godt være det lyder dramatisk. Men jeg tænkte om det mon var sådan dødsdømte havde det, når de var på vej til nålen med giften, der skulle sprøjte dem ud af livet?

Jeg blev kørt afsted af portøren til kardiologisk ambulatorium hvor overbrændingen skulle finde sted. Min mor og 2 veninder småløb efter mig og forsikrede mig om, at det hele nok skulle gå. De jokede med lægerne – om de måtte komme med ind hvor det foregik osv..Men selvfølgelig skulle de blive udenfor døren.

Jeg blev kørt ind på stuen hvor det hele skulle foregå. Lægen der var midt i fyrrene og som skulle foretage indgrebet bød mig smilende velkommen. Der blev lagt drop (venflon) i min arm så evt. medicin kunne sprøjtes direkte ind (blodfortyndende medicin). Jeg følte mig fuldkommen prisgivet og tænkte – så nu dør jeg, om lidt!

Jeg blev dækket til med grønt klæde – hovedet kiggede dog frem, men jeg var ikke i stand til at se hvad der blev lavet ved min lyske. Lægen forklarede dog, at nu ville jeg få en lokalbedøvende sprøjte i både højre og venstre lyske og han lovede, at intet blev ført ind i kroppen på mig før bedøvelsen virkede.

At få stikket i lysken gjorde ikke ondt. Det strammede kun lidt, da det lokalbedøvende stof trængte ind i vævet. Så snakkede lægen lidt med mig og min bevidsthed fangede musik fra en lille radio, der stod i lokalet.

- På den skærm dér, vil du kunne se dit hjerte fordi vi har et lille kamera som vi om lidt fører ind i venen – i den ene lyske. Og i den anden indfører vi brænder og pacer. Men jeg kan se på din puls, at det vist ikke er nødvendigt, at fremkalde takykardi med paceren – du har det allerede! Så meget desto nemmere bliver det, at finde det punkt i hjertet, der skal brændes.

Jeg lyttede og lyttede ikke. Radioen spillede stadig.

- Kan du mærke det her?

Jeg kunne intet mærke. Og lægen sagde, at nu ville han indsætte katetrene i årerne. Det begyndte at bløde lidt, som han sagde. Men det var ok. Jeg kunne ikke mærke andet end at der blev hevet lidt i mit skind.

- Hm, jeg synes det bløder lidt vel rigeligt..Jeg må nok ha assistance!

En lille kineser havde stået og vasket hænder i et tilstødende lokale og kom nu løbende ud og sagde, at det her overtog han. Jeg bemærkede en lille sitren i den anden læges ansigt.

- Men du har lige været på i over 6 timer Chen?

Chen? Det var søreme den berømte Chen, der stod der og ville overtage det hele selv om det betød overarbejde for ham. Han smilede beroligende til mig og tryllede krisen væk!

- Når du kommer herfra, så får du aldrig mere takykardi!

Han sagde det så overbevisende til mig, at jeg – midt i min underlige tilstand – kun kunne smile og nikke. Katetrene blev ført ind i kroppen på mig via højre og venstre lyske – og det gjorde overhovedet ikke ondt! Det eneste jeg mærkede i kroppen, var en svag kildrende fornemmelse. Den var mere behagelig end ubehagelig.

- Dit hjerte kan du se på skærmen!

Chen pegede med panden over på en skærm hvor et hjerte, der skulle forestille mit – pumpede som besat. Jeg kunne se hvordan isenkrammet løb ubesværet igennem årene.

- Det er jo meget bløde og bøjelige kabler vi bruger!

Chen smilede og sagde noget på engelsk til en fyr der betjente elektronikken (radiobølgerne) ved et lille bord. Han sagde, at nu ville de prøve, at brænde – det var ikke svært at se, hvor impulserne stammede fra.

- Mens vi brænder skal du ligge mussestille. Du må slet ikke røre dig, for så risikerer vi at katetret rykker sig i hjertet og så brænder vi et forkert sted.

Jeg lå stiv som en pind. Og så advarede Chen – at nu brændte de. Det strammede en anelse i brystet, men egentlig var der ingen smerte. Hjertet hoppede lidt forvirret rundt og kom ind i normal sinusrytme. Jeg smilede og udbrød ahh, takykardien stoppede! Lidt efter kom den dog igen.

- Vi brænder igen – og du ligger musestille!

Jeg adlød. Min respekt var stor. Den mand, Chen, havde været på job i mange timer og så tog han alligevel over – sådan bare lige – sådan! Det strammede igen lidt i brystet og takykardien holdt inde. Nu gik et par minutter med normal sinusrytme. Chen var tilfreds.

- Er jeg færdig?

Chen rystede på hovedet og sagde at nu skulle der brændes godt og grundigt så jeg ville få noget smertestillende – da det kunne gøre lidt ondt. Jeg nægtede og sagde, nej – jeg kan sagtens holde det ud! Men sygeplejersken gav mig noget smertestillende i droppet og Chen bad mig endnu engang om at ligge mussestille mens de brændte.

Jeg fik det pludselig dårligt og følte det som om jeg skulle besvime. Sygeplejersken, der havde siddet og holdt mig på skuldrene for at berolige mig, gav mig ilt i en maske og så fik jeg det bedre.

