Posts Tagged ‘depression’

he most commonly prescribed antidepressant barely relieves symptoms of modern depression, a major study reveals.

The largest independent investigation ever undertaken found patients taking sertraline experienced negligible improvements in mood.

Published in the Lancet Psychiatry, the study comes amid mounting controversy over increased use of antidepressants by GPs in recent decades, with roughly 7.3 million people in England issued a prescription each year.

Its authors said they were “shocked and surprised” by the results, and called for the development of new classes of medication.

However, in the absence of better drugs, they do not want current prescribing practice to be changed because the trial also showed sertraline is effective in reducing anxiety, which often accompanies depression.

The new trial is by far the largest to be conducted without the involvement of the pharmaceutical industry.

It is also the most in-depth examination of sertraline – a type of selective serotonin reuptake inhibitor (SSRI) – in patients with a range of depression severities, rather than just in severely depressed patients in specialist mental health units.

The study included 654 people aged 18 to 74 who were given either the antidepressant for 12 weeks or a placebo.

The results showed depressive symptoms were five per cent lower after six weeks in the sertraline group, which was “no convincing evidence” of an effect.

After 12 weeks, there was a 13 per cent reduction, a finding the experts described as “weak”.

But the drug did offer clear benefits in reducing anxiety, with a 21 per cent reduction in symptoms at six weeks and 23 per cent at 12 weeks.

This is likely to explain why patients taking sertraline were twice as likely to say they felt generally better compared to the placebo group, even once questioned on specific symptoms of depression the benefit was far weaker.

Symptoms of depression include poor concentration, low mood, trouble with sleep, lack of enjoyment, whereas anxiety is presents as worry, nervousness, irritability and restlessness.

Professor Glyn Lewis, who led the research at University College London, said: “We were shocked and surprised when we did our analysis.

“There is absolutely no doubt this is an unexpected result.’

“Our primary hypothesis was that it would affect those depressive symptoms at six weeks and we didn’t find that.

“We definitely need better treatments for depression, and we need more research in this area.”

He suggested that new, more effective classes of antidepressants could be based on ketamine, psilocybin, the psychedelic in magic mushrooms, and anti-inflammatories.

It is thought that roughly four million people in England are long-term users of antidepressants.

Prescribing data shows that SSRI’s such as sertraline make up 54 per cent of antidepressant prescriptions.

Scientists have responded to the new study by pointing out that some of the patients had very mild symptoms of depression to start with, making it less likely that sertraline would cause an improvement.

However, others have pointed out that this is exactly the basis upon which GPs tend to hand out the drugs in practice.

Dr Gemma Lewis, who co-authored the new research, said: “I think it’s really important to understand that anxiety symptoms are very, very common among people with depression.”

She added: “It appears that people taking the drug are feeling less anxious, so they feel better overall, even if their depressive symptoms were less affected.

“We hope that we have cast new light on how antidepressants work, as they may be primarily affecting anxiety symptoms such as nervousness, worry and tension, and taking longer to affect depressive symptoms.”

Professor Helen Stokes-Lampard, Chair of the Royal College of GPs, said: “It is well-established that it often takes a while for patients to feel the full benefits of modern antidepressants and that they work best when taken for significant periods of time, which is one reason why doctors will often review patients after several weeks of use and then prescribe a fairly long course of the drugs, if they appear to be beneficial.”

https://www.telegraph.co.uk/science/2019/09/19/common-antidepressant-barely-helps-improve-depression-symptoms/

Thanks to Kebmodee for bringing this to the It’s Interesting community.

by David N. Osser, MD

Current estimates are that 4% to 5% of the population is at risk for a disorder on the bipolar spectrum. Among the patients in the so-called soft portion of that spectrum are those with a disturbance of temperament in the direction of hypomania.

The concept of temperament is a product of German nosological research from a century ago starting with Kraepelin. In the US, the concept has been championed by Hagop Akiskal, MD and his colleagues. Akiskal is now the editor emeritus of the Journal of Affective Disorders. The notion of depressive temperament has been incorporated into DSM-5 nosology in the form of “persistent depressive disorder” (previously called dysthymia). The other pole was called hyperthymia by the Germans. DSM committees have considered adding hyperthymia but have not done so. The research base on it is still, to many, unconvincing. However, it seems that in clinical practice one encounters individuals who have chronic low-grade hypomanic symptoms—high energy, need for less sleep than others, chronic optimism, chronic risk taking. These individuals can be prone to major depressions and can become severely suicidal.

