The mysterious dancing mania and mass psychogenic illness

Try to imagine yourself walking along the streets of a city (maybe the one you live in, or one you’ve visited, or one you simply make up in your head—as long as you can picture it clearly it doesn’t matter much). Think of the shops and businesses you might pass as you stroll down the sidewalk, the smells of food emanating from nearby restaurants, and the noises you’d hear—intermittent car horns, snippets of conversation, the discordant sounds of construction equipment. Now, imagine you approach a street corner, and as you do you begin to hear some rhythmic music playing from just out of view—on what sounds like bagpipes (to really set the mood, click play on the video below for some appropriate background music). As you turn the corner, curious to find the source of the music, you see a large city park. It charmingly interrupts the asphalt and concrete of the city with expansive green grasses, dense leafy trees, and a bubbling decorative fountain. But despite its beauty, the park is also the backdrop to one of the strangest spectacles you’ve ever witnessed.

The park is filled with people—perhaps a hundred, maybe more. Many of them are naked. Others are wearing clothes that are dirty, ripped, and often hanging loosely from their undernourished bodies. A large group of them have formed a circle by holding hands, and many others are contained within the circle. Someone you can’t see is playing the aforementioned upbeat (almost eerily so, now that you can see the whole picture) tune on the bagpipes, and nearly everyone is dancing—but not in a choreographed manner you might see from a flash mob today. Instead, this dancing is convulsive and jerky, and almost out of control—like there is a maniacal puppet master manipulating their movements from above.

As you cautiously take a few steps closer to this bizarre scene, you see that many of the dancers are staring blankly up at the sky, as if in a trance. Occasionally, they yell—shriek might be the more appropriate word—unintelligibly into the air. Some of these shrieks become agonized screams, and you can clearly make out the word “help!” shouted at least once or twice. You notice that, in the middle of the circle, several couples are on the ground having sex with one another. The whole thing looks like a drug-fueled ritual/orgy, but it’s taking place right out in the open, for everyone to see.

One of the dancers suddenly falls to the ground and starts convulsing. He’s clearly having some sort of seizure, his body thrashing about wildly and uncontrollably—but everyone just ignores him. After what must be about 30 seconds, he recovers, slowly gets up, and begins dancing again.

Think of the shock and horror you would feel when you encountered this scene. Now consider that if you lived in certain parts of Europe between the fourteenth and seventeenth centuries, this spectacle may not even have been cause for alarm. These types of dancing displays were not unheard of, and it’s very possible you would have seen one before.

In those days, the people who participated in the dancing rituals were thought to be afflicted by some malady (often assumed to be demonic possession) that led to compulsive dancing. The ailment was deemed contagious, and it was believed onlookers could be overcome and compelled to join the dancing at any moment. The condition was often called the dancing mania or St. Vitus’ dance, the latter name coming into use because the afflicted would often dance near the churches or shrines of St. Vitus, the patron saint of dancers. Priests from these churches frequently tried to intercede, frantically attempting to exorcise the demons from those who were affected before they were able to pass the sickness on to members of the clergy.

A depiction of dancing mania by Pieter Brueghel the Younger.

One such event occurred in 1374 and spread across a large area of Europe that included western Germany, Belgium, the Netherlands, Luxembourg, and northeastern France. Dozens of independent chroniclers of the events agree that thousands of people were affected, and the dancing went on for weeks. Another incident in Strasbourg in 1518 involved around 400 people, a number of whom were reported to have died while dancing in oppressively high summer temperatures. There were many other smaller occurrences of dancing mania, and sporadic reports of it persisted up until the mid-1600s.

While it’s possible some of the details of these events have been embellished, the number of independent verifications of them suggest they did occur in some form. So what could have caused this strange behavior? To this day, scientists are stumped. Some have suggested the culprit might have been widespread ergot poisoning. Ergot is a fungus that grows on rye; it has strong psychoactive effects when it’s ingested, and it can cause hallucinations, tremors, and convulsions (a constituent of ergot, lysergic acid, can be used to synthesize LSD). Is it possible, then, that widespread consumption of tainted rye could have led to these “epidemics?”

