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A Blood Test May Help Pinpoint the Right Antidepressant for You

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When doctors determine the best medication for a person with depression, they generally rely upon little more than guesswork and patient self-reports, due to insufficient medical evidence. Research out of UT Southwestern Medical Center (UTSMC) previously suggested that such practices were insufficient, and a new study, published in Psychoneuroendocrinology, provides additional diagnostic information that may change the way depression is treated.

The research team drew upon a large body of research that links low levels of inflammation in the body with depression. They say a blood test for an inflammatory biomarker, known as C-reactive protein (CRP), can significantly improve the success rate of two common antidepressants for depressed patients.

Lead author Madhukar Trivedi, a professor of psychiatry at UTSMC and director of the Center for Depression Research and Clinical Care, says doctors typically pick an antidepressant for their patients in one of three ways: personal experience; matching the perceived benefits of one drug with a certain type of patient’s needs; or having the patient pick a drug by ruling out the unwanted side effects of other drugs. “There isn’t a strong evidence base to support one way [of choosing an antidepressant] over another,” he tells mental_floss.

Trivedi says that because many doctors are pressed for time and overloaded with patients, they don't thoroughly address a depressed patient’s needs. “If you have diabetes, the doctor spends a lot of time explaining that it’s a serious illness—there are consequences for ignoring it, and there are treatments you need to do. In depression, that does not happen as much. Patient engagement is not that strong,” he says.

Trivedi led a landmark study more than a decade ago that revealed how serious the medication problem is: Up to one-third of depressed patients don’t see an improvement in their first month of medication, and approximately 40 percent of people who take antidepressants quit within the first three months.

This failure rate is exacerbated by the lingering social stigma accompanying the illness. “It is not fashionable to say, ‘I have depression,’ so people around you may put in their uninformed advice … 'Just go for a walk,' or 'Why are you depressed?'” says Trivedi.

The CRP blood test is traditionally used as a measure of inflammation for such diseases as cardiovascular disease, diabetes, and rheumatoid arthritis, among others, where doctors are looking for high levels of C-reactive protein—approximately 3 to 5 milligrams per blood liter. In the new study, which Trivedi refers to as a “secondary analysis” of a study he led in 2011 (the Co-MED trial), he says, “Our hypothesis was that for depression there may be stress related inflammation in lower levels.”

Trivedi’s lab measured depression remission rates of 106 patients, culled from 440 patients involved in the 2011 study, each of whom had given blood samples. Fifty-one of them had been prescribed only escitalopram (Lexapro), while 55 of them had been prescribed escitalopram plus bupriopion (Wellbutrin), both commonly prescribed SSRI antidepressant drugs.

After analyzing blood samples, the researchers found that for patients whose CRP levels were less than 1 milligram per liter of blood, escitalopram alone was more effective—patients experienced a 57 percent remission rate of their depression versus 30 percent on the other drug. For patients with higher CRP levels, escitalopram plus bupropion was more effective. These patients experienced a 51 percent remission rate, compared to 33 percent on only escitalopram.

Not only do these SSRI antidepressant drugs promote higher levels of retention of the “feel good” neurotransmitters serotonin and dopamine, they trigger an immune response that blocks inflammatory molecules called cytokines.

“The magnitude of the effect was really thrilling,” Trivedi says. “The bottom line in depression is we have not had objective tests that help us with any component of diagnosis or treatment matching—and this is a very solid first step.”

His next step will be to do a clinical trial in which researchers will go to primary care practices and randomize patients, so that half of the participants will get “the best care the provider is willing to do,” he says, and the other half will do the blood test and then get matched with one of the two drug approaches. “We want to show that if you have the treatment matching based on the blood tests, that group of patients will have significantly better outcomes than those who do usual care.”

He hopes that other studies will use the CRP test with other antidepressant drugs, as well. “It’s not a perfect solution for 100 percent of patients, but it helps.”

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Scientists Identify Cells in the Brain That Control Anxiety
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People plagued with the uncomfortable thoughts and sensations characteristic of anxiety disorders may have a small group of cells in the brain to blame, according to a new study. As NPR reports, a team of researchers has identified a class of brain cells that regulates anxiety levels in mice.

The paper, published in the journal Neuron, is based on experiments conducted on a group of lab mice. As is the case with human brains, the hippocampus in mouse brains is associated with fear and anxiety. But until now, researchers didn't know which neurons in the hippocampus were responsible for feelings of worry and impending danger.

To pinpoint the cells at work, scientists from Columbia University, the University of California, San Francisco, and other institutions placed mice in a maze with routes leading to open areas. Mice tend to feel anxious in spacious environments, so researchers monitored activity in the hippocampus when they entered these parts of the maze. What the researchers saw was a specialized group of cells lighting up when the mice entered spaces meant to provoke anxiety.

To test if anxiety was really the driving factor behind the response, they next used a technique called optogenetics to control these cells. When they lowered the cells' activity, the mice seemed to relax and wanted to explore the maze. But as they powered the cells back up, the mice grew scared and didn't venture too far from where they were.

Anxiety is an evolutionary mechanism everyone experiences from time to time, but for a growing portion of the population, anxiety levels are debilitating. Generalized anxiety disorder, social anxiety disorder, and panic disorder can stem from a combination of factors, but most experts agree that overactive brain chemistry plays a part. Previous studies have connected anxiety disorders to several parts of the brain, including the hippocampus, which governs memory as well as fear and worry.

By uncovering not just how the brain produces symptoms of anxiety but the individual cells behind them, scientists hope to get closer to a better treatment. There's more work to be done before that becomes a possibility. The anxiety cells in mice aren't necessarily a perfect indicator of which cells regulate anxiety in humans, and if a new treatment does eventually come from the discovery, it will be one of many options rather than a cure-all for every patient with the disorder.

[h/t NPR]

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Wilder Penfield: The Pioneering Brain Surgeon Who Operated on Conscious Patients
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Public Domain, Wikimedia Commons

For centuries, epilepsy was a source of mystery to scientists. Seizures were thought to be caused by everything from masturbation to demonic possession, and it wasn’t until the 1930s that a neurosurgeon showed the condition could sometimes be boiled down to specific spots in the brain. To do it, he had to open up patients’ heads and electrocute their brain tissue—while they were still conscious.

Wilder Penfield, the subject of today’s Google Doodle, was born on January 26, 1891 in Spokane, Washington. According to Vox, the Canadian-American doctor revolutionized the way we think about and treat epilepsy when he pioneered the Montreal Procedure. The operation required him to remove portions of the skulls of epilepsy sufferers to access their brains. He believed seizures were connected to small areas of brain tissue that were somehow damaged, and by removing the affected regions he could cure the epilepsy. His theory was based on the fact that people with epilepsy often experience “auras” before a seizure: vivid recollections of random scents, tastes, or thoughts.

To pinpoint the damaged brain tissue, he would have to locate the part of the brain tied to his patient’s aura. This meant that the patient would need to be awake to tell him when he struck upon the right sensation. Penfield stimulated the exposed brain tissue with an electrode, causing the patient to either feel numbness in certain limbs, experience certain smells, or recall certain memories depending on what part of the brain he touched. A local anesthetic reduced pain in the head; shocking the brain didn’t cause any pain because the organ doesn’t contain pain receptors.

During one of his surgeries, a patient famously cried, “I smell burnt toast!” That was the same scent that visited her before each seizure, and after Penfield removed the part of her brain associated with the sensation, her epilepsy went away.

Brain surgery isn’t a cure-all for every type of epilepsy, but treatments similar to the one Penfield developed are still used today. In some cases, as much as half of the brain is removed with positive results.

[h/t Vox]

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