Posts tagged depression
Articles and news from the latest research reports.
Personal reflection triggers increased brain activity during depressive episodes
Research by the University of Liverpool has found that people experiencing depressive episodes display increased brain activity when they think about themselves.
Using functional magnetic resonance imaging (fMRI) brain imaging technologies, scientists found that people experiencing a depressive episode process information about themselves in the brain differently to people who are not depressed.
British Queen
Researchers scanned the brains of people in major depressive episodes and those that weren’t whilst they chose positive, negative and neutral adjectives to describe either themselves or the British Queen - a figure significantly removed from their daily lives but one that all participants were familiar with.
Professor Peter Kinderman, Head of the University’s Institute of Psychology, Health and Society, said: “We found that participants who were experiencing depressed mood chose significantly fewer positive words and more negative and neutral words to describe themselves, in comparison to participants who were not depressed.
“That’s not too surprising, but the brain scans also revealed significantly greater blood oxygen levels in the medial superior frontal cortex – the area associated with processing self-related information – when the depressed participants were making judgments about themselves.
“This research leads the way for further studies into the psychological and neural processes that accompany depressed mood. Understanding more about how people evaluate themselves when they are depressed, and how neural processes are involved could lead to improved understanding and care.”
Dr May Sarsam, from the Mersey Care NHS Trust, said: “This study explored the difference in medical and psychological theories of depression. It showed that brain activity only differed when depressed people thought about themselves, not when they thought about the Queen or when they made other types of judgements, which fits very well with the current psychological theory.
Equally important
“Thought and neurochemistry should be considered as equally important in our understanding of mental health difficulties such as depression.”
Depression is associated with extensive negative feelings and thoughts. Nearly one-fifth of adults experience anxiety or depression, with the conditions affecting a higher proportion of women than men.
The research, in collaboration with the Mersey Care NHS Trust and the Universities of Manchester, Edinburgh and Lancaster, is published in PLOS One.
Depression twice as likely in migraine sufferers
The prevalence of depression among those with migraine is approximately twice as high as for those without the disease (men: 8.4% vs. 3.4%; women 12.4% vs. 5.7%), according to a new study published by University of Toronto researchers.
In a paper published online this week in the journal Depression Research and Treatment, investigators reported that younger migraine sufferers were particularly at risk for depression. Women with migraines who were younger than 30 had six times the odds of depression in comparison to sufferers who were aged 65 and over, said lead author, Professor Esme Fuller-Thomson, Sandra Rotman Endowed Chair at the University of Toronto’s Factor-Inwentash Faculty of Social Work. Unmarried individuals and migraine sufferers who had difficulties with daily activities also had high odds of depression.
Data drawn from a representative sample of more than 67,000 Canadians, the 2005 Canadian Community Health Survey, were used to examine gender-specific associations between migraine and depression. More than 6,000 respondents reported that they had been diagnosed by a health professional with migraines. Consistent with prior research, the prevalence of migraines was much higher in women than men, with one in every seven women, compared to one in every 16 men, reporting that they had migraines.
The study also investigated the relationship between migraine and suicidal ideation. For both men and women, those with migraines were much more likely to have “ever seriously considered suicide or taking (their) own life” than were those without migraines (men: 15.6% versus 7.9%; women: 17.6% versus 9.1%). Migraineurs under age 30 had four times the odds of lifetime suicidal ideation in comparison to migraineurs aged 65 and over. Other factors associated with suicidal ideation among those with migraines included unmarried status, lower household income and greater activity limitations.
Co-author and former graduate student Meghan Schrumm commented “We are not sure why younger migraineurs have such a high likelihood of depression and suicidal ideation. It may be that younger people with migraines have not yet managed to find adequate treatment or develop coping mechanisms to minimize pain and the impact of this chronic illness on the rest of their lives. The much lower prevalence of depression and suicidal ideation among older migraineurs suggests a promising area for future research.”
Dr. Fuller-Thomson adds that this study “draws further attention to the need for routine screening and targeted interventions for depression and suicidality, particularly among the most vulnerable migraineurs: Individuals who are young, unmarried and those with activity limitations.”
