Vascular dementia

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Vascular dementia
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  (Redirected from Multi-infarct dementia)
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Vascular dementia
Classification and external resources
eMedicinemed/3150 neuro/227

Vascular dementia or "multi-infarct dementia" is dementia caused by problems in the supply of blood to the brain, typically by a series of minor strokes. Vascular dementia is the second most common form of dementia after Alzheimer's disease (AD) in older adults.[1][2] Multi-infarct dementia (MID) is thought to be an irreversible form of dementia, and its onset is caused by a number of small strokes or, sometimes, one large stroke preceded or followed by other smaller strokes.[3] The term refers to a group of syndromes caused by different mechanisms all resulting in vascular lesions in the brain. Early detection and accurate diagnosis are important, as vascular dementia is at least partially preventable.

The main subtypes of this disease are: mild cognitive impairment, multi-infarct dementia, vascular dementia due to a strategic single infarct (affecting the thalamus, the anterior cerebral artery, the parietal lobes or the cingulate gyrus), vascular dementia due to hemorrhagic lesions, and mixed Alzheimer's and vascular dementia.

Vascular lesions can be the result of diffuse cerebrovascular disease, such as small vessel disease, or focal lesions; usually both. Mixed dementia is diagnosed when patients have evidence of AD and cerebrovascular disease, either clinically or based on neuroimaging evidence of ischemic lesions. In fact vascular dementia and Alzheimer's disease often coexist, especially in older patients with dementia.

MID is sometimes triggered by cerebral amyloid angiopathy, which involves accumulation of beta amyloid plaques in the walls of the cerebral arteries, leading to breakdown and rupture of the vessels. Since amyloid plaques are a characteristic feature of AD, vascular dementia may occur as a side effect of it. However, cerebral amyloid angiopathy can also appear in people with no prior dementia condition and a small amount of beta amyloid plaques are often present in cognitively normal older persons.

Signs and symptoms[edit]

Multi-infarct dementia and Alzheimer's disease, despite the fact that the two organic disorders have different causes, can be almost impossible to tell apart clinically and are often misdiagnosed.[4] Patients suffering from vascular dementia present with cognitive impairment, acutely or subacutely, after an acute cerebrovascular event. After the onset a stepwise progression is typical.

In small vessel disease the incidence peaks between the 4th and the 7th decades of life and 80% will have a history of hypertension. Patients develop progressive cognitive, motor and behavioral signs and symptoms. A significant proportion of them also develop affective symptoms. These changes occur over a period of 5–10 years. If the frontal lobes are affected, which is often the case, patients may present as apathetic or abulic. This is often accompanied by problems with attention, orientation and urinary incontinence.

As already stated, small vessel disease and focal lesions often overlap, so these two patterns may be evident in the same individual concurrently. Although atheroma of the major cerebral arteries is typical in MID, the condition mainly affects smaller vessels and arterioles.

Rare genetic disorders which result in vascular lesions in the brain have other patterns of presentation. As a rule of thumb they tend to present earlier in life and have a more aggressive course. In addition, infectious disorders such as syphilis lead to artery damage and strokes along with bacterial inflammation of the brain.


Several specific diagnostic criteria can be used to diagnose vascular dementia,[5] including the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria, the International Classification of Diseases, Tenth Edition (ICD-10) criteria, the National Institute of Neurological Disorders and Stroke- Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN) criteria,[6] the Alzheimer's Disease Diagnostic and Treatment Center criteria, and the Hachinski ischemic score.[7]

Lateralizing signs such as hemiparesis, bradykinesia, hyperreflexia, extensor plantar reflexes, ataxia, pseudobulbar palsy, and gait and swallowing difficulties may be observed.

Signs may include cognitive decline from a previously higher level of functioning; impairment of memory and two or more other cognitive areas; sufficient severity as to interfere with activities of daily living; cerebrovascular disease is present, defined by the presence of focal neurologic signs (e.g., hemiparesis, sensory deficit, hemianopsia, Babinski sign, etc.); evidence of relevant features consistent with cerebrovascular disease on brain imaging (CT or MRI).[8]

In terms of cognitive testing patients have patchy deficits. They tend to have better free recall and fewer recall intrusions compared with patients with Alzheimer's disease. As small vessel disease often affects the frontal lobes, apathy early in the disease is more suggestive of vascular dementia because it usually occurs in the later stages of Alzheimer's. Consequently patients with vascular dementia perform worse than their Alzheimer's disease counterparts in frontal lobe tasks such as verbal fluency. They also tend to exhibit more perseverative behavior. They may also present with general slowing of processing ability, difficulty shifting sets and impairment in abstract thinking. In the more severe patients, or those patients affected by strategic infarcts in the Wernicke or Broca areas, dysarthrias and aphasias may be present.

