The Moral Brain

Consider a failed murder attempt. Or a simple mistake that causes another to die. Is one of these more acceptable than the other?

Neuroscientists don’t pretend to hold the answers as to how people know what is right and what is wrong. But studies show individual biology may influence the ways people process the actions of others.

It turns out we judge others not only for what they do, but also for what we perceive they are thinking while they do it.

Consider the following scenario: Grace and Sally are touring a chemical factory when Grace decides to grab a cup of coffee. Sally asks Grace to pour her a cup as well. Grace spots a container of white powder next to the coffee maker and, knowing that her friend takes sugar in her coffee, she pours some into Sally’s cup. As it turns out, the powder is poison, and Sally dies after a few sips.

Most of us would understand and maybe forgive Grace for accidentally poisoning — or even killing — her friend. But what would you think of Grace if you were to learn that she had a hunch that the powder was toxic, yet decided to add it to her friend’s cup anyway?

“Often, what determines moral blame is not what the outcome is, but what [we think] is going on in the mind of the person performing the act,” says Rebecca Saxe, a neuroscientist at the Massachusetts Institute of Technology who studies how the brain casts judgment.

Scientists are learning the ways the brain responds when we attempt to determine right from wrong. Ultimately, they hope such information will help show how the brain processes difficult situations.

What was she thinking?

One way scientists study how we make right-or-wrong judgments is to look at brain regions that are most active when people attempt to interpret the thoughts of others.

In some studies, participants read stories about characters that either accidentally or intentionally cause harm to others while scientists use functional magnetic resonance imaging (fMRI) to track how brain activity changes. Such studies show that thinking about another’s thoughts increases the activity of nerve cells in a brain region known as the right temporo-parietal junction located behind the right ear.

As it turns out, some of these cells respond differently when presented with an intentional harm versus an accident. By zeroing in on the distinct patterns of activity in these cells, Saxe’s group discovered that they could accurately predict how forgiving the participants would be.

“People who say accidents are forgivable have really different [activity] patterns” than those less willing to overlook the unintentional harm, Saxe says.

Thinking about harm

Neuroscientists also study how people respond when asked how they themselves would act in morally challenging scenarios.

In one popular moral dilemma scenario, scientists ask participants to imagine the following: A runaway train is barreling down on five people. The only way to save these people is to hit a switch that would redirect the train onto tracks where it will kill only one person. Would you hit the switch?

What if, instead, you had to push a man off of a bridge to stop the train, knowing that doing so will kill him but save the lives of the others?

Studies ran these scenarios by people with damage to the ventromedial prefrontal cortex — a region believed to be involved in the processing of emotions — and those without damage. Both groups equally support the decision to hit the switch to redirect the train to save more lives.

However, those with damage to the ventromedial prefrontal cortex are much more likely to endorse pushing the man in front of the train, a more direct and personal harm. These studies, led by neuroscientist Antonio Damasio of the University of Southern California, suggest the important role of emotion in the generation of such judgments.

To test how important the ventromedial prefrontal cortex is when we judge the actions of others, Damasio along with neuroscientist Liane Young of Boston asked a small group of people with damage to this region to evaluate variations of the Grace and Sally story.

When told that Grace deliberately puts powder she believes is toxic into Sally’s cup, only to later learn the powder was sugar, healthy adults regularly condemn Grace’s failed attempt to harm her friend. However, people with ventromedial prefrontal cortex damage shrug off Grace’s action. As they see it, as long as Sally survives, Grace’s actions are no big deal.

Damasio says these results, along with others, reveal the role of the ventromedial prefrontal cortex and emotion in evaluating harmful intent.

That’s not fair

There is also evidence that changes in the chemistry of the brain influence how we behave when others treat us unfairly.

To measure how changes in brain chemistry affect people’s reactions to unfairness, University College London neuroscientist Molly Crockett and others gave study participants a drink to drive down levels of the neurotransmitter serotonin in the brain before asking them to play the ultimatum game.

In the ultimatum game, participants are paired with strangers they are told have been given a lump sum of money to share with them. The stranger determines how to divvy up the money, and proposes a split to the participant. The participant decides whether or not to accept the stranger’s offer. If the participant accepts, both players walk away with some money. However, a participant may reject the offer, believing it to be unfair, leaving both players empty-handed. Crockett found that people with lower levels of serotonin were more likely than others to reject offers they deemed to be unfair.

