Myofascial Trigger Points Comorbidity in Headache

Fig. 11.1
Referred pain elicited by TrPs in the cervical muscles: (a) sternocleidomastoid, (b) splenius capitis, (c) semispinalis capitis, (d) suboccipital and (e) upper trapezius

Myofascial TrP pain referral patterns in the head, neck and shoulder muscles are to the occipital, parietal, temporal, frontal and vertex regions of the head, in other words, to every part of the head that can be described as painful in headache, whether tension-type headache or migraine [7]. This includes pain referred to the eye, a common site of headache pain. The association of TrPs specifically in migraine headache is well described. Calandre et al. found that 93.9 % of migraineurs have trigger points in relevant muscles compared to 29 % of controls [10]. The number of TrPs in a patient with migraine headaches is directly related to the intensity and duration of the headaches. Migraineurs who had more numerous TrPs had more severe and longer-duration migraine headaches. Active TrPs, defined as TrPs that spontaneously produce pain, are more common in migraineurs with unilateral headache than in non-headache control subjects and are ipsilateral to the headache more than contralateral or bilateral, except for the suboccipital muscles [11, 12]. In the author’s clinic, 54 consecutive headache patients were evaluated for active TrPs that reproduced all or part of their headache pain. Thirty-six (67 %) met the criteria for migraine headaches, of whom 40 % had 15 or more headache days a month. Active TrPs relevant to their headache complaints were found in 100 % of these migraine sufferers, most commonly in the upper trapezius muscles in the shoulders (Gerwin RD, unpublished data 1995). Active myofascial TrPs relevant to the headache complaint are likely to be found in migraine patients when they are properly examined. Active and latent TrPs in the sternocleidomastoid muscle and in the trapezius muscle are more common in migraineurs than in control subjects [13].

The association of myofascial TrPs with migraine is of interest etiologically as TrPs can be considered either as a consequence of migraine headache, unrelated epiphenomena or causative in the sense that they can be one of the many triggers that activate the trigeminovascular cascade that initiates a migraine attack [14]. This issue is of importance, because if they are either unrelated or are secondary to migraine, they do not necessarily need to be treated. However, if they are a potential trigger of migraine, then treatment of these TrPs might well diminish the frequency and intensity of migraine. An early exploration of this question showed that activation of TrPs in the neck and shoulder muscles of migraineurs elicited referred pain to the head in 73 % of subjects. Inactivation of myofascial trigger sites in the neck and shoulder muscles by injection of either lidocaine or saline eliminated headache pain (symptom-free) in 26 of 48 subjects (54 %) at 70 min. This was significantly better than medical therapy [15]. A more recent, landmark study showed that treatment of active TrPs in the neck that referred pain to migraine headache pain sites in the head, in other words, that reproduced migraine headache pain, reduced local pain, decreased the sensitivity of referred pain areas and reduced the number and maximal intensity of migraine headaches [16]. Local TrPs in the neck and in the referred pain areas in the head were evaluated at days 0, 3, 10, 30 and 60 for their electrical pain threshold. The cervical triggers were injected with lidocaine on day 0 after obtaining baseline measurements. The electrical pain thresholds in the skin, subcutaneous tissue and muscle in the TrP sites in the neck and in the referred pain areas in the head were reduced at baseline in the migraine subjects compared to the values in the normal control subjects, meaning that they were more sensitive in the migraineurs. The sensitivity (electrical pain threshold) of all three tissue layers, as measured by their electrical pain threshold, returned to normal in the treated group compared to controls over the treatment period, but did not change in the untreated migraine subjects. The number of migraine attacks in the treated subjects decreased by 46.8 %, and the maximal intensity of migraine headaches was reduced by 17.6 %, compared to pretreatment, a significant change [16]. Thus, proper management of cervical myofascial TrPs can reduce not only local cervical pain sensitivity but can also reduce pain sensitivity in related headache regions and also reduce headache frequency and intensity. This strongly suggests that cervical myofascial TrPs can operate either as triggers of the migraine-inducing trigeminovascular cascade or that myofascial TrPs are potent activators of central sensitization that can make migraine headache more likely. A more recent study further confirms this hypothesis since migraine patients receiving drug treatment combined with TrP therapy experienced greater reduction in migraine intensity and frequency than those patients who received drug treatment alone [17].

