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Cognitive and Motor Impairment Severity Related to Signs of Subclinical Wernicke's Encephalopathy in HIV Infection

Le Berre, Anne-Pascale PhDa; Fama, Rosemary PhDa,b; Sassoon, Stephanie A. PhDb; Pfefferbaum, Adolf MDa,b; Sullivan, Edith V. PhDa; Zahr, Natalie M. PhDa,b

JAIDS Journal of Acquired Immune Deficiency Syndromes: July 1, 2019 - Volume 81 - Issue 3 - p 345–354
doi: 10.1097/QAI.0000000000002043
Clinical Science
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Background: Wernicke's encephalopathy (WE) is a neurological condition resulting from thiamine deficiency. Although commonly associated with alcoholism, nonalcoholic WE has been described in individuals with HIV infection, but subclinical WE may be underdiagnosed. The current study questioned whether the presence of subclinical WE signs underlies cognitive and motor deficits in HIV individuals as observed in alcoholism.

Setting: Fifty-six HIV-positive individuals (HIV+) and 53 HIV-negative controls (HIV−) were assessed on 6 cognitive and motor domains: attention/working memory, production, immediate and delayed episodic memory, visuospatial abilities, and upper-limb motor function.

Methods: Based on a rating scheme by Caine et al, HIV+ individuals were categorized by subclinical WE risk factors (dietary deficiency, oculomotor abnormality, cerebellar dysfunction, and altered mental state). Performance was expressed as age- and education-corrected Z-scores standardized on controls.

Results: Sorting by Caine criteria yielded 20 HIV+ as Caine 0 (ie, meeting no criteria), 22 as Caine 1 (ie, meeting one criterion), and 14 as Caine 2 (ie, meeting 2 criteria). Comparison among HIV+ Caine subgroups revealed a graded effect: Caine 0 performed at control levels, Caine 1 showed mild to moderate deficits on some domains, and Caine 2 showed the most severe deficits on each domain.

Conclusion: This graded severity pattern of performance among Caine subgroups suggests that signs of subclinical WE can partly explain the heterogeneity in HIV-related cognitive and motor impairment. This study highlights the utility of Caine criteria in identifying potential causes of HIV-related neurocognitive disorders and has implications for disease management.

aDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA; and

bNeuroscience Program, Biosciences Division, Center for Health Science, SRI International, Menlo Park, CA.

Correspondence to: Anne-Pascale Le Berre, PhD, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Road Stanford, CA 94305 (e-mail: aleberre@stanford.edu).

Supported by the US National Institute on Alcohol Abuse and Alcoholism grants AA017347, AA017168, AA017923, AA010723, AA005965, and the Moldow Women's Hope and Healing Fund.

The authors have no conflicts of interest to disclose.

A.-P.L.B., R.F., E.V.S., N.M.Z., and A.P. were responsible for the study concept and design. S.A.S. and N.M.Z. contributed to the acquisition of data. A.-P.L.B., R.F., E.V.S., S.A.S., and N.M.Z. assisted with data analyses and collection. A.-P.L.B., R.F., E.V.S., S.A.S., A.P., and N.M.Z. interpreted the findings. A.-P.L.B. and E.V.S. drafted the manuscript. E.V.S., S.A.S., N.M.Z., R.F., and A.P. provided critical revision of the manuscript for important intellectual content. All authors have critically reviewed content and approved final version submitted for publication.

Received December 06, 2018

Accepted March 11, 2019

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