Posts Tagged ‘hallucination’


A mouse exploring one of the custom hologram generators used in the experiments at Stanford. By stimulating particular neurons, scientists were able to make engineered mice see visual patterns that weren’t there.

By Carl Zimmer

In a laboratory at the Stanford University School of Medicine, the mice are seeing things. And it’s not because they’ve been given drugs.

With new laser technology, scientists have triggered specific hallucinations in mice by switching on a few neurons with beams of light. The researchers reported the results on Thursday in the journal Science.

The technique promises to provide clues to how the billions of neurons in the brain make sense of the environment. Eventually the research also may lead to new treatments for psychological disorders, including uncontrollable hallucinations.

“This is spectacular — this is the dream,” said Lindsey Glickfeld, a neuroscientist at Duke University, who was not involved in the new study.

In the early 2000s, Dr. Karl Deisseroth, a psychiatrist and neuroscientist at Stanford, and other scientists engineered neurons in the brains of living mouse mice to switch on when exposed to a flash of light. The technique is known as optogenetics.

In the first wave of these experiments, researchers used light to learn how various types of neurons worked. But Dr. Deisseroth wanted to be able to pick out any individual cell in the brain and turn it on and off with light.

So he and his colleagues designed a new device: Instead of just bathing a mouse’s brain in light, it allowed the researchers to deliver tiny beams of red light that could strike dozens of individual brain neurons at once.

To try out this new system, Dr. Deisseroth and his colleagues focused on the brain’s perception of the visual world. When light enters the eyes — of a mouse or a human — it triggers nerve endings in the retina that send electrical impulses to the rear of the brain.

There, in a region called the visual cortex, neurons quickly detect edges and other patterns, which the brain then assembles into a picture of reality.

The scientists inserted two genes into neurons in the visual cortices of mice. One gene made the neurons sensitive to the red laser light. The other caused neurons to produce a green flash when turned on, letting the researchers track their activity in response to stimuli.

The engineered mice were shown pictures on a monitor. Some were of vertical stripes, others of horizontal stripes. Sometimes the stripes were bright, sometimes fuzzy. The researchers trained the mice to lick a pipe only if they saw vertical stripes. If they performed the test correctly, they were rewarded with a drop of water.

As the mice were shown images, thousands of neurons in their visual cortices flashed green. One population of cells switched on in response to vertical stripes; other neurons flipped on when the mice were shown horizontal ones.

The researchers picked a few dozen neurons from each group to target. They again showed the stripes to the mice, and this time they also fired light at the neurons from the corresponding group. Switching on the correct neurons helped the mice do better at recognizing stripes.

Then the researchers turned off the monitor, leaving the mice in darkness. Now the scientists switched on the neurons for horizontal and vertical stripes, without anything for the rodents to see. The mice responded by licking the pipe, as if they were actually seeing vertical stripes.

Anne Churchland, a neuroscientist at Cold Spring Harbor Laboratory who was not involved in the study, cautioned that this kind of experiment can’t reveal much about a mouse’s inner experience.

“It’s not like a creature can tell you, ‘Oh, wow, I saw a horizontal bar,’” she said.

Dr. Churchland said that it would take more research to better understand why the mice behaved as they did in response to the flashes of red light. Did they see the horizontal stripes more clearly, or were they less distracted by misleading signals?

One of the most remarkable results from the study came about when Dr. Deisseroth and his colleagues narrowed their beams of red light to fewer and fewer neurons. They kept getting the mice to lick the pipe as if they were seeing the vertical stripes.

In the end, the scientists found they could trigger the hallucinations by stimulating as few as two neurons. Thousands of other neurons in the visual cortex would follow the lead of those two cells, flashing green as they became active.

Clusters of neurons in the brain may be tuned so that they’re ready to fire at even a slight stimulus, Dr. Deisseroth and his colleagues concluded — like a snowbank poised to become an avalanche.

But it doesn’t take a fancy optogenetic device to make a few neurons fire. Even when they’re not receiving a stimulus, neurons sometimes just fire at random.

That raises a puzzle: If all it takes is two neurons, why are we not hallucinating all the time?

Maybe our brain wiring prevents it, Dr. Deisseroth said. When a neuron randomly fires, others may send signal it to quiet down.