(Image: Shutterstock)
Schizophrenia linked to abnormal brain waves
Neuroscientists discover neurological hyperactivity that produces disordered thinking
Schizophrenia patients usually suffer from a breakdown of organized thought, often accompanied by delusions or hallucinations. For the first time, MIT neuroscientists have observed the neural activity that appears to produce this disordered thinking.
The researchers found that mice lacking the brain protein calcineurin have hyperactive brain-wave oscillations in the hippocampus while resting, and are unable to mentally replay a route they have just run, as normal mice do.
Mutations in the gene for calcineurin have previously been found in some schizophrenia patients. Ten years ago, MIT researchers led by Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, created mice lacking the gene for calcineurin in the forebrain; these mice displayed several behavioral symptoms of schizophrenia, including impaired short-term memory, attention deficits, and abnormal social behavior.
In the new study, which appears in the Oct. 16 issue of the journal Neuron, Tonegawa and colleagues at the RIKEN-MIT Center for Neural Circuit Genetics at MIT’s Picower Institute for Learning and Memory recorded the electrical activity of individual neurons in the hippocampus of these knockout mice as they ran along a track.
Previous studies have shown that in normal mice, “place cells” in the hippocampus, which are linked to specific locations along the track, fire in sequence when the mice take breaks from running the course. This mental replay also occurs when the mice are sleeping. These replays occur in association with very high frequency brain-wave oscillations known as ripple events.
In mice lacking calcineurin, the researchers found that brain activity was normal as the mice ran the course, but when they paused, their ripple events were much stronger and more frequent. Furthermore, the firing of the place cells was abnormally augmented and in no particular order, indicating that the mice were not replaying the route they had just run.
This pattern helps to explain some of the symptoms seen in schizophrenia, the researchers say.
“We think that in this mouse model, we may have some kind of indication that there’s a disorganized thinking process going on,” says Junghyup Suh, a research scientist at the Picower Institute and one of the paper’s lead authors. “During ripple events in normal mice we know there is a sequential replay event. This mutant mouse doesn’t seem to have that kind of replay of a previous experience.”
The paper’s other lead author is David Foster, a former MIT postdoc. Other authors are Heydar Davoudi and Matthew Wilson, the Sherman Fairchild Professor of Neuroscience at MIT and a member of the Picower Institute.
The researchers speculate that in normal mice, the role of calcineurin is to suppress the connections between neurons, known as synapses, in the hippocampus. In mice without calcineurin, a phenomenon known as long-term potentiation (LTP) becomes more prevalent, making synapses stronger. Also, the opposite effect, known as long-term depression (LTD), is suppressed.
“It looks like this abnormally high LTP has an impact on activity of these cells specifically during resting periods, or post exploration periods. That’s a very interesting specificity,” Tonegawa says. “We don’t know why it’s so specific.”
The researchers believe the abnormal hyperactivity they found in the hippocampus may represent a disruption of the brain’s “default mode network” — a communication network that connects the hippocampus, prefrontal cortex (where most thought and planning occurs), and other parts of the cortex.
This network is more active when a person (or mouse) is resting between goal-oriented tasks. When the brain is focusing on a specific goal or activity, the default mode network gets turned down. However, this network is hyperactive in schizophrenic patients before and during tasks that require the brain to focus, and patients do not perform well in these tasks.
Further studies of these mice could help reveal more about the role of the default mode network in schizophrenia, Tonegawa says.
To pinpoint why depression messes with memory, researchers took a page from Sesame Street’s book.
The show’s popular game “One of these things is not like the others” helps young viewers learn to differentiate things that are similar – a process known as “pattern separation.”
A new Brigham Young University study concludes that this same skill fades in adults in proportion to the severity of their symptoms of depression. The more depressed someone feels, the harder it is for them to distinguish similar experiences they’ve had.
If you’ve ever forgotten where you parked the car, you know the feeling (though it doesn’t mean you have depression).
“That’s really the novel aspect of this study – that we are looking at a very specific aspect of memory,” said Brock Kirwan, a psychology and neuroscience professor at BYU.
Depression has been generally linked to poor memory for a long time. To find out why, Kirwan and his former grad student D.J. Shelton put people through a computer-aided memory test. The participants viewed a series of objects on the screen. For each one, they responded whether they had seen the object before on the test (old), seen something like it (similar), or not seen anything like it (new).
