Highlights
- •New-onset headache following COVID-19 is a heterogenous condition.
- •New daily persistent headache represents the most frequent initial diagnosis.
- •Response to therapy is variable.
- •COVID-19 may act as a trigger for idiopathic headaches.
Abstract
Objective
To describe the characteristics of patients with new-onset headache following SARS-CoV-2 infection.
Background
SARS-CoV-2 infection leads to several neurological manifestations, and headache is a frequent and disabling symptom, both exacerbating pre-existing headache syndromes and causing new-onset ones.
Methods
Patients with new-onset headache after SARS-CoV-2 infection with consent to participate were included, while those ones with previous headaches were excluded. The temporal latency of headache after infection, pain characteristics, and concomitant symptoms were analysed. Moreover, the efficacy of acute and preventive medications was explored.
Results
Eleven females (median age 37.0 [10.0–60.0] years old) were included. In most cases, headache onset occurred with the infection, the location of pain varied, and the quality was either pulsating or tightening. Headache was persistent and daily in 8 patients (72.7%), while it occurred in episodes in the remaining subjects. Baseline diagnoses were new daily persistent headache (36.4%), probable new daily persistent headache (36.4%), probable migraine (9.1%), and migraine-like headache secondary to COVID-19 (18.2%). Ten patients received one or more preventive treatments and six of them showed an improvement.
Conclusion
New-onset headache following COVID-19 is a heterogenous condition with uncertain pathogenesis. This type of headache can become persistent and severe, with a wide spectrum of manifestations (new daily persistent headache being the most represented one) and variable response to treatment.
Keywords
1. Introduction
SARS-CoV-2 pandemic considerably influenced the prevalence and clinical course of pre-existing headache disorders both due to social distancing [
[1]
] and to several (mainly psychological) pandemic associated factors, that worsened headache frequency and intensity [[2]
]. Moreover, headache is the most common neurological symptom of SARS-CoV-2 infection, and it is overall among its five most common symptoms [[3]
]. Indeed, it has been reported as a prodromal symptom of COVID-19, as part of the acute symptomatology of the disease or, in some cases, it may persist even in the long term after the end of the disease [4
, 5
, 6
, 7
]. Headache associated with COVID-19 (HCoV) is heterogeneous, although it usually presents at the beginning of the infection with a tension-type form in more than 50% of cases [[8]
]. This condition may even become long lasting, as showed in a meta-analysis conducted on hospitalized COVID-19 survivors; this study reported that HCoV may persist for up to 90 days from discharge in 10.6%, and for more than 180 days in 8.4% of patients [[9]
]. Furthermore, acute treatment options for HCoV are not defined, with analgesic and steroidal approach being among the most used ones [[6]
].Sometimes, patients seek medical attention complaining of a new-onset persistent headache. In patients without a clinical history of headache, this condition is addressed as new daily persistent headache (NDPH) [
[10]
]. It is a rare headache disorder (ranging from 0.03 to 0.1% in general adult population), which has been found to be more frequent among children and adolescents [[11]
]. Typically, NPDH is characterized by a sudden onset of headache with continuous, unremitting pain, lasting for over 3 months that usually has a poor response to common headache treatments, often requiring an aggressive therapeutic regimen with intravenous steroids [[10]
,[11]
]. Very little is known about NDPH pathogenetic mechanisms, but infections or flu-like syndromes are the most referred triggers (22%) [[12]
]. It has been proposed that NDPH may arise because of the activation of the pro-inflammatory cascade after an infection; however, the very low frequency of NDPH in comparison to the high prevalence of infectious diseases in general population suggests that other still unknown factors might play a relevant role in the genesis of the condition. Particularly, viral infections are described among the triggers of NDPH [[11]
], and, among them, even SARS-CoV-2 [[6]
].Here, a multicentre case series of patients presenting with new-onset headache following COVID-19 infection is presented.
