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Myofascial trigger points in the suboccipital muscles in episodic tension-type headache
ARTICLE IN PRESS
Manual Therapy 11 (2006) 225–230 www.elsevier.com/locate/math
Original article
Myofascial trigger points in the suboccipital muscles in episodic tension-type headache Ce´sar Ferna´ndez-de-las-Pen˜asa,b,, Cristina Alonso-Blancoa, Maria Luz Cuadradob,c, Juan A. Parejab,c a
Department of Physical Therapy, Occupational Therapy, Physical Medicine and Rehabilitation of Universidad Rey Juan Carlos, Alcorco´n, Madrid, Spain b Esthesiology Laboratory of Universidad Rey Juan Carlos, Alcorco´n, Madrid, Spain c Department of Neurology of Fundacio´n Hospital Alcorco´n and Universidad Rey Juan Carlos, Alcorco´n, Madrid, Spain
Abstract Referred pain evoked by suboccipital muscle trigger points (TrPs) spreads to the side of the head over the occipital and temporal bones and is usually perceived as bilateral headache. This paper describes the presence of referred pain from suboccipital muscle TrPs in subjects with episodic tension-type headache (ETTH) and in healthy controls. Ten patients presenting with ETTH and 10 matched controls without headache were examined by a blinded assessor for the presence of suboccipital muscle TrPs. Diagnostic criteria described by Simons and Gerwin were adapted to diagnose TrPs, i.e. presence of tenderness in the suboccipital region, referred pain evoked by maintained pressure for 10 s, and increased referred pain on muscle contraction. Six ETTH patients (60%) had active TrPs and 4 had latent TrPs (40%). On the other hand, 2 control subjects also had latent TrPs. Differences in the presence of suboccipital muscle TrPs between both groups were significant for active TrPs (Po0:001), but not for latent TrPs. Active TrPs were only present in ETTH patients, although TrP activity was not related to any clinical variable concerning the intensity and the temporal profile of headache. Myofascial TrPs in the suboccipital muscles might contribute to the origin and/or maintenance of headache, but a comprehensive knowledge of the role of these muscles in tension-type headache awaits further research. r 2006 Elsevier Ltd. All rights reserved. Keywords: Tension-type headache; Myofascial trigger points; Suboccipital muscles; Referred pain
1. Background Headache disorders are one of the most common problems seen in medical practice. Among the many types of headache disorders, tension-type headache (TTH) is the most frequent in adults. Population-based studies suggest 1-year prevalence rates of 38.3% for episodic TTH, and 2.2% for chronic TTH (Schwartz et al., 1998). TTH is considered to be the prototype of headache with myofascial tissues playing an important Corresponding author. Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avenida de Atenas s/n, 28922 Alcorco´n, Madrid, Spain. Tel.: +34 91 488 88 84; fax: +34 91 488 89 57. E-mail addresses: [email protected], [email protected] (C. Ferna´ndez-de-las-Pen˜as).
1356-689X/$ - see front matter r 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2006.07.003
role (Jensen and Olesen, 1996). Gerwin (2005) and Jensen (1999) have claimed that pain from pericranial head; neck and shoulder muscles might be referred to the head, and be experienced as headache. Simons et al. (1999) described the referred pain patterns from different myofascial trigger points (TrPs) in head and neck muscles, which produced pain features that are usually found in subjects presenting with TTH. Simons et al. (1999) define a TrP as a hyperirritable spot associated with a taut band of a skeletal muscle that is painful on compression, palpation and/or stretch, and that usually gives rise to a typical referred pain pattern. Active TrPs are cause of clinical symptoms, i.e. spontaneous referred pain and restricted motion of the affected tissues, whereas latent TrPs may not be an immediate source of pain, but might produce other muscle dysfunctions such as fatigue
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and restricted range of motion (Simons et al., 1999). This clinical distinction has been strongly substantiated by histochemical findings, since higher levels of concentration of bradykinin, calcitonin gene-related peptide, substance P, tumour necrosis factor-a, interleukin-1b, serotonin and norepinephrine have been recently found in active TrPs (Shah et al., 2005). TTH is characterized by bilateral, pressing and tightening head pain, of mild-to-moderate intensity, that is not aggravated during routine physical activity. In the episodic form, patients suffer from headache less than 15 days per month, whereas in the chronic form patients experience headache at least 15 days per month (IHS, 2004). Some characteristics of TTH, such as pressure or band-like tightness (IHS, 1988, 2004), and increased tenderness on palpation of neck and shoulder muscles (Jensen and Olesen, 1996; Lipchik et al. 1997), resemble the descriptions of referred pain originating in TrPs (Simons et al. 1999). Marcus et al. (1999) found that subjects suffering from TTH showed a greater number of either active or latent TrPs in different muscles than healthy subjects. On the other hand, we have already found that TTH subjects, either chronic or episodic, show a greater number of TrPs in the superior oblique muscle than controls (Ferna´ndez-de-las-Pen˜as et al., 2005). Therefore, it seems plausible that TrPs might play an important role in the genesis of TTH. Within the cervical musculature, suboccipital muscles can develop TrPs, accounting for a referred pain pattern that spreads to the side of the head over the occipital and temporal bones (Fig. 1). This referred pain extends to both sides, thus being perceived as bilateral headache (Simons et al., 1999). In a series of patients with chronic TTH (CTTH), our research group recently demonstrated that this disorder was associated with suboccipital active TrPs and forward head posture, and that those CTTH subjects with active TrPs had greater headache intensity and frequency than those with latent TrPs (Ferna´ndez-de-lasPen˜as et al., 2006). Moreover, we have previously found that the management of suboccipital muscle TrPs may produce significant pain relief in subjects presenting with episodic TTH (ETTH) (Ferna´ndez-de-las-Pen˜as et al., 2004). After such early observations, we have extended our former study in CTTH subjects (Ferna´ndez-de-las-Pen˜as et al., 2006) to subjects suffering from ETTH. This paper describes the presence of referred pain stemming from suboccipital muscle TrPs in subjects with ETTH and in healthy control subjects.
