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September 3, 2007 THE NEW YORK TIMES http://www.nytimes.com/2007/09/03/business/03drug.html?_r=1&n=Top/News/Business/Companies/Lilly,%20Eli,%20&%20Company&oref=slogin
In a clinical trial of about 200 patients, an experimental drug from Eli Lilly reduced schizophrenia symptoms without the serious side effects of current treatments, according to a paper published yesterday in the journal Nature Medicine.
The drug must still be evaluated on many more patients to test for the possibility of side effects that have not yet emerged, and it is at least three to four years from completing regulatory review.
But schizophrenia researchers said the trial’s results were surprising and impressive, especially since the drug works in a different way from existing antipsychotic medicines, all of which have serious side effects, including substantial weight gain and tremors.
Lilly will begin a larger clinical trial for the drug this month. If that trial confirms the results seen so far, the new drug could mark a breakthrough in the treatment of schizophrenia — and open the way to a broad new class of treatments for the disease. Schizophrenia, a devastating mental illness that affects 1 percent of adults, or about 2.5 million in the United States, usually begins in the late teens or 20s and is marked by psychotic delusions as well as social withdrawal and cognitive impairment.
“This is potentially one giant step forward for patients,” said Dr. Jeffrey Lieberman, chairman of the psychiatry department at Columbia and the lead investigator on a federally sponsored clinical trial of schizophrenia medicines. “This drug may turn out to be not just a comparably good antipsychotic agent, but a better antipsychotic agent.”
Dr. Lieberman has not been involved with the development of the medicine and does not receive any payments or consulting fees from Lilly.
The new drug also has the potential to be a blockbuster for Lilly. Medicines for schizophrenia and bipolar disorder are the fourth-best selling class of medicines in the United States, with sales of $12 billion in the United States and $18 billion worldwide last year.
The troubled history of Zyprexa, another antipsychotic medicine from Lilly, will lead regulators and psychiatrists to scrutinize the new medicine closely for hidden dangers, Dr. Lieberman said. When it introduced Zyprexa in 1996, Lilly hailed it as a breakthrough with fewer side effects than older drugs. But Zyprexa causes severe weight gain, and the American Diabetes Association has linked it to diabetes. Internal Lilly documents show that the company played down Zyprexa’s side effects, worrying they would hurt sales.
Despite that history, psychiatrists will be eager to see whether the new Lilly medicine works, since the existing drugs are of limited help for many patients. Existing schizophrenia medicines, whether older drugs such as Thorazine or newer medicines like Zyprexa, all work by blocking the brain’s dopamine receptors.
But the new Lilly drug does not directly affect dopamine. Instead, it modulates brain activity through a different set of receptors. As a result, it has the potential to be the first truly novel treatment for schizophrenia since Thorazine was introduced 1954, Dr. Lieberman and other researchers said.
Lilly’s new drug — which does not have a name yet and is referred to as LY2140023 — emerged from almost two decades of research by Dr. Darryle D. Schoepp, a toxicologist and pharmacologist who joined Lilly in 1988.
For decades, psychiatrists have known that users of PCP, a street drug sometimes called angel dust, have symptoms nearly identical to those of people with schizophrenia. By the 1980s, scientists had discovered that PCP blocked brain receptors that are triggered by an amino acid called glutamate. This led some companies and scientists to study ways to stimulate glutamate receptors as a treatment for schizophrenia.
But the brain has many different kinds of glutamate receptors, and figuring out how to stimulate or block them in medically beneficial ways has proved complicated. Instead of focusing on the receptors blocked by PCP, Dr. Schoepp concentrated on modulating the action of glutamate receptors in the brain’s prefrontal cortex, an area responsible for personality and learning.
“This is a system that is so fundamental to the function of your brain that it is quite powerful,” said Dr. Schoepp.
