Medicine:Vascular dementia

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Short description: Dementia due to the brain's blood supply
Vascular dementia
Other namesDementia due to cerebrovascular disease [1]
Vascular cognitive impairment
SymptomsCognitive impairment

Vascular dementia (VaD) is dementia caused by problems in the blood supply to the brain, resulting from a cerebrovascular disease. Restricted blood supply (ischemia) leads to cell and tissue death in the affected region, known as an infarct. The three types of vascular dementia are subcortical vascular dementia, multi-infarct dementia, and stroke related dementia.[2] Subcortical vascular dementia is brought about by damage to the small blood vessels in the brain. Multi-infarct dementia is brought about by a series of mini-strokes where many regions have been affected. The third type is stroke related where more serious damage may result.[2] Such damage leads to varying levels of cognitive decline. When caused by mini-strokes, the decline in cognition is gradual.[3] When due to a stroke, the cognitive decline can be traced back to the event.[4]

ICD-11 lists vascular dementia as dementia due to cerebrovascular disease.[1] DSM-5 lists vascular dementia as either major or mild vascular neurocognitive disorder.[5]

Signs and symptoms

Differentiating dementia syndromes can be challenging, due to the frequently overlapping clinical features and related underlying pathology. Mixed dementia, involving two types of dementia can occur, in particular, Alzheimer's disease often co-occurs with vascular dementia.[6]

People with vascular dementia present with progressive cognitive impairment, acutely or sub-acutely as in mild cognitive impairment, frequently step-wise, after multiple cerebrovascular events (strokes). Some people may appear to improve between events and decline after further silent strokes. A rapidly deteriorating condition may lead to death from a stroke, heart disease, or infection.[7]

The disease is described as both a mental and behavioural disorder within the ICD-11.[8] Signs and symptoms are cognitive, motor, behavioral, and for a significant proportion of patients, also affective. These changes typically occur over a period of 5–10 years. Signs are typically the same as in other dementias, but mainly include cognitive decline and memory impairment of sufficient severity as to interfere with activities of daily living, sometimes with presence of focal neurologic signs, and evidence of features consistent with cerebrovascular disease on brain imaging (CT or MRI).[9] The neurologic signs localizing to certain areas of the brain that can be observed are hemiparesis, bradykinesia, hyperreflexia, extensor plantar reflexes, ataxia, pseudobulbar palsy, as well as gait problems and swallowing difficulties. People have patchy deficits in terms of cognitive testing. They tend to have better free recall and fewer recall intrusions when compared with patients with Alzheimer's disease.[10] In the more severely affected patients, or patients affected by infarcts in Wernicke's or Broca's areas, specific problems with speaking called dysarthria and aphasias may be present.[citation needed]

In small vessel disease, the frontal lobes are often affected. Consequently, patients with vascular dementia tend to perform worse than their Alzheimer's disease counterparts in frontal lobe tasks, such as verbal fluency, and may present with frontal lobe problems: apathy, abulia (lack of will or initiative), problems with attention, orientation, and urinary incontinence. They tend to exhibit more perseverative behavior. VaD patients may also present with general slowing of processing ability, difficulty shifting sets, and impairment in abstract thinking. Apathy early in the disease is more suggestive of vascular dementia.[citation needed]

Rare genetic disorders that cause vascular lesions in the brain have other presentation patterns. As a rule, they tend to occur earlier in life and have a more aggressive course. In addition, infectious disorders, such as syphilis, can cause arterial damage, strokes, and bacterial inflammation of the brain.[11]

Causes

Vascular dementia can be caused by ischemic or hemorrhagic infarcts affecting multiple brain areas, including the anterior cerebral artery territory, the parietal lobes, or the cingulate gyrus. On rare occasion, infarcts in the hippocampus or thalamus are the cause of dementia.[12] A history of stroke increases the risk of developing dementia by around 70%, and recent stroke increases the risk by around 120%.[13] Brain vascular lesions can also be the result of diffuse cerebrovascular disease, such as small vessel disease.[citation needed]

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.[14]

Vascular dementia can sometimes be 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 Alzheimer's disease, vascular dementia may occur as a consequence. Cerebral amyloid angiopathy can, however, appear in people with no prior dementia condition. Amyloid beta accumulation is often present in cognitively normal elderly people.[15][16]

Two reviews of 2018 and 2019 found a potential association between celiac disease and vascular dementia.[17][18]

Diagnosis

Several specific diagnostic criteria can be used to diagnose vascular dementia,[19] 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 criteria, Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN) criteria,[20] the Alzheimer's Disease Diagnostic and Treatment Center criteria, and the Hachinski Ischemic Score (after Vladimir Hachinski).[21]