When the scientists examined the brain activity of participants with depleted serotonin levels as they accepted or rejected the offers, they found that rejecting offers led to increased activity in the dorsal striatum — a region involved in processing reward. Crockett says the findings suggest that dips in serotonin can shift people’s motivations to punish unfairness. For instance, when you deplete serotonin, people who are normally more forgiving may become happier with revenge, she says.

Crockett notes that serotonin levels may fluctuate when people are hungry or stressed. The findings illustrate how individual differences in biology might influence the way people view, and respond to, the actions of others.

Giving White People The Illusion Of Darker Skin Makes Them Less Racist

An optical illusion can change the implicit biases of Caucasian people against people with darker skin, according to a study published in the August 2013 edition of Cognition.

The research, a collaboration between Royal Holloway University of London, the Central European University in Budapest and Radboud University Nijmegen in the Netherlands, analyzed the implicit racial biases of 34 Caucasian participants, then subjected them to something called the Rubber Hand Illusion, where they watched a rubber hand being touched by a paintbrush as they felt their own hand being stimulated out of sight. The illusion creates the sense that the fake hand is part of the subject’s body, even when it’s of a completely different skin color.

The more the participants felt like the darker skinned fake hand was their own, the less racist they came off in a second implicit bias test.

In another test, participants underwent the same process, but some saw a white hand, while others saw a dark hand. The implicit bias test showed that the opinions of those who saw the white hand didn’t change, while again those who felt ownership of the darker hand felt less racial bias.

"Across two experiments, the more intense the participants’ illusion of ownership over the dark-skinned rubber hand, the more positive their implicit racial attitudes became," the authors write.

“It comes down to a perceived similarity between white and dark skin,” lead author Lara Maister of Royal Holloway University of London said in a press statement. “The illusion creates an overlap, which in turn helps to reduce negative attitudes because participants see less difference between themselves and those with dark skin.”

The study suggests that racial biases aren’t necessarily cemented by adulthood, but that they can be altered. “Changes in body-representation may therefore constitute a core, previously unexplored, dimension that in turn changes social cognition processes,” the authors write. They suggest that future research into different social groups and stereotypes could expand on their work, since this research only explored the attitudes of white individuals.

Can Brain Scans Really Tell Us What Makes Something Beautiful?

When art meets neuroscience, strange things happen.

Consider the Museum of Scientifically Accurate Fabric Brain Art in Oregon which features rugs and knitting based on a brain scan motif. Or the neuroscientist at the University of Nevada-Reno who scanned the brain of a portrait artist while he drew a picture of a face.

And then there’s the ongoing war of words between scientists who think it’s possible to use analysis of brain activity to define beauty–or even art–and their critics who argue that it’s absurd to try to make sense of something so interpretive and contextual by tying it to biology and the behavior of neurons.

Beauty and the brain

On one side you have the likes of Semir Zeki, who heads a research center called the Institute of Neuroesthetics at London’s University College. A few years ago he started studying what happens in a person’s brain when they look at a painting or listen to a piece of music they find beautiful. He looked at the flip side, too–what goes on in there when something strikes us as ugly.

What he found is that when his study’s subjects experienced a piece of art or music they described as beautiful, their medial orbito-frontal cortex–the part of the brain just behind the eyes–”lit up” in brain scans. Art they found ugly stimulated their motor cortex instead. Zeki also discovered that whether the beauty came through their ears, in music, or their eyes, in art, the brain’s response was the same–it had increased blood flow to what’s known as its pleasure center. Beauty gave the brains a dopamine reward.

Zeki doesn’t go so far as to suggest that the essence of art can be captured in a brain scan. He insists his research really isn’t about explaining what art is, but rather what our neurons’ response to it can tell us about how brains work. But if, in the process, we learn about common characteristics in things our brains find beautiful, his thinking goes, what harm is there in that?

Beware of brain rules?

Plenty, potentially, responds the critics’ chorus. Writing recently in the journal Nature, Philip Ball makes the point that this line of research ultimately could lead to rule-making about beauty, to “creating criteria of right or wrong, either in the art itself or in individual reactions to it.” It conceivably could devolve to “scientific” formulas for beauty, guidelines for what, in music or art or literature, gets the dopamine flowing.

Adds Ball:

Although it is worth knowing that musical ‘chills’ are neurologically akin to the responses invoked by sex or drugs, an approach that cannot distinguish Bach from barbiturates is surely limited.

Others, such as University of California philosophy professor Alva Noe, suggest that to this point at least, brain science is too limiting in what it can reveal, that it focuses more on beauty as shaped by people’s preferences, as opposed to addressing the big questions, such as “Why does art move us?” and “Why does art matter?”

