Secondary Otalgia: Referred Pain Pathways and Pathologies.

Otalgia is very common, and when the cause of ear pain is not identified on otoscopy and physical examination, cross-sectional imaging is routinely used to evaluate for potential sources of referred ear pain (secondary otalgia). Innervation of the ear structures is complex, involving multiple upper cervical, lower cranial, and peripheral nerves, which transit and innervate a large anatomic territory involving the brain, spine, skull base, aerodigestive tract, salivary glands, paranasal sinuses, face, orbits, deep spaces of the neck, skin, and viscera. Interpreting radiologists must be familiar with these neural pathways and potential sources of secondary otalgia. The purposes of this review are to detail the currently proposed mechanisms of referred ear pain, review the salient neuroanatomy of the complex pathways responsible for secondary otalgia, highlight important benign and malignant etiologies of referred ear pain, and provide a structured search pattern for approaching these challenging cases on cross-sectional imaging.

The local and referred pain patterns of the longus colli muscle.

The longus colli muscle is a neck flexor believed to play an important role in pain originating in the neck region, including pain resulting from whiplash injuries. Despite the clinical importance attributed to it, the pain referral pattern of the longus colli has previously been described only in a small cohort of subjects. Here, we aim to delineate the pain referral pattern of the longus colli muscle. Thirty-five healthy volunteers underwent deep massage of the longus colli followed by dry needling of the muscle. The subjects depicted the distribution of the pain they experienced on a blank manikin. Their drawings were digitized and used to produce pain pattern histogram maps. The pain referral pattern during deep massage and needling of the longus colli was primarily local, with referral to the ipsilateral ear and lateral to the ipsilateral eye. Some subjects reported pain on the contralateral side of the neck.

Monosynaptic convergence of somatic and visceral C-fiber afferents on projection and local circuit neurons in lamina I: a substrate for referred pain.

Referred pain is a phenomenon of feeling pain at a site other than the site of the painful stimulus origin. It arises from a pathological mixing of nociceptive processing pathways for visceral and somatic inputs. Despite numerous studies based on unit recordings from spinal and supraspinal neurons, the exact mechanism and site of this mixing within the central nervous system are not known. Here, we selectively recorded from lamina I neurons, using a visually guided patch-clamp technique, in thoracic spinal cord preparation with preserved intercostal (somatic) and splanchnic (visceral) nerves. We show that somatic and visceral C fibers converge monosynaptically onto a group of lamina I neurons, which includes both projection and local circuit neurons. Other groups of lamina I neurons received inputs from either somatic or visceral afferents. We have also identified a population of lamina I local circuit neurons showing overall inhibitory responses upon stimulation of both nerves. Thus, the present data allow us to draw two major conclusions. First, lamina I of the spinal cord is the first site in the central nervous system where somatic and visceral pathways directly converge onto individual projection and local circuit neurons. Second, the mechanism of somatovisceral convergence is complex and based on functional integration of monosynaptic and polysynaptic excitatory as well as inhibitory inputs in specific groups of neurons. This complex pattern of convergence provides a substrate for alterations in the balance between visceral and somatic inputs causing referred pain.

Pain referral and regional deep tissue hyperalgesia in experimental human hip pain models.

Hip disorder patients typically present with extensive pain referral and hyperalgesia. To better understand underlying mechanisms, an experimental hip pain model was established in which pain referrals and hyperalgesia could be studied under standardized conditions. In 16 healthy subjects, pain was induced by hypertonic saline injection into the gluteus medius tendon (GMT), adductor longus tendon (ALT), or gluteus medius muscle (GMM). Isotonic saline was injected contralaterally as control. Pain intensity was assessed on a visual analogue scale (VAS), and subjects mapped the pain distribution. Before, during, and after injections, passive hip joint pain provocation tests were completed, together with quantitative sensory testing as follows: pressure pain thresholds (PPTs), cuff algometry pain thresholds (cuff PPTs), cutaneous pin-prick sensitivity, and thermal pain thresholds. Hypertonic saline injected into the GMT resulted in higher VAS scores than hypertonic injections into the ALT and GMM (P<.05). Referred pain areas spread to larger parts of the leg after GMT and GMM injections compared with more regionalized pain pattern after ALT injections (P<.05). PPTs at the injection site were decreased after hypertonic saline injections into GMT and GMM compared with baseline, ALT injections, and isotonic saline. Cuff PPTs from the thigh were decreased after hypertonic saline injections into the ALT compared with baseline, GMT injections, and isotonic saline (P<.05). More subjects had positive joint pain provocation tests after hypertonic compared with isotonic saline injections (P<.05), indicating that this provocation test also assessed hyperalgesia in extra-articular soft tissues. The experimental models may open for better understanding of pain mechanisms associated with painful hip disorders.

