Abstract
In the current issue of Cephalalgia, Fernández-de-las-Peñas and colleagues report decreased pressure pain thresholds in children with frequent episodic tension-type headache (TTH). The degree of pain hypersensitivity was similar at pericranial and extracranial locations. The finding of wide-spread pressure pain hypersensitivity, also at non-symptomatic locations, suggests that the central nervous system is sensitised in these children.
The study is important because, for the first time, it examines wide-spread pressure pain sensitivity in children with frequent episodic TTH. Only 25 children with frequent episodic TTH were investigated. The findings should, therefore, be confirmed in other studies, and also other types of nociceptive stimuli should be investigated. However, the study has several strengths: (i) the diagnosis was ensured though headache diaries; (ii) a well-defined group was investigated, i.e. only children with frequent headaches (8–14 days per month); and (iii) investigations were performed in a blinded design.
The results of Fernández-de-las-Peñas and colleagues are in line with the findings from numerous studies performed in the last two decades in adults with TTH (1). These studies initially demonstrated that patients with episodic TTH had increased tenderness of their pericranial muscles and normal general pain sensitivity, while patients with chronic TTH had both increased pericranial tenderness and a generalised, wide-spread pain hypersensitivity (2). After the division of episodic TTH into infrequent and frequent subtypes in the second edition of the International Classification of Headache Disorders in 2004 (3), several studies have demonstrated also that patients with frequent episodic TTH have a generalised pain hypersensitivity (4,5).
The studies of pain sensitivity in TTH led to the hypothesis that nociceptive input from pericranial myofascial tissues is important for the development of single episodes of TTH, while continuous nociceptive input from these structures may lead to increased excitability of nociceptive pathways and impaired pain inhibition in the central nervous system and, thereby, to headache chronification (2). This has been supported not only by a number of cross-sectional pain studies (1), but also by imaging studies (6), neurophysiological studies (7–9) and pharmacological studies (10,11). Most importantly, a recent longitudinal 12-year follow-up study (12) demonstrated that subjects who developed episodic TTH had increased pericranial myofascial tenderness but normal general pain sensitivity at follow-up, whereas subjects who developed chronic TTH had normal pain sensitivity at baseline but developed increased central pain sensitivity at follow-up. The investigators concluded that increased pain sensitivity is a consequence of frequent TTH, not a risk factor, and that central sensitisation plays an important role for the chronification of TTH (12).
The present study by Fernández-de-las-Peñas and colleagues suggests that central sensitisation can occur already in childhood and underlines the need for further research into the mechanisms responsible for headache chronification. Two major targets for future treatment strategies should be to: (i) identify the source of peripheral nociception in order to prevent the development of central sensitization and, thereby, the conversion of episodic into chronic TTH; and (ii) reduce established central sensitisation.