Brain Scans Could Become EKGs for Mental Disorders

  • Share
  • Read Later
Getty Images / Getty Images

If EKGs can detect potential problems in heart function, then doctors are asking why brain scans can’t be used in the same way, to identify disorders like depression, autism or schizophrenia.

Doctors have long relied on EKGs, or electrocardiograms, to track the electrical activity of the heart and find any potential aberrations in the normal pattern of blips and valleys that could indicate distress. It’s not invasive, not that expensive, and for the patient, only involves getting hooked up to a few leads with patches on the chest.

Now researchers say that a similarly patient-friendly technique could scour brain activity for signs of trouble. The idea is to look for any changes in the normal “resting state” of multiple brain regions recorded by functional magnetic resonance imaging (fMRI) machines. And so far, promising evidence suggests that it may be possible to detect when communication between these regions is out of sync, or otherwise different from the norm. Even more encouraging, say scientists, various mental disorders, such as depression and autism, may involve different aberrant patterns of activity, providing a type of visual fingerprint for the condition. Finding such signatures could not only lead to better diagnosis of certain neurological or developmental diseases but also track how well patients respond to treatment.

And — just as with a standard EKG test — all the patient has to do is lie still. “With resting-state fMRI, they just have to hold still for eight minutes in the scanner,” says Dr. Michael Greicius, medical director of the Stanford Center for Memory Disorders. “That’s the main practical advantage.”

(MORE: Unique Brain Pattern Could Predict Autism in Youngest Children)

In the latest demonstration of this approach, appearing in the journal JAMA Psychiatry, researchers compared the resting-state brain activity of children with autism to that of similarly aged youngsters without the developmental disorder. The autistic children showed a distinctive pattern of hyperconnected signaling in what the authors call the brain’s “salience network,” a collection of regions that appear to regulate attention.

Other researchers have found evidence that such fMRI scans might also help diagnose attention-deficit/hyperactivity disorder (ADHD), schizophrenia and depression. In an experiment appearing in the forthcoming July issue of Psychiatry Research, Dr. Jonathan Posner of Columbia University and his colleagues looked at 22 children with ADHD who were not yet on medication and compared them with 20 youngsters around the same age without the disorder. Compared with the healthy children, those with ADHD had, on average, less coordinated brain activity between regions such as the prefrontal cortex, an area at the front of the brain thought to be involved in decisionmaking, and the caudate, a region located toward the base of the brain involved in controlling impulses. Such patterns could one day help identify children at highest risk of developing ADHD and provide them with behavioral or educational support to address symptoms early on, when such interventions might have the biggest impact.

And such scans aren’t limited to diagnosing disease but could help improve treatment of mental disorders as well. “I am most interested in us[ing] resting-state fMRI to really examine the effects of treatment,” says Posner. He also published a paper in JAMA Psychiatry last spring showing that antidepressants successfully quieted hyperconnectivity in the brains of individuals with chronic depression.

(MORE: Concussion and Alzheimer’s Patients Show Similar Brain Changes)

That trial compared brain scans from 32 people with depression with those from 25 healthy counterparts and confirmed that the former group had more activity in what is known as the default mode network, a collection of disparate brain regions that makes up the baseline, or default level of brain activity necessary to keep a body functioning. When a person performs a mental task, this default network is suppressed. But in the depressed patients, this network was overactive, and that was associated with increased rumination — or overfixating on a thought that could contribute to depression.

The patients with depression were then given a 10-week course of either the antidepressant Cymbalta (duloxetine) or a placebo. At the end of the trial, patients who received the drug showed similar connectivity patterns to those seen in healthy individuals, but the depressed participants who received placebo did not. (The study received some funding support from the pharmaceutical company Eli Lilly, which markets Cymbalta.)

(MORE: Your Brain on Laughter)

Similar differences were found among those with schizophrenia. In these patients, both the default network and the salience network appear disrupted compared with those without the disorder, according to French neuroscientists who published their results in the journal Schizophrenia Research. They noted that lack of synchronicity involving a part of the brain called the left striatum, which wasn’t seen in healthy individuals, was associated with symptoms of schizophrenia like delusions.

Other research has pointed to differences in resting-state abnormalities in illnesses such as Alzheimer’s, Tourette syndrome and anxiety disorder.

So why are such brain scans not used for clinical diagnosis? Until recently, limited computing power often meant that scientists could only analyze fMRI data from one brain region at a time, and many of these patterns require a more global view to understand how certain networks interact with others.