With old and new items, participants with depression did just fine. They often got it wrong, however, when looking at objects that were similar to something they had seen previously. The most common incorrect answer was that they had seen the object before.
“They don’t have amnesia,” Kirwan said. “They are just missing the details.”
This can be a challenge in a number of everyday situations, such as trying to remember which friends and family members you’ve told about something personal – and which ones are still in the dark.
The findings also give an important clue about what is happening in the brain that might explain this.
“There are two areas in your brain where you grow new brain cells,” Kirwan said. “One is the hippocampus, which is involved in memory. It turns out that this growth is decreased in cases of depression.”
Because of this study, we know a little more about what these new brain cells are for: helping us see and remember new experiences. The study appears in the journal Behavioral Brain Research.
Experiments with neutrons at the Technische Universität München (TUM) show that the antidepressant lithium accumulates more strongly in white matter of the brain than in grey matter. This leads to the conclusion that it works differently from synthetic psychotropic drugs. The tissue samples were examined at the Research Neutron Source Heinz Maier-Leibnitz (FRM II) with the aim of developing a better understanding of the effects this substance has on the human psyche.
At present lithium is most popular for its use in rechargeable batteries. But for decades now, lithium has also been used to treat various psychological diseases such as depressions, manias and bipolar disorders. But, the exact biological mode of action in certain brain regions has hardly been understood. It is well known that lithium lightens moods and reduces aggression potential.
Because it is so hard to dose, doctors have been reluctant to prescribe this “universal drug”. Nonetheless, a number of international studies have shown that a higher natural lithium content in drinking water leads to a lower suicide rate in the general population. Lithium accumulates in the brains of untreated people, too. This means that lithium, which has so far been regarded as unimportant, could be an essential trace element for humans.
Lithium detection with neutrons
This is what Josef Lichtinger is studying in his doctoral thesis at the Chair for Hadron and Nuclear Physics (E12) at the Technische Universität München. From the Institute for Forensic Medicine at the Ludwig-Maximilians-Universität Munich (LMU) he received tissue samples taken from patients treated with lithium, untreated patients and healthy test persons. The physicist exposed these to a focused cold neutron beam of greatest intensity at the measuring station for prompt gamma activation analysis at FRM II.
Lithium reacts with neutrons in a very specific manner and decays to a helium and a tritium atom. Using a special detector developed by Josef Lichtinger, traces as low as 0.45 nanograms of lithium per gram of tissue can be measured. “It is impossible to make measurements as precise as those using the neutrons with any other method,” says Jutta Schöpfer, forensic scientist at the LMU in charge of several research projects on lithium distribution in the human body.
Lithium concentrates at the nerve-tracts
Lichtinger’s results are surprising: Only in the samples of a depressive patient treated with lithium did he observe a higher accumulation of lithium in the so-called white matter. This is the area in the brain where nerve tracts run. The lithium content in the neighboring grey matter was 3 to 4 times lower. Lithium accumulation in white matter was not observed in a number of untreated depressive patients. This points to the fact that lithium does not work in the space between nerve cells, like other psychotropic drugs, but within the nerve tracts themselves.
In a next step Josef Lichtinger plans to examine further tissue samples at TUM’s Research Neutron Source in order to confirm and expand his results. The goal is a space-resolved map showing lithium accumulation in the brain of a healthy and a depressive patient. This would allow the universal drug lithium to be prescribed for psychological disorders with greater precision and control. The project is funded by the German Research Foundation (DFG).
Publication:
J. Lichtinger et. al, „Position sensitive measurement of lithium traces in brain tissue with neutrons“, Med. Phys. 40, 023501 (2013)
New Study Shows How ICU Ventilation May Trigger Mental Decline
Researchers from Penn Medicine and University of Oviedo Identify Molecular Pathway Linking ICU Ventilation to Brain Damage
At least 30 percent of patients in intensive care units (ICUs) suffer some form of mental dysfunction as reflected in anxiety, depression, and especially delirium. In mechanically-ventilated ICU patients, the incidence of delirium is particularly high, about 80 percent, and may be due in part to damage in the hippocampus, though how ventilation is increasing the risk of damage and mental impairment has remained elusive.