And he wonders if a science built around analyzing events in an individual’s brain can ever answer them. As he wrote in the New York Times:

…there can be nothing like a settled, once-and-for-all account of what art is, just as there can be no all-purpose account of what happens when people communicate or when they laugh together. Art, even for those who make it and love it, is always a question, a problem for itself. What is art? The question must arise, but it allows no definitive answer.

Fad or fortune?

So what of neuroaesthetics? Is it just another part of the “neuro” wave, where brain scans are being billed as neurological Rosetta Stones that proponents claim can explain or even predict behavior–from who’s likely to commit crimes to why people make financial decisions to who’s going to gain weight in the next six months.

More jaded souls have suggested that neuroaesthetics and its bulky cousin, neurohumanities, are attempts to capture enough scientific sheen to attract research money back to liberal arts. Alissa Quart, writing in The Nation earlier this month, cut to the chase:

Neurohumanities offers a way to tap the popular enthusiasm for science and, in part, gin up more funding for humanities. It may also be a bid to give more authority to disciplines that are more qualitative and thus are construed, in today’s scientized and digitalized world, as less desirable or powerful.

Samir Zeki, of course, believes this is about much more than research grants. He really isn’t sure where neuroaesthetics will lead, but he’s convinced that only by “understanding the neural laws,” as he puts it, can we begin to make sense of morality, religion and yes, art.

Ketamine Shows Significant Therapeutic Benefit in People with Treatment-Resistant Depression

Patients with treatment-resistant major depression saw dramatic improvement in their illness after treatment with ketamine, an anesthetic, according to the largest ketamine clinical trial to-date led by researchers from the Icahn School of Medicine at Mount Sinai. The antidepressant benefits of ketamine were seen within 24 hours, whereas traditional antidepressants can take days or weeks to demonstrate a reduction in depression.

The research will be discussed at the American Psychiatric Association meeting on Monday, May 20, 2013 at 12:30 pm in the Press Briefing Room at the Moscone Center in San Franscico.

Led by Dan Iosifescu, MD, Associate Professor of Psychiatry at Mount Sinai; Sanjay Mathew, MD, Associate Professor of Psychiatry at Baylor College of Medicine; and James Murrough, MD Assistant Professor of Psychiatry at Mount Sinai, the research team evaluated 72 people with treatment-resistant depression—meaning their depression has failed to respond to two or more medications—who were administered a single intravenous infusion of ketamine for 40 minutes or an active placebo of midazolam, another type of anesthetic without antidepressant properties. Patients were interviewed after 24 hours and again after seven days. After 24 hours, the response rate was 63.8 percent in the ketamine group compared to 28 percent in the placebo group. The response to ketamine was durable after seven days, with a 45.7 percent response in the ketamine group versus 18.2 percent in the placebo group. Both drugs were well tolerated.

“Using midazolam as an active placebo allowed us to independently assess the antidepressant benefit of ketamine, excluding any anesthetic effects,” said Dr. Murrough, who is first author on the new report. “Ketamine continues to show significant promise as a new treatment option for patients with severe and refractory forms of depression.”

Major depression is caused by a breakdown in communication between nerve cells in the brain, a process that is controlled by chemicals called neurotransmitters. Traditional antidepressants such as selective serotonin reuptake inhibitors (SSRIs) influence the activity of the neurotransmitters serotonin and noreprenephrine to reduce depression. In these medicines, response is often significantly delayed and up to 60 percent of people do not respond to treatment, according to the U.S Department of Health and Human Services. Ketamine works differently than traditional antidepressants in that it influences the activity of the glutamine neurotransmitter to help restore the dysfunctional communication between nerve cells in the depressed brain, and much more quickly than traditional antidepressants.

Future studies are needed to investigate the longer term safety and efficacy of a course of ketamine in refractory depression. Dr. Murrough recently published a preliminary report in the journal Biological Psychiatry on the safety and efficacy of ketamine given three times weekly for two weeks in patients with treatment-resistant depression.

“We found that ketamine was safe and well tolerated and that patients who demonstrated a rapid antidepressant effect after starting ketamine were able to maintain the response throughout the course of the study,” Dr. Murrough said. “Larger placebo-controlled studies will be required to more fully determine the safety and efficacy profile of ketamine in depression.”

The potential of ketamine was discovered by Dennis S. Charney, MD, Anne and Joel Ehrenkranz Dean of the Icahn School of Medicine at Mount Sinai, and Executive Vice President for Academic Affairs of The Mount Sinai Medical Center, in collaboration with John H. Krystal, MD, Chair of the Department of Psychiatry at Yale University.

