article · QJM
Abstract Background Essential tremor (ET) is the most common adult movement disorder, affecting about 4.6% of those aged 65 years and older. Recent studies have also demonstrated an association between ET and hearing impairment. Although different neuroanatomical structures and pathways are emphasized as possible explanations for essential tremor (ET), there is still an ongoing debate. This study aimed to assess the role of brainstem auditor responses and reflex pathways with ABR & vestibular-evoked myogenic potentials (VEMP) in patients with ET. Aim of the Work 1. To assess peripheral & central vestibulocochlear function in patients with ET in comparison to controls & To correlate the degree of vestibulocochlear and brainstem pathway dysfunction to disease characteristics and severity. Patients and Methods 24 patients were included, selected from outpatient clinics at recruited from movement disorders clinic at Ain Shams University Hospitals and fulfilled the criteria of diagnosis of ET (ET criteria were set forth in the Consensus Statement of the Movement Disorder Society) (Bhatia et al. 2018) and 24 healthy controls who were age and sex matched, selected from workers at outpatient clinic, Fahn Tolosa tremor scale (FTM) was used for assessment of severity of tremors in patients, in addition ABR parameters were recorded for both groups for assessment of upper & lower vestibular pathways. Results Our study showed that there was non-significant difference as regards the age and gender between the two groups, on the other hand there was significant difference between the patients and controls regarding prolongation of wave III & V latencies than healthy controls, with statistically significant positive correlation between wave length and the severity of tremor (p = 0.015). Conclusion The findings in our study highlight the involvement of vestibular pathway by utilizing the vestibular studies which justify the increasingly noticed hearing impairment in ET patients population & help us to further understand the pathophysiology of ET.
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DOI: 10.1093/qjmed/hcae175.499
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