But because drugs that blocked dopamine had been the only successful schizophrenia treatments, many researchers viewed the glutamate pathway as unlikely to produce useful medicines, said Dr. P. Jeffrey Conn, director of the Vanderbilt University drug discovery program and an expert on glutamate research.
Dr. Schoepp deserved praise for persuading Lilly to invest in a field that appeared to be a long shot, Dr. Conn said, adding, “He locked in very early.”
As a result, Lilly appears to have a multiyear lead over its competitors in glutamate drugs, Dr. Conn said. Dr. Schoepp left Lilly in March to become the head of neuroscience research for Merck. Dr. Schoepp and Dr. Steven Paul, the president of Lilly Research Laboratories, both said that his departure would not hurt the development of Lilly’s new medicine
Dr. Joseph T. Coyle, a professor of psychiatry and neuroscience at Harvard Medical School, said the Lilly trial validated the theory that modulating glutamate receptors might control the symptoms of schizophrenia. Even if this drug fails in later trials, companies and scientists are likely to pursue glutamate research more aggressively, he said.
“When you see a company that comes up with something that’s completely different, completely out of the box, that attracts attention,” Dr. Coyle said.
Existing drugs are reasonably good at treating the hallucinations and delusions of schizophrenia. But they are far less effective at treating the so-called negative symptoms of the disease — the lack of motivation and emotion that leave many patients unable to work or have normal social relationships. The side effects of existing medicines, which affect nearly all patients, are also severe. Older drugs like Thorazine often cause tics and movement disorders, while newer medicines typically have fewer effects on movement but can cause weight gain and other metabolic changes.
In the clinical trial whose results were reported yesterday, LY2140023 had none of those side effects and appeared to work about as well as Zyprexa at reducing symptoms. In the trial, which was conducted in Russia from August 2005 to June 2006, patients were given the experimental drug, Zyprexa or a placebo. About 100 patients received the experimental medicine.
For the drug to be approved, Lilly will need to replicate the results in larger trials. This month, Lilly will begin a trial with 870 patients to determine the most effective dose of the drug. That trial is expected to be complete in January 2009, and if it is successful Lilly will probably start a large Phase III trial that could cover at least 2,000 patients.
“We have to confirm safety and efficacy with multiple studies,” Dr. Paul of Lilly said. He said he did not want to offer a prediction of when Lilly might ask the FDA Food and Drug Administration for approval. But he said Lilly intended to develop the drug aggressively.
“We are very actively working on this target and related targets because we believe that this mechanism is now validated,” he said.
SIZOFRENIDE GORULEN INTAHARLARA MEYILLI DAVRANISLARI ONLEYEBILECEK/ TEDAVI EDEBILECEK OLAN ANTIPSIKOTIK ILAC ONAYLANDI- December 20, 2002, Friday The New York Times-Anti-Psychotic Approved To Treat Suicidal Behavior
By ERICA GOODE (NYT) 692 words
Late Edition - Final , Section A , Page 30 , Column 5
LEAD PARAGRAPH - Clozapine, one of a new generation of anti-psychotic drugs, has become the first psychiatric medication to win federal approval as a treatment for suicidal behavior.
The Food and Drug Administration announced yesterday that the agency had approved the drug for treating recurrent suicidal thoughts or suicide attempts in patients with schizophrenia, a devastating illness that afflicts 1 of 100 Americans. Yazinin kalani 2.95 dolara satin alinabilir gazetden.
Yazi ozetle soyle diyor;…
Sizofrenide genler faktor olabilir http://www.nytimes.com/2002/12/13/national/13GENE.html Gene May Play a Role in Schizophrenia-By NICHOLAS WADE
The long search for a gene that helps cause schizophrenia may at last be bearing fruit after many false starts and disappointments, scientists are reporting.
An errant gene first implicated among schizophrenic patients in Iceland has now turned up in a survey of Scottish patients, too, giving a clear confirmation of the earlier result.
