Poverty's most insidious damage is to a child's brain

An alarming 22 percent of U.S. children live in poverty, which can have long-lasting negative consequences on brain development, emotional health and academic achievement. Now, even more compelling evidence has been provided suggesting that growing up in poverty has detrimental effects on the brain.

Low-income children have irregular brain development and lower standardized test scores, with as much as an estimated 20 percent gap in achievement explained by developmental lags in the frontal and temporal lobes of the brain.

Credit: © Phils Photography / Fotolia

An alarming 22 percent of U.S. children live in poverty, which can have long-lasting negative consequences on brain development, emotional health and academic achievement. A new study, published July 20 in JAMA Pediatrics, provides even more compelling evidence that growing up in poverty has detrimental effects on the brain.

In an accompanying editorial, child psychiatrist Joan L. Luby, MD, at Washington University School of Medicine in St. Louis, writes that "early childhood interventions to support a nurturing environment for these children must now become our top public health priority for the good of all."

In her own research in young children living in poverty, Luby and her colleagues have identified changes in the brain's architecture that can lead to lifelong problems with depression, learning difficulties and limitations in the ability to cope with stress.

However, her work also shows that parents who are nurturing can offset some of the negative effects on brain anatomy seen in poor children. The findings suggest that teaching nurturing skills to parents -- particularly those who live below the poverty line -- may provide a lifetime of benefit for children.

"Our research has shown that the effects of poverty on the developing brain, particularly in the hippocampus, are strongly influenced by parenting and life stresses experienced by the children," said Luby, the Samuel and Mae S. Ludwig Professor of Child Psychiatry and director of Washington University's Early Emotional Development Program.

The study in JAMA Pediatrics, by a team of researchers at the University of Wisconsin-Madison, found that low-income children had irregular brain development and lower standardized test scores, with as much as an estimated 20 percent gap in achievement explained by developmental lags in the frontal and temporal lobes of the brain.

"In developmental science and medicine, it is not often that the cause and solution of a public health problem become so clearly elucidated," Luby wrote in the editorial. "It is even less common that feasible and cost-effective solutions to such problems are discovered and within reach."

Based on this new research and what already is known about the damaging effects of poverty on brain development in children, as well as the benefits of nurturing during early childhood, "we have a rare roadmap to preserving and supporting our society's most important legacy, the developing brain," Luby writes. "This unassailable body of evidence taken as a whole is now actionable for public policy."

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The above post is reprinted from materials provided by Washington University in St. Louis

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Study Questions Statin, Memory Loss Connection

Statin and nonstatin use both associated with increased complaints of memory loss

Beginning treatment with a statin was associated with a nearly fourfold increased risk of developing acute memory loss within 30 days in a retrospective cohort study, but a similar increase in risk was seen in patients starting non-statin lipid-lowering drugs.

Compared with non-users, both statin and non-statin lipid-lowering drug (LLD) use was found to be associated with acute memory loss in the weeks following treatment initiation, but there was no difference in memory loss when statins and non-statins were compared with each other, researcher Brian L. Strom, MD, of Rutgers University in Newark, N.J., and colleagues wrote online June 8 in JAMA Internal Medicine.

The observation that all LLDs were associated with memory loss suggests that either all drugs used to lower lipid levels cause acute memory loss or that the observed memory loss in the study was due to detection bias, Strom said.

In a telephone interview with MedPage Today, Strom said it makes sense that patients on a new drug would be more likely to notice symptoms and attribute them to the drug, and they are also more likely to report such symptoms to their physician.

"Patients might report a memory loss to me that they would otherwise pay little attention to because I am seeing them more often and I ask them about it," he said.

Earlier Statin, Memory Studies Mixed

Several previous studies have shown acute memory loss associated with the use of statins, but others have not shown the association or have even shown improved memory in long-term statin users compared with non-users.

Strom noted that without the non-statin LLD control group in his study, the findings would have shown a strong association between statin initiation and short-term memory loss.

"In the absence of this control group, the finding would have been completely misleading," he said.

The study included data obtained between early 1987 through late 2013 from The Health Improvement Network (THIN), which is a comprehensive database of medical records from general practitioners in the U.K. Patients were excluded from the analysis if they had a diagnosis of Alzheimer's disease or dementia, if they had received medications used for dementia, or if they had other conditions affecting cognition, such as Parkinson's disease, Huntington's disease, or vascular dementia.

The analysis compared 482,543 statin users with 482,543 matched non-users of any lipid-lowering drug (control group 1) and with 26,484 users of non-statin LLDs, such as cholestyramine, colestipol hydrochloride, colesevelam, clofibrate, gemfibrozil, and niacin (control group 2).