Fig. 1. Referred pain from myofascial trigger points in the suboccipital muscles (rectus capitis posterior minor and major muscles). Adapted from Simons DG, Travell JG, Simons LS. Travell and Simons’ Myofascial Pain and dysfunction: The trigger point manual. Volume 1: upper half of the body. (2nd edition) Ed Baltimore: Williams & Wilkins, 1999. Fig. 17.1 (p. 473).
2. Material and methods
subjects without headache during the previous year participated in this study from June to November of 2004. Patients were recruited from the Neurology Department of Fundacio´n Hospital Alcorco´n, whereas controls were recruited from the hospital staff. Patients with ETTH were diagnosed according to the criteria of the International Headache Society (IHS) by an experienced neurologist (IHS, 2004). ETTH patients had to have headache less than 15 days per month. A headache diary was kept for 4 weeks in order to substantiate the diagnosis (Russell et al., 1992). The health status of all participants was clinically stable, without current symptoms of any other concomitant disease. This study was supervised by the Departments of Physical Therapy and Neurology of Rey Juan Carlos University and Fundacio´n Hospital Alcorco´n, and it was also approved by the local human research Committee. All subjects signed an informed consent prior to their inclusion.
2.1. Subjects
2.2. Myofascial trigger point examination
Ten patients presenting with episodic tension-type headache (ETTH) and 10 healthy age- and sex-matched
TrPs were sought in the suboccipital muscles by an assessor who had more than 4 years’ experience in TrPs
ARTICLE IN PRESS C. Ferna´ndez-de-las-Pen˜as et al. / Manual Therapy 11 (2006) 225–230
diagnosis, and who was also blinded to the subjects’ condition. Diagnostic criteria as described by Simons et al. (1999) and by Gerwin et al. (1997) were adapted for the suboccipital muscles and used to diagnose TrPs. These modified criteria have been employed in previous studies (Ferna´ndez-de-las-Pen˜as et al., 2005, 2006). Specifically, the TrP diagnosis was made when there was tenderness in the suboccipital region; referred pain evoked by maintained pressure for 10 s (Fig. 1), and increased referred pain on muscle contraction, i.e. active extension of the upper cervical spine. The suboccipital muscles that extend the neck at the occipital–atlas junction (rectus capitis posterior major and minor, and the oblique capitis superior) are not directly palpable. To evaluate the effect of muscle contraction on referred pain intensity, subjects lay supine with the cervical spine in a neutral position. The assessor palpated the suboccipital region, that is, the anatomical projection of the rectus capitis posterior major and minor muscles between the posterior arch of the atlas and the occiput bone (Fig. 2), for 10 s. If referred pain was evoked upon compression, subjects were asked to extend the neck. This movement produced a palpable contraction of the most superficial posterior cervical muscles, and conceivably a contraction of the suboccipital muscles, that are not directly palpable. Subjects were asked to keep the neck straight and only extend at the cervical– occipital junction, to focus the contraction on both rectus capitis posterior muscles. The assumption that the suboccipital muscles were involved during the exploration was based on the characteristic referred pain pattern of these muscles (Fig. 1), in contrast to the referred pain patterns characteristic of other posterior cervical muscles. TrPs were considered active if the subject recognized the evoked referred pain as familiar, i.e. if it reproduced the pain that he or she perceived during spontaneous headache attacks; conversely, TrPs were considered latent if the subject did not recognize the evoked referred pain as a familiar pain (Simons et al., 1999; Gerwin et al., 1997). Since referred pain from suboccipital muscle TrPs is elicited bilaterally (Simons et al., 1999), we did not classify TrPs as either right or left. Then, we considered the presence of a unique TrP if manual palpation of suboccipital muscles evoked bilateral referred pain (Simons et al., 1999; Gerwin, 2005; Ferna´ndez-de-las-Pen˜as et al., 2006). 2.3. Study protocol All subjects had to be headache-free on the day of the examination. A first assessor gave a headache diary to ETTH patients. Patients had to register on this diary the daily headache intensity, on a 10-cm horizontal visual analogue scale (VAS; range: 0 ¼ no pain, to 10 ¼ maximum pain) (Jensen et al., 1999), the headache
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Fig. 2. Topography of the rectus capitis posterior minor (RCPmin) and major (RCPmaj) muscles.