It doesn’t seem very likely. Ergot poisoning is characterized by spasms and convulsions, but also by symptoms like nausea and diarrhea, making it improbable sufferers could have danced for days on end. Additionally, ergot poisoning often involves the appearance of gangrene (i.e. tissue dying due to a lack of blood flow—it causes gruesome blackened skin that’s difficult to overlook) on the toes and fingers, but reports of dancing manias don’t include such descriptions. Finally, outbreaks of dancing mania also sometimes occurred in regions where rye wasn’t a common crop.

Of course it’s possible there was some other environmental exposure we haven’t identified that had a widespread influence on behavior, but such things are difficult to ascertain so long after-the-fact. And due to the lack of viable alternative explanations, many scientists have begun to believe the dancing mania was a manifestation of something called mass psychogenic illness, or MPI.

MPI involves the appearance of symptoms that spread throughout a population, but don’t have a clear physical origin. In other words, in MPI the brain is causing the patient to think they are afflicted by some ailment—even though the brain itself is the creator and orchestrator of the illness. This doesn’t mean that the symptoms aren’t real; there can be legitimate physical manifestations of MPI. But there’s no evidence the symptoms are produced by something (like a poison or a germ) other than the nervous system.

MPI is surprisingly common throughout history. Before dancing mania, there was a condition known as tarantism that occurred during the Middle Ages in Southern Italy. Victims of tarantism suffered from a number of symptoms ranging from headache to difficulty breathing, which, according to the victims, began immediately after the bite of a tarantula. (In those days, tarantula referred to a wolf spider, not the spiders we typically think of as tarantulas. Regardless, whether a spider bite was really involved was usually difficult to verify; it’s suspected that in many cases, the spider—like the resultant condition—was a phantom of the mind.) Once the malady took hold, however, the victims didn’t seek out antidotes to spider venom. Instead, they immediately began to take part in the only recognized cure: dancing. Patients would dance on and off for hours, days, or even weeks to upbeat melodies now known as tarantellas (this is what you heard in the video clip above).

Since these dancing disorders of the Middle Ages and early modern times, there have been hundreds of other potential instances of MPI as well. But, you might be thinking, perhaps MPI occurred in the distant past because people were more superstitious and easily-duped than they are today. Surely, we must have advanced past this era of gullibility, right?

Wrong. There is a long list of examples of possible MPI in modern times. For instance, in 2011, twenty classmates at a high school outside Buffalo, NY suddenly began to experience tics, verbal outbursts, and other symptoms that resembled those of Tourette syndrome. Despite investigations by doctors and state health department officials, no environmental cause of the condition was identified, and most doctors eventually agreed that the students’ conditions were brought on by psychological factors. Some doctors even suggested that social and mainstream media contributed to the “spread” of the affliction. Those who were more inclined to post frequently about their ailment on sites like Facebook and those that gave frequent interviews to the press were thought to have the most aggravated conditions. The students who avoided these practices tended to improve more quickly.

Havana syndrome is potentially an even more recent example. Havana syndrome began in late 2016 in Cuba, when American and Canadian diplomatic personnel started reporting a number of symptoms—like headaches, nausea, dizziness, memory problems, hearing loss, and even “mild brain trauma”— which typically appeared after hearing a prolonged harsh, high-pitched noise. Strangely, other people nearby usually didn’t report hearing anything. By 2018, up to 40 cases of Havana syndrome had been documented among American and Canadian diplomatic personnel in Cuba. And in early 2018, similar claims began to be made by U.S. diplomats in China.

At first, many thought this was a case of international espionage at its finest—perhaps Moscow testing a secret acoustical weapon. But evidence to support that theory is lacking, and a number of scientists have now decided it’s more likely the diplomats were experiencing MPI. (Some have even suggested the high-pitched noise the diplomats heard was actually the sound of a particularly noisy type of cricket.)

