Neuroscience

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Posts tagged depression

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Lack of nutrients and metabolic syndrome linked to different subtypes of depression
A low intake of folate and vitamin B12 increases the risk of melancholic depressive symptoms, according to a study among nearly 3,000 middle-aged and elderly Finnish subjects. On the other hand, non-melancholic depressive symptoms are associated with an increased risk for the metabolic syndrome. Based on these new observations, melancholic and non-melancholic depression may be separate depressive subtypes with different etiologies in terms of proinflammation and diet. The study was the first to look at these depressive sub-types separately.
"The findings have practical implications in the care of patients with depressive symptoms. For example, it may be wise to avoid medication causing weight gain among patients with non-melancholic depression, whereas melancholic depressive symptoms may call for a closer look at the quality of the patient’s diet," says Mr Jussi Seppälä, MD, Chief of the Department of Psychiatry of the Hospital District of Southern Savo.
Melancholic depression involves typical depressive symptoms, such as a depressed mood. Non-melancholic depression is characterized by other types of symptoms, such as low self-esteem and feelings of worry and anxiety.
Among subjects with the highest folate intake, the risk for melancholic depressive symptoms was almost 50 per cent lower than among those with the lowest intake. In addition, among those with the highest vitamin B12 levels, the risk for melancholic depressive symptoms was almost three times lower than among those with the lowest levels. Both findings are new. A similar association with non-melancholic depressive symptoms was not observed.
Another novel observation is that the risk for the metabolic syndrome was twofold among those with non-melancholic depressive symptoms, as compared to those with melancholic symptoms or those with no depressive symptoms.
Mr Seppälä’s doctoral thesis “Depressive symptoms, metabolic syndrome and diet" was published at the University of Eastern Finland. The study was conducted as part of the Finnish Type 2 Diabetes Prevention Programme. The findings were originally published in Journal of Affective Disorders.

Lack of nutrients and metabolic syndrome linked to different subtypes of depression

A low intake of folate and vitamin B12 increases the risk of melancholic depressive symptoms, according to a study among nearly 3,000 middle-aged and elderly Finnish subjects. On the other hand, non-melancholic depressive symptoms are associated with an increased risk for the metabolic syndrome. Based on these new observations, melancholic and non-melancholic depression may be separate depressive subtypes with different etiologies in terms of proinflammation and diet. The study was the first to look at these depressive sub-types separately.

"The findings have practical implications in the care of patients with depressive symptoms. For example, it may be wise to avoid medication causing weight gain among patients with non-melancholic depression, whereas melancholic depressive symptoms may call for a closer look at the quality of the patient’s diet," says Mr Jussi Seppälä, MD, Chief of the Department of Psychiatry of the Hospital District of Southern Savo.

Melancholic depression involves typical depressive symptoms, such as a depressed mood. Non-melancholic depression is characterized by other types of symptoms, such as low self-esteem and feelings of worry and anxiety.

Among subjects with the highest folate intake, the risk for melancholic depressive symptoms was almost 50 per cent lower than among those with the lowest intake. In addition, among those with the highest vitamin B12 levels, the risk for melancholic depressive symptoms was almost three times lower than among those with the lowest levels. Both findings are new. A similar association with non-melancholic depressive symptoms was not observed.

Another novel observation is that the risk for the metabolic syndrome was twofold among those with non-melancholic depressive symptoms, as compared to those with melancholic symptoms or those with no depressive symptoms.

Mr Seppälä’s doctoral thesis “Depressive symptoms, metabolic syndrome and diet" was published at the University of Eastern Finland. The study was conducted as part of the Finnish Type 2 Diabetes Prevention Programme. The findings were originally published in Journal of Affective Disorders.