A secondary case-crossover analysis was performed that included 68,028 patients with incident acute memory loss whose exposure to statins was evaluated during the period immediately before the outcome versus three earlier periods (31 to 60 days prior, 150 to 180 days prior, and 270 to 300 days prior).

Non-statin LLD Users Had 3.6-Fold Risk Increase

The analysis revealed that:

• When compared with matched non-users of any LLDs, there was a strong association between first exposure to statins and acute memory loss within 30 days immediately following exposure (fully adjusted odds ratio 4.40, 95% CI 3.01-6.41).
• The association was not seen in the comparison of statin versus non-statin LLDs (fully adjusted OR 1.03, 95% CI 0.63-1.66).
• The association was seen in the first 30 days following exposure in non-statin LLD users compared with matched non-user controls (adjusted OR 3.60, 95% CI 1.34-9.70).
• Both atorvastatin and simvastatin showed an increased OR within the first 30 days after exposure compared with non-users (adjusted OR 2.40, 95% CI 1.42-4.04 and 3.53, 95% CI 2.79 -4.48, respectively).
• The case-crossover analysis showed a weak negative association, which was not found to be clinically meaningful.

A potential study limitation cited by the researchers involved a substantial difference in baseline characteristics between users of statins and users of non-statin LLDs, and differences among users of the various statin drugs.

"Bias from confounding by indication is the most serious potential problem in this study, even though we attempted to control for indication variables and a large number of other underlying conditions," the researchers wrote.

The case-crossover analysis was conducted to address this issue because each patient served as his or her own control.

Statin, Memory Issue 'Tempest in Teapot'

The researchers also noted that potential confounding could exist for variables not recorded in the medical records database.

Strom said the study findings should reassure both patients and physicians who prescribe statins.

"This whole issue of short-term memory loss with statins is really a tempest in a teapot," he said. "Statins are very effective drugs, and people should not veer away from them for fear of a short-term memory effect, especially given the data suggesting that long-term statin use improves memory."

The research was funded by the National Institutes of Health.

Strom reported receiving research funding from AstraZeneca and Bristol-Myers Squibb and serving as a consultant to Abbott, AstraZeneca, Bayer Healthcare, Bristol-Myers Squibb, Novartis and Pfizer. A co-author reported receiving research funding from AstraZeneca and Bristol-Myers Squibb and serving as a consultant to AstraZeneca, Bayer Healthcare, Bristol-Myers Squibb, and Merck.

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Emotional brains 'physically different' from rational ones

Researchers have found physical differences in the brains of people who respond emotionally to others' feelings, compared to those who respond more rationally.

Illustration. Rationally-based brains are physically different from emotionally-based brains, according to new research.

Credit: © olly / Fotolia

Researchers at Monash University have found physical differences in the brains of people who respond emotionally to others' feelings, compared to those who respond more rationally, in a study published in the journal NeuroImage.

The work, led by Robert Eres from the University's School of Psychological Sciences, pinpointed correlations between grey matter density and cognitive and affective empathy. The study looked at whether people who have more brain cells in certain areas of the brain are better at different types of empathy.

"People who are high on affective empathy are often those who get quite fearful when watching a scary movie, or start crying during a sad scene. Those who have high cognitive empathy are those who are more rational, for example a clinical psychologist counselling a client," Mr Eres said.

The researchers used voxel-based morphometry (VBM) to examine the extent to which grey matter density in 176 participants predicted their scores on tests that rated their levels for cognitive empathy compared to affective -- or emotional -- empathy.

The results showed that people with high scores for affective empathy had greater grey matter density in the insula, a region found right in the 'middle' of the brain. Those who scored higher for cognitive empathy had greater density in the midcingulate cortex -- an area above the corpus callosum, which connects the two hemispheres of the brain.

"Taken together, these results provide validation for empathy being a multi-component construct, suggesting that affective and cognitive empathy are differentially represented in brain morphometry as well as providing convergent evidence for empathy being represented by different neural and structural correlates," the study said.

The findings raise further questions about whether some kinds of empathy could be increased through training, or whether people can lose their capacity for empathy if they don't use it enough.

"Every day people use empathy with, and without, their knowledge to navigate the social world," said Mr Eres.

"We use it for communication, to build relationships, and consolidate our understanding of others."

However, the discovery also raises new questions -- like whether people could train themselves to be more empathic, and would those areas of the brain become larger if they did, or whether we can lose our ability to empathise if we don't use it enough.

