Juan A. Pareja

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.

Sunct syndrome. A clinical review

The clinical features of SUNCT syndrome have been reviewed in 21 patients. There were 17 men and 4 women, rendering a clear male preponderance (ratio of 4.25). The mean age at onset was around 51 years. Attacks were experienced mostly in the orbital/periorbital area and always recurred on the same side, with an erratic temporal pattern and remissions of varying lengths. Most attacks were moderate to severe in intensity and burning, electrical, or stabbing in character. The attacks were regularly accompanied by prominent, ipsilateral, conjunctival injection, tearing; and rhinorrhea or nasal obstruction. There were many precipitating mechanisms. Exclusively spontaneous attacks were described in 3 patients. The usual duration of paroxysms ranged from 10 to 60 seconds, whereas the longest duration varied from 60 to 300 seconds. The frequency of attacks during the symptomatic periods varied from less than I attack daily to more than 30 per hour. hi the majority of patients, supplementary examinations failed to show any notable abnormality. However, 2 patients were documented to have a symptomatic form of SUNCT, with a vascular malformation in the ipsilateral cerebellopontine angle. A variety of drugs and local anesthetic blockades. inclusive of tic douloureux drugs, were tried, but a persistent, convincingly beneficial effect was generally lacking SUNCT syndrome is in the differential diagnosis when encountering unilateral, orbital/periorbital headache syndromes.

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.

Nonconvulsive status epilepticus associated with cephalosporins in patients with renal failure

PURPOSE Nonconvulsive status epilepticus is an unusual complication of cephalosporin therapy, with only a few isolated cases reported. SUBJECTS AND METHODS We reviewed the clinical and electroencephalographic (EEG) characteristics of 10 patients with renal failure in whom developed alteration of consciousness without convulsions associated with continuous epileptiform EEG activity while being treated with cephalosporins. RESULTS Nonconvulsive status epilepticus developed in 5 men and 5 women, with a mean (+/- SD) age of 69 +/- 14 years, while receiving intravenous cephalosporins (ceftriaxone, 2 patients; ceftazidime, 2; and cefepime, 6). All patients had renal failure; 1 also had hepatic failure. Patients presented with progressive disorientation or agitation, sometimes associated with mild facial or limb myoclonus, that had begun 1 to 10 days (mean, 5 +/- 2 days) after starting cephalosporin treatment. The EEG showed continuous or intermittent bursts of generalized, high-voltage, 1 to 2 Hz sharp wave activity or sharp and slow wave activity that resembled, but could be differentiated from, the triphasic waves seen in metabolic encephalopathies. Intravenous clonazepam suppressed the epileptiform activity completely in 5 patients and partially in the other 5. Cephalosporins were withdrawn, and antiepileptic therapy was started for all patients. All patients improved, 2 in less than 24 hours and the remainder within 2 to 7 days. CONCLUSIONS Cephalosporins can cause nonconvulsive status epilepticus in patients with renal failure. The clinical picture is difficult to differentiate from a that of metabolic encephalopathy unless an EEG is obtained. Physicians should be aware of this potentially dangerous complication.

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.