The gene may be involved in remodeling the connections that brain cells make with one another, called synapses. Many of the Icelandic and Scottish patients have the same variant pattern in the gene, supporting the idea that when the gene does not work as designed, wrongly formed nerve-to-nerve wiring accumulates in the brain, giving rise to schizophrenia.
Not all schizophrenics carry the variant and many people carry it without a problem, an expected pattern in diseases caused by several genes. But in both populations, inheriting the variant form of the gene appears to double the risk of schizophrenia.
The finding, if correct, would bolster the strategy followed by Decode Genetics, a company based in Reykjavik that is using the Icelandic population to search for the genetic roots of common diseases like cancer, diabetes, heart disease and Parkinson's. The schizophrenia-related gene is one of the first it has found.
Dr. Kari Stefansson, a former Harvard neuropathologist who is the company's chief executive, said Decode and its partner, the drug company Roche, were developing new drugs to counteract the aberrant gene's effects but could not say when any would be ready for clinical testing.
The variant form of the gene in Icelanders was reported in July this year by Decode Genetics. But many scientists have grown skeptical of claims about a schizophrenia gene because some have not been confirmed by later studies.
In the current issue of The American Journal of Human Genetics, Dr. Hreinn Stefansson (no relation to Kari Stefansson), with colleagues at Decode Genetics and in Scotland, reports that the same variant is common among Scottish schizophrenics.
Dr. Kenneth Kendler, a psychiatric geneticist at Virginia Commonwealth University, said the replication was "impressively robust" and that "it all looks very good." Another schizophrenia expert, Dr. Ann Pulver of Johns Hopkins University, called the new data "pretty convincing" and "really nice evidence to support the original finding."
Speaking from a conference on mind drugs in Puerto Rico, Dr. Kari Stefansson said other researchers had recently found the same variant in German, Welsh and American schizophrenics.
The gene at issue is called neuregulin-1. It makes a signaling protein that influences the receptivity of brain cells to several types of neurotransmitters, the chemicals that convey messages between nerve cells. Dr. Stefansson said neuregulin-1 may govern the process by which the synapses are made and unmade in response to the brain's experiences.
A defect in neuregulin-1, he suggested, might lead to an accumulation of wrongly formed synapses, accounting for the progressive nature of the disease. It might also explain why environmental factors as well as heredity contribute to schizophrenia, as shown by the fact that if one identical twin has the disease the other has only a 30 to 50 percent chance of developing it.
Dr. Stefansson said he had a considerable emotional investment in the disease because his elder brother has schizophrenia.
The variation discovered by Decode Genetics is a set of seven genetic differences that spans the beginning of the neuregulin gene, which is located on the eighth of the 23 pairs of human chromosomes. Dr. Stefansson said he guessed that the seven changes might in some unexplained way be altering the amount of protein the gene could produce.
Recently another gene possibly related to schizophrenia-related gene was discovered on chromosome 6 by Dr. Kendler and colleagues among Irish patients. The gene, known as dysbindin, may represent a different way of causing schizophrenia.
Alternatively, both dysbindin, neuregulin-1, and perhaps other genes yet to be discovered may all operate in the same task or pathway, so that a defect in any one of them could cause schizophrenia. If the disease has a single cause, it should be much easier to find treatments that work for all schizophrenics.
Dr. Kendler said the progress with the two genes "induces a bit more optimism in a field that has had some difficult times."
BEYINDEN FOTOGRAFLAR SIZOFRENIDE ERKEN TESHISE YARDIM EDEBILIR-http://www.nytimes.com/2002/12/11/health/11BRAI.html Brain Imaging May Detect Schizophrenia in Early Stages-By ERICA GOODE
Scientists have known for some time that people who suffer from schizophrenia show abnormalities in the structure of their brains.
