Dynamic assessment of abnormalities in central pain transmission and modulation in tension-type headache sufferers

OBJECTIVE: To examine and compare central pain processing and modulation in young tension-type headache sufferers with that of matched healthy controls using an induced headache "challenge" paradigm. BACKGROUND: Recent research has suggested that abnormalities in central pain processing and descending pain modulation may contribute to chronic tension-type headache. These abnormalities, if they contribute to headache pathogenesis, should be present in young adult tension-type headache sufferers. Recent research using static measures of physiological variables, such as muscle tenderness and exteroceptive suppression, has identified chronic muscle tenderness as a characteristic of young tension-type headache sufferers, but other central nervous system functional abnormalities may require a dynamic "challenge" to be observed. METHODS: Twenty-four young women meeting the International Headache Society diagnostic criteria for tension-type headache (headache-prone) and a matched group of 24 healthy women who reported fewer than 10 problem headaches per year (control) participated in a double-blind, placebo-controlled, crossover study. Subjects completed jaw clenching and a placebo condition on different days in counterbalanced order. Pericranial muscle tenderness, pressure-pain thresholds on the temporalis, and exteroceptive suppression periods were assessed before and after each procedure. Head pain was recorded for 12 to16 hours following each condition. RESULTS: Headache-prone subjects were more likely than controls to experience headaches after both the jaw clenching and placebo procedures, but neither group was significantly more likely to experience headaches following jaw clenching than placebo. In pretreatment measurements, headache-prone subjects exhibited greater muscle tenderness than controls, but pressure-pain detection thresholds and exteroceptive suppression periods did not differ in the two groups. Control subjects showed increases in muscle tenderness and exteroceptive suppression periods following both the clenching and placebo procedures, whereas headache-prone subjects exhibited no significant changes in any of the physiological measures following either experimental manipulation. CONCLUSIONS: These results confirm previous findings indicating abnormally high pericranial muscle tenderness in young tension headache sufferers even in the headache-free state. In addition, the results suggest that the development of headaches following noxious stimulation is more strongly related to headache proneness and associated abnormalities in central pain transmission or modulation (indexed by pericranial muscle tenderness and exteroceptive suppression responses) than muscle strain induced by jaw clenching.     

Amitriptyline reduces myofascial tenderness in patients with chronic tension-type headache

The tricyclic anti-depressant amitriptyline is widely used in the treatment of chronic tension-type headache. The aim of the present study was to investigate whether the analgesic effect is caused by a reduction of muscle pain or by a general reduction of pain sensitivity. Thirty-three non-depressed patients with chronic tension-type headache were treated with amitriptyline 75 mg/day and with the highly selective serotonin reuptake inhibitor citalopram 20 mg/day in a 32-week, double-blind, placebo-controlled, three-way crossover study. At the end of each treatment period, actual headache intensity and pericranial myofascial tenderness were recorded, pressure pain detection and tolerance thresholds were measured in the finger and in the temporal region and the electrical pain threshold was measured at the labial commissure. Amitriptyline reduced tenderness and headache intensity significantly more than placebo (P=0.01 and P=0.04, respectively). The reduction in tenderness could be ascribed solely to the group of patients who responded to amitriptyline treatment by at least 30% reduction in headache while tenderness was unchanged in non-responders. Amitriptyline did not affect pressure or electrical pain thresholds at any of the examined locations. Citalopram had no significant effect on any of the examined parameters. These findings indicate that amitriptyline elicits its analgesic effect in chronic myofascial pain by reducing the transmission of painful stimuli from myofascial tissues rather than by reducing overall pain sensitivity. We suggest that this effect is caused by a segmental reduction of central sensitization in combination with a peripheral anti-nociceptive action.     

