Research criteria for subcortical vascular dementia in clinical trials.

Vascular dementia (VaD) incorporate different vascular mechanisms and changes in the brain, and have different causes and clinical manifestations. Variation in defining the cognitive syndrome, in vascular etiologies, and allowable brain changes in current clinical definitions of VaD have resulted in variable estimates of prevalence, of groups of subjects, and of the types and distribution of putative causal brain lesions. Thus current criteria for VaD select an etiologically and clinically heterogeneous group. This definitional heterogeneity may have been a factor in "negative" clinical trials. An alternative for clinical drug trials is to focus on a more homogeneous group, such as those with subcortical (ischemic) VaD. This designation incorporates two small vessel clinical entities "Binswanger's disease" and "the lacunar state". It comprises small vessel disease as the primary vascular etiology, lacunar infarct(s) and ischaemic white matter lesions as the primary type of brain lesions, and subcortical location as the primary location of lesions. The subcortical clinical syndrome is the primary clinical manifestation, a definition which still requires additional empirical data. We expect that subcortical VaD show a more predictable clinical picture, natural history, outcome, and treatment responses. We propose a modification of the NINDS-AIREN criteria as a new research criteria for subcortical VaD.

[1]  W. Markesbery,et al.  Brain infarction and the clinical expression of Alzheimer disease. The Nun Study. , 1997, JAMA.

[2]  T. Tatemichi,et al.  How acute brain failure becomes chronic , 1990, Neurology.

[3]  H. Chui Dementia. A review emphasizing clinicopathologic correlation and brain-behavior relationships. , 1989, Archives of neurology.

[4]  A. Paetau,et al.  Accuracy of the clinical diagnosis of vascular dementia: a prospective clinical and post-mortem neuropathological study. , 1988, Journal of neurology, neurosurgery, and psychiatry.

[5]  J. Garcìa,et al.  Pathogenesis of leukoaraiosis: a review. , 1997, Stroke.

[6]  J. Cummings,et al.  Behavioral neurology of multi-infarct dementia. , 1991, Alzheimer disease and associated disorders.

[7]  K Herholz,et al.  Severity of vascular dementia is related to volume of metabolically impaired tissue. , 1992, Archives of neurology.

[8]  V. Hachinski,et al.  Rethinking Vascular Dementia (Part 1 of 2) , 1993 .

[9]  V Hachinski,et al.  The effect of different diagnostic criteria on the prevalence of dementia. , 1997, The New England journal of medicine.

[10]  R. Mayeux,et al.  Risk of dementia after stroke in a hospitalized cohort , 1994, Neurology.

[11]  K. Blennow,et al.  The clinical diagnosis of vascular dementia. , 1994, Dementia.

[12]  K. Rockwood,et al.  Spectrum of Disease in Vascular Cognitive Impairment , 1999, Neuroepidemiology.

[13]  M. Kaste,et al.  Dementia three months after stroke. Baseline frequency and effect of different definitions of dementia in the Helsinki Stroke Aging Memory Study (SAM) cohort. , 1997, Stroke.

[14]  J. Cummings,et al.  Vascular subcortical dementias: clinical aspects. , 1994, Dementia.

[15]  J. Garcìa,et al.  The significance of cerebral white matter abnormalities 100 years after Binswanger's report. A review. , 1995, Stroke.

[16]  Florence Pasquier,et al.  Why are stroke patients prone to develop dementia? , 1997, Journal of Neurology.

[17]  V. Hachinski,et al.  Subcortical Vascular Dementia: Survey of Treatment Patterns and Research Considerations , 1998, Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques.

[18]  D. W. Desmond,et al.  Vascular dementia: a construct in evolution. , 1996, Cerebrovascular and brain metabolism reviews.

[19]  G. Wilcock,et al.  Fortnightly Review: Vascular dementia , 1996 .

[20]  J. Cummings Frontal-subcortical circuits and human behavior. , 1993, Journal of psychosomatic research.

[21]  T. Wetterling,et al.  Comparison of different diagnostic criteria for vascular dementia (ADDTC, DSM-IV, ICD-10, NINDS-AIREN). , 1996, Stroke.

[22]  C. DeCarli,et al.  Imaging of static brain lesions in vascular dementia: implications for clinical trials. , 1999, Alzheimer disease and associated disorders.

[23]  T. Erkinjuntti Cerebrovascular Dementia , 1999 .

[24]  I. Skoog Status of Risk Factors for Vascular Dementia , 1998, Neuroepidemiology.

[25]  A. Brun,et al.  Pathology and pathophysiology of cerebrovascular dementia: pure subgroups of obstructive and hypoperfusive etiology. , 1994, Dementia.

[26]  T. Erkinjuntti Types of multi‐infarct dementia , 1987, Acta neurologica Scandinavica.

[27]  G. C. Román,et al.  Vascular dementia , 1993, Neurology.

[28]  I. Skoog,et al.  A population-based study of dementia in 85-year-olds. , 1993, The New England journal of medicine.

[29]  V. Babikian,et al.  Binswanger's disease: a review. , 1987, Stroke.

[30]  A Brun,et al.  White matter changes in dementia of Alzheimer's type. Biochemical and neuropathological correlates. , 1988, Brain : a journal of neurology.

[31]  G. Román,et al.  Senile dementia of the Binswanger type. A vascular form of dementia in the elderly. , 1987, JAMA.

[32]  Yasuo Nishihara,et al.  Why do frontal lobe symptoms predominate in vascular dementia with lacunes? , 1986, Neurology.