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June 14, 2010
Letter to the Editor

Intellectual enrichment lessens the effect of brain atrophy on learning and memory in multiple sclerosis

June 15, 2010 issue
74 (24) 1942-1945

Abstract

Objective: Learning and memory impairments are prevalent among persons with multiple sclerosis (MS); however, such deficits are only weakly associated with MS disease severity (brain atrophy). The cognitive reserve hypothesis states that greater lifetime intellectual enrichment lessens the negative impact of brain disease on cognition, thereby helping to explain the incomplete relationship between brain disease and cognitive status in neurologic populations. The literature on cognitive reserve has focused mainly on Alzheimer disease. The current research examines whether greater intellectual enrichment lessens the negative effect of brain atrophy on learning and memory in patients with MS.
Methods: Forty-four persons with MS completed neuropsychological measures of verbal learning and memory, and a vocabulary-based estimate of lifetime intellectual enrichment. Brain atrophy was estimated with third ventricle width measured from 3-T magnetization-prepared rapid gradient echo MRIs. Hierarchical regression was used to predict learning and memory with brain atrophy, intellectual enrichment, and the interaction between brain atrophy and intellectual enrichment.
Results: Brain atrophy predicted worse learning and memory, and intellectual enrichment predicted better learning; however, these effects were moderated by interactions between brain atrophy and intellectual enrichment. Specifically, higher intellectual enrichment lessened the negative impact of brain atrophy on both learning and memory.
Conclusion: These findings help to explain the incomplete relationship between multiple sclerosis disease severity and cognition, as the effect of disease on cognition is attenuated among patients with higher intellectual enrichment. As such, intellectual enrichment is supported as a protective factor against disease-related cognitive impairment in persons with multiple sclerosis.

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REFERENCES

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Chiaravalloti ND, DeLuca J. Cognitive impairment in multiple sclerosis. Lancet Neurol 2008;7:1139–1151.
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Letters to the Editor
4 October 2010
Intellectual enrichment lessens the effect of brain atrophy on learning and memory in multiple scler
Melissa Bonnet, EA 2966, Université de Bordeaux (Victor Segalen, Bordeaux 2),
Mathilde Deloire ([email protected]), Bruno Brochet ([email protected])

Sumowski et al. [1] showed that greater intellectual enrichment lessened the negative effect of brain atrophy on cognitive performance in Multiple Sclerosis (MS). MS patients with high intellectual enrichment performed similarly in memory tasks regardless of brain atrophy values on MRI while brain atrophy was associated with lower performances in patients with low intellectual enrichment.

We previously showed that educational background protects cognitive efficiency in patients with newly diagnosed patients with relapsing-remitting MS (RRMS). [2] Low-educated (LE) RRMS patients, but not high-educated (HE) patients, had lower performances than matched healthy controls on most neuropsychological tests including the memory test used by Sumowski et al. However, cognitive scores between LE and HE controls showed no difference. LE and HE RRMS patients did not differ regarding age, gender, disability, or MRI measures, so the effect of education on cognition was not attributable to a different distribution by chance.

Sumowski et al. only observed a correlation between brain atrophy and cognitive performance in patients with low intellectual enrichment. In our study, almost none of the MRI measures correlated with cognitive scores in LE patients, which suggests that a limited amount of tissue damage could be sufficient to induce cognitive disturbances in these patients. In addition, lower compensatory capacities in these patients could not counteract the cognitive deficits related to brain involvement. By contrast, cognitive performances of HE patients were negatively correlated with MRI measures indicating that education-dependent cognitive compensation—as we showed for cognitive compensation in RRMS [3]—could be limited by tissue damage accumulation and disease progression.

Both studies demonstrated two different intellectual enrichment variables and the protective effect of a strong intellectual background on brain damage. However, we obtained different results according to MRI correlations, which could be explained by differences in the two MS populations including: disease course (we studied only early RRMS); number of years of education (16.1±2.3 years [1] vs 13±2.9 years) [2]); or the disease duration (10.5±7 years [1] vs 2±2.19 years [2]).

Further studies are needed to understand the compensatory effect of intellectual background on cognitive efficiency preservation in MS patients. The ceiling effect due to the progression of the disease should also be elucidated.