2. Materials and methods
A multicentre prospective observational study, including patients evaluated at three different Italian Headache Centres (Referral Centre for the Study of Headaches, AOUP “Paolo Giaccone” of Palermo; Regional Headache Referral Centre - ASL 1 Abruzzo; Child Neurology and Psychiatry Unit - ISMEP, “G. Di Cristina” Children's Hospital - ARNAS Civico of Palermo) was carried out in the period from July 2020 to July 2022. The inclusion criteria were: 1) the presence of a new-onset headache started during or within three months after SARS-CoV-2 infection in patients without a history of previous headache disorders; 2) informed consent for participation. The onset of the SARS-CoV-2 infection was defined as the day in which patients started to complain flu-like symptoms (then positive for SARS-CoV-2), while the end of the infection was defined as the day of the first negative antigenic or molecular nasal swab. The only exclusion criterion was a previous history of primary or secondary headache disorders. The study was approved from Palermo 1 ethical committee on 13th July 2020 (record n.7/2020).
Baseline and follow-up data including demographic information (age, sex) and comorbidities were recorded during routine neurological evaluations at the headache centres. During the baseline clinical evaluation, the following characteristics about COVID-19 infection were recorded: disease duration (number of days from the onset of symptoms to the negative result of the oropharyngeal swab), disease severity (e.g., asymptomatic, mild oropharyngeal symptoms with or without fever, or hospital admission for more severe cases), and the presence of other neurological symptoms apart from headache (e.g., hyposmia, dysgeusia or paraesthesia). Finally, for patients included after the advent of anti-SARS-CoV-2 vaccination, data on the patient's vaccination protocol and timing in relation related to infection were collected.
Regarding headache, information about its onset in relationship to the infection (i.e., concurrently or after it, with the latency in days), its location (e.g., frontal, temporal, parietal, occipital), intensity (on a visual analogue scale – VAS – from 1 to 10), quality (e.g., pulsating or tightening), duration (in hours), frequency (days/month), and concurrent symptoms (e.g., nausea, photophobia, phonophobia, worsening with physical exercise) were recorded. The above-mentioned headache characteristics were used to attribute a diagnosis using the International Classification of Headache Disorders, 3rd edition (ICHD-3) criteria [
[10]
]. Moreover, data regarding any preventive and acute treatments for headache control and their efficacy were recorded. Also, when a brain imaging exam was performed, relevant findings were reported.At follow-up evaluation (performed within 3 months in most cases), headache characteristics and treatment response were assessed. Regarding acute medications, patients' subjective response was recorded. Regarding preventive treatment response, patients were classified as: 1) responders (i.e., reduction of headache days more than 50%), 2) partial responders (i.e., reduction between 30 and 50%), and 3) non-responders (i.e., headache days reduction below 30%); following the same criterion, preventive treatment were classified as 1) effective, 2) partially effective, or 3) ineffective.
All categorical variables were given as percentages. Quantitative variables were reported as medians and interquartile ranges (IQR), and were analysed with Mann-Whitney U test and Kruskal-Wallis non-parametric tests for independent samples. All analyses were carried out using IBM SPSS v.26 software.
3. Results
During the study period, 3030 first visits were performed at the three headache centres (1620 at the Referral Centre for the Study of Headaches, AOUP “Paolo Giaccone” of Palermo; 1080 at the Regional Headache Referral Centre - ASL 1 Abruzzo; 330 at the Child Neurology and Psychiatry Unit - ISMEP, “G. Di Cristina” Children's Hospital - ARNAS Civico of Palermo). After the analysis of medical records for inclusion and exclusion criteria, 11 female patients, aged 37.0 (10.0–60.0) years old were included. Regarding reported comorbidities, 3 patients (27.3%) were affected by arterial hypertension, one (9.1%) by hypothyroidism, one (9.1%) suffered from left ear hearing loss and had a history of insomnia, while another one (9.1%) suffered from paroxysmal tachycardia (see Table 1 for patients' characteristics).
Table 1Population characteristics.
| Population characteristics (n = 11) | ||
|---|---|---|
| Median age | 37 y (10–60) | |
| Sex | Female | 11 (100%) |
| Comorbidities | Cardiologic Endocrinologic Other None | 4 (36%) 1 (9%) 1 (9%) 6 (54%) |
COVID-19 lasted a median of 9.0 (7.0–15.0) days, presenting with mild symptoms in all patients (rhinorrhoea, sore throat, non-productive cough). Four patients (36.4%) showed transient hyposmia. Four patients (36.4%) presented the infection during 2020, hence they were not vaccinated against COVID-19, while only one of the remaining patients was unvaccinated (9.1%).