(MORE: Brain Scans Can Predict Which Criminals Are Likely to Get Rearrested)

But as imaging technologies become more robust, such scans could increasingly become useful diagnostic tools for doctors. With autism, for example, doctors are “really desperate for a biological marker to help with diagnosis and [measuring] treatment response,” says Daniel Smith, senior director of discovery neuroscience at Autism Speaks. Currently, most children are diagnosed around the age of 2, when the behavioral symptoms of inattention and repetitive actions tend to emerge. More studies suggest, however, that intervening with behavioral therapy in children as young as 6 months old could reduce, or even normalize, some of the aberrant brain changes responsible for the disorder, so diagnosing the condition as early as possible could become critical.

For other conditions affecting the brain, fMRI may not be as helpful. “I don’t think this is going to yield insights into every neurologic disorder,” says Greicius, who is dubious that abnormalities in resting-state connectivity exist in disorders such as multiple sclerosis — in which neuronal deterioration is “willy-nilly” — or traumatic brain injury, which can disproportionately affect an isolated area. But for conditions like autism, it could provide valuable opportunities to both understand and improve treatments. First, however, as with any new technique, scientists will have to replicate and confirm the early results. If they hold up, he says, “That’s going to help shore up recent exciting preliminary findings” — and hopefully pave the way for assigning certain mental illnesses their own imaging fingerprint that could give doctors and patients a head start on treatments.

5 comments
AlainCouvier
AlainCouvier

As researchers from the Children’s Hospital, Boston elegantly showed the brain , epilepsy and autism are intimately linked. Their study published as "The Interaction between Early Life Epilepsy and Autistic-Like Behavioral Consequences: A Role for the Mammalian Target of Rapamycin (mTOR) Pathway" may become one of those landmark studies particularly over the last two years.

In this study the researchers showed that in an animal model,  early life seizures were linked with the development in later life of not only epilepsy but also autistic like behaviors.

They also were able to unpack a relationship with the mTOR pathway - the drug Rapamycin can block the mTOR pathway and as showed once again in animal models were less likely to have seizures and had less 'autistic' symptoms.

Interestingly  mTOR is also implicated in the regulation of both the innate and adaptive immune responses.

It's been an exciting time in ASD research we are on the verge on making big inroads into what can be for some families a devestating condition.


Krzysztof
Krzysztof

Could brain scans become EKGs for mental disorder (epilepsy) ?

Krzysztof

km48@op.pl

dnaada
dnaada

There are 2 problems with this type of research, particularly in regard to a disorder such as ADHD (as one example). First is the fact that comparing ADHD kids to a normal control group is inadequate. A key issue is differential diagnosis, or in other words discriminating ADHD from other disorders (oppositional defiant disorder, autism spectrum disorders, etc.).  This is more difficult than simply showing that ADHD kids differ from normal controls on a particular measure, and critically important for accurate diagnosis.

A second issue for demonstrating any diagnostic technique is clinically useful involves the rates of false negatives and false positives. How many kids tested with a particular instrument (fMRI or whatever) are either falsely identified with ADHD when they in fact don't have the disorder, as well as how many kids are determined not to have the disorder when in fact they do.

Thus research like this is preliminary at best, and articles like this tend to mislead the public into thinking such techniques are "ready for prime time".


FrancisMulhare
FrancisMulhare like.author.displayName 1 Like

Finally psychiatry, psychology and psychotherapy  is on the outer orbits of becoming a real science with objective data and measurable results, instead of studies comprised of subjective reports about how patients feel better today than they did  2 weeks ago before they started  drug X with multibillion dollar selling potential.

JarlathCoady
JarlathCoady

Wow, interesting how a 10-week study on Cymbalta found that the Eli Lilly-funded research showed a significant difference between the drug and a placebo when the majority of studies show anti-depressants are almost mythological in their treatment of depression. If anti-depressants were designed during a time when they simply knew there was a link between serotonin and norepenephrine levels in the brain and not much more, and anti--depressants have not wandered far from the practice of tackling this abnormal pattern rather than focusing more money on directly exploring causes of depression, then any recent studies with this outdated chemical and it's similar offshoots are completely redundant. 


This article very briefly mentions behavioural and educational attempts and interventions to certain disorders when most current resources should be on those interventions rather than the biological (and failed) approach.. Identifying a link in depression is just not good enough anymore. Far too much medication has been sold on the illusion of a link. By citing studies funded by pharmaceutical companies is astonishingly naive. How many studies which showed negative results have been lost behind a filing cabinet in the offices of Eli Lilly? For now, psychiatry is a pseudoscience, and will remain that way until they directly treat disorders and not indirect symptoms of disorders.