Scientists advance the art of magic with a study of Penn and Teller’s ‘cups and balls’ illusion

Cognitive brain researchers have studied a magic trick filmed in magician duo Penn & Teller’s theater in Las Vegas, to illuminate the neuroscience of illusion. Their results advance our understanding of how observers can be misdirected and will aid magicians as they work to improve their art.

The research team was led by Dr. Stephen Macknik, Director of the Laboratory of Behavioral Neurophysiology at Barrow Neurological Institute, in collaboration with fellow Barrow researchers Hector Rieiro and Dr. Susana Martinez-Conde, Director of the Laboratory of Visual Neuroscience. The study, titled “Perceptual elements in Penn and Teller’s “Cups and Balls” magic trick” was published today, Feb 12th 2013, as part of the launch of PeerJ, a new peer reviewed open access journal in which all articles are freely available to everyone. “Cups and Balls,” a magic illusion in which balls appear and disappear under the cover of cups, is one of the oldest magic tricks in history, with documented descriptions going back to Roman conjurors in 3 B.C. “But we still don’t know how it really works in the brain,” says Macknik, “because this is the first, long overdue, neuroscientific study of the trick.”

The discovery concerns the way magicians manipulate human cognition and perception. The “Cups and Balls” trick has many variations, but the most common one uses three balls and three cups. The magician makes the balls pass through the bottom of cups, jump from cup to cup, disappear from a cup and turn up elsewhere, turn into other objects, and so on. The cups are usually opaque and the balls brightly colored. Penn & Teller’s variant is performed with three opaque and then with three transparent cups. “The transparent cups mean that visual information about the loading of the balls is readily available to the brain, yet still the spectators cannot see how the trick is done!” said Martinez-Conde.

Magicians have performed and systematically developed the art and theory of this illusion for thousands of years, but each new generation of conjurers offers new insights and hypotheses about how and why it works for the audience. Here the scientists turned the power of the scientific method to the illusion. The experiments tracked when and where observers looked during video clips portraying specific element of the performance, filmed by a NOVA scienceNOW TV crew. By quantifying how well observers tracked the loading and unloading of balls with and without transparent cups, the scientists determined that some aspects of the illusion were even more powerful at controlling attention than aspects originally predicted by the magician.

The end result is that cognitive scientists now have an improved understanding of how (and by how much) observers can be misdirected. In addition, this knowledge can help magicians further hone their art.

In Some Dystonia Cases, Deep Brain Therapy Benefits May Linger After Device Turned Off

Two patients freed from severe to disabling effects of dystonia through deep brain stimulation therapy continued to have symptom relief for months after their devices accidentally were fully or partly turned off, according to a report published online Feb. 11 in the journal Movement Disorders.

“Current thought is that symptoms will worsen within hours or days of device shut-off, but these two young men continued to have clinical benefit despite interruption of DBS therapy for several months. To our knowledge, these two cases represent the longest duration of retained benefit in primary generalized dystonia. Moreover, when these patients’ symptoms did return, severity was far milder than it was before DBS,” said senior author Michele Tagliati, MD, director of the Movement Disorders Program at Cedars-Sinai’s Department of Neurology.

Dystonia causes muscles to contract, with the affected body part twisting involuntarily and symptoms ranging from mild to crippling. If drugs – which often have undesirable side effects, especially at higher doses – fail to give relief, neurosurgeons and neurologists may work together to supplement medications with deep brain stimulation, aimed at modulating abnormal nerve signals. Electrical leads are implanted in the brain – one on each side – and an electrical pulse generator is placed near the collarbone. The device is then programmed with a remote, hand-held controller. Tagliati is an expert in device programming, which fine-tunes stimulation for individual patients.

Few studies have looked at the consequences of interrupted DBS therapy, although one found “fairly rapid worsening of dystonia in 14 patients after interruption of stimulation for 48 hours, with symptom severity at times becoming worse than the pre-operative baseline.” In another study of 10 patients with generalized dystonia, however, symptoms did not return in four patients when stimulation was discontinued for 48 hours.

Findings from the 10-patient study correlate well with these two cases, Tagliati said.

“It appears that several factors – age, duration of disease, length of time the patient has received DBS treatment and stimulation parameters – determine which patients may retain symptom relief after prolonged DBS interruption. Our two patients were young, 20 years old. They both began DBS therapy a relatively short time after disease onset; one at four years and the other at seven years. One had received continuous stimulation for five years and the other for 18 months before stimulation was interrupted,” Tagliati said.