11.1.2 Temporomandibular Joint Dysfunction, Trigger Points and Migraine

Temporomandibular joint dysfunction is a disorder of the facial muscles associated with mastication. Temporomandibular disorder (TMD) and migraine are associated as a common comorbidity [18]. Tomaz-Morais reported that 71.4 % of migraineurs had comorbid TMD (OR, 4.1, P = 0.03) and that the prevalence of more than six signs and symptoms of TMD were present in 54.8 % of subjects with primary headache (migraine or tension-type headache) [19]. Moreover, patients with both TMD and migraine tend to have hypertrophy of the lateral pterygoid muscle (58.7 %), and abnormal mandibular movements (61.2 %) and temporomandibular joint disc displacement (70 %) [20]. Muscle hyperactivity may be a result of migraine, a result of TMD or an aggravating factor in both conditions. Twin studies in women with both migraine and TMD showed that additive genetic effects contributed 27 % of the variance in TMD pain and 49 % of the variance in migraine headache. The model revealed that 12 % of the genetic component of TMD pain is shared with migraine [21]. The authors suggest that the association between TMD and migraine in women may be partially due to modest shared risk for both conditions. This idea has greater implications than shared genetic risk, because a number of conditions that coexist or that are comorbid with migraine are more common in women than men. Migraine itself is more frequent in women than men. TMD, fibromyalgia, irritable bowel syndrome, fibromyalgia and hypothyroidism are all more common in women than in men. Treatment of both conditions, TMD and migraine, at the same time, is more effective than treating either condition alone [22].

11.1.3 Otalgia

Otalgia is also associated with migraine. Subjects with chronic otalgia of more than 3 months duration, and who had no identifiable cause of their otalgia, were treated with migraine therapies. Sixty-five per cent of the 29 patients studied met the International Headache Society criteria for migraine. Improvement in symptom intensity, frequency and duration was reported in 92 % of subjects. This association is notable because TrPs in both the clavicular head of the sternocleidomastoid muscle and the deep masseter muscle refer pain deep into the ipsilateral ear and TrPs in the clavicular head of the sternocleidomastoid muscle can cause tinnitus [7]. In fact, inactivation of TrPs in the cervical muscles was effective for tinnitus [23]. Although TrPs are more common in the sternocleidomastoid muscle in migraineurs than in non-headache controls [13], the authors did not investigate this possible relationship, but given the frequency with which we see TrPs in these muscles in TMD and in migraine patients, the association could explain this association.

11.1.4 Fibromyalgia Syndrome

Fibromyalgia syndrome has already been mentioned as a condition in which migraine is a common comorbidity. Myofascial TrPs are common in fibromyalgia patients [4, 5]. Thus, one expects to find TrPs in patients with both fibromyalgia and migraine. This possibility has not been studied specifically, but the possible association is consistent with what we see in our patients with both migraine and fibromyalgia.

11.1.5 Sleep Disorders

Sleep disorders are well known as provocative factors for muscle pain [24, 25]. Persons with chronic myofascial pain often have sleep disorders that result in insomnia, or reduced stage 3 and stage 4 sleep, resulting in non-restful or non-restorative sleep. These conditions have certainly been described in fibromyalgia, a condition known to be comorbid with myofascial pain. The adjusted hazard ratio for persons with a sleep-related breathing disorder developing migraine was 2.34 (95 %CI 1.72–3.44) and interestingly was higher in men than in women [26], even though migraine is more common in women than in men.

