Why Do We Blink So Frequently?

We all blink. A lot. The average person blinks some 15-20 times per minute—so frequently that our eyes are closed for roughly 10% of our waking hours overall.

Although some of this blinking has a clear purpose—mostly to lubricate the eyeballs, and occasionally protect them from dust or other debris—scientists say that we blink far more often than necessary for these functions alone. Thus, blinking is physiological riddle. Why do we do it so darn often? In a paper published in the Proceedings of the National Academy of Sciences, a group of scientists from Japan offers up a surprising new answer—that briefly closing our eyes might actually help us to gather our thoughts and focus attention on the world around us.

The researchers came to the hypothesis after noting an interesting fact revealed by previous research on blinking: that the exact moments when we blink aren’t actually random. Although seemingly spontaneous, studies have revealed that people tend to blink at predictable moments. For someone reading, blinking often occurs after each sentence is finished, while for a person listening to a speech, it frequently comes when the speaker pauses between statements. A group of people all watching the same video tend to blink around the same time, too, when action briefly lags.

As a result, the researchers guessed that we might subconsciously use blinks as a sort of mental resting point, to briefly shut off visual stimuli and allow us to focus our attention. To test the idea, they put 10 different volunteers in an fMRI machine and had them watch the TV show “Mr. Bean” (they had used the same show in their previous work on blinking, showing that it came at implicit break points in the video). They then monitored which areas of the brain showed increased or decreased activity when the study participants blinked.

Their analysis showed that when the Bean-watchers blinked, mental activity briefly spiked in areas related to the default network, areas of the brain that operate when the mind is in a state of wakeful rest, rather than focusing on the outside world. Momentary activation of this alternate network, they theorize, could serve as a mental break, allowing for increased attention capacity when the eyes are opened again.

To test whether this mental break was simply a result of the participants’ visual inputs being blocked, rather than a subconscious effort to clear their minds, the researchers also manually inserted “blackouts” into the video at random intervals that lasted roughly as long as a blink. In the fMRI data, though, the brain areas related to the default network weren’t similarly activated. Blinking is something more than temporarily not seeing anything.

It’s far from conclusive, but the research demonstrates that we do enter some sort of altered mental state when we blink—we’re not just doing it to lubricate our eyes. A blink could provide a momentary island of introspective calm in the ocean of visual stimuli that defines our lives.

Simple eye scan can reveal extent of Multiple Sclerosis

A simple eye test may offer a fast and easy way to monitor patients with multiple sclerosis (MS), medical experts say in the journal Neurology. Optical Coherence Tomography (OCT) is a scan that measures the thickness of the lining at the back of the eye - the retina. It takes a few minutes per eye and can be performed in a doctor’s surgery.

In a trial involving 164 people with MS, those with thinning of their retina had earlier and more active MS. The team of researchers from the Johns Hopkins University School of Medicine say larger trials with a long follow up are needed to judge how useful the test might be in everyday practice. The latest study tracked the patients’ disease progression over a two-year period.

Unpredictable disease

Multiple sclerosis is an illness that affects the nerves in the brain and spinal cord causing problems with muscle movement, balance and vision. In MS, the protective sheath or layer around nerves, called myelin, comes under attack which, in turn, leaves the nerves open to damage.

There are different types of MS - most people with the condition have the relapsing remitting type where the symptoms come and go over days, weeks or months. Usually after a decade or so, half of patients with this type of MS will develop secondary progressive disease where the symptoms get gradually worse and there are no or very few periods of remission.

Another type of MS is primary progressive disease where symptoms get worse from the outset. There is no cure but treatments can help slow disease progression. It can be difficult for doctors to monitor MS because it has a varied course and can be unpredictable.

Brain scans can reveal inflammation and scarring, but it is not clear how early these changes might occur in the disease and whether they accurately reflect ongoing damage.

Scientists have been looking for additional ways to track MS, and believe OCT may be a contender. OCT measures the thickness of nerve fibres housed in the retina at the back of the eye. Unlike nerve cells in the rest of the brain which are covered with protective myelin, the nerve cells in the retina are bare with no myelin coat. Experts suspect that this means the nerves here will show the earliest signs of MS damage.

The study at Johns Hopkins found that people with MS relapses had much faster thinning of their retina than people with MS who had no relapses. So too did those whose level of disability worsened. Similarly, people with MS who had inflammatory lesions that were visible on brain scans also had faster retinal thinning than those without visible brain lesions. Study author Dr Peter Calabresi said OCT may show how fast MS is progressing.

"As more therapies are developed to slow the progression of MS, testing retinal thinning in the eyes may be helpful in evaluating how effective those therapies are," he added.

In an accompanying editorial in the same medical journal that the research is published in, MS experts Drs Robert Bermel and Matilde Inglese say OCT “holds promise” as an MS test.

(Image courtesy: Boston University Eye Associates, Inc.)

Kim Peek, The Real Rain Man

Kim Peek, who lent inspiration to the fictional character Raymond Babbitt—played by Dustin Hoffman—in the movie Rain Man, was a remarkable savant. A savant is an individual who—with little or no apparent effort—completes intellectual tasks that would be impossible for ordinary people to master.

Kim Peek’s special abilities started early, around the age of a year and a half. He could read both pages of an open book at once, one page with one eye and the other with the other eye. This style of reading continued until his dead in 2009. His reading comprehension was impressive. He would retain 98 percent of the information he read. Since he spent most of his days in the library with his dad, he quickly made it through thousands of books, encyclopedia and maps. He could read a thick book in an hour and remember just about anything in it. Because he could quickly absorb loads of information and recall it when necessary, his condition made him a living encyclopedia and a walking GPS. He could provide driving directions between almost any two cities in the world. He could also do calendar calculations (“which day was June 15, 1632?”) and remember old baseball scores and a vast amount of musical, historical and political facts. His memory abilities were astounding.