“We can’t say for certain why these factors make the difference,” he added, “But we theorize that a younger brain with shorter exposure to the negative effects of dystonia may be more responsive to therapy and have greater ‘plasticity’ to adapt back to normal. Both of our patients received DBS therapy at a lower energy than most patients experience, suggesting the possibility that low-frequency stimulation over an extended time may help retrain the brain’s low-frequency electrical activity.”

Both instances of device shut-off were accidental and were discovered during doctor visits after mild symptoms returned. The patient who had undergone five years of DBS therapy had only one stimulator turned off for about three months; the one stimulating the left side of his brain remained active. In the other patient, the left device had been off for about seven months and the right one for two months, Tagliati said.

Tagliati was senior author of a 2011 Journal of Neurology article on a study showing that for patients suffering from dystonia, deep brain therapy tends to get better, quicker results when started earlier rather than later.

“We knew from earlier work that younger patients with shorter disease duration had better clinical outcomes in the short term. In our 2011 article, we reported that they fare best in the long term, as well. That study uniquely showed that age and disease duration play complementary roles in predicting long-term clinical outcomes. The good news for older patients is that while they may not see the rapid gains of younger patients, their symptoms may gradually improve over several years,” Tagliati said.

Identification of abnormal protein may help diagnose, treat ALS and frontotemporal dementia

Amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, and frontotemporal dementia (FTD) are devastating neurodegenerative diseases with no effective treatment. Researchers are beginning to recognize ALS and FTD as part of a spectrum disorder with overlapping symptoms. Now investigators reporting online February 12 in the Cell Press journal Neuron have discovered an abnormal protein that first forms as a result of genetic abnormalities and later builds up in the brains of many patients with either disease.

"In identifying the novel protein that abnormally accumulates in the brains of affected patients, we have uncovered a potentially new therapeutic target and biomarker that would allow clinicians to confirm diagnosis of the diseases," says senior author Dr. Leonard Petrucelli, Chair of Neuroscience at Mayo Clinic in Florida.

By analyzing brain tissue from patients with ALS or FTD, Dr. Petrucelli and his team discovered that the abnormal protein, which they call C9RANT, is generated as a result of repeat expansions of nucleotides in the noncoding region of the C9ORF72 gene. These expansions are the most common cause of ALS and FTD. “Simply put, an error in the highly regulated cellular process through which proteins are generated causes the abnormal production of C9RANT,” explains Dr. Petrucelli.

The researchers discovered the protein C9RANT after creating a novel antibody to specifically detect it. The ability to detect C9RANT in individuals’ cerebrospinal fluid may provide a valuable diagnostic and prognostic tool for identifying patients carrying the C9ORF72 repeat expansion and for then tracking the progression of the disease in these at-risk individuals.

"Although it remains to be shown whether C9RANT is causing the cell death or toxicity associated with disease symptoms, our discovery offers a potential target to prevent neuronal loss in patients carrying the C9ORF72 repeat expansion," says Dr. Petrucelli.

The concept that abnormal proteins accumulate and can be toxic to cells is not new. In fact, tau protein forms tangles in Alzheimer’s disease and alpha-synuclein forms clumps in Parkinson’s disease. Just as new therapies are being developed to break down the protein aggregates associated with these diseases, developing a therapeutic strategy to target C9RANT aggregates may also prove beneficial.

Neuroprosthesis gives rats the ability to ‘touch’ infrared light

Researchers have given rats the ability to “touch” infrared light, normally invisible to them, by fitting them with an infrared detector wired to microscopic electrodes implanted in the part of the mammalian brain that processes tactile information. The achievement represents the first time a brain-machine interface has augmented a sense in adult animals, said Duke University neurobiologist Miguel Nicolelis, who led the research team.

The experiment also demonstrated for the first time that a novel sensory input could be processed by a cortical region specialized in another sense without “hijacking” the function of this brain area said Nicolelis. This discovery suggests, for example, that a person whose visual cortex was damaged could regain sight through a neuroprosthesis implanted in another cortical region, he said.

Although the initial experiments tested only whether rats could detect infrared light, there seems no reason that these animals in the future could not be given full-fledged infrared vision, said Nicolelis. For that matter, cortical neuroprostheses could be developed to give animals or humans the ability to see in any region of the electromagnetic spectrum, or even magnetic fields. “We could create devices sensitive to any physical energy,” he said. “It could be magnetic fields, radio waves, or ultrasound. We chose infrared initially because it didn’t interfere with our electrophysiological recordings.”