Pathophysiological mechanisms of tension-type headache: a review of epidemiological and experimental studies

In this present thesis I have discussed the epidemiology and possible pathophysiological mechanisms of tension-type headache. A population-based study of 1000 subjects randomly selected from a general population, two clinical studies, and a method study of EMG recordings, were conducted. Tension-type headache was the most prevalent form of headache, with a life-time prevalence of 78% in a general adult population. Thirty percent were affected more than 14 days per year and 3% were chronically affected, i.e. had headache at least every other day. Females were more frequently affected than males, and young subjects more frequently affected than older subjects. Females were more sensitive to mechanical pressure pain and revealed more tenderness from pericranial muscles and tendon insertions than males, and young subjects were more pain-sensitive than older subjects. Significantly higher tenderness in pericranial muscles was found in subjects with tension-type headache compared to migraineurs and to subjects without any experience of headache. Tenderness increased significantly with increasing frequency of tension-type headache in both males and females, whereas no such relation was found for mechanical pain thresholds. The applied EMG methodology was fairly reliable and nonpainful, but due to intersubject variability paired studies should be preferred. Subjects with chronic tension-type headache had slightly increased EMG levels during resting conditions and decreased levels during maximal voluntary contraction compared with headache-free subjects, indicating insufficient relaxation at rest and impaired recruitment at maximal activity. In a subsequent clinical, controlled study, the effect of 30 min of sustained tooth clenching was studied. Within 24 h, 69% of patients and 17% of controls developed a tension-type headache. Shortly after clenching, tenderness was increased in the group who subsequently developed headache, whereas tenderness was stable in the group of patients who remained headache-free, indicating that tenderness might be a causative factor of the headache. Likewise, psychophysical and EMG parameters were studied in 28 patients with tension-type headache, both during and outside of a spontaneous episode of tension-type headache. It was concluded that a peripheral mechanism of tension-type headache is most likely in the episodic subform, whereas a secondary, segmental central sensitization and/or an impaired supraspinal modulation of incoming stimuli seems to be involved in subjects with chronic tension-type headache. Prolonged nociceptive stimuli from myofascial tissue may be of importance for the conversion of episodic into chronic tension-type headache. The author emphasizes that tension-type headache is a multifactorial disorder with several concurrent pathophysiological mechanisms, and that extracranial myofascial nociception may constitute only one of them. The present thesis supplements the understanding of the balance between peripheral and central components in tension-type headache, and thereby, hopefully, leads us to a better prevention and treatment of the most prevalent type of headache.     

Muscular Factors are of Importance in Tension-Type Headache

Recent studies have indicated that muscular disorders may be of importance for the development of increased pain sensitivity in patients with chronic tension-type headache. The objective of the present study was to investigate this hypothesis by examining the pain perception in tension-type headache with and without muscular disorders defined as increased tenderness. We examined 28 patients with episodic tension-type headache, 28 patients with chronic tension-type headache, and 30 healthy controls. Pericranial myofascial tenderness was recorded with manual palpation, and pressure pain detection and tolerances in cephalic and extracephalic locations with an electronic pressure algometer. In addition, thermal pain sensitivity and electromyographic activity were recorded. The main result was significantly lower pressure pain detection thresholds and tolerances in all the examined locations in patients with chronic tension-type headache with a muscular disorder compared to those without a muscular disorder. There were no such differences in any of the examined locations when the two subgroups of patients with episodic tension-type headache were compared. Thermal pain sensitivity did not differ between patients with and without a muscular disorder, while electromyographic activity levels were significantly higher in patients with chronic tension-type headache with than in those without a muscular disorder. Our results strongly indicate that prolonged nociceptive stimuli from the pericranial myofascial tissue sensitize the central nervous system and, thereby, lead to an increased general pain sensitivity. Muscular factors may, therefore, be of major importance for the conversion of episodic into chronic tension-type headache. The present study complements the understanding of the important interactions between peripheral and central factors in tension-type headache and may lead to a better prevention and treatment of the most prevalent type of headache.     

Muscular disorders in tension-type headache

In order to evaluate the diagnostic criteria for muscular disorders in tension-type headache, pericranial muscle tenderness and pressure pain thresholds were studied in a random sample population of 735 adults aged 25–64. In addition, quantitative EMGs were recorded in 547 of these subjects. The correlation between the three diagnostic tests was assessed and the discriminality and cut-off points were analysed using Receiver Operating Characteristics analysis. Local tenderness from the temporal muscles was closely related to the total tenderness scores from 14 pairs of muscles. In chronic tension-type headache, tenderness was positively related to EMG and inversely related to pain thresholds. In the episodic form the total tenderness score was inversely related to pain thresholds, whereas no significant relation to EMG was noted. The Receiver Operating Characteristics curves indicated that tenderness recorded by manual palpation was the most specific and sensitive test, whereas EMG and pain thresholds were of limited diagnostic value. Eighty-seven percent of subjects with the chronic, and 66% of subjects with the episodic form were found to have a "muscular disorder" defined as increased tenderness recorded by either manual palpation or pressure algometry and/or increased EMG levels. However, muscle tenderness increased significantly during pain, so the headache state should be considered in future studies. Suggestions for revision of the present diagnostic criteria for muscular disorders are given.     