The recommended investigations for cognitive impairment should be carried out, including a dementia screening blood test, chest X-Ray, ECG, and some type of neuroimaging, preferably a scan with a functional or metabolic sensitivity beyond simple CT or MRI. When available as a diagnostic tool, single photon emission computed tomography (SPECT) and positron emission tomography (PET) neuroimaging may be used to confirm a diagnosis of multi-infarct dementia in conjunction with evaluations involving mental status examination.[9] In a person already having dementia, SPECT appears to be superior in differentiating multi-infarct dementia from Alzheimer's disease, as compared with the usual attempts to differentiate the dementing processes by employing mental testing and medical history analysis.[10] Advances have led to the proposal of new diagnostic criteria.[11][12]

The screening blood test would typically include full blood count, liver function tests, thyroid function tests, lipid profile, erythrocyte sedimentation rate, C reactive protein, syphilis serology, calcium serum level, fasting glucose, urea and electrolytes, vitamin B-12, folate. In selected patients HIV serology and autoantibody testing may be done.

Pathology and necropsy[edit]

Gross examination of the brain may reveal noticeable lesions and artery damage. Accumulation of various substances such as lipid deposits and clotted blood appear on microscopic views. The white matter is most affected, with noticeable atrophy and tissue loss, in addition to calcification of the arteries. Microinfarcts may also be present in the gray matter (cerebral cortex), sometimes in large numbers. On rare occasion, infarcts in the hippocampus or thalamus are the cause of dementia.[13]


Risk factors for vascular dementia include age, hypertension, smoking, hypercholesterolemia, diabetes mellitus, cardiovascular disease, and cerebrovascular disease.

Other risk factors include geographic origin, genetic predisposition, and prior strokes. Further strokes must be prevented through surgical or medical therapy to lessen the chance of developing Multi-Infarct Dementia.[14]


The goal of the management is the prevention of further cerebrovascular lesions. This includes administering antiplatelet drugs and controlling major vascular risk factors such as hypertension, hypercholesterolemia, smoking and diabetes mellitus.

The general management of dementia includes referral to community services, judgment and decision-making regarding legal and ethical issues (e.g., driving, capacity, advance directives), and consideration of caregiver stress.

Cholinesterase inhibitors such as galantamine have shown to be helpful in various randomized controlled trials. However their use is not licensed yet for this indication.

Behavioral and affective symptoms are particularly important in this patient group and deserve special consideration. These problems, if they develop, tend to be resistant to conventional psychopharmacological treatment and in many cases lead to hospital admission and placement in permanent care.


The 5-year survival rate is 39% for patients with vascular dementia compared with 75% for age-matched controls. Unlike Alzheimer's Disease, which merely weakens the victim to the point where he succumbs to bacterial infections like pneumonia, vascular dementia is a direct cause of death due to the possibility of a fatal interruption in the brain's blood supply.

The prognosis for MID is usually not very promising. Symptoms may begin suddenly with the onset of the disease and steadily become more prevalent with each progressive small stroke. Even though it may seem that people with MID improve over time, their condition often steadily declines after ensuing silent strokes. A rapidly deteriorating condition may lead to death from a stroke, heart disease, or infection.[15]


Vascular dementia is the second most common type of dementia in the United States and Europe in the elderly, but it is the most common form in some parts of Asia. The prevalence of the illness is 1.5% in Western countries and approximately 2.2% in Japan. It accounts for 50% of all dementias in Japan, 20% to 40% in Europe and 15% in Latin America. The incidence of dementia is 9 times higher in patients who have had a stroke than in controls. 25% of stroke patients develop new-onset dementia within 1 year of their stroke. The relative risk of incident dementia is 5.5% within 4 years of suffering a stroke.

