Wyss Center
Wyss Center

New Technology "Reads" the Thoughts of ALS Patients

Wyss Center
Wyss Center

Communication can be incredibly limited in patients with advanced amyotrophic lateral sclerosis (ALS), a degenerative motor neuron disease also known as Lou Gehrig’s disease. Those who can communicate minimally with eye movements are considered “locked in,” and those who can no longer communicate with eye blinks or eye rolls are referred to as having complete locked-in syndrome, or CLIS. Most of these patients are believed to remain cognitively aware but cannot communicate any thoughts or feelings to caregivers.

For CLIS patients, “quality of life depends on social care by the family and positive social attention from caretakers and friends,” Niels Birbaumer, senior research fellow in neuroscience and psychology at the Wyss Center in Geneva, Switzerland, tells mental_floss.

Researchers have continued to look for ways to offer these patients noninvasive methods of communicating with their caregivers and loved ones. Birbaumer and his colleagues’ new clinical trial offers some fresh hope to CLIS ALS patients with a new brain-computer technology that can essentially “read” the thoughts of these patients and translate their answers to caregivers through a computer interface. Their results were published today in the journal PLOS Biology [PDF].

The system takes the form of a noninvasive cap, worn on the head. Functional near-infrared spectroscopy (fNIRS) determines changes in blood flow in the brain, and an electroencephalogram (EEG) hookup monitors sleep and electrical activity in the brain. It is not the first brain-computer interface that exists to help paralyzed patients communicate, but near-infrared spectroscopy is the only approach that has successfully enabled communication for CLIS patients.

The trial focused specifically on four patients with advanced ALS—two of them in permanent CLIS, and two who were close to entering CLIS, with unreliable communication. Three patients completed more than 46 sessions spread over several weeks, and one patient completed 20 sessions.

The participants trained over the course of several weeks by responding to 500 questions, such as "The capital of Germany is Paris." They also answered personal questions with known answers ("Your husband's name is Joachim") and unknown answers ("You want to be moved from left to right").

All questions were formatted to require either a true/false or yes/no response, which the patient gave by thinking the answer. “'Yes' and 'no' thinking produces different brain blood flow answers in the frontal part of the brain,” Birbaumer explains. “Each patient has a different answer pattern.”

The questions elicited correct responses 70 percent of the time.

Birbaumer says he was surprised by the results: “I had previously thought that people with complete locked-in syndrome are not capable of communication. In fact, we found that all four people we tested were able to answer the personal questions we asked them, using their thoughts alone.”

The next phase of the team's research will be to attempt to build a brain-computer interface “which allows CLIS patients to select letters and words with their brain,” for more robust and individualized communication. While this may involve invasive implantation, they will also try non-invasive methods, although “so far this was not possible.”

Birbaumer and his team would also like to take the knowledge they’ve gained with ALS CLIS patients and extend it to those who experience chronic strokes.

Whatever their next steps, this technology may allow people living in the silence of their own minds a chance to engage in life-improving social interaction.

The Real Reason the Lyme Disease Vaccine Had No Shot

With the potential for causing a variety of lingering symptoms ranging from lethargy to nervous system damage, Lyme disease has become a perennial concern for people venturing outdoors in the summer months. Carried by deer ticks, the Borrelia burgdorferi bacteria can challenge our immune systems and prove frustrating to treat. About 30,000 cases are reported to the CDC each year, although the total cases of unreported transmissions could be ten times that number.

So why don’t we have a vaccine for it? We did. And it disappeared.

According to Vox, the spread of Lyme cases in the 1990s compelled pharmaceutical company GlaxoSmithKline to research and develop a vaccine called LYMErix that attacked the outer protein present in the bacteria. It did so by becoming proactively aggressive, killing off the bacteria while it was still in the body of the attached and feeding tick. More than 1.5 million people were given the vaccine before 2000. Clinical trials demonstrated up to a 90 percent success rate.

While that kind of efficacy and protection would be welcome today, at the time doctors weren’t quite certain what kind of demographic they should be recommending the vaccine to: There was less information about regional areas of tick concentrations than there is now. The vaccine also required three doses in the span of a year, making it slightly inconvenient; some health insurers resisted the $50 cost for each injection.

Those issues were surmountable over time. But some members of the Food and Drug Administration (FDA) panel that had approved the vaccine voiced concern that LYMErix might potentially attack healthy proteins in the body. This autoimmune reaction was never demonstrated in trials, but the theory made consumers wary when it was publicized in the media, and some of those treated complained of arthritis symptoms. Coupled with increasing scrutiny and apprehension over vaccines in general, LYMErix failed to become a staple of vaccination schedules. Sales dropped and GlaxoSmithKline stopped production. With the patent having expired, it’s not likely drug companies will be interested in resurrecting it, only to face additional bad press. Alternative vaccines are being considered, but could take years before coming to market.