Bladder pain relief by HMGB1 neutralization and soluble thrombomodulin in mice with cyclophosphamide-induced cystitis.

High mobility group box 1 (HMGB1), one of damage-associated molecular patterns (DAMPs), plays roles in not only inflammation but also processing of somatic pain. Given that no evidence for roles of HMGB1 in visceral pain signaling is available, we asked if HMGB1 participates in bladder pain accompanying cystitis caused by cyclophosphamide in mice, using the anti-HMGB1 neutralizing antibody and recombinant human soluble thrombomodulin (rhsTM) that sequesters HMGB1 and promotes its degradation by thrombin. Cyclophosphamide, administered i.p., caused bladder pain-like nociceptive behavior and referred hyperalgesia accompanying cystitis symptoms including increased bladder weight, an indicator of edema, in mice. The cyclophosphamide-induced bladder pain and referred hyperalgesia, but not increased bladder weight, were prevented by i.p. preadministration of the anti-HMGB1 neutralizing antibody or rhsTM. HMGB1, given i.p., facilitated the bladder pain and referred hyperalgesia caused by a subeffective dose of cyclophosphamide, an effect blocked by rhsTM. In the cyclophosphamide-treated mice, HMGB1 levels greatly decreased in the bladder tissue, particularly in the urothelial cells, but did not change in the plasma. Low molecular weight heparin, known to inhibit the receptor for advanced glycation end products (RAGE), but not lipopolysaccharide from Rhodobacter sphaeroides, an inhibitor of toll-like receptor 4 (TLR4), blocked the cyclophosphamide-induced bladder pain and referred hyperalgesia. Thus, our data indicate involvement of HMGB1 in the cyclophosphamide-induced bladder pain signaling, but not cystitis itself, and suggest that targeting HMGB1 with rhsTM or blocking RAGE might serve as a novel therapeutic strategy for the management of bladder pain.

Thermographic and clinical correlation of myofascial trigger points in the masticatory muscles.

OBJECTIVES: The aim of the study was to identify and correlate myofascial trigger points (MTPs) in the masticatory muscles, using thermography and algometry. METHODS: 26 female volunteers were recruited. The surface facial area over the masseter and anterior temporalis muscles was divided into 15 subareas on each side (n=780). This investigation consisted of three steps. The first step involved thermographic facial examination, using lateral views. The second step involved the pressure pain threshold (PPT), marking the MTP pattern areas for referred pain (n=131) and local pain (n=282) with a coloured pencil, and a photograph of the lateral face with the head in the same position as the infrared imaging. The last step was the fusion of these two images, using dedicated software (Reporter® 8.5-SP3 Professional Edition and QuickReport® 1.2, FLIR Systems, Wilsonville, OR); and the calculation of the temperature of each point. RESULTS: PPT levels measured at the points of referred pain in MTPs (1.28±0.45 kgf) were significantly lower than the points of local pain in MTPs (1.73±0.59 kgf; p<0.05). Infrared imaging indicated differences between referred and local pain in MTPs of 0.5 °C (p<0.05). Analysis of the correlation between the PPT and infrared imaging was done using the Spearman non-parametric method, in which the correlations were positive and moderate (0.4≤r<0.7). The sensitivity and specificity in MTPs were 62.5% and 71.3%, respectively, for referred pain, and 43.6% and 60.6%, respectively, for local pain. CONCLUSION: Infrared imaging measurements can provide a useful, non-invasive and non-ionizing examination for diagnosis of MTPs in masticatory muscles.

Effect of ischemic pressure using a Backnobber II device on discomfort associated with myofascial trigger points.

OBJECTIVE: The purpose of this study was to assess the effectiveness of ischemic pressure on myofascial trigger point (MTrP) sensitivity. DESIGN: Randomized, controlled study with the researcher assessing MTrP sensitivity blinded to the intervention. PARTICIPANTS: Twenty-eight people with two MTrPs in the upper back musculature. INTERVENTION: The sensitivity of two MTrPs in the upper back was assessed with a JTECH algometer. One of the two MTrPs was randomly selected for treatment with a Backnobber II, while the other served as a control. OUTCOME MEASURES: Pre- and post-test pressure-pain thresholds of the MTrPs RESULTS: There was a significant difference between the pre- and post-test sensitivities of the treated and non-treated MTrPs (p=0.04). CONCLUSIONS: The results of this study confirm that the protocol of six repetitions of 30-s ischemic compression with the Backnobber II rendered every other day for a week was effective in reducing MTrP irritability.