Experimental induction of muscle tenderness and headache in tension-type headache patients

The aim of the present study was to investigate the impact of static contraction of the shoulder and neck muscles on muscle tenderness and headache in patients with tension-type headache. Twenty patients with frequent episodic tension-type headache and 20 healthy age- and sex-matched controls were examined using a placebo-controlled cross-over design. The subjects performed static contraction of the trapezius muscles (active procedure) or the anterior tibial muscles (placebo procedure) with 10% of maximal force for 30 min. Total tenderness score, local tenderness score and headache intensity were evaluated before and after the static work. Changes in headache intensity were followed for 24 h. Pericranial tenderness increased significantly more in patients than in controls after the active procedure (P = 0.04). The increase in pericranial tenderness tended to be higher after the active procedure than after the placebo procedure in patients (P = 0.08) and in controls (P = 0.07). Sixty per cent of the patients and 20% of the healthy controls developed headache after the active procedure. Fifty per cent of the patients and none of the controls developed headache after the placebo procedure. There was no significant difference in headache development between the active and the placebo procedure in patients or controls. These findings demonstrate that tension-type headache patients are more liable to develop shoulder and neck pain in response to static exercise than healthy controls.     

Pain perception studies in tension-type headache

Tension-type headache (TTH) is a disorder with high prevalence and significant impact on society. Understanding of pathophysiology of TTH is paramount for development of effective treatments and prevention of chronification of TTH. Our aim was to review the findings from pain perception studies of pathophysiology of TTH as well as to review the research of pathophysiology of TTH. Pain perception studies such as measurement of muscle tenderness, pain detection thresholds, pain tolerance thresholds, pain response to suprathreshold stimulation, temporal summation and diffuse noxious inhibitory control (DNIC) have played a central role in elucidating the pathophysiology of TTH. It has been demonstrated that continuous nociceptive input from peripheral myofascial structures may induce central sensitization and thereby chronification of the headache. Measurements of pain tolerance thresholds and suprathreshold stimulation have shown presence of generalized hyperalgesia in chronic tension-type headache (CTTH) patients, while DNIC function has been shown to be reduced in CTTH. One imaging study showed loss of gray matter structures involved in pain processing in CTTH patients. Future studies should aim to integrate pain perception and imaging to confirm this finding. Pharmacological studies have shown that drugs like tricyclic anti-depressant amitriptyline and nitric oxide synthase inhibitors can reverse central sensitization and the chronicity of headache. Finally, low frequency electrical stimulation has been shown to rapidly reverse central sensitization and may be a new modality in treatment of CTTH and other chronic pain disorders.     

Muscle tenderness in pericranial and neck-shoulder region in children with headache. A controlled study

Increased pericranial muscle tenderness is connected with tension-type headache in adults. In children, the importance of muscle tenderness in the pericranial or neck-shoulder region in the pathogenesis of different types of headache is unknown. The present study evaluated muscle tenderness in the pericranial and neck-shoulder region in children with migraine, those with tension-type headache and those without headache. An unselected population-based questionnaire study concerning headache was carried out in 1135 Finnish schoolchildren aged 12 years. Of them, 183 children were randomly selected for a face-to-face interview and a clinical examination. Muscle tenderness was recorded by manual palpation and dolorimeter. Children with migraine had increased overall tenderness, recorded by manual palpation, compared with those without headache. They also self-reported tenderness in the neck-shoulder region during daily activities more often than the children of the other groups. Muscle tenderness was not associated with paediatric tension-type headache. The mean pressure pain thresholds did not differ among the three groups. However, a negative correlation between the total tenderness score and the dolorimeter score was found in each group. In conclusion, children with migraine had increased muscle tenderness at palpation of the pericranial and neck-shoulder muscles and they also reported pain symptoms in the neck-shoulder region most frequently. Instead, increased pericranial and neck-shoulder muscle tenderness was not associated with tension-type headache in children.     