In the absence of an effective vaccine, the best way to ward off Lyme remains prevention. If you’re going to be in wooded areas where the ticks tend to congregate, wearing light-colored clothing will help you spot the small nymphs. Insect repellent is important, and examining your body—particularly behind the ears and armpits—for ticks after being outside is also a must. If you find one, remove it with a pair of tweezers.

For more information about Lyme disease, check out our 15 Useful Facts.

[h/t Vox]

6 Things You Might Not Know About Ebola

There's been a new outbreak of Ebola in the Democratic Republic of the Congo. Eleven people have been sickened by the disease, and one has died. Here are some things you might not have known about Ebola.


Five species of Ebolavirus have been identified, each named after the place they sprung up: Ebola (formerly Zaire), Bundibugyo, Sudan, Taï Forest, and Reston. All but one—Reston—arose in Africa. The Reston subtype is named after a town in Virginia where an outbreak occurred in 1989, followed by incidents in Texas and Pennsylvania; all three were tied to infected monkeys exported by a single facility in the Philippines. All Ebolavirus species affect people and nonhuman primates—monkeys, gorillas, and chimpanzees—but Reston doesn't cause detectable disease in humans.


Researchers are finding out just how clever Ebola is. One key to its lethal success is the stealth way it shuts down immune system defenses, the same way an air force will disable air defenses before sending in the bombers. Ebola obstructs parts of an immune system that are activated by molecules called interferons. These interferons have a vital role in fighting Ebola, usually with scorched-earth tactics such as apoptosis, or cell self-destruction. A 2014 study found that Ebola disables signals the cells use to defend against its attack using a protein called VP24, which binds to a specific protein that takes signaling molecules in and out a cell's nucleus. Blocked from communication, the cell can't call for help or get the order to self-destruct. The virus then hijacks the cell, uses it to make more viruses, and spreads them to more cells. It also produces ebolavirus glycoprotein, which binds to cells inside blood vessels, increasing their permeability and leading to leakage. This contributes to the catastrophic bleeding characteristic of late-stage Ebola infection.


CDC illustration of cycle of ebola infection from bats to humans and animals

Scientists believe that Ebola's natural host species, or "reservoir hosts," are bats. Infected bats can pass the virus to other mammals, including rats, primates, and us. No one is sure how people first became exposed to Ebola, but the best guess is that monkeys were the conduit. Local hunters in Africa likely became infected while butchering the animals. Anyone who became sick likely infected their family and, if hospitalized in an unsanitary facility, other patients. When the illness spreads from person to person, it does so through direct contact with the bodily fluids of someone who is sick with or has died from Ebola.


It takes the investigative skill of a homicide detective to stop an outbreak. Professionals call it contact tracing. Here's how it works: Ebola victim A is isolated and interviewed. Anyone who had close contact with A is put into quarantine for 21 days. If they exhibit no symptoms, they're free to go when the three weeks are up. If they come down with Ebola, they become victim B, and another contact trace begins. If the investigators miss anyone, the outbreak will continue.


Researchers analyzing the the 2014 outbreak of Ebola in West Africa made a surprising finding: patients who had an active malaria parasite infection were actually more likely to survive the Ebola virus, and by a significant degree. While just over half (52 percent) of Ebola patients not infected with malaria survived, those co-infected with malaria had a survival rate of 72 to 83 percent, depending on their ages and the amount of Ebola virus in their blood. The researchers aren't yet sure why, but the prevailing theory is that malaria somehow modifies the immune response to Ebola by toning down a phenomenon called the "cytokine storm"—the body's own response to an Ebola infection, which inadvertently kills the host while attempting to eliminate the pathogen. If malaria can dampen this response, infected patients may have a better chance of surviving.


We do not yet have a vaccine or antiviral drug to treat Ebola, but many scientists are working to find one. One source is the National Institute of Allergy and Infectious Diseases (NIAID)'s BEI Resources, which gives research facilities access to microbiological materials called reagents that can help them develop diagnostics and vaccines for emerging diseases, including Ebola. Scientists must be registered with BEI to request materials. Reagents are not active viruses, so they can't spread; on the biosafety level, or BSL, scale—which ranks the severity of infectious disease and sets required safety protocols for working with them in a lab—the Ebola-related reagents are considered BLS 1—the lowest risk. (Live Ebola virus is BLS 4—the highest.) Ordering is limited to one Ebola-related reagent at a time, and can be ordered only twice per year.


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