Filed under depression metabolic syndrome non-melancholic depression nutrition neuroscience science

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Researchers find decline in availability and use of key treatment for depression
Electroconvulsive therapy (ECT) is considered the most effective treatment option for patients with severe depression who cannot find symptom relief through antidepressant medications or psychotherapy. In a new study, researchers at Butler Hospital and Bradley Hospital in Rhode Island found a sharp decline in the availability and use of ECT in general hospitals across the U.S. The findings were published online in the journal Biological Psychiatry on October 10, 2012.
The researchers analyzed data from a nationally representative survey of US general hospitals, the Nationwide Inpatient Sample (NIS), conducted annually by the Agency for Healthcare Research and Quality (AHRQ). They took information from between five and eight million patient discharge records at 1,000 hospitals nationwide between the years 1993 through 2009 and found that the annual number of hospital stays in which ECT was administered fell 43 percent over the 17 year period, from more than 1.2 million to 720,000. Researchers also found a dramatic decline in the percentage of hospitals conducting ECT, from 55 percent to 35 percent of facilities with a psychiatric unit. The percentage of inpatients with severe, recurrent major depression treated in hospitals conducting ECT fell from 71 to 45 percent. But for depressed patients treated in hospitals that conduct ECT, the proportion who received the procedure remained stable.
"The data strongly support the impression that psychiatric units in general hospitals are discontinuing use of ECT and that this is driving the decline in the number of severely depressed inpatients receiving the procedure," said Brady Case, MD, an assistant professor of psychiatry and human behavior at Brown University and director of the Health Services Research Program at Bradley Hospital. "Growing pressures to avoid the inpatient treatment costs and length of stay associated with ECT may be one factor associated with this trend. We didn’t have information on provider and patient attitudes, but as facilities cease conducting ECT, we can expect that fewer clinicians and inpatients are exposed to the option, reinforcing the turn away from ECT." Researchers also note the FDA approval of new treatment alternatives, like vagus nerve stimulation and transcranial magnetic stimulation, as possible influences.

Researchers find decline in availability and use of key treatment for depression

Electroconvulsive therapy (ECT) is considered the most effective treatment option for patients with severe depression who cannot find symptom relief through antidepressant medications or psychotherapy. In a new study, researchers at Butler Hospital and Bradley Hospital in Rhode Island found a sharp decline in the availability and use of ECT in general hospitals across the U.S. The findings were published online in the journal Biological Psychiatry on October 10, 2012.

The researchers analyzed data from a nationally representative survey of US general hospitals, the Nationwide Inpatient Sample (NIS), conducted annually by the Agency for Healthcare Research and Quality (AHRQ). They took information from between five and eight million patient discharge records at 1,000 hospitals nationwide between the years 1993 through 2009 and found that the annual number of hospital stays in which ECT was administered fell 43 percent over the 17 year period, from more than 1.2 million to 720,000. Researchers also found a dramatic decline in the percentage of hospitals conducting ECT, from 55 percent to 35 percent of facilities with a psychiatric unit. The percentage of inpatients with severe, recurrent major depression treated in hospitals conducting ECT fell from 71 to 45 percent. But for depressed patients treated in hospitals that conduct ECT, the proportion who received the procedure remained stable.

"The data strongly support the impression that psychiatric units in general hospitals are discontinuing use of ECT and that this is driving the decline in the number of severely depressed inpatients receiving the procedure," said Brady Case, MD, an assistant professor of psychiatry and human behavior at Brown University and director of the Health Services Research Program at Bradley Hospital. "Growing pressures to avoid the inpatient treatment costs and length of stay associated with ECT may be one factor associated with this trend. We didn’t have information on provider and patient attitudes, but as facilities cease conducting ECT, we can expect that fewer clinicians and inpatients are exposed to the option, reinforcing the turn away from ECT." Researchers also note the FDA approval of new treatment alternatives, like vagus nerve stimulation and transcranial magnetic stimulation, as possible influences.

Filed under brain depression electroconvulsive therapy ECT neuroscience psychology science

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“Obese but Happy Gene” Challenges the Common Perception of Link Between Depression and Obesity

Researchers at McMaster University have discovered new genetic evidence about why some people are happier than others.

McMaster scientists have uncovered evidence that the gene FTO – the major genetic contributor to obesity – is associated with an eight per cent reduction in the risk of depression. In other words, it’s not just an obesity gene but a “happy gene” as well.

The research appears in a study published in the journal Molecular Psychiatry. The paper was produced by senior author David Meyre, associate professor in clinical epidemiology and biostatistics at the Michael G. DeGroote School of Medicine and a Canada Research Chair in genetic epidemiology; first author Dr. Zena Samaan, assistant professor, Department of Psychiatry and Behavioural Neurosciences, and members of the Population Health Research Institute of McMaster University and Hamilton Health Sciences.

