Posts Tagged ‘anxiety’

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

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The Food and Drug Administration (FDA) has approved a new cranial electrotherapy stimulator (CES) device for the treatment of anxiety, depression, and insomnia.

The Cervella Cranial Electrotherapy Stimulator by Innovative Neurological Devices is operated using noise-cancelling, Bluetooth-enabled headphones and an app. The device delivers a low-level, constant current to the patient’s cranium via a pair of conductive electrodes incorporated into ear pads of the headphones.

Patients will need a prescription from a licensed healthcare provider in order to purchase the device, which will cost $695, and is due to launch at the end of March (2019).

“We hope that by incorporating treatment electrodes into a noise-cancelling headset, patient compliance will significantly increase and, consequently, treatment outcomes will improve,” said Bart Waclawik, President and CEO of Innovative Neurological Devices. “Also, by making the Cervella device appear indistinguishable from ordinary over-ear headphones, patients will have the freedom to use the device in anxiety-inducing situations without curious looks from onlookers.”

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Waclawik added that patients will be able to share treatment data with providers through the app, which provides automated data recordings and treatment reminders.

For more information visit Cervella.us.

by PETER DOCKRILL

When bad things happen, we don’t want to remember. We try to block, resist, ignore – but we should perhaps be doing the opposite, researchers say.

A new study led by scientists in Texas suggests the act of intentionally forgetting is linked to increased cerebral engagement with the unwanted information in question. In other words, to forget something, you actually need to focus on it.

“A moderate level of brain activity is critical to this forgetting mechanism,” explains psychologist Tracy Wang from the University of Texas at Austin.

“Too strong, and it will strengthen the memory; too weak, and you won’t modify it.”

Trying to actively forget unwanted memories doesn’t just help prevent your brain from getting overloaded.

It also lets people move on from painful experiences and emotions they’d rather not recall, which is part of the reason it’s an area of active interest to neuroscientists.

“We may want to discard memories that trigger maladaptive responses, such as traumatic memories, so that we can respond to new experiences in more adaptive ways,” says one of the researchers, Jarrod Lewis-Peacock.

“Decades of research has shown that we have the ability to voluntarily forget something, but how our brains do that is still being questioned.”

Much prior research on intentional forgetting has focussed on brain activity in the prefrontal cortex, and the brain’s memory centre, the hippocampus.

In the new study, the researchers monitored a different part of the brain called the ventral temporal cortex, which helps us process and categorise visual stimuli.

In an experiment with 24 healthy young adults, the participants were shown pictures of scenes and people’s faces, and were instructed to either remember or forget each image.

During the experiment, each of the participants had their brain activity monitored by functional magnetic resonance imaging (fMRI) machines.

When the researchers examined activity in the ventral temporal cortex, they found that the act of forgetting effectively uses more brain power than remembering.

“Pictures followed by a forget instruction elicited higher levels of processing in [the] ventral temporal cortex compared to those followed by a remember instruction,” the authors write in their paper.

“This boost in processing led to more forgetting, particularly for items that showed moderate (vs. weak or strong) activation.”

Of course, forgetting specific images on demand in a contrived laboratory experiment is very different to moving on from painful or traumatic memories of events experienced in the real world.

But the mechanisms at work could be the same, researchers say, and figuring out how to activate them could be a huge benefit to people around the world who need to forget things, but don’t know how.

Especially since this finding in particular challenges our natural intuition to suppress things; instead, we should involve more rather than less attention to unwanted information, in order to forget it.

“Importantly, it’s the intention to forget that increases the activation of the memory,” Wang says.

“When this activation hits the ‘moderate level’ sweet spot, that’s when it leads to later forgetting of that experience.”

The findings are reported in JNeurosci.

https://www.sciencealert.com/to-forget-something-you-need-to-think-about-it-neuroscientists-reveal

by Carly Cassella

Sticks and stones may break your bones, but name-calling could actually change the structure of your brain.

