Frequency of headache is related to sensitization: A population study

Abstract

Central sensitization is thought to play an important role in the chronification of tension-type headache and in the maintenance and exacerbation of the migraine attack. It has, however, almost exclusively been studied in highly selected patients from headache clinics. The aim of the present study was to evaluate pain perception in primary headaches in the general population. Stimulus-response functions for pressure versus pain, tenderness and pressure pain thresholds were studied in a random sample of 523 adults from the general population. All results were controlled for the effects of age and gender. The area under the stimulus-response function was increased in chronic- and frequent episodic tension-type headache compared with subjects without headache (p<0.001, p<0.001) and in chronic tension-type headache compared with migraine (p=0.01). Increasing slope (p<0.0001) and displacement towards lower pressures was found in the following order: no headache, migraine, frequent episodic tension-type headache, chronic tension-type headache. The displacement of the stimulus-response function was closely associated with frequency of headache. Finally, the stimulus-response function tended to be qualitatively altered in patients with frequent headache. The findings demonstrate, for the first time in a population-based study, a close relation between altered pain perception and chronification of headache, which most likely can be explained by central sensitization.

Pressure pain threshold in the craniocervical muscles of women with episodic and chronic migraine: a controlled study

“…In disagreement with our results, Buchgreitz et al 4 reported an association between increased muscle tenderness and headache chronification, but the authors did not evaluate episodic and chronic migraine patients. Our findings also disagree with a large populational study, where central sensitization was assessed using a validated questionnaire 29 .…”

“…Prolonged nociceptive input from the periphery may be associated to the onset of central sensitization, may exacerbate already established central sensitization, and may impair supraspinal pain modulation, since the hyperexcitability could contribute to an amplification of the nociceptive signal coming from the periphery 4,27 . As a result peripheral nociceptive inputs from the face and cervical sites, contributing or not to central sensitization may have influenced the lower PPT values showed in EM and CM groups.…”

“…Finally to the best of our knowledge, PPT values for masticatory and cervical sites as a function of headache status are missing. The mechanism responsible for the transition from episodic to chronic pain are clinically very important for prevention and treatment strategies, but unfortunately poorly understood 4 . Differently from previous results 8 , our results failed to demonstrate a correlation between headache laterality and PPT values as observed by Fernandez-de-las-Peñas et al 9 .…”

“…Migraine is currently conceptualized as a chronic condition with episodic attacks 2 with the potential for progression, meaning that in some individuals, migraine evolves into a stage in which patients have headaches on more days than not, a condition called chronic migraine (CM) 3 . Prolonged nociceptive input from the periphery may result in central sensitization of the incoming stimuli 4 and this may be of relevance to migraine 5 . In migraine, central sensitization is associated with refractoriness to treatment 5 and is a risk factor for chronic migraine 6 .…”

Altered processing of sensory stimuli in patients with migraine

“…This amplification also occurs during migraine attacks 108 and worsens with increasing attack frequency. 109 One mechanism underlying central sensi tization is the activity dependent change in excitability of central nociceptors, which results in abnormal ampli fication of pain sensation in physiological nociceptiona phenomenon referred to as temporal summation of pain stimuli 110 that is equivalent to 'wind up' phenomenon (facilitation of wide dynamic range nociceptive neurons located in the deep laminae of the spinal cord dorsal horn and the spinal trigeminal nucleus after constant intensity stimulation of C fibres) in animal experiments. 111 The nociceptive flexion or withdrawal reflex (NWR) is a reliable measure of spinal nociception, as demon strated by the fact that it requires Aδ fibre activation, that the reflex threshold is related to the pain percep tion threshold, and that the reflex magnitude correlates positively with pain intensity ratings.…”