She sits on the cold plastic folding chair with arms crossed. Her eyes are slightly narrowed in suspicion.
“What brings you here today?” The psychologist asks.
She glances around the crowded emergency room before responding. “You know why I’m here,” she whispers, as if they were sharing something private, “I’ve been infected.”
She carries on the interview in hushed tones. The psychologist learns that she has no prior psychiatric history whatsoever. Her speech is fast-paced and her thought processes are clearly tangential. She interrupts the psychologist to quietly respond to a voice that only she hears. When asked who she is talking to, she states that, “the government can hear everything. They know I’ve been infected with the virus. It was their plan all along.”
What is psychosis?
Psychosis is not a disorder in and of itself but rather refers to a group of symptoms that indicate a loss of touch with reality. Psychosis is predominantly categorized into positive and negative symptoms. Positive symptoms include auditory and visual hallucinations, delusions, suspiciousness, hostility, and conceptual disorganization, while negative symptoms include blunted affect, emotional withdrawal, apathy, stereotyped thinking, and poor rapport with others.
More recently, a third category of psychosis has been introduced: cognitive deficits. Cognitive deficits seem to predate disease onset and correlate with psychotic symptom type and severity.
Schizophrenia is arguably the most notable neuropsychiatric disorder that is characterized by psychotic symptoms- and remains one of the most severe types of mental illness- yet researchers and clinicians alike still know very little about what causes schizophrenia and related psychotic disorders.
One of the more popular theories that attempts to understand the origins of psychotic processes is the neural diathesis-stress model. Simply put, this model posits that a genetic predisposition coupled with environmental stressors gives way to the manifestation of psychotic symptoms. But this doesn’t explain the link between psychosis and primarily physical viral illnesses, such as COVID-19.
Linking Viral Illness to Psychosis
Perhaps the first better-known correlation between the onset of psychotic symptoms in response to viral illness was documented during the Spanish influenza pandemic of 1918. Individuals infected with influenza at that time were noted to have a variety of psychiatric sequelae, including hysteria, melancholy, and insanity. Similar findings were noted in later influenza pandemics, so much so that they were termed, "psychoses of influenza" (Kępińska et al., 2020). These accounts were the first to acknowledge viral illnesses as impacting more than just the respiratory system.
At present, the literature suggests the incidence of psychosis in confirmed COVID-19 cases to range from 0.9% to 4% (Brown et al., 2020). It is important to note, however, that this data is derived from observational and case studies with limited sample sizes.
At present, there appears to be a tripartite relationship between COVID-19 and psychotic symptoms:
- Primary: The virus itself is producing psychosis.
- Secondary: The consequences of the virus’ symptoms are producing psychosis.
- Tertiary: The impact of social isolation, coupled with an increase in fear and vigilance, is producing psychosis.
As with past influenza pandemics, there is some evidence to suggest that the COVID-19 virus has capability to penetrate the central nervous system, leading to inflammation of the brainstem. The medulla in particular is apt to be compromised in severe cases of respiratory failure. A strong correlation between neural inflammation and psychotic illness has been well-documented since the eighteenth century, making it likely that the onset of psychosis in a small subset of COVID-19 patients could be traced back to this etiological process.
Additionally, there is a wide subset of literature describing the hypercoagulability in COVID-19 cases ( Connors & Levy, 2020; Panigada et al., 2020; Spiezia et al., 2020). Essentially, these studies describe the abnormality of blood coagulation in COVID-19 patients, which increases the risk for blood clots in the circulatory system. Interestingly, the same global hypercoagulability is noted in individuals with schizophrenia (Chow et al., 2015).
Similarly, Acute Respiratory Distress Syndrome (ARDS) is a common complication in cases of COVID-19. ARDS has been associated with cerebral atrophy which occurs by way of hypoxic injury to neural (and other) tissue. Essentially, there is a reduction of oxygenated blood reaching essential organs. The deleterious effects of hypoxia has been associated with residual hyperglycemia, delirium, and hypotension—all of which can produce psychotic symptoms and lasting cognitive changes. There is some evidence to suggest mild-to-moderate global cerebral atrophy is occurring in severe COVID-19 cases. In particular, CT scans illustrate atrophy of the ventricles—a classic neurological finding in patients with psychotic illness (Li & Hashikawa, 2020).