duration (in hours per day), and the days with headache. This headache diary was kept for 4 weeks. This assessor also informed control subjects about physical therapy and headache (health education), but did not give them a headache diary. A second assessor, blinded to the subjects’ condition, examined the suboccipital muscles for the presence of TrPs. Four weeks later, ETTH subjects returned the headache diary to the first assessor, who calculated the following variables: 1, headache intensity, which was calculated from the mean of the VAS of the days with headache; 2, headache frequency, which was calculated dividing the number of days with headache by 4 weeks (days per week); and 3, headache duration, which was calculated dividing the sum of the total hours of headache by the number of days with headache (hours per day). 2.4. Statistical analysis Data were analysed with the SPSS statistical package (12.0 Version). The Kolmogorov–Smirnov test showed a
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normal distribution of the quantitative outcomes. The chi-square (w2) test was used to compare the presence of either latent or active TrPs between both study groups. The unpaired t-test was used to analyse the differences in the clinical variables relating to headache (headache intensity, frequency and/or duration) between ETTH subjects with either latent or active TrPs. The statistical analysis was conducted at a 95% confidence level. A Pvalue less than 0.05 was considered statistically significant.
4. Discussion All patients presenting with ETTH in this series had suboccipital muscle TrPs, either active or latent. The referred pain evoked by suboccipital TrPs reproduced usual headache in 6 (60%) of them, which was consistent with active TrPs, while the remaining 4 (40%) had latent TrPs. Within the control group, no one had active TrPs, but 2 healthy subjects (20%) had latent TrPs. Therefore, both groups had latent TrPs, while active TrPs were only present in the ETTH group. Our results are in agreement with Chaiamnuay et al. (1998), who also observed some latent TrPs in healthy subjects. On the other hand, current findings in ETTH subjects complete our previous findings for subjects with the chronic form of TTH (CTTH), in whom, suboccipital muscle TrPs were also more common than in healthy controls (Ferna´ndez-de-las-Pen˜as et al., 2006). However, in CTTH patients the presence of active TrPs was related to greater headache intensity and greater headache frequency than the presence of latent TrPs. These latter results have not been replicated in this study, since none of the clinical variables concerning the intensity and the temporal profile of headache differed with TrP activity in our group of ETTH patients (Table 2). Previous (Ferna´ndez-de-las-Pen˜as et al., 2006) and current findings support the hypothesis that suboccipital muscle TrPs might play an important role in the genesis of TTH, either episodic or chronic. Bendtsen (2000) reported that both peripheral mechanisms, i.e.
3. Results A total of 10 ETTH patients, 2 men and 8 women, aged 18–66 years old, and 10 healthy volunteers, 3 men and 7 women, aged 18–66 years old, were studied. No significant differences were found for gender or age between both study groups. ETTH subjects were headache-free on the day of the evaluation. Demographic and clinical data of each group are given in Table 1. All ETTH patients showed TrPs in the suboccipital muscles. Six of them (60%) had active TrPs, whereas the remaining 4 (40%) had latent TrPs. On the other hand, 2 (20%) control subjects had latent TrPs. Differences in the presence of suboccipital muscle TrPs between both groups were significant for active TrPs (Po0:001), but not for latent TrPs. Within the ETTH group, headache intensity, frequency and duration outcomes did not differ depending on TrP activity, whether the TrPs were active or latent (Table 2).
Table 1 Demographic and clinical data of both groups
Gender (male/female) Age (years) Length of headache history (years) Headache intensity (VAS) Headache frequency (days/week) Headache duration (hours per headache day)
ETTH (n ¼ 10)
Controls (n ¼ 10)
P-value
2/8 35715 5.573.5 4.371.5 2.970.5 572.7
3/7 34713 — — — —
NS NS — — — —
Values are expressed as mean7SD. ETTH ¼ episodic tension-type headache. VAS ¼ Visual Analogue Scale (0–10). NS ¼ Non-significant.