Central sensitization in tension-type headache--possible pathophysiological mechanisms

The aim of the present thesis was to investigate the pathophysiology of chronic tension-type headache with special reference to central mechanisms. Increased tenderness to palpation of pericranial myofascial tissues is the most apparent abnormality in patients with tension-type headache. A new piece of equipment, a so-called palpometer, that makes it possible to control the pressure intensity exerted during palpation, was developed. Thereafter, it was demonstrated that the measurement of tenderness could be compared between two observers if the palpation pressure was controlled, and that the Total Tenderness Scoring system was well suited for the scoring of tenderness during manual palpation. Subsequently, it was found that pressure pain detection and tolerance thresholds were significantly decreased in the finger and tended to be decreased in the temporal region in chronic tension-type headache patients compared with controls. In addition, the electrical pain threshold in the cephalic region was significantly decreased in patients. It was concluded that the central pain sensitivity was increased in the patients probably due to sensitization of supraspinal neurones. The stimulus-response function for palpation pressure vs. pain was found to be qualitatively altered in chronic tension-type headache patients compared with controls. The abnormality was related to the degree of tenderness and not to the diagnosis of tension-type headache. In support of this, the stimulus-response function was found to be qualitatively altered also in patients with fibromyalgia. It was concluded that the qualitatively altered nociception was probably due to central sensitization at the level of the spinal dorsal horn/trigeminal nucleus. Thereafter, the prophylactic effect of amitriptyline, a non-selective serotonin (5-HT) reuptake inhibitor, and of citalopram, a highly selective 5-HT reuptake inhibitor, was examined in patients with chronic tension-type headache. Amitriptyline reduced headache significantly more than placebo, while citalopram had only a slight and insignificant effect. It was concluded that the blockade of 5-HT reuptake could only partly explain the efficacy of amitriptyline in tension-type headache, and that also other actions of amitriptyline, e.g. reduction of central sensitization, were involved. Finally, the plasma 5-HT level, the platelet 5-HT level and the number of platelet 5-HT transporters were found to be normal in chronic tension-type headache. On the basis of the present and previous studies, a pathophysiological model for tension-type headache is presented. According to the model, the main problem in chronic tension-type headache is central sensitization at the level of the spinal dorsal horn/trigeminal nucleus due to prolonged nociceptive inputs from pericranial myofascial tissues. The increased nociceptive input to supraspinal structures may in turn result in supraspinal sensitization. The central neuroplastic changes may affect the regulation of peripheral mechanisms and thereby lead to, for example, increased pericranial muscle activity or release of neurotransmitters in the myofascial tissues. By such mechanisms the central sensitization may be maintained even after the initial eliciting factors have been normalized, resulting in the conversion of episodic into chronic tension-type headache. Future basic and clinical research should aim at identifying the source of peripheral nociception in order to prevent the development of central sensitization and at ways of reducing established sensitization. This may lead to a much needed improvement in the treatment of chronic tension-type headache and other chronic myofascial pain conditions.     

Photophobia and phonophobia in tension-type and cervicogenic headache

Light and sound-induced discomfort and pain thresholds were measured in 26 patients with cervicogenic headache, in 40 patients with tension-type headache, and in 100 headache-free controls. Neither headache group was significantly different as to photophobia and phonophobia, but both were significantly more sensitive to light and sound than controls ( p <0.0001), even when patients were tested in the headache-tree period ( p <0.05). Episodic and chronic tension-type headache had similar photo- and phonophobia thresholds ( p ≥0.7). Tension-type headache patients were more photo- and phonophobic during headache than outside attack ( p <0.05), but this was not true for cervicogenic headache ( p ≥0.56). In cervicogenic headache patients, photophobia ( p <0.05) but not phonophohia ( p =0.28) was greater on the symptomatic side than on the non-symptomatic side.     

