La Demenza Vascolare - GrG

La Demenza Vascolare 

Luca ROZZINI

Dementia is the clinical syndrome 

characterised by acquired losses of 

cognitive and emotional abilities severe 

enough to interfere with daily functioning 

and the quality of life. 

DS Geldmacher, PJ Whitehouse 

N Engl J Med, 335:330-336, 1996

I criteri diagnostici della demenza 

(DSM-IV) 

• Presenza di deficit cognitivi multipli caratterizzati da: 

1) Compromissione mnesica (deficit dell’abilità ad apprendere nuove 

informazioni o a richiamare informazioni precedentemente apprese)e 

almeno 

2) uno o più deficit cognitivi: afasia (disturbo del linguaggio); aprassia 

(incapacità ad eseguire attività motorie nonostante l’integrità della 

comprensione e della motricità); agnosia (incapacità a riconoscere o 

identificare oggetti in assenza di deficit sensoriali); deficit del pensiero 

astratto e della capacità critica 

• I deficit cognitivi interferiscono significativamente nel lavoro, nelle attività sociali, 

nelle relazioni con gli altri, e determinano un peggioramento significativo rispetto 

al precedente livello funzionale

The ICD-10 Classification of Mental and Behavioural Disorders 

World Health Organization, Geneva, 1992 

• Dementia is a syndrome due to disease of the brain, usually of a chronic or progressive nature, in 

which there is disturbance of multiple higher cortical functions, including memory, thinking, 

orientation, comprehension, calculation, learning capacity, language, and judgment. 

Consciousness is not clouded. Impairments of cognitive function are commonly accompanied, and 

occasionally preceded, by deterioration in emotional control, social behaviour, or motivation. This 

syndrome occurs in Alzheimer's disease, in cerebrovascular disease, and in other conditions primarily 

or secondarily affecting the brain. 

• Dementia produces an appreciable decline in intellectual functioning, and usually some 

interference with personal activities of daily living, such as washing, dressing, eating, 

personal hygiene, excretory and toilet activities. How such a decline manifests itself will depend 

largely on the social and cultural setting in which the patient lives. Changes in role performance, such 

as lowered ability to keep or find a job, should not be used as criteria of dementia because of the 

large cross-cultural differences that exist in what is appropriate, and because there may be frequent, 

externally imposed changes in the availability of work within

The criteria for MCI are those previously proposed by Petersen et al. 

(i) presence of a subjective memory complaint; 

(ii) Preserved general intellectual functioning (as estimated in this study by performance on 

a vocabulary test); 

(iii) demonstration of a memory impairment by cognitive testing; 

(iv) intact ability to perform activities of daily living; 

(v) absence of dementia.

(i) presence of a cognitive complaint from either the subject and/or a family 

member; 

(ii) absence of dementia; 

(iii) change from normal functioning; 

(iv) decline in any area of cognitive functioning; 

(v) preserved overall general functioning but possibly with increasing difficulty in 

the performance of activities of daily living.

La Demenza Vascolare

…In the Italian study VaD was more prevalent than 

AD in subjects 70 years old and older. 

Rocca et al.

DSM-III criteria for the diagnosis of multi-infarcts 

dementia 

A. Demenza 

B. Deteroramento a gradini (cioè non uniformemente 

progressivo) con distribuzione dei deficit a scacchiera 

(cioè con interessamento di certe funzioni ma non di altre) 

all’inizio del decorso 

C. Sintomi e segni neurologici focali (per esempio aumento 

dei riflessi tendinei profondi, Babinski, paralisi 

pseudobulbare, alterazioni della marcia, debolezza di un 

arto ecc. ) 

D. Dimostrazione, fondata sull’anamnesi, sull’esame clinico, 

o sugli esami di laboratorio, di una vasculopatia cerebrale 

eziologicamente correlata al disturbo.

DSM-IV-R criteria for the diagnosis of vascular 

dementia 

A. The development of multiple cognitive deficits manifested by 

both: 

1. Memory impairment (impaired ability to learn new information or to recall 

previously learned information) 

2. One or more of the following cognitive disturbances: 

(a) aphasia (language disturbance) 

(b) apraxia (impaired ability to carry out motor activities despite intact 

motor function) 

(c) agnosia (failure to recognize or identify objects despite intact sensory 

function) 

(d) disturbance in executive functioning (i.e., planning, organizing, 

sequencing, abstracting)

DSM-IV criteria for the diagnosis of vascular 

dementia 

B. The cognitive deficits in criteria A1 and A2 each cause significant 

impairment in social or occupational functioning and represent a 

significant decline from a previous level of functioning. 