Now, a new study published in the American Journal of Respiratory and Critical Care Medicine fromresearchers at the University of Oviedo in Spain, St. Michael’s Hospital in Toronto, Canada, and the Perelman School of Medicine at the University Pennsylvaniafound a molecular mechanism that may explain the connection between mechanical ventilation and hippocampal damage in ICU patients.
The investigators, including Adrian González-López, PhD, in the laboratory of Guillermo M. Albaiceta, MD, PhD at the University of Oviedo , and co-authored by Konrad Talbot, PhD, an assistant research professor in Neurobiology in the Department of Psychiatry at Penn Medicine, began by studying the hippocampus in control mice and in mice on low or high-pressure mechanical ventilation for 90 minutes. Compared to the controls, those on either low- or high-pressure ventilation showed evidence of neuronal cell death in the hippocampus, as a result of a cell suicide program called apoptosis.
Searching for the molecular cause of the ventilation-induced apoptosis, the team discovered that a well-known apoptosis trigger had been set off in the hippocampus of the ventilated animals. That trigger is dopamine-induced suppression of a molecule known as Akt, which normally acts to prevent neuronal apoptosis. Akt suppression was clearly evident in the hippocampus of the ventilated mice and was associated with a hyperdopaminergic state (increased levels of dopamine) in that brain area. The ventilated mice had elevated gene expression of the enzyme tyrosine hydroxylase, which is critical in synthesizing dopamine. The resulting rise in dopamine increases the strength of dopamine receptor activation in the hippocampus.
The investigators hypothesized that ventilation-induced apoptosis in the hippocampus was at least partly mediated by elevated activation of dopamine receptors in that brain area. This was confirmed by showing that pretreatment of mice with type 2 (D2) dopamine receptor blockers injected into the ventricles of the brain significantly reduced ventilation-induced apoptosis in the hippocampus.
How mechanical ventilation manages to affect the hippocampus was answered by experiments on mice in which the vagus cranial nerve connecting the lungs with the brain was severed. In these mice, mechanical ventilation had virtually no effect on levels of the dopamine-synthesizing enzyme or on apoptosis in the hippocampus.
The investigators then studied the consequences of ventilation and elevated hippocampal dopamine on dysbindin-1, a protein known to affect levels of cell surface D2 dopamine receptors, cognition, and possibly the risk of psychosis. High-pressure ventilation in mice caused an increase in gene expression of dysbindin-1C, and later, in protein levels of dysbindin-1C. Dopamine alone had similar effects on dysbindin-1C in hippocampal slice preparations, effects that were inhibited by D2 receptor blockers.
Since dysbindin-1 can lower cell-surface D2 receptors and protect against apoptosis, the authors speculate that increased dysbindin-1C expression in the ventilated mice may reflect compensatory responses to ventilation-induced hippocampal apoptosis. That possibility applies to ICU cases given the additional finding by the authors that total dysbindin-1 was increased in hippocampal neurons of ventilated compared to non-ventilated humans who died in the ICU.
The findings could lead to new therapeutic uses of established drugs and targets for new drugs that activate a molecular pathway mediating adverse effects of ICU ventilation on brain function.
“The results prove the existence of a pathogenic mechanism of lung stretch-induced hippocampal apoptosis that could explain the development of neurobehavioral disorders in patients exposed to mechanical ventilation,” the authors write. One of the coauthors, Dr. Talbot, adds: “The study indicates the need to reevaluate use of D2 receptor antagonists in minimizing the negative cognitive effects of mechanical ventilation in ICU patients and to evaluate the novel possibility that elevation in dysbindin-1C expression can also reduce those effects.”
The corresponding author, Dr. Albaiceta, offered a look at future research on this topic: “Now that we have established the mouse model, we are mainly looking for therapeutic approaches aimed at avoiding the vagal activation caused by mechanical ventilation and therefore prevent the deleterious effects observed in the hippocampus,” he said. “We are also interested in studying the relationship between the different described gene polymorphisms of dysbindin, Akt, and type 2 dopamine receptor versus the incidence of neurological disorders in patients on ventilation in ICUs. This could help us to identify susceptible individuals to in which a preventive treatment could be effective.”
(Source: uphs.upenn.edu)
A shot of anxiety and the world stinks
In evolutionary terms, smell is among the oldest of the senses. In animals ranging from invertebrates to humans, olfaction exerts a primal influence as the brain continuously and subconsciously processes the steady stream of scent molecules that waft under our noses.