“The difference of eight per cent is modest and it won’t make a big difference in the day-to-day care of patients,” Meyre said. “But, we have discovered a novel molecular basis for depression.”

In the past, family studies on twins, and brothers and sisters, have shown a 40 per cent genetic component in depression. However, scientific studies attempting to associate genes with depression have been “surprisingly unsuccessful” and produced no convincing evidence so far, Samaan said.

The McMaster discovery challenges the common perception of a reciprocal link between depression and obesity: That obese people become depressed because of their appearance and social and economic discrimination; depressed individuals may lead less active lifestyles and change eating habits to cope with depression that causes them to become obese.

“We set out to follow a different path, starting from the hypothesis that both depression and obesity deal with brain activity. We hypothesized that obesity genes may be linked to depression,” Meyre said.

The McMaster researchers investigated the genetic and psychiatric status of patients enrolled in the EpiDREAM study led by the Population Health Research Institute, which analyzed 17,200 DNA samples from participants in 21 countries.

In these patients, they found the previously identified obesity predisposing genetic variant in FTO was associated with an eight per cent reduction in the risk of depression. They confirmed this finding by analyzing the genetic status of patients in three additional large international studies.

Meyre said the fact the obesity gene’s same protective trend on depression was found in four different studies supports their conclusion. It is the “first evidence” that an FTO obesity gene is associated with protection against major depression, independent of its effect on body mass index, he said.

This is an important discovery as depression is a common disease that affects up to one in five Canadians, said Samaan.

(Source: newswise.com)

Filed under depression obesity brain activity genetics neuroscience psychology science

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Optogenetics illuminates pathways of motivation through brain
Whether you are an apple tree or an antelope, survival depends on using your energy efficiently. In a difficult or dangerous situation, the key question is whether exerting effort — sending out roots in search of nutrients in a drought or running at top speed from a predator — will be worth the energy.
In a paper published online Nov. 18 in Nature, Karl Deisseroth, MD, PhD, a professor of bioengineering and of psychiatry and behavioral sciences at Stanford University, and postdoctoral scholar Melissa Warden, PhD, describe how they have isolated the neurons that carry these split-second decisions to act from the higher brain to the brain stem. In doing so, they have provided insight into the causes of severe brain disorders such as depression.
In organisms as complex as humans, the neural mechanisms that help answer the question, “Is it worth my effort?” can fail, leading to debilitating mental illnesses. Major depressive disorder, for instance, which affects nearly 20 percent of people at some point in life, is correlated with underperformance in the parts of the brain involved in motivation. But researchers have struggled to work out the exact cause and effect.
“It’s challenging because we do not have a fundamental understanding of the circuitry that controls this sort of behavioral pattern selection. We don’t understand what the brain is doing wrong when these behaviors become dysfunctional, or even what the brain is supposed to be doing when things are working right,” Deisseroth said. “This is the level of the mystery we face in this field.”
Clinicians refer to this slowing down of motivation in depressed patients as “psychomotor retardation.” According to Deisseroth, who is also a practicing psychiatrist, patients may experience this symptom mentally, finding it hard to envision the positive results of an action, or, he said, they may feel physically heavy, like their limbs just do not want to move.
“This is one of the most debilitating aspects of depression, and motivation to take action is something that we can model in animals. That’s the exciting opportunity for us as researchers,” said Deisseroth, who also holds the D.H. Chen Professorship.

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Optogenetics illuminates pathways of motivation through brain

Whether you are an apple tree or an antelope, survival depends on using your energy efficiently. In a difficult or dangerous situation, the key question is whether exerting effort — sending out roots in search of nutrients in a drought or running at top speed from a predator — will be worth the energy.

In a paper published online Nov. 18 in Nature, Karl Deisseroth, MD, PhD, a professor of bioengineering and of psychiatry and behavioral sciences at Stanford University, and postdoctoral scholar Melissa Warden, PhD, describe how they have isolated the neurons that carry these split-second decisions to act from the higher brain to the brain stem. In doing so, they have provided insight into the causes of severe brain disorders such as depression.

