Editor, Editors, USER, admin, Bureaucrats, Check users, dev, editor, founder, Interface administrators, member, oversight, Suppressors, Administrators, translator
11,073
edits
Line 2: | Line 2: | ||
{{ArtBy|autore=Gianni Frisardi}} | {{ArtBy|autore=Gianni Frisardi}} | ||
'''Abstract:'''This chapter delves into the complex and often debated topic of electromyography (EMG) in resting muscles, especially in patients with Orofacial Pain (OP) and Temporomandibular Disorders (TMDs). The central question revolves around whether a muscle at rest is truly silent or exhibits motor unit activity. Several studies, including those by Zieliński et al. and Fernández-de-Las-Peñas et al., have shown that changes in electromyographic patterns of masticatory muscles may be linked to myofascial trigger points (MTrPs) and TMDs. The presence of altered EMG activity in muscles at rest could be indicative of associated pain or dysfunction in masticatory and neck-shoulder muscles. | |||
The article explores the relationship between depression and resting masticatory muscle activity, as depression is known to affect the stomatognathic system. However, a key question remains: how relevant is EMG activity in resting muscles to a patient’s psychological state? This article presents the 5th clinical case study of a 65-year-old female patient suffering from Orofacial Pain and TMD, where traditional diagnostic approaches failed to uncover the true underlying condition. Through advanced EMG techniques, including surface and needle EMG, spontaneous motor unit activity was observed, revealing the presence of "involuntary EMG activity" that likely originated from a central pacemaker, rather than muscle fiber or motor neuron damage. | |||
An experimental pharmacological study using Propofol was conducted to decouple brainstem activity from cortical control. The study's results demonstrated that the patient’s EMG activity ceased upon Propofol administration, providing evidence of a central origin of the pacemaker activity, independent of brainstem functions. This led to a final diagnosis of Focal Oromandibular Dystonia rather than TMD. | |||
The article concludes by emphasizing the importance of considering neurological factors, such as involuntary EMG activity driven by a central pacemaker, in diagnosing and treating OP and TMD. It advocates for a more comprehensive neuro-electrophysiological approach, integrating techniques like bilateral trigeminal motor evoked potentials (bRoot-MEPs) to better understand the functional and organic aspects of TMDs. This case underscores the potential for misdiagnosis when relying solely on traditional gnathological and EMG methods without deeper neurophysiological exploration. | |||
===Introduction === | ===Introduction === | ||
edits