"In the future we want to investigate causation by testing whether training people on empathy related tasks can lead to changes in these brain structures and investigate if damage to these brain structures, as a result of a stroke for example, can lead to empathy impairments," said Mr Eres.

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The above post is reprinted from materials provided by Monash University.

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Missing link found between brain, immune system; major disease implications

In a stunning discovery that overturns decades of textbook teaching, researchers have determined that the brain is directly connected to the immune system by vessels previously thought not to exist. The discovery could have profound implications for diseases from autism to Alzheimer's to multiple sclerosis.

Maps of the lymphatic system: old (left) and updated to reflect UVA's discovery.

Credit: University of Virginia Health System

In a stunning discovery that overturns decades of textbook teaching, researchers at the University of Virginia School of Medicine have determined that the brain is directly connected to the immune system by vessels previously thought not to exist. That such vessels could have escaped detection when the lymphatic system has been so thoroughly mapped throughout the body is surprising on its own, but the true significance of the discovery lies in the effects it could have on the study and treatment of neurological diseases ranging from autism to Alzheimer's disease to multiple sclerosis.

"Instead of asking, 'How do we study the immune response of the brain?' 'Why do multiple sclerosis patients have the immune attacks?' now we can approach this mechanistically. Because the brain is like every other tissue connected to the peripheral immune system through meningeal lymphatic vessels," said Jonathan Kipnis, PhD, professor in the UVA Department of Neuroscience and director of UVA's Center for Brain Immunology and Glia (BIG). "It changes entirely the way we perceive the neuro-immune interaction. We always perceived it before as something esoteric that can't be studied. But now we can ask mechanistic questions."

"We believe that for every neurological disease that has an immune component to it, these vessels may play a major role," Kipnis said. "Hard to imagine that these vessels would not be involved in a [neurological] disease with an immune component."

New Discovery in Human Body

Kevin Lee, PhD, chairman of the UVA Department of Neuroscience, described his reaction to the discovery by Kipnis' lab: "The first time these guys showed me the basic result, I just said one sentence: 'They'll have to change the textbooks.' There has never been a lymphatic system for the central nervous system, and it was very clear from that first singular observation -- and they've done many studies since then to bolster the finding -- that it will fundamentally change the way people look at the central nervous system's relationship with the immune system."

Even Kipnis was skeptical initially. "I really did not believe there are structures in the body that we are not aware of. I thought the body was mapped," he said. "I thought that these discoveries ended somewhere around the middle of the last century. But apparently they have not."

'Very Well Hidden'

The discovery was made possible by the work of Antoine Louveau, PhD, a postdoctoral fellow in Kipnis' lab. The vessels were detected after Louveau developed a method to mount a mouse's meninges -- the membranes covering the brain -- on a single slide so that they could be examined as a whole. "It was fairly easy, actually," he said. "There was one trick: We fixed the meninges within the skullcap, so that the tissue is secured in its physiological condition, and then we dissected it. If we had done it the other way around, it wouldn't have worked."

After noticing vessel-like patterns in the distribution of immune cells on his slides, he tested for lymphatic vessels and there they were. The impossible existed. The soft-spoken Louveau recalled the moment: "I called Jony [Kipnis] to the microscope and I said, 'I think we have something.'"

As to how the brain's lymphatic vessels managed to escape notice all this time, Kipnis described them as "very well hidden" and noted that they follow a major blood vessel down into the sinuses, an area difficult to image. "It's so close to the blood vessel, you just miss it," he said. "If you don't know what you're after, you just miss it."

"Live imaging of these vessels was crucial to demonstrate their function, and it would not be possible without collaboration with Tajie Harris," Kipnis noted. Harris, a PhD, is an assistant professor of neuroscience and a member of the BIG center. Kipnis also saluted the "phenomenal" surgical skills of Igor Smirnov, a research associate in the Kipnis lab whose work was critical to the imaging success of the study.

Alzheimer's, Autism, MS and Beyond

The unexpected presence of the lymphatic vessels raises a tremendous number of questions that now need answers, both about the workings of the brain and the diseases that plague it. For example, take Alzheimer's disease. "In Alzheimer's, there are accumulations of big protein chunks in the brain," Kipnis said. "We think they may be accumulating in the brain because they're not being efficiently removed by these vessels." He noted that the vessels look different with age, so the role they play in aging is another avenue to explore. And there's an enormous array of other neurological diseases, from autism to multiple sclerosis, that must be reconsidered in light of the presence of something science insisted did not exist.