A new study has found that persistent bullying in high school is not just psychologically traumatising, it could also cause real and lasting damage to the developing brain.

The findings are drawn from a long-term study on teenage brain development and mental health, which collected brain scans and mental health questionnaires from European teenagers between the ages of 14 and 19.

Following 682 young people in England, Ireland, France and Germany, the researchers tallied 36 in total who reported experiencing chronic bullying during these years.

When the researchers compared the bullied participants to those who had experienced less intense bullying, they noticed that their brains looked different.

Across the length of the study, in certain regions, the brains of the bullied participants appeared to have actually shrunk in size.

In particular, the pattern of shrinking was observed in two parts of the brain called the putamen and the caudate, a change oddly reminiscent of adults who have experienced early life stress, such as childhood maltreatment.

Sure enough, the researchers found that they could partly explain these changes using the relationship between extreme bullying and higher levels of general anxiety at age 19. And this was true even when controlling for other types of stress and co-morbid depressive symptoms.

The connection is further supported by previous functional MRI studies that found differences in the connectivity and activation of the caudate and putamen activation in those with anxiety.

“Although not classically considered relevant to anxiety, the importance of structural changes in the putamen and caudate to the development of anxiety most likely lies in their contribution to related behaviours such as reward sensitivity, motivation, conditioning, attention, and emotional processing,” explains lead author Erin Burke Quinlan from King’s College London.

In other words, the authors think all of this shrinking could be a mark of mental illness, or at least help explain why these 19-year-olds are experiencing such unusually high anxiety.

But while numerous past studies have already linked childhood and adolescent bullying to mental illness, this is the very first study to show that unrelenting victimisation could impact a teenager’s mental health by actually reshaping their brain.

The results are cause for worry. During adolescence, a young person’s brain is absolutely exploding with growth, expanding at an incredible place.

And even though it’s normal for the brain to prune back some of this overabundance, in the brains of those who experienced chronic bullying, the whole pruning process appears to have spiralled out of control.

The teenage years are an extremely important and formative period in a person’s life, and these sorts of significant changes do not bode well. The authors suspect that as these children age, they might even begin to experience greater shrinkage in the brain.

But an even longer long-term study will need to be done if we want to verify that hunch. In the meantime, the authors are recommending that every effort be made to limit bullying before it can cause damage to a teenager’s brain and their mental health.

This study has been published in Molecular Psychiatry.

https://www.sciencealert.com/chronic-bullying-could-actually-reshape-the-brains-of-teens

largest-ever-study-of-genetic-links-to-depression-and-anxiety-launched-309700

The NIHR and King’s College London are calling for 40,000 people diagnosed with depression or anxiety to enrol online for the Genetic Links to Anxiety and Depression (GLAD) Study and join the NIHR Mental Health Bioresource.

Researchers hope to establish the largest ever database of volunteers who can be called up to take part in research exploring the genetic factors behind the two most common mental health conditions – anxiety and depression.

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The GLAD study will make important strides towards better understanding of these disorders and provide a pool of potential participants for future studies, reducing the time-consuming process of recruiting patients for research.

Research has shown 30-40% of the risk for both depression and anxiety is genetic and 60-70% due to environmental factors. Only by having a large, diverse group of people available for studies will researchers be able to determine how genetic and environmental triggers interact to cause anxiety and depression.

Leader of the GLAD study and the NIHR Mental Health BioResource, Dr Gerome Breen of King’s College London, said: “It’s a really exciting time to become involved in mental health research, particularly genetic research which has made incredible strides in recent years – we have so far identified 46 genetic links for depression and anxiety.

“By recruiting 40,000 volunteers willing to be re-contacted for research, the GLAD Study will take us further than ever before. It will allow researchers to solve the big unanswered questions, address how genes and environment act together and help develop new treatment options.”

The GLAD Study, a collaboration between the NIHR BioResource and King’s College London, has been designed to be particularly accessible, with a view to motivating more people to take part in mental health research.