Restless leg syndrome (RLS) is another condition that both causes sleep disturbance and is a comorbid condition of migraine. Restless leg syndrome was found in 1.4 % of migraine patients [27]. Migraine patients with RLS had a poorer sleep quality than migraineurs without RLS. There is a bidirectional relationship between migraine and RLS, with each capable of triggering the other [27]. The association between the two conditions is more common in younger persons aged 19–29 than in older persons aged 50–59 [28]. Restless leg syndrome is related to iron deficiency in some subjects. Iron deficiency is also a predisposing factor for headache. This aspect of the relationship was not explored in the cited studies. However, RLS is certainly a cause for sleep disturbance. The association between migraine and sleep disturbance has already been noted. The relationship between sleep disturbance and muscle pain has likewise already been noted [24, 25].

11.1.6 Hypermobility Syndromes

Ehlers-Danlos syndrome (EDS) is a connective tissue disorder in which there is a hypermobile form that is associated with migraine. Migraine is the most common headache type in the hypermobile form of EDS [29]. Headache is complex in EDS patients and may be due to many different mechanisms, including posterior fossa compression syndrome, intracranial hypertension and intracranial hypotension, and cervical and temporomandibular joint instability. The latter two conditions, instability of the temporomandibular joint and cervical spine instability, are both associated with myofascial TrPs that can contribute to the headache picture and that can trigger migraine headache in these patients.

In conclusion, clinicians should be aware that there is an established relationship of migraine headache and myofascial TrPs. Current evidence strongly suggests that myofascial TrPs play a role in triggering migraine attacks, either directly by nociceptive input to the trigeminal nerve or through the mechanism of central sensitization. Examination of the migraine patient for myofascial TrPs in the muscles of the head, neck and shoulders can lead to productive therapeutic measures that address both myofascial pain and migraine. Moreover, there are conditions associated with migraine, enumerated in this chapter, that are also associated with myofascial TrPs. Therefore, it is productive to evaluate patients for these conditions as well when managing patients with migraine. The approach to migraine headache must be comprehensive and extend beyond considering the important, commonly investigated issues of diet, allergy, stress and familial basis of migraine.

11.2 Trigger Point Comorbidity in Temporomandibular Disorders

Temporomandibular pain disorder (TMD) is a term including different pain conditions involving the temporomandibular joint (TMJ), the masticatory muscles and their associated tissues, e.g. ligaments, or disc. Diagnostic criteria of TMD have been recently updated (DC/TMD) including group I (myofascial TMD) and group II (disc displacement) [30]. The overall prevalence of TMD pain is 4.6 %, with 6.3 % for women and 2.8 % for men (ratio 2:1) [31]. A meta-analysis including a total of 3,463 subjects with orofacial pain concluded that the overall prevalence for myofascial TMD (group I muscle disorder-DC/TMD criteria) was 45.3 % and the prevalence of disc displacement (group II-DC/TMD criteria) was 41.1 % [32].

The most common clinical features of TMD include spontaneous face pain or pain with mandibular motion. Patient-based drawings show symptoms concentrated around the masseter muscle, the mouth, including the teeth, and spread up to the temporalis muscle [33]. The pain is felt to be deep. “Spreading pain” is a descriptive phrase commonly used by the patients. This constellation of pain symptoms is a cardinal symptom complex in patients presenting with myofascial TMD pain, although not exclusive of this condition. The words describing the pain of patients suspected to have myofascial TMD resemble the pain features of muscle pain and TrPs in general, as described by Simons et al. [7]. Another typical clinical sign of myofascial TMD is tenderness or pain on muscle palpation particularly of the masticatory muscles.

