Home > Riviste > Panminerva Medica > Fascicoli precedenti > Panminerva Medica 2004 December;46(4) > Panminerva Medica 2004 December;46(4):207-15





Rivista di Medicina Interna

Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,6




Panminerva Medica 2004 December;46(4):207-15

lingua: Inglese

Vascular dementia. Advances in nosology, diagnosis, treatment and prevention

Román G. C.

Department of Medicine/Neurology University of Texas Health Science Center at San Antonio and the Audie Murphy Veterans Administration Hospital San Antonio, TX, USA


Ischemic or hemor­rhag­ic cereb­ro­vas­cu­lar dis­ease (CVD) pro­duc­es inju­ry of ­brain ­regions impor­tant for exec­u­tive func­tion, behav­ior, and mem­o­ry lead­ing to ­decline in cog­ni­tive func­tions and vas­cu­lar demen­tia (VaD). Cardiovascular dis­ease may ­cause VaD ­from hypo­per­fu­sion of sus­cep­ti­ble ­brain are­as. CVD may wors­en degen­er­a­tive demen­tias ­such as Alzheimer dis­ease (AD). Currently, the glo­bal diag­nos­tic cat­e­go­ry for cog­ni­tive impair­ment of vas­cu­lar ori­gin is vas­cu­lar cog­ni­tive dis­or­der (VCD). VCD rang­es ­from vas­cu­lar cog­ni­tive impair­ment (VCI) to VaD. The ­term VCI is lim­it­ed to cas­es of cog­ni­tive impair­ment of vas­cu­lar eti­ol­o­gy, with­out demen­tia; VCI is equiv­a­lent to vas­cu­lar ­mild cog­ni­tive impair­ment (MCI). Risk fac­tors for VaD ­include age, hyper­ten­sion, dia­betes, smok­ing, car­di­o­vas­cu­lar dis­ease (cor­o­nary ­heart dis­ease, con­ges­tive ­heart fail­ure, periph­er­al vas­cu­lar dis­ease), atri­al fib­ril­la­tion, ­left ven­tric­u­lar hyper­tro­phy, hyper­hom­o­cys­tei­ne­mia, orthos­tat­ic hypo­ten­sion, car­diac arrhyth­mi­as, hyper­fib­ri­nog­e­ne­mia, ­sleep ­apnea, infec­tion, and ­high C-reac­tive pro­tein. Research on bio­mark­ers ­revealed ­increased CSF-NFL lev­els in VaD, where­as CSF-τ was nor­mal. CSF-TNF-α, ­VEGF, and TGF-β ­were ­increased in ­both AD and VaD. VaD ­shows low CSF ace­tyl­chol­i­nes­te­rase lev­els. This con­di­tion ­responds to ace­tyl­chol­i­nes­te­rase inhib­i­tors, con­firm­ing the cen­tral ­role of chol­i­ner­gic def­i­cit in its path­o­gen­e­sis. Evidence strong­ly sug­gests ­that con­trol of vas­cu­lar ­risk fac­tors, in par­tic­u­lar hyper­ten­sion, ­could pre­vent VaD.

inizio pagina

Publication History

Per citare questo articolo

Corresponding author e-mail