And while odors — whether the aroma of stinky socks or the sweet smell of baking bread — are known to stir the emotions, how they exert their influence biologically on the emotional centers of the human brain, evoking passion or disgust, has been a black box.
Now, however, researchers using powerful new brain imaging technologies are peeling back some of the mystery, revealing how anxiety or stress can rewire the brain, linking centers of emotion and olfactory processing, to make typically benign smells malodorous.
Writing today (Sept. 24, 2013) in the Journal of Neuroscience, a team led by Wen Li, a professor of psychology at the UW-Madison Waisman Center, reports that the brains of human subjects experience anxiety induced by disturbing pictures and text of things like car crashes and war transform neutral odors to distasteful ones, fueling a feedback loop that could heighten distress and lead to clinical issues like anxiety and depression.
The finding is important because it may help scientists understand the dynamic nature of smell perception and the biology of anxiety as the brain rewires itself under stressful circumstances and reinforces negative sensations and feelings.
"After anxiety induction, neutral smells become clearly negative," explains Li, who conducted the study with UW-Madison colleagues Elizabeth Krusemark and Lucas Novak, and Darren Gitelman of Northwestern University’s Feinberg School of Medicine. "People experiencing an increase in anxiety show a decrease in the perceived pleasantness of odors. It becomes more negative as anxiety increases."
Using behavioral techniques and functional magnetic resonance imaging (fMRI), Li’s group looked at the brains of a dozen human subjects with induced anxiety as they processed known neutral odors.
Functional MRI is a technology that enables clinicians and researchers to observe the working brain in action. Before entering the MRI where screens cycle through a series of disturbing pictures and text, subjects were exposed to and rated a panel of neutral smells.
In the course of the experiment, the Wisconsin team observed that two distinct and typically independent circuits of the brain — one dedicated to olfactory processing, the other to emotion — become intimately intertwined under conditions of anxiety. Subsequent to anxiety induction and the imaging process, subjects were asked again to rate the panel of neutral smells, most assigning negative responses to smells they previously rated as neutral.
"In typical odor processing, it is usually just the olfactory system that gets activated," says Li. "But when a person becomes anxious, the emotional system becomes part of the olfactory processing stream."
Although those two systems of the brain are right next to each other, under normal circumstances there is limited crosstalk between the two. However, under conditions of induced anxiety, the Wisconsin team observed the emergence of a unified network cutting across the two systems.
The results may have clinical implications in the sense that it begins to uncover the biological mechanisms at play during periods of anxiety. “We encounter anxiety and as a result we experience the world more negatively. The environment smells bad in the context of anxiety. It can become a vicious cycle, making one more susceptible to a clinical state of anxiety as the effects accumulate. It can potentially lead to a higher level of emotional disturbances with rising ambient sensory stress.”
Electro-shock therapy sees a resurgence
The procedure is widely accepted by the medical community, although it lingers in the public imagination as a crude medical holdover.
The patients are rolled on gurneys into a small screened-off area at Park Royal Hospital every 15 minutes with assembly line regularity.
One is a woman in her 60s, who, like the others, gets a momentary jolt of electricity sent through her head, causing a brain seizure and her body to tense for several seconds. The hope: That this treatment — the electroconvulsive, or “electro-shock,” therapy — will ease the symptoms of her bipolar disorder that has so far not responded well to drugs.
The procedure, one of thousands performed at Park Royal since the 76-bed hospital opened last year, has worked on the woman in the past, says Dr. Ivan Mazzorana, who performs all of them on patients here. And, he said, it’s likely to do so again.
These days, the treatment goes by its more clinical-sounding acronym, “ECT.”
"When you bring it up, most people say, ‘Oh my God! Not ECT, that’s something from the past,’" Mazzorana said. "It’s a very simple procedure, safer, and it’s a lot quicker than the medication."
Electroconvulsive therapy today is a procedure widely accepted by the medical community and one, absent a rare court order, that is done with patient consent. But it is also a treatment that lingers in the public imagination as a crude medical holdover almost as dated as bloodletting. Many outside of psychiatry are surprised to learn that the procedure still exists at all.