In organisms as complex as humans, the neural mechanisms that help answer the question, “Is it worth my effort?” can fail, leading to debilitating mental illnesses. Major depressive disorder, for instance, which affects nearly 20 percent of people at some point in life, is correlated with underperformance in the parts of the brain involved in motivation. But researchers have struggled to work out the exact cause and effect.

“It’s challenging because we do not have a fundamental understanding of the circuitry that controls this sort of behavioral pattern selection. We don’t understand what the brain is doing wrong when these behaviors become dysfunctional, or even what the brain is supposed to be doing when things are working right,” Deisseroth said. “This is the level of the mystery we face in this field.”

Clinicians refer to this slowing down of motivation in depressed patients as “psychomotor retardation.” According to Deisseroth, who is also a practicing psychiatrist, patients may experience this symptom mentally, finding it hard to envision the positive results of an action, or, he said, they may feel physically heavy, like their limbs just do not want to move.

“This is one of the most debilitating aspects of depression, and motivation to take action is something that we can model in animals. That’s the exciting opportunity for us as researchers,” said Deisseroth, who also holds the D.H. Chen Professorship.

Read more

Filed under brain neuron neural mechanisms depression major depression neuroscience science

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Study links exposure to light at night to depression, learning issues
For most of history, humans rose with the sun and slept when it set. Enter Thomas Edison, and with a flick of a switch, night became day, enabling us to work, play, and post cat and kid photos on Facebook into the wee hours.
However, according to a new study led by a Johns Hopkins biologist, this typical 21st- century scenario comes at a serious cost: When people routinely burn the midnight oil, they risk suffering depression and learning issues, and not only because of lack of sleep. The culprit could also be exposure to bright light at night from lamps, computers, and even iPads.
"Basically, what we found is that chronic exposure to bright light—even the kind of light you experience in your own living room at home or in the workplace at night if you are a shift worker—elevates levels of a certain stress hormone in the body, which results in depression and lowers cognitive function,” said Samer Hattar, a biology professor in the Krieger School of Arts and Sciences.
The study, published in the Nov. 14 Advance Online Publication of the journal Nature, used mice to demonstrate how special cells in the eye (called intrinsically photosensitive retinal ganglion cells, or ipRGCs) are activated by bright light, affecting the brain’s center for mood, memory, and learning.

Study links exposure to light at night to depression, learning issues

For most of history, humans rose with the sun and slept when it set. Enter Thomas Edison, and with a flick of a switch, night became day, enabling us to work, play, and post cat and kid photos on Facebook into the wee hours.

However, according to a new study led by a Johns Hopkins biologist, this typical 21st- century scenario comes at a serious cost: When people routinely burn the midnight oil, they risk suffering depression and learning issues, and not only because of lack of sleep. The culprit could also be exposure to bright light at night from lamps, computers, and even iPads.

"Basically, what we found is that chronic exposure to bright light—even the kind of light you experience in your own living room at home or in the workplace at night if you are a shift worker—elevates levels of a certain stress hormone in the body, which results in depression and lowers cognitive function,” said Samer Hattar, a biology professor in the Krieger School of Arts and Sciences.

The study, published in the Nov. 14 Advance Online Publication of the journal Nature, used mice to demonstrate how special cells in the eye (called intrinsically photosensitive retinal ganglion cells, or ipRGCs) are activated by bright light, affecting the brain’s center for mood, memory, and learning.

Filed under depression learning difficulties light exposure ipRGCs neuroscience psychology science

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The Mysterious Motivational Functions of Mesolimbic Dopamine
Nucleus accumbens dopamine is known to play a role in motivational processes, and dysfunctions of mesolimbic dopamine may contribute to motivational symptoms of depression and other disorders, as well as features of substance abuse. Although it has become traditional to label dopamine neurons as “reward” neurons, this is an overgeneralization, and it is important to distinguish between aspects of motivation that are differentially affected by dopaminergic manipulations. For example, accumbens dopamine does not mediate primary food motivation or appetite, but is involved in appetitive and aversive motivational processes including behavioral activation, exertion of effort, approach behavior, sustained task engagement, Pavlovian processes, and instrumental learning. In this review, we discuss the complex roles of dopamine in behavioral functions related to motivation.