Dr. Glickfeld speculated that attention may be crucial to triggering the avalanche of neuronal action only at the right times. “Attention allows you to ignore a lot of the background activity,” she said.

Dr. Deisseroth hopes to see what other hallucinations he can trigger with light. In other parts of the brain, he might be able to cause mice to perceive more complex images, such as the face of a cat. He might be able to coax neurons to create phantom sounds, or even phantom smells.

As a psychiatrist, Dr. Deisseroth has treated patients who have suffered from visual hallucinations. In his role as a neuroscientist, he’d like to find out more about how individual neurons give rise to these images — and how to stop them.

“Now we know where those cells are, what they look like, what their shape is,” he said. “In future work, we can get to know them in much more detail.”

In a small study of patients referred to the Johns Hopkins Early Psychosis Intervention Clinic (EPIC), researchers report that about half the people referred to the clinic with a schizophrenia diagnosis did not actually have schizophrenia. People who reported hearing voices or having anxiety were the ones more likely to be misdiagnosed, according to the study published in the Journal of Psychiatric Practice.

The researchers say that therapies can vary widely for people with schizophrenia, bipolar disorder, major depression or other serious types of mental illness, and that misdiagnosis can lead to inappropriate or delayed treatment.

The findings, the researchers say, suggest that second opinions at a specialised schizophrenia clinic after initial diagnosis are wise efforts to reduce the risk of misdiagnosis, and ensure prompt and appropriate patient treatment.

“Because we’ve shined a spotlight in recent years on emerging and early signs of psychosis, diagnosis of schizophrenia is like a new fad, and it’s a problem especially for those who are not schizophrenia specialists because symptoms can be complex and misleading,” says Krista Baker, LCPC, Johns Hopkins Medicine, Baltimore, Maryland. “Diagnostic errors can be devastating for people, particularly the wrong diagnosis of a mental disorder,” she adds.

According to the National Institute of Mental Health, schizophrenia affects an estimated 0.5% of the world population, and is more common in men. It typically arises in the late adolescences, 20s and even as late as the early 30s in women. Symptoms such as disordered thinking, hallucinations, delusions, reduced emotions and unusual behaviours can be disabling, and drug treatments often create difficult side effects.

The new study was prompted in part by anecdotal evidence among healthcare providers in Baker’s specialty clinic that a fair number of people were being seen who were misdiagnosed. These patients usually had other mental illnesses, such as depression.

To see if there was rigorous evidence of such a trend, the researchers looked at patient data from 78 cases referred to EPIC for consultation between February 2011 and July 2017. Patients were an average age of 19, and about 69% were men, 74% were white, 12% African American and 14% were another ethnicity. Patients were referred to the clinic by general psychiatrists, outpatient psychiatric centres, primary care physicians, nurse practitioners, neurologists or psychologists.

Each consultation by the clinic took 3 to 4 hours, and included interviews with the patient and the family, physical exams, questionnaires, and medical and psychosocial histories.

Of the patients referred to the clinic, 54 people came with a predetermined diagnosis of a schizophrenia spectrum disorder. Of those, 26 received a confirmed diagnosis of a schizophrenia spectrum disorder following their consultation with the EPIC team, which is composed of clinicians and psychiatrists. Of the 54 cases, 51% were rediagnosed by clinic staff as having anxiety or mood disorders. Anxiety symptoms were prominent in 14 of the misdiagnosed patients.

One of the other most common symptoms that the researchers believe may have contributed to misdiagnosis of schizophrenia was hearing voices, as almost all incorrectly diagnosed patients reported auditory hallucinations.

“Hearing voices is a symptom of many different conditions, and sometimes it is just a fleeting phenomenon with little significance,” says Russell L. Margolis, MD, Johns Hopkins Schizophrenia Center, Johns Hopkins University School of Medicine, Baltimore, Maryland. “At other times when someone reports ‘hearing voices’ it may be a general statement of distress rather than the literal experience of hearing a voice. The key point is that hearing voices on its own doesn’t mean a diagnosis of schizophrenia.”

In speculating about other reasons why there might be so many misdiagnoses, the researchers say that it could be due to overly simplified application of criteria listed in the Diagnostic Statistical Manual of Mental Disorders, a standard guide to the diagnosis of psychiatric disorders.

“Electronic medical record systems, which often use pull-down diagnostic menus, increase the likelihood of this type of error,” says Dr. Margolis, who refers to the problem as “checklist psychiatry.”