Akiskal and colleagues have been describing these patients for almost 40 years. Their research criteria for hyperthymic temperament include onset before age 21, habitual sleep of less than 6 hours even on weekends, excessive use of denial, and traits (described originally by Schneider et al) that include being overoptimistic, self-assured, grandiose, overtalkative, warm and people-seeking, uninhibited, promiscuous, and meddlesome (1). Neurobiological studies have suggested the individuals have dopaminergic dysregulation (2),

Treatment issues have focused on what medications to use when hyperthymic individuals become depressed. The studies have all been uncontrolled. However, it seems that antidepressants are ineffective for these depressions and often trigger a mixed state or frank mania at times. Mood stabilizers and medications effective for bipolar depression may be more appropriate for the depressions in these patients.Usually their sunny temperament itself doesn’t require treatment and may, in fact, foster excellent productivity and creativity during much of their lifespan.

Disclosures:
Dr Osser is a Consulting Psychiatrist, US Department of Veterans Affairs, National Telemental Health Center, Bipolar Disorders Telehealth Program, Brockton, MA.

References:
1. Akiskal HS, Mallya G. Criteria for the “soft” bipolar spectrum: treatment implications. Psychopharmacol Bull. 1987;23:68-73.

2. Rihmer Z, Akiskal KK, Rihmer A, Akiskal HS. Current research on affective temperaments. Curr Opin Psychiatry. 2010;23:12-18.

by Bruce Jancin

The tantalizing prospect that statins could be repurposed as adjunctive antidepressant drugs in a defined subgroup of patients with major depression is finally about to undergo rigorous testing.

Several lines of preliminary evidence, including large observational cohort studies as well as three small, short-duration randomized trials, suggest that this might indeed be the case. It’s an extremely attractive possibility, since patients and physicians wish that antidepressant therapy were more effective, statins are among the most widely prescribed drugs worldwide, and their safety profile is thoroughly established. The expectation is that a definitive answer as to whether repurposing of statins as antidepressants is worthwhile will be provided by the SIMCODE trial, recently approved for funding by the German Federal Ministry of Education and Research, Christian Otte, MD, announced at the annual congress of the European College of Neuropsychopharmacology.

SIMCODE is a multicenter, double-blind, placebo-controlled randomized trial to be conducted at eight German academic medical centers. Participants, all of whom must have major depressive disorder and comorbid obesity, will be randomized to simvastatin or placebo on top of standard antidepressant therapy with escitalopram, an SSRI which, like simvastatin, is available as a relatively inexpensive generic, explained Dr. Otte, professor and vice director of the department of psychiatry and psychotherapy at Charite University in Berlin.

For Dr. Otte, SIMCODE will close a circle he helped open with his 2012 report from the Heart and Soul Study, a prospective longitudinal study of nearly 1,000 San Francisco Bay Area patients with coronary heart disease who were assessed annually for depressive symptoms for 6 years. The 65% of patients who were on statin therapy, albeit in nonrandomized fashion, had an adjusted 38% lower risk of developing depression (J Clin Psychiatry. 2012 May;73[5]:610-5).

His was one of seven observational studies involving more than 9,000 patients included in a subsequent meta-analysis showing that statin users were 37% less likely to develop depression than were nonusers (J Affect Disord. 2014 May;160:62-7).

At a symposium on repurposing statins as antidepressants held at ECNP 2019, Dr. Otte was joined by other researchers who have made key contributions in this area. All agreed that the verdict isn’t in yet as to statins’ effectiveness as adjunctive antidepressants, and that the subgroup of patients with major depression who are most likely to gain added antidepressive effect from a statin are those with what the speakers variously described as comorbid cardiometabolic disease, immunometabolic disease, or simply, as in SIMCODE, obesity. These are patients with a high degree of systemic inflammation, which often makes their depression less responsive to standard antidepressant therapies. The working hypothesis is that the pleiotropic anti-inflammatory effects of statins will result in a greater response to conventional antidepressants.