References

1. Sumowski JF, Wylie GR, Chiaravalloti N, et al. Intellectual enrichment lessens the effect of brain atrophy on learning and memory in multiple sclerosis. Neurology 2010;74:1942-1945.

2. Bonnet M, Deloire M, Salort E, Dousset V, Petry KG, Brochet B. Evidence of cognitive compensation associated with educational level in early relapsing-remitting multiple sclerosis. J Neurol Sci 2006;251:23-28.

3. Bonnet M, Allard M, Dilharreguy B, Deloire M, Petry KG, Brochet B. Cognitive compensation failure in multiple slcerosis. Neurology, 2010 in press.

Disclosures: Dr. Bonnet has received speaker honoraria from Bayer Schering Pharma. Dr. Brochet serves on scientific advisory boards for Bayer Schering Pharma, Novartis, and Merck Serono; received funding for travel or speaker honoraria from Bayer Schering Pharma, Merck Serono, Biogen Idec, Novartis, and Teva Pharmaceutical Industries Ltd./Sanofi-Aventis; serves as LEN editor for SEP et Neurosciences; and has received institutional research support from Biogen Idec, Novartis, Roche, Sanofi-Aventis, Bayer Schering Pharma, Teva Pharmaceutical Industries Ltd., Peptimmune, Eli Lilly and Company, and AB Science.

4 October 2010
Reply from the author
James F. Sumowski, Kessler Foundation Research Center
NONE

We reported negative correlations between brain atrophy and cognition in MS patients with lower reserve, but not patients with higher reserve. [1,4] In contrast, Bonnet et al. found only one correlation between MRI measures and cognition in patients with lower reserve, but several correlations among patients with higher reserve. [2]

The cognitive reserve hypothesis states that patients with higher reserve can withstand more severe neurologic disease before suffering cognitive decline. [5] The negative impact of neuropathology on cognition is weaker among higher reserve patients, as we have shown in MS [1,4] and others have shown in aging and Alzheimer disease. [6-7] In this context, Bonnet et al.’s [2] findings conflict with the cognitive reserve literature, and therefore prompted this review of their study.

Bonnet et al. defined low reserve as educational attainment as less than 12 years. However, the LE MS group had much lower verbal intelligence than the LE control group. Considering that verbal intellectual decline is very rare in MS, [8] the MS group probably had lower intelligence before disease onset. The observed cognitive differences between the LE MS and control groups likely represent premorbid differences rather than disease-induced cognitive decline—especially given the short disease duration of the MS group.

Because lower cognition among MS patients was likely developmental rather than disease-induced, a correlation between MRI measures and cognition cannot be expected. Among HE MS patients, Bonnet et al. reported correlations between MRI parameters and performance on eight cognitive tasks. However, MS patients only differed from controls on one task, suggesting that most of the correlations were due to an uncontrolled non-disease variable, such as age—which likely correlates with both cognition and MRI measures. If so, correlations should also be evident among controls but these analyses were not performed. Finally, differential statistical power is another explanation for fewer correlations among LE patients (N = 19) relative to HE patients (N = 24), especially given the high risk of Type I error (5 MRI parameters * 15 cognitive scores = 75 correlations performed for each group, with an uncorrected alpha of .05).

The cognitive reserve literature supports the notion that neuropathology is more likely related to cognition among patients with lesser reserve, [1,4-7] and the exception posed by Bonnet and colleagues [2] appears confounded.

References

4. Sumowski JF, Chiaravalloti N, Wylie GR, DeLuca J. Cognitive reserve moderates the negative effect of brain atrophy on cognitive efficiency in multiple sclerosis. J Int Neuropsychol Soc 2009;15:606-612.

5. Stern Y. Cognitive reserve. Neuropsychologia 2009; 47:2015-2028.

6. Bennett DA, Wilson RS, Schneider JA, et al. Education modifies the relation of AD pathology to level of cognitive function in older persons. Neurology 2003;60:1909-1915.

7. Rentz DM, Locascio JL, Becker JA, et al. Cognition, reserve, and amyloid deposition in normal aging. Ann Neurol 2010; 67: 353-364.