Table 2 Headache intensity, frequency and duration depending on the activity of suboccipital muscle trigger points
Active TrPs (n ¼ 6) Latent TrPs (n ¼ 4)
Headache intensity (VAS)
Headache frequency (days/week)
Headache duration (hours/day)
4.871.4 3.671.4
2.970.5 370.5
4.273.4 6.370.4
Values are expressed as mean7SD. VAS ¼ Visual Analogue Scale (0–10). TrPs ¼ Myofascial trigger points. Non-significant in comparison with the latent TrP subgroup (unpaired t-test, Po0:05).
ARTICLE IN PRESS C. Ferna´ndez-de-las-Pen˜as et al. / Manual Therapy 11 (2006) 225–230
myofascial tenderness of pericranial structures, and central mechanisms, i.e. sensitization of supraspinal neurones and decreased anti-nociceptive activity from supraspinal structures, might be involved in the pathogenesis of TTH. These phenomena could be interconnected, since continuous or prolonged nociceptive inputs from myofascial tissues may contribute to the central sensitization in CTTH (Jensen, 1999). Nociceptive inputs from suboccipital muscle TrPs may produce a continuous afferent bombardment to the trigeminal nerve nucleus caudalis. Such repeated nociceptive activation of the nucleus caudalis could produce central sensitization in CTTH (Bendtsen, 2000). If there were a lesser degree of central sensitization in ETTH, because of the intermittent nature of this condition, one would expect fewer active and more latent TrPs in ETTH subjects than in CTTH subjects. Our findings do not support this hypothesis, as suboccipital active TrPs were present in a similar proportion in both ETTH subjects (60%) and CTTH subjects (65%). However, headache intensity and frequency were related to TrPs activity in CTTH (Ferna´ndez-de-las-Pen˜as et al., 2006), but not in ETTH. Since TrPs are responsible for the liberation of nociceptive mediators (Shah et al., 2005), it seems plausible that TrP activity originated in the suboccipital muscles might be a triggering factor for central sensitization seen in chronic headaches. In such way, the presence of TrPs could contribute to the evolution of the episodic form to the chronic form of TTH. There are some limitations to our studies. First, only subjects with TTH have been evaluated. Hence, our results cannot be extrapolated to other headache disorders. It would be interesting to repeat the same procedure with patients suffering from other disorders in order to explore the relevance of suboccipital muscle TrPs in headache. The second limitation was the sample size. To our knowledge, our studies are the first ones to analyse the relationship between suboccipital muscle TrPs and clinical features in TTH. However, it would be necessary to repeat the same procedure with a greater number of subjects so as to confirm our findings in both ETTH and CTTH patients. Third, it is possible that other structures of the upper cervical region, e.g. atlanto-axial joint or C2 nerve trunk, could be palpated during the exploration and then responsible for the perceived referred pain. However, our palpation was done next to the occipital bone (Fig. 2), so the possibility to palpate these structures was minimal. Moreover, since muscle contraction increased referred pain in all patients, it is most likely that the elicited referred pain was originated in the muscle tissue, that is, in the suboccipital muscles. 5. Conclusions Active myofascial TrPs in the suboccipital muscles were more common in ETTH subjects than in healthy
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controls, although TrP activity was not related to any clinical variable concerning the intensity and the temporal profile of headache. Suboccipital TrPs might contribute to the origin and/or maintenance of headache, but a comprehensive knowledge of the role of these muscles in TTH awaits further research.
Acknowledgements We would like to thank Dr. David Simons and Dr. Robert D. Gerwin for their kind encouragement and support.
References Bendtsen L. Central sensitization in tension-type headache: possible patho-physiological mechanisms. Cephalalgia 2000;29: 486–508. Chaiamnuay P, Darmawan J, Muirden KD, Assawatanabodee P. Epidemiology of rheumatic disease in rural Thailand: a WHOILAR COPCORD study. Community Oriented Programme for the Control of the Rheumatic Disease. Journal of Rheumatology 1998;25:1382–7. Ferna´ndez-de-las-Pen˜as C, Alonso-Blanco C, Cuadrado ML, Pareja JA, Barriga FJ, Miangolarra JC. Adverse tension in cranial dura mater and Myofascial trigger points in suboccipital muscles in patients with episodic tension type headache. Journal of Musculoskeletal Pain 2004;12(Suppl 9):75 (abstract). Ferna´ndez-de-las-Pen˜as C, Cuadrado ML, Gerwin RD, Pareja JA. Referred pain from the trochlear region in tension-type headache: a Myofascial trigger point from the superior oblique muscle. Headache 2005;45:731–7. Ferna´ndez-de-las-Pen˜as C, Alonso-Blanco C, Cuadrado ML, Gerwin RD, Pareja JA. Trigger points in the suboccipital muscles and forward head posture in chronic tension type headache. Headache 2006;46:454–60. Gerwin R. Headache. In: Ferguson L, Gerwin R, editors. Clinical mastery in the treatment of myofascial pain. Philadelphia: Lippincott Williams & Wilkins; 2005. p. 1–24. Gerwin RD, Shanon S, Hong CZ, Hubbard D, Gevirtz R. Interrater reliability in myofascial trigger point examination. Pain 1997;69: 65–73. IHS: Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain—1st edition. Cephalalgia 1988;8(Suppl 7):29–34. IHS: Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders–2nd edition. Cephalalgia 2004;24(Suppl 1):9–160. Jensen R. Pathophysiological mechanism of tension-type headache: a review of epidemiological and experimental studies. Cephalalgia 1999;19:602–21. Jensen R, Olesen J. Initiating mechanism of experimentally induced tension-type headache. Cephalalgia 1996;16:175–82. Jensen MP, Turbner JA, Romano JM, Fisher L. Comparative reliability and validity of chronic pain intensity measures. Pain 1999;83:157–62. Lipchik GL, Holroyd KA, Talbot F, Greer M. Pericranial muscle tenderness and exteroceptive suppression of temporalis muscle activity: a blind study of chronic tension-type headache. Headache 1997;37:368–76.