Possible mechanisms of glyceryl-trinitrate-induced immediate headache in patients with chronic tension-type headache

Nitric oxide (NO) plays an important role in the pathophysiology of primary headaches including chronic tension-type headache (CTTH). Thus, a NO synthase inhibitor reduces headache and muscle hardness while the NO donor glyceryl trinitrate (GTN) causes more headache in patients than in healthy controls. Sensitization of myofascial pain pathways is important in CTTH, and the aim of the present study was to investigate if such mechanisms may also explain GTN-induced immediate headache in patients with CTTH. In a randomized, double-blind, crossover study 16 patients with CTTH and 16 healthy subjects received intravenous infusion of GTN (0.5 microg/kg per min for 20 min) or placebo on two headache-free days separated by at least 1 week. Muscle hardness, myofascial tenderness, mechanical and heat pain thresholds were measured at baseline and at 60 min and 120 min after start of infusion. In patients, GTN infusion resulted in a biphasic response with immediate headache and more pronounced delayed headache. A similar but less pronounced response was seen in controls. There was no difference between GTN and placebo regarding muscle hardness, myofascial tenderness or pressure and heat pain thresholds in either patients or controls (P>0.05). The unchanged sensitivity of pericranial myofascial pain pathways indicates that peripheral and central sensitization is not involved in the mechanisms of GTN-induced immediate headache.     

Pressure pain thresholds and thermal nociceptive thresholds in chronic tension-type headache

The nociceptive thresholds to mechanical and thermal stimuli in patients with chronic tension-type headache were compared. Palpation of pericranial tenderness was performed in 50 patients and a total tenderness score (TTS) was calculated. Palpation was repeated, and pressure pain thresholds (PPTs) were determined with a pressure algometer in the temporal and occipital regions. In 32 of the patients, pain thresholds for heat and cold and limens for detection of non-painful temperature changes were determined in the hands and the temporal regions. Twenty-four healthy volunteers served as controls. Scores obtained by manual palpation (TTS) at the first and second visit were positively correlated. A negative correlation between headache severity and PPT was found in the temporal region. A positive correlation between PPT in the temporal and occipital region was found, and PPT and TTS were negatively correlated. Thermal pain thresholds were consistently less extreme in patients compared to controls, and patients reporting severe headache on the examination day were those most sensitive to thermal pain. No difference was found between patients and controls with respect to detection of temperature changes. A correlation was found between PPT and the corresponding cold pain thresholds, but no correlation could be demonstrated between TTS and thermal pain thresholds. In conclusion, headache patients had decreased pain perception thresholds. Chronic tension-type headache might be a result of dysmodulation of nociceptive impulses, but it is likely that sensitized nociceptors also play a role.     

Increased pain sensitivity is not a risk factor but a consequence of frequent headache: a population-based follow-up study

Altered pain sensitivity is believed to play an important role for chronification of headache. It has however mainly been evaluated in highly selected patients from headache clinics and never in longitudinal studies. The present study is a 12-year follow-up of a population-based study of primary headache disorders and pain perception, combining a diagnostic headache interview with examination of muscle tenderness and measurement of pressure pain thresholds in 1000 subjects drawn randomly from the general population in Denmark. The aim of the study was to explore the cause–effect relationship between the increased pain sensitivity and the development of headache. The pressure pain thresholds were normal at baseline but had decreased at follow-up in subjects who developed chronic tension-type headache over the 12-year period (p = 0.025). In subjects who developed frequent episodic tension-type headache the tenderness was normal at baseline but had increased at follow-up (p < 0.01) while the pain thresholds were normal both at baseline and at follow-up. The findings demonstrate that increased pain sensitivity is a consequence of frequent tension-type headache, not a risk factor, and support that central sensitization plays an important role for the chronification of tension-type headache.     

Perceptions of pain in women with headache: a laboratory investigation of the influence of pain-related anxiety and fear

The present study compared the responses of women with headache (chronic tension-type, n = 27; migraine, n = 27) and controls (n = 27) to an acute pain laboratory task, the cold pressor test. Participants' pain perception (i.e., threshold and tolerance) and their fear/anxiety associated with pain were assessed during days 1, 2, or 3 of menses. Analyses pertaining to participants' responses to the cold pressor test (ie, pain threshold and tolerance) failed to show statistically significant group differences, even when covarying pain-related anxiety/fear. Analyses did, however, reveal significant group differences between migraineurs and controls in cognitive anxiety. Correlational analyses also revealed that cognitive anxiety, somatic anxiety, fear, and escape/avoidance were all significantly correlated with pain tolerance in the group with chronic tension-type headache, but not in the other two groups. Subsequent multiple regressions, however, showed that the relationship between anxiety and pain tolerance was primarily a function of somatic anxiety. These results suggest that headache frequency plays a role in mediating the relationship between fear of pain and pain tolerance and that the models by Lethem and colleagues and McCracken may be relevant for understanding tension headache sufferers' responses to head pain.     