“The big take-home message from our study is that careful consultative services by experts are important and likely underutilised in psychiatry,” says Dr. Margolis. “Just as a primary care clinician would refer a patient with possible cancer to an oncologist or a patient with possible heart disease to a cardiologist, it’s important for general mental health practitioners to get a second opinion from a psychiatry specialty clinic like ours for patients with confusing, complicated or severe conditions. This may minimise the possibility that a symptom will be missed or overinterpreted.”

Dr. Margolis cautioned that the study was limited to patients evaluated in 1 clinic. Nonetheless, he was encouraged by the willingness of so many patients, their families and their clinicians to ask for a second opinion from the Johns Hopkins clinic. If further study confirms their findings, it would lend support to the belief by the Johns Hopkins team that overdiagnosis may be a national problem, because they see patients from across the country who travel to Johns Hopkins for an opinion. They hope to examine the experience of other specialty consultation clinics in the future.

Reference: doi: 10.1097/PRA.0000000000000363

SOURCE: Johns Hopkins Medicine

https://dgnews.docguide.com/reported-symptoms-anxiety-hearing-voices-most-common-reasons-misdiagnosis-schizophrenia?overlay=2&nl_ref=newsletter&pk_campaign=newsletter&nl_eventid=20124


St. Jude Children’s Research Hospital scientists have linked disruption of a brain circuit associated with schizophrenia to an age-related decline in levels of a single microRNA in one brain region

St. Jude Children’s Research Hospital scientists have identified a small RNA (microRNA) that may be essential to restoring normal function in a brain circuit associated with the “voices” and other hallucinations of schizophrenia. The microRNA provides a possible focus for antipsychotic drug development. The findings appear today in the journal Nature Medicine.

The work was done in a mouse model of a human disorder that is one of the genetic causes of schizophrenia. Building on previous St. Jude research, the results offer important new details about the molecular mechanism that disrupts the flow of information along a neural circuit connecting two brain regions involved in processing auditory information. The findings also provide clues about why psychotic symptoms of schizophrenia are often delayed until late adolescence or early adulthood.

“In 2014, we identified the specific circuit in the brain that is targeted by antipsychotic drugs. However, the existing antipsychotics also cause devastating side effects,” said corresponding author Stanislav Zakharenko, M.D., Ph.D., a member of the St. Jude Department of Developmental Neurobiology. “In this study, we identified the microRNA that is a key player in disruption of that circuit and showed that depletion of the microRNA was necessary and sufficient to inhibit normal functioning of the circuit in the mouse models.

“We also found evidence suggesting that the microRNA, named miR-338-3p, could be targeted for development of a new class of antipsychotic drugs with fewer side effects.”

There are more than 2,000 microRNAs whose function is to silence expression of particular genes and regulate the supply of the corresponding proteins. Working in a mouse model of 22q11 deletion syndrome, researchers identified miR-338-3p as the microRNA that regulates production of the protein D2 dopamine receptor (Drd2), which is the prime target of antipsychotics.

Individuals with the deletion syndrome are at risk for behavior problems as children. Between 23 and 43 percent develop schizophrenia, a severe chronic disorder that affects thinking, memory and behavior. Researchers at St. Jude are studying schizophrenia and other brain disorders to improve understanding of how normal brains develop, which provides insights into the origins of diseases like cancer.

The scientists reported that Drd2 increased in the brain’s auditory thalamus when levels of the microRNA declined. Previous research from Zakharenko’s laboratory linked elevated levels of Drd2 in the auditory thalamus to brain-circuit disruptions in the mutant mice. Investigators also reported that the protein was elevated in the same brain region of individuals with schizophrenia, but not healthy adults.

Individuals with the deletion syndrome are missing part of chromosome 22, which leaves them with one rather than the normal two copies of more than 25 genes. The missing genes included Dgcr8, which facilitates production of microRNAs.

Working in mice, researchers have now linked the 22q11 deletion syndrome and deletion of a single Dgcr8 gene to age-related declines in miR-338-3p in the auditory thalamus. The decline was associated with an increase in Drd2 and reduced signaling in the circuit that links the thalamus and auditory cortex, a brain region implicated in auditory hallucination. Levels of miR-338-3p were lower in the thalamus of individuals with schizophrenia compared to individuals of the same age and sex without the diagnosis.