Research psychologist and study lead Professor Thalia Eley, King’s College London, said: “We want to hear from all different backgrounds, cultures, ethnic groups and genders, and we are especially keen to hear from young adults. By including people from all parts of the population, what we learn will be relevant to everyone. This is a unique opportunity to participate in pioneering medical science.”

https://www.nihr.ac.uk/news/nihr-launches-largest-ever-study-of-genetic-links-to-depression-and-anxiety/9201

inhaled-version-of-blood-pressure-drug-shows-promise-in-treating-anxiety-pain-309437

An inhaled form of a high blood pressure medication has potential to treat certain types of anxiety as well as pain, according to a new study by the Centre for Addiction and Mental Health (CAMH).

Anxiety disorders are usually treated with different types of medications, such as antidepressants, and psychotherapy. Amiloride is a medication offering a new approach, as a short-acting nasal spray that could be used to prevent an anxiety attack.

“Inhaled amiloride may prove to have benefits for panic disorder, which is typically characterized by spells of shortness of breath and fear, when people feel anxiety levels rising,” says lead author Dr. Marco Battaglia, Associate Chief of Child and Youth Psychiatry and Clinician Scientist in the Campbell Family Mental Health Research Institute at CAMH.

The study was based on understanding the key physiological changes in brain functioning that are linked to anxiety and pain sensitivity. The researchers then tested a molecule, amiloride, which targets this functioning.

Amiloride was inhaled so that it could immediately access the brain. The study showed that it reduced the physical respiratory signs of anxiety and pain in a preclinical model of illness. This therapeutic effect didn’t occur when amiloride was administered in the body, as it didn’t cross the blood-brain barrier and did not reach the brain.

Results were published in the Journal of Psychopharmacology.

The role of early life adversity
The study is based on years of research into how a person’s early life experiences affect their genes, says Dr. Battaglia. Childhood adversity, such as loss or separation from parents, increases the risk of anxiety disorders and pain, among other health issues.

At a molecular level, these negative life experiences are linked to changes in some genes of the ASIC (acid-sensing-ion-channels) family. While the DNA itself doesn’t change, the way it functions is affected.

DNA is converted into working proteins through a process called gene expression. As a result of childhood adversity, some ASIC genes showed increased expression and epigenomic changes. (“Epigenomic” refers to changes in gene regulation that can inherited by children). Overlapping genetic changes were also seen in blood taken from twins who responded to specific tests designed to provoke panic.

These genetic changes are linked to physical symptoms. Breathing can be affected, due to over-sensitivity to higher carbon dioxide levels in the air. In such situations, a person might hyperventilate and experience growing anxiety. Preclinical and human data are strikingly similar in this regard. “As a treatment, amiloride turned out to be very effective preclinically,” says Dr. Battaglia.

The next step in his research is to test whether it eases anxiety symptoms. Dr. Battaglia is now launching a pilot clinical trial, supported through a seed grant from CAMH’s new Discovery Fund. Collaborators at the University of Utah are testing the drug’s safety.

Amiloride has been used as an oral treatment for decades for hypertension, and as an inhaled spray in a few experimental studies of cystic fibrosis, he notes. The researchers are therefore further ahead than if they had to develop and test an entirely new medication.

https://www.technologynetworks.com/neuroscience/news/inhaled-version-of-blood-pressure-drug-shows-promise-in-treating-anxiety-pain-309437

anewmapofthe
A 3-D rendering of the serotonin system in the left hemisphere of the mouse brain reveals two groups of serotonin neurons in the dorsal raphe that project to either cortical regions (blue) or subcortical regions (green) while rarely crossing into the other’s domain.

As Liqun Luo was writing his introductory textbook on neuroscience in 2012, he found himself in a quandary. He needed to include a section about a vital system in the brain controlled by the chemical messenger serotonin, which has been implicated in everything from mood to movement regulation. But the research was still far from clear on what effect serotonin has on the mammalian brain.

