Trilobites: Owls See the World Much Like We Do

Barn owls have simpler brains than primates, but they can process information about things moving in their environment in a similarly complex way.

Even though barn owls have simple brains, a new study suggests they can visually process objects in ways similar to that of animals with more sophisticated perception.CreditJean-Christophe Verhaegen/Agence France-Presse — Getty Images

Owl eyes are round, but not spherical. These immobile, tubular structures sit on the front of an owl’s face like a pair of built-in binoculars. They allow the birds to focus in on prey and see in three dimensions, kind of like humans — except we don’t have to turn our whole heads to spot a slice of pizza beside us.

Although owls and humans both have binocular vision, it has been unclear whether these birds of prey process information they collect from their environments like humans, because their brains aren’t as complex. But in a study published in the Journal of Neuroscience on Monday, scientists tested the ability of barn owls to find a moving target among various shifting backgrounds, a visual processing task earlier tested only in primates.

The research suggests that barn owls, with far simpler brains than humans and other primates, also group together different elements as they move in the same direction, to make sense of the world around them.

“Humans are not so different from birds as you may think,” said Yoram Gutfreund, a neuroscientist at Technion Israel Institute of Technology who led the study with colleagues from his university and RWTH Aachen University in Germany.

The owls were able to spot the target. They were better at finding it when the contrasting dot direction was uniform rather than scattered. Even though the elements were all black dots, the direction they were moving made a big difference in the owl’s perception of the world — and how its brain responded.

The researchers also recorded activity from the ocular tectum, a brain area involved in basic visual processing in owls and many other vertebrates. They found that it activated more or less depending on the movement of the dots, suggesting it was responsible for performing this seemingly complex task.

“What we find is considered higher level processing in an area that is not traditionally considered a higher level area,” Dr. Gutfreund said. He thinks this ability was conserved through evolution in a similar part of the human brain called the superior colliculus, which helps direct attention among other functions.

The researchers found that an owl’s ocular tectum, a brain area involved in basic visual processing in vertebrates, activated according to the movement of dots in the experiment.CreditRonaldo Schemidt/Agence France-Presse — Getty Images

But how the ability evolved, or how it may play out differently in birds and mammals is still a mystery, Dr. Gutfreund said. For now, they want to determine the path traveled through the owl’s brain by these movement-grouping signals.

“It’s not so easy to do these experiments,” said Dr. Gutfreund, but he believes this motion grouping ability is widespread in the animal kingdom. “I think that the visual system basically evolved to identify targets for behavior. This is why we have the brain.”

Mind: Antidepressants and Withdrawal: Readers Tell Their Stories

Readers in my age group and older (I’m 58) often came of age in an era in which depression was considered somehow a lapse in character. These readers typically reported having started on Prozac or one of its early competitors — Paxil, Zoloft — very often after a major setback like divorce, or the loss of a job, spouse or child.

“My G.P. put me on Zoloft 28 years ago to deal with my husband’s cancer diagnosis,” wrote Carole Wilson, 74, of Alburnett, Iowa. Her husband has since died. “I have cut down from 200 milligrams to 100, but when I go lower I get horrible side effects, like nausea, jumpiness, crying a lot which I never do. I’m nearly 75; at this point I will continue because I cannot go through the withdrawal.”

James Midkiff, 75, of Vienna, W.V., wrote: “I was sole caretaker for my dying wife and was a law enforcement officer and under a great deal of stress.” Mr. Midkiff said he tapered off Lexapro gradually, about a month ago, “but I am having withdrawal symptoms of shaking, panic attacks, flulike symptoms, nausea, fatigue, night sweats, tingling and numbness in the arms and legs. I am determined to get off antidepressant drugs; however it is disheartening to note that other folks are still having withdrawal symptoms after a year.”

Hundreds of others, in their 60s and 70s, told us similar stories about starting a prescription in the wake of terrible loss. The drugs helped ease the emotional turmoil initially, many said.

Their reasons for wanting to stop taking them were rooted in part in the understanding that antidepressants were supposed to be a short-term solution, a bridge over troubled waters. But by the mid-1990s, drug makers had convinced government regulators that when taken long-term, the medications sharply reduced the risk of relapse in people with chronic, recurrent depression.

Thus began the era of indefinite or open-ended prescribing, and not just for the most severe cases of depression. The change in practice roughly coincided with the promotion of the “chemical imbalance” theory of depression: Marketers and some researchers implied that antidepressants corrected deficits in brain levels of serotonin, a neurotransmitter.

In truth, the theory has scant basis. No one knows the underlying biology of depression or any mood disorder. But that shift — along with a change in federal regulations, in 1997, allowing drug makers to advertise directly to consumers — helped undermine the stigma associated with depression and mood disorders generally.

Depression, anxiety and bipolar disorder came out of the closet, if gingerly, and the generation that came of age during this time — people now in their 40s, give or take — did so in a culture that no longer automatically presumed that depression was a character flaw.

The condition had some biological basis, it was felt, and antidepressants became a vastly popular option. Everyone knew someone taking them. Long-term prescription rates surged.