But in a new study, researchers for the first time have detected similar abnormalities in brain scans of people who were considered at high risk for schizophrenia or other psychotic illnesses but who did not yet have full-blown symptoms. Those abnormalities, the study found, became even more marked once the illness was diagnosed. The subjects in the study who went on to develop psychoses had less gray matter in brain areas involved in attention and higher mental processes like planning, emotion and memory, the researchers found.
Experts said the study's results, reported yesterday in an online version of The Lancet, the medical journal, offered the possibility that imaging techniques might eventually be used to predict who will develop schizophrenia, a devastating illness that affects more than 2.8 million Americans. Doctors could then offer treatment while the disease was still in its earliest stages, possibly preventing further damage to the brain.
But Dr. Christos Pantelis, an associate professor of psychiatry at the University of Melbourne and the lead author of the report, cautioned that much more research was needed before magnetic resonance imaging, the method used in the study, could serve as a diagnostic tool for individual people with schizophrenia.
"I think it's still too early to say how helpful it will be," Dr. Pantelis said.
Still, other researchers called the study's findings exciting and said that the areas of the brain in which the abnormalities were found would now be an active focus for study.
"This is a terrific first step," said Dr. Paul Thompson, a professor of neurology at the University of California at Los Angeles and an expert on brain imaging and schizophrenia.
Dr. Herbert Y. Meltzer, a professor of psychiatry at Vanderbilt University and an expert on schizophrenia, said, "It proves that the psychosis is almost a late stage in the evolution of the disease process."
He added, "The key message is that this is a neurodevelopmental disorder and that changes in memory, learning, attention and executive decision-making precede the experience of the psychosis."
People who suffer from schizophrenia typically experience auditory hallucinations and have blunted emotional responses and difficulty with activities that require planning or other higher-level processes.
Some studies have suggested that the earlier the illness is treated with antipsychotic drugs the better the prognosis. At least two research groups, one led by Dr. Patrick McGorry, an author of the Lancet report, and another at Yale, are conducting studies in which young people who are experiencing some symptoms but have not yet developed schizophrenia are treated with antipsychotic drugs. But the studies have been controversial because it is not yet clear which symptoms predict later illness.
In the new study, the researchers used magnetic resonance imaging to scan the brains of 75 people who were deemed "at high risk" for psychosis because they had a strong family history of severe mental illness or had other risk factors, including transient or mild symptoms of mental disturbance or a decline in mental functioning.
Over the next 12 months, 23 of the subjects developed a full-blown psychosis and 52 did not fall ill, the researchers found.
A comparison of the brain scans from the two groups revealed significant differences in the volume of gray matter in areas of the frontal and temporal lobes and the cingulate gyrus. All three regions have been linked to schizophrenia by previous research, Dr. Pantelis said.
When the researchers conducted additional brain scans on some subjects who developed psychoses, they found further reductions in gray matter not seen in the scans taken before the illnesses were diagnosed.
http://query.nytimes.com/gst/abstract.html?res=FB0712F939550C778CDDAE0894DA404482&fta=y Schizophrenia May Be Tied To 2 Genes, Research Finds -National Desk | July 4, 2002, Thursday
Schizophrenia May Be Tied To 2 Genes, Research Finds
By NICHOLAS WADE (NYT) 1067 words
Late Edition - Final , Section A , Page 11 , Column 5
ABSTRACT - Study of 270 Irish families, each with several schizophrenic members, suggests to researchers that mutuation of gene known as dysbindin may be involved in disease; separately, mutations of gene called neuregulin-1, located on different chromosome, are found to be highly correlated with schizophrenia in about 15 percent of Icelandic patients; geneticists believe many different mutated genes contribute to schizophrenia (M)
Not;yaziyi NYTimes’dan satin alabilirisniz.
http://www.msnbc.com/news/558493.asp#BODY Son arastirmaya gore babanin gec yasta cocuk sahibi olmasi,cocukta sizofreni riskini arttirmaktadir.