The Mysterious Motivational Functions of Mesolimbic Dopamine

Nucleus accumbens dopamine is known to play a role in motivational processes, and dysfunctions of mesolimbic dopamine may contribute to motivational symptoms of depression and other disorders, as well as features of substance abuse. Although it has become traditional to label dopamine neurons as “reward” neurons, this is an overgeneralization, and it is important to distinguish between aspects of motivation that are differentially affected by dopaminergic manipulations. For example, accumbens dopamine does not mediate primary food motivation or appetite, but is involved in appetitive and aversive motivational processes including behavioral activation, exertion of effort, approach behavior, sustained task engagement, Pavlovian processes, and instrumental learning. In this review, we discuss the complex roles of dopamine in behavioral functions related to motivation.

Filed under mesolimbic dopamine depression dopamine neuron motivation neuroscience science

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The Brain An Electric Cure for the Mind

Why does shock therapy beat back depression? New experiments show how such a blunt 
treatment can have such positive effects.

Ian Reid, a psychiatrist at the Royal Cornhill Hospital in the Scottish city of Aberdeen, has treated people with severe depression for 25 years. “It’s a very nasty illness, depression,” he says. “I have worked with people who have cancer and depression, and more than one of them has said, ‘If I had to choose one of those two diseases, I’d go for the cancer.’ ”

When patients come to Royal Cornhill with major depression, they’re first treated with psychotherapy and antidepressants. Only about 40 percent respond to their first medication. Sometimes a different one will do the trick, but in Reid’s experience, about 10 to 20 percent of depressed people respond to no drug at all. In those cases, Reid regularly shifts to a third option. It’s officially called electroconvulsive therapy, or ECT—better known by its unofficial name, shock therapy.

Reid is an expert on ECT, and over the years he has received plenty of grief for it. “There are people on the Internet who describe me as a Nazi, as a barbarian,” he says. “And there’s one person who suggested I should get ECT so I know what I’m doing.”

Reid is not surprised by the reactions. For many people, the sum of their knowledge about ECT comes from the 1975 movie One Flew Over the Cuckoo’s Nest. Jack Nicholson plays Randle McMurphy, a criminal hoping to escape hard labor by spending his term in a mental institution. But McMurphy gets more than he bargained for, including a harrowing session of ECT. The hospital staff straps him down, puts a piece of rubber in his mouth so he won’t bite off his own tongue, and delivers a blast of electricity to his temples. He writhes in agony and then slumps back, his body limp.

That scene bears no resemblance to what Reid does for his patients. For one thing, he gives them anesthesia and muscle relaxants so they don’t experience any flailing. But most crucially, ECT works. “You can watch someone going from being unresponsive and soiling themselves to being completely transformed,” Reid says.

In Scotland, a country of 5 million, 400 people receive the treatment each year. And for about 75 percent of them, it brings relief. “ECT outperforms psychotherapeutic treatments and antidepressant drugs,” Reid notes. Yet its effectiveness is a mystery. “It doesn’t sound intuitive at all,” he admits. “Making someone have a seizure, giving them an electric shock, and making something as complex as depression better just seems crazy.”

Read more …

Filed under brain depression electroconvulsive therapy shock therapy neuroscience psychology science

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Genes, depression and life satisfaction

Vulnerability to major depression is linked with how satisfied we are with our lives. This association is largely due to genes.

This is the main finding of a new twin study from the Norwegian Institute of Public Health in collaboration with the University of Oslo. The researchers compared longitudinal information from identical and fraternal twins to determine how vulnerability to major depression is associated with dispositional (overall) lifetime satisfaction.

Previous studies have systematically shown that life satisfaction is considerably stable over time. People who are satisfied at any one point in life are often also satisfied at other times in their lives. This stability—the dispositional life satisfaction—is often said to reflect an underlying positive mood or a positive disposition. Previous studies have also shown that people with such a positive disposition are less depressed, but very few studies have examined the mechanisms behind this relationship.

Results

• Both men and women who met the criteria for lifetime major depression (15.8% and 11.1% respectively) reported lower life satisfaction.