Despite that, ECT has seen a resurgence at many health centers in recent decades, experts say.
Park Royal, the only inpatient psychiatric hospital in Lee County, Fla., has already treated nearly 200 people with ECT, most receiving multiple treatments. The number represents roughly 10 percent of all of Park Royal’s admissions since it opened in early 2012.
The hospital is a for-profit facility owned by the Tennessee-based Acadia Healthcare Co.
Most of those who have received ECT at Park Royal — patient ages have ranged from 18 years to those in their 90s — suffer from severe depression or bi-polar disorders. About 90 percent are inpatients. Others are referred from other parts of Florida, according to the hospital. A few are snowbirds who come in for ETC “maintenance” treatments.
The Mayo Clinic calls the treatment, which has a reported success rate of 70 percent to 80 percent, the “gold standard” treatment for severe depression. The most common side effect, according to proponents, is temporary short-term memory loss.
"I was afraid, to be honest with you," said Ron Spesia, a 71-year-old Fort Myers Beach retiree who suffered a deep, multiyear depression that did not respond to medication. He had 12 treatments and said he started feeling better after the third. "Then one day I decided, ‘Hey, you know what? It’s time to put the big boy pants on and pursue this.’ Smartest move I ever made."
Still, ECT has its critics. Some, including patients of decades past and anti-ECT groups, say it is little more than intentional brain damage. This, despite the psychiatric community’s endorsement of it and positive testimonials from many of the estimated 100,000 Americans who get the treatment each year.
A Fort Myers News-Press reporter was recently allowed to witness about a half dozen such procedures at Park Royal.
But even hospital administrators remain sensitive to the ECT stigma. Though a patient agreed to be photographed during one such procedure, and to have it recorded on video, the hospital overruled that consent.
The hospital also prohibited patient interviews inside the building, though other medical facilities routinely allow such interactions if patients are willing. David Edson, Park Royal’s director of business development, cited concerns about privacy and “the very delicate nature of the ECT treatment.”
Despite that, Mazzorana said he wants to demystify the treatment and those who get it.
"It seems like an extreme, dramatic treatment," Mazzorana said. "It’s a matter of really educating the psychiatric community, so then we can educate patients."
Mundane process
The treatments at Park Royal begin at 7 a.m. Mondays, Wednesdays and Fridays, and continue throughout the mornings. Staff usually see up to 10 ECT patients on these days.
The process bears little resemblance to its horrific depictions in popular culture. At Park Royal, it starts when patients come to a medical preparation area adjacent to the ECT treatment room, where staff hook them up to IVs — they will eventually get medication to paralyze their muscles during the treatment — as well as heart and brain monitors attached to their skin.
After a quick chat with medical staff, who assess their conditions, patients bite down on foam “bite blocks” before they are put fully under.
Flashlight-shaped paddles coated with a blue conductive gel are placed on each temple (bilateral treatment) or one goes on the right temple and one on the top of the head (unilateral treatment), depending on the type of ECT the patients need. Bilateral ECT is recommended in more severe cases of mental illness and may produce more memory loss, experts say.
Following a quick buzzing sound, patients’ bodies tense for about five seconds. Patients typically wake a minute or so after the procedure and are sent off to a recovery area until the anesthesia fully wears off. They remember nothing of the treatment itself.
New patients must typically stay in the hospital for the first half of the standard dozen ECT treatments.
Spesia, the former ECT patient, said the IV injection was the most painful part of the process. The most unpleasant, he said was the hospital stay. Now, months after the process, he said the only lingering side effect has been some short-term memory loss.
"All I can remember is them giving me the rubber bite block and then them putting the (anesthesia) mask on and telling me to breathe deeply." he said. "Absolutely painless."
Nancy Kish, a 74-year-old Fort Myers resident who has received dozens of treatments over the years, said her memory of treatments from years past is fuzzy but her mind is otherwise as sharp as it has ever been. She said the treatment is a better alternative to the high doses of medication she otherwise took, drugs that largely left her bed-ridden.
"I feel pretty good," said Kish. "I get upset easy, and I get anxiety attacks. But other than that, I’m better than what I was."
Much like the therapeutic mystery behind anti-depressant medication experts are not exactly sure why ECT works for some patients.
