Central pain processing in chronic tension-type headache

2009 ◽  
Vol 120 (7) ◽  
pp. 1364-1370 ◽  
Author(s):  
Kim Lindelof ◽  
Jens Ellrich ◽  
Rigmor Jensen ◽  
Lars Bendtsen
Cephalalgia ◽  
2010 ◽  
Vol 30 (10) ◽  
pp. 1250-1267 ◽  
Author(s):  
Stuart Cathcart ◽  
Anthony H Winefield ◽  
Kurt Lushington ◽  
Paul Rolan

Stress is widely demonstrated as a contributing factor in tension-type headache (TTH). The mechanisms underlying this remain unclear at present. Recent research indicates the importance of central pain processes in tension-type headache (TTH) pathophysiology. Concurrently, research with animals and healthy humans has begun to elucidate the relationship between stress and pain processing in the central nervous system, including central pain processes putatively dysfunctional in TTH. Combined, these two fields of research present new insights and hypotheses into possible mechanisms by which stress may contribute to TTH. To date, however, there has been no comprehensive review of this literature. The present paper provides such a review, which may be valuable in facilitating a broader understanding of the central mechanisms by which stress may contribute to TTH.


Brain ◽  
2008 ◽  
Vol 131 (12) ◽  
pp. 3232-3238 ◽  
Author(s):  
L. Buchgreitz ◽  
L.L. Egsgaard ◽  
R. Jensen ◽  
L. Arendt-Nielsen ◽  
L. Bendtsen

Cephalalgia ◽  
1993 ◽  
Vol 13 (1) ◽  
pp. 11-14 ◽  
Author(s):  
Thomas-Martin Wallasch ◽  
Hartmut Göbel

Exteroceptive suppression of temporalis muscle activity was proposed by Schoenen and co-workers in 1987 as a tool in headache diagnosis and research. Their finding of a decreased or abolished second silent period (ES2) in chronic tension-type headache sufferers has been confirmed by several independent laboratories during the last five years. Temporalis silent periods have also been studied in various other types of headaches. Their modulation by neuropsychological factors and pharmacological agents has also been investigated as well as their retest reliability. The pathophysiological concept of muscle contraction in tension-type headache has been challenged by studies using temporalis silent periods. The exterocepfive suppression of temporalis muscle activity points unequivocally towards a central pathogenetic mechanism, although it remains unclear whether the abnormalities of temporalis ES2 represent the primary dysfunction or a secondary phenomenon in chronic tension-type headache.


2007 ◽  
Vol 23 (9) ◽  
pp. 786-792 ◽  
Author(s):  
César Fernández-de-las-Peñas ◽  
Hong-You Ge ◽  
Lars Arendt-Nielsen ◽  
Maria Luz Cuadrado ◽  
Juan A. Pareja

PLoS ONE ◽  
2018 ◽  
Vol 13 (5) ◽  
pp. e0197381 ◽  
Author(s):  
Elena Benito-González ◽  
Maria Palacios-Ceña ◽  
Juan J. Fernández-Muñoz ◽  
Matteo Castaldo ◽  
Kelun Wang ◽  
...  

Cephalalgia ◽  
2001 ◽  
Vol 21 (8) ◽  
pp. 830-836 ◽  
Author(s):  
Ishaq Abu-Arafeh

