Unpacking the Medical Mystery of Encephalitis Lethargica
Written by Nicholas Kwok June 20, 2024
Written by Nicholas Kwok June 20, 2024
Imagine lying in a cold hospital bed, shivering under the bare white blankets with your eyes wide open but unseeing, unable to move in your own body—frozen. Numerous medical professionals surround you but cannot diagnose you. Your heartbeat rises, and precious memories revolve around your mind. Was this a dark journey into the great unknown? A path shrouded in mystery?
Encephalitis Lethargica, or the ‘sleeping sickness,’ has remained a great medical mystery. “Encephalitis Lethargica (EL) was a mysterious and devastating early 20th-century epidemic that killed, by one estimate, 500,000 people worldwide” [4]. How were 500,000 individuals mysteriously murdered? Why has the current medical industry still not found a cure? Nonetheless, what caused the spread of this morbid sickness throughout Europe?
Although many theories surround the diffusion of sleeping sickness, a combination theory of a bacterial streptococcal infection associated with an autoimmune disorder and brain manipulation originating in the Romanian Kingdom is the most credible.
The Romanian Kingdom of 1916, which once was a communal home to many, mysteriously shriveled into nothingness — a possible plotline of a grotesque nightmare. However, what could have caused the disaster, which rapidly spread throughout Europe, mass killing countless individuals? Encephalitis Lethargica, more commonly known as the sleeping sickness, provided a slow, painful death for thousands — manipulating the consciousness of the host’s minds, limiting speech and even laughter for up to years.
This severe disease, characterized by high fevers, double vision, and delayed mental responses, leads to paralysis. Although many theories surround the diffusion of Encephalitis Lethargica, a combination theory of a bacterial streptococcal infection associated with an autoimmune disorder and brain manipulation originating in the Romanian Kingdom is the most credible.
A streptococcal infection affecting the respiratory system diffuses Encephalitis Lethargica. Numerous EL patients previously experienced a streptococcal infection before death [1]. Countless studies have also shown that EL correlates to brain inflammation. In the 1920s, doctors conducted autopsies on EL patient brains and found streptococcal antibodies in the cerebrospinal fluid.
The cerebrospinal fluid surrounds the brain tissue and aids in nutrition. Antibodies meant to protect the body against streptococcal infection eventually began manipulating the brain [6]. “Furthermore, western immunoblotting showed that 95% of EL patients had autoantibodies reactive against human basal ganglia antigens” [1]. The basal ganglia aided in movement and cognition, which were uncontrollable functions in EL, antibody-manipulated patients. The patient's autoimmune system weakens because of the negative connection between both EL and respiratory infection symptoms.
Encephalitis Lethargica manipulates antibody functions as an autoimmune disorder. The disorder occurs when the body’s antibodies begin attacking healthy cells in the brain. Several studies have found that individuals have higher levels of antibodies in some brain regions, such as the basal ganglia, thalamus, and brainstem [1].
These three vital brain sections support the body’s motor skills, emotions, and consciousness. “The thalamus is composed of different nuclei that each serve a unique role, ranging from relaying sensory and motor signals, as well as regulation of consciousness and alertness” [5]. An abundance of thalamus antibodies may lead to Encephalitis Lethargica. The offset of antibodies in the brain caused individuals to appear unstable and sleep-deprived, almost statue-like.
Encephalitis Lethargica’s symptom of increased inflammation in the thalamus and basal ganglia caused excessive sleepiness. As a result, patients suffered from hallucinations, insomnia, and many other neuropsychiatric symptoms.
The deterioration of healthy cells in the brain led patients to severe mental disorders that impacted both their personalities and consciousness. Insomnia leads to neurological imbalances throughout the host’s body. The side effects of insomnia resulted in malnutrition and an increased risk for other infections. These long-term symptoms often lead to a reduced quality of life or even possible death [1].
The most credible theory links all three possible approaches through a common thread: antibodies. The double-edged sword (antibodies), which supposedly helps protect the body from harm, became the culprit responsible for over 500,000 deaths in Europe. Instead of helping fight the infection, they destroyed the brain’s protective cells. The streptococcal infection triggers an autoimmune response, causing the immune system to attack the brain. [6].
Although many theories surround the diffusion of EL, the most accurate is a combination theory of a bacterial streptococcal infection associated with an autoimmune disorder and brain manipulation originating in the Romanian Kingdom. Research has shown that the disease affects the brain’s regulation of sleep-wake cycles [6].
Imbalanced sleep cycles influence negative symptoms such as excessive sleepiness and insomnia. Furthermore, the neurological after-effects of survivors support the correlation to the neuropsychiatric nature of the sleeping sickness. Like the common cold, the disease spread rapidly throughout Europe as a bacterial infection first transmitted throughout the respiratory system, then upwards to the brain, causing damaged neurons and manipulative contact among them [2].
Ultimately, Encephalitis Lethargica remains one of the most fascinating medical mysteries of the 20th century. While the disease may not have created a pandemic outbreak that caused the world to plunge into the abyss of obscurity, it did strike as a sporadic streptococcal bacterial jolt, affecting countless lives both physically and mentally.
Unfortunately, this disease is still prevalent in today’s society and remains mostly unknown. In the future, it is vital to study the background of Encephalitis Lethargica to decrease the risk of exposure to individuals globally. Ongoing research will be required to unravel more truths about Encephalitis Lethargica and its dark realm of secrets.
REFERENCES
Dale, Russell C et al. “Encephalitis lethargica syndrome: 20 new cases and evidence of basal ganglia autoimmunity.” Brain: a journal of neurology vol. 127, Pt 1 (2004): 21-33. doi:10.1093/brain/awh008 Retrieved June 10, 2024
Devinsky, Orrin. “Encephalitis Lethargica.” Seminars in Neurology, vol. 29, no. 4, 2009, pp. 361-375. Retrieved June 11, 2024
Hoffman, L.A., & Vilnesky, J.A. (2017, July 14). Encephalitis lethargica: 100 years after the epidemic. Retrieved June 8, 2024
Ravenholt, R. T., & Foege, W. H. (1982). 1918 influenza, encephalitis lethargica, parkinsonism. Lancet (London, England), 2(8303), 860–864. https://doi.org/10.1016/s0140-6736(82)90820-0. Retrieved June 8, 2024
Torrico TJ, Munakomi S, “Neuroanatomy, Thalamus - Statpearls - NCBI Bookshelf.” Neuroanatomy, Thalamus, NIH Library, https://www.ncbi.nlm.nih.gov/books/NBK542184/. Retrieved June 10, 2023
Vilensky, J. A., & Gilman, M. R. (2012). Encephalitis lethargica: The mind and brain virus. Journal of the History of the Neurosciences, 21(1), 46-63. Retrieved June 10, 2024