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Blink Reflex May Help Discriminate Alzheimer Disease From Vascular Dementia Publisher Pubmed



Mohammadian F1 ; Noroozian M2 ; Nafissi S3 ; Fatehi F3
Authors
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Authors Affiliations
  1. 1. Department of Neurology, Shariati Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Iranian Center of Neurological Research, Department of Neurology, Shariati Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, 14117-13135, Iran

Source: Journal of Clinical Neurophysiology Published:2015


Abstract

Purpose: Dementia has several different etiologies, and vascular dementia (VaD) is considered the second leading cause of dementia after Alzheimer disease (AD). Various studies used blink reflex in different spectrum of neurological diseases as a complementary diagnostic test. We performed blink test in AD, VaD, and mixed dementia to investigate different usefulness of blink reflex in differentiating these types of dementia. Methods: Blink reflex was performed for patients with AD (n = 18), VaD (n = 17), mixed dementia (n = 19), and normal subjects (n = 20). The absolute latency of R1, R2, and contralateral R2 (R2c) was determined and then compared with normal values. We used ROC curve to determine the screening cut-off value for R2 and R2c to discriminate dementia with vascular component and AD. Results: The mean age ± SD of patients was 71.61 ± 8.23, 66.71 ± 11.48, 75.26 ± 8.32, and 66.60 ± 3.91 years in 4 groups of AD, VaD, mixed dementia, and normal, respectively. R2 and R2c were recorded in fewer number of subjects with VaD or mixed dementia than AD and normal subjects. For mean R2 latency higher than 45 milliseconds, the sensitivity and specificity were 42% and 100%, respectively, and for latency higher than 45 milliseconds, the sensitivity and specificity were 72% and 89%, respectively. Conclusions: R2 and R2c components of blink reflex could specifically discriminate between Alzheimer and dementia with vascular component. The interruption of descending corticoreticular pathways by small infarcts could explain it. © Copyright 2015 by the American Clinical Neurophysiology Society.