Background: Vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are used to reduce the risk of developing Coronavirus Disease 2019 (COVID-19). Despite the significant benefits in terms of reduced risk of hospitalization and death, different adverse events may present after vaccination: among them, headache is one of the most common, but nowadays there is no summary presentation of its incidence and no description of its main features. Methods: We searched PubMed and EMBASE covering the period between January 1^st 2020 and August 6^th, 2021, looking for record in English and with an abstract and using three main search terms (with specific variations): COVID-19/SARS-CoV-2; Vaccination; headache/adverse events. We selected manuscript including information on subjects developing headache after injection, and such information had to be derived from a structured form (i.e. no free reporting). Pooled estimates and 95% confidence intervals were calculated. Analyses were carried out by vaccine vs. placebo, by first vs. second dose, and by mRNA-based vs. “traditional” vaccines; finally, we addressed the impact of age and gender on post-vaccine headache onset. Results: Out of 9338 records, 84 papers were included in the review, accounting for 1.57 million participants, 94% of whom received BNT162b2 or ChAdOx1. Headache was generally the third most common AE: it was detected in 22% (95% CI 18–27%) of subjects after the first dose of vaccine and in 29% (95% CI 23–35%) after the second, with an extreme heterogeneity. Those receiving placebo reported headache in 10–12% of cases. No differences were detected across different vaccines or by mRNA-based vs. “traditional” ones. None of the studies reported information on headache features. A lower prevalence of headache after the first injection of BNT162b2 among older participants was shown. Conclusions: Our results show that vaccines are associated to a two-fold risk of developing headache within 7 days from injection, and the lack of difference between vaccine types enable to hypothesize that headache is secondary to systemic immunological reaction than to a vaccine-type specific reaction. Some descriptions report onset within the first 24 h and that in around one-third of the cases, headache has migraine-like features with pulsating quality, phono and photophobia; in 40–60% of the cases aggravation with activity is observed. The majority of patients used some medication to treat headache, the one perceived as the most effective being acetylsalicylic acid.

Objective. The aim of this study was to investigate pain patterns and the distribution of myofascial trigger points (MTPs) in whiplash-associated disor

Purpose: The purpose of this study was to investigate the test-retest reliability of ultrasound (US) thickness measurements and the muscle contraction ratio (CR) of lumbar multifidus (LM) and transversus abdominis (TA) muscles in participants with and without nonspecific chronic low back pain (NCLBP). Methods: A total of 62 participants (37 with NCLBP, 25 without NCLBP) with participated in the study. The within-day and between-day reliability of US thickness measurements and CR in a lying (supine for TA and prone for LM) and sitting positions for both muscles (sitting on a gym ball with both feet on the ground or lifting one foot off the floor) were assessed. Reliability analysis was performed with intraclass correlations (ICCs) for these two static and dynamic positions. Results: Test-retest reliability was calculated to be good to high for the static position (ICC = 0.72–0.95) and the dynamic position (ICC = 0.74–0.94) sonographic measurements in both group of TA measurement. Test-retest reliability of LM measurements was good to high for the static position (ICC = 0.82–0.95) and the dynamic position (ICC = 0.85–0.97) sonographic measurements in both groups. Conclusions: US imaging is a highly reliable method for the assessment of TA and LM thickness muscles in the dynamic position in participants with and without NCLBP. The CR measures may be adequately reliable in assessing the function of the TA and LM muscles in participants with NCLBP and healthy ones.

A better understanding of potential relationship between mood disorders, sleep quality, pain, and headache frequency may assist clinicians in determining optimal therapeutic programs. The aim of the current study was to analyze the effects of sleep quality, anxiety, depression on potential relationships between headache intensity, burden of headache, and headache frequency in chronic tension type headache (CTTH). One hundred and ninety-three individuals with CTTH participated. Headache features were collected with a 4-weeks headache diary. The Hospital Anxiety and Depression Scale was used for assessing anxiety and depression. Headache Disability Inventory evaluated the burden of headache. Pain interference was determined with the bodily pain domain (SF-36 questionnaire). Sleep quality was assessed with Pittsburgh Sleep Quality Index. Path analyses with maximum likelihood estimations were conducted to determine the direct and indirect effects of depression, anxiety, and sleep quality on the frequency of headaches. Two paths were observed: the first with depression and the second with sleep quality as mediators. Direct effects were noted from sleep quality, emotional burden of disease and pain interference on depression, and from depression to headache frequency. The first path showed indirect effects of depression from emotional burden and from sleep quality to headache frequency (first model R 2 = 0.12). Direct effects from the second path were from depression and pain interference on sleep quality and from sleep quality on headache frequency. Sleep quality indirectly mediated the effects of depression, emotional burden and pain interference on headache frequency (second model R 2 = 0.18). Depression and sleep quality, but not anxiety, mediated the relationship between headache frequency and the emotional burden of disease and pain interference in CTTH.

Tension-type headache (TTH) is a common condition but the underlying etiology is not understood. Episodic TTH may develop into chronic TTH, and some possible triggers may be involved in generation and maintenance. Nociceptive generators and hyperexcitable spots in neck and shoulder regions may to some degree contribute to TTH. The current paper highlights some of the possible triggers and associated pain mechanisms involved in TTH and discusses whether inhibition of these possible triggers may provide new treatment options. This paper presents possible pathophysiological factors in TTH, the role of muscle pain, and how referred pain from triggers can contribute to development, maintenance of sensitization, or both. Referred pain patterns from trigger points and associated muscle hyperalgesia seem to be clinically important factors. Damping the nociceptive peripheral drive may not only reduce the number of TTH attacks but may also prevent, delay the transition from episodic into more chronic TTH, or both. The role of muscle triggers in driving TTH is debated as the pathogenesis of such triggers is not fully understood. Furthermore, inhibiting the drive from the triggers does not consistently modulate TTH. Understanding the possible triggers in TTH, muscle hyperalgesia, and widespread pain sensitization, may help to develop better management regimes and possibly prevent TTH from developing into more chronic conditions. Currently, there is a striking difference between the clinical observational studies favoring the role of muscle triggers in TTH and the intervention studies generally not supporting the role of muscle triggers in TTH.

To investigate the association between trigger points (TrPs) and widespread pressure pain sensitivity in people with tension-type headache (TTH) and to determine if this association is different between frequent episodic (FETTH) or chronic (CTTH) headache. A cross-sectional study. One hundred and fifty-seven individuals (29% male) with TTH participated. Clinical features of headache, i.e., intensity, duration, and frequency, were recorded in a headache diary. Active and latent TrPs were bilaterally explored in the temporalis, masseter, suboccipital, upper trapezius, sternocleidomastoid, and splenius capitis muscles. Pressure pain thresholds (PPT) were assessed over the trigeminal area (i.e., temporalis muscle), extra-trigeminal (i.e., C5/C6 zygapophyseal joint), and two distant pain-free points (i.e., second metacarpal and tibialis anterior muscle). Eighty (51%) patients were classified as FETTH, whereas 77 (49%) were classified as CTTH. No differences in the number of either active or latent TrPs (all p > 0.171) or widespread pressure pain sensitivity (all p > 0.351) were observed between FETTH and CTTH groups. The number of active and latent TrPs was significantly and negatively associated with PPTs: The higher the number of active or latent TrPs, the lower the widespread PPT, and the more generalized sensitization. This association was stronger within the FETTH group than the CTTH group. This study found that the number of TrPs in head and neck/shoulder muscles was associated with widespread pressure hypersensitivity independently of the frequency of headache.