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Marcus DA, Scharff L, Mercer S, Turk DC. Musculoskeletal abnormalities in chronic headache: a controlled comparison of headache diagnostic groups. Headache 1999;39:21–7. Russell MB, Rasmussen BK, Brennum J, Iversen HK, Jensen RA, Olesen J. Presentation of a new instrument: the diagnostic headache diary. Cephalalgia 1992;12:369–74. Schwartz BS, Stewart WF, Simon D, et al. Epidemiology of tensiontype headache. Journal of the American Medical Association 1998;279:381–3.
Shah JP, Phillips TM, Danoff JV, Gerber LH. An in vitro microanalytical technique for measuring the local biochemical milieu of human skeletal muscle. Journal of Applied Physiology 2005;99:1977–84. Simons DG, Travell J, Simons LS. Myofascial pain and dysfunction: the trigger point manual: vol. 1. 2nd ed. Baltimore: Williams & Wilkins; 1999.
Manual Therapy 11 (2006) 225–230 www.elsevier.com/locate/math
Original article
Myofascial trigger points in the suboccipital muscles in episodic tension-type headache Ce´sar Ferna´ndez-de-las-Pen˜asa,b,, Cristina Alonso-Blancoa, Maria Luz Cuadradob,c, Juan A. Parejab,c a
Department of Physical Therapy, Occupational Therapy, Physical Medicine and Rehabilitation of Universidad Rey Juan Carlos, Alcorco´n, Madrid, Spain b Esthesiology Laboratory of Universidad Rey Juan Carlos, Alcorco´n, Madrid, Spain c Department of Neurology of Fundacio´n Hospital Alcorco´n and Universidad Rey Juan Carlos, Alcorco´n, Madrid, Spain
Abstract Referred pain evoked by suboccipital muscle trigger points (TrPs) spreads to the side of the head over the occipital and temporal bones and is usually perceived as bilateral headache. This paper describes the presence of referred pain from suboccipital muscle TrPs in subjects with episodic tension-type headache (ETTH) and in healthy controls. Ten patients presenting with ETTH and 10 matched controls without headache were examined by a blinded assessor for the presence of suboccipital muscle TrPs. Diagnostic criteria described by Simons and Gerwin were adapted to diagnose TrPs, i.e. presence of tenderness in the suboccipital region, referred pain evoked by maintained pressure for 10 s, and increased referred pain on muscle contraction. Six ETTH patients (60%) had active TrPs and 4 had latent TrPs (40%). On the other hand, 2 control subjects also had latent TrPs. Differences in the presence of suboccipital muscle TrPs between both groups were significant for active TrPs (Po0:001), but not for latent TrPs. Active TrPs were only present in ETTH patients, although TrP activity was not related to any clinical variable concerning the intensity and the temporal profile of headache. Myofascial TrPs in the suboccipital muscles might contribute to the origin and/or maintenance of headache, but a comprehensive knowledge of the role of these muscles in tension-type headache awaits further research. r 2006 Elsevier Ltd. All rights reserved. Keywords: Tension-type headache; Myofascial trigger points; Suboccipital muscles; Referred pain
1. Background Headache disorders are one of the most common problems seen in medical practice. Among the many types of headache disorders, tension-type headache (TTH) is the most frequent in adults. Population-based studies suggest 1-year prevalence rates of 38.3% for episodic TTH, and 2.2% for chronic TTH (Schwartz et al., 1998). TTH is considered to be the prototype of headache with myofascial tissues playing an important Corresponding author. Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avenida de Atenas s/n, 28922 Alcorco´n, Madrid, Spain. Tel.: +34 91 488 88 84; fax: +34 91 488 89 57. E-mail addresses: [email protected], [email protected] (C. Ferna´ndez-de-las-Pen˜as).