Unlike many individuals with savant syndrome, Kim Peek was not afflicted with autistic spectrum disorder. Though he was strongly introverted, he did not have difficulties with social understanding and communication. The main cause of his remarkable abilities seems to have been the lack of connections between his brain’s two hemispheres. An MRI scan revealed an absence of the corpus callosum, the anterior commissure and the hippocampal commissure, the parts of the neurological system that transfer information between hemispheres. In some sense Kim was a natural born split-brain patient.

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Brain displays an intrinsic mechanism for fighting infection

White blood cells have long reigned as the heroes of the immune system. When an infection strikes, the cells, produced in bone marrow, race through the blood to fight off the pathogen. But new research is emerging that individual organs can also play a role in immune system defense, essentially being their own hero. In a study examining a rare and deadly brain infection, scientists at The Rockefeller University have found that the brain cells of healthy people likely produce their own immune system molecules, demonstrating an “intrinsic immunity” that is crucial for stopping an infection.

Shen-Ying Zhang, a clinical scholar in the St. Giles Laboratory of Human Genetics of Infectious Diseases, has been studying children with Herpes simplex encephalitis, a life-threatening brain infection from the herpes virus, HSV-1, that can cause significant brain damage. The scientists already knew from previous work that children with this encephalitis have a genetic defect that impairs the function of an immune system receptor — toll-like receptor 3 (TLR3) — in the brain. For this study they wanted to see how the defect in TLR3 was hampering the brain’s ability to fight the herpes infection.

When TLR3 detects a pathogen it triggers an immune response causing the release of proteins called interferons to sound the alarm and “interfere” with the pathogen’s replication. It’s most commonly associated with white blood cells, found throughout the body, but here the researchers were examining the receptor’s presence on neurons and other brain cells.

“One interesting thing about these patients is that they didn’t have any of the other, more common herpes symptoms. They didn’t have an infection on their skin or their mouths, just in their brains. We therefore hypothesized that the TLR3 response must be specifically responsible for keeping the herpes virus from infecting the brain and not necessary in other parts of the body,” says Zhang.

The lab, headed by Jean-Laurent Casanova, collaborated with scientists at Harvard Medical School and Memorial Sloan-Kettering Cancer Institute to create induced pluripotent stem cells. Made from the patients’ own tissue, the stem cells were developed into central nervous system cells that carried the patients’ genetic defects. Zhang exposed the cells to HSV-1 and to synthetic double-stranded RNA, which mimics a byproduct of the virus that spurs the toll-like receptors into action. By measuring levels of interferon, Zhang showed that the patients’ TLR3 response was indeed faulty; their cells weren’t making these important immune system proteins, leaving them unable to fight off the infection.

Zhang also exposed the patients’ blood cells to the virus and found that the TLR3 defect was not an issue there as it was in the brain — interferons were released by other means.

Because the toll-like receptors on neurons proved to be vital in preventing the encephalitis infection, the researchers concluded that brain cells use it as an in-house mechanism to fight infection, rather than relying on white blood cells. When its function was impaired, patients couldn’t get better.

“This is evidence of an intrinsic immunity, a newly-discovered function of the immune system,” says Zhang. “It’s likely that other organs also have their own specific tools for fighting infection.”

The researchers are putting together a pilot study to test an interferon-based treatment in patients with the encephalitis, believing it will help speed recovery and increase the survival rate when used alongside antiviral drugs. They’ll also explore whether the brain displays an intrinsic immunity to other types of viral infection.

Scientists Map Initial Anti-Aging Formula

A new study indicates that scientists have found a new way of delaying the aging process in mice, and they hope to replicate the finding in people.

The scientists published their findings in the journal Cell Metabolism. The research was built upon an earlier study that shed light on progeria, a rare genetic disease that prematurely ages one in four million babies.

A mutation was found in the Lamin A protein, which lines the nucleus in human cells, disrupting the repair process and accelerating aging. They also found that normal and healthy Lamin A binds to and activates the gene SIRT1, which has been long associated with longevity. If scientists can develop drugs that mimic Lamin A or increase the binding between Lamin A and SIRT1, this may lead to anti-aging drugs.

The team also examined if the binding efficiency was boosted with resveratrol, a compound found in the skin of red grapes. Mice fed with concentrated resveratrol fared significantly better than healthy mice that weren’t given it and the onset of aging was delayed and the life expectancy was extended. Mice with progeria lived 30% longer when fed with resveratrol compared with progerial mice not given the compound.

Why overlearned sequences are special: distinct neural networks for ordinal sequences

Several observations suggest that overlearned ordinal categories (e.g., letters, numbers, weekdays, months) are processed differently than non-ordinal categories in the brain. In synesthesia, for example, anomalous perceptual experiences are most often triggered by members of ordinal categories (Rich et al., 2005; Eagleman, 2009). In semantic dementia (SD), the processing of ordinal stimuli appears to be preserved relative to non-ordinal ones (Cappelletti et al., 2001). Moreover, ordinal stimuli often map onto unconscious spatial representations, as observed in the SNARC effect (Dehaene et al., 1993; Fias, 1996). At present, little is known about the neural representation of ordinal categories. Using functional neuroimaging, we show that words in ordinal categories are processed in a fronto-temporo-parietal network biased toward the right hemisphere. This differs from words in non-ordinal categories (such as names of furniture, animals, cars, and fruit), which show an expected bias toward the left hemisphere. Further, we find that increased predictability of stimulus order correlates with smaller regions of BOLD activation, a phenomenon we term prediction suppression. Our results provide new insights into the processing of ordinal stimuli, and suggest a new anatomical framework for understanding the patterns seen in synesthesia, unconscious spatial representation, and SD.