C. Focal neurological signs and symptoms (e.g., exageration of deep 

tendon reflexes, extensor plantar response, psuedobulbar palsy, gait 

abnormalities, weakness of an extremity) or laboratory evidence 

indicative of cerebrovascular disease (e.g., multiple infarctions involving 

cortex and underlyig white matter) that are judged to be etiologically 

related to the disturbance. 

D. The deficits do not ocurr exclusively during the course of a delirium.

Criteri OMS per la diagnosi di demenza vascolare 

(Classificazione Internazionale delle Malattie, ICD-10) 

• deficit della memoria soprattutto quella a breve termine presente da 

almeno sei mesi; 

• capacità di giudizio e ideazione relativamente conservate; 

• relativa conservazione della personalità e dello stato di coscienza; 

• storia di ipertensione arteriosa; 

• danno cerebrale focale (in particolare, nelle forme sottocorticali, a livello 

della sostanza bianca sottocorticale degli emisferi cerebrali)

Dementia syndrome 

It was decided to adopt here the definition of dementia from the 10th revision of 

The Neurological Adaptation of the International Classification of Diseases 

(ICD-10 NA). 

Diagnosis of dementia requires the presence of a decline in memory and 

intellectual abilities that causes impaired functioning in daily living. 

“Impaired functioning in daily living” was accepted as a criterion for 

epidemiologic studies of VaD because it would ensure that the changes are more 

than incidental and would increase specificity. Chui et al. also included 

“interference with the conduct of the patient’s customary affairs of life” as a 

requirement for the diagnosis of ischemic VaD. 

The impairment should be due to cognitive deficits and not to physical handicaps 

produced by stroke.

Dementia syndrome 

For the diagnosis of VaD, cognitive decline should 

be demonstrated by loss of memory and deficits 

in at least two other domains, including 

orientation, attention, language-verbal skills, 

visuospatial abilities, calculations, executive 

functions, motor control, praxis, abstraction, and 

judgment.

The criteria for the clinical diagnosis of 

probable vascular dementia include all 

of the following:

1. Dementia defined by cognitive decline from a 

previously higher level of functioning and manifested by 

impairment of memory and of two or more cognitive 

domains (orientation, attention, language,visuospatial 

functions, executive functions,motor control, and praxis), 

preferably established by clinical examination and 

documented by neuropsychological testing; deficits should be 

severe enough to interfere with activities of daily living not due 

to physical effects of stroke alone.

2. Cerebrovascular disease, defined by the presence of focal 

signs on neurologic examination, such as hemiparesis, lower 

facial weakness, Babinski sign, sensory deficit, hemianopia, and 

dysarthria consistent with stroke (with or without history of stroke), 

and 

evidence of relevant CVD by brain imaging (CT or MRI) including 

multiple large-vessel infarcts or a single strategically placed infarct 

(angular gyrus, thalamus, basal forebrain, or PCA or ACA 

territories), as well as multiple basal ganglia and white matter 

lacunes or extensive periventricular white matter lesions, or 

combinations thereof.

3. A relationship between the above two disorders, 

manifested or inferred by the presence of one or 

more of the following: 

(a) onset of dementia within 3 months following a 

recognized stroke; 

(b) abrupt deterioration in cognitive functions; or 

fluctuating, stepwise progression of cognitive 

deficits.

Clinical features consistent with the diagnosis of probable vascular 

dementia include the following: 

(a) Early presence of a gait disturbance (small step gait or marche a 

petits pas, or magnetic, apraxic-ataxic or parkinsonian gait); 

(b) history of unsteadiness and frequent, unprovoked falls; 

(c) early urinary frequency, urgency, and other urinary symptoms 

not explained by urologic disease; 

(d) pseudobulbar palsy; and 

(e) personality and mood changes, abulia, depression, emotional 

incontinence, or other subcortical deficits including psychomotor 

retardation and abnormal executive function.

Clinical diagnosis of possible vascular dementia 

may be made in the presence of dementia with 

focal neurologic signs in patients in whom brain 

imaging studies to confirm definite CVD are 

missing; or in the absence of clear temporal 

relationship between dementia and stroke; or in 

patients with subtle onset and variable course 

(plateau or improvement) of cognitive deficits and 

evidence of relevant CVD.

Dementia is a deterioration from a known or estimated prior level 

of intellectual function sufficient to interfere broadly with the 

conduct of the patient’s customary affairs of life, which is not 

isolated to a single narrow category of intellectual performance, 

and which is independent of level of consciousness. 

This deterioration should be supported by historical evidence and 

documented by either bedside mental status testing or ideally by 

more detailed neuropsychological examination, using tests that 

are quantifiable, reproducible, and for which normative data are 

available.