“Major depression is one of the most prevalent and costly illnesses in the world, and yet currently available treatments fall far short of alleviating this burden,” said Dr. Charney. “There is an urgent need for new, fast-acting therapies, and ketamine shows important potential in filling that void.”

Dr. Murrough will present his research on Sunday, May 19, 2013 from 1:00 pm to 3:00 pm in the Moscone exhibit hall at the APA meeting.

Temporal Processing in the Olfactory System: Can We See a Smell?

Sensory processing circuits in the visual and olfactory systems receive input from complex, rapidly changing environments. Although patterns of light and plumes of odor create different distributions of activity in the retina and olfactory bulb, both structures use what appears on the surface similar temporal coding strategies to convey information to higher areas in the brain. We compare temporal coding in the early stages of the olfactory and visual systems, highlighting recent progress in understanding the role of time in olfactory coding during active sensing by behaving animals. We also examine studies that address the divergent circuit mechanisms that generate temporal codes in the two systems, and find that they provide physiological information directly related to functional questions raised by neuroanatomical studies of Ramon y Cajal over a century ago. Consideration of differences in neural activity in sensory systems contributes to generating new approaches to understand signal processing.

For combat veterans suffering from post-traumatic stress disorder, ‘fear circuitry’ in the brain never rests

Chronic trauma can inflict lasting damage to brain regions associated with fear and anxiety. Previous imaging studies of people with post-traumatic stress disorder, or PTSD, have shown that these brain regions can over-or under-react in response to stressful tasks, such as recalling a traumatic event or reacting to a photo of a threatening face. Now, researchers at NYU School of Medicine have explored for the first time what happens in the brains of combat veterans with PTSD in the absence of external triggers.

Their results, published in Neuroscience Letters, and presented today at the annual meeting of the American Psychiatry Association in San Francisco, show that the effects of trauma persist in certain brain regions even when combat veterans are not engaged in cognitive or emotional tasks, and face no immediate external threats. The findings shed light on which areas of the brain provoke traumatic symptoms and represent a critical step toward better diagnostics and treatments for PTSD.

A chronic condition that develops after trauma, PTSD can plague victims with disturbing memories, flashbacks, nightmares and emotional instability. Among the 1.7 million men and women who have served in the wars in Iraq and Afghanistan, an estimated 20% have PTSD. Research shows that suicide risk is higher in veterans with PTSD. Tragically, more soldiers committed suicide in 2012 than the number of soldiers who were killed in combat in Afghanistan that year.

"It is critical to have an objective test to confirm PTSD diagnosis as self reports can be unreliable," says co-author Charles Marmar, MD, the Lucius N. Littauer Professor of Psychiatry and chair of NYU Langone’s Department of Psychiatry. Dr. Marmar, a nationally recognized expert on trauma and stress among veterans, heads The Steven and Alexandra Cohen Veterans Center for the Study of Post-Traumatic Stress and Traumatic Brain Injury at NYU Langone Medical Center.

The study, led by Xiaodan Yan, a research fellow at NYU School of Medicine, examined “spontaneous” or “resting” brain activity in 104 veterans of combat from the Iraq and Afghanistan wars using functional MRI, which measures blood-oxygen levels in the brain. The researchers found that spontaneous brain activity in the amygdala, a key structure in the brain’s “fear circuitry” that processes fearful and anxious emotions, was significantly higher in the 52 combat veterans with PTSD than in the 52 combat veterans without PTSD. The PTSD group also showed elevated brain activity in the anterior insula, a brain region that regulates sensitivity to pain and negative emotions.

Moreover, the PTSD group had lower activity in the precuneus, a structure tucked between the brain’s two hemispheres that helps integrate information from the past and future, especially when the mind is wandering or disengaged from active thought. Decreased activity in the precuneus correlates with more severe “re-experiencing” symptoms—that is, when victims re-experience trauma over and over again through flashbacks, nightmares and frightening thoughts.

Individuals who drink heavily and smoke may show ‘early aging’ of the brain

• Alcohol treatment interventions work best when patients understand and are actively involved in the process.
• A first-of-its-kind study looks at the interactive effects of smoking status and age on neurocognition in one-month-abstinent alcohol dependent (AD) individuals in treatment.
• Results show that AD individuals who currently smoke have more problems with memory, ability to think quickly and efficiently, and problem-solving skills than those who do not smoke, effects which seem to become greater with increasing age.