April 12 — Children fathered by older men run a much higher risk of developing schizophrenia, researchers said Thursday in a finding that provides strong evidence that men, like women, have a “biological clock” when it comes to having children…………
http://www.nytimes.com/2001/04/12/health/12DADS.html April 12, 2001
Father's Age Linked to Risk of Schizophrenia-By ERICA GOODE
The risk of having a child with schizophrenia may increase with a father's advancing age, researchers reported yesterday.
The researchers, who examined the relationship between the fathers' ages and schizophrenia among 87,907 Israelis born from 1964 through 1976, found that the older the father, the more likely he was to have a child who suffered from schizophrenia, a devastating mental illness.
Men who were 45 through 49, for example, were twice as likely to have offspring with schizophrenia or a related disorder as were men under 25, the researchers found. The overall risk of having a child with the illness, however, remained small.
"The finding is a very strong association of schizophrenia risk and father's age," said Dr. Delores Malaspina, an associate professor of clinical psychiatry at the Columbia University College of Physicians and Surgeons and the lead author of the report, which appears in this month's issue of the journal Archives of General Psychiatry.
Other scientists were more skeptical. They noted that confirmation through other studies was needed before such a link could be said to be established, and they cautioned that in the history of schizophrenia research, many apparent associations had eventually proved spurious or impossible to replicate.
If the results of the study hold up to scrutiny, Dr. Malaspina said, "The next question is, `What might explain that finding?' " One possibility, the researchers argue in their report, is that some cases of schizophrenia are a result of genetic abnormalities in sperm cells that become more likely as a man ages.
Stem cells in the testicles divide throughout a man's life in a process that leads to the production of sperm. Each cell division carries the chance for copying errors in reproducing the DNA. By the age of 40, research suggests, about 660 such divisions have taken place. Genetic mutations can also occur from exposure to radiation or chemicals over a man's life.
In contrast, the divisions of cells that produce a woman's eggs occur only before birth.
A number of physical illnesses and birth defects have been linked to genetic mutations during sperm production in older fathers, including Apert syndrome, a rare congenital deformity of the skull, fingers and toes, and achondroplasia, the most common form of dwarfism.
Some cases of schizophrenia, the researchers suggested, might be associated with similar mutations.
The illness runs in families, and is known to have a strong genetic component, though efforts to identify the specific gene or genes that predispose a person to schizophrenia have so far been inconclusive. The disease affects 1 of every 100 Americans and is more common in men. Full-blown symptoms often first appear in late adolescence or early adulthood.
In some cases, people who do not have a family history of schizophrenia also develop the illness. Dr. Malaspina said that the findings of her study "suggest that relevant mutations are there" in such sporadic cases "as well as in familial cases."
Dr. James F. Crow, a professor emeritus of genetics at the University of Wisconsin, said, "I think this is very strong evidence for a mutation component to schizophrenia, but it's quite an open question as to how much of a component."
But other scientists cautioned that other explanations beside spontaneous genetic mutation could also account for the study's results.
For example, said Dr. Ann Pulver, director of the epidemiology and genetics program in psychiatry at Johns Hopkins University, "It may be that the fathers of schizophrenics have unusual characteristics that delay reproduction."
"I think this is an interesting contribution to the epidemiological literature, that paternal age may be a risk factor for a subgroup of schizophrenic patients," Dr. Pulver said. "And it may be that advanced paternal age is associated with a mutation. But that is a hypothesis and one would need to test it.
In the study, Dr. Malaspina and her colleagues took advantage of the Jerusalem Perinatal Study, a research archive that includes information about all births in one area of Jerusalem. Records from the study were correlated with those of a national registry of psychiatric illness kept by the Israeli government.