While some individuals will display psychotic symptoms in association with a COVID-19 diagnosis, a number of individuals without the virus can display these symptoms as well. A recent case series documented four individuals who presented with acute psychosis in response to the psychosocial stressors associated with COVID-19 (Valdes-Florido et al., 2020). Moreover, an observational study suggests a 25% increase in acute psychoses for individuals living in areas with a high prevalence of COVID-19 cases (Hu et al., 2020). This data is in addition to a growing number of case studies that document similar findings.
Albeit a rare complication, the prevalence of psychosis in non-infected individuals appears to be occurring in response to quarantine and social distancing. While these measures are necessary and life-saving, living in quarantine and socially distancing oneself has been known to trigger psychotic episodes- particularly in individuals with a genetic predisposition. Solitary confinement, especially in extreme forms, has been used as a method of punishment since the early nineteenth century. Human beings require some form of social contact. In fact, it has been purported that psychosis derived from social isolation occurs, at least in part, due to the brain’s attempt to manifest a more comfortable, social experience; hence, auditory hallucinations. Excessive vigilance about hand-washing and personal health, conspiracy theories regarding the etiology of the virus, and general fear generated by the pandemic are additional factors that contribute to the manifestation of psychosis in a variety individuals.
What can we learn from this?
While the literature regarding psychosis in COVID-19 cases is flawed in terms of methodology and sample sizes, these studies still call to examine an interesting link between viral illness and psychosis, and further highlight the likelihood of multi-system involvement.
With regard to long-term outcomes for psychosis-linked COVID-19 cases, there appears to be some concern for lasting neuropsychological change. This is likely due to the association between cognitive deficits and psychosis. As aforementioned, cognitive deficits are a primary factor in psychosis and psychotic illness that tend to predate disease onset and persist beyond symptom resolve. It should not be surprising, then, that there is potential for long-term neuropsychological impairment in resolved COVID-19 cases. Specifically, researchers and clinicians suggest particular susceptibility to deficits in attention, processing speed (how quickly we can complete tasks), memory, and executive function (higher-order processing) (Li & Hashikawa, 2020).
The incidence of psychosis in viral illness gives credence to the mind-body connection. Physical health and mental health are so intertwined that you cannot attend wholly to one without consideration of the other—suggesting, perhaps, a false distinction between physical illness and psychological illness. The future of healthcare, and society at large, would likely benefit from the eradication of this distinction, as doing so would foster the betterment of medical outcomes, improve access to care, and reduce stigma. Future studies examining the relationship between viral illness and neuropsychiatric changes are warranted.
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Kępińska, A. P., Iyegbe, C. O., Vernon, A. C., Yolken, R., Murray, R. M., & Pollak, T. A. (2020). Schizophrenia and influenza at the centenary of the 1918-1919 Spanish influenza pandemic: mechanisms of psychosis risk. Frontiers in Psychiatry, 11, 72.
Valdés-Florido, M. J., López-Díaz, Á., Palermo-Zeballos, F. J., Martínez-Molina, I., Martín-Gil, V. E., Crespo-Facorro, B., & Ruiz-Veguilla, M. (2020). Reactive psychoses in the context of the COVID-19 pandemic: clinical perspectives from a case series.
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Hu W., Su L., Qiao J., Zhu J., Zhou Y. COVID-19 outbreak increased risk of schizophrenia in aged adults. 2020. Chinaxiv.org (preprint)
Li, Y. C., Bai, W. Z., & Hashikawa, T. (2020). The neuroinvasive potential of SARS‐CoV2 may play a role in the respiratory failure of COVID‐19 patients. Journal of medical virology, 92(6), 552-555.
Connors, J. M., & Levy, J. H. (2020). Thromboinflammation and the hypercoagulability of COVID‐19. Journal of Thrombosis and Haemostasis.
Panigada, M., Bottino, N., Tagliabue, P., Grasselli, G., Novembrino, C., Chantarangkul, V., ... & Tripodi, A. (2020). Hypercoagulability of COVID‐19 patients in intensive care unit. A report of thromboelastography findings and other parameters of hemostasis. Journal of Thrombosis and Haemostasis.
Spiezia, L., Boscolo, A., Poletto, F., Cerruti, L., Tiberio, I., Campello, E., ... & Simioni, P. (2020). COVID-19-related severe hypercoagulability in patients admitted to intensive care unit for acute respiratory failure. Journal of Thrombosis and haemostasis.