The clinical signs taken altogether suggest that TrPs may be clinically related to TMD pain. Several experimental pain models have demonstrated that injection of an irritant substance in the masseter muscle mimics the symptoms experienced by individuals with TMD [3436]. Any of the masticatory muscles, including the masseter, temporalis, lateral pterygoid, medial pterygoid and hyoid muscles, can refer pain to the orofacial region (Fig. 11.2) and can contribute to TMD pain symptoms. Clinical evidence to support this referral pattern is scarce, although scientific data from human pain models clearly support the notion that referred pain from masticatory muscles is involved in myofascial TMD [37]. An early study reported that myofascial pain from head and neck muscles was the most prevalent diagnosis in a sample of 164 patients [38]. The referred pain pattern following manual examination of TrPs in the masticatory muscles in one non-blinded study was similar to the pain pattern experienced by subjects with TMD [39]. The lateral pterygoid and masseter muscles were the most common sources of referred pain to the craniofacial region in a sample of 230 patients with TMD pain in this study. In a blinded-controlled study, Fernández-de-las-Peñas et al. reported the existence of multiple active TrPs in the masticatory and neck-shoulder musculature in women with myofascial TMD [40]. Local and referred pain, elicited from manual palpation of active TrPs, together reproduced the symptoms in all TMD patients. Temporalis and masseter muscles were the most affected by active TrPs in women with TMD; but it is noticeable that they also exhibited TrPs in the upper trapezius and sternocleidomastoid muscles [40].


Fig. 11.2
Referred pain elicited by TrPs within the masticatory muscles: (a) masseter, (b) temporalis, (c) lateral pterygoid, (d) medial pterygoid and (e) hyoids

It has been suggested that different muscles may be involved in TMD and tension-type headache (TTH), since TMD pain is clinically more similar to the pain patterns produced by stimulation of the masseter muscle, whereas TTH is more similar to the pain patterns evoked by stimulation of cervical muscles, e.g. upper trapezius [41]. This assumption is supported by another study comparing the prevalence of TrPs between women with TMD and fibromyalgia [42]. This study revealed that women with TMD had greater number of active TrPs in head/neck muscles than women with fibromyalgia and that the neck muscles were more affected in fibromyalgia whereas the masticatory muscles were more affected in TMD pain [42].

Patients with TMD exhibit multiple TrPs supporting the assumption that spatial summation plays a significant role in this condition. Each patient showed at least five active TrPs in the neck/head musculature [41, 42]. It is likely that nociceptive activity from active TrPs contributes to central sensitization mechanisms seen in subjects experiencing TMD pain. We postulate that ongoing nociceptive input originating from active muscle TrPs [43, 44] perpetuates or promotes sensitization of central pathways in TMD. This hypothesis agrees with a study reporting lower pressure pain thresholds, i.e. higher pressure pain sensitivity, at the referred pain area in TrPs in the masticatory muscles [45] and other studies in which dry needling of active TrPs within the masseter muscle induced significant increases in pressure pain thresholds when compared to sham dry needling in myofascial TMD [46, 47]. Finally, the role of active TrPs in TMD pain is also supported by some studies suggesting that treatment of active TrPs with dry needling in the masticatory muscles (Fig. 11.3) is effective in the management of these patients [48, 49]. Other authors proposed that manual therapies targeting the masticatory muscles are also effective in the management of TMD pain (Fig. 11.4) [50].


Fig. 11.3
Dry needling of masseter muscle TrPs (Copyright, David G Simons Academy™, Switzerland©, with permission)


Fig. 11.4
Manual therapy applied over temporalis muscle TrPs (Copyright, David G Simons Academy™, Switzerland©, with permission)

11.3 Trigger Points in Tension-Type Headache

There has been an increasing interest in the pathogenic mechanism of headache disorders since they constitute a serious health problem [51]. Tension-type headache (TTH) has a prevalence of almost 60 % in the general population [52] and is one of the most common headaches, but it is also the most neglected [53]. It is accepted that TTH has a muscular origin and that peripheral and central nervous system factors play a crucial role in its development and persistence [54, 55].

Pain features of TTH (deep, pressing, tightening or dull pain) resemble the descriptions of referred pain originating in TrPs. In fact, TTH is considered as the prototype of headache where the main factor responsible for the pain is TrP referred pain [56]. Additionally, headaches involving a significant component of pain referred from TrPs have been called myogenic headaches, to indicate the role of muscle pain in the genesis of the headache [57], although this term in not widely accepted in the literature.