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The above post is reprinted from materials provided by University of Virginia Health System. Note: Materials may be edited for content and length.

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Journal Reference:

1. Antoine Louveau, Igor Smirnov, Timothy J. Keyes, Jacob D. Eccles, Sherin J. Rouhani, J. David Peske, Noel C. Derecki, David Castle, James W. Mandell, Kevin S. Lee, Tajie H. Harris, Jonathan Kipnis. Structural and functional features of central nervous system lymphatic vessels. Nature, 2015; DOI: 10.1038/nature14432

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Missing link found between brain, immune system; major disease implications

In a stunning discovery that overturns decades of textbook teaching, researchers have determined that the brain is directly connected to the immune system by vessels previously thought not to exist. The discovery could have profound implications for diseases from autism to Alzheimer's to multiple sclerosis.

Maps of the lymphatic system: old (left) and updated to reflect UVA's discovery.

Credit: University of Virginia Health System

In a stunning discovery that overturns decades of textbook teaching, researchers at the University of Virginia School of Medicine have determined that the brain is directly connected to the immune system by vessels previously thought not to exist. That such vessels could have escaped detection when the lymphatic system has been so thoroughly mapped throughout the body is surprising on its own, but the true significance of the discovery lies in the effects it could have on the study and treatment of neurological diseases ranging from autism to Alzheimer's disease to multiple sclerosis.

"Instead of asking, 'How do we study the immune response of the brain?' 'Why do multiple sclerosis patients have the immune attacks?' now we can approach this mechanistically. Because the brain is like every other tissue connected to the peripheral immune system through meningeal lymphatic vessels," said Jonathan Kipnis, PhD, professor in the UVA Department of Neuroscience and director of UVA's Center for Brain Immunology and Glia (BIG). "It changes entirely the way we perceive the neuro-immune interaction. We always perceived it before as something esoteric that can't be studied. But now we can ask mechanistic questions."

"We believe that for every neurological disease that has an immune component to it, these vessels may play a major role," Kipnis said. "Hard to imagine that these vessels would not be involved in a [neurological] disease with an immune component."

New Discovery in Human Body

Kevin Lee, PhD, chairman of the UVA Department of Neuroscience, described his reaction to the discovery by Kipnis' lab: "The first time these guys showed me the basic result, I just said one sentence: 'They'll have to change the textbooks.' There has never been a lymphatic system for the central nervous system, and it was very clear from that first singular observation -- and they've done many studies since then to bolster the finding -- that it will fundamentally change the way people look at the central nervous system's relationship with the immune system."

Even Kipnis was skeptical initially. "I really did not believe there are structures in the body that we are not aware of. I thought the body was mapped," he said. "I thought that these discoveries ended somewhere around the middle of the last century. But apparently they have not."

'Very Well Hidden'

The discovery was made possible by the work of Antoine Louveau, PhD, a postdoctoral fellow in Kipnis' lab. The vessels were detected after Louveau developed a method to mount a mouse's meninges -- the membranes covering the brain -- on a single slide so that they could be examined as a whole. "It was fairly easy, actually," he said. "There was one trick: We fixed the meninges within the skullcap, so that the tissue is secured in its physiological condition, and then we dissected it. If we had done it the other way around, it wouldn't have worked."

After noticing vessel-like patterns in the distribution of immune cells on his slides, he tested for lymphatic vessels and there they were. The impossible existed. The soft-spoken Louveau recalled the moment: "I called Jony [Kipnis] to the microscope and I said, 'I think we have something.'"

As to how the brain's lymphatic vessels managed to escape notice all this time, Kipnis described them as "very well hidden" and noted that they follow a major blood vessel down into the sinuses, an area difficult to image. "It's so close to the blood vessel, you just miss it," he said. "If you don't know what you're after, you just miss it."

"Live imaging of these vessels was crucial to demonstrate their function, and it would not be possible without collaboration with Tajie Harris," Kipnis noted. Harris, a PhD, is an assistant professor of neuroscience and a member of the BIG center. Kipnis also saluted the "phenomenal" surgical skills of Igor Smirnov, a research associate in the Kipnis lab whose work was critical to the imaging success of the study.

Alzheimer's, Autism, MS and Beyond

The unexpected presence of the lymphatic vessels raises a tremendous number of questions that now need answers, both about the workings of the brain and the diseases that plague it. For example, take Alzheimer's disease. "In Alzheimer's, there are accumulations of big protein chunks in the brain," Kipnis said. "We think they may be accumulating in the brain because they're not being efficiently removed by these vessels." He noted that the vessels look different with age, so the role they play in aging is another avenue to explore. And there's an enormous array of other neurological diseases, from autism to multiple sclerosis, that must be reconsidered in light of the presence of something science insisted did not exist.