[Differences between myofascial trigger points and tender points]. / Unterschiede zwischen myofazialen Triggerpunkten und "tender points".

The article describes and compares the characteristics of myofascial trigger points (MTrPs) of the myofascial pain syndrome and the tender points (TePs) of the fibromyalgia syndrome. Many statements are hypothetical, because not all aspects of the disorders have been clarified in solid studies. Signs and symptoms of MTrPs: (1) palpable nodule, often located close to the muscle belly, (2) often single, (3) allodynia and hyperalgesia at the MTrP, (4) referral of the MTrP pain, (5) normal pain sensitivity outside the MTrPs, (6) local twitch response, (7) local contracture in biopsy material, (8) peripheral mechanism probable. Signs and symptoms of TePs: (1) no palpable nodule, (2) location often close to the muscle attachments, (3) multiple by definition, (4) allodynia and hyperalgesia also outside the TePs, (5) enhanced pain under psychic stress, (6) unspecific histological changes in biopsy material, (7) central nervous mechanism probable. The multitude of differences speak against a common aetiology and pathophysiology.

Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome.

The generalized hypersensitivity associated with fibromyalgia syndrome (FMS) may in part be driven by peripheral nociceptive sources. The aim of the study was to investigate whether local and referred pain from active myofascial trigger points (MTrPs) contributes to fibromyalgia pain. FMS patients and healthy controls (n=22 each, age- and gender-matched) were recruited. The surface area over the upper trapezius muscle on each side was divided into 13 sub-areas (points) of 1cm in diameter for each point. Pressure pain threshold (PPT) and the local and referred pain pattern induced by manual palpation at 13 points bilaterally in the upper trapezius were recorded. Results showed that PPT levels at all measured points were significantly lower in FMS than controls. Multiple active MTrPs (7.4+/-2.2) were identified bilaterally in the muscle in FMS patients, but no active MTrPs were found in controls. The mid-fiber region of the muscle had the lowest PPT level with the largest number of active MTrPs in FMS and with the largest number of latent MTrPs in controls. The local and referred pain pattern induced from active MTrPs bilaterally in the upper trapezius muscle were similar to the ongoing pain pattern in the neck and shoulder region in FMS. In conclusion, active MTrPs bilaterally in the upper trapezius muscle contribute to the neck and shoulder pain in FMS. Active MTrPs may serve as one of the sources of noxious input leading to the sensitization of spinal and supraspinal pain pathways in FMS.

Multiple active myofascial trigger points and pressure pain sensitivity maps in the temporalis muscle are related in women with chronic tension type headache.

OBJECTIVE: To describe the common locations of active trigger points (TrPs) in the temporalis muscle and their referred pain patterns in chronic tension type headache (CTTH), and to determine if pressure sensitivity maps of this muscle can be used to describe the spatial distribution of active TrPs. METHODS: Forty women with CTTH were included. An electronic pressure algometer was used to assess pressure pain thresholds (PPT) from 9 points over each temporalis muscle: 3 points in the anterior, medial and posterior part, respectively. Both muscles were examined for the presence of active TrPs over each of the 9 points. The referred pain pattern of each active TrP was assessed. RESULTS: Two-way analysis of variance detected significant differences in mean PPT levels between the measurement points (F=30.3; P<0.001), but not between sides (F=2.1; P=0.2). PPT scores decreased from the posterior to the anterior column (P<0.001). No differences were found in the number of active TrPs (F=0.3; P=0.9) between the dominant side the nondominant side. Significant differences were found in the distribution of the active TrPs (chi2=12.2; P<0.001): active TrPs were mostly found in the anterior column and in the middle of the muscle belly. The analysis of variance did not detect significant differences in the referred pain pattern between active TrPs (F=1.1, P=0.4). The topographical pressure pain sensitivity maps showed the distinct distribution of the TrPs indicated by locations with low PPTs. CONCLUSIONS: Multiple active TrPs in the temporalis muscle were found, particularly in the anterior column and in the middle of the muscle belly. Bilateral posterior to anterior decreased distribution of PPTs in the temporalis muscle in women with CTTH was found. The locations of active TrPs in the temporalis muscle corresponded well to the muscle areas with lower PPT, supporting the relationship between multiple active muscle TrPs and topographical pressure sensitivity maps in the temporalis muscle in women with CTTH.

Exertional headache as unusual presentation of the syndrome of an elongated styloid process.

We present the case of a 34-year-old man with a 2-year history of pain related to efforts in heavy lifting, beginning in the right ear and radiating to the neck and to the vertex. He underwent multiple negative neuroimaging examinations, until a 3-dimensional computerized tomography scan of the pharyngeal region evidenced an elongated styloid process. A diagnosis of Eagle's syndrome was made. The excision of the elongated styloid process was performed, resulting in complete and lasting pain relief. We focus on Eagle's syndrome and in particular on this atypical presentation.