The headache started during COVID-19 infection in 54.5% of cases and its clinical features assessed during the first patient evaluation are summarised in Table 2. The localization of the pain was varied, with either pulsating (54.5%) or tightening quality (45.5%). More than half of the patients complained of some symptoms associated with headache (Table 2), among which nausea was the most frequent (54.5%). In 8 cases (72.7%) the headache was persistent and daily, while in the remaining cases it occurred in an episodic form. Lastly, according to ICHD-3 criteria, baseline diagnoses were distributed as follows: NDPH (36.4%), probable NDPH (36.4%), migraine-like headache secondary to COVID-19 (18.2%), and probable migraine (9.1% - see Table 2). All patients showed a normal neurologic physical examination.
Table 2Headache characteristics and diagnosis at baseline.
| Headache characteristics | ||
|---|---|---|
| Onset from COVID-19 (days) | 0.0 (0.0–10.0) | |
| Localization, n (%) | frontal | 3 (27.3%) |
| fronto-temporal | 2 (18.2%) | |
| temporal | 1 (9.1%) | |
| parietal | 1 (9.1%) | |
| occipital | 1 (9.1%) | |
| periorbital | 1 (9.1%) | |
| holocranic | 2 (18.2%) | |
| Lateralization, n (%) | bilateral | 10 (90.9%) |
| unilateral | 1 (9.1%) | |
| Irradiation, n (%) | from bilateral occipital to temporal | 1 (9.1%) |
| from bilateral frontal to the whole head | 1 (9.1%) | |
| Quality, n (%) | pulsating | 6 (54.5%) |
| tightening | 5 (45.5%) | |
| Intensity (VAS) | 8.0 (7.0–8.0) | |
| Associated symptoms, n (%) | nausea | 6 (54.5%) |
| photophobia | 3 (27.3%) | |
| phonophobia | 2 (18.2%) | |
| tearing | 2 (18.2%) | |
| burning eye | 2 (18.2%) | |
| brief episodes of stabbing pain | 2 (18.2%) | |
| worsening with physical activity | 2 (18.2%) | |
| vomiting | 1 (9.1%) | |
| brain fog | 1 (9.1%) | |
| tinnitus | 1 (9.1%) | |
| Duration (hours) | persistent in 8 (72.7%) | 18.0 (8.0–24.0) in 3 (27.3%) |
| Headache days/month | daily in 8 (72.7%) | 16.0 (11.0–22.0) in 3 (27.3%) |
| Proposed diagnosis, n (%) | NDPH | 4 (36.4%) of which: |
| 3 tension-type like (75.0%) | ||
| 1 migraine like (25.0%) | ||
| probable NDPH | 4 (36.4%) of which: | |
| 3 migraine-like (75.0%) | ||
| 1 tension-type like (25.0%) | ||
| migraine-like headache secondary to COVID-19 | 2 (18.2%) | |
| probable migraine | 1 (9.1%) | |
| Latency from headache onset and first evaluation (days) | 47 (26–158) | |
VAS Visual Analogue Scale; NDPH New Daily Persistent Headache.
Table 3List of drugs used both for acute and preventive treatment.