One study found that in the United States specifically, the prevalence of vascular dementia in all individuals over the age of 71 is 2.43%, and another found that the prevalence of the dementias doubles with every 5.1 years of age.[16][17]

See also[edit]


  1. ^ Battistin L, Cagnin A (December 2010). "Vascular cognitive disorder. A biological and clinical overview". Neurochem. Res. 35 (12): 1933–8. doi:10.1007/s11064-010-0346-5. PMID 21127967. 
  2. ^ "Vascular Dementia: A Resource List". 
  3. ^ Antai-Otong, D. 2008. Psychiatric Nursing: Biological and Behavioral Concepts. 2nd ed. Canada: Thompson Delmar Learning.
  4. ^ Marks, D. and Sykes, C. 2000. Dealing with Dementia: Recent European Research. London: Middlesex University Press.
  5. ^ Wetterling T, Kanitz RD, Borgis KJ (January 1996). "Comparison of different diagnostic criteria for vascular dementia (ADDTC, DSM-IV, ICD-10, NINDS-AIREN)". Stroke 27 (1): 30–6. doi:10.1161/01.str.27.1.30. PMID 8553399. 
  6. ^ Tang W, Chan S, Chiu H, Ungvari G, Wong K, Kwok T, Mok V, Wong K, Richards P, Ahuja A (2004). "Impact of applying NINDS-AIREN criteria of probable vascular dementia to clinical and radiological characteristics of a stroke cohort with dementia". Cerebrovasc. Dis. 18 (2): 98–103. doi:10.1159/000079256. PMID 15218273. 
  7. ^ Pantoni L, Inzitari D (1993). "Hachinski's ischemic score and the diagnosis of vascular dementia: a review". Italian journal of neurological sciences 14 (7): 539–46. doi:10.1007/BF02339212. PMID 8282525. 
  8. ^ . "Dementia associated with depression". Encyclopedia of the Human Brain. Oxford: Elsevier Science & Technology, 2002. Credo Reference. 19 May 2010. Web. 20 Sept. 2012. <>.
  9. ^ Bonte FJ, Harris TS, Hynan LS, Bigio EH, White CL. Tc-99m HMPAO SPECT in the differential diagnosis of the dementias with histopathologic confirmation. Clin Nucl Med. 2006;31(7):376–8. doi:10.1097/01.rlu.0000222736.81365.63. PMID 16785801.
  10. ^ Dougall NJ, Bruggink S, Ebmeier KP. Systematic review of the diagnostic accuracy of 99mTc-HMPAO-SPECT in dementia. Am J Geriatr Psychiatry. 2004;12(6):554–70. doi:10.1176/appi.ajgp.12.6.554. PMID 15545324.
  11. ^ Waldemar G. Recommendations for the diagnosis and management of Alzheimer's disease and other disorders associated with dementia: EFNS guideline. Eur J Neurol. 2007;14(1):e1–26. doi:10.1111/j.1468-1331.2006.01605.x. PMID 17222085.
  12. ^ From NINCDS-ADRDA Alzheimer's Criteria: Dubois B, Feldman HH, Jacova C, et al. (2007). "Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDS-ADRDA criteria". Lancet Neurol 6 (8): 734–46. doi:10.1016/S1474-4422(07)70178-3. PMID 17616482. 
  13. ^
  14. ^ Arvanitakis, Zoe. "Dementia And Vascular Disease". 
  15. ^ Office of Communications and Public Liaison. "NINDS Multi-Infarct Dementia Information Page". Retrieved 6 December 2011. 
  16. ^ Plassman, B.L.; Langa, K. M.; Fisher, G. G.; Heeringa, S. G.; Weir, D. R.; Ofstedal, M. B.; Burke, J. R.; Hurd, M. D.; Potter, G. G.; Rodgers, W. L.; Steffens, D. C.; Willis, R. J.; Wallace, R. B. (2007). "Prevalence of dementia in the United States: The aging, demographics, and memory study.". Neuroepidemiology 29 (1-2): 125–132. doi:10.1159/000109998. Retrieved 17 December 2012. 
  17. ^ Jorm, A.F.; Korten, A. E.; Henderson, A. S. (1987). "The prevalence of dementia: A quantitative integration of the literature.". Acta Psychiatrica Scandinavica 76 (5): 465–479. doi:10.1111/j.1600-0447.1987.tb02906.x. Retrieved 17 December 2012. 

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