There are many more examples of MPI in both modern times and the distant past. So, what is actually going on here? Well, first it’s important to point out that it’s almost impossible to completely eliminate other potential causes in these cases. There’s always the chance the unexplained symptoms linked to occurrences of putative MPI could be better explained by a toxin in the environment, a pathogen, or something else altogether that we just haven’t been able to identify. Perhaps, for example, Havana syndrome really was caused by some new weapon being surreptitiously tested by the Russians. We don’t know for sure.

But it’s also likely that at least some of these cases of potential MPI are due mainly to psychological factors. And if so, we’re at a loss to explain how, exactly, that might occur.

Some have suggested that extreme stress, pushing the brain to its cognitive breaking-point, might be a risk factor. Dancing mania, for instance, often affected areas that had recently been ravaged by harsh societal blights like food shortages, devastating diseases, etc. Others have argued that MPI preys primarily on the most suggestible people in the population. According to this hypothesis, there are some who are simply more inclined to believe a mysterious illness is taking hold of them, especially after they’ve heard about or seen someone else affected by that “illness.” (These might also be the same people who are most likely to be susceptible to the influence of something like hypnosis.) And still others are unconvinced that MPI is a viable diagnosis in many cases, since it implies a certainty we can’t possess (that there is no other cause of the condition) and assumes we have the ability to explain behavior that might have been prompted by any number of factors ranging from actual physical illness to cultural elements we may not completely understand.

Thus, at this point, MPI is controversial. We can’t explain why it might happen, and we also can’t say for sure how often it really does. But, there are many scientists who believe this type of mass hysteria is a legitimate phenomenon that has the potential to affect anyone, given the right circumstances. That’s a sobering thought, although it’s still unclear if it’s grounded in reality or if it, like the condition in question, is merely an example of the inherent fallibility of the brain.

References (in addition to linked text above):

Bartholomew RE. Tarantism, dancing mania and demonopathy: the anthro-political aspects of 'mass psychogenic illness'. Psychol Med. 1994 May;24(2):281-306.

Waller J. A forgotten plague: making sense of dancing mania. Lancet. 2009 Feb 21;373(9664):624-5.

Know Your Brain: Alzheimer's Disease

Background

Auguste Deter, the subject of Alois Alzheimer’s case study describing what would come to be known as Alzheimer’s disease.

In 1906, at a meeting of psychiatrists in Germany, Alois Alzheimer gave a lecture in which he detailed the unusual case of Auguste Deter. Alzheimer had encountered Deter about five years prior, when he was working as an assistant physician at a psychiatric institution in Frankfurt am Main in Germany. Deter had made an impression on Alzheimer because she was relatively young, but was suffering from a unique constellation of severe, dementia-like symptoms.

Deter was 51 years old when Alzheimer met her. Her most noticeable symptoms had begun in the previous year, when her behavior became alarmingly erratic. First, she began displaying uncharacteristic jealousy of her husband. Then, her memory started to deteriorate rapidly. She would easily become disoriented, and often lose touch with reality, consumed with paranoid delusions. As Alzheimer described it:

“…sometimes she thought somebody was trying to kill her and started to cry loudly… Sometimes she greets the attending physician like company…sometimes she protests loudly that he intends to cut her…Then again she is completely delirious, drags around her bedding, calls her husband and daughter and seems to suffer from auditory hallucinations. Often she screamed for many hours.”

Alzheimer was intrigued by the case. Deter seemed to be afflicted with a form of senile psychosis, which was probably a symptom of dementia. But it was rare to see dementia this severe in someone so young.

In addition to being a physician, Alzheimer was also an industrious researcher. He was intensely interested in pathological changes in the nervous system that accompanied psychiatric and neurological illnesses. Thus, when Deter died at the age of 55, Alzheimer requested her brain be sent to him for study. Upon examination, Alzheimer found the brain had suffered widespread neuronal loss and was riddled with abnormal structures (later learned to be the protein deposits discussed below).