The miR-338-3p depletion did not disrupt other brain circuits in the mutant mice, and the findings offer a possible explanation. Researchers found that miR-338-3p levels were higher in the thalamus than in other brain regions. In addition, miR-338-3p was one of the most abundant microRNAs present in the thalamus.

Replenishing levels of the microRNA in the auditory thalamus of mutant mice reduced Drd2 protein and restored the circuit to normal functioning. That suggests that the microRNA could be the basis for a new class of antipsychotic drugs that act in a more targeted manner with fewer side effects. Antipsychotic drugs, which target Drd2, also restored circuit function.

The findings provide insight into the age-related delay in the onset of schizophrenia symptoms. Researchers noted that microRNA levels declined with age in all mice, but that mutant mice began with lower levels of miR-338-3p. “A minimum level of the microRNA may be necessary to prevent excessive production of the Drd2 that disrupts the circuit,” Zakharenko said. “While miR-338-3p levels decline as normal mice age, levels may remain above the threshold necessary to prevent overexpression of the protein. In contrast, the deletion syndrome may leave mice at risk for dropping below that threshold.”

The study’s first authors are Sungkun Chun, Fei Du and Joby Westmoreland, all formerly of St. Jude. The other authors are Seung Baek Han, Yong-Dong Wang, Donnie Eddins, Ildar Bayazitov, Prakash Devaraju, Jing Yu, Marcia Mellado Lagarde and Kara Anderson, all of St. Jude.

https://www.stjude.org/media-resources/news-releases/2016-medicine-science-news/small-rna-identified-that-offers-clues-for-quieting-the-voices-of-schizophrenia.html

An international team of researchers has linked specific symptoms of schizophrenia with various anatomical characteristics in the brain, according to research published in NeuroImage.

By analyzing the brain’s anatomy with magnetic resonance imaging (MRI), researchers from the University of Granada, Washington University in St. Louis, and the University of South Florida have demonstrated the existence of distinctive subgroups among patients with schizophrenia who suffer from different symptoms.

These findings could herald a significant step forward in diagnosing and treating schizophrenia.

To perform the study, the researchers conducted the MRI technique “diffusion tensor imaging” on 36 healthy participants and 47 schizophrenic participants.

The researchers found that tests on schizophrenic participants revealed various abnormalities in parts of the corpus callosum, a bundle of neural fibers that connects the left and right cerebral hemispheres and is essential for effective interhemispheric communication.

Different anomalies in the corpus callosum were associated with different symptoms in the schizophrenic participants. An anomaly in one part of the brain structure was associated with strange and disorganized behavior; another anomaly was associated with disorganized thought and speech, as well as negative symptoms such as a lack of emotion; and other anomalies were associated with hallucinations.

In 2014, this same research group proved that schizophrenia is not a single illness. The team demonstrated the existence of 8 genetically distinct disorders, each with its own symptoms. Igor Zwir, PhD, and Javier Arnedo from the University of Granada’s Department of Computer Technology and Artificial Intelligence found that different sets of genes were strongly linked with different clinical symptoms.

“The current study provides further evidence that schizophrenia is a heterogeneous group of disorders, as opposed to a single illness, as was previously thought to be case,” Dr Zwir said in a statement.

While current treatments for schizophrenia tend to be generic regardless of the symptoms exhibited by each patient, the researchers believe that in the future, analyzing how specific gene networks are linked to various brain features and specific symptoms will help develop treatments that are adapted to each patient’s individual disorder.

To conduct the analysis of the gene groups and brain scans, the researchers developed a new, complex analysis of the relationships between different types of data and recommendations regarding new data. The system is similar to that used by companies such as Netflix to determine what movies they want to broadcast.

“To conduct the research, we did not begin by studying individuals who had certain schizophrenic symptoms in order to determine whether they had the corresponding brain anomalies,” said Dr Zwir in a statement. “Instead, we first analyzed the data, and that’s how we discovered these patterns. This type of information, combined with data on the genetics of schizophrenia, will someday be of vital importance in helping doctors treat the disorders in a more precise and effective way.”