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The above story is based on materials provided by University of Virginia Health System. Note: Materials may be edited for content and length.

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Surgical anesthesia in young children linked to effects on IQ, brain structure

Children who received general anesthesia for surgery before age 4 had diminished language comprehension, lower IQ and decreased gray matter density in posterior regions of their brain, according to a new study. The authors of the study recommend additional studies to determine anesthesia's precise molecular effects on the brain and contribution to diminished brain function and composition.

Young children who received general anesthesia for surgery had diminished language comprehension, lower IQ and decreased gray matter density in posterior regions of their brain, according to a new study. (stock image)

Credit: © garagundi / Fotolia

Children who received general anesthesia for surgery before age 4 had diminished language comprehension, lower IQ and decreased gray matter density in posterior regions of their brain, according to a new study in the journal Pediatrics.

Researchers from Cincinnati Children's Hospital Medical Center report their findings in the journal's June 8 online edition. The authors recommend additional studies to determine anesthesia's precise molecular effects on the brain and contribution to diminished brain function and composition. Researchers say this knowledge could make it possible to develop mitigating strategies for what the authors describe as a potential dilemma for child health.

"The ultimate goal of our laboratory and clinical research is to improve safety and outcomes in young children who have no choice but to undergo surgery with anesthesia to treat their serious health concerns," said Andreas Loepke, MD, PhD, FAAP, lead study author and an anesthesiologist in the Department of Anesthesiology at Cincinnati Children's. "We also have to better understand to what extent anesthetics and other factors contribute to learning abnormalities in children before making drastic changes to our current practice, which by all measures has become very safe."

Loepke and his research colleagues have published previous studies showing widespread cell death, permanent deletion of neurons and neurocognitive impairment in laboratory rats and mice after exposure to general anesthesia. Those studies have raised concerns about similar effects in young children during a particularly sensitive neurodevelopmental period in early life, which researchers say could interfere with the refinement of neuronal networks and lead to long-term functional abnormalities.

For their current retrospective study, the authors compared the scores of 53 healthy participants of a language development study (ages 5 to 18 years with no history of surgery) with the scores of 53 children in the same age range who had undergone surgery before the age of 4.

The authors stress that average test scores for all 106 children in the study were within population norms, regardless of surgical history. Still, compared with children who had not undergone surgery, children exposed to anesthesia scored significantly lower in listening comprehension and performance IQ. Researchers also report that decreased language and IQ scores were associated with lower gray matter density in the occipital cortex and cerebellum of the brain.

Researchers, who used extensive analysis of surgical and other medical records, said the children were matched for age, gender, handedness and socioeconomic status -- all confounding factors of cognition and brain structure. The authors also factored into their calculations the types of surgeries and length of exposure to anesthetics. The anesthetics used during the surgeries included common agents such as sevoflurane, isoflurane or halothane (used alone or in combination) and nitrous oxide.

Children included in the study did not have a history of neurologic or psychological illness, head trauma or any other associated conditions. Neurocognitive assessments included the Oral and Written Language Scales and the Wechsler Intelligence Scale. Brain structural comparisons were conducted by MRI scans.

Estimated Social Cost

Extending their study a step beyond the medical data, the research team also considered the potential societal impact of their findings. Earlier research from 2008 had estimated the loss of 1 IQ point to decrease a person's lifetime earnings potential by $18,000. Factoring in the potential loss of 5 or 6 IQ points found in their current study, the researchers report that, based on the estimated 6 million children who undergo surgery in the United States each year the lifetime potential earnings loss could total $540 billion.

Emphasis on Safety

Although data in the current study highlight the need to look for improved methods of administering anesthesia, Loepke and his colleagues emphasize that current methods are very safe. Loepke advises parents who are concerned to discuss with their pediatrician and surgeon the risks of a surgical procedure -- and the potential risk of anesthetic exposure -- versus the risks of not having a surgery.

"It is important to note that no surgeries are truly elective in young children," Loepke said. "Many surgical procedures early in life treat life-threatening conditions, avert serious health complications, or improve quality of life. These cannot be easily postponed or avoided."

Loepke also stressed that researchers at Cincinnati Children's are actively looking for alternative anesthetic techniques in their ongoing laboratory studies. Drugs are being tested that show potential for lessening the harmful effects of anesthetics in laboratory rats and mice, and this research is ongoing. Additionally, the medical center is participating in an international clinical trial to test an alternative anesthetic regimen in young children undergoing urological procedures.