The recommended investigations for cognitive impairment include: blood tests (for anemia, vitamin deficiency, thyrotoxicosis, infection, etc.), chest X-Ray, ECG, and neuroimaging, preferably a scan with a functional or metabolic sensitivity beyond a 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.[22] In a person already having dementia, SPECT appears to be superior in differentiating multi-infarct dementia from Alzheimer's disease, compared to the usual mental testing and medical history analysis.[23] Advances have led to the proposal of new diagnostic criteria.[24][25]

The screening blood tests 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, electrolytes, vitamin B-12, and folate. In selected patients, HIV serology and certain autoantibody testing may be done.[citation needed]

Mixed dementia is diagnosed when people have evidence of Alzheimer's disease and cerebrovascular disease, either clinically or based on neuro-imaging evidence of ischemic lesions.[26]

Pathology

Gross examination of the brain may reveal noticeable lesions and damage to blood vessels. Accumulation of various substances such as lipid deposits and clotted blood appear on microscopic views. The white matter is most affected, with noticeable atrophy (tissue loss), in addition to calcification of the arteries.[27] Microinfarcts may also be present in the gray matter (cerebral cortex), sometimes in large numbers. Although atheroma of the major cerebral arteries is typical in vascular dementia, smaller vessels and arterioles are mainly affected.[citation needed]

Prevention

Early detection and accurate diagnosis are important,[28] as vascular dementia is at least partially preventable. Ischemic changes in the brain are irreversible, but the patient with vascular dementia can demonstrate periods of stability or even mild improvement.[29] Since stroke is an essential part of vascular dementia,[13] the goal is to prevent new strokes. This is attempted through reduction of stroke risk factors, such as high blood pressure, high blood lipid levels, atrial fibrillation, or diabetes mellitus. Meta-analyses have found that medications for high blood pressure are effective at prevention of pre-stroke dementia, which means that high blood pressure treatment should be started early.[30] These medications include angiotensin converting enzyme inhibitors, diuretics, calcium channel blockers, sympathetic nerve inhibitors, angiotensin II receptor antagonists or adrenergic antagonists. Elevated lipid levels, including HDL, were found to increase risk of vascular dementia. However, six large recent reviews showed that therapy with statin drugs was ineffective in treatment or prevention of this dementia.[30][31] Aspirin is a medication that is commonly prescribed for prevention of strokes and heart attacks; it is also frequently given to patients with dementia. However, its efficacy in slowing progression of dementia or improving cognition has not been supported by studies.[30][32] Smoking cessation and Mediterranean diet have not been found to help patients with cognitive impairment; physical activity was consistently the most effective method of preventing cognitive decline.[30]

Treatment

Currently, there are medications that have been approved specifically for prevention or treatment of vascular dementia. The use of medications for treatment of Alzheimer's dementia, such as cholinesterase inhibitors and memantine, has shown small[quantify] improvement of cognition in vascular dementia. This is most likely due to the drugs' actions on co-existing AD-related pathology. Multiple studies found a small[quantify] benefit in VaD treatment with: memantine, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist; cholinesterase inhibitors galantamine, donepezil, rivastigmine;[33] Studies have been proposed to evaluate whether an extract of Ginkgo biloba EGb761 improves cognition, daily activities, and quality of life in treating vascular dementia.[34]

In those with celiac disease or non-celiac gluten sensitivity, a strict gluten-free diet may relieve symptoms of mild cognitive impairment.[17][18] It should be started as soon as possible. There is no evidence that a gluten free diet is useful against advanced dementia. People with no digestive symptoms are less likely to receive early diagnosis and treatment.[18]

General management of dementia includes referral to community services, aid with judgment and decision-making regarding legal and ethical issues (e.g., driving, capacity, advance directives), and consideration of caregiver stress. Behavioral and affective symptoms deserve special consideration in this patient group. These problems tend to resist conventional psychopharmacological treatment, and often lead to hospital admission and placement in permanent care.[citation needed]

Prognosis

Many studies have been conducted to determine average survival of patients with dementia. The studies were frequently small and limited, which caused contradictory results in the connection of mortality to the type of dementia and the patient's gender. A very large study conducted in Netherlands in 2015 found that the one-year mortality was three to four times higher in patients after their first referral to a day clinic for dementia, when compared to the general population.[35] If the patient was hospitalized for dementia, the mortality was even higher than in patients hospitalized for cardiovascular disease.[35] Vascular dementia was found to have either comparable or worse survival rates when compared to Alzheimer's Disease;[36][37][38] another very large 2014 Swedish study found that the prognosis for VaD patients was worse for male and older patients.[39]