Probable IVD 

A. The criteria for the clinical diagnosis of PROBABLE IVD include ALL of 

the following: 

1. Dementia; 

2. Evidence of two or more ischemic strokes by history, neurologic signs, 

and/or neuroimagingstudies (CT or T,-weighted MRI); 

or 

Occurrence of a single stroke with a clearly documented temporal 

relationship to the onset ofdementia; 

3. Evidence of at least one infarct outside the cerebellum by CT or TIweighted 

MRI.

Probable IVD 

B. The diagnosis of PROBABLE IVD is supported by 

1. Evidence of multiple infarcts in brain regions known to 

affect cognition; 

2. A history of multiple transient ischemic attacks; 

3. History of vascular risk factors (eg, hypertension,heart 

disease, diabetes mellitus); 

4. Elevated Hachinski Ischemia Scale (original or modified 

version).

C. Clinical features that are thought to be associated with IVD, but await 

further research, include 

1. Relatively early appearance of gait disturbance and urinary 

incontinence; 

2. Periventricular and deep white matter changes on T,-weighted MRI that 

are excessive for age; 

3. Focal changes in electrophysiologx studies (eg, EEG, evoked 

potentials) or physiologic neuroimaging studies (eg, SPECT, PET, NMR 

spectroscopy). 

D. Other clinical features that do not constitute strong evidence either for 

or against a diagnosis of PROBABLE IVD include 

1. Periods of slowly progressive symptoms; 

2. Illusions, psychosis, hallucinations, delusions; 

3. Seizures.

Possible IVD 

A clinical diagnosis of POSSIBLE IVD may be made when there is 

1. Dementia; and one or more of the following: 

2a. A history or evidence of a single stroke (but not multiple strokes) without a 

clearly documented temporal relationship to the onset of dementia; 

Or 

2b. Binswanger’s syndrome (without multiple strokes) that includes all of the 

following: 

i. Early-onset urinary incontinence not explained by urologic disease, or 

gait disturbance (eg, parkinsonian, magnetic, apraxic, or “senile” gait) not 

explained by peripheral cause, 

ii. Vascular risk factors, and 

iii. Extensive white matter changes on neuroimaging.

Conclusions—Current criteria of VaD identify different frequencies and clusters of patients 

and are not interchangeable. Optimally, prospective studies with clinicopathological 

correlation could identify new criteria. Meanwhile, focus on more homogeneous subtypes 

(eg, small-vessel subcortical VaD) and detailed neuroimaging criteria could improve the 

diagnostics.

Conclusions: None of the clinical criteria for VaD identified the same group 

of subjects. The diagnosis of vascular dementia is difficult in epidemiologic 

studies because poststroke dementia can be due to Alzheimer disease (AD) 

and evidence of vascular disease can be found in the MRI of dementia cases 

without clinical strokes. Whether the clinical progression is related to AD 

pathology or vascular disease is difficult to establish.

Clinicopathological Validation Study of Four Sets 

of Clinical Criteria for Vascular Dementia 

Gold et al. 

Am J Psychiatry 2002; 159:82–87 

Conclusions: Clinical criteria for vascular dementia are not 

interchangeable. The ADDTC criteria for possible vascular dementia 

are the most sensitive for the detection of vascular dementia; however, 

the DSM-IV criteria for vascular dementia and the NINDS-AIREN 

criteria for possible vascular dementia may be more effective in 

excluding mixed dementia. Given their inability to detect the vast 

majority of cases of vascular dementia, the ICD-10 criteria for vascular 

dementia and the ADDTC and NINDS-AIREN criteria for probable 

vascular dementia should be revised.

…about a quarter of 3660 participants aged 65 or older had one or more 

lacunes on magnetic resonance imaging (MRI)… 

…According to several population-based studies, the prevalence of 

cerebral white-matter hyperintensities on MRI in elderly people is in the 

range of 62–95%...

Subcortical ischaemic vascular dementia 

Gustavo C Román, Timo Erkinjuntti, Anders Wallin, Leonardo Pantoni, and Helena C Chui 

Lancet Neurology 2002;1:426-436



The criteria for the clinical diagnosis include all of the following: 

Cognitive syndrome 

Dysexecutive syndrome —impairment in goal formulation, 

initiation,planning, organising, sequencing, executing, set-shifting 

and maintenance, abstracting 

Memory deficit —impaired recall, relatively intact recognition, 

moderate forgetfulness, and benefit from cues; may be mild 

Deterioration from a previous higher level of functioning, interference 

with complex (executive) occupational and social activities not 

due to physical effects of cerebrovascular disease alone



Cerebrovascular disease 

Evidence of relevant cerebrovascular disease by brain imaging 

Presence or history of neurological signs consistent with subcortical 

cerebrovascular disease (such as hemiparesis, lower facial 

weakness, Babinski sign, sensory deficit, dysarthria, gait disorder, 

and extrapyramidal signs)



