BACKGROUND The abnormal movements seen in motor conversion disorder are affected by distraction and entrainment, similar to voluntary movement. Unlike voluntary movement, however, patients lack a sense of control for the abnormal movements, a failure of “self-agency.” The action-effect binding paradigm has been used to quantify the sense of self-agency, because subjective contraction of time between an action and its effect only occurs if the subject feels that they are the agent responsible for the action. We used this paradigm, coupled with emotional stimuli, to investigate the sense of agency with voluntary movements in patients with motor conversion disorder. METHODS Twenty patients with motor conversion disorder and 20 age- and gender-matched healthy volunteers used a rotating clock to judge the time of their own voluntary keypresses (action) and a subsequent auditory tone (effect), after completing conditioning blocks in which high, medium and low tones were coupled to images of happy, fearful and neutral faces. RESULTS The results replicate those shown previously: an effect following a voluntary action was reported as occurring earlier, and the preceding action later, compared to trials of only keypresses or tones. Patients had reduced overall binding scores relative to healthy volunteers, suggesting a reduced sense of agency. There was no effect of the emotional stimuli (faces) or other interaction effects. Healthy volunteers with subclinical depressive symptoms had higher overall binding scores. CONCLUSIONS We show that motor conversion disorder patients have decreased action-effect binding for normal voluntary movements compared to healthy volunteers, consistent with the greater experience of lack of control.
Background: The term middle ear myoclonus (MEM) has been invoked to explain symptoms of tinnitus presumably caused by the dysfunctional movement of either of the two muscles that insert in the middle ear: tensor tympani and stapedius. MEM has been characterized through heterogeneous case reports in the otolaryngology literature, where clinical presentation is variable, phenomenology is scarcely described, the pathogenic muscle is usually not specified, natural history is unknown, and the presumptive definitive treatment, tensor tympani or stapedius tendon lysis, is inconsistently effective. It is not surprising that no unique acoustogenic mechanism or pathophysiologic process has been identified to explain MEM, one of several descriptive diagnoses associated with the complicated disorders of myogenic tinnitus.Methods: Here, we explore MEM from the neurologist's perspective. Following the detailed descriptions of two informative cases from our clinic, we systematically evaluate the different mechanisms and movement disorder phenomena that could lead to a diagnosis of MEM.Results: From a functional neuroanatomic perspective, we explain how tensor tympani MEM is best explained as a form of peritubal myogenic tinnitus, similar to the related disorder of essential palatal tremor. From a pathogenic perspective, we discuss how MEM symptomatology may reflect different mechanical and neurologic processes. We emphasize the diagnostic imperative to recognize when myogenic tinnitus is consistent with a psychogenic origin.Discussion: Both individual patient care and further elucidation of MEM will rely on more detailed clinical characterization as well as multidisciplinary input from neurology, otolaryngology, and dentistry.
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