Bilateral myofascial trigger points in the forearm muscles in patients with chronic unilateral lateral epicondylalgia: a blinded, controlled study.

OBJECTIVE: The aim of the present study was to investigate the presence of active and latent muscle trigger points (TrPs) in the forearm musculature on both affected and unaffected sides in patients with lateral epicondylalgia (LE) and healthy controls. METHODS: Twenty-five patients with LE and 20 healthy matched controls participated. Both groups were examined for the presence of TrPs in the extensor carpi radialis brevis, extensor carpi radialis longus, extensor digitorum communis, and brachioradialis muscles in a blinded fashion. TrPs were identified in both affected and unaffected sides within the patient group. In the control group, TrPs were explored around the dominant side. Pressure pain thresholds (PPTs) were assessed on both affected and unaffected arms. RESULTS: In the patient group, the number of active muscle TrPs in the affected side was 3.1 [95% confidence interval (CI): 2.8-3.4], whereas in the unaffected arm, only latent TrPs were found (mean: 2.2; 95% CI: 1.8-2.6). Active TrPs were only located on the affected side (P<0.001). Within the control group, the number of latent TrPs in the dominant arm was 0.4 (95% CI: 0.0-0.7), which was significantly lower than the number of latent TrPs in the unaffected arm (P<0.001) in patients. Therefore, latent muscle TrPs in the forearm musculature were associated with the unaffected side in the patient group as compared with the dominant arm in healthy controls: extensor carpi radialis brevis [odds ratio (OR)=66 (95% CI: 9.9-48.8)], extensor carpi radialis longus [OR=16 (95% CI: 3.7-29.6)], brachioradialis [OR=2.6 (95% CI: 0.3-27.1)], and extensor digitorum communis [OR=0.5 (95% CI: 0.4-0.8)]. PPTs were lower around the affected side than around the unaffected arm in patients (mean+/-SD: 274.5+/-90.4 KPa vs. 465.4+/-140.7 KPa; P<0.001) in the patient group. Finally, PPT from the extensor digitorum muscle in those patients with active TrPs (mean+/-SD: 244+/-70.4 KPa) was significantly lower (P<0.001) than PPT levels of patients with no TrP in the same muscle (mean+/-SD: 370+/-83.4 KPa). CONCLUSIONS: Latent TrPs are present in forearm muscles on the unaffected side in patients with LE where active TrPs contribute to the pain on the affected arm. The presence of latent TrPs on the unaffected side in unilateral LE may be related to central sensitization and be a mechanism explaining bilateral pain in some patients with unilateral pathologies.

Association of cross-sectional area of the rectus capitis posterior minor muscle with active trigger points in chronic tension-type headache: a pilot study.

OBJECTIVE: To investigate whether cross-sectional area (CSA) of the suboccipital muscles was associated with active trigger points (TrPs) in chronic tension-type headache (CTTH). DESIGN: Magnetic resonance imaging (MRI) of the cervical spine was performed in 11 females with CTTH aged from 26 to 50 yrs old. CSA for both rectus capitis posterior minor (RCPmin) and rectus capitis posterior major (RCPmaj) muscles were measured from axial T1-weighted images, using axial MRI slices aligned parallel to the C2/3 intervertebral disc. A headache diary was kept for 4 wks to record the pain history. TrPs in the suboccipital muscle were identified by eliciting referred pain to palpation, and increased referred pain with muscle contraction. TrPs were considered active if the elicited referred pain reproduced the head pain pattern and features of the pattern seen during spontaneous headache attacks. RESULTS: Active TrPs were found in six patients (55%), whereas the remaining five patients showed latent TrPs. CSA of the RCPmin was significantly smaller (F = 13.843; P = 0.002) in the patients with active TrPs (right side: 55.9 +/- 4.4 mm; left side: 61.1 +/-: 3.8 mm) than in patients with latent TrPs (right side: 96.9 +/- 14.4 mm; left side: 88.7 +/- 9.7 mm). No significant differences were found for CSA of the RCPmaj between the patients with either active or latent TrP (P > 0.5). CONCLUSIONS: It seems that muscle atrophy in the RCPmin, but not in the RCPmaj, was associated with suboccipital active TrPs in CTTH, although studies with larger sample sizes are now required. It may be that nociceptive inputs in active TrPs could lead to muscle atrophy of the involved muscles. Muscle disuse or avoidance behavior can also be involved in atrophy.