Objective
Recent reports of hearing impairment in Parkinson’s disease (PD) have suggested that auditory dysfunction could be a non-motor manifestation of PD. These reports were based on observations of elderly patients for whom presbycusis may, to some extent, have contributed to hearing dysfunction. Therefore, we aimed to explore the auditory functions in younger patients with PD.
Methods
We conducted a case-control study in a relatively younger (< 55 years of age at study time) population of PD patients and healthy volunteers to test whether auditory dysfunction is a significant non-motor dysfunction in PD. Pure tone audiometry (PTA) and brainstem evoked response audiometry (BERA) were performed in all participants.
Results
None of the patients or controls reported hearing deficits. Fifty-one patients with PD and 50 healthy volunteers who were age- and gender-matched to the patients participated. PTA-detected hearing impairment was found in 64.7% of patients and 28% of controls (
p
< 0.001) for both low-mid and/or high frequencies. Hearing impairment was more frequent in the younger subgroups of patients than age-matched controls, while the frequency of hearing impairment was similar in older groups of subjects. BERA was not different between patients and controls.
Conclusion
Asymptomatic auditory dysfunction is a common non-motor manifestation of early-onset PD and more frequent in younger patients, indicating that it may be independent of aging. The mechanism underlying this dysfunction appears to be peripheral, although a central dysfunction cannot be ruled out based on the findings of this study.
Neurological manifestations of coronavirus disease (COVID-19) have increasingly been reported since the onset of the pandemic. Herein, we report a relatively new presentation. A patient in the convalescence period following a febrile illness with lower respiratory tract infection (fever, myalgia, nonproductive cough) presented with generalized disabling myoclonus, which is phenotypically suggestive of brainstem origin, along with additional truncal cerebellar ataxia. His neurology work-ups, such as brain MRI, electroencephalography, serum autoimmune and paraneoplastic antibody testing, were normal. His CT chest scan revealed right lower lung infiltrates, and serological and other laboratory testing did not show evidence of active infection. COVID-19 titers turned out to be strongly positive, suggestive of post-COVID-19 lung sequelae. He responded partially to antimyoclonic drugs and fully to a course of steroids, suggesting a para- or postinfectious immune-mediated pathophysiology. Myoclonusataxia syndrome appears to be a neurological manifestation of COVID-19 infection, and knowledge regarding this phenomenon should be increased among clinicians for better patient care in a pandemic situation.
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