Clinical features supporting the diagnosis of SIVD include the following: 

-Episodes of mild upper motor-neuron involvement such as drift, reflex 

asymmetry, and incoordination 

-Early presence of a gait disturbance (small-step gait or marche à petits pas 

magnetic, apraxic-ataxic, or Parkinsonian gait) 

-History of unsteadiness and frequent, unprovoked falls 

-Early urinary frequency, urgency, and other urinary symptoms not explained 

by urological disease 

-Dysarthria, dysphagia, extrapyramidal signs (hypokinesia, rigidity) 

-Behavioural and psychological symptoms such as depression, personality 

change, emotional incontinence, and psychomotor retardation



Features that make the diagnosis of SIVD uncertain or unlikely 

include: 

Early onset of memory deficit and progressive worsening of memory 

and other cognitive cortical functions, such as language 

(transcortical sensory aphasia), motor skills (apraxia), and perception 

(agnosia), in the absence of corresponding focal lesions on brain 

imaging. 

Absence of relevant cerebrovascular disease lesions on brain CT 

scan or MRI.



CT 

Extensive periventricular and deep white-matter lesions: patchy or diffuse symmetrical areas of low 

attenuation, of intermediate density between normal white matter and CSF, with ill-defined margins 

extending to the centrum semiovale, and at least one lacunar infarct 

MRI 

Binswanger-type white matter lesions: hyperintensities extending into periventricular and deep white 

matter; extending caps (>10 mm as measured parallel to ventricle) or irregular halo (>10 mm with broad, 

irregular margins and extending into deep white matter); and diffusely confluent hyperintensities (>25 

mm, irregular shape) or extensive white matter change (diffuse hyperintensity without focal lesions); and 

lacune(s) in the deep grey matter 

OR 

Lacunar cases: multiple lacunes (>5) in the deep grey matter and at least moderate white-matter 

lesions; extending caps, irregular halo, diffusely confluent hyperintensities, or extensive white-matter 

changes 

AND 

Absence of haemorrhages, cortical and/or corticosubcortical non-lacunar territorial infarcts and 

watershed infarcts; signs of normal pressure hydrocephalus; and specific causes of white-matter lesions 

(eg, multiple sclerosis, sarcoidosis, and brain irradiation)

Neuropathology Lessons in Vascular Dementia 

Helena Chui, MD 

(Alzheimer Dis Assoc Disord 2005;19:45–52) 

The hippocampus is the key enabler of episodic memory. 

Hippocampal sclerosis (HS) refers to selective neuronal loss in the absence of 

cystic cavitation or neurofibrillary degeneration. HS is most prominent in the CA-1 

sector of the hippocampus, extending into the subiculum. It has been reported to 

be a common neuropathologic finding in persons with dementia who are very old 

(80+ yrs),9 among 12% of elderly persons with dementia10 or with cardiac 

disease.11 The pathogenesis of HS is still disputed, but systemic hypoxiaischemia 

12 and ischemia due to intrinsic cerebrovascular disease are hypothesized, as CA- 

1 neurons have a relatively high metabolic rate but relatively poor vascular supply

Conclusions—Our findings suggest that the presence and the 

progression of WML are associated with progression of Medial 

temporal lobe atrophy in AD. WML may be a predictor of the course 

of the disease and a potential treatment target in AD.

Caratteristiche socio demografiche di un campione di 442 pazienti 

consecutivamente valutati presso UVA Spedali Civili di Brescia 

SIVD 

N=71 

AD 

N=371 

Media DS % Media DS 

Età 78,6 7,0 74,9 7,2 

Sesso 47 71 

Scolarità 6,2 3,1 6,4 3,4 

CDR 1,1 0,8 1,8 15,9 

MMSE 22,0 5,6 21,0 4,4 

ADAS 12,1 6,9 17,4 9,2 

GDS 5,3 3,7 4,2 3,2 

IADL 4,3 2,3 5,1 2,2 

BADL 5,0 1,4 5,3 1,1 

NPI 16,8 14,9 16,4 12,5 

APOE 4 39 53 

Ipertensione 75 47 

Diabete 17 11 

Colesterolo 225,8 41,8 208,7 45,7 

Albumina gr 4,2 0,4 4,2 0,4

Although small, the mechanism of action of cholinesterase inhibitors in vascular 

dementia is still worth investigating. Vascular lesions, particularly 

those that affect subcortical areas, might disrupt the cholinergic pathways to the 

cortex, and this might explain why cholinesterase inhibitors are also eff ective in 

vascular disease. 

Amos D Korczyn 

The Lancet Neurology 6 September 2007

La Demenza Vascolare - GrG

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