The Outbreak Narrative: What has changed this time around?

EDITOR’S NOTE: Points is delighted to welcome past guest contributor, Jessica Diller Kovler (check out her previous post here). Kovler is part of the History of Science program at Harvard University and currently teaches at John Jay College of Criminal Justice, the City University of New York. Her work has appeared in The New York Times, Forbes, and Discover magazines. 

Unless you’ve had your head buried in the sand for the past month, you’ve undoubtedly thought of the recent Ebola outbreak. Even if you have a background in public health, you would probably avoid the New York bowling alley visited by Dr. Craig Spencer (even though the City shut it down the day the news of his illness hit the papers). You’re probably using extra Purell, even though we’re relatively knowledgeable about the pathogen’s mode of transmission.

News reporters have scrambled to assemble our patient zero. Even our most liberal friends are arguing for shutting down the borders. We are blaming and looking for answers.

Bloomberg Buisnessweek, September 24, 2014
Bloomberg Buisnessweek, September 24, 2014

As my grandfather would ask at our Passover Seder: “Manishtana?” (What has changed?) As a social historian, I wonder what makes the societal response to Ebola any different than our collective response to the Black Death, typhoid, polio, and HIV? In the past few weeks, people have compared the response to Ebola to the first cholera pandemic of the early-19th century, the 1918 Spanish Flu epidemic, the polio epidemic of the first half of the 20th century, and AIDS in the early 1980s. Perhaps, as some have argued, there is a formulaic narrative in how we respond to outbreak of disease. But does this narrative also apply to epidemics involving alcohol abuse (or, in the case of the disease I’m about to describe, suspected alcohol abuse)?

From 1915 to 1927, a mysterious illness befell millions worldwide. Its symptoms were wide-ranging—no two patients presented exactly the same—and the illness left many of its survivors in a catatonic, semi-conscious state. Those who “awakened” were left with Parkinsonism, psychiatric sequelae, and severe behavior disturbance. Almost as quickly as Encephalitis Lethargica appeared in 1915, it seemingly vanished 12 years later. Thousands around the world, however, lived long past 1927, imprisoned—some for decades—in their own bodies. The lack of attention to this disorder beyond its peak, has, in recent years, earned the disease the moniker “The Forgotten Epidemic.” (Perhaps you’ve heard of the disease thanks to the 1990 Oscar-nominated film, Awakenings, starring Robin Williams and Robert DeNiro, based on the work of Oliver Sacks.)

Yet the history of Encephalitis Lethargica is more than the tale of a forgotten epidemic. It is an illness narrative evoking shifting socio-medical paradigms in the second half of the 20th century that is uniquely tied to the sociomedical response to alcoholism.

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One night in 1926, Sylvia dreamt that the world had come to a stop, and that she was a living statue of stone. By morning, her nightmare had come true. In France, not even childbirth could awaken one mother. In Switzerland, a bride “fell frozen” at the altar. In Vienna, a man playing cricket froze as he lifted his arm up to catch a ball and found himself stuck in that position. A young man awoke from a trance-like state, only to feel a compulsion to steal. Another man wrote: “I am certain I have been given another character. Mine died in my sleep.”

These bizarre and seemingly unrelated symptoms were signs of one of the most mysterious epidemics in modern history. The story of Encephalitis Lethargica—and its victims—is important to examine within the context of the widely observed and accepted “outbreak narrative” as identified in the historiographic literature by Priscilla Wald, professor at Duke University and author of Contagious (2008). Such narratives dictate how a society usually responds, often in a formulaic fashion, to an unknown or poorly understood pathogen or disease. In general, according to Wald, these narratives proceed as follows: Fear and uncertainty define the beginning stages of an epidemic. This is followed by the race to identify a mysterious pathogen, subsequent recognition of the illness, identifying “global networks of contact and contagion,” and then “containment,” and “subsequent epidemiological analysis.”

Encephalitis Lethargica seems to defy this formulaic narrative. Symptoms varied so greatly, as did the incubation period, that many doctors were unable to recognize the disease in its earliest stages. (Some patients reached a level of extreme severity within a matter of hours, while others reached the most acute phase over many years. Some recovered in a matter of days, others over many decades, while others succumbed quickly and died.) That the disease did not follow a prescribed pattern made only its misdiagnosis predictable. And—as I’ve argued for some time—due to its inconsistent symptomology and presentation, doctors often confused and conflated Encephalitis Lethargica with symptoms of a more familiar condition: the Tardive Dyskinesia observed during alcohol withdrawal.