Deter’s age, symptom profile, and neural deterioration convinced Alzheimer that she was a unique case. The psychiatrists present at his lecture on the topic didn’t seem to feel the same way, however, as there were no questions, comments, or other indications of interest following his presentation (the attendees seemed much more intrigued by the next presentation on compulsive masturbation). But little did Alzheimer know that his lecture would mark a historic moment, as only a few years later the renowned psychiatrist (and Alzheimer’s colleague) Emil Kraepelin introduced the term Alzheimer’s disease (AD) to describe an early-onset form of senile dementia.

It wasn’t until the late 1970s that researchers began to recognize that most cases of AD are not early-onset, and occur in patients over the age of 65. Today, AD is one of the greatest health concerns for people in this age group, and due to the fact that this population continues to increase in number (which is, ironically, a result of our improved ability to keep people alive longer), it is a rapidly growing problem. Today, about 1 in every 10 people over the age of 65 suffers from AD, and the number of people with AD in the United States is expected to nearly triple by the year 2050.

What are the symptoms of Alzheimer’s disease?

AD is a type of dementia, a term used to describe a condition that involves memory loss and other cognitive difficulties. There are a number of different types of dementia, however—each with its own causes and specific symptom profile. AD is just one variation.

The best-recognized sign of mental decline in AD is problems with memory. In the early stages of the disease, this often manifests as difficulties creating new memories, and problems are especially noticeable with declarative memories, or memories about information and events (as opposed to memories for how to do routine things like tie your shoes or eat with utensils, which are known as non-declarative memories). Early on, patients are typically able to maintain older memories and non-declarative memories. Over time, however, all memory can be affected, and even the most enduring memories may deteriorate.

But memory deficits are just one aspect of AD symptomatology. Patients can also experience problems with communication, and the ability to read and write may be impaired. Unpredictable mood disturbances, ranging from apathy and depression to angry outbursts, can occur. Thinking often becomes delusional, and a substantial subset of patients (up to 20%) even experience visual hallucinations.

It’s not just cognition that’s affected, though. Movement is hindered, causing patients to begin to lose mobility and have trouble performing even the simplest acts of self-care. Basic motor functions like chewing and swallowing become faulty, and incontinence eventually occurs.

In the end (if a patient survives this long), there aren’t many brain functions that haven’t been affected in some way, and patients become completely dependent on caregivers to help with even the most basic daily activities like eating and going to the bathroom. The disease is always fatal.

What happens in the brain in Alzheimer’s disease?

When Alois Alzheimer examined the brain of Auguste Deter, he noted a few distinct pathological changes. The first was that the brain had undergone significant atrophy. It appeared somewhat shrunken compared to a healthy brain.

This atrophying of the AD brain is due to the death of brain cells that occurs in the disease. AD is what is known as a neurodegenerative disease, which is a classification used to refer to diseases that cause the degeneration and death of neurons. A number of diseases fall into this category (e.g. Parkinson’s disease, amyotrophic lateral sclerosis), but AD is the most common of the group.

Alzheimer also noted unusual formations both within and surrounding neurons. He remarked that “distributed all over the cortex…there are…foci which are caused by the deposition of a special substance,” and he also mentioned “many fibrils located next to each other…they appear one by one at the surface of the cell.” Alzheimer was describing what today are the two hallmark neurological signs of AD: amyloid plaques and neurofibrillary tangles.

The first of these structures, amyloid plaques, consist of collections of small peptides (essentially a smaller version of a protein) known as amyloid beta, or Aβ, that form large clusters outside of neurons. Normally, enzymes called proteases can help to get rid of unwanted peptides and proteins in the brain. But amyloid plaques are especially resistant to degradation by proteases. Thus, they build up in the brain as the disease progresses; their presence is a defining feature of an AD brain.

Watch this 2-Minute Neuroscience video for a summary of the way Alzheimer’s disease affects the brain.

The other structure observed by Alzheimer, neurofibrillary tangles, also consist of abnormal deposits of proteins. In this case, the protein culprit is called tau. Tau normally plays an important role in helping to transport materials throughout the cell, but in AD it loses its normal function and clusters together in the tangles Alzheimer described. Like amyloid plaques, normal mechanisms the brain uses to remove unwanted protein deposits fail to effectively clear away neurofibrillary tangles. In fact, even after an affected neuron dies, the tangles found within it remain like a reminder of the neuron that was.