8 Chiaravalloti ND, DeLuca J. Cognitive impairment in multiple sclerosis. Lancet Neurol 2008;7:1139-1151.

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Published In

Neurology®
Volume 74Number 24June 15, 2010
Pages: 1942-1945
PubMed: 20548040

Publication History

Published online: June 14, 2010
Published in print: June 15, 2010

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Authors

Affiliations & Disclosures

James F. Sumowski, PhD
From the Kessler Foundation Research Center (J.F.S., G.R.W., N.C., J.D.), West Orange; and Departments of Physical Medicine and Rehabilitation (J.F.S., G.R.W., N.C., J.D.) and Neurology and Neurosciences (J.D.), UMDNJ–New Jersey Medical School, Newark, NJ.
Glenn R. Wylie, DPhil
From the Kessler Foundation Research Center (J.F.S., G.R.W., N.C., J.D.), West Orange; and Departments of Physical Medicine and Rehabilitation (J.F.S., G.R.W., N.C., J.D.) and Neurology and Neurosciences (J.D.), UMDNJ–New Jersey Medical School, Newark, NJ.
Nancy Chiaravalloti, PhD
From the Kessler Foundation Research Center (J.F.S., G.R.W., N.C., J.D.), West Orange; and Departments of Physical Medicine and Rehabilitation (J.F.S., G.R.W., N.C., J.D.) and Neurology and Neurosciences (J.D.), UMDNJ–New Jersey Medical School, Newark, NJ.
John DeLuca, PhD
From the Kessler Foundation Research Center (J.F.S., G.R.W., N.C., J.D.), West Orange; and Departments of Physical Medicine and Rehabilitation (J.F.S., G.R.W., N.C., J.D.) and Neurology and Neurosciences (J.D.), UMDNJ–New Jersey Medical School, Newark, NJ.

Notes

Address correspondence and reprint requests to Dr. James F. Sumowski, Neuropsychology & Neuroscience Laboratory, Kessler Foundation Research Center, 300 Executive Drive, Suite 10, West Orange, NJ 07052 [email protected]

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  1. Depressive symptoms, anxiety and cognitive impairment: emerging evidence in multiple sclerosis, Translational Psychiatry, 13, 1, (2023).https://doi.org/10.1038/s41398-023-02555-7
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  2. Systematic review of cognitive reserve in multiple sclerosis: Accounting for physical disability, fatigue, depression, and anxiety, Multiple Sclerosis and Related Disorders, 79, (105017), (2023).https://doi.org/10.1016/j.msard.2023.105017
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  3. Exploring the relation between reserve and fatigue in multiple sclerosis, Multiple Sclerosis and Related Disorders, 76, (104842), (2023).https://doi.org/10.1016/j.msard.2023.104842
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  4. Differential associations of mentally-active and passive sedentary behaviours and physical activity with putative cognitive decline in healthy individuals and those with bipolar disorder: Findings from the UK Biobank cohort, Mental Health and Physical Activity, 24, (100514), (2023).https://doi.org/10.1016/j.mhpa.2023.100514
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  5. What Is the True Impact of Cognitive Impairment for People Living with Multiple Sclerosis? A Commentary of Symposium Discussions at the 2020 European Charcot Foundation, Neurology and Therapy, 12, 5, (1419-1429), (2023).https://doi.org/10.1007/s40120-023-00519-z
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  6. Non-pharmacological Approaches Based on Mind-Body Medicine to Enhancement of Cognitive and Brain Reserve in Humans, Neurobiological and Psychological Aspects of Brain Recovery, (151-175), (2023).https://doi.org/10.1007/978-3-031-24930-3_7
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  7. Psychological-health correlates of physical activity and sedentary behaviour during the COVID pandemic, Mental Health and Physical Activity, 23, (100481), (2022).https://doi.org/10.1016/j.mhpa.2022.100481
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  8. Associations of social network structure with cognition and amygdala volume in multiple sclerosis: An exploratory investigation, Multiple Sclerosis Journal, 28, 2, (228-236), (2021).https://doi.org/10.1177/13524585211018349
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  9. Cognitive rehabilitation, Neurologie pro praxi, 21, 1, (55-59), (2020).https://doi.org/10.36290/neu.2020.005
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  10. Association of social network structure and physical function in patients with multiple sclerosis, Neurology, 95, 11, (e1565-e1574), (2020)./doi/10.1212/WNL.0000000000010460
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