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Stroke. 2006;37:2197
Published online before print August 17, 2006, doi: 10.1161/01.STR.0000237144.29980.9c
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(Stroke. 2006;37:2197.)
© 2006 American Heart Association, Inc.


Editorials

Welcome Harmonizations

José M. Ferro, MD, PhD

From the Department of Neurosciences, Hospital de Santa Maria, University of Lisboa, Lisboa, Portugal.

Correspondence to José M. Ferro, MD, PhD, the Department of Neurosciences, Hospital de Santa Maria, University of Lisboa, Av. Egas Moniz, 1649-035 Lisboa, Portugal. E-mail jmferro{at}fm.ul.pt


Key Words: vascular dementia

See related article, pages 2220–2241

Cerebrovascular disease is the second most common cause of acquired cognitive impairment and dementia and contributes to cognitive decline in the neurodegenerative dementias.1 The narrow definition of vascular dementia was broadened to include any cognitive impairment associated not only with clinically evident stroke, but also with neuroimaging or neuropathological evidence of brain lesions, related to vascular and circulatory diseases and to vascular risk factors, including genetic ones. Cerebrovascular disease impacts the whole brain, causing cognitive deficits, mood and personality changes, and gait and balance problems. Focus has moved from the "end-stage" condition—vascular dementia—to the "brain-at-risk" concept—individuals exposed to vascular risk factors or whose neuroimaging tests show mild assymptomatic lesions of vascular origin.

Significant progress in the field of vascular dementia resulted from the publication of the NINDS-AIREN diagnostic criteria for vascular dementia.2 Time has come to produce a similar document in relation to the broader concept of vascular cognitive impairment. In fact, harmonization standards are a prerequisite to observational or experimental studies in vascular cognitive impairment.

The publication of the NINDS-CNS Vascular Cognitive Impairment Harmonization standards3 is therefore an important step forward. Both the authors and the NIH deserve to be congratulated by this initiative.

The publication successively addresses clinical and epidemiological issues, neuropsychology, neuroimaging, neuropathology, experimental models, biomarkers, genetics and methodological aspects of clinical trials. An innovative aspect of the proposed standards is their possibility to be adapted to different setting of research. For example, in the clinical section an abbreviated clinical evaluation that can "be performed in the context of a busy physician’s practice" is suggested. In the neuropsychological section, both 60-minute, 30-minute and 5-minute protocols are described.

The present harmonization standards have, however, 2 general methodological limitations. They were produced following a meeting of experts, predominantly from North America. A larger representation of scientists from other parts of the world would have enriched the current standards, expressing the transcultural issues pertaining to cognitive impairment and behavioral changes caused by vascular brain damage.4 The limitations of the quality of evidence obtained from expert consensus are well known for a long time.5 Throughout the text and its different sections, there is never mention to a systematic review or a critical appraisal of the available evidence, namely to previous proposals of harmonization. For instance, in the neuropsychological section the validity, sensitivity and specificity, and the crucial issue of availability of validated versions of the proposed tests in different languages is not indicated.

Some detail remarks, again relating to the neuropsychological section, probably the most difficult to harmonize. The phonemic fluency task COWA cannot be used in several Latin languages, because W does not exist in these languages. The Rey figure is in our opinion an unfortunate choice to test visual spatial functions because its performance is strongly influenced by education and poor vision. A scale of apathy would be important to include, detecting and quantifying apathic personality changes, which are a rather common early manifestation of subcortical vascular disease.

Nevertheless, we completely agree with the authors’ conclusion that "using the same standards will help identify individuals in the early stages of cognitive impairment, will make studies comparable and by integrating knowledge, accelerate the pace of progress". The publication of standards will open the road for fruitful multicenter, multinational and multicultural networks and research collaboration in this growing field.

Footnotes

The opinions in this editorial are not necessarily those of the editors or of the American Heart Association.

References

1. O’Brien JT, Erkinjuntti T, Reisberg B, Roman G, Sawada T, Pantoni L, Bowler JV, Ballard C, DeCarli C, Gorelick PB, Rockwood K, Burns A, Gauthier S, DeKosky ST. Vascular cognitive impairment. Lancet Neurol. 2003; 2: 89–98.[CrossRef][Medline] [Order article via Infotrieve]

2. Roman GC, Tatemichi TK, Erkinjuntti T, Cummings JL, Masdeu JC, Garcia JH, Amaducci L, Orgogozo JM, Brun A, Hofman A. Vascular dementia: diagnostic criteria for research studies. Report of the NINDS-AIREN International Workshop. Neurology. 1993; 43: 250–260.[Abstract/Free Full Text]

3. Hachinski V, Iadecola C, Petersen RC, Breteler MMB, Nyenhuis DL, Black SE, Powers WJ, DeCarli C, Merino JG, Kalaria R, Vinters H, Holtzman D, Rosenberg GA, Dichgans M, Marler J, Leblanc GG. NINDS-CSN vascular cognitive impairment harmonization standards. Stroke. 2006; 37: 2220–2241.[Abstract/Free Full Text]

4. Chen CP. Transcultural expression of subcortical vascular disease. J Neurol Sci. 2004; 226: 45–47.[CrossRef][Medline] [Order article via Infotrieve]

5. Sackett DL, Haynes RB, Tugwell P. Clinical epidemiology. A basic science for clinical medicine. Boston/Toronto: Little Brown and Company; 1985: 178–179.


Related Article:

National Institute of Neurological Disorders and Stroke–Canadian Stroke Network Vascular Cognitive Impairment Harmonization Standards
Vladimir Hachinski, Costantino Iadecola, Ron C. Petersen, Monique M. Breteler, David L. Nyenhuis, Sandra E. Black, William J. Powers, Charles DeCarli, Jose G. Merino, Raj N. Kalaria, Harry V. Vinters, David M. Holtzman, Gary A. Rosenberg, Anders Wallin, Martin Dichgans, John R. Marler, and Gabrielle G. Leblanc
Stroke 2006 37: 2220-2241. [Abstract] [Full Text] [PDF]




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