1356-689X/$ - see front matter r 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2006.07.003
role (Jensen and Olesen, 1996). Gerwin (2005) and Jensen (1999) have claimed that pain from pericranial head; neck and shoulder muscles might be referred to the head, and be experienced as headache. Simons et al. (1999) described the referred pain patterns from different myofascial trigger points (TrPs) in head and neck muscles, which produced pain features that are usually found in subjects presenting with TTH. Simons et al. (1999) define a TrP as a hyperirritable spot associated with a taut band of a skeletal muscle that is painful on compression, palpation and/or stretch, and that usually gives rise to a typical referred pain pattern. Active TrPs are cause of clinical symptoms, i.e. spontaneous referred pain and restricted motion of the affected tissues, whereas latent TrPs may not be an immediate source of pain, but might produce other muscle dysfunctions such as fatigue
ARTICLE IN PRESS 226
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and restricted range of motion (Simons et al., 1999). This clinical distinction has been strongly substantiated by histochemical findings, since higher levels of concentration of bradykinin, calcitonin gene-related peptide, substance P, tumour necrosis factor-a, interleukin-1b, serotonin and norepinephrine have been recently found in active TrPs (Shah et al., 2005). TTH is characterized by bilateral, pressing and tightening head pain, of mild-to-moderate intensity, that is not aggravated during routine physical activity. In the episodic form, patients suffer from headache less than 15 days per month, whereas in the chronic form patients experience headache at least 15 days per month (IHS, 2004). Some characteristics of TTH, such as pressure or band-like tightness (IHS, 1988, 2004), and increased tenderness on palpation of neck and shoulder muscles (Jensen and Olesen, 1996; Lipchik et al. 1997), resemble the descriptions of referred pain originating in TrPs (Simons et al. 1999). Marcus et al. (1999) found that subjects suffering from TTH showed a greater number of either active or latent TrPs in different muscles than healthy subjects. On the other hand, we have already found that TTH subjects, either chronic or episodic, show a greater number of TrPs in the superior oblique muscle than controls (Ferna´ndez-de-las-Pen˜as et al., 2005). Therefore, it seems plausible that TrPs might play an important role in the genesis of TTH. Within the cervical musculature, suboccipital muscles can develop TrPs, accounting for a referred pain pattern that spreads to the side of the head over the occipital and temporal bones (Fig. 1). This referred pain extends to both sides, thus being perceived as bilateral headache (Simons et al., 1999). In a series of patients with chronic TTH (CTTH), our research group recently demonstrated that this disorder was associated with suboccipital active TrPs and forward head posture, and that those CTTH subjects with active TrPs had greater headache intensity and frequency than those with latent TrPs (Ferna´ndez-de-lasPen˜as et al., 2006). Moreover, we have previously found that the management of suboccipital muscle TrPs may produce significant pain relief in subjects presenting with episodic TTH (ETTH) (Ferna´ndez-de-las-Pen˜as et al., 2004). After such early observations, we have extended our former study in CTTH subjects (Ferna´ndez-de-las-Pen˜as et al., 2006) to subjects suffering from ETTH. This paper describes the presence of referred pain stemming from suboccipital muscle TrPs in subjects with ETTH and in healthy control subjects.
Fig. 1. Referred pain from myofascial trigger points in the suboccipital muscles (rectus capitis posterior minor and major muscles). Adapted from Simons DG, Travell JG, Simons LS. Travell and Simons’ Myofascial Pain and dysfunction: The trigger point manual. Volume 1: upper half of the body. (2nd edition) Ed Baltimore: Williams & Wilkins, 1999. Fig. 17.1 (p. 473).
2. Material and methods
subjects without headache during the previous year participated in this study from June to November of 2004. Patients were recruited from the Neurology Department of Fundacio´n Hospital Alcorco´n, whereas controls were recruited from the hospital staff. Patients with ETTH were diagnosed according to the criteria of the International Headache Society (IHS) by an experienced neurologist (IHS, 2004). ETTH patients had to have headache less than 15 days per month. A headache diary was kept for 4 weeks in order to substantiate the diagnosis (Russell et al., 1992). The health status of all participants was clinically stable, without current symptoms of any other concomitant disease. This study was supervised by the Departments of Physical Therapy and Neurology of Rey Juan Carlos University and Fundacio´n Hospital Alcorco´n, and it was also approved by the local human research Committee. All subjects signed an informed consent prior to their inclusion.