“Scientists were reporting divergent findings,” said Luo, who is the Ann and Bill Swindells Professor in the School of Humanities and Sciences at Stanford University. “Some found that serotonin promotes pleasure. Another group said that it increases anxiety while suppressing locomotion, while others argued the opposite.”

Fast forward six years, and Luo’s team thinks it has reconciled those earlier confounding results. Using neuroanatomical methods that they invented, his group showed that the serotonin system is actually composed of at least two, and likely more, parallel subsystems that work in concert to affect the brain in different, and sometimes opposing, ways. For instance, one subsystem promotes anxiety, whereas the other promotes active coping in the face of challenges.

“The field’s understanding of the serotonin system was like the story of the blind men touching the elephant,” Luo said. “Scientists were discovering distinct functions of serotonin in the brain and attributing them to a monolithic serotonin system, which at least partly accounts for the controversy about what serotonin actually does. This study allows us to see different parts of the elephant at the same time.”

The findings, published online on August 23 in the journal Cell, could have implications for the treatment of depression and anxiety, which involves prescribing drugs such as Prozac that target the serotonin system – so-called SSRIs (selective serotonin reuptake inhibitors). However, these drugs often trigger a host of side effects, some of which are so intolerable that patients stop taking them.

“If we can target the relevant pathways of the serotonin system individually, then we may be able to eliminate the unwanted side effects and treat only the disorder,” said study first author Jing Ren, a postdoctoral fellow in Luo’s lab.

Organized projections of neurons

The Stanford scientists focused on a region of the brainstem known as the dorsal raphe, which contains the largest single concentration in the mammalian brain of neurons that all transmit signals by releasing serotonin (about 9,000).

The nerve fibers, or axons, of these dorsal raphe neurons send out a sprawling network of connections to many critical forebrain areas that carry out a host of functions, including thinking, memory, and the regulation of moods and bodily functions. By injecting viruses that infect serotonin axons in these regions, Ren and her colleagues were able to trace the connections back to their origin neurons in the dorsal raphe.

This allowed them to create a visual map of projections between the dense concentration of serotonin-releasing neurons in the brainstem to the various regions of the forebrain that they influence. The map revealed two distinct groups of serotonin-releasing neurons in the dorsal raphe, which connected to cortical and subcortical regions in the brain.

“Serotonin neurons in the dorsal raphe project to a bunch of places throughout the brain, but those bunches of places are organized,” Luo said. “That wasn’t known before.”

Two parts of the elephant

In a series of behavioral tests, the scientists also showed that serotonin neurons from the two groups can respond differently to stimuli. For example, neurons in both groups fired in response to mice receiving rewards like sips of sugar water but they showed opposite responses to punishments like mild foot shocks.

“We now understand why some scientists thought serotonin neurons are activated by punishment, while others thought it was inhibited by punishment. Both are correct – it just depends on which subtype you’re looking at,” Luo said.

What’s more, the group found that the serotonin neurons themselves were more complex than originally thought. Rather than just transmitting messages with serotonin, the cortical-projecting neurons also released a chemical messenger called glutamate – making them one of the few known examples of neurons in the brain that release two different chemicals.

“It raises the question of whether we should even be calling these serotonin neurons because neurons are named after the neurotransmitters they release,” Ren said.

Taken together, these findings indicate that the brain’s serotonin system is not made up of a homogenous population of neurons but rather many subpopulations acting in concert. Luo’s team has identified two groups, but there could be many others.

In fact, Robert Malenka, a professor and associate chair of psychiatry and behavioral sciences at Stanford’s School of Medicine, and his team recently discovered a group of serotonin neurons in the dorsal raphe that project to the nucleus accumbens, the part of the brain that promotes social behaviors.

“The two groups that we found don’t send axons to the nucleus accumbens, so this is clearly a third group,” Luo said. “We identified two parts of the elephant, but there are more parts to discover.”

https://medicalxpress.com/news/2018-08-brain-serotonin.html