| Response to medication | |||
|---|---|---|---|
| Acute treatment, n (%) | acetaminophen | 5 (45.5%) | 3 (27.3%), effective |
| 2 (18.2%) ineffective | |||
| NSAIDs (ibuprofen, naproxen, indomethacin) | 7 (63,7%) | 5 (45.5%) partially effective | |
| 2 (18.2%) ineffective | |||
| Preventive treatment, n (%) | amitriptyline | 4 (36.4%) | 3 (27.3%) ineffective |
| 1 (9.1%) not tolerated | |||
| magnesium | 4 (36.4%) | ineffective | |
| corticosteroids (prednisone, dexamethasone) | 3 (27.3%) | 2 (18.2%) effective | |
| 1 (9.1%) ineffective | |||
| topiramate | 2 (18.2%) | ineffective | |
| cinnarizine | 2 (18.2%) | 1 (9.1%) partially effective | |
| 1 (9.1%) ineffective | |||
| B-vitamins drugs | 2 (18.2%) | 1 (9.1%) effective | |
| 1 (9.1%) partially effective | |||
| propranolol | 1 (9.1%) | ineffective | |
| lamotrigine | 1 (9.1%) | ineffective | |
| carbamazepine | 1 (9.1%) | ineffective | |
| bilateral greater occipital anaesthetic nerve block | 1 (9.1%) | ineffective | |
| adjustment of antihypertensive therapy | 1 (9.1%) | effective | |
| no therapy | 1 (9.1%) | effective | |
NSAIDs: Non-Steroidal Anti-inflammatory Drugs; n: number of patients who underwent the treatment; the right column shows the efficacy of each treatment.
Table 4Headache characteristics at follow-up and response to treatment.
| Headache at follow-up | |||||
|---|---|---|---|---|---|
| Group (n) | Baseline days/month (IQR) | follow-up days/month (IQR) | % reduction (IQR) | p-value | |
| Frequency | total sample (11) | 30.0 (22.0–30.0) | 15.0 (2.0–30.0) | 40.0 (0–93.3) | 0.06 |
| responders (4) | 26.0 (17.5–30.0) | 5.0 (0.5–13.3) | 71.7 (50.0–98.3) | 0.02 | |
| partial responders (2) | 20.5 (11.0–30.0) | 12.5 (7.0–18.0) | 38.2 (36.4–40.0) | 0.44 | |
| non-responders (4) | 30.0 (30.0–30.0) | 30.0 (30.0–30.0) | 0.0 (0.0–0.0) | 1.00 | |
| autoresolution (1) | 30.0 | 1.0 | 96.7 | 0.32 | |
| Group (n) | Baseline VAS (IQR) | follow-up VAS (IQR) | % reduction (IQR) | p-value | |
| Intensity | all sample (11) | 8.0 (7.0–8.0) | 6.0 (3.0–8.0) | 14.3 (0.0–57.1) | 0.02 |
| responders (4) | 7.5 (7.0–8.0) | 4.0 (0.8–6.5) | 42.9 (16.5–89.3) | 0.04 | |
| partial responders (2) | 8.5 (8.0–9.0) | 6.0 (4.0–8.0) | 27.8 (0.0–55.6) | 0.22 | |
| non-responders (4) | 8.0 (7.3–8.0) | 7.5 (3.3–8.0) | 6.3 (0.0–56.7) | 0.41 | |
| autoresolution (1) | 7.00 | 6.00 | 14.3 | 0.32 | |
| Diagnoses at follow-up, n (%) | |||||
| Diagnosis | NDPH | 3 (27.3) | |||
| Probable NDPH | 1 (9.1) | ||||
| Migraine-like headache secondary to COVID-19 | 2 (18.2) | ||||
| Migraine without aura | 1 (9.1) | ||||
| Probable migraine | 1 (9.1) | ||||
| Frequent episodic tension-type headache | 1 (9.1) | ||||
| Infrequent episodic tension-type headache | 1 (9.1) | ||||
| No headache | 1 (9.1) | ||||
| Latency from first evaluation and follow-up (days) | 76 (29–96) | ||||
VAS: visual analogue scale; n: number of patients of each group.
Ten patients received one or more preventive headache treatments, showing a variable response to therapy (see Table 3), while one patient decided to not undergo any treatment. At follow-up evaluation, according to the reduction in headache days/month, patients were classified into responders (36.4%), partial responders (18.2%), and non-responders (36.4%); in addition, one patient (9.1%) achieved a spontaneous resolution of headache without any treatment. Table 4 details the change of patients' headache characteristics between baseline and follow-up and response to therapy. Regarding the diagnoses at follow-up, some patients received a different classification: one patient with a previous NDPH diagnosis was reclassified as “frequent episodic tension-type headache”, one probable NDPH as “migraine-like headache secondary to COVID-19”, while another changed to “infrequent episodic tension-type headache”; lastly, one of the two patients with a first diagnosis of migraine-like headache secondary to COVID-19 was reclassified as “migraine without aura”, while the other one showed no more headache at follow-up (follow-up diagnoses are summarised in Table 4). Finally, 8 patients (72.7%) underwent brain magnetic resonance imaging (MRI), which showed no significant changes. The supplementary material provides details on individual patients' pain features, response to treatment, follow-up assessment, and COVID-19 infection (see Supplementary Table 1, Supplementary Table 2, Supplementary Table 3).