2.1. Subjects
2.2. Myofascial trigger point examination
Ten patients presenting with episodic tension-type headache (ETTH) and 10 healthy age- and sex-matched
TrPs were sought in the suboccipital muscles by an assessor who had more than 4 years’ experience in TrPs
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diagnosis, and who was also blinded to the subjects’ condition. Diagnostic criteria as described by Simons et al. (1999) and by Gerwin et al. (1997) were adapted for the suboccipital muscles and used to diagnose TrPs. These modified criteria have been employed in previous studies (Ferna´ndez-de-las-Pen˜as et al., 2005, 2006). Specifically, the TrP diagnosis was made when there was tenderness in the suboccipital region; referred pain evoked by maintained pressure for 10 s (Fig. 1), and increased referred pain on muscle contraction, i.e. active extension of the upper cervical spine. The suboccipital muscles that extend the neck at the occipital–atlas junction (rectus capitis posterior major and minor, and the oblique capitis superior) are not directly palpable. To evaluate the effect of muscle contraction on referred pain intensity, subjects lay supine with the cervical spine in a neutral position. The assessor palpated the suboccipital region, that is, the anatomical projection of the rectus capitis posterior major and minor muscles between the posterior arch of the atlas and the occiput bone (Fig. 2), for 10 s. If referred pain was evoked upon compression, subjects were asked to extend the neck. This movement produced a palpable contraction of the most superficial posterior cervical muscles, and conceivably a contraction of the suboccipital muscles, that are not directly palpable. Subjects were asked to keep the neck straight and only extend at the cervical– occipital junction, to focus the contraction on both rectus capitis posterior muscles. The assumption that the suboccipital muscles were involved during the exploration was based on the characteristic referred pain pattern of these muscles (Fig. 1), in contrast to the referred pain patterns characteristic of other posterior cervical muscles. TrPs were considered active if the subject recognized the evoked referred pain as familiar, i.e. if it reproduced the pain that he or she perceived during spontaneous headache attacks; conversely, TrPs were considered latent if the subject did not recognize the evoked referred pain as a familiar pain (Simons et al., 1999; Gerwin et al., 1997). Since referred pain from suboccipital muscle TrPs is elicited bilaterally (Simons et al., 1999), we did not classify TrPs as either right or left. Then, we considered the presence of a unique TrP if manual palpation of suboccipital muscles evoked bilateral referred pain (Simons et al., 1999; Gerwin, 2005; Ferna´ndez-de-las-Pen˜as et al., 2006). 2.3. Study protocol All subjects had to be headache-free on the day of the examination. A first assessor gave a headache diary to ETTH patients. Patients had to register on this diary the daily headache intensity, on a 10-cm horizontal visual analogue scale (VAS; range: 0 ¼ no pain, to 10 ¼ maximum pain) (Jensen et al., 1999), the headache
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Fig. 2. Topography of the rectus capitis posterior minor (RCPmin) and major (RCPmaj) muscles.
duration (in hours per day), and the days with headache. This headache diary was kept for 4 weeks. This assessor also informed control subjects about physical therapy and headache (health education), but did not give them a headache diary. A second assessor, blinded to the subjects’ condition, examined the suboccipital muscles for the presence of TrPs. Four weeks later, ETTH subjects returned the headache diary to the first assessor, who calculated the following variables: 1, headache intensity, which was calculated from the mean of the VAS of the days with headache; 2, headache frequency, which was calculated dividing the number of days with headache by 4 weeks (days per week); and 3, headache duration, which was calculated dividing the sum of the total hours of headache by the number of days with headache (hours per day). 2.4. Statistical analysis Data were analysed with the SPSS statistical package (12.0 Version). The Kolmogorov–Smirnov test showed a
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normal distribution of the quantitative outcomes. The chi-square (w2) test was used to compare the presence of either latent or active TrPs between both study groups. The unpaired t-test was used to analyse the differences in the clinical variables relating to headache (headache intensity, frequency and/or duration) between ETTH subjects with either latent or active TrPs. The statistical analysis was conducted at a 95% confidence level. A Pvalue less than 0.05 was considered statistically significant.
4. Discussion All patients presenting with ETTH in this series had suboccipital muscle TrPs, either active or latent. The referred pain evoked by suboccipital TrPs reproduced usual headache in 6 (60%) of them, which was consistent with active TrPs, while the remaining 4 (40%) had latent TrPs. Within the control group, no one had active TrPs, but 2 healthy subjects (20%) had latent TrPs. Therefore, both groups had latent TrPs, while active TrPs were only present in the ETTH group. Our results are in agreement with Chaiamnuay et al. (1998), who also observed some latent TrPs in healthy subjects. On the other hand, current findings in ETTH subjects complete our previous findings for subjects with the chronic form of TTH (CTTH), in whom, suboccipital muscle TrPs were also more common than in healthy controls (Ferna´ndez-de-las-Pen˜as et al., 2006). However, in CTTH patients the presence of active TrPs was related to greater headache intensity and greater headache frequency than the presence of latent TrPs. These latter results have not been replicated in this study, since none of the clinical variables concerning the intensity and the temporal profile of headache differed with TrP activity in our group of ETTH patients (Table 2). Previous (Ferna´ndez-de-las-Pen˜as et al., 2006) and current findings support the hypothesis that suboccipital muscle TrPs might play an important role in the genesis of TTH, either episodic or chronic. Bendtsen (2000) reported that both peripheral mechanisms, i.e.