Pain sensitivity and pain reactivity of pericranial muscles in migraine and tension-type headache

We investigated whether experimentally determined, suprathreshold pain sensitivity of pericranial musculature in patients with tension-type headache differs from that of migraine patients or from that of healthy subjects. Furthermore, we looked to see whether differences could be found in the effects of experimental pain induction on EMG activity of pericranial musculature and whether subgroups could be discovered with higher and lower pericranial pain sensitivity within the three diagnostic groups in terms of neurophysiological, psychological and clinical variables. In 20 patients with tension-type headache, 23 patients with migraine without aura, and 29 healthy individuals experimental pain was induced in the temporal muscle by mechanical pressure; pain sensitivity in the entire metrically subdivided suprathreshold pain sensitivity range was measured. Surface EMG activity of pericranial muscles was determined before, during and after experimental pain induction. In addition, headache characteristics as well as personality and mood states were determined and recorded in a standardized fashion. There were no significant differences in pain sensitivity of pericranial musculature between the three groups. Patients with tension-type headache showed significantly higher EMG scores during suprathreshold pain stimulation than did migraine patients. EMG scores of healthy subjects fell between these two groups. With respect to pericranial tenderness significant differences in clinical, neurophysiological and psychological variables were found only between subgroups within the group of patients with tension-type headache. The results indicate that significant differences in the examined groups are found not in pain perception but in the processing or reaction to experimental headache stimuli. In patients with tension-type headache subgroups evolve based on pericranial pain sensitivity with quantitatively and/or qualitatively impaired reactions; for this reason diagnostic grouping according to the IHS classification seems to be pathophysiologically relevant. The intraindividual phasic comparison of pain reactions appears to be more important than the absolute interindividual tonic comparison.     

Bilateral pressure pain sensitivity mapping of the temporalis muscle in chronic tension-type headache

Purpose.— To analyze pressure pain sensitivity maps in chronic tension-type headache (CTTH) and healthy controls over nine locations covering the temporalis muscle.
Background.— Lower pressure pain thresholds (PPT) have been found in craniofacial muscles in patients with CTTH. Since the temporalis muscle can play a relevant role in the genesis or maintenance of headache, the determination of pressure pain sensitivity maps of this muscle is needed.
Methods.— A pressure algometer was used to measure PPT over 9 points of the temporalis muscle (3 points in the anterior part of the muscle, another 3 in the middle of the muscle, and the remaining 3 in the posterior part) in 15 females suffering from CTTH and 10 healthy women. A pressure pain sensitivity map of both dominant and nondominant sides in patients and controls was calculated.
Results.— Chronic tension-type headache patients showed lower PPT as compared with healthy subjects ( P  < .01). Further, PPT levels of the nondominant side were lower than those on the dominant side for controls ( P  < .01). Within the CTTH group, more bilaterally homogeneous pressure pain sensitivity maps with PPT decreased from the posterior to anterior column were found, whereas among controls, PPT distribution maps were inhomogeneous with side-to-side differences.
Conclusions.— Our data may provide preliminary new key information about muscle sensitivity, since it seems that pressure pain sensitivity maps could be different between CTTH patients and healthy subjects. Further studies with greater sample sizes and other headache populations are now required to confirm our results.     

Clinical features of headache patients with fibromyalgia comorbidity

Our previous study assessed the prevalence of fibromyalgia (FM) syndrome in migraine and tension-type headache. We aimed to update our previous results, considering a larger cohort of primary headache patients who came for the first time at our tertiary headache ambulatory. A consecutive sample of 1,123 patients was screened. Frequency of FM in the main groups and types of primary headaches; discriminating factor for FM comorbidity derived from headache frequency and duration, age, anxiety, depression, headache disability, allodynia, pericranial tenderness, fatigue, quality of life and sleep, and probability of FM membership in groups; and types of primary headaches were assessed. FM was present in 174 among a total of 889 included patients. It prevailed in the tension-type headache main group (35%, p < 0.0001) and chronic tension-type headache subtype (44.3%, p < 0.0001). Headache frequency, anxiety, pericranial tenderness, poor sleep quality, and physical disability were the best discriminating variables for FM comorbidity, with 81.2% sensitivity. Patients presenting with chronic migraine and chronic tension-type headache had a higher probability of sharing the FM profile (Bonferroni test, p < 0.01). A phenotypic profile where headache frequency concurs with anxiety, sleep disturbance, and pericranial tenderness should be individuated to detect the development of diffuse pain in headache patients.     