Reference
Arnedo J, Mamah D, Baranger DA, et al. Decomposition of brain diffusion imaging data uncovers latent schizophrenias with distinct patterns of white matter anisotropy. NeuroImage. 2015; doi:10.1016/j.neuroimage.2015.06.083.

http://www.psychiatryadvisor.com/schizophrenia-and-psychoses/types-subgroups-schizophrenia-linked-various-different-brain-anomalies-corpus-callosum/article/470226/?DCMP=EMC-PA_Update_rd&cpn=psych_md&hmSubId=&hmEmail=5JIkN8Id_eWz7RlW__D9F5p_RUD7HzdI0&NID=&dl=0&spMailingID=13630678&spUserID=MTQ4MTYyNjcyNzk2S0&spJobID=720090900&spReportId=NzIwMDkwOTAwS0

Schizophrenia is associated with structural and functional alterations of the visual system, including specific structural changes in the eye. Tracking such changes may provide new measures of risk for, and progression of the disease, according to a literature review published online in the journal Schizophrenia Research: Cognition, authored by researchers at New York Eye and Ear Infirmary of Mount Sinai and Rutgers University.

Individuals with schizophrenia have trouble with social interactions and in recognizing what is real. Past research has suggested that, in schizophrenia, abnormalities in the way the brain processes visual information contribute to these problems by making it harder to track moving objects, perceive depth, draw contrast between light and dark or different colors, organize visual elements into shapes, and recognize facial expressions. Surprisingly though, there has been very little prior work investigating whether differences in the retina or other eye structures contribute to these disturbances.

“Our analysis of many studies suggests that measuring retinal changes may help doctors in the future to adjust schizophrenia treatment for each patient,” said study co-author Richard B. Rosen, MD, Director of Ophthalmology Research, New York Eye and Ear Infirmary of Mount Sinai, and Professor of Ophthalmology, Icahn School of Medicine at Mount Sinai. “More studies are needed to drive the understanding of the contribution of retinal and other ocular pathology to disturbances seen in these patients, and our results will help guide future research.”

The link between vision problems and schizophrenia is well established, with as many as 62 percent of adult patients with schizophrenia experience visual distortions involving form, motion, or color. One past study found that poorer visual acuity at four years of age predicted a diagnosis of schizophrenia in adulthood, and another that children who later develop schizophrenia have elevated rates of strabismus, or misalignment of the eyes, compared to the general population.

Dr. Rosen and Steven M. Silverstein, PhD, Director of the Division of Schizophrenia Research at Rutgers University Behavioral Health Care, were the lead authors of the analysis, which examined the results of approximately 170 existing studies and grouped the findings into multiple categories, including changes in the retina vs. other parts of the eye, and changes related to dopamine vs. other neurotransmitters, key brain chemicals associated with the disease.

The newly published review found multiple, replicated, indicators of eye abnormalities in schizophrenia. One of these involves widening of small blood vessels in the eyes of schizophrenia patients, and in young people at high risk for the disorder, perhaps caused by chronic low oxygen supply to the brain. This could explain several key vision changes and serve as a marker of disease risk and worsening. Also important in this regard was thinning of the retinal nerve fiber layer in schizophrenia, which is known to be related to the onset of hallucinations and visual acuity problems in patients with Parkinson’s disease. In addition, abnormal electrical responses by retinal cells exposed to light (as measured by electroretinography) suggest cellular-level differences in the eyes of schizophrenia patients, and may represents a third useful measure of disease progression, according to the authors.

In addition, the review highlighted the potentially detrimental effects of dopamine receptor-blocking medications on visual function in schizophrenia (secondary to their retinal effects), and the need for further research on effects of excessive retinal glutamate on visual disturbances in the disorder.

Interestingly, the analysis found that there are no reports of people with schizophrenia who were born blind, suggesting that congenital blindness may completely or partially protect against the development of schizophrenia. Because congenitally blind people tend to have cognitive abilities in certain domains (e.g., attention) that are superior to those of healthy individuals, understanding brain re-organization after blindness may have implications for designing cognitive remediation interventions for people with schizophrenia.

“The retina develops from the same tissue as the brain,” said Dr. Rosen. “Thus retinal changes may parallel or mirror the integrity of brain structure and function. When present in children, these changes may suggest an increased risk for schizophrenia in later life. Additional research is needed to clarify these relationships, with the goals of better predicting emergence of schizophrenia, and of predicting relapse and treatment response and people diagnosed with the condition.”

