Clinical diagnosis of vascular dementia

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Abstract

Vascular dementia (VaD) is a heterogeneous clinical entity based on various vascular pathophysiological processes underlying the subtypes of cerebrovascular disease (CVD). Several diagnostic criteria are currently being used for the clinical diagnosis of VaD, but they are mostly more than 10 years old and need to be renovated including the use of functional brain imaging methods such as single photon emission computerized tomography (SPECT). There is a limitation in the diagnosis based on the strict dichotomy between AD and VaD, and the concept of “AD with CVD” or “mixed dementia” should be included in the clinical diagnosis of VaD.

Introduction

Vascular dementia (VaD) is the second most common cause of dementia next to Alzheimer's disease (AD). Although there are several diagnostic criteria of VaD, the differential diagnosis between VaD and AD is not so easy because VaD is a heterogeneous clinical entity including various subtypes of cerebrovascular disease (CVD) based on different vascular pathology: lacunar infarction, cortical infarction, subcortical infarction, white matter lesions, cardiogenic emboli, hemodynamic (hypotensive) infarction, hypertensive intracerebral hemorrhage, lobar hemorrhage, and subarachnoid hemorrhage (Fig. 1). In addition, neuropathological studies revealed that vascular and neurodegenerative pathologies coexist, and global neuropsychological scales which are commonly used in the evaluation of dementia are emphasized toward memory deficits and cortical signs, and this may bias the clinical diagnosis of VaD towards concomitant AD pathology in the attempt to exclude pure vascular dementia [1], [2], [3]. Thus it seems difficult to make a firm diagnosis of VaD using current clinical diagnostic criteria [1], [4], [5].

Section snippets

Overview of diagnostic criteria

Current clinical diagnostic criteria of VaD were constructed based on the expert opinion about risk factors, neurological manifestations and pathogenetic mechanisms, and designed to achieve high sensitivity and specificity in contrast to the clinical features of AD (Table 1). They are, however, mostly more than 10 years old and need to be updated.

Those diagnostic criteria were basically designed to differentiate VaD from AD, but the strict dichotomy between VaD and AD is often difficult because

Clinical course and temporal relationship

A temporal relationship between dementia and CVD in post-stroke dementia (VaD) is inferred from the onset of dementia within 3 months following the recent stroke event in NINDS-AIREN criteria. Otherwise, abrupt onset of cognitive dysfunctions, or fluctuating or stepwise deterioration of cognitive deficits is regarded as a characteristic clinical course for VaD. The ADDTC criteria require a clearly documented temporal relationship between onset of dementia and the occurrence of a stroke event by

Subcategories of VaD

Although there are several subtypes of VaD listed in the current diagnostic criteria, no detailed guidelines are given for those subcategories. In the ICD-10 criteria, there are 6 subtypes of VaD with unequal clinical description such as acute onset, multi-infarct, subcortical, mixed cortical and subcortical, other and unspecified.

Case 1 is a right-handed patient with paroxysmal atrial fibrillation who suddenly developed a left unilateral space neglect, anosognosia, inattention, memory deficits

Diagnostic brain imaging

Structural brain imaging techniques such as X-ray CT and MRI have been applied to the discriminative diagnosis of VaD and AD by detecting organic changes including cortical or subcortical infarcts and/or ischemic white matter lesions. Although large infarcts can be easily detected on such structural imaging, mild ischemia may cause partial neuronal loss (incomplete infarction) and consequently result in undetectable structural changes on such brain images.

With regard to the diagnostic

References (29)

  • T. Wetterling et al.

    The ICD-10 criteria for vascular dementia

    Dementia

    (1994)
  • T. Wetterling et al.

    Clinical evaluation of the ICD-10 criteria for vascular dementia

    Eur Arch Psychiatry Clin Neurosci

    (1993)
  • H.C. Chui et al.

    Criteria for the diagnosis of ischemic vascular dementia proposed by the State of California Alzheimer's Disease Diagnostic and Treatment Centers

    Neurology

    (1992)
  • G.C. Roman et al.
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