Effect of mental stress on cold pain in chronic tension-type headache sufferers

Mental stress is a noted contributing factor in chronic tension-type headache (CTH), however the mechanisms underlying this are not clearly understood. One proposition is that stress aggravates already increased pain sensitivity in CTH sufferers. This hypothesis could be partially tested by examining effects of mental stress on threshold and supra-threshold experimental pain processing in CTH sufferers. Such studies have not been reported to date. The present study measured pain detection and tolerance thresholds and ratings of supra-threshold pain stimulation from cold pressor test in CTH sufferers (CTH-S) and healthy Control (CNT) subjects exposed to a 60-min stressful mental task, and in CTH sufferers exposed to a 60-min neutral condition (CTH-N). Headache sufferers had lower pain tolerance thresholds and increased pain intensity ratings compared to controls. Pain detection and tolerance thresholds decreased and pain intensity ratings increased during the stress task, with a greater reduction in pain detection threshold and increase in pain intensity ratings in the CTH-S compared to CNT group. The results support the hypothesis that mental stress contributes to CTH through aggravating already increased pain sensitivity in CTH sufferers.     

Changing headache from preschool age to puberty. A controlled study

The characteristics of disturbing primary headache and the occurrence of headache types were studied by sending a questionnaire to 1132 Finnish families of 6-year-old children. Children with headache in the preceding 6 months and their controls were clinically examined at the ages of 6 and 13. During the follow-up, half of the headaches, classified as migraine at age 6 years, were unchanged and 32% turned into tension-type headache. In children with tension-type headache, the situation was unchanged in 35%, and in 38% of children the headache type had changed to migraine. At preschool age the most common location of headache was bilateral and supraorbital, and at puberty bilateral and temporal. During the follow-up, symptoms concurrent with headache, such as odour phobia, dizziness and balance disturbances became more typical, whereas restlessness, flushing and abdominal symptoms became less marked. The early manifestation of both migraine and tension-type headache predict equally often migraine in puberty with marked changes in concurrent symptoms and pain localization.     

Central pain modulation and scalp tenderness in frequent episodic tension-type headache

Objective.— To determine whether the inhibitory effect of acute limb pain on pain to mechanical stimulation of the forehead is compromised in individuals with frequent episodes of tension‐type headache. Background.— Central pain modulation processes are disrupted in patients with chronic tension‐type headache. This deficit in pain modulation might be a predisposing characteristic that increases vulnerability to tension‐type headache and to symptoms such as scalp tenderness, or could be a feature that develops secondarily during attacks and that persists for a few days afterward. To distinguish between these 2 possibilities in the present study, inhibitory pain control was investigated in participants with episodic rather than chronic tension‐type headache. Methods.— Pressure‐pain thresholds and sensitivity to sharpness in the forehead were measured in 34 individuals with 1‐10 episodes of tension‐type headache per month and in 32 controls before and after immersion of their hand in painfully cold water. Results.— Before the cold pressor test, pressure‐pain thresholds and sensitivity to the sharp stimulus were similar in both groups. Mild headache developed and pressure‐pain thresholds in the forehead decreased from 631 ± 178 g to 579 ± 196 g (mean ± SD) after the cold water immersion in the episodic tension‐type headache group (P < .05). However, sharpness ratings did not change (mean rating 3.2 ± 1.4 on a 0‐10 scale). In contrast, headache did not develop, pressure‐pain thresholds did not change, and sharpness ratings decreased from 3.0 ± 1.3 to 2.3 ± 1.1 after the immersion in controls (P < .01). Conclusions.— These findings suggest that endogenous pain modulation processes are compromised in individuals with frequent episodic tension‐type headache. This deficit could increase vulnerability to scalp tenderness and recurrent episodes of headache.