Dr. Silverstein points out that, to date, vision has been understudied in schizophrenia, and studies of the retina and other ocular structures in the disorder are in their infancy. However, he added, “because it is much faster and less expensive to obtain data on retinal structure and function, compared to brain structure and function, measures of retinal and ocular structure and function may have an important role in both future research studies and the routine clinical care of people with schizophrenia.”

http://www.eurekalert.org/pub_releases/2015-08/tmsh-rcm081715.php

Deep in the Amazon rainforest, a group of veterans chokes down a gritty, gut-wrenching shot of liquid absolution. They try to drink away their severe mental disturbances, but not the way you drink away your ex-girlfriend with a bottle of whiskey. They’re looking for a cure. Their leader: 27-year-old retired infantryman Ryan LeCompte. Their goal: to hallucinate away their terrible memories.

From a few fringe psychiatrists to veterans like LeCompte, there is a budding belief that extreme hallucination can save our brains from themselves. Several organizations, including the Multidisciplinary Association for Psychedelic Studies (MAPS), and adventurous doctors around the world test out psychedelics such as MDMA, psilocybin and ayahuasca for possible medical uses.

Ayahuasca is a devilish brew. It’s made of vines and roots found in the Amazon; drinking it equals a heavy psychedelic experience and profuse vomiting. “As the shapes and colors continued to move about, they sometimes converged to create the face of a woman, who of course I immediately labeled as Aya,” says an ayahuasca user on the underground drug website Erowid. Aya is known as the spirit or soul of the ayahuasca world. LeCompte described having kaleidoscope vision during his ayahuasca trip, and he even began to dance and went to look at leaves and other pieces of the nature around him at points.

Ryan LeCompte is a scruffy former Marine who, today, is studying at the eccentric Naropa University in Boulder. The school was founded by Tibetan Buddhist teacher and Oxford University scholar Chögyam Trungpa and includes schools such as the Jack Kerouac School of Disembodied Poetics. The beat poets used to flock to there. It’s a Buddhist-inspired school infamous for attracting people who are looking for an alternative education in an attractive location.

For his part, LeCompte didn’t ever face a PTSD diagnosis during his time in service. But he’s lucky, because many of his peers did. What he did experience still shook him. In 2008, while stationed in 8th and I Marine Barracks in Washington, D.C., LeCompte walked into the room of a good friend in his barracks one morning to find Sgt. Jorge Leon-Alcivar dead—a suicide. He was not the only Marine LeCompte encountered who would take his own life. At least 22 veterans kill themselves every day. Leon-Alcivar’s death was the final straw, and three years later LeCompte retired from the Marines to start fighting PTSD. He received his End of Active Service honorable discharge after four years in the Marines and didn’t look back.

LeCompte began traveling to the VA hospital in Birmingham, Alabama, where he was living, to learn what was ailing disturbed veterans and soldiers. He hung around in waiting rooms, cautiously approaching the soldiers, wheedling their stories out. But it didn’t take much persuasion; the men were “so beat,” he recalls, that they opened up to him instantly. This took course over several years, during his free time, while he did contract work building helicopters.

Soon, LeCompte had amassed the information from about 100 cases in Birmingham; Veterans spilled almost everything to him: their meds, their dosages, their choice of therapy. It all added up. Over and over again, he discovered his peers were taking the same types of medicines such Zoloft and Paxil, in the same dosages, 50 to 200mg of Zoloft a day or 20 to 60mg of Paxil a day were common, and with the same form of EMDR therapy. EMDR is a somatic therapy that follows eye movements and dream states.

LeCompte didn’t see anything wrong with the therapy. How about the drugs? Yeah, it’s probably the drugs. LeCompte’s complaints ring of an old story these days in American psychiatry: we’re too drugged up, we’re overdosed and overdiagnosed. It’s a complaint plenty of professionals agree with, but only a handful of psychiatrists are taking alternate routes. “There are some veterans who actually do respond to those meds, but it’s rare,” Dr. Sue Sisley, an expert on PTSD in veterans who has studied treating the illness with marijuana, told ATTN:. “The vets who respond to the standard FDA approved meds like Zoloft or Paxil is probably less than 10 percent. The rest come in looking like zombies.”

