A 26-year-old right-handed man presented with progressive gait imbalance over the last 6 years. He was in his usual state of health until his junior year of college. He noticed having trouble with his balance while playing intramural sports. When he was a senior in college, he started noticing intermittent difficulty with his balance while standing or walking, especially when walking a straight line. He felt jerky and had intermittent shaking of his legs. He also complained of worsening instability in the dark. He had numerous falls over the last 1 year. Over the months prior to presentation, he started to notice tremors and mild incoordination.Tremors were worse at the end of tasks, especially while eating or drinking. He also complained of mild slurring of his speech. He denied any weakness, numbness, tingling, drooping of the eyelids, double vision, bowel or bladder incontinence, and trouble swallowing.His medical history was otherwise unremarkable for any known contributing factors. He reported no travel history, history of developmental delay, or toxin exposure. He was taking sertraline, multivitamins, and coenzyme Q10. He drank approximately 15 to 20 beers per week and endorsed binge drinking during college years, but he denied tobacco or other illicit drug use. His maternal side of the family was of Irish descent and paternal side, French-Canadian descent. There was no consanguinity between his parents and no known history of neurological disease in his family, and he had 3 siblings who were asymptomatic.His general and mental status examinations were normal. Cranial nerves were normal, other than mild dysarthria. Motor examination showed normal tone, bulk, and strength. He was hyperreflexic in his arms and legs, with bilateral Hoffman sign and clonus at the ankles. Plantar reflex and sensory examination were normal. He had kinetic tremors with end point worsening. Gait examination was normal. Mild dystonic posturing of the right upper extremity was noticed while walking.
To the Editor We read with interest the article by Zissimopoulos et al 1 that found that Alzheimer disease (AD) risk was 10% lower among Medicare beneficiaries exposed to higher levels of statins compared with lower levels of statins. While the authors have designed the study to address certain biases, we are concerned that they overlooked other potential biases in ascertaining AD after the submission of Medicare claims for statins that may have contributed to the lower observed incidence among people using high levels of statins.Ascertainment biases arise from the particular complexities of Medicare claims for medical conditions, such as AD, that are only available for periods when the beneficiary is covered by fee-for-service plans and not participating in a health management organization. Zissimopolous et al 1 limit their cohort to those covered by fee-for-service for 2 or more years. It is, however, possible that after the 2006 to 2008 period used to define statin use, some beneficiaries could have switched from fee-for-service to health management organizations, which would prevent the ability to ascertain their claims for AD. This could bias results, if, for example, those with higher statin use more often switched to health management organizations, possibly because they were healthier. While we do not know if this occurred, it would be informative to at least partially address this potential bias by adjusting for months covered by fee-forservice among cases and controls during the entire follow-up period.Additionally, we suggest adjusting for the number of visits to doctors (only knowable during fee-for-service coverage). 2 Because statin use may be related to the subsequent frequency of visits to doctors and an AD diagnosis cannot be made without a doctor's visit, controlling for medical surveillance intensity could affect the observed associations between statins and AD. Finally, in evaluating ascertainment bias, it may be useful to examine the relationship between AD and cholesterol-lowering medications other than statins that affect circulating cholesterol levels through mechanisms of action that differ from statins. Thus, if the relationship between statins and AD reflects the particular mechanism of action of statins, one would not expect to replicate the association with medications reliant on other biological processes.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.