As the disease progresses, amyloid plaques and neurofibrillary tangles accumulate more and more in the brain. Thus, the appearance of these abnormal structures is correlated with the severity of the symptoms of AD. At the same time, exactly what role these structures play in the development of the disease remains unclear. For example, researchers are still unsure if amyloid plaques themselves are damaging to neurons, or if they represent an effort by the brain to sequester toxic Aβ peptides to protect neurons from their detrimental effects. There are similar questions about neurofibrillary tangles. Their appearance seems to be disruptive to neuronal function, and their spread throughout the brain correlates even better with neurodegeneration and symptoms than the proliferation of amyloid plaques. Nevertheless, their specific contribution to the progression of AD remains uncertain.

Causes and treatments

Thus, there are a lot of questions still surrounding the disease process of AD. Similarly, uncertainty surrounds why the disease affects some people but not others. In a small fraction of AD cases, the disease can be linked to mutations in a handful of identified genes whose protein products are involved in the production of the Aβ peptides mentioned above. But for most patients, there is no clear genetic or environmental cause of the disease.

There are, however, some known risk factors. For example, a variant of a gene called Apolipoprotein E, or ApoE, is known to increase the risk of AD by 10 to 20 times. ApoE encodes for a protein that is involved with the transport of cholesterol and other lipids in the blood, but it’s not yet clear why it might be involved with AD risk. High lipid and cholesterol levels, however, have also been identified as possible risk factors for the disease.

There are a number of other potential risk factors, like smoking, repetitive head injuries, poor cardiovascular health, and diabetes. Researchers are still unsure, however, just how these factors might increase the chances of developing AD. And by far the greatest risk factor remains one that we can’t avoid: old age.

Thus, the causes of AD remain somewhat obscure, which perhaps makes it unsurprising that our treatments are similarly unsatisfying. The most common treatment for the disease involves drugs that raise levels of the neurotransmitter acetylcholine in the brain. Acetylcholine is thought to play important roles in learning and memory, and large repositories of acetylcholine neurons (e.g. the nucleus basalis) are decimated during AD—likely contributing to memory loss.

Drugs called acetylcholinesterase inhibitors (AChEIs) suppress the activity of an enzyme called acetylcholinesterase, whose normal function is to remove acetylcholine from the synapse—in effect reducing the effect the neurotransmitter can have at that synapse. By inhibiting acetylcholinesterase activity, AChEIs cause acetylcholine levels to increase. In the process, these drugs can lead to modest improvements in memory. Because the effects are modest, however, AChEIs are often not very useful in the later stages of the disease. In fact, clear improvement in cognitive symptoms is only seen in less than 10% of patients taking the drugs. Additionally, AChEIs can only treat the symptoms of AD—they don’t do anything to stop the disease from progressing.

There are a handful of other treatments, and many others being explored, but at this point we don’t have any means of halting the neurodegeneration that underlies the symptoms of AD. Thus, we remain somewhat limited in our ability to treat the disease. Hopefully, continued neuroscience research allows us to one day develop better methods of addressing the pathological changes that occur in the AD brain.

References (in addition to linked text above):

Alzheimer A, Stelzmann RA, Schnitzlein HN, Murtagh FR. An English translation of Alzheimer's 1907 paper, "Uber eine eigenartige Erkankung der Hirnrinde". Clin Anat. 1995;8(6):429-31.

Cipriani G, Dolciotti C, Picchi L, Bonuccelli U. Alzheimer and his disease: a brief history. Neurol Sci. 2011 Apr;32(2):275-9. doi: 10.1007/s10072-010-0454-7.

Sanes JR, Jessell TM. The Aging Brain. In: Kandel ER, Schwartz JH, Jessell TM, eds. Principles of Neural Science, 5th ed. New York: McGraw-Hill.