Mazzorana said two theories dominate: One says that electroconvulsive therapy enhances certain beneficial brain chemicals that are lacking in different parts of the brain. Another states that it causes the release of hormones that have a beneficial effect on mood and promote the growth of healthy brain cells, he said. Other recent research suggests that ECT works by reducing “hyper-connectivity” in the minds of severely depressed patients.
Endorsements
Whatever the exact mechanism, ECT’s endorsements include the American Psychiatric Association, the American Medical Association, and the U.S. Surgeon General.
"When you raise ECT, people’s eyes always roll up in their heads and their family says, ‘Oh my God, you’re a monster!’" said Fort Myers psychiatrist Steve Machlin, who performed the procedure more than a decade ago. "There’s always going to be people on the outside who say it’s not proven but, if you’ve looked at the science, it’s been proven to be effective."
Another Southwest Florida psychiatrist and researcher, Fred Schaerf, said opposition to the treatment is largely anti-psychiatry bias and from the treatment’s early days, when it was performed without anesthesia.
"I think there is a misconception about the treatment — that it’s barbaric, cruel," Schaerf said. "It has to do with that stigma and people’s belief system with psychiatry."
Most insurance, including Medicare, covers the treatment.
Edson, the Park Royal Hospital business development director, said the health center generally charge insurers $500 a treatment, though that does not include the costs of the anesthesiologist and hospital stay. Mazzorana said the total cost is about $1,000.
Opposition
Medical and patient endorsements aside, some patient groups believe it does little more than cause brain damage. A quick Internet search turns up a long list of anti-ECT websites, many of which include testimonials from people claiming to have suffered negative effects from the treatments.
Among the most vocal opponents is the Philadelphia-based National Mental Health Consumers’ Self Help Clearinghouse, which urged the U.S. Food and Drug Administration in 2011 not to reduce federal oversight of ECT devices. It also sharply criticized the Surgeon General’s endorsement of ECT in 1999.
The group points to published studies suggesting that ECT leads to memory loss and may be far more dangerous for the elderly than medication alone. Susan Rogers, the organization’s director, said patients aren’t warned enough about the risks.
"People are not given the opportunity for truly informed consent," said Rogers, who has not had the procedure herself. "People are not advised of the enormous risks as well as the benefits. They’re given a whitewashed version of the facts. They’re not told it might cause permanent cognitive impairment, and I think that’s wrong."
She said she is not opposed to the treatment itself.
"Apparently about 100,000 people a year receive ECT in the United States and, I’m sure for many of those people, they’re satisfied with those results," she said. "There are also many people who feel that ECT has destroyed their lives."
The psychiatric community commonly uses the one in 10,000 patients mortality figure (or one per 80,000 treatments), figures anti-ECT groups say dramatically under-estimate the risk, particularly among older patients. A 1995 USA TODAY investigation found that it may have been as high as one in 200 among elderly patients, based on some state reports at the time and some earlier studies.
A recent Department of Veterans Affairs review of ECT between 1999 and 2010 found no ECT deaths at VA hospitals during that period. It placed the mortality risk at one per 14,000 patients, or one per 73,400 treatments.
Florida does not closely track ECT usage. But Texas, which does, reported that none of the 2,079 patients receiving ECT last year died during the procedure. Two died shortly after treatment in 2012, the state report noted, but neither case was related to the treatment.
Five years of reports show that roughly 2 percent of patients experience some level of memory loss shortly after treatment.
None of Park Royal’s ECT patients have died during the procedure, said Christina Brownwood, the hospital’s ECT coordinator. Nor have any needed emergency medical care immediately after a treatment, she said.
Shutting off Neurons Helps Bullied Mice Overcome Symptoms of Depression
Findings Point to New Potential Drug Target—GABA Neurons—to Treat Patients with Depression and Other Mood Disorders
A new drug target to treat depression and other mood disorders may lie in a group of GABA neurons (gamma-aminobutyric acid –the neurotransmitters which inhibit other cells) shown to contribute to symptoms like social withdrawal and increased anxiety, Penn Medicine researchers report in a new study in the Journal of Neuroscience.
Experts know that people suffering from depression and other mood disorders often react to rejection or bullying by withdrawing themselves socially more than the average person who takes it in strides, yet the biological processes behind these responses have remained unclear.