- Er du klar? Vi brænder nu!

Jeg var klar og lå stiv som en pind. Og det var godt jeg fik smertestillende. Det her gjorde ondt. Man brændte også længere end de andre gange. Jeg kiggede op i loftet med min iltmaske om næse og mund og tænkte, at den smerte kunne beskrives, som hvis man havde ondt i musklerne efter et marathonløb – blot var det en vedvarende smerte og fornemmelse af, at lungerne blev hevet ud af ryggen på mig. Så var det pludselig overstået. Smerten holdt op. Chen smilede og hev mig ud af mit mentale blackout.

- Se hvor fint dit hjerte slår!

Jeg bemærkede, at det var overstået. Og det var sandt. Mit hjerte slog helt normalt. Efter en hel dag med takykardi var hjertet roligt. Indgrebet havde varet 3 timer. Man må sige, at det var gået super godt – takket være Chen.

- Nu er vi færdige! Vi trækker katetrene ud af dig nu. Er du glad?

Jeg kunne tude. Men var stadig i sådan en slags ingenmandsland rent mentalt. Men ja, jeg var glad. Og taknemmelig. Jeg kunne ikke få mine øjne væk fra Chen – jeg måtte vise min taknemmelighed med øjnene – jeg kunne ikke sige noget. Jeg var så rørt.

Så blev jeg kørt tilbage til min stue af en portør. Min mor havde siddet udenfor rummet og spurgte hvordan jeg havde det. Heldigvis var mine veninder gået og min mor skulle hente min datter i fritidsordningen, så hun blev også nødt til at gå. Jeg smilede og lå mussestille. Turde ikke røre mig. Ovenpå min mave og lyske havde de placeret sandsække så der blev holdt et konstant pres mod indstiksstederne (af hensyn til blødningsrisiko). Sygeplejersken satte hjerteovervågning til og sagde at nu skulle jeg ligge helt stille i 5 timer. Intet problem. Jeg ville gøre lige hvad de sagde! Jeg levede!

Jeg sprang fra ablation alle gode gange 2

80imin — Mon, 10 Mar 2008 17:25:47 +0000

Jeg havde taget en taxa til Riget. Jeg var fastende. Ikke engang et stykke tyggegummi havde angang til de tørre slimhinder. Min datter blev passet af sine bedsteforældre så hun var da i det mindste ok. Det var vist det sidste man kunne sige om mig.

Så fik jeg mit værelse på hospitalet og besked om at trække i hospitalets ikke-charmerende tøj. Inden radiofrekvensablation skulle der måles blodtryk – i bad skulle jeg også og bagefter skulle jeg have barberet hårene i lysken. Der skulle der tages EKG og lægges kanyle i en blodåre i armen – hvis det blev nødvendigt at give mig medicin under behandlingen.

Jeg gjorde det jeg blev bedt om. Gik i bad – barberede lysken og og lagde mig i sengen.

En overlæge kom forbi og ønskede mig held og lykke og så gik han igen.

Så var jeg indlagt. Og skide bange. Jeg tillader mig, at bande her – fordi – INGEN ord kan beskrive hvordan jeg havde det. Alt gik sandsynligvis som det skulle. Men ingen tænkte på, at jeg var ved at gå fuldstændigt i stykker af angst indeni.

Og – jeg ved ikke hvad der skete. Men Fanden tog ved mig. Jeg slugte en propranolol for at dæmpe mit plagede hjerte og stod ud af sengen. Så tog jeg hospitalstøjet af og iførte mig mit civile tøj. En sygeplejerske kom forbi og spurgte hvad jeg lavede.

- Jeg tager hjem!

Hun kiggede forskrækket på mig og forsikrede mig om, at dét kunne jeg bare ikke gøre nu. Lægerne ventede på mig i Kardiologisk laboratorium!

- Det er jeg ked af. Men det er aflyst! Jeg er aflyst. Det kan du godt fortælle dem. Og jeg har lige taget en betablogger!

Hun snurrede rundt på hælen og skyndte sig ud af værelset. Jeg var lettet. Satte mig i en stol og ventede på, at pillen ville virke.

Pludselig kom overlægen stormende ind i værelset og så meget stram ud i betrækket.

- Hvad i alverden har du tænkt dig!?

- Jeg vil ikke gennemføre ablationen. Jeg er bange for, at det går galt..

- Du laver sjov med mig ikke?

Jeg måtte fortælle den vantro læge at jeg ikke jokede. Og han var mildest talt shokeret. Jeg fik at vide, at nu hvor jeg sprang fra i sidste øjeblik havde jeg brugt af resourcer, som jeg slet ikke var klar over og jeg skulle ikke tro, at jeg bare kunne komme og kræve ablation i morgen!

- Jeg ved det godt. Men jeg vil bare hjem og undskyld.

Den der blev mest skuffet over, at jeg var sprunget fra ablationen i sidste øjeblik, var nok min kæreste. Han havde jo set hvor slemt jeg sommetider havde det med takykardien. Men jeg var lettet – for min angst havde været meget slemmere end et takykardianfald plejede at være

Syntes jeg på dét tidspunkt.