Nicolelis and colleagues Eric Thomson and Rafael Carra published their findings February 12, 2013 in the online journal Nature Communications. Their research was sponsored by the National Institute of Mental Health.

Stopping cold: USC scientists turn off the ability to feel cold

USC neuroscientists have isolated chills at a cellular level, identifying the sensory network of neurons in the skin that relays the sensation of cold.

David McKemy, associate professor of neurobiology in the USC Dornsife College of Letters, Arts and Sciences, and his team managed to selectively shut off the ability to sense cold in mice while still leaving them able to sense heat and touch.

In prior work, McKemy discovered a link between the experience of cold and a protein known as TRPM8 (pronounced trip-em-ate), which a sensor of cold temperatures in neurons in the skin, as well as a receptor for menthol, the cooling component of mint. Now, in a paper appearing in the Journal of Neuroscience on February 13, McKemy and his co-investigators have isolated and ablated the neurons that express TRPM8, giving them the ability to test the function of these cells specifically.

Using mouse-tracking software program developed by one of McKemy’s students, the researchers tested control mice and mice without TRPM8 neurons on a multi-temperature surface. The surface temperature ranged from 0 degrees to 50 degrees Celsius (32 to 122 degrees Farenheit), and mice were allowed to move freely among the regions.

The researchers found that mice depleted of TRPM8 neurons could not feel cold, but still responded to heat. Control mice tended to stick to an area around 30 degrees Celsius (86 degrees Fahrenheit) and avoided both colder and hotter areas. But mice without TRPM8 neurons avoided only hotter plates and not cold — even when the cold should have been painful or was potentially dangerous.

In tests of grip strength, responses to touch, or coordinated movements, such as balancing onto a rod while it rotated, there was no difference between the control mice and the mice without TRPM8-expressing neurons.

By better understanding the specific ways in which we feel sensations, scientists hope to one day develop better pain treatments without knocking out all ability to feel for suffering patients.

"The problem with pain drugs now is that they typically just reduce inflammation, which is just one potential cause of pain, or they knock out all sensation, which often is not desirable," McKemy said. "One of our goals is to pave the way for medications that address the pain directly, in a way that does not leave patients completely numb."

Some Autism Behaviors Linked to Altered Gene

Scientists at Washington University School of Medicine in St. Louis have identified a genetic mutation that may underlie common behaviors seen in some people with autism, such as difficulty communicating and resistance to change.

An error in the gene, CELF6, leads to disturbances in serotonin, a chemical that relays messages in the brain and has long been suspected to be involved in autism.

The researchers identified the error in a child with autism and then, working in mice, showed that the same genetic alteration results in autism-related behaviors and a sharp drop in the level of serotonin circulating in the brain.

While the newly discovered mutation appears to be rare, it provides some of the first clues to the biological basis of the disease, the scientists report Feb. 13 in the Journal of Neuroscience.

“Genetically, autism looks very complicated, with many different genetic routes that lead to the disease,” says lead author Joseph D. Dougherty, PhD, an assistant professor of genetics at Washington University. “But it’s not possible to design a different drug for every child. The real key is to find the common biological pathways that link these different genetic routes and target those pathways for treatment.”

Autism is known to have a strong genetic component, but the handful of genes implicated in the condition so far explain only a small number of cases or make a small contribution to symptoms.

This led Dougherty and senior author Nathaniel Heintz, PhD, a Howard Hughes Medical Institute investigator at Rockefeller University, to speculate that some of the most common behavioral symptoms of autism may be caused by disruptions in a common biological pathway, like the one involved in serotonin signaling.

Research finds protein that prevents light-induced retinal degeneration

Research led by Minghao Jin, PhD, Assistant Professor of Ophthalmology and Neuroscience at the LSU Health Sciences Center New Orleans Neuroscience Center of Excellence, has found a protein that protects retinal photoreceptor cells from degeneration caused by light damage. This protein may provide a new therapeutic target for both an inherited retinal degenerative disease and age-related macular degeneration. The paper is published in the February 13, 2013 issue of the Journal of Neuroscience.