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The above story is based on materials provided by Cincinnati Children's Hospital Medical Center. Note: Materials may be edited for content and length.

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Seeing Isn’t Believing

How motion illusions trick the visual system, and what they can teach us about how our eyes and brains evolved.

© ISTOCK.COM/ATYPEEK

Animal vision has not evolved as one might think. In contrast to the invention of photography and film—which began with the first black-and-white daguerreotypes in 1839, then added color in 1861, and finally motion in 1891—motion perception in animals appears to have evolved long before color vision. Indeed, as vision researcher Gordon Walls declared in 1942, perceiving motion is one of the most ancient and primitive forms of vision.

Even the humble housefly, which can only distinguish four to six different colors, is remarkably good at seeing motion. Try to swat a fly with your hand, and it will be gone long before you even get close. (The best way is to clap your hands above it so that it flies up between your hands. Wear gloves.) Oddly, however, while a fly is quick to register these fast movements, it cannot recognize slow movement at all. Move your hand very, very slowly toward a fly, and you can tap its back before it knows that you are there.

As good as animals are at detect­ing motion, they can also be fooled. Seeing the errors that a system makes can help us to understand how that system works nor­mally.

Much of the early research on motion perception was performed on insects,¹ but similar results have been found for a huge range of species, from fishes to birds to mammals. Frogs, which eat insects, respond to small, rapidly moving prey, as well as to overall dimming or darkening that likely signals an approaching predator, but they often ignore stationary objects, perhaps because they cannot see them.²

Mammals are likewise tuned in to motion. Although many people believe that it is the bright red color of the matador’s cape that enrages the bull, the popular TV program Mythbusters found that the color made no difference; it was the motion of the cape’s fabric that mattered. Red, blue, and white capes got equal, half-hearted attacks when they were motionless, but waving the capes elicited an aggressive charge. In fact, most mammals, including domestic and big cats, deer, cattle, and dogs, appear to be color-blind. Apes may have evolved color vision in order to find the ripe fruit among green leaves (see “The Rainbow Connection,” The Scientist, October 2014), but lions eat other mammals, most of which have evolved to match their surroundings, rendering color vision useless in finding prey. When a gazelle runs away, however, it becomes a strong stimulus for the lion’s keen motion vision. It’s no wonder that young deer will often freeze when they sense danger. Correspondingly, prey animals would find color vision of little use, but they are extremely good at seeing the motion of an approaching predator.

UNCOVERING STEALTH: Many animals are camouflaged to match their surroundings. Predator and prey animals thus rely heavily on motion to detect one another. A moving object pops out from the fixed background though a process called motion segmentation. Motion has broken the camouflage.

But as good as animals are at detecting motion, they can also be fooled. I study visual illusions of motion because seeing the errors that a system makes can help us to understand how that system works normally. Visual perception goes far beyond our retinal images, which provide only partial sensory information. We use our knowledge and expectations of the world to fill in the gaps, for instance, when an object is partly hidden. Ambiguous illusions that can be interpreted in two different ways, but not both ways at the same time, can also shed light on how we perceive the world around us.

Illusions of movement

Visual movement can be thought of as a change in brightness, or luminance, over space and time. A white spot that glides across a black screen shows real movement. If the same spot jumps back and forth between two positions, or makes a series of intermittent forward jumps, the brain can still perceive movement. Small, fast jumps give the smoothest impression of movement, but even large, slow jumps give a strong impression that the spot is, in fact, moving across the screen.

MINIMAL MOTION: The static oblique pairs of dots look random, but in fact are a minimum stimulus for seeing motion. Run your finger from left to right across the arrow at the bottom, following your finger with your eyes, and the dots will almost magically segregate and move up and down.

Why does the visual system treat this jumping dot as a single object in motion, instead of seeing one spot disappear while an unrelated spot appears nearby at the same instant? First, the brain usually treats “suspicious coincidences” as being more than coincidences: it is more likely that this is a single spot in motion rather than two separate events. Second, the visual system is tolerant of brief gaps in stimuli, filling in those gaps when necessary. This perception of apparent motion is, of course, the basis of the entire movie and TV industries, as viewers see a smooth motion picture when in reality they are simply watching a series of stationary stills.

