Multi-infarct dementia

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Multi-infarct dementia
ICD-10 F01.1
ICD-9 290.4
DiseasesDB 8393
MedlinePlus 000746
MeSH D015161

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2]

Overview

Multi-infarct dementia, also known as vascular dementia, is the second most common form of dementia after Alzheimer disease (AD) in the elderly (persons over 65 years of age). 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 described at the moment are: vascular 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, small vessel disease (which includes vascular dementia due to lacunar lesions and Binswanger's disease), and mixed Alzheimer's and vascular dementia.

Vascular lesions can be the result of diffuse cerebrovascular disease or focal lesions (or a combination of both, which is what is observed in the majority of cases). 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.

Etiology

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

Differential Diagnosis

Cause of dementia Clinical features Associated features Nature of progression Histopathological findings
Cognitive impairment
Recall Recollection Cue requirement for recall Infirngement of thoughts Semantic memory Procedural memory Working memory Awareness Attention Executive functioning issues Visuo-spatial skills
Alzheimer's disease +++

(Slow cognitive and functional decline with early loss of awareness)

+++ Not helpful +++ ++ - ++ +++ ++ ++ ++ Has the following clinical stages:
Lewy body dementia ++ - Helpful +++ + + +++ + +++ +++ +++
Frontotemporal lobar degeneration +/- - Helpful +++ + - +++ +++ ++ +++ -
  • Onset in young age
Vascular dementia + (Dysexecutive syndrome) - Helpful + + + ++ - ++ +++ +
  • Other medical conditions
  • Other mental disorders

Epidemiology and Demographics

Prevalence

The prevalence of major or mild vascular neurocognitive disorder is:

200 per 100,000 (0.2%) in the ages 65-70 years

16,000 per 100,000 (16%)in the ages 80 years and older.[17]

vascular dementia is the second most common cause 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% percent 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.

Risk Factors

Diagnosis

Several specific diagnostic criteria can be used to diagnose vascular dementia, including the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria, the International Classification of Diseases, Tenth Edition criteria, the National Institute of Neurological Disorders and Stroke-Association International pour la Recherché at L'Enseignement en Neurosciences (NINDS-AIREN) criteria,[18] the Alzheimer's Disease Diagnostic and Treatment Center criteria, and the Hachinski ischemic score.[19]

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

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 that their Alzheimer's disease counterparts in frontal lobe tasks such as verbal fluency. They also tend to exhibit more perseverative behaviour. 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, dysphasias and aphasias may be present.

Symptoms

The onset of multi-infarct dementia often goes unnoticed in the early stages, particularly if the strokes are minor. If the strokes are minor, symptoms caused by each stroke may include mild weakness in the limbs, slurred speech, dizziness and a slight impairment to the short-term memory, though these do not last for long.

However, the cumulative effects of these strokes will eventually result in noticeable symptoms being displayed. These symptoms include:

  • problems with recent memory
  • wandering or getting lost in familiar places
  • walking with rapid, shuffling steps
  • loss of bladder or bowel control
  • emotional lability
  • difficulty following instructions
  • problems handling money

Clinical presentation

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. However this pattern may not be observed in small vessel disease (Binswanger disease or vascular dementia due to small lacunar infarcts).

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 they very often are) 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.

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.

Investigations

The recommended investigations for cognitive impairment should be carried out, including a dementia screening blood test, chest X-Ray, CAT scan and EKG. The screening blood test should 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.

Diagnostic Criteria

DSM-V Diagnostic Criteria for Major or Mild Vascular Neurocognitive Disorder[17]

  • A.The criteria are met for major or mild neurocognitive disorder.

AND

  • B.The clinical features are consistent with a vascular etiology, as suggested by either of the following:
  • 1.Onset of the cognitive deficits is temporally related to one or more cerebrovascular events.
  • 2.Evidence for decline is prominent in complex attention (including processing speed) and frontal-executive function.

AND

  • C.There is evidence of the presence of cerebrovascular disease from history, physical examination, and/or neuroimaging considered sufficient to account for the neurocognitive

deficits.

AND

  • D.The symptoms are not better explained by another brain disease or systemic disorder.Probable vascular neurocognitive disorder is diagnosed if one of the following is present;otherwise possible vascular neurocognitive disorder should be diagnosed:
  • 1.Clinical criteria are supported by neuroimaging evidence of significant parenchymal injury attributed to cerebrovascular disease (neuroimaging-supported).
  • 2.The neurocognitive syndrome is temporally related to one or more documented cerebrovascular events.

