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Neurology India
Medknow Publications on behalf of the Neurological Society of India
ISSN: 0028-3886 EISSN: 1998-4022
Vol. 54, Num. 4, 2006, pp. 349-349

Neurology India, Vol. 54, No. 4, October-December, 2006, pp. 349

Invited Commentaries

Recognition of impaired cognition in multiple sclerosis

Dept. of Neurology and Section of Neuroradiology, Medical University Graz, Auenbruggerplatz 22, 8036 Graz
Correspondence Address:Dept. of Neurology and Section of Neuroradiology, Medical University Graz, Auenbruggerplatz 22, 8036 Graz, chris.enzinger@meduni-graz.at

Code Number: ni06122

Cognitive dysfunction has been reported to be frequent in multiple sclerosis (MS), with prevalence rates ranging from 40 to 60%. Current evidence suggests that cognitive disturbances might already occur at early stages of the disease. While patients frequently complain about attention and memory problems or a decreased ability to cope with multiple tasks, cognitive functioning in MS still receives little attention by treating physicians. To some extent, this certainly relates to the common appraisal that specific therapeutic options are limited. Recent reports have challenged this notion, indicating that acetylcholinesterase inhibitors might represent a therapeutic strategy in this condition.[1]

Against this background, clinicians are facing several issues. How frequent is this condition among my patients? How can it be detected at the earliest? Can it be treated? The study[2] gives some answers. It confirms that cognitive dysfunction in MS patients is a frequent problem. Moreover, it provides indirect evidence that there is a gradual though differential worsening of cognitive functioning with disease progression. Importantly, the authors failed to identify clinical predictors of cognitive dysfunction in their study. Although distinct differences in the cognitive profiles of RR- and SP-MS patients were found, unexpectedly, there was no correlation with disease duration and only a loose correlation with the degree of disability as reflected by EDSS scores. This dissociation can be partly explained by the findings of a large imaging study which demonstrated a clear distinction between lesion locations causing physical and cognitive disability.[3]

Together, this emphasises the need to define factors that allow early identification of MS patients at risk for developing cognitive impairment. However, the clinical diagnosis of cognitive dysfunction at these earlier stages might be rather insensitive until a characteristic pattern of "subcortical cognitive impairment" becomes apparent.[4] Extensive neuropsychological testing still remains a challenge and less straining screening tests are currently under investigation.

Functional imaging studies have demonstrated functional reorganisation with cognitive tasks in MS, with some indication that compensatory mechanisms might exhaust with disease progression.[5] Interestingly, the behavioural data reported by Drake and colleagues also seem to suggest that MS patients - despite generally impaired recall - might have a relatively intact capacity of learning and storing new information. Therefore, specific cognitive training techniques aiming at reinforcement of plasticity might be feasible.

Clearly, such an approach would be facilitated by surrogate markers of cognitive dysfunction in MS. In subjects pre-selected for cognitive impairment, a high correlation between cognition and central brain atrophy has been reported, but this only accounted for approximately half the variance in overall cognitive performance.[6] Lesion location might represent an additional important factor, evidenced by a correlation between cognitive dysfunction with lesions at the grey-white junction of associative, limbic and prefrontal cortices.[3]

Cautious optimism that the importance of cognitive dysfunction in MS will be increasingly recognised in future therefore appears justified. Research endeavours to limit the burden of cognitive impairment in MS should focus on timely identification of a target population whose cognitive abilities can still be enhanced by pharmacological intervention or specific training techniques.

References

1.Christodoulou C, Melville P, Scherl WF, MacAllister WS, Elkins LE, Krupp LB. Effects of donepezil on memory and cognition in multiple sclerosis. J Neurol Sci 2006;245:127-36.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Drake MA, Carrα A, Allegri RF, Luetic G. Differential patterns of memory performance in relapsing remitting and secondary progressive multiple sclerosis. Neurol India 2006;54:370-6  Back to cited text no. 2    
3.Charil A, Zijdenbos AP, Taylor J, Boelman C, Worsley KJ, Evans AC, et al . Statistical mapping analysis of lesion location and neurological disability in multiple sclerosis: Application to 452 patient data sets. Neuro Image 2003;19:532-44.  Back to cited text no. 3    
4.Schmidt R, Enzinger C, Ropele S, Schmidt H, Fazekas F. Subcortical vascular cognitive impairment: similarities and differences with multiple sclerosis. J Neurol Sci 2006;245:3-7.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Penner IK, Kappos L, Rausch M, Opwis K, Radu EW. Therapy-induced plasticity of cognitive functions in MS patients: Insights from fMRI. J Physiol Paris 2006;99:455-62.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Christodoulou C, Krupp LB, Liang Z, Huang W, Melville P, Roque C, et al . Cognitive performance and MR markers of cerebral injury in cognitively impaired MS patients. Neurology 2003;60:1793-8.  Back to cited text no. 6    

Copyright 2006 - Neurology India

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