4. Discussion
Several authors have attempted to estimate headache prevalence during COVID-19 [
[13]
]. Studies conducted in hospitalized COVID-19 patients and outpatients describe a prevalence of HCoV up to 47% [[9]
,[13]
]. Data from literature have shown that pain usually begins during the first day of COVID-19 infection (39% to 55%) [[6]
]. Similarly, data from the present sample reported that the onset of headache was concomitant with COVID-19 infection in 54.5% of cases. Caronna et al. found that headache was more prevalent in females and in younger COVID-19 patients; also, females complained of more severe and persistent headache [[4]
]. Of interest, in our cohort, all included subjects were female and, in addition, it included 5 patients that were children or adolescents, demonstrating how HCoV can even occur in the developmental age.In the present study, 4 patients (36.4%) reported hyposmia during SARS-CoV-2 infection, which completely receded from days to weeks after recovery from the infection. Central nervous system (CNS) invasion through the olfactory bulbs might represent a pathogenetic mechanism for the onset of headache in COVID-19 patients [
[14]
]. Regarding vaccines against COVID-19, no significant correlation could be found, since 45.5% of patients was not vaccinated and the remaining ones completed their vaccination cycle several months before COVID-19 and the onset of headache.Headache in the course of COVID-19 infection is usually described with a tension-type phenotype in most cases (around 54%) and with a migraine-like phenotype in 25% of cases [
[8]
,[15]
]. Considering the headache features showed by the whole population in this study, 54.5% patients showed a migraine-like phenotype, while 45.5% a tension-type-headache phenotype. However, the sample included in this research is different from the general COVID-19 population, probably due to a selection bias of specialized headache centres. Regarding the number of first evaluations performed at the headache centres in the study period, HCoV showed a prevalence of 0.26% among adult centres and of 1.21% at the paediatric one; thus, this condition might be more represented in younger ages.- Caronna E.
- Pozo-Rosich P.
Headache as a symptom of COVID-19: narrative review of 1-year research.
Curr Pain Headache Rep [Internet]. 2021; 25 (Available from:)https://doi.org/10.1007/s11916-021-00987-8
Persistent headache after COVID-19 has already been described, and a migraine-like phenotype was reported to be more associated with longer symptom duration [
[16]
]. Regarding its classification, a few considerations should be made. Because of the temporal relation with SARS-CoV-2 infection, HCoV could be classified as “9. Headache attributed to infection”, but there is no evidence of any intracranial localization of the virus (e.g., encephalitis, meningitis, abscess) in almost all cases. The specific sub-diagnosis could be “9.2.2 Headache attributed to systemic viral infection”, but, in this case, a systemic viral infection should be confirmed and headache should improve with improvement or remission of the infection [[10]
]. In the studied population, patients experienced COVID-19 with only upper respiratory tract symptoms and mild fever or arthralgia, none presented with pneumonia or severe systemic infection. Moreover, headache did not improve after the end of the infection but persisted for several weeks or months (see supplementary material). Therefore, we believe that the diagnosis “9.2.2 Headache attributed to systemic viral infection” does not adequately describe the patients in the present case series. Another nosologic entity that can be found in ICHD-3 classification is “7.3.3 Headache attributed to other non-infectious inflammatory intracranial disease”, but, although systemic inflammation is described in COVID-19 (especially in more severe cases) [[17]
], this group principally refers to systemic autoimmune diseases (e.g. systemic lupus erythematosus, acute disseminated encephalomyelitis, Behçet syndrome) [[10]
] and, as per definition, it should be restricted to non-infectious causes of systemic inflammation. Finally, headache is one of the most represented symptoms of the so called “long COVID”, the pathogenesis of which is still unclear, although a prolonged pathologic inflammation is one of the main suggested hypotheses [[18]
]. In the present study, patients referred to the tertiary headache centres at different timing after COVID-19; since there is no specific classification for HCoV, headaches assessed within three months from the end of the infection were classified as secondary to COVID-19, while those ones which persisted beyond that period were considered idiopathic (i.e., considering the infection as a triggering factor). Regarding NDPH, an infection is one of the main triggers already well described in the literature [[6]
