Orophangeal dysphagia in polymyositis/dermatomyositis

Department of Clinical Neurophysiology, Medical School Hospital Ege University, Bornova, Izmir, Turkey.
Clinical Neurology and Neurosurgery (Impact Factor: 1.13). 01/2005; 107(1):32-7. DOI: 10.1016/j.clineuro.2004.02.024
Source: PubMed


The nature of the oropharyngeal dysphagia in polymyositis/dermatomyositis (PM/DM) has been investigated by EMG methods. Nineteen patients with PM/DM were studied. The oropharyngeal phase of swallowing was evaluated by the electrophysiological methods measuring the laryngeal relocation time, pharyngeal transit time and the triggering of the pharyngeal phase of swallowing reflex. The EMG of cricopharyngeal muscle of the upper esophageal sphincter was also recorded in 10 patients. The patients have been compared with a group of 22 healthy controls matched with age and gender. Dysphagia limit was also measured for all patients and control subjects. Fourteen out of 19 patients could not swallow 20 ml or less amount of water at one go and divided the bolus into two or more pieces (piecemeal deglutition) in comparison to normal subjects. In PM/DM patients, the triggering of the swallowing reflex for the voluntarily initiated swallow was normal while the pharyngeal phase of swallowing was significantly prolonged. The cricopharyngeal sphincter muscle EMG demonstrated severe abnormalities in halves of the patients investigated. These findings demonstrated the weakness of the striated oropharyngeal muscles. Cricopharyngeal sphincter muscle was affected less frequently and showed either hyperreflexic or hyporeflexic states during swallowing. It is concluded that the pharyngeal stage of oropharyngeal swallowing is mainly involved in patients with PM/DM.