Treatment for alcohol use disorders works best if the patient actively understands and incorporates the interventions provided in the clinic. Multiple factors can influence both the type and degree of neurocognitive abnormalities found during early abstinence, including chronic cigarette smoking and increasing age. A new study is the first to look at the interactive effects of smoking status and age on neurocognition in treatment-seeking alcohol dependent (AD) individuals. Findings show that AD individuals who currently smoke show more problems with memory, ability to think quickly and efficiently, and problem-solving skills than those who don’t smoke, effects which seem to become exacerbated with age.

Results will be published in the October 2013 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

"Several factors – nutrition, exercise, comorbid medical conditions such as hypertension and diabetes, psychiatric conditions such as depressive disorders and post-traumatic stress disorder, and genetic predispositions – may also influence cognitive functioning during early abstinence," explained Timothy C. Durazzo, assistant professor in the department of radiology and biomedical imaging at the University of California San Francisco, and corresponding author for the study. "We focused on the effects of chronic cigarette smoking and increasing age on cognition because previous research suggested that each has independent, adverse affects on multiple aspects of cognition and brain biology in people with and without alcohol use disorders. This previous research also indicated that the adverse effects of smoking on the brain accumulate over time. Therefore, we predicted that AD, active chronic smokers would show the greatest decline in cognitive abilities with increasing age."

"The independent and interactive effects of smoking and other drug use on cognitive functioning among individuals with AD are largely unknown," added Alecia Dager, associate research scientist in the department of psychiatry at Yale University. "This is problematic because many heavy drinkers also smoke. Furthermore, in treatment programs for alcoholism, the issue of smoking may be largely ignored. This study provides evidence of greater cognitive difficulties in alcoholics who also smoke, which could offer important insights for treatment programs. First, individuals with AD who also smoke may have more difficulty remembering, integrating, and implementing treatment strategies. Second, there are clear benefits for thinking skills as a result of quitting both substances."

Durazzo and his colleagues compared the neurocognitive functioning of four groups of participants, all between the ages of 26 and 71 years of age: never-smoking healthy individuals or “controls” (n=39); and one-month abstinent, treatment-seeking AD individuals, who were never-smokers (n = 30), former-smokers (n = 21) and active-smokers (n = 68). Evaluated cognitive abilities included cognitive efficiency, executive functions, fine motor skills, general intelligence, learning and memory, processing speed, visuospatial functions, and working memory.

"We found that, at one month of abstinence, actively smoking AD [individuals] had greater-than-normal age effects on measures of learning, memory, processing speed, reasoning and problem-solving, and fine motor skills," said Durazzo. "AD never-smokers and former-smokers showed equivalent changes on all measures with increasing age as the never-smoking controls. These results indicate the combination of alcohol dependence and active chronic smoking was related to an abnormal decline in multiple cognitive functions with increasing age."

"These results indicate the combined effects of these drugs are especially harmful and become even more apparent in older age," said Dager. "In general, people show cognitive decline in older age. However, it seems that years of combined alcohol and cigarette use exacerbate this process, contributing to an even greater decline in thinking skills in later years."

Durazzo agreed. “Chronic cigarette smoking, excessive alcohol consumption, and increasing age are all associated with increased oxidative damage to brain tissue,” he said. “Oxidative damage results from increased levels of free radicals and other compounds that directly injure neurons and other cells that make up the brain. Cigarette smoking and excessive alcohol consumption expose the brain to a tremendous amount of free radicals. We hypothesize that chronic, long-term exposure to cigarette smoke and excessive alcohol consumption interacts with the normal aging process to produce greater neurocognitive decline in the active-smoking AD group.”

Cigarette smoking is a “modifiable health risk” that is directly associated with at least 440,000 deaths every year in the United States, Durazzo noted. “Chronic smoking, and to a lesser extent, alcohol use disorders are also associated with an increased risk for Alzheimer’s disease,” he said. “So, the combination of these modifiable health risks may place an individual at even greater risk for development of Alzheimer’s disease. Given the above, in conjunction with the findings from our cognitive and neuroimaging research, we completely support programs that routinely offer smoking cessation programs to all individuals seeking treatment for alcohol/substance abuse disorders.”

Deep brain stimulation: a fix when the drugs don’t work

Neurological disorders can have a devastating impact on the lives of sufferers and their families.

Symptoms of these disorders differ extensively – from motor dysfunction in Parkinson’s disease, memory loss in Alzheimer’s disease to inescapable cravings in drug addiction.

