Medical hypotheses. 2021;146:110469
Plain language summary
A proportion of COVID-19 patients develop post-COVID-19 syndrome, with long-term symptoms such as persistent fatigue, muscle pains, depressive symptoms, and non-restorative sleep, similar to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In this article the author presents his medical hypothesis that, in a subset of patients at least, post-COVID-19 fatigue syndrome may result from damage to olfactory (smell) sensory neurons, which in turn may lead to toxic build-up within the central nervous system (CNS) through congestion of the glymphatic system (the waste clearance system of the CNS). Loss of smell and altered sensation of taste have been reported in 33–80% of COVID-19 patients but the underlying mechanisms are not yet known. Most of these patients regain their sense of smell within 1-3 weeks, suggesting that the virus does not affect the olfactory neurons but their surrounding supporting cells. Some patients, however, do not regain their sense of smell for months which may point to the destruction of neurons. A decrease in olfactory neurons may affect the flow of the cerebrospinal fluid (CSF) in an area important for CSF drainage. This may cause an increase in intracranial pressure (idiopathic intracranial hypertension, IIH) and congestion of the glymphatic system, which have been associated with chronic fatigue syndrome, as well as with headaches and tinnitus, symptoms also commonly seen in COVID-19 patients. The author states that if this hypothesis is confirmed, glymphatic-lymphatic drainage therapies, such as osteopathy, should be recommended as early treatment for patients with post-COVID-19 fatigue syndrome.