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Available from: Cumhur Ertekin,
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    • "Orofacial persistent pain following trigeminal nerve injury or orofacial inflammation is known to cause various motor as well as sensory disorders in the orofacial regions such as mastication or swallowing dysfunction [1]. Orofacial dysesthesia is known as the secondary hyperalgesia often associated with pulpitis and/or periapical periodontitis [2], suggesting that oral and craniofacial organs are target regions for ectopic pain following intraoral inflammation. "
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    ABSTRACT: A rat model of pulpitis/periapical periodontitis was used to study mechanisms underlying extraterritorial enhancement of masseter response associated with tooth inflammation. Periapical bone loss gradually increased and peaked at 6 weeks after complete Freund's adjuvant (CFA) application to the upper molar tooth pulp (M1). On day 3, the number of Fos-immunoreactive (IR) cells was significantly larger in M1 CFA rats compared with M1 vehicle (veh) rats in the trigeminal subnucleus interpolaris/caudalis transition zone (Vi/Vc). The number of Fos-IR cells was significantly larger in M1 CFA and masseter (Mass) capsaicin applied (M1 CFA/Mass cap) rats compared with M1 veh/Mass veh rats in the contralateral Vc and Vi/Vc. The number of phosphorylated extracellular signal-regulated kinase (pERK)-IR cells was significantly larger in M1 CFA/Mass cap and M1 veh/Mass cap rats compared to Mass-vehicle applied rats with M1 vehicle or CFA in the Vi/Vc. Pulpal CFA application caused significant increase in the number of Fos-IR cells in the Vi/Vc but not Vc on week 6. The number of pERK-IR cells was significantly lager in the rats with capsaicin application to the Mass compared to Mass-vehicle treated rats after pulpal CFA- or vehicle-application. However, capsaicin application to the Mass did not further affect the number of Fos-IR cells in the Vi/Vc in pulpal CFA-applied rats. The digastric electromyographic (d-EMG) activity after Mass-capsaicin application was significantly increased on day 3 and lasted longer at 6 weeks after pulpal CFA application, and these increase and duration were significantly attenuated by i.t. PD98059, a MEK1 inhibitor. These findings suggest that Vi/Vc and Vc neuronal excitation is involved in the facilitation of extraterritorial hyperalgesia for Mass primed with periapical periodontitis or acute pulpal-inflammation. Furthermore, phosphorylation of ERK in the Vi/Vc and Vc play pivotal roles in masseter hyperalgesia after pulpitis or periapical periodontitis.
    PLoS ONE 10/2014; 9(10):e109168. DOI:10.1371/journal.pone.0109168 · 3.23 Impact Factor
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    • "It is well-known that intraoral pain and masticatory or swallowing-related muscle pain frequently cause severe dysfunction of mastication and/or swallowing (Ertekin et al., 2004; Vaiman et al., 2006). The noxious information from the intraoral tissue, masticatory and swallowing-related muscles are conveyed to the brainstem neurons (Hu et al., 1992; Noma et al., 2008; Yu et al., 1993). "
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    ABSTRACT: Many phosphorylated extracellular signal-regulated kinase (pERK)-immunoreactive (IR) cells are expressed in the trigeminal spinal subnucleus caudalis (Vc), upper cervical spinal cord (C1-C2), nucleus tractus solitarii (NTS) and paratrigeminal nucleus (Pa5) after capsaicin injection into the whisker pad (WP), masseter muscle (MM), digastric muscle (DM) or sternohyoideus muscle (SM). The pERK-IR cells also showed NeuN immunoreactivity, indicating that ERK phosphorylation occurs in neurons. The pERK-IR cells were significantly reduced after intrathecal injection of MEK 1/2 inhibitor PD98059. The pERK-IR cells expressed bilaterally in the Vc and C1-C2 after capsaicin injection into the unilateral DM or SM, whereas unilaterally in the Vc and C1-C2 after unilateral WP or MM injection. After capsaicin injection into the WP or MM, the pERK-IR cell expression in the Vc was restricted rostrocaudally within a narrow area. However, the distribution of pERK-IR cells was more wide spread without a clear peak in the Vc and C1-C2 after capsaicin injection into the DM or SM. In the NTS, the unimodal pERK-IR cell expression peaked at 0-720μm rostral from the obex following capsaicin injection into WP, MM, DM or SM. In the ipsilateral Pa5, many pERK-IR cells were observed following capsaicin injection into the SM. The number of swallows elicited by distilled water administration was significantly smaller after capsaicin injection into the WP, MM or DM but not SM compared to that of vehicle-injected rats. Various noxious inputs due to the masticatory or swallowing-related muscle inflammation may be differentially involved in muscle pain and swallowing reflex activity.
    Brain research 08/2011; 1417:45-54. DOI:10.1016/j.brainres.2011.08.032 · 2.84 Impact Factor
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    • "These findings suggest that the trigeminal nociceptive inputs may be involved in the modulation of orofacial reflex function, including swallowing. Some previous reports have described that inflammatory myopathy or severe oral pain after dental extraction is involved in swallowing abnormalities (Ertekin et al. 2004; Vaiman et al. 2006), and so it is "
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    ABSTRACT: In order to evaluate the neuronal mechanisms underlying functional abnormalities of swallowing in orofacial pain patients, this study investigated the effects of noxious orofacial stimulation on the swallowing reflex, phosphorylated extracellular signal-regulated kinase (pERK) and gamma-aminobutyric acid (GABA) immunohistochemical features in brainstem neurons, and also analysed the effects of brainstem lesioning and of microinjection of GABA receptor agonist or antagonist into the nucleus tractus solitarii (NTS) on the swallowing reflex in anaesthetized rats. The swallowing reflex elicited by topical administration of distilled water to the pharyngolaryngeal region was inhibited after capsaicin injection into the facial (whisker pad) skin or lingual muscle. The capsaicin-induced inhibitory effect on the swallowing reflex was itself depressed after the intrathecal administration of MAPK kinase (MEK) inhibitor. No change in the capsaicin-induced inhibitory effect was observed after trigeminal spinal subnucleus caudalis lesioning, but the inhibitory effect was diminished by paratrigeminal nucleus (Pa5) lesioning. Many pERK-like immunoreactive neurons in the NTS showed GABA immunoreactivity. The local microinjection of the GABA(A) receptor agonist muscimol into the NTS produced a significant reduction in swallowing reflex, and the capsaicin-induced depression of the swallowing reflex was abolished by microinjection of the GABA(A) receptor antagonist bicuculline into the NTS. The present findings suggest that facial skin-NTS, lingual muscle-NTS and lingual muscle-Pa5-NTS pathways are involved in the modulation of swallowing reflex by facial and lingual pain, respectively, and that the activation of GABAergic NTS neurons is involved in the inhibition of the swallowing reflex following noxious stimulation of facial and intraoral structures.
    The Journal of Physiology 02/2009; 587(Pt 4):805-17. DOI:10.1113/jphysiol.2008.165324 · 5.04 Impact Factor
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