Vascular dementia

Vascular dementia
Classification and external resources
Specialty psychiatry, neurology
ICD-10 F01.1
ICD-9-CM 290.4
DiseasesDB 8393
MedlinePlus 000746
eMedicine med/3150 neuro/227
MeSH D015161

Vascular dementia, also known as multi-infarct dementia (MID) and vascular cognitive impairment (VCI), is dementia caused by problems in the supply of blood to the brain, typically a series of minor strokes, leading to worsening cognitive decline that occurs step by step.[1] The term refers to a syndrome consisting of a complex interaction of cerebrovascular disease and risk factors that lead to changes in the brain structures due to strokes and lesions, and resulting changes in cognition. The temporal relationship between a stroke and cognitive deficits is needed to make the diagnosis.[2]

Signs and symptoms

Differentiating the different dementia syndromes can be challenging, due to the frequently overlapping clinical features and related underlying pathology. In particular, Alzheimer's dementia often co-occurs with vascular dementia.[3]

People with vascular dementia present with progressive cognitive impairment, acutely or subacutely as in mild cognitive impairment, frequently step-wise, after multiple cerebrovascular events (strokes). Some people may appear to improve between events and decline after more silent strokes. A rapidly deteriorating condition may lead to death from a stroke, heart disease, or infection.[4]

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).[5] 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 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. In the more severely affected patients, or patients affected by infarcts in Wernicke's or Broca's areas, dysarthrias and aphasias may be present (problems with speaking).

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, 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.

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

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.[6] Brain vascular lesions can also be the result of diffuse cerebrovascular disease, such as small vessel disease.

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.[7]

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. However, cerebral amyloid angiopathy can appear in people with no prior dementia condition. Some beta amyloid plaques are often present in cognitively normal elderly persons.

Diagnosis

Several specific diagnostic criteria can be used to diagnose vascular dementia,[8] 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,[9] the Alzheimer's Disease Diagnostic and Treatment Center criteria, and the Hachinski ischemic score.[10]

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.[11] 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.[12] Advances have led to the proposal of new diagnostic criteria.[13][14]

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

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

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. 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.

Prevention

Early detection and accurate diagnosis are important, as vascular dementia is at least partially preventable. Ischemic changes in the brain are irreversible, however the patient with vascular dementia can demonstrate periods of stability or even mild improvement.[15] Since stroke is an essential part of vascular dementia, 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.[16] 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, four large recent reviews showed that therapy with statin drugs was ineffective in treatment or prevention of this dementia.[16] 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.[16] Smoking cessation and Mediterranean diet have not been found to help patients with cognitive impairment, however physical activity was consistently the most effective method of preventing cognitive decline.[16]

Treatment

Currently, there are no 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 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 benefit in VaD treatment with: memantine, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist; cholinesterase inhibitors galantamine, donepezil, rivastigmine; and ginkgo biloba extract.[16]

The 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 be resistant to conventional psychopharmacological treatment and often lead to hospital admission and placement in permanent care.

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.[17] If the patient was hospitalized for dementia, the mortality was even higher than in patients hospitalized for cardiovascular disease.[17] Vascular dementia was found to have either comparable or worse survival rates when compared to Alzheimer's Disease,[18][19][20] however another very large 2014 Swedish study found that prognosis was worse for male and older patients.[21]

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.

Epidemiology

Vascular dementia is the second-most-common form of dementia after Alzheimer's disease (AD) