Additionally, neuroinvasion of SARS-CoV-2 via the olfactory nerve has been demonstrated in the animal model, which is supported by the characteristic symptom of anosmia commonly suffered by patients with COVID-19. Furthermore, many viruses, including human coronaviruses, use retrograde axonal transport to allow CNS invasion via peripheral nerves. Another possible mechanism of neuroinvasion includes the entry of SARS-CoV-2 via the endothelial cells of the blood brain barrier in the setting of viremia, which has been demonstrated with other viruses. It has been demonstrated that the binding of SARS-CoV-2 to angiotensin-converting enzyme 2 (ACE2) receptors results in cellular invasion, and the ACE2 receptors are located on cells of the CNS including neurons and glia of various structures including olfactory groove and trigeminal ganglia. However, there have been many hypothesized mechanisms describing the ability of SARS-CoV-2 to invade the central nervous system, and therefore headache due to direct CNS invasion may be the causal mechanism in some patients. Headaches may also occur as a result of complications of viral infection, such as hypoxia and dehydration. Interleukin-6 (IL-6), a proinflammatory cytokine which also has been implicated in migraine, has also been studied in the COVID-infected population retrospectively with some associations found with pain in frontal regions, though another study noted that levels were found to be lower in a headache group presenting for emergency care. Support for an underlying cytokine-driven mechanism is reinforced by the findings of increased levels of IL-10 in patients with headache, along with the trend towards elevation of other interleukins (including IL-23 and PIGF1) in an exploratory study comparing cytokine profiles in patients with and without headache in SARS-CoV-2 infection. Respiratory viral infections are associated with headache even without direct CNS infection, and although the exact mechanism has yet to be elucidated, this is likely a result of fever and activation of inflammatory cytokines and cytokine release storm. Given the extent of impact headache has on patients who have had SARS-CoV-2 infection, the need for timely diagnosis of associated headache disorders, investigation of underlying mechanisms, and ultimately optimization of treatment is prudent. It is also becoming apparent that patients with long-term effects from COVID-19, so-called COVID long haulers, experience headache as one of the most common persistent symptoms. Although the literature describes many types of headaches occurring in the setting of COVID-19, common features include a moderate to severe persistent headache that is often refractory to treatment. Ĭurrent literature suggests that headache associated with COVID-19 may be unique, often presenting as a new phenotype in patients with a history of a primary headache disorder or resulting in a new headache syndrome in those without history of headache. described in their retrospective cohort study that the most frequent neurological manifestation of COVID-19 in younger patients was headache, in contrast to stroke and confusion in older adults. It should be noted that studies that cite higher frequency of headache are often using healthcare professionals as their population, and therefore these individuals may be better able to recognize their symptoms. Reported rates of headache in the setting of COVID-19 are variable, ranging from 6.5 to 71% in various studies. As our literature search revealed that the bulk of original research centers on our understanding of headache after COVID-19, we have centered our review on this specific topic.
Covid headache update#
In this review, we will provide an update on headache post virus, with an emphasis on reports published within the last 3 years. In the current coronavirus disease 2019 (COVID-19) pandemic, headache has been found to be one of the most common neurological symptoms of SARS-CoV-2 infection and has even been included as one of the presenting cardinal symptoms. This has also been seen more recently in 2009 during the H1N1 pandemic, in which the most frequent neurological sign reported was headache.
Historically, headache has been observed as a complication of many viral epidemics, including Spanish influenza in 1918 and the Russian or Asiatic flu in 1890. Headache in association with viral infection, either in accompaniment with or post-infectious, is a well-documented phenomenon that is acknowledged by the International Classification of Headache Disorders, 3rd edition (ICHD-3), and may be a result of neuroinvasive disease or systemic infection.
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