Unlike Alzheimer's disease, which weakens the patient, causing them to succumb to bacterial infections like pneumonia, vascular dementia can be a direct cause of death due to the possibility of a fatal interruption in the brain's blood supply.[citation needed]

Epidemiology

Vascular dementia is the second-most-common form of dementia after Alzheimer's disease (AD) in older adults.[40] 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. 25% of stroke patients develop new-onset dementia within one year of their stroke. One study found that in the United States, the prevalence of vascular dementia in all people 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.[41][42] The incidence peaks between the fourth and the seventh decades of life and 80% of patients have a history of hypertension.[43][44]

A recent meta-analysis identified 36 studies of prevalent stroke (1.9 million participants) and 12 studies of incident stroke (1.3 million participants).[13] For prevalent stroke, the pooled hazard ratio for all-cause dementia was 1.69 (95% confidence interval: 1.49–1.92; P < .00001; I2 = 87%). For incident stroke, the pooled risk ratio was 2.18 (95% confidence interval: 1.90–2.50; P < .00001; I2 = 88%). Study characteristics did not modify these associations, with the exception of sex, which explained 50.2% of between-study heterogeneity for prevalent stroke. These results confirm that stroke is a strong, independent, and potentially modifiable risk factor for all-cause dementia.[13]

See also

References

  1. ↑ 1.0 1.1 "ICD-11 for Mortality and Morbidity Statistics". https://icd.who.int/browse11/l-m/en#/http://id.who.int/icd/entity/1365258270?data=%7B%22dataType%22%3A%22pc%22%2C%22postcoordinationCodeSet%22%3A%7B%22stemId%22%3A%22http%3A%2F%2Fid.who.int%2Ficd%2Fentity%2F1365258270%22%2C%22axisToValueIds%22%3A%7B%22associatedWith%22%3A%5B%7B%22stemId%22%3A%22http%3A%2F%2Fid.who.int%2Ficd%2Fentity%2F688029844%22%7D%5D%7D%7D%7D. 
  2. ↑ 2.0 2.1 "Types of vascular dementia | Alzheimer's Society". 2022-06-21. https://www.alzheimers.org.uk/about-dementia/types-dementia/types-of-vascular-dementia#1. 
  3. ↑ MedlinePlus Encyclopedia Multi-infarct dementia
  4. ↑ "Dementia". The Ulster Medical Journal 84 (2): 79–87. May 2015. PMID 26170481. 
  5. ↑ American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders : DSM-5 (5th ed.). Washington, DC: American Psychiatric Association. pp. 591–603. ISBN 978-0-89042-554-1. https://archive.org/details/diagnosticstatis0005unse/page/621. 
  6. ↑ "What is mixed dementia". https://www.dementiauk.org/understanding-dementia/types-and-symptoms/mixed-dementia/. 
  7. ↑ Office of Communications and Public Liaison. "NINDS Multi-Infarct Dementia Information Page". https://www.ninds.nih.gov/Disorders/All-Disorders/Multi-Infarct-Dementia-Information-Page. 
  8. ↑ "ICD-11 for Mortality and Morbidity Statistics". https://icd.who.int/browse11/l-m/en#/http://id.who.int/icd/entity/334423054. 
  9. ↑ Encyclopedia of the Human Brain - Dementia Associated with Depression. Oxford: Elsevier Science and Technology. 2002. http://www.credoreference.com/entry/esthumanbrain/vi_dementia_associated_with_depression. Retrieved 2012-09-20. 
  10. ↑ Alagiakrishnan, Kannayiram. "Vascular Dementia Clinical Presentation: History, Physical, Causes". https://emedicine.medscape.com/article/292105-clinical#b4. 
  11. ↑ Cannistraro, Rocco J.; Badi, Mohammed; Eidelman, Benjamin H.; Dickson, Dennis W.; Middlebrooks, Erik H.; Meschia, James F. (2019-06-11). "CNS small vessel disease: A clinical review". Neurology 92 (24): 1146–1156. doi:10.1212/WNL.0000000000007654. ISSN 1526-632X. PMID 31142635. 
  12. ↑ "Neuropathological investigation of dementia: a guide for neurologists". Journal of Neurology, Neurosurgery, and Psychiatry 76 Suppl 5 (supplement 5): v8-14. December 2005. doi:10.1136/jnnp.2005.080754. PMID 16291923. 