Simons et al. [7] described several neck and shoulder muscles from which referred pain can mimic TTH, including the upper trapezius, sternocleidomastoid, splenius capitis, splenius cervicis, semispinalis capitis, semispinalis cervicis or suboccipital (see Fig. 11.1). There was little scientific evidence before this century about the association between TrPs and TTH. Some early studies found active TrPs in neck and shoulder muscles in subjects with TTH, particularly in the splenius capitis, semispinalis capitis, upper trapezius and suboccipital muscles [58, 59]. However, these were noncontrolled and non-blinded studies. An updated series of blinded-controlled clinical studies observed that active TrPs in the suboccipital [60], upper trapezius [61, 62], sternocleidomastoid [63] and temporalis [64] muscles and extraocular muscles such as the superior oblique [65] and lateral rectus [66] are highly prevalent in subjects with TTH and reproduce the headache pain pattern. In addition, the presence of active TrPs in these muscles was associated with headaches of greater intensity, frequency and duration and also to greater pressure pain hypersensitivity [6064]. The fact that patients with chronic TTH who had active TrPs had more severe headache characteristics than those with latent TrPs is evidence of temporal integration of signals from TrPs [67]. This suggests temporal integration of nociceptive inputs from active TrPs by central nociceptive neurons, leading to sensitization of central pathways in patients with TTH. Nevertheless, it has been questioned if active TrPs are consequence and not a causative factor of central sensitization in chronic pain conditions (see “The Exchange Between Dodick and Gerwin in Letters to the Editor”, N Eng J Med 2006;354:1958). The data supports peripheral sensitization associated with elevated levels of chemical mediators that have been found in active TrPs regions, as well as central sensitization produced by active TrPs [68, 69]. In fact, there is good evidence that TrPs cause peripheral and central sensitization, but there is no evidence that central sensitization predisposes to the development of TrPs. This is an important point, because the two concepts are diametrically opposed and are central to two mutually exclusive ways of looking at the role of TrPs in TTH.

It is also important to note that active TrPs in the same neck and shoulder muscles reproduce the headache in children with TTH [70]. Alonso-Blanco et al. showed that the referred pain elicited from active TrPs shared similar pain patterns as spontaneous headache in both adults and children with TTH, but slight differences in TrP prevalence and location of the referred pain areas could be observed between adults and children [71]. Current evidence clearly supports a relevant role of TrPs in the pathogenesis of TTH. Abboud et al. assert that understanding TrP mechanisms, in association with other musculoskeletal disorders, provides insight into TTH pathophysiology, diagnosis and interdisciplinary patient care [72].

TrPs have been postulated to play a pathogenic role in TTH in an updated pain model for this condition [73]. The updated model is based on previous models considering that the main problem in TTH is the sensitization of central pain pathways due to prolonged peripheral nociceptive inputs. The peripheral nociceptive inputs are provoked by the liberation of algogenic substances and chemical mediator at the periphery in pericranial tender tissues [74]. Fernández-de-las-Peñas et al. postulated that TTH could be explained by referred pain from active TrPs that is mediated through the spinal cord and trigeminocervical nucleus caudalis [73]. Thus, active TrPs located in muscles innervated by C1–C3 or by the trigeminal nerve would initiate the peripheral nociceptive input and could produce a continuous afferent negative barrage into the trigeminal nerve nucleus caudalis. Sensitization of nociceptive pain pathways in the central nervous system due to prolonged nociceptive stimuli from TrPs is likely to be responsible for the conversion of episodic to chronic TTH [75]. According to this updated model, referred pain elicited by TrPs would be one (but not the only one) of the main causes of the headache experienced by patients with TTH. Needless to say, this updated model needs further confirmation and verification.

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Oct 25, 2017 | Posted by in NEUROLOGY | Comments Off on Myofascial Trigger Points Comorbidity in Headache
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