The researchers found that in 1,337 people admitted to psychiatric hospitals before 1998, the fathers' ages were strongly associated with a diagnosis of schizophrenia or a related disorder. The risk of schizophrenia increased steadily with the father's increasing age. Advancing age of the fathers, the investigators reported, accounted for 26 percent of the cases of schizophrenia in the study; for fathers over 50, two out of every three cases of the illness could be attributed to the father's age.
http://www.abcnews.go.com/onair/2020/2020_000225_schizophrenia_feature.html 25 Subat 2000 de, WABC TV 20/20 de “Inside a Tortured Mind-The Voices Within” (Iskence edilen Aklin Icinden, Icindeki sesler) adli programda ilk defa “TIPTA ONEMLI GELISME “ haberiyle Virtuel Sizofreni Halusinasyon aleti (TLF;ABD Janssen Customer Action Center at 1-800-JANSSEN den) tanitilmistir ve asagidaki deneme asamasindaki ses halusinasyonlarini yok edebilecek beyne manyetik stimulasyon uygulamasi,TMS anlatilmistir. Asagidaki transkriptle,TV izlerken tutulan notlarin karisimidir.
“Sizofreni hala bilinmeyenlerle dolu,sebebi bilinmeyen bir mechul beyin hastaligidir . Doktorlar hastalarin niye halusinasyonlar ve paranoya yasadiklarini bilemiyorlar.Hatta niye dehset verici halusinasyonlarin onlari etkiledigini,neden % 25 si olmayan garip,urkutucu seyler goruyorlar,% 60 si ise sesler duyuyorlar bunu da bilmiyorlar.Uzmanlar ses olarak duyulan halusinasyonlarin genelde daha tehlikeli oldugunu cunku sozle konusarak verilen mesajlarin sizofreni kurbanlarinin kendilerine zarar vermelerine yol acan davranislara neden oldugunu,cok azinda da siddete sebep oldugunu bildiriyorlar.Her 10 kisiden biri intahar ederler. Hastalik kadin vee rkekleri esit sekilde etkilemektedir.Kadinlar cogunlukla 20 li ve 30lu yaslarda sizofreni hastasi olurken,erkeklerde tipik olarak12-14 lu yaslar ve erken yirmili yaslarda sizofreni gorulmektedir. Dr.Ralph Hoffman Yale psikiyatri Enstitusunun direktor vekilidir ve sizofreni uzmanidir.Hastalarinin cogunun bu olmayan ama onlarin beyinlerinde kesinlikle duyduklari sesleri bloke etmek icin,yok etmek icin,duymamak icin basarisizca caba sarfedislerine tanik olmustur.”Akillarina,beyinlerine ve hayatlarina el koyuyor bu hastalik,istenmeyen mudahale gibi…Bir hastamdan mektup aldim, sizofreniye “BEYNIN .AKLIN SUREKLI TECAVUZ EDILMESIDIR ” diyor Dr.Hoffman.Peki bu garip seyleri gormek ve dehset verici sesleri duymak nasil birseydir? Doktorlar uzun yillardir bu hastaligi tarif eden,karakterize eden parcalanmis dusunceleri anlamaga cebellestirler.Ama doktorlar sizofreni olmadiklarindan,sadece hastalarinin tarif ettigi seyleri hayal edebiliyorlardi.AMA SIMDI GERCEKTEN SIZOFRENI HASTALARININ AKLINDA,BEYNINDE OLUP BITENLERI GORMESI,DUYMASI,ANLAMASI MUMKUN UZMANLARIN.
Virtuel realite denen teknikle, Janssen Farmokoloji sirketi sizofreni hastasinin duydugu ve gordugu halusinasyonlari simule/taklit eden bir alet gelistirdi.