  13. ↑ 13.0 13.1 13.2 13.3 "Stroke and dementia risk: A systematic review and meta-analysis" (in English). Alzheimer's & Dementia 14 (11): 1416–1426. November 2018. doi:10.1016/j.jalz.2018.06.3061. PMID 30177276. 
  14. ↑ Arvanitakis, Zoe. "Dementia And Vascular Disease". http://www.dcmsonline.org/jax-medicine/2000journals/February2000/vascdement.htm. 
  15. ↑ "Amyloid-beta plaque growth in cognitively normal adults: longitudinal [11CPittsburgh compound B data"]. Annals of Neurology 70 (5): 857–61. November 2011. doi:10.1002/ana.22608. PMID 22162065. 
  16. ↑ "Longitudinal patterns of β-amyloid deposition in nondemented older adults". Archives of Neurology 68 (5): 644–9. May 2011. doi:10.1001/archneurol.2011.77. PMID 21555640. 
  17. ↑ 17.0 17.1 "Cognitive impairment in celiac disease and non-celiac gluten sensitivity: review of literature on the main cognitive impairments, the imaging and the effect of gluten free diet.". Acta Neurol Belg 118 (1): 21–27. 2018. doi:10.1007/s13760-017-0870-z. PMID 29247390. 
  18. ↑ 18.0 18.1 18.2 "Treatment of Neurological Manifestations of Gluten Sensitivity and Coeliac Disease.". Curr Treat Options Neurol 21 (3): 10. 2019-02-26. doi:10.1007/s11940-019-0552-7. PMID 30806821. 
  19. ↑ "Comparison of different diagnostic criteria for vascular dementia (ADDTC, DSM-IV, ICD-10, NINDS-AIREN)". Stroke 27 (1): 30–6. January 1996. doi:10.1161/01.str.27.1.30. PMID 8553399. http://stroke.ahajournals.org/cgi/pmidlookup?view=long&pmid=8553399. [yes|permanent dead link|dead link}}]
  20. ↑ "Impact of applying NINDS-AIREN criteria of probable vascular dementia to clinical and radiological characteristics of a stroke cohort with dementia". Cerebrovascular Diseases 18 (2): 98–103. 2004. doi:10.1159/000079256. PMID 15218273. 
  21. ↑ "Hachinski's ischemic score and the diagnosis of vascular dementia: a review". Italian Journal of Neurological Sciences 14 (7): 539–46. October 1993. doi:10.1007/BF02339212. PMID 8282525. 
  22. ↑ Bonte FJ, Harris TS, Hynan LS, Bigio EH, White CL (July 2006). "Tc-99m HMPAO SPECT in the Differential Diagnosis of the Dementias with Histopathologic Confirmation". Clinical Nuclear Medicine 31 (7): 376–378. doi:10.1097/01.rlu.0000222736.81365.63. PMID 16785801. 
  23. ↑ Dougall NJ, Bruggink S, Ebmeier KP (2004). "Systematic Review of the Diagnostic Accuracy of 99mTc-HMPAO-SPECT in Dementia". American Journal of Geriatric Psychiatry 12 (6): 554–570. doi:10.1176/appi.ajgp.12.6.554. PMID 15545324. 
  24. ↑ Waldemar G.; Dubois B.; Emre M. et al. (January 2007). "Recommendations for the Diagnosis and Management of Alzheimer's Disease and Other Disorders Associated with Dementia: EFNS guideline". European Journal of Neurology 14 (1): e1–26. doi:10.1111/j.1468-1331.2006.01605.x. PMID 17222085. 
  25. ↑ From NINCDS-ADRDA Alzheimer's Criteria: "Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDS-ADRDA criteria". The Lancet. Neurology 6 (8): 734–46. August 2007. doi:10.1016/S1474-4422(07)70178-3. PMID 17616482. 
  26. ↑ Custodio, Nilton; Montesinos, Rosa; Lira, David; Herrera-Pérez, Eder; Bardales, Yadira; Valeriano-Lorenzo, Lucía (2017). "Mixed dementia: A review of the evidence". Dementia & Neuropsychologia 11 (4): 364–370. doi:10.1590/1980-57642016dn11-040005. ISSN 1980-5764. PMID 29354216. 
  27. ↑ Hase, Yoshiki; Horsburgh, Karen; Ihara, Masafumi; Kalaria, Raj N. (2018). "White matter degeneration in vascular and other ageing-related dementias". Journal of Neurochemistry 144 (5): 617–633. doi:10.1111/jnc.14271. PMID 29210074. 
  28. ↑ McVeigh, Catherine; Passmore, Peter (September 2006). "Vascular dementia: prevention and treatment". Clinical Interventions in Aging 1 (3): 229–235. doi:10.2147/ciia.2006.1.3.229. ISSN 1176-9092. PMID 18046875. 