,[11]
]. NDPH has already been described after COVID-19 [[5]
,[19]
,[20]
], but here, together with probable NDPH, it accounted for 72.8% of the diagnoses. Furthermore, it is worth noting that NDPH or probable NDPH were present in the 100% of the paediatric population in the presented sample. The pathogenesis of this condition is still uncertain, even if a long-lasting CNS inflammation is one of the main hypothesis, as demonstrated by elevated TNF-alpha cerebrospinal fluid levels in patients with NPDH [[21]
]. This theory could be supported by the clinical response that some patients of the present study achieved with corticosteroids rather than with anti-migraine preventive drugs (see Table 3 and supplementary material) [[19]
]. Nevertheless, three patients diagnosed with NDPH and another with probable NDPH found no relief from any treatment, although steroids were only used in one case. As with the clinical findings of NDPH patients, COVID-19 leads to a presentation consistent with other post-viral infection described in literature, without showing any peculiar feature of this enigmatic disorder [[22]
,[23]
].Lastly, in one case of migraine-like headache secondary to COVID-19 in which blood pressure was not well controlled after infection, complete regression of headache was observed with proper adjustment of the antihypertensive therapy. An alternative diagnosis for the patient could have been “10.3 Hypertension-related headache”, although it usually occurs during uncontrolled arterial hypertension with systolic values above 180 mmHg and/or diastolic values above 120 mmHg [
[10]
]. The patient presented in the series showed only one initial peak of systolic blood pressure of 180 mmHg, while in the following weeks the pressure remained much lower (around 140/85 mmHg, however more than usual), and headache was still present. The regression of headache with normalization of blood pressure supports the diagnosis of “10.3 Hypertension-related headache”, so perhaps COVID-19 only acted by dysregulating pressure control. The latter issue suggests that is crucial to properly investigate comorbidities when evaluating patients with new-onset headache following COVID-19.The present study has some strengths as it is a multicentre case series of patients followed by tertiary headache centres, where the treating physicians are specialized in the care of headache disorders. Therefore, the diagnoses, treatments, and follow-up visits were performed within an expert and standardized setting. Nevertheless, several limitations should be pointed out. First, the low number of patients included and the relatively limited follow-up time. Second, it was not possible to assess the exact causal role of COVID-19 in the onset of headache, therefore a time-based criterion was chosen. Third, the end of the infection criterion was also subject to variability, as antigenic and molecular nasal swabs have different times thresholds for negative results. Finally, although other causes of secondary headache were ruled out in most cases by brain MRI, further laboratory testing were not performed.
5. Conclusion
Headache persisting after COVID-19 infection is not uncommon and can become severe, lasting up to several months, with poor response to therapy. Among COVID-19 related headache, NDPH and probable NDPH were the most frequent new-onset conditions in the present sample. Data from the present series need to be confirmed and extended to larger populations. These data will have relevant prognostic and therapeutic implications for all clinicians managing headache patients in the COVID-19 setting.
The following are the supplementary data related to this article.
- Supplementary Table 1
Patients' pain features and baseline diagnoses. VAS: visual analogue scale; N: nausea; V: vomit; FN: phonophobia; FT: photophobia; BE: burning eyes; L: lacrimation; DT: stabbing pain; CD: concentration difficulties; AF: worsening with physical activity; T: tinnitus.
- Supplementary Table 2
Patients’ treatment response and follow-up characteristics.
- Supplementary Table 3
COVID-19 features.
Financial support
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Declaration of Competing Interest
None.
Acknowledgements
None.
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Article info
Publication history
Published online: February 15, 2023
Accepted:
February 13,
2023
Received in revised form:
February 10,
2023
Received:
November 22,
2022
Identification
Copyright
© 2023 Elsevier B.V. All rights reserved.