Animal studies point to multiple potential mechanisms by which statins might have antidepressant efficacy in clinical practice, according to Dr. Otte. Beyond their anti-inflammatory effects, these include the drugs’ documented effects on glutamatergic N-methyl-D-aspartate (NMDA) receptors, dopamine receptors, brain-derived neurotrophic factor, glucocorticoid receptors, and hippocampal serotonin 2A receptors.

https://www.the-hospitalist.org/hospitalist/article/207875/depression/statins-may-do-double-duty-antidepressants?channel=51329

An ambitious research project aims to assess the state of mental-health resources and support for graduate students. The 22-month initiative is a joint venture of the Council of Graduate Schools (CGS) in Washington DC and the Jed Foundation, a non-profit organization in New York City that focuses on the mental health of young adults. The initiative will explore current schemes and programmes centred on student wellness at CGS member universities in the United States and Canada, and provide recommendations for future approaches to promote mental and emotional well-being in students.

“We want to create a road map for moving forward,” says Suzanne Ortega, CGS president and the principal investigator of the project, called Supporting Mental Health and Wellness of Graduate Students. “We’ll be offering advice about policies and resources that will help students in crisis while also creating an environment where graduate students can thrive.”

The project, supported by nearly US$280,000 in grants from the Alfred P. Sloan Foundation and the Andrew W. Mellon Foundation, will gather input through surveys of administrators at CGS’s 500 or so member institutions across the world, along with focus groups that will probably involve students as well as those advocating on behalf of students. A key part of the conversation will take place at a workshop for students, administrators and mental-health specialists that is tentatively scheduled for October next year in Washington DC. An initial report of findings and recommendations for policies is scheduled to be published in December next year.

Unmet needs

The pressure, competition and stress experienced by graduate students puts them at high risk for mental-health issues, Ortega says. Precise estimates of the prevalence of anxiety and depression in this population remain elusive, she notes, and graduate students need and deserve thoughtful, evidence-based support. “We’re convinced by the need,” she says. “We know that a significant minority of graduate students have clinical symptoms of distress.”

Nance Roy, the Jed Foundation’s chief clinical officer, says that few effective mental-health programmes aimed at graduate students are currently offered at academic institutions. The Jed Foundation assisted universities in developing guidelines that will help to address undergraduate mental health, but Roy points out that graduate students have different needs and life situations that could require tailored approaches. For example, graduate students might find it especially difficult to take time off when they’re feeling overwhelmed. “They may not be able to just step away from a research project,” she says. “We want to promote people taking time off if they need it.”

Roy is also concerned about mentorship, a crucial aspect of graduate training that doesn’t always receive much scrutiny. “That relationship needs a tremendous amount of attention,” she says.

Ortega and other investigators have identified some innovative approaches that deserve a closer look. Boston University in Massachusetts, for example, instituted a holiday policy this year that ensures two weeks, or ten working days, of paid holiday every year for PhD students on annual stipends. “The idea is that this will foster work–life balance, which is a big part of student wellness,” says Ortega.

Another is the Mental Health Bill of Rights and Responsibilities that was adopted by the graduate education department at Vanderbilt University in Nashville, Tennessee, in February. The document states that, among other things, any student who seeks mental-health treatment through the university will be assigned a care coordinator who can help them to navigate the system and connect with resources.

Mark Wallace, a neuroscientist and dean of the Vanderbilt University Graduate School, says that the bill of rights was a product of many discussions between graduate students and university leaders. “This approach ensures that everyone has a role to play in tackling mental-health issues on our campus, whether they be students, faculty or staff,” he says.

Covering new ground

Ortega says that the CGS initiative is the first of its kind in the United States and Canada. She and other investigators were partly inspired by other mental-health schemes, including the UK Council For Graduate Education’s first International Conference on the Mental Health & Wellbeing of Postgraduate Researchers, which took place in May (and was supported by Nature Research).

The CGS will co-host a global summit, Cultural Contexts of Health and Well-Being in Graduate Education, at the University of Manchester, UK, on 1–3 September. “There’s a growing recognition of these issues in Europe,” Ortega says.