Now, a preclinical study, from the labs of Olivier Berton, PhD, an assistant professor in the department of Psychiatry, with Collin Challis of the Neuroscience Graduate Group, and Sheryl Beck, PhD, a professor in the department of Anesthesiology at Children’s Hospital of Philadelphia, found that bullying and other social stresses triggered symptoms of depression in mice by activating GABA neurons, in a never-before-seen direct relationship between social stimuli and this neural circuitry. Activation of those neurons, they found, directly inhibited levels of serotonin, long known to play a vital role in behavioral responses—without it, a depressed person is more likely to socially withdrawal.
Conversely, when the researchers successfully put the brake on the GABA neurons, mice became more resilient to bullying and didn’t avoid once -perceived threats.
“This is the first time that GABA neuron activity—found deep in the brainstem—has been shown to play a key role in the cognitive processes associated with social approach or avoidance behavior in mammals,” said Dr. Berton. “The results help us to understand why current antidepressants may not work for everyone and how to make them work better—by targeting GABA neurons that put the brake on serotonin cells.”
Less serotonin elicits socially defensive responses such as avoidance or submission, where enhancement—the main goal of antidepressants—induces a positive shift in the perception of socio-affective stimuli, promoting affiliation and dominance. However, current antidepressants targeting serotonin, like SSRIs, are only effective in about 50 percent of patients.
These new findings point to GABA neurons as a new, neural drug target that could help treat the other patients who don’t respond to today’s treatment.
For the study, “avoidant” mice were exposed to brief bouts of aggression from trained “bully” mice. By comparing gene expression in the brains of resilient and avoidant mice, Berton and colleagues discovered that bullying in avoidant mice puts GABA neurons in a state where they become more excitable and the mice exhibit signs of social defeat. Resilient mice, however, had no change in neuron levels and behavior.
To better understand the link between GABA and the development of stress resilience, Berton, Beck, and colleagues also devised an approach to directly manipulate levels: Lifting GABA inhibition of serotonin neurons reduced social and anxiety symptoms in mice exposed to bullies and also fully prevented neurobiological changes due to stress.
“Our paper provides a novel cellular understanding of how social defensiveness and social withdrawal develop in mice and gives us a stepping stone to better understand the basis of similar social symptoms in humans,” said Berton. “This has important implications for the understanding and treatment of mood disorders.”
(Source: uphs.upenn.edu)
Depressed people have a more accurate perception of time
People with mild depression underestimate their talents. However, new research carried out researchers at the University of Limerick and the University of Hertfordshire shows that depressed people are more accurate when it comes to time estimation than their happier peers.
Depressed people often appear to distort the facts and view their lives more negatively than non-depressed people. Feelings of helplessness, hopelessness and worthlessness and of being out of control are some of the main symptoms of depression. For these people time seems to pass slowly and they will often use phrases such as “time seems to drag” to describe their experiences and their life. However, depressed people sometimes have a more accurate perception of reality than their happier friends and family who often look at life through rose-tinted glasses and hope for the best.
Dr Rachel Msetfi, senior lecturer in psychology, University of Limerick and one of the studies authors, said: “We found that depressed people tended to be more accurate when estimating time whereas non-depressed people tended to be less accurate. This finding, along with some of our other work, suggests that depression leads to more attention paid to time passing. Sometimes this might lead to a phenomenon known as ‘depressive realism’, though on other occasions time might seem to be moving more slowly than usual.”
In the study, volunteers, who were classified as mildly depressed or non-depressed, made estimates of the length of different time intervals of between two and sixty-five seconds. Overall, those volunteers who were mildly–depressed were more accurate in their time estimations.
Dr Msetfi noted that: “Time is a very important part of everyday experience, it flies when we are having fun or enjoying ourselves. One of the commonest experiences of depression is that people feel that time passes slowly and sometimes painfully. Our findings may help to shed a little light on how people with depression can be treated. People with depression are often encouraged to check themselves against reality, but maybe this timing skill can be harnessed to help in the treatment of mildly-depressed people. These findings may also link to successful mindfulness based treatments for depression which focus on encouraging present moment awareness.”
The paper, “Time perception and depressive realism: Judgement type, psychophysical functions and bias”, is published in PLOS ONE.
(Source: ul.ie)