• 74% of the relationship between major depression and life satisfaction could be explained by genes.

• The remaining association (26%) could be explained by unique environmental factors.

• The researchers also calculated the heritability of dispositional life satisfaction and major depression separately. The heritability of dispositional life satisfaction, which has not previously been reported, was estimated to be 72%. In other words, it is largely genes that explain why we differ in our tendency to be satisfied and content with our lives.

• Major depression had a heritability of 34%, which is highly consistent with previous studies.

“The stable tendency to see the bright side of life is associated with lower risk of major depression because some genetic factors influence both conditions”, says researcher Ragnhild Bang Nes from the Division of Mental Health. Genes involved in satisfaction and positivity thus give protection against major depression. Nes is the main author of the study that was recently published in the Journal of Affective Disorders.

Susceptibility to both depression and overall life satisfaction is partly influenced by the same set of genes, but is also influenced by genes that are unique to each.

“The heritability figures mean that 72% of the individual differences in overall satisfaction, and 34% of the differences in depression, are caused by genes. These figures do not provide information on the importance of specific genes for an individual’s life satisfaction or risk of major depression. Traits and propensities like dispositional life satisfaction and vulnerability to major depression are not heritable in themselves. Heritability refers to the importance of genes for explaining the differences between people and the estimates may vary across time and place”, explains Nes.

Although the heritability of major depression was lower than that of life satisfaction, this does not necessarily mean that life satisfaction is far more heritable than depression. The researchers used questionnaire data from two time points to measure dispositional life satisfaction, and a single clinical interview to measure the prevalence of lifetime major depression. The use of only a single assessment to measure depression may partly explain why the heritability of depression is so much lower than life satisfaction.

Can we prevent depression by promoting life satisfaction?

“We found that depression and life satisfaction did not share as many environmental factors as genetic factors. This means that environmental factors of importance to life satisfaction (for example, activities and interventions that make you happy and content) only to a small extent protect against depression”, says Nes.

“Although our underlying disposition to life satisfaction and positivity appears to be relatively stable, small actions in our daily lives may provide temporary pleasures, and these are also important. How we spend our time is tremendously important for our happiness and well-being. It is therefore important to encourage and follow up on activities that make us happy”.

Nes adds:

“To some extent, positive experiences may also accumulate over time and create favorable conditions for our quality of life”.

(Source: fhi.no)

Filed under depression life satisfaction major depression well-being genes genetics neuroscience psychology science

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Magnetic brain stimulation treats depression independent of sleep effect

While powerful magnetic stimulation of the frontal lobe of the brain can alleviate symptoms of depression, those receiving the treatment did not report effects on sleep or arousal commonly seen with antidepressant medications, researchers say.

“People’s sleep gets better as their depression improves, but the treatment doesn’t itself cause sedation or insomnia.” said Dr. Peter B. Rosenquist, Vice Chair of the Department of Psychiatry and Health Behavior at the Medical College of Georgia at Georgia Health Sciences University.

The finding resulted from a secondary analysis of a study of 301 patients at 23 sites comparing the anti-depressive effects of the Neuronetics Transcranial Magnetic Stimulation Therapy System to sham (placebo) treatment in patients resistant to antidepressant medications. TMS sessions were given for 40 minutes, five days a week for six weeks. Initial findings, published in the journal Biological Psychiatry in 2007, were the primary evidence in the Food and Drug Administration’s approval of TMS for depression.  The secondary review reaffirmed TMS’s effectiveness in depression but revealed no differences in rates of insomnia or sleepiness among those who got actual and sham (placebo) therapy. Patients in the treatment group were also no more likely to request medication for insomnia or anxiety.

“It’s important for us to understand the full range of the effects of any treatment we give,” said Rosenquist, corresponding author of the study in the journal Psychiatric Research. The new findings will assuage worries of sleep-related side effects and remind physicians to remain alert to residual insomnia in depressed patients they are treating with TMS, the researchers report.

Sleep problems are a common side effect of major antidepressants: some drugs sedate patients while others stimulate them and increase insomnia. Insomnia occurs in 50-90 percent of patients with major depressive disorder. Other depressed patients complain they sleep too much. The good news is that TMS does not contribute to insomnia or oversleeping.