Identifying the emerging infection, vital to the standard outbreak narrative, proved difficult in the case of Encephalitis Lethargica. Doctors were baffled over the cause and mode of transmission. One doctor in New Orleans told a medical journal that it was “difficult to make a positive diagnosis of the disease,” in large part because his patient was an “alcoholic” with a “wet brain on account of alcoholic history.” Some reported that it was easier to make a diagnosis in people who denied alcohol use, yet, as clinicians then and now recognize, patients typically underreport or deny drug or alcohol use. Women were typically not diagnosed as alcoholics until the late 20th century. Thus, when women presented with Encephalitis Lethargica’s Parkinsonian tremors, doctors were likelier to correctly diagnose the disease. (More women than men were diagnosed with the disease, leading historians to question how many men were misdiagnosed as alcoholics.)

During the 1920s, many catatonic Encephalitis Lethargica patients were confined to specially built facilities or transitioned to hospitals previously designed to quarantine those with other epidemic diseases, e.g. smallpox. Additional wards were created in hospitals to care for the “chronically insane.” This is because some victims spontaneously awoke from their catatonia, seemingly without warning, and were left with Parkinsonism symptoms (both physical and mental presentation) and previously undocumented psychiatric sequelae including delirium, hysteria, uncontrolled rage, lethargy, and compulsive behaviors. In his analysis of patient records, neuroscience researcher Paul Foley noted that had the afflicted “not at some time exhibited symptoms that allowed a diagnosis of Encephalitis Lethargica, [it] would have resulted in their being classified as schizophrenic or hysteric.” To quell their psychiatric symptoms, some patients turned to alcohol, and would eventually become alcoholics.

Encephalitis Lethargica patient
Encephalitis Lethargica patient

In addition, misdiagnosis of the psychiatric symptomology confounded the ability of clinicians to properly assess patients once they recovered. For example, some early patient reports suggested no clinical reason for a patient’s symptoms, and no reportable pathology. Concluding remarks in these reports include directives to “immediately cease consumption of alcohol,” tremors again clinically interpreted as the effects of chronic alcoholism. This Sontagian practice of victim-blaming was as common as blatant misdiagnosis. A 1925 New York Herald Tribune report lamented how “Sleepy Sickness Victims Are Often Made Martyrs to Injustice,” as “the dread[ed] disease is mistaken for [the] trick of lazy.” One patient self-report noted how her seemingly mild bout with Encephalitis Lethargica caused her “extreme humiliation” because her symptoms were seen as drunken behavior or drug addiction—not post-encephalitic syndrome. Her symptoms persisted for the better part of a decade, and her employers threatened termination for suspected addiction. As she wrote, “Life was nothing but a command to ‘wake up’ when all I wanted in the world was to be left entirely alone and to be allowed to continue sleeping.” Doctors were quick to diagnose her with melancholia/depression. She lived her life “humiliated,” she wrote, the result of her somnolence and instability.

For the Encephalitis Lethargica patient suffering psychiatric symptoms, life proved difficult to navigate. While victims of other outbreaks were isolated for fear of contagion, these patients were warehoused for fear of antisocial behaviors that could not be explained or treated through known interventions. Again, Encephalitis Lethargica proves an exception to the outbreak narrative, with no pathogen to blame, no method to control the disease, and, in the case of extreme psychiatric symptoms, no way to control the patients. Yet as a simulacrum of the disease, alcoholism served as a believable conclusion for doctors following the outbreak narrative.

It has been no formidable challenge to track down Ebola’s “patient zero.” But when little is understood about disease causality and transmission, and where misdiagnosis is rampant because of the disease’s symptomological similarity to a social problem like alcoholism, it’s much more difficult.

The outbreak narratives for other epidemics are defined by social reactions to the disease. Omnipresent is the impulse to blame a segment of society for the outbreak (e.g. the poor during cholera outbreaks or anyone from West Africa in 2014) and stigmatize the behaviors of groups that either carried or ran a higher risk of transmission (e.g. the sexual activities of gay men during the early days of the HIV/AIDS epidemic). Encephalitis Lethargica flouts this aspect of the outbreak narrative, as its immediate social component was alcoholism, if anything at all.