Drug treatments are often ineffective in these disorders. But what if there was a way to simply switch off a devastating tremor, or boost a fading memory?

Recent advances using Deep Brain Stimulation (DBS) in selective brain regions have provided therapeutic benefits and have allowed those affected by these neurological disorders freedom from their symptoms, in absence of an existing cure.

A pacemaker for the brain

Artificial cardiac pacemakers are typically associated with controlling and resynchronising heartbeats by electrical stimulation of the heart muscle.

In a similar manner, DBS sends electrical impulses to specific parts of the brain that control discrete functions. This stimulation evokes control over the neural activity within these regions.

Prior to switching on the electrical stimulation, electrodes are surgically implanted within precise brain regions to control a specific function.

The neurosurgery is conducted under local anaesthetic to maintain consciousness in the patient. This ensures that the electrode does not damage critical brain regions.

The brain itself has no pain receptors so does not require anaesthetic.

Following recovery from surgery the electrodes are activated and the current calibrated by a neurologist to determine the optimal stimulation parameters.

The patient can then control whether the electrodes are on or off by a remote battery-powered device.

Turning off tremors

Perhaps the most documented success of DBS is in the control of tremors and motor coordination in Parkinson’s disease.

This is caused by the degeneration of neurons in an area of the brain called the substantia nigra. These neurons secrete the neurotransmitter dopamine.

Deterioration of these neurons reduces the amount of dopamine available to be released in a brain area involved in movement, the basal ganglia.

Drug therapy for Parkinson’s disease involves the use of levodopa (L-DOPA), a form of dopamine that can cross the blood brain barrier and then be synthesised into dopamine.

The administration of L-DOPA temporarily reduces the motor symptoms by increasing dopamine concentrations in the brain. However, side effects of this treatment include nausea and disordered movement.

DBS has been shown to provide relief from the motoric symptoms of Parkinson’s disease and essential tremors.

For the treatment of Parkinson’s disease electrodes are implanted into regions of the basal ganglia – the subthalamic nucleus or globus pallidus, to restore control of movement.

These are regions innervated by the deteriorating substantia nigra, therefore the DBS boosts stimulation to these areas.

Patients can then switch on the electrodes, stimulating these brain regions to enhance control of movement and diminish tremors.

Restoring fading memories

Recently, DBS has been used to diminish memory deficits associated with Alzheimer’s disease, a progressive and terminal form of dementia.

The pathologies associated with Alzheimer’s disease involve the formation of amyloid plaques and neurofibrillary tangles within the brain leading to dysfunction and death of neurons.

Brain regions primarily affected include the temporal lobes, containing important memory structures including the hippocampus.

Recent clinical trials with DBS involve the implantation of electrodes within the fornix – a structure connecting the left and right hippocampi together.

By stimulating neural activity within the hippocampi via the fornix, memory deficits associated with Alzheimer’s disease can be improved, enhancing the daily functioning of patients and slowing the progression of cognitive decline.

Deactivating addiction

Another use of DBS is in the treatment of substance abuse and drug addiction. Substance-related addictions constitute the most frequently occurring psychiatric disease category and patients are prone to relapse following rehabilitative treatment.

Persistent drug use leads to long term changes in the brain’s reward system.

Understanding of the reward systems affected in addiction has created a range of treatment options that directly target dysregulated brain circuits in order to normalise functionality.

One of the key reward regions in the brain is the nucleus accumbens and this has been used as a DBS target to control addiction.

Translational animal research has indicated that stimulation of the nucleus accumbens decreases drug seeking in models of addiction. Clinical studies have shown improved abstinence in both heroin addicts and alcoholics.

Studies have extended the use of DBS to potentially restore control of maladaptive eating behaviours such as compulsive binge eating.

In a recent study, binge eating of a high fat food in mice was decreased by DBS of the nucleus accumbens. This is the first study demonstrating that DBS can control maladaptive eating behaviours and may be a potential therapeutic tool in obesity.

Despite its therapeutic use for more than a decade, the neural mechanism of DBS is still not yet fully understood.

The remedial effect is proposed to involve modulation of the dopamine system – and this seems particularly relevant in the context of Parkinson’s disease and addiction.

DBS potentially has effects on the functional activity of other interconnected brain systems. While it can provide therapeutic relief from symptoms of neurological diseases, it does not treat the underlying pathology.

But it provides both effective and rapid intervention from the effects of debilitating illnesses, restoring activity in deteriorating brain regions and aids understanding of the brain circuits involved in these disorders.