Bu aleti takiyorsunuz ve aynen sizofrenili bir hastanin 24 saat,haftalarca,aylarca,yillarca katlanmak zorunda kaldigi beynindeki kotu sesler ve goruntulerle siz de 1-2 dakika icin de olsa tanisiyorsunuz-bu goruntuler ornek olarak ekranda da gosterildi,sesler de verildi. Janssen firmasi animasyonlu virtuel senaryoya “Onlarin Yerinde Olsaniz” adini vermis . Alet oyle yapilmis ki,kullanan kisi sizofreni hastalarinin normal bir karsilikli konusma yaparken, halusinasyon goruntu ve diger seslerle mucadelesini anlatiyor size.Bu gozlugu takan kisi sizofreni hastasinin hayatinin ne kadar zor ve inanilmaz dikkat dagitici oldugunu anliyor.Janssen bu virtuel aleti bir tek sebepten dolayi yapmis- doktorlarin ve aile uyelerinin, sizofrenili hastadaki inanilmaz felaket zor yasamlarini,stresi anlamalarina yardimci olmak icin.
Sizofrenili kisiler her an kafalarinin icinde konusan,kotu, onlara emirler veren, cogunlukla kendilerine zarar vermelerini emreden inanilmaz kotu bir veya birden cok fazla sesler duymaktadirlar.Bunlara inanilmaz dikkat cekici,urkutucu,korkunc goruntuler de eslik etmektedir.Ve bu sesler ilaclarla bazen kismen susturulabilmekteyse de her hastada degisik neticeler elde edilmektedir, tamamen yok edilememektedir-surekli hortlamaktadirlar.Ustelik bu sesler (bazen tek ses,cogunlukla da birden fazla ses) gittikce daha cok gurultu yaparlar ve goruntulerdeki renkler ve carpikliklar da ise karisinca ;sizofrenili kisi karsisindakini,sizi dahi duyamayabilir-cunku dikkatini dagitan,sizi duymamasina sebep olan inanilmaz cok dikkat dagitici faktor vardir beyninde ve hicbir seye konsantre olamaz dogal olarak !Ustelik gozunun onundeki ve beynindeki goruntuler de surekli degiskendir,var olmayan seyler gorebilir;yataginin altinda yilan, bogazinda fare, sizin alninizda goz, pencerede vahsi bir hayvan, uzayan gariplesmis sekiller/insanlar , cilgin renkler vs gibi.Hastalarin halusinasyonlarinin % 25 si goruntu, % 65 si ise duyulan seslerdir.Sikinti veren, en kotusu ve kisinin kendisi icin daha tehlikeli olan ise duyulan seslerdir cunku “kendini yarala,ise yaramazsin, oldur, assagiliksin” gibi cok agir tahrik edici ve surekli olmesini emreden seslerdir bunlar.Ve de bunlar simdilik bilebildigimiz kadariyla beyindeki fiziksel,kimyevi dengelerdeki degisikliklerin sonucunda ortaya cikmaktadir.Yani kanser,diyabet,kalp gibi bir beyin hastaligidir sizofreni.Ve beyinde bu hastalik neticesinde acimasiz bir kisa devreler trajedisi yasanmaktadir.Yale Universitesindeki bu arastirmaya ayrica asagidaki 3 hasta da katildilar ve bu bilgiler onlarin yasadiklarindan ve doktorun anlattiklarindan ozetlenmistir.Mesela bu aletteki goruntu ile edinilen tecrubenin aynen kendi yasadiklarinin benzeri oldugunu soyleyen erkek hasta 14 yasindan beri sizofreni hastasiymis.Ilk defa bir gun “radyo dinlerken,araya giren bir sesin direkt kendisiyle konusmaga baslamasiyla” ilk defa bu seslerle tanistigini anlatti.Simdi yeni ilac Risperidon ile duyma ve goruntu halusinasyonlari simdilik tamamen yok olmus ve de New York’ta “City Voices” gazetesini cikariyormus simdi.Ama her hastada ilaclarla ayni neticeler alinamiyabiliyormus. Donald ise 38 yasina kadar basarili bir kimya arastirmacisiymis ve aniden hastalanmis.Kafasinin icindeki ses devamli”Hic bir ise yaramazsin,oldur kendini ‘diyormus hala.Ailesi ayni masada yemek yerken,Donald’in baska seslerle konusmasina alistik diyorlar.Bu sesler ve goruntuler nedeniyle hastalarin 24 saat,omur boyu dunyalari kararmaktadir.Onun icin de sizofreni hastalarin kisisel trajedisidir.