3. Results A total of 10 ETTH patients, 2 men and 8 women, aged 18–66 years old, and 10 healthy volunteers, 3 men and 7 women, aged 18–66 years old, were studied. No significant differences were found for gender or age between both study groups. ETTH subjects were headache-free on the day of the evaluation. Demographic and clinical data of each group are given in Table 1. All ETTH patients showed TrPs in the suboccipital muscles. Six of them (60%) had active TrPs, whereas the remaining 4 (40%) had latent TrPs. On the other hand, 2 (20%) control subjects had latent TrPs. Differences in the presence of suboccipital muscle TrPs between both groups were significant for active TrPs (Po0:001), but not for latent TrPs. Within the ETTH group, headache intensity, frequency and duration outcomes did not differ depending on TrP activity, whether the TrPs were active or latent (Table 2).
Table 1 Demographic and clinical data of both groups
Gender (male/female) Age (years) Length of headache history (years) Headache intensity (VAS) Headache frequency (days/week) Headache duration (hours per headache day)
ETTH (n ¼ 10)
Controls (n ¼ 10)
P-value
2/8 35715 5.573.5 4.371.5 2.970.5 572.7
3/7 34713 — — — —
NS NS — — — —
Values are expressed as mean7SD. ETTH ¼ episodic tension-type headache. VAS ¼ Visual Analogue Scale (0–10). NS ¼ Non-significant.
Table 2 Headache intensity, frequency and duration depending on the activity of suboccipital muscle trigger points
Active TrPs (n ¼ 6) Latent TrPs (n ¼ 4)
Headache intensity (VAS)
Headache frequency (days/week)
Headache duration (hours/day)
4.871.4 3.671.4
2.970.5 370.5
4.273.4 6.370.4
Values are expressed as mean7SD. VAS ¼ Visual Analogue Scale (0–10). TrPs ¼ Myofascial trigger points. Non-significant in comparison with the latent TrP subgroup (unpaired t-test, Po0:05).
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myofascial tenderness of pericranial structures, and central mechanisms, i.e. sensitization of supraspinal neurones and decreased anti-nociceptive activity from supraspinal structures, might be involved in the pathogenesis of TTH. These phenomena could be interconnected, since continuous or prolonged nociceptive inputs from myofascial tissues may contribute to the central sensitization in CTTH (Jensen, 1999). Nociceptive inputs from suboccipital muscle TrPs may produce a continuous afferent bombardment to the trigeminal nerve nucleus caudalis. Such repeated nociceptive activation of the nucleus caudalis could produce central sensitization in CTTH (Bendtsen, 2000). If there were a lesser degree of central sensitization in ETTH, because of the intermittent nature of this condition, one would expect fewer active and more latent TrPs in ETTH subjects than in CTTH subjects. Our findings do not support this hypothesis, as suboccipital active TrPs were present in a similar proportion in both ETTH subjects (60%) and CTTH subjects (65%). However, headache intensity and frequency were related to TrPs activity in CTTH (Ferna´ndez-de-las-Pen˜as et al., 2006), but not in ETTH. Since TrPs are responsible for the liberation of nociceptive mediators (Shah et al., 2005), it seems plausible that TrP activity originated in the suboccipital muscles might be a triggering factor for central sensitization seen in chronic headaches. In such way, the presence of TrPs could contribute to the evolution of the episodic form to the chronic form of TTH. There are some limitations to our studies. First, only subjects with TTH have been evaluated. Hence, our results cannot be extrapolated to other headache disorders. It would be interesting to repeat the same procedure with patients suffering from other disorders in order to explore the relevance of suboccipital muscle TrPs in headache. The second limitation was the sample size. To our knowledge, our studies are the first ones to analyse the relationship between suboccipital muscle TrPs and clinical features in TTH. However, it would be necessary to repeat the same procedure with a greater number of subjects so as to confirm our findings in both ETTH and CTTH patients. Third, it is possible that other structures of the upper cervical region, e.g. atlanto-axial joint or C2 nerve trunk, could be palpated during the exploration and then responsible for the perceived referred pain. However, our palpation was done next to the occipital bone (Fig. 2), so the possibility to palpate these structures was minimal. Moreover, since muscle contraction increased referred pain in all patients, it is most likely that the elicited referred pain was originated in the muscle tissue, that is, in the suboccipital muscles. 5. Conclusions Active myofascial TrPs in the suboccipital muscles were more common in ETTH subjects than in healthy
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controls, although TrP activity was not related to any clinical variable concerning the intensity and the temporal profile of headache. Suboccipital TrPs might contribute to the origin and/or maintenance of headache, but a comprehensive knowledge of the role of these muscles in TTH awaits further research.
Acknowledgements We would like to thank Dr. David Simons and Dr. Robert D. Gerwin for their kind encouragement and support.
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