Maria Luz Cuadrado

Myofascial trigger points and sensitization: an updated pain model for tension-type headache.

Present pain models for tension-type headache suggest that nociceptive inputs from peripheral tender muscles can lead to central sensitization and chronic tension-type headache (CTTH) conditions. Such models support that possible peripheral mechanisms leading to pericranial tenderness include activation or sensitization of nociceptive nerve endings by liberation of chemical mediators (bradikinin, serotonin, substance P). However, a study has found that nonspecific tender points in CTTH subjects were not responsible for liberation of algogenic substances in the periphery. Assuming that liberation of algogenic substances is important, the question arising is: if tender muscle points are not the primary sites of on-going neurogenic inflammation, which structure can be responsible for liberation of chemical mediators in the periphery? A recent study has found higher levels of algogenic substances, and lower pH levels, in active myofascial trigger point (TrPs) compared with control tender points. Clinical studies have demonstrated that referred pain elicited by head and neck muscles contribute to head pain patterns in CTTH. Based on available data, an updated pain model for CTTH is proposed in which headache can at least partly be explained by referred pain from TrPs in the posterior cervical, head and shoulder muscles. In this updated pain model, TrPs would be the primary hyperalgesic zones responsible for the development of central sensitization in CTTH.

Myofascial trigger points and their relationship to headache clinical parameters in chronic tension-type headache.

Objective.—To assess the presence of trigger points (TrPs) in several head and neck muscles in subjects with chronic tension‐type headache (CTTH) and in healthy subjects; and to evaluate the relationship of these TrPs with forward head posture (FHP), headache intensity, duration, and frequency.

Myofascial trigger points, neck mobility and forward head posture in unilateral migraine.

This paper describes the differences in the presence of myofascial trigger points (TrPs) in the upper trapezius, sternocleidomastoid, temporalis and suboccipital muscles between unilateral migraine subjects and healthy controls, and the differences in the presence of TrPs between the symptomatic side and the nonsymptomatic side in migraine subjects. In addition, we assess the differences in the presence of both forward head posture (FHP) and active neck mobility between migraine subjects and healthy controls and the relationship between FHP and neck mobility. Twenty subjects with unilateral migraine without side-shift and 20 matched controls participated. TrPs were identified when there was a hypersensible tender spot in a palpable taut band, local twitch response elicited by the snapping palpation of the taut band and reproduction of the referred pain typical of each TrP. Side-view pictures were taken in both sitting and standing positions to measure the cranio-vertebral angle. A cervical goniometer was employed to measure neck mobility. Migraine subjects showed a significantly greater number of active TrPs (P < 0.001), but not latent TrPs, than healthy controls. Active TrPs were mostly located ipsilateral to migraine headaches (P < 0.01). Migraine subjects showed a smaller cranio-vertebral angle than controls (P < 0.001), thus presenting a greater FHP. Neck mobility in migraine subjects was less than in controls only for extension (P = 0.02) and the total range of motion in flexion/extension (P = 0.01). However, there was a positive correlation between the cranio-vertebral angle and neck mobility. Nociceptive inputs from TrPs in head and neck muscles may produce continuous afferent bombardment of the trigeminal nerve nucleus caudalis and, thence, activation of the trigeminovascular system. Active TrPs located ipsilateral to migraine headaches might be a contributing factor in the initiation or perpetuation of migraine.

Trigger points in the suboccipital muscles and forward head posture in tension-type headache.

Objective.—To assess the presence of trigger points (TrPs) in the suboccipital muscles and forward head posture (FHP) in subjects with chronic tension‐type headache (CTTH) and in healthy subjects, and to evaluate the relationship of TrPs and FHP with headache intensity, duration, and frequency.

Forward head posture and neck mobility in chronic tension‐type headache: a blinded, controlled study

Forward head posture (FHP) and neck mobility were objectively assessed in 25 patients with chronic tension-type headache (CTTH) and 25 healthy controls. Side-view pictures were taken in a sitting position to measure the craniovertebral angle. A cervical goniometer was employed to measure the range of all cervical motions. Patients with CTTH showed a smaller cranio-vertebral angle (45.3° ± 7.6°) than controls (54.1° ± 6.3°), thus presenting a greater FHP (P < 0.001). Patients also had lesser neck mobility for all cervical movements, except for right lateral flexion (P < 0.01). There was a positive correlation between the craniovertebral angle and neck mobility. Within the CTTH group, a negative correlation was found between the cranio-vertebral angle and headache frequency, but neck mobility did not correlate with headache parameters. Further research is needed to define a potential role of FHP and restricted neck mobility in the origin or maintenance of TTH.

Referred pain from trapezius muscle trigger points shares similar characteristics with chronic tension type headache

Referred pain and pain characteristics evoked from the upper trapezius muscle was investigated in 20 patients with chronic tension‐type headache (CTTH) and 20 age‐ and gender‐matched controls. A headache diary was kept for 4 weeks in order to confirm the diagnosis and record the pain history. Both upper trapezius muscles were examined for the presence of myofascial trigger points (TrPs) in a blinded fashion. The local and referred pain intensities, referred pain pattern, and pressure pain threshold (PPT) were recorded. The results show that referred pain was evoked in 85% and 50% on the dominant and non‐dominant sides in CTTH patients, much higher than 55% and 25% in controls (P<0.01). Referred pain spread to the posterior‐lateral aspect of the neck ipsi‐lateral to the stimulated muscle in both patients and controls, with additional referral to the temple in most patients, but none in controls. Nearly half of the CTTH patients (45%) recognized the referred pain as their usual headache sensation, i.e. active TrPs. CTTH patients with active TrPs in the right upper trapezius muscle showed greater headache intensity and frequency, and longer headache duration than those with latent TrPs. CTTH patients with bilateral TrPs reported significantly decreased PPT than those with unilateral TrP (P<0.01). Our results showed that manual exploration of TrPs in the upper trapezius muscle elicited referred pain patterns in both CTTH patients and healthy subjects. In CTTH patients, the evoked referred pain and its sensory characteristics shared similar patterns as their habitual headache pain, consistent with active TrPs. Our results suggest that spatial summation of perceived pain and mechanical pain sensitivity exists in CTTH patients.