We can pose a riddle to the visual system by presenting two apparent motions in opposite directions simultaneously. For example, an image of a white horse and an image of a black horse suddenly exchange positions. But you do not see each horse independently changing in color. Rather, you see the horses jumping from one location to the other. The coincidence is too great, and, instead of two independent events, the visual system economically infers a single event: the jumping horse.

CONTRAST DRIVES MOTION: In both panels, the jumping horses are identical, only the backgrounds differ. In the upper panel, the white horse has higher contrast against the dark background and appears to jump back and forth. In the lower panel, the black horse has higher contrast against the light background and appears to jump.

But which horse jumps? The answer depends on the context. On a dark background, the white horse appears to jump back and forth; on a light background, the black horse appears to move. In other words, the horse with the higher contrast wins. This is because the strength of a motion signal in the brain of the observer is equal to the product of the contrast of each horse against the background color, a measure called motion energy.³ Interestingly, if contrast is held constant, the color of the horses makes no difference because color has little or no input into the motion pathways of the brain.⁴

Contrast can also explain why a black or white object on a background of the opposite color seems to move faster than a gray object on a gray background, and why cars appear to move more slowly in the fog. Indeed, we tend to judge motion not in absolute terms, but relative to the background: the perceived strength and speed of motion depend on the contrast of the moving object against its surroundings.⁵ In fact, a driver partly judges his own speed by the rate at which landmarks such as trees flash past him. In the fog, the trees appear slowed down, so he underestimates the speed of all cars, including his own, with potentially disastrous consequences.⁶

BABY STEPS: Two squares, one dark blue and one light yellow, move smoothly together at constant speed across a grey background. But when the background is changed to black and white vertical stripes, the motion seems to change as well. The little squares appear to hesitate and speed up in alternation, a little like the feet of a walking person (Anstis 2001, 2004: Howe et al. 2006).

Combining movement and changes in contrast results in an even more complex outcome. Suppose that a black spot on a medium-gray background makes a small jump to the right—a total distance much smaller than the diameter of the spot itself—and, at the same time, instantaneously changes to white. Instead of seeing a slight motion to the right, one sees something quite unexpected: the spot appears to move to theleft, toward the starting position and opposite to the physical displacement.

MOTION IN CONTEXT: A yellow bug and a red bug both fly around in perfect clockwise circles of the same size, though the red bug moves much more rapidly. When a background is added that also circles clockwise, the yellow bug’s orbit, which syncs up with the motion of the background, seems to shrink to about half the size of the red bug's orbit.

This effect, known as reverse phi, is particularly strong in peripheral vision: if someone fixes his gaze on a small stationary cross and observes the moving spot out of the corner of his eye, the backwards leap will be even more pronounced.^7,8 Once again, this phenomenon is consistent with the idea that perceived motion depends on motion energy, or the product of the contrasts of moving objects.³ If the spot makes a long series of jumps to the right, changing between black and white on each jump, one still sees steady motion to the left, but after a while the observer will recognize that, paradoxically, the spot is now farther to the right, demonstrating that position and motion are signaled independently.

RIGHT OR LEFT: The lion on the left moves to the right, then back to the left, in successive movie frames. Because the contrast is held constant, an observer accurately sees this movement. The lion on the right actually moves in the same direction, but since the lion on the right is alternately positive and negative, it seems to move in the opposite direction, as a result of a visual phenomenon known as reverse phi.

Why we are fooled

The phenomena described above are “low-level” illusions that are probably based on “bottom-up” sensory signals from brain cells in the visual system that are specialized to detect motion. Normally, sensory information agrees. If a cat is partly hidden behind a tree, for example, all the cues of color, shadows, and texture tell the same story—that the hidden part of the cat exists out of view behind the tree. The brain acts like a judge, confirming the same story as told by independent witnesses. The brain also strengthens this verdict with “top-down” information based upon prior learning: if the cat’s whiskers stick out on one side of the tree, and its tail on the other, the brain automatically “fills in” that there is a continuous cat partly hidden by the tree, not two unrelated cat bits. This interpolation process, called visual amodal completion, starts from a representation of the visible features of the stimulus in early visual cortex, probably an area called V1, and ends with a completed representation of the stimulus in the inferior temporal cortex.⁹ Jay Hegdé of the University of Minnesota and colleagues even found two regions in the object-processing pathways of the brain that actually responded more strongly to partly hidden objects than to complete ones.¹⁰

Visual object recognition thus involves two stages: a bottom-up inputting of perceptual information, and a top-down memory stage in which perceptual information is matched with an object’s stored representation. Tomoya Taminato of Tohoku University School of Medicine in Japan and colleagues last year presented volunteers with blurry pictures that gradually became sharper. Observers responded once when they could guess the identity of the object in the image, representing the perception stage, and a second time when they were certain of the identity, the memory stage. Their results attributed the perception stage to the right medial occipitotemporal region of the brain, and the memory stage to the posterior part of the rostral medial frontal cortex.¹¹

If a cat’s whiskers stick out on one side of the tree, and its tail on the other, the brain auto­matically “fills in” that there is a continu­ous cat partly hidden by the tree, not two unrelated cat bits.