“One of the many bad things about depression is that often patients cannot sleep. We think it’s a significant symptom,” Rosenquist said. “If patients can’t sleep, it really adds to their distress, and even increases the likelihood of suicide.  We need antidepressant treatments that patients can tolerate so that they will stay with the treatment, which takes weeks to fully achieve.  Our study adds to the evidence showing that TMS has remarkably few side effects.” Patients often seek TMS as an option or adjunct to medication to avoid medication side effects.

“Mood disorders are associated with widespread structural and functional changes in the human brain, which can be reversed with successful treatment,” Rosenquist said.  “Clinical researchers are working to find the optimal way to restore normal brain function.”

TMS targets the prefrontal cortex of the brain, involved in mood regulation as well as other higher-order functions like planning, evaluating and decision-making. In this procedure, patients sit in a recliner and receive brief pulses of a MRI strength magnet held against the front of the head. The magnetic energy of TMS causes the brain cells closest to the surface of the brain to increase their activity which in turn influences the activity of the brain as a whole.

Major Depressive Disorder affects approximately 14.8 million, or about 6.7 percent of American adults in a given year, according to the National Institute of Mental Health. It’s the leading cause of disability in ages 15 to 44. Despite the numbers, Rosenquist concedes that it’s not clear what causes depression or exactly how antidepressants and other therapies, such as TMS, work.  “It’s an important puzzle and the work continues.  We are excited to be a part of this effort at Georgia Health Sciences University.”

(Source: news.georgiahealth.edu)

Filed under brain magnetic stimulation depression sleep sleep problems neuroscience psychology science

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New depression treatment may avoid side-effects

In an Australian first, researchers are studying Magnetic Seizure Therapy (MST) as an alternative treatment for the 30 per cent of patients suffering from depression who don’t respond to traditional treatment.

The treating team; Anne Maree Clinton, Dr Kate Hoy and Professor Paul Fitzgerald with the MST machine

The study, led by researchers from the Monash Alfred Psychiatry Research Centre (MAPrc) and funded by beyondblue and the National Health and Medical Research Council (NHMRC), has been published in two leading journals: Psychiatry Research: Neuroimaging and Depression and Anxiety. Both papers are a result of the same study.

MAPrc Deputy Director Professor Paul Fitzgerald, who led the study, said depression was a common and disabling disorder, affecting up to one in five Australians during their lifetime.

“Electroconvulsive Therapy (ECT) is one of the only established interventions for treatment resistant depression,” Professor Fitzgerald said.

“But use of ECT is limited due to the presence of memory-related side effects and associated stigma.”

For this reason, the MAPrc researchers began exploring new treatment options. MST is a brain-stimulation technique that may have similar clinical effects to ECT without the unwanted side effects.

“In MST, a seizure is induced through the use of magnetic stimulation rather than a direct electrical current like ECT. Magnetic fields are able to pass freely into the brain, making it possible to more precisely focus stimulation,” Professor Fitzgerald said.

“By avoiding the use of direct electrical currents and inducing a more focal stimulation, it is thought that MST will result in an improvement of depressive symptoms without the memory difficulties seen with ECT.”

Research is still at an early stage and MST is only available in a handful of locations worldwide. The MAPrc is the only centre in Australia conducting trials with this therapy.

The study found that MST resulted in an overall significant reduction in depression symptoms; 40 per cent showed overall improvement and 30 per cent showed some improvement. None of the trial participants complained of cognitive side effects.

“MST shows antidepressant efficacy without apparent cognitive side effects. However, substantial research is required to understand the optimal conditions for stimulation and to compare MST to established treatments, including ECT,” Professor Fitzgerald said.

“In order to accurately assess the comparable efficacy of MST to ECT, large-scale randomised controlled trials are required. There remains considerable work to be done before statements of the relative efficacy of these treatments can be made.”

Professor Fitzgerald and his team have received more funding from beyondblue and the NHMRC to carry out a large-scale trial on MST as an alternative treatment for depression.

(Source: monash.edu.au)

Filed under depression magnetic seizure therapy treatment neuroscience psychology science

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