Subcortical vascular cognitive impairment: Similarities and differences with multiple sclerosis

    * Reinhold Schmidt
            Affiliations
          o Department of Neurology, Medical University Graz, Auenbruggerplatz 22, A-8036 Graz, Austria
          o Corresponding Author InformationCorresponding author. Tel.: +43 316 385 83397; fax: +43 316 32 55 20.
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    * , Christian Enzinger
            Affiliations
          o Department of Neurology, Medical University Graz, Auenbruggerplatz 22, A-8036 Graz, Austria
    * , Stefan Ropele
            Affiliations
          o Department of Neurology, Medical University Graz, Auenbruggerplatz 22, A-8036 Graz, Austria
          o Division of Neuroradiology, Department of Radiology, Medical University Graz, Auenbruggerplatz 22, A-8036 Graz, Austria
    * , Helena Schmidt
            Affiliations
          o Institute of Medical Molecular Biology and Medical Biochemistry, Medical University Graz, A-8036 Graz, Austria
    * , Franz Fazekas
            Affiliations
          o Department of Neurology, Medical University Graz, Auenbruggerplatz 22, A-8036 Graz, Austria
          o Division of Neuroradiology, Department of Radiology, Medical University Graz, Auenbruggerplatz 22, A-8036 Graz, Austria

Received 29 April 2005; received in revised form 6 June 2005; accepted 28 June 2005.

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Abstract

Subcortical vascular cognitive impairment is caused by lacunes and widespread ischemic white matter damage which closely resembles white matter abnormalities seen in multiple sclerosis. Recent evidence suggests that the progression rate of ischemic white matter lesions on MRI is very similar to that observed in multiple sclerosis. Consequently, it has been proposed to use MRI for monitoring disease activity not only in multiple sclerosis but also in vascular dementia trials. There is first evidence from magnetization transfer imaging studies that other than in MS normal appearing white matter is not affected in cerebral small vessel disease. This contrasts the hypothesis that ischemic white matter damage extends far beyond changes visible on conventional MR. The cognitive consequences of both diseases are strikingly similar which is at least partly caused by damage to frontal–subcortical circuits. Involvement of these common functional anatomical structures and their modulatory transmitter systems has now led to common interventional approaches such as the use of cholinesterase inhibitors.

Keywords: Vascular dementia, Cognition, Dementia, MRI, White matter lesions, Frontal lobe dysfunction, Cholinesterase inhibitors