Visualizing motion is similarly subject to both bottom-up and top-down processes. Reverse phi, in which an object that changes contrast as it travels is viewed as moving in the reverse direction, is a bottom-up illusion that happens early in the brain’s visual processing pathway. Researchers have tracked the origin of this illusion to V1 cells, which in awake monkeys respond to the reverse phi illusion in the same way they respond to backwards-moving objects.¹² Meanwhile, top-down processes predict what objects these signals probably represent, based upon memory and previous learning. Object parsing, for example, is a process that guides perception by deciding what objects are likely to be present based upon prior knowledge of the world.¹³

Consider the closing blades of a pair of scissors. The intersection itself is not an object; only the blades are. This distinction is not lost on the visual system. Observers make 10 times the tracking errors—their eyes deviating from the target—when they attempt to follow a sliding rather than a rigid intersection.¹⁴ Although you can sense the movement of a sliding intersection, you do not interpret it as an object.

FOLLOW THE CENTER: In the top-left panel, a vertical bar and an overlapping horizontal bar both move in a clockwise circular path without rotating. Most observers correctly see each bar as moving clockwise, but falsely view the central intersection as going clockwise too. In fact, the intersection of the bars moves counterclockwise, as becomes apparent in the top-right panel, in which a red outline surrounds the bars.

This phenomenon stems from the fact that smooth eye movements require a smoothly moving target. Move your thumb from side to side in front of you and ask a friend to follow your thumb with his eyes. Watch his eyes and you will see them move smoothly from side to side. Now hold up both your thumbs a yard apart and ask him to move his eyes smoothly from one stationary thumb to the other. He cannot do it! You will see his eyes moving in a series of jerky eye movements called saccades. This shows that a moving object is necessary to drive smooth-pursuit eye movements.

Visual signals flow forward from the visual cortex at the back of the brain, then travel along the ventral stream for the decision about what objects are present, and also up along the dorsal stream to the medial temporal area, which analyzes motion. Finally, the nerve signals travel forward to the frontal eye fields that control eye movements. A sliding intersection is not parsed as a real object, and it cannot support smooth eye movements.

The visual system can also flip between local and global motions, but it cannot see both at once. The brain considers incompatible interpretations—Are there many small groups, or a few large groups?—and adopts them in alternation, but never both at the same time. The shape and spacing of spots on a screen, the duration and position of your fixations, and other factors can all influence which percept you see.

LOCAL OR GLOBAL: At first, viewers see pairs of spots, each pair rotating about their common center. But if you watch for a while, you will suddenly see it reorganize into two larger squares on top, or eight interdigitating octagons on the bottom. The visual system can alternate between either percept, but it cannot see both at once.

Motion can shift an object’s perceived position. If an image of an upright cross flashes briefly on a textured wheel that is rotating clockwise, the cross itself will appear to be tilted clockwise, and it sometimes even looks distorted. Notably, only the motion of the background that occurs after the flash can drag the cross along: motion beforehand has no effect.¹⁵

SPINNING BACKGROUND: Red and green crosses flashing in alternation look bent out of shape, with the right angles no longer looking like right angles. This is because the vertical arms of the crosses lie on the edge of a pie-shaped sector of the moving background, while the horizontal arms lie on the middle of a sector. The edge of a sector has more pulling power than the middle of a sector.

In sum, illusions teach us that perception goes far beyond the information picked up by our senses. Perception is an indirect, interpretive top-down process that is not driven simply by stimulus patterns, but is instead a dynamic, active search for the best interpretation of the available sensory data.
UNDERESTIMATING MOVEMENT: When it moves slowly, it is correctly seen as moving through 180°, from 12 o’clock to 6 o’clock. But at faster speeds, the length of its motion path is underestimated and it seems to move only from 1 o’clock to 5 o’clock. Spots that flash at its turnaround points simply provide milestones that mark this underestimation.

Stuart Anstis is a professor of psychology at the University of California, San Diego, and a visiting fellow at Pembroke College in Oxford, U.K. Working with international collaborators, he has published some 170 articles on visual perception.

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