Ortega and Roy hope that their project will inspire universities around the United States to take a closer look at at what they’re doing — or not doing — to promote the mental health of graduate students. The results should also lay the foundation for a future of better support for graduate students, including more scientifically rigorous studies of issues that this group faces, Ortega says.

“Graduate-student mental health and well-being has become one of the hottest topics that our graduate dean members want to see addressed,” Ortega says. “Clearly, we have a lot of work to do in the next 22 months.”

https://www.nature.com/articles/d41586-019-02584-7?utm_source=Nature+Briefing&utm_campaign=0a58fd4efb-briefing-dy-20190902&utm_medium=email&utm_term=0_c9dfd39373-0a58fd4efb-44039353

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

By Simon Makin

The Food and Drug Administration’s approval last month of a depression treatment based on ketamine generated headlines, in part, because the drug represents a completely new approach for dealing with a condition the World Health Organisation has labelled the leading cause of disability worldwide. The FDA’s approval marks the first genuinely new type of psychiatric drug—for any condition—to be brought to market in more than 30 years.

Although better known as a party drug, the anesthetic ketamine has spurred excitement in psychiatry for almost 20 years, since researchers first showed that it alleviated depression in a matter of hours. The rapid reversal of symptoms contrasted sharply with the existing set of antidepressants, which take weeks to begin working. Subsequent studies have shown ketamine works for patients who have failed to respond to multiple other treatments, and so are deemed “treatment-resistant.”

Despite this excitement, researchers still don’t know exactly how ketamine exerts its effects. A leading theory proposes that it stimulates regrowth of synapses (connections between neurons), effectively rewiring the brain. Researchers have seen these effects in animals’ brains, but the exact details and timing are elusive.

A new study, from a team led by neuroscientist and psychiatrist Conor Liston at Weill Cornell Medicine, has confirmed that synapse growth is involved, but not in the way many researchers were expecting. Using cutting-edge technology to visualize and manipulate the brains of stressed mice, the study reveals how ketamine first induces changes in brain circuit function, improving “depressed” mice’s behavior within three hours, and only later stimulating regrowth of synapses.

As well as shedding new light on the biology underlying depression, the work suggests new avenues for exploring how to sustain antidepressant effects over the long term. “It’s a remarkable engineering feat, where they were able to visualize changes in neural circuits over time, corresponding with behavioral effects of ketamine,” says Carlos Zarate, chief of the Experimental Therapeutics and Pathophysiology Branch at the National Institute of Mental Health, who was not involved in the study. “This work will likely set a path for what treatments should be doing before we move them into the clinic.”

Another reason ketamine has researchers excited is that it works differently than existing antidepressants. Rather than affecting one of the “monoamine” neurotransmitters (serotonin, norepinephrine, and dopamine), as standard antidepressants do, it acts on glutamate, the most common chemical messenger in the brain. Glutamate plays an important role in the changes synapses undergo in response to experiences that underlie learning and memory. That is why researchers suspected such “neuroplasticity” would lie at the heart of ketamine’s antidepressant effects.

Ketamine’s main drawback is its side effects, which include out-of-body experiences, addiction and bladder problems. It is also not a “cure.” The majority of recipients who have severe, difficult-to-treat depression will ultimately relapse. A course of multiple doses typically wears off within a few weeks to months. Little is known about the biology underlying depressive states, remission and relapse. “A big question in the field concerns the mechanisms that mediate transitions between depression states over time,” Liston says. “We were trying to get a better handle on that in the hopes we might be able to figure out better ways of preventing depression and sustaining recovery.”

Chronic stress depletes synapses in certain brain regions, notably the medial prefrontal cortex (mPFC), an area implicated in multiple aspects of depression. Mice subjected to stress display depressionlike behaviors, and with antidepressant treatment, they often improve. In the new study, the researchers used light microscopes to observe tiny structures called spines located on dendrites (a neuron’s “input” wires) in the mPFC of stressed mice. Spines play a key role because they form synapses if they survive for more than a few days.