  29. ↑ Erkinjuntti, Timo (February 2012). Gelder, Michael; Andreasen, Nancy; Lopez-Ibor, Juan et al.. eds. New Oxford Textbook of Psychiatry (2 ed.). Oxford: Oxford University Press. doi:10.1093/med/9780199696758.001.0001. ISBN 9780199696758. http://oxfordmedicine.com/view/10.1093/med/9780199696758.001.0001/med-9780199696758-chapter-48. Retrieved 2015-09-07. 
  30. ↑ 30.0 30.1 30.2 30.3 "Pharmacological prevention and treatment of vascular dementia: approaches and perspectives". Experimental Gerontology 47 (11): 887–91. November 2012. doi:10.1016/j.exger.2012.07.002. PMID 22796225. 
  31. ↑ "Post-stroke dementia - a comprehensive review". BMC Medicine 15 (1): 11. January 2017. doi:10.1186/s12916-017-0779-7. PMID 28095900. 
  32. ↑ Rands, Gianetta; Orrell, Martin (2000-10-23). "Aspirin for vascular dementia". Cochrane Database of Systematic Reviews 2012 (4): CD001296. doi:10.1002/14651858.cd001296. PMID 11034710. 
  33. ↑ J, Birks; B, McGuinness; D, Craig (2013-05-31). "Rivastigmine for Vascular Cognitive Impairment". The Cochrane Database of Systematic Reviews (5): CD004744. doi:10.1002/14651858.CD004744.pub3. PMID 23728651. https://pubmed.ncbi.nlm.nih.gov/23728651/. Retrieved 2020-05-29. 
  34. ↑ Wang, MExpression error: Unrecognized word "et". (2020-09-11). "Efficacy and safety of ginkgo preparation in patients with vascular dementia: A protocol for systematic review and meta-analysis.". Medicine 99 (37): e22209. doi:10.1097/MD.0000000000022209. PMID 32925798. 
  35. ↑ 35.0 35.1 "Prognosis of patients with dementia: results from a prospective nationwide registry linkage study in the Netherlands". BMJ Open 5 (10): e008897. October 2015. doi:10.1136/bmjopen-2015-008897. PMID 26510729.  open access
  36. ↑ "Mortality in dementia". Neuroepidemiology 25 (3): 153–62. 2005. doi:10.1159/000086680. PMID 15990446. 
  37. ↑ "Alzheimer disease with cerebrovascular disease and vascular dementia: clinical features and course compared with Alzheimer disease". Journal of Neurology, Neurosurgery, and Psychiatry 80 (2): 133–9. February 2009. doi:10.1136/jnnp.2007.137851. PMID 18977819. 
  38. ↑ "Dementia-associated mortality at thirteen years in the NEDICES Cohort Study". Journal of Alzheimer's Disease 26 (3): 543–51. 2011. doi:10.3233/JAD-2011-110443. PMID 21694455. 
  39. ↑ "Mortality risk after dementia diagnosis by dementia type and underlying factors: a cohort of 15,209 patients based on the Swedish Dementia Registry". Journal of Alzheimer's Disease 41 (2): 467–77. 2014. doi:10.3233/JAD-131856. PMID 24625796. 
  40. ↑ "Vascular cognitive disorder. A biological and clinical overview". Neurochemical Research 35 (12): 1933–8. December 2010. doi:10.1007/s11064-010-0346-5. PMID 21127967. 
  41. ↑ "Prevalence of dementia in the United States: the aging, demographics, and memory study". Neuroepidemiology 29 (1–2): 125–32. 2007. doi:10.1159/000109998. PMID 17975326. 
  42. ↑ "The prevalence of dementia: a quantitative integration of the literature". Acta Psychiatrica Scandinavica 76 (5): 465–79. November 1987. doi:10.1111/j.1600-0447.1987.tb02906.x. PMID 3324647. 
  43. ↑ Sova, Maria-Roxana; Dobrin, R P; Chiriţă, V (2009). "Aspects regarding the incidence and prevalence of vascular dementia forms" (in ro). Revista Medico-Chirurgicala a Societatii de Medici Si Naturalisti Din Iasi (Rev Med Chir Soc Med Nat Iasi) 113 (1): 53–58. PMID 21495296. https://pubmed.ncbi.nlm.nih.gov/21495296/. Retrieved 2021-03-31. 
  44. ↑ Wolters, Frank J.; Ikram, M Arfan (2019). "Epidemiology of Vascular Dementia". Arteriosclerosis, Thrombosis, and Vascular Biology (Arterioscler Thromb Vasc Biol) 39 (8): 1542–1549. doi:10.1161/ATVBAHA.119.311908. PMID 31294622. 

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