Myofascial Trigger Points, Neck Mobility, and Forward Head Posture in Episodic Tension‐Type Headache

Objective.—To assess the differences in the presence of trigger points (TrPs) in head and neck muscles, forward head posture (FHP) and neck mobility between episodic tension‐type headache (ETTH) subjects and healthy controls. In addition, we assess the relationship between these muscle TrPs, FHP, neck mobility, and several clinical variables concerning the intensity and the temporal profile of headache.

Bilateral widespread mechanical pain sensitivity in carpal tunnel syndrome: evidence of central processing in unilateral neuropathy

The aim of this study was to investigate whether bilateral widespread pressure hypersensitivity exists in patients with unilateral carpal tunnel syndrome. A total of 20 females with carpal tunnel syndrome (aged 22-60 years), and 20 healthy matched females (aged 21-60 years old) were recruited. Pressure pain thresholds were assessed bilaterally over median, ulnar, and radial nerve trunks, the C5-C6 zygapophyseal joint, the carpal tunnel and the tibialis anterior muscle in a blinded design. The results showed that pressure pain threshold levels were significantly decreased bilaterally over the median, ulnar, and radial nerve trunks, the carpal tunnel, the C5-C6 zygapophyseal joint, and the tibialis anterior muscle in patients with unilateral carpal tunnel syndrome as compared to healthy controls (all, P < 0.001). Pressure pain threshold was negatively correlated to both hand pain intensity and duration of symptoms (all, P < 0.001). Our findings revealed bilateral widespread pressure hypersensitivity in subjects with carpal tunnel syndrome, which suggest that widespread central sensitization is involved in patients with unilateral carpal tunnel syndrome. The generalized decrease in pressure pain thresholds associated with pain intensity and duration of symptoms supports a role of the peripheral drive to initiate and maintain central sensitization. Nevertheless, both central and peripheral sensitization mechanisms are probably involved at the same time in carpal tunnel syndrome.

The local and referred pain from myofascial trigger points in the temporalis muscle contributes to pain profile in chronic tension-type headache

ObjectiveTo assess the local and referred pain areas and pain characteristics evoked from temporalis muscle trigger points (TrPs) in chronic tension-type headache (CTTH). MethodsThirty CTTH patients and 30 age and sex-matched controls were studied. A headache diary was kept for 4 weeks to substantiate the diagnosis and record the pain history. Both temporalis muscles were examined for the presence of myofascial TrPs in a blinded fashion. The local and referred pain intensities, referred pain pattern, and pressure pain threshold were recorded. ResultsReferred pain was evoked in 87% and 54% on the dominant and nondominant sides in CTTH patients, which was significantly higher (P<0.001) than in controls (10% vs. 17%, respectively). Referred pain spread to the temple ipsilateral to the stimulated muscle in both patients and controls, with additional referral behind the eyes in most patients, but none in controls. CTTH patients reported a higher local [visual analog scale (VAS): 5.6±1.2 right side, 5.3±1.4 left side] and referred pain (VAS: 4.7±2 right side, 3.5±2.8 left side) intensity than healthy controls (VAS: 0.8±0.7 right side, 0.7±0.7 left side for local pain; and 0.3±0.2 right side, 0.4±0.3 left side for referred pain) in both temporalis muscles (both, P<0.001). The local and referred pain areas were larger in patients than in controls (P<0.001). Twenty-three out of 30 CTTH patients (77%) had active TrPs in the temporalis muscle leading to their usual headache (17 patients on the right side; 12 on the left side, whereas 6 with bilateral active TrPs). CTTH patients with active TrPs in either right or left temporalis muscle showed longer headache duration than those with latent TrPs (P=0.004). CTTH patients showed significantly (P<0.001) lower pressure pain threshold (1.1±0.2 right side, 1.2±0.3 left side) as compared with controls (2.5±0.5 right side, 2.6±0.4 left side). ConclusionsIn CTTH patients, the evoked local and referred pain from active TrPs in the temporalis muscle and its sensory characteristics shared similar patterns as their habitual headache pain. Local and referred pain from active TrPs in the temporalis muscles may constitute one of the sources contributing to the pain profile of CTTH.

Increased pericranial tenderness, decreased pressure pain threshold, and headache clinical parameters in chronic tension-type headache patients.

ObjectiveThe aim was to investigate whether increased pericranial tenderness or decreased pressure pain threshold (PPT) was related to headache intensity, duration, and frequency in chronic tension-type headache (CTTH). MethodsTwenty-five CTTH patients and 25 matched controls were studied. A headache diary was kept for 4 weeks to substantiate the diagnosis and record the pain history. Three tenderness (total, cephalic, and neck) scores and PPT at both cephalic and neck points were objectively and blinded assessed. Bodily pain perceived by the patients was assessed with the Short Form-36 questionnaire. ResultsCTTH patients showed decreased PPT and increased tenderness as compared with controls (P<0.001). Negative correlations were found between PPT on each point and their respective tenderness scores. Within the CTTH group, neither increased tenderness nor decreased PPT seemed to directly influence headache intensity, frequency or duration; or vice versa. DiscussionIncreased tenderness may predispose the patients to other perpetuating factors in inducing headache attacks. Further research is needed to clearly define the role of pericranial tender tissues or other factors in the genesis and maintenance of CTTH.