The visual cycle is essential for regenerating visual pigments that sense light for vision. However, abnormal visual cycles promote formation of toxic byproducts that contribute to the development of age-related macular degeneration (AMD), the leading cause of vision loss in elderly people that affects an estimated 2 million Americans. The mechanisms that regulate the visual cycle have been unclear. Identification and characterization of regulators of the visual cycle enzymes are critical for understanding these mechanisms.

RPE65 is a key enzyme involved in the visual cycle. RPE65 mutations have been linked to early onset vision loss, retinal degeneration, and blinding eye diseases. Despite such importance, the mechanisms that regulate the function of RPE65 are unknown. To identify and characterize previously unknown inhibitors of RPE65, the scientists tested five candidate proteins. Using gene screening, the LSUHSC research team discovered that one of them – fatty acid transport protein 4 (FATP4) – is a negative regulator; it inhibits RPE65.

"We found that FATP4 protects retinal photoreceptor cells from experimentally-induced retinal degeneration," notes Nicolas Bazan, MD, PhD, Boyd Professor, Ernest C. and Yvette C. Villere Endowed Chair of Retinal Degeneration, and Director of the LSU Health Sciences Center New Orleans Neuroscience Center of Excellence, who is a co-author of the paper.

Recently, mutations in the human FATP4 gene have been identified in patients with a certain recessive disorder which also features one of the toxic byproducts associated with abnormal visual cycles. This byproduct, called A2E accumulates in retinal pigment epithelial cells with age, prompting a call for further investigation to determine whether FATP4 mutations cause age-related vision impairment and retinal degeneration.

"These findings suggest that FATP4 may be a therapeutic target for the inherited retinal degenerative disease caused by RPE65 mutations and AMD," concludes Dr. Jin.

(Image: Eyeland Design Network)

Long memories in brain activity explain streaks in individual behaviour

Even with a constant task, human performance fluctuates in time-scales from seconds to minutes in a fractal manner. In a recent study a Finnish research group found that the individual variability in the brain dynamics as indexed by the neuronal scaling laws predicted the individual behavioral variability and the conscious detection of very weak sensory stimuli. These data indicate that individual neuronal dynamics underlie the individual variability in human cognition and performance. Results may also have a strong impact in understanding the neuronal mechanism of neuropsychiatric diseases in which behavioral dynamics are abnormal.

Human performance in cognitive tasks varies from moment-to-moment so that the similar behavioral performance is clustered into streaks. The neuronal dynamics underlying this behavioral variability has remained unknown.

Similar scale-free and power-law distributed “avalanche dynamics” is observed in many natural systems such as sand piles, earthquakes, gene regulation, and also brain activity. However, the functional significance of the neuronal scale-free behavior has remained unknown. It is also unclear whether it is just epiphenomena without any further significance. 

"We investigated whether the individual variability in the scaling-laws governing the detection of auditory and visual stimuli presented in the threshold of detection could be predicted by the variability in the neuronal scaling laws", explains Matias Palva, project leader in the Neuroscience Center of the University of Helsinki, Finland.

The researchers used magneto- and electroencephalography to record non-invasively human brain activity during the task performance. They found that both the behavioral and neuronal dynamics were characterized by scale-free dynamics. Individual variability in the neuronal scaling laws predicted the individual scaling laws in behavioral performance.

"These results suggest that the individual behavioral and psychophysical variability in task performance is largely a result of the inherent variability in the individual neuronal dynamics", says project leader Satu Palva.

(Image: Harry Sieplinga, HMS/Getty Images)

Early music lessons boost brain development

If you started piano lessons in grade one, or played the recorder in kindergarten, thank your parents and teachers. Those lessons you dreaded – or loved – helped develop your brain. The younger you started music lessons, the stronger the connections in your brain.

A study published last month in the Journal of Neuroscience suggests that musical training before the age of seven has a significant effect on the development of the brain, showing that those who began early had stronger connections between motor regions – the parts of the brain that help you plan and carry out movements.

This research was carried out by students in the laboratory of Concordia University psychology professor Virginia Penhune, and in collaboration with Robert J. Zatorre, a researcher at the Montreal Neurological Institute and Hospital at McGill University.

The study provides strong evidence that the years between ages six and eight are a “sensitive period” when musical training interacts with normal brain development to produce long-lasting changes in motor abilities and brain structure. “Learning to play an instrument requires coordination between hands and with visual or auditory stimuli,” says Penhune. “Practicing an instrument before age seven likely boosts the normal maturation of connections between motor and sensory regions of the brain, creating a framework upon which ongoing training can build.”

(Image credit)