For the experiment, some mice became stressed when repeatedly restrained, others became so after they were administered the stress hormone corticosterone. “That’s a strength of this study,” says neuroscientist Anna Beyeler, of the University of Bordeaux, France, who was not involved in the work, but wrote an accompanying commentary article in Science. “If you’re able to observe the same effects in two different models, this really strengthens the findings.” The team first observed the effects of subjecting mice to stress for 21 days, confirming that this resulted in lost spines. The losses were not random, but clustered on certain dendrite branches, suggesting the damage targets specific brain circuits.

The researchers then looked a day after administering ketamine and found that the number of spines increased. Just over half appeared in the same location as spines that were previously lost, suggesting a partial reversal of stress-induced damage. Depressionlike behaviors caused by the stress also improved. The team measured brain circuit function in the mPFC, also impaired by stress, by calculating the degree to which activity in cells was coordinated, a measure researchers term “functional connectivity.” This too improved with ketamine.

When the team looked closely at the timing of all this, they found that improvements in behavior and circuit function both occurred within three hours, but new spines were not seen until 12 to 24 hours after treatment. This suggests that the formation of new synapses is a consequence, rather than cause, of improved circuit function. Yet they also saw that mice who regrew more spines after treatment performed better two to seven days later. “These findings suggest that increased ensemble activity contributes to the rapid effects of ketamine, while increased spine formation contributes to the sustained antidepressant actions of ketamine,” says neuroscientist Ronald Duman, of the Yale School of Medicine, who was not involved in the study. Although the molecular details of what happens in the first hours are not yet fully understood, it seems a restoration of coordinated circuit activity occurs first; this is then entrenched by neuroplasticity effects in synapses, which then maintain behavioral benefits over time.

To prove that new synapses were a cause of antidepressant effects, rather than just coinciding with the improved behaviors, the team used a newly developed optogenetic technique, which allowed them to eliminate newly formed spines using light. Optogenetics works by introducing viruses that genetically target cells, causing them to produce light-sensitive proteins. In this case, the protein is expressed in newly formed synapses, and exposure to blue light causes the synapse to collapse. The researchers found that eliminating newly formed synapses in ketamine-treated mice abolished some of the drug’s positive effects, two days after treatment, confirming that new synapses are needed to maintain benefits. “Many mechanisms are surely involved in determining why some people relapse and some don’t,” Liston says, ” but we think our work shows that one of those involves the durability of these new synapses that form.”

And Liston adds: “Our findings open up new avenues for research, suggesting that interventions aimed at enhancing the survival of these new synapses might be useful for extending ketamine’s antidepressant effects.” The implication is that targeting newly formed spines might be useful for maintaining remission after ketamine treatment. “This is a great question and one the field has been considering,” Duman says. “This could include other drugs that target stabilization of spines, or behavioral therapies designed to engage the new synapses and circuits, thereby strengthening them.”

The study used three behavioral tests: one involving exploration, a second a struggle to escape, and a third an assessment of how keen the mice are on a sugar solution. This last test is designed to measure anhedonia—a symptom of depression in which the ability to experience pleasure is lost. This test was unaffected by deleting newly formed spines, suggesting that the formation of new synapses in the mPFC is important for some symptoms, such as apathy, but not others (anhedonia)—and that different aspects of depression involve a variety of brain circuits.

These results could relate to a study published last year that found activity in another brain region, the lateral habenula, is crucially involved in anhedonia, and injecting ketamine directly into this region improves anhedonia-related behavior in mice. “We’re slowly identifying specific regions associated with specific behaviors,” Beyeler says. “The factors leading to depression might be different depending on the individual, so these different models might provide information regarding the causes of depression.”

One caveat is that the study looked at only a single dose, rather than the multiple doses involved in a course of human treatment, Zarate says. After weeks of repeated treatments, might the spines remain, despite a relapse, or might they dwindle, despite the mice still doing well? “Ongoing effects with repeated administration, we don’t know,” Zarate says. “Some of that work will start taking off now, and we’ll learn a lot more.” Of course, the main caution is that stressed mice are quite far from humans with depression. “There’s no real way to measure synaptic plasticity in people, so it’s going to be hard to confirm these findings in humans,” Beyeler says.

https://www.scientificamerican.com/article/behind-the-buzz-how-ketamine-changes-the-depressed-patients-brain/

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.