In this study, the causes, predisposing factors and clinical features of chronic daily headache in children and adolescents were studied within the population of patients attending a specialist headache. The International Headache Society's (IHS) criteria for the diagnosis of chronic tension type headache (CTTH) were assessed for their applicability in the paediatric age group. Over a period of three years, demographic and clinical data were collected prospectively on all children who attended the clinic and suffered from daily attacks of headache. One hundred and fifteen children and adolescents (32% of all clinic population) had chronic daily headache, of whom 93 patients (81%) fulfilled the IHS criteria for the diagnosis of CTTH. They were between 3-15 years of age (mean: 11.1, SD: 2.3) and their female to male ratio was 1.2: 1. Around one third of the patients also suffered from migraine (mainly migraine without aura). The headache was described as mild in 60.9%, moderate 36.5% and severe 2.6%. Headache was located at the forehead in 53% or over the whole of the head in 29.6%. Pain was described as ‘just sore’ or dull by 73.9%. During attacks of headache, at least half the patients reported light intolerance, noise intolerance, anorexia or nausea. Thirty-two percent of patients had at least one underlying chronic disease that may have contributed to the pathogenesis of the CTTH. Eleven percent had serious stressful events related to family illnesses and in four patients headaches were triggered by family bereavement. Fourteen percent were investigated with neuroimaging and 22% were referred for clinical psychology assessment and management. In conclusion, CTTH is a common cause of headache in children attending a specialist headache clinic. The clinical features closely match those of adult population and the IHS criteria for the diagnosis of CTTH can be adapted for use in children. Predisposing stressful risk factors, physical or emotional, are present in a large proportion.


CNS Drugs ◽  
1995 ◽  
Vol 4 (2) ◽  
pp. 90-98 ◽  
Author(s):  
Alessandro S. Zagami

2017 ◽  
Vol 14 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Dagmar C. van Rijckevorsel ◽  
Oliver B. Boelens ◽  
Rudi M. Roumen ◽  
Oliver H. Wilder-Smith ◽  
Harry van Goor

AbstractBackground10–30% of chronic abdominal pain originates in the abdominal wall. A common cause for chronic abdominal wall pain is the Anterior Cutaneous Nerve Entrapment Syndrome (ACNES), in which an intercostal nerve branch is entrapped in the abdominal rectus sheath. Treatment consists of local anaesthetics and neurectomy, and is ineffective in 25% of cases for yet unknown reasons.In some conditions, chronic pain is the result of altered pain processing. This so-called sensitization can manifest as segmental or even generalized hyperalgesia, and is generally difficult to treat.ObjectiveThe aim of this study was to assess pain processing in ACNES patients responsive and refractory to treatment by using Quantitative Sensory Testing, in order to explore whether signs of altered central pain processing are present in ACNES and are a possible explanation for poor treatment outcomes.Methods50 patients treated for ACNES with locally orientated treatment were included. They were allocated to a responsive or refractory group based on their response to treatment. Patients showing an improvement of the Visual Analogue Scale (VAS) pain score combined with a current absolute VAS of <40 mm were scored as responsive.Sensation and pain thresholds to pressure and electric skin stimulation were determined in the paravertebral bilateral ACNES dermatomes and at four control areas on the non-dominant side of the body, i.e. the musculus trapezius pars medialis, musculus rectus femoris, musculus abductor hallucis and the thenar. The ACNES dermatomes were chosen to signal segmental hyperalgesia and the sum of the control areas together as a reflection of generalized hyperalgesia. Lower thresholds were interpreted as signs of sensitized pain processing. To test for alterations in endogenous pain inhibition, a conditioned pain modulation (CPM) response to a cold pressor task was determined. Also, patients filled in three pain-related questionnaires, to evaluate possible influence of psychological characteristics on the experienced pain.ResultsPatients refractory to treatment showed significantly lower pressure pain thresholds in the ACNES dermatomes and for the sum of as well as in two individual control areas. No differences were found between groups for electric thresholds or CPM response. Duration of complaints before diagnosis and treatment was significantly longer in the refractory compared to the responsive group, and refractory patients scored higher on the pain-related psychological surveys.Conclusion and ImplicationsIn this hypothesis-generating exploratory study, ACNES patients refractory to treatment showed more signs of sensitized segmental and central pain processing. A longer duration of complaints before diagnosis and treatment may be related to these alterations in pain processing, and both findings could be associated with less effective locally orientated treatment. In order to validate these hypotheses further research is needed.Registration numberNCT01920880 (Clinical Trials Register; http://www.clinicaltrials.gov).


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