Ilaclarla tedavi edilerek sizofrenideki sikca gorulen paranoya ve deluzyonlari regule etmek,minimuma indirmekte etkili olunmustur.Goruntuler ve sesler icinse genellikle ,ilac tedavisi en iyi sekliyle, ancak gecici cozum olabilmektedir halen.
ABD de agir sekilde hasta olan 2.5 milyon sizofreni hastasinin, dortte birinde ise ilaclar duyduklari sesleri ve gordukleri halusinasyonlari yok edememistir hala.Goruntu halusinasyonlari icin ilaclar tek tedavidir ama simdi duyulan sesleri tedavi edebilecek Yale Psikiyatri Enstitusunde Dr.Hoffman tarafindan yonetilen yeni metodla tedavi yaklasimi vardir.
Hoffman ve ekibi “Transcranial Magnetic Stimulation=TMS” denen yeni yontemi test ettiler.Bu yontem beynin sol tarafinda konusmayi aktive eden bolgeye kisa manyetik stimulasyonlar gondermek seklindedir.Bazi bilimsel bulgulara gore bu bolgenin duyulan seslerle ilgili oldugu anlasilmaktadir, ve Hoffman ve ekibi de bu bolgeye fokus oldular TMS ile. Hoffman bu deneme mahiyetindeki islemi 12 hastaya uyguladi.Bunlara 4 gunde 40 dakika TMS uygulandi.12 hastadan 8 zinde basarili sonuc alindi-bazilarinda hemen etkisi goruldu,bazilari ise gunlerce stimule edildiklerinde netice alindi.Bu yeni TMs uygulamasinin ise yaradigini anlamalari kolaydi cunku aniden hastalarin iclerindeki ses sustu.
HOFFMAN TMS IN HALA DENEME ASAMASINDA OLDUGUNU SOYLUYOR.Eger uzun donemde etkili olacagi ispatlanirsa,TMS yuzbinlerce ses halusinasyonlarindan ceken sizofreni hastasina ilacsiz tedavi alternatifi olabilir .”
Onumuzdeki yakin gelecekte yeni arastirma sonuclari aciklanincaya kadar, simdilik tek careleri ise hastaya cevap verecek en uygun ilaci ve en uygun dozu bularak, surekli omur boyu ilac tedavisi ve terapiler uygulanmasidir-bu uzunca zaman alabilmektedir.Yale Universitesi psikiyatri bolumu direktoru Dr.Hoffman’in anlattigina gore, ILACLA SES HALUSINASYONU TEDAVISINE ALTERNATIF OLABILECEK arastirma safhasindaki TMS aleti http://info.med.yale.edu/psych/clinics/rTMS.html ile yapilan ilacsiz deneylere bu 3 hasta da da katilmaktaymislar.Beynin sol tarafindaki konusmayi aktive eden,harekete geciren noktaya 4 gunde 40 titresim ,stimulasyoon veriliyor (herkesde degisik uygulaniyor) ve hastada halusinasyon azaliyor veya yok olabiliyormus.Bir hastada 3 ay sonra yeniden baslamis sesler.Simdi tekrar beynini stimule ediyorlar.Eger arastirma neticelenirse,kesinlesirse hastalara yeni umitler dogacak.VE DE EN ONEMLISI; UMIT VERICI BU HABERLERIN BIR BASLANGIC OLDUGUNU VE SIZOFRENININ TEDAVISINDE,ONLENMESINDE ONUMUZDEKI 10 YILDA COK BUYUK GELISMELER ORTAYA CIKACAGINI SOYLEDILER. 26 Subat 2000