LeCompte had tried almost all the drugs they were offering, from “highly addictive anxiolytics like Klonopin, and … Prozac as an anti-depressant and Ambien for a sleep aid,” he said. “These different drugs sort of mixed together in a cocktail just as a recipe for disaster,” he said. He never tried to contact U.S. Veteran’s Affairs to inform them of these problems, because he didn’t think they would do anything about it. VA psychiatrists like Dr. Basimah Khulusi of Missouri have been fired for simply refusing to increase medication dosages that they didn’t think their patients needed shows the kind of system LeCompte was dealing with.

LeCompte looked into how these drugs work and found they’re just mind blockers, they’re not helping you deal with your problems. “Medications do not entirely eliminate symptoms but provide a symptom reduction and are sometimes more effective when used in conjunction with an ongoing program of trauma specific psychotherapy,” according to the VA website.

LeCompte looked at research from people like Julie D. Megler, watched videos of the academic conferences focusing on psychedelics called Psychedemia from Penn State and went on websites like Erowid to look at ayahuasca experiences people had posted to the site. What did he learn? “Something like ayahuasca or MDMA is used to bridge severed connections in the brain that trauma plays a big part in creating,” he said.

“Ayahuasca opens the limbic pathways of the brain to affect the emotional core of the trauma in a way similar to affective psychotherapy for trauma, and also impacts higher cortical areas … to allow the patient to assign a new context to their trauma,” wrote brain experts J. L. Nielson and J. D. Megler, in the book The Therapeutic Use of Ayahuasca.

Soon, LeCompte started having conversations with veterans and began informing people of the possible benefits of ayahuasca, wondering if anyone else was daring enough to start considering the idea of drinking a shot of psychedelics for their PTSD. LeCompte had never tried ayahuasca, but he was willing to try anything to help his comrades. Eventually he heard of an ayahuasca retreat, the Phoenix Ayahuasca retreat in Peru, where he could test out his medicine.

It took him six months to do what any sane person would do before planning a group outing to South America to hallucinate in a forest together… he started a nonprofit. Its name? The Veterans for Entheogenic Therapy. Other vets started to find him; some were suicidal, exhausted by the daily challenge of deciding whether or not they wanted to be alive. He didn’t know them, but he felt he intimately understood – or at least sympathized with – their minds. He rounded up a trip: five other vets, and him. MAPS helped pay for two of the trips for veterans who couldn’t afford it, and the rest paid for themselves.

The prep was strangely regimented: LeCompte had to ensure the veterans were off their medication for a month leading up to the trip; anti-depressants plus ayahuasca equal a lethal mix. That task amounted to phone therapy and keeping a close eye on everyone: He called the guys every day, even their friends and family, to make sure the men had quit their pills, he said. But he made it work. The families may have thought the idea was strange, but LeCompte says none of them tried to stop their family members because of their knowledge that the drugs weren’t helping treat the PTSD symptoms, and they just wanted to help their family.

The veterans flew into Iquitos, Peru, from Lima – from Iquitos, they sat in a van all the way to the Amazon, winding past motorbikes and rickshaws “on back roads in the middle of bum fuck,” LeCompte says.

Then their lives collided and things got weird.

They were stationed for 10 days at Phoenix Ayahuasca. The camp was little more than a set of huts in the jungle, made from wood and leaves. They would drink the ayahuasca on ceremony nights and be led through their experience by the shaman, and they would stay in their personal huts on days off to reflect on their experiences alone.

LeCompte said the ayahuasca drink “tastes like shit.” The shaman leading the experience dressed in all white scrub-like clothes, like a nurse lost in the jungle. After you drink the brew, the shaman’s job is simply to observe. He diagnoses: Is anyone losing it? Some people have been known to begin convulsing. Is this the moment they need to hear a song that will send them burrowing into a different dimension? “I don’t know how he does it. It’s beyond my rational mind,” LeCompte said. “It” amounts to singing, blowing smoke on trippers’ faces and using instruments like a rattler to change their state of mind.

For his part, LeCompte only wanted two out of the four drink ceremonies, since they were so powerful. It certainly wasn’t about the PTSD for LeCompte; he was trying to get past his experiences of fallen friends and broken relationships. He says just returning home to family and friends from military service or an ayahuasca trip is a difficult experience of its own. “You’re a changed person and there’s no doubting or denying that.”