3.Both clinical and genetic (e.g., cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) evidence of cerebrovascular disease is present.

Possible vascular neurocognitive disorder is diagnosed if the clinical criteria are met but neuroimaging is not available and the temporal relationship of the neurocognitive syndrome with one or more cerebrovascular events is not established.

Treatment

The aim of the management is the prevention of further cerebrovascular lesions. This includes administering antiplatelet drugs and controlling major vascular risk factors (hypertension, hypercholesterolemia, smoking and diabetes mellitus to mention a few).

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

Cholinesterase inhibitors have shown to be helpful in various randomised 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. Agents that may be useful include antidepressants, neuroleptics and mood-stabilizers. Electroconvulsive therapy may be indicated in extreme cases provided a medical contraindication does not exist.

Mortality/Morbidity

The 5-year survival rate is 39% for patients with vascular dementia compared with 75% for age-matched controls. Vascular dementia is associated with a higher mortality than 'Alzheimer's', presumably because of the excess in cardiovascular risk factors.

References

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  3. Hodges JR, Patterson K (1996). "Nonfluent progressive aphasia and semantic dementia: a comparative neuropsychological study". J Int Neuropsychol Soc. 2 (6): 511–24. PMID 9375155.
  4. Hodges JR, Patterson K, Oxbury S, Funnell E (1992). "Semantic dementia. Progressive fluent aphasia with temporal lobe atrophy". Brain. 115 ( Pt 6): 1783–806. PMID 1486461.
  5. "Dementia, Globalization and Contemporary Art".
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  8. Goldman JG, Williams-Gray C, Barker RA, Duda JE, Galvin JE (2014). "The spectrum of cognitive impairment in Lewy body diseases". Mov. Disord. 29 (5): 608–21. doi:10.1002/mds.25866. PMC 4126402. PMID 24757110.
  9. Metzler-Baddeley C (2007). "A review of cognitive impairments in dementia with Lewy bodies relative to Alzheimer's disease and Parkinson's disease with dementia". Cortex. 43 (5): 583–600. PMID 17715794.
  10. Uversky VN (2008). "Alpha-synuclein misfolding and neurodegenerative diseases". Curr. Protein Pept. Sci. 9 (5): 507–40. PMID 18855701.
  11. Bennett DA, Schneider JA, Wilson RS, Bienias JL, Arnold SE (2004). "Neurofibrillary tangles mediate the association of amyloid load with clinical Alzheimer disease and level of cognitive function". Arch. Neurol. 61 (3): 378–84. doi:10.1001/archneur.61.3.378. PMID 15023815.
  12. Brion JP (1998). "Neurofibrillary tangles and Alzheimer's disease". Eur. Neurol. 40 (3): 130–40. PMID 9748670.
  13. Lee JS, Jung NY, Jang YK, Kim HJ, Seo SW, Lee J, Kim YJ, Lee JH, Kim BC, Park KW, Yoon SJ, Jeong JH, Kim SY, Kim SH, Kim EJ, Park KC, Knopman DS, Na DL (2017). "Prognosis of Patients with Behavioral Variant Frontotemporal Dementia Who have Focal Versus Diffuse Frontal Atrophy". J Clin Neurol. 13 (3): 234–242. doi:10.3988/jcn.2017.13.3.234. PMC 5532319. PMID 28748674.
  14. Pao WC, Dickson DW, Crook JE, Finch NA, Rademakers R, Graff-Radford NR (2011). "Hippocampal sclerosis in the elderly: genetic and pathologic findings, some mimicking Alzheimer disease clinically". Alzheimer Dis Assoc Disord. 25 (4): 364–8. doi:10.1097/WAD.0b013e31820f8f50. PMC 3107353. PMID 21346515.
  15. Tsolaki M, Kokarida K, Iakovidou V, Stilopoulos E, Meimaris J, Kazis A (2001). "Extrapyramidal symptoms and signs in Alzheimer's disease: prevalence and correlation with the first symptom". Am J Alzheimers Dis Other Demen. 16 (5): 268–78. doi:10.1177/153331750101600512. PMID 11603162.
  16. McGuinness B, Barrett SL, Craig D, Lawson J, Passmore AP (2010). "Executive functioning in Alzheimer's disease and vascular dementia". Int J Geriatr Psychiatry. 25 (6): 562–8. doi:10.1002/gps.2375. PMID 19810010.
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See also

it:Demenza vascolare fi:Vaskulaarinen dementia



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