Robin Hempel began taking an antidepressant on the advice of her gynecologist. “Had I been told the risks of trying to come off this drug, I never would have started it,” she said.

Cheryl Senter for The New York Times

In their responses to us, many readers in this age group were much more likely than older readers to cite specific psychiatric diagnoses: social anxiety, panic disorder, PTSD, as well as depression. And their decisions to taper off were less tied to the presumption that the drugs are short-term bridges; most cited practical concerns like lingering side effects (sexual dysfunction is common, as is weight gain), pregnancy or the passing of postpartum despair.

“When I became pregnant I chose to stop taking Effexor because I was uncomfortable using it during pregnancy,” wrote Katie Slattery, 39, of Orlando, Fla. “When I stopped cold turkey, I felt extremely unwell and had to go back on and wean off slowly. I would break open my pill capsules and reduce my dose by one milligram at a time every couple of days. It was a lengthier process, but it prevented the dizziness, headache and fogginess I felt when I originally stopped the medication.”

Amy Cannon, 42, of Philadelphia wrote: “I started taking Zoloft after experiencing moderate postpartum depression, and after about a year I felt my symptoms weren’t as severe.” But she had “brain zaps” — electric-shock sensations in her head — and mood swings after trying to quit cold turkey, so she resumed taking the drug.

“Eventually I was able to wean down slowly without severe consequences, but it took six months and was still really unpleasant.” Nonetheless, she said that she was very grateful that the drugs were available when she needed them.

Women taking antidepressants who become pregnant, or are planning to, often prefer not to expose the developing fetus to any prescriptions. The evidence that exposure in utero causes problems for a child is fairly weak.

And untreated depression poses risks indeed, both before birth and after, when the child needs an energetic, vigilant caregiver.

As the stigma associated with mood disorders faded, so too did the social barriers to taking a daily prescription. By 2000, when doctors began prescribing antidepressants to children, prevailing views were vastly different from those of the first Prozac generation.

Nearly 1,000 young people in their 20s or younger responded the The Times’s invitation. They did not come of age during the rise of long-term use — their parents did, and often it was their parents who decided the medications could help them.

Many told us they were too young to know what the drugs were at the time, and didn’t learn until much later. As they enter high school and college, their understanding of the prescription culture is far different from that of generations before.

For one thing, many of their friends have been on antidepressants or other psychiatric medications for long periods. “I live in a college house of six girls, two of whom are on antidepressants,” wrote Julian O., 21, of Seattle.

“When brought up in conversation, the medications are discussed with vanity, as if they are veterans trying out the newest medication prescribed to them.”

Emma Dreyfus, 28, of Boston, said the “one mistake her parents had made” was putting her on Paxil at age 10 to treat anxiety. She weaned herself off slowly at age 23.

“I don’t blame them, but I wish we’d all understood the long-term effects.” She said she is starting graduate work in the fall, in social work, to help others facing similar challenges.

Others in this youngest cohort wondered about the effect of the medications on brain development; the drugs cause biological adjustments in the brain, but so do persistent mood problems.

For now, no one has good answers for them. The drugs are a brand new cultural development, historically speaking, and their diffuse biological effects — especially in the developing brain — are largely unknown.

Whatever their ages, all of us are part of Generation Rx — a huge, uncontrolled experiment with little precedent and few guideposts.

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For Many Strokes, There’s an Effective Treatment. Why Aren’t Some Doctors Offering It?

It’s a perspective with real-world consequences. Close to 700,000 patients have strokes caused by blood clots each year and could be helped by T.P.A. Yet up to 30 percent of stroke victims who arrive at hospitals on time and are perfect candidates for the clot-buster do not receive it.

The result: paralysis and muscle weakness; impaired cognition, speech or vision; emotional and behavioral dysfunction; and many other permanent neurological injuries.

Stroke treatment guidelines issued by the American Heart Association and the American Stroke Association strongly endorse T.P.A. for patients after they’ve been properly evaluated. But treatment must start within three hours (in some cases, four-and-a-half hours) of the stroke’s onset, and the sooner, the better.

A number of medical societies also endorse the treatment as highly effective in reducing disability. The drug can cause or exacerbate cerebral hemorrhage, or bleeding in the brain — a real risk. But in most stroke patients it prevents brain injury, and in any event, rates of cerebral hemorrhage have declined as doctors have gained experience over the years.

Without treatment, “many patients end up permanently disabled,” said Dr. Gregg C. Fonarow, a cardiologist at the University of California, Los Angeles. “The stroke neurologists who are involved in chronic care see the devastating consequences.”

“For some reason, the emergency medicine doctors are not factoring this in,” he added.

While the vocal disbelievers are a minority, it is increasingly easy for them to spread their message on social media, said Dr. Edward C. Jauch, a professor of neurosciences at the Medical University of South Carolina.

“The way information and opinion is now communicated to the younger generation of physicians is much more through web and social media and less through peer review journals, journal clubs or live debates,” Dr. Jauch said.