“Most people get a cut, and they put a bandaid on it,” he said. “These people have had these wounds for so long that they’ve become infected. The infection can’t be fought off with a bandaid.” LeCompte sees ayahuasca as an antibiotic, not a bandaid.

LeCompte is now planning to do an official study to look at how ayahuasca could treat PTSD, which will serve as his thesis for Naropa University. It is being sponsored by MAPS, and it will focus on 12 veterans with treatment resistant PTSD who will try using ayahuasca to treat it. The plan is to conduct the study over 10 days in early 2016. LeCompte is currently running an Indiegogo campaign to fund research and education around the medicinal use of ayahuasca.

http://www.stumbleupon.com/su/2KDuBh/:1EfXhqlsu:Y+0NYw4t/www.attn.com/stories/2301/semicolon-tattoo-mental-health


Parasitic worm normally found in amphibians and crustaceans in China may have scavenged nutrients from patient’s brain

A man who went to see his doctor after suffering headaches and experiencing strange smells was found to have been living for more than four years with a rare parasitic worm in his brain.

In the first case of its kind in Britain, the ribbon-shaped tapeworm was found to have burrowed from one side of the 50-year-old man’s brain to the other.

Doctors were left baffled after spotting strange ring-like patterns moving 5cm through his brain tissue in a series of scans taken over four years.

Surgeons only discovered the 1cm worm while carrying out a biopsy at Addenbrooke’s hospital in Cambridge and took it to parasite experts to be identified.

Geneticists at the Wellcome Trust Sanger Institute in Cambridge found the creature was a rare species of tapeworm known as Spirometra erinaceieuropaei.

Only 300 cases of infection by this parasite in humans have been reported since 1953, with only two previous cases identified in Europe.

The worm is normally found in amphibians and crustaceans in China and as it goes through its life cycle it later infects the guts of cats and dogs, where it can grow into 1.5-metre adult worms. Even in China, where the parasite is normally found, there have only been 1,000 cases reported in humans since 1882.

The unfortunate patient, who was of Chinese descent but lived in East Anglia, is thought to have picked up the parasite while on a visit to China, where he visited regularly. However, exactly how he came to be infected is not known, but he could have picked it up from infected meat or water and the worm then burrowed through his body to his brain.

Now scientists believe they have been able to learn new information about this rare parasite after studying its DNA.

Rather than living on the brain tissue of its unknowing victim, the parasite is thought to have simply absorbed nutrients from the man’s brain through its body as the worm has no mouth.

Dr Hayley Bennett said they hoped to use the result of the study to help diagnose infections in humans more quickly in the future and even find ways of treating it.

She said: “This worm is quite mysterious and we don’t know everything about what species it can infect or how. Humans are a rare and accidental host. for this particular worm. It remains as a larva throughout the infection. We know from the genome that the worm has fatty acid binding proteins that might help it scavenge fatty acids and energy from its environment, which may be one the mechanisms for how it gets its food.

“This genome will act as a reference, so that when new treatments are developed for the more common tapeworms, scientists can cross-check whether they are also likely to be effective against this very rare infection.” The research is published in the journal Genome Biology.

The patient first noticed something was wrong in 2008 when he began suffering headaches, seizures, memory flashbacks and strange smells.

After visiting his doctor, an MRI scan revealed a cluster of rings in the right medial temporal lobe.

He was given tests for a wide range of other diseases including syphilis, HIV and tuberculosis but tested negative for them all. Later scans showed the rings moving through his brain.

After undergoing two biopsies, surgeons found the worm moving around in his brain and removed it in 2012. The man was then given drugs to help treat the infection but he continues to suffer from problems associated with having had the worm living in his brain.

It is not known how he first became infected, but one source of infection is the use of frog poultice, a traditional Chinese remedy where raw frog meat is used to calm sore eyes.

“We did not expect to see an infection of this kind in the UK, but global travel means that unfamiliar parasites do sometimes appear,” said Dr Effrossyni Gkrania-Klotsas, one of the clinicians involved in the man’s treatment at Addenbrooke’s NHS Trust.

“We can now diagnose sparganosis using MRI scans, but this does not give us the information we need to identify the exact tapeworm species and its vulnerabilities.

“Our work shows that, even with only tiny amounts of DNA from clinical samples, we can find out all we need to identify and characterise the parasite.”

http://www.theguardian.com/science/2014/nov/21/tapeworm-parasite-mans-brain-four-years-china