Dr. Charles R. Wira III, a professor of emergency medicine at Yale, said that when he talked to residents about T.P.A., they often start citing blogs and podcasts “as the divine word for why T.P.A. is harmful,” he said. “They have not read the articles or practice guidelines.”

Skepticism has spread around the world, Dr. Jauch said, and he has come to expect naysayers wherever he goes. In Saudi Arabia, where he was lecturing at a conference, a Saudi doctor said over dinner that he simply did not believe in T.P.A.

A leader of the skeptical contingent, Dr. Jerome Hoffman, an emergency medicine specialist and emeritus professor at U.C.L.A., believes that while the initial trial and a second one were positive, both were flawed.

He reviewed the raw data from the federal study and concluded that more patients who got T.P.A. had the least severe type of stroke and fewer had the most severe type. The treatment and control groups were dissimilar — that is, those getting T.P.A. were less badly affected from the start. Experts disagree with this analysis.


A CT scan of a stroke patient. The brain tissue that died from reduced blood flow is in red.

Zephyr/Science Source

And 11 other studies did not show a benefit, Dr. Hoffman claims. But supporters note that those studies were meant to investigate whether T.P.A. might help patients with more severe strokes or those outside the recommended window of time.

The failure of those efforts, they say, does not mean T.P.A. cannot help patients like those in the original clinical trials.

A charismatic, riveting speaker, Dr. Hoffman has given educational courses across the country and sold informational tapes expounding his theory. And his influence has spread.

At U.C.L.A., he said in an interview, he has spoken to stroke patients and their families even as their medical teams headed into the emergency room. He has told the patients that although the stroke team would strongly recommend T.P.A., there actually was debate over whether the treatment benefits patients in the long term.

In addition, no study suggested that a clot-buster was lifesaving, he told them, and it may cause bleeding in the brain in a small number of patients.

“In my experience, almost no one — after hearing a neutral version and then a positive version — chose T.P.A.,” Dr. Hoffman said.

Dr. Hoffman said he has debated renowned neurologists about the benefits of T.P.A. at several meetings. Afterward, audiences voted overwhelmingly against the drug.

“This is not a testament to any debating skill of mine, but reflects how people react when they are shown the actual evidence,” he said.

At Sierra Vista Regional Medical Center in San Luis Obispo, Calif., Dr. Scott Bisheff, an emergency medical physician, tells patients there is great uncertainty about whether T.P.A. helps or harms. If it caused bleeding in a patient’s brain, the consequences could be catastrophic.

About half of his stroke patients decline the treatment, Dr. Bisheff said.

For neurologists, the worst scenario by far is the patient who is never even asked if he or she wants the clot-buster. At Yale, Dr. Wira said, patients sometimes are transferred from community hospitals where they have not received T.P.A. Usually, it’s far too late to try.

Dr. Wira and other staff do not tell the family about the missed opportunity. “We try not to raise issues that may lead to litigation,” he said.

But sometimes family members cannot help knowing what went on. It happened to Dr. Lewandowski.

About a decade ago, Dr. Lewandowski was at work when he got a call that his father had had a stroke — his right side was paralyzed. But his father had gotten to the hospital within 45 minutes, well inside the window to receive T.P.A.

Dr. Lewandowski told his mother to make the family’s wishes very clear. They wanted the emergency room doctor to give the clot-buster to his dad. The doctor refused.

“He told my mom that he doesn’t believe in the drug and he is not giving it. He doesn’t care who I am,” Dr. Lewandowski said.

“I got in my car and drove 400 miles to the hospital,” he recalled. But by the time he got there, it was too late. The treatment window had closed.

His father had a facial droop and slurred speech. His right arm and right leg flopped about uselessly. His stroke scale was 7, moderately disabling, but he survived for a few more years.

“It was very difficult for me personally,” Dr. Lewandowski recalled. “I had spent so much of my professional life working on this treatment. It actually worked.”

“I felt like I had let my dad down.”

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Sketch Guy: Resistance Is Futile. To Change Habits, Try Replacement Instead.


Carl Richards

Let’s play a little game. Clear your mind. Go ahead, clear it.

O.K., now, as soon as you finish reading this sentence, try not to picture a white bear.


O.K., let’s try again. On the count of three. One … two …

White bear! Dang it!

If you’re having trouble with this, don’t worry. You’re not alone. The harder people try not to think of something, the more they end up thinking about it. Ironic, no?

It turns out this experience has a name. It’s called the ironic process theory, and it almost guarantees that your efforts to change bad habits by resisting those habits will fail. Research shows that “thought suppression has counterproductive effects on behaviors.” If you’ve ever desperately told yourself not to scratch that mosquito bite or buy another cactus on Amazon, I’m sure this comes as no surprise.

This inconvenient little bit of neuroscience has bothered me ever since I came across a famous Carl Jung quote: “What you resist not only persists but will grow in size.” If resisting a behavior I want to change is not only ineffective but harmful, then what should I do instead?

One trick is to pull a little bait and switch on your own brain. It goes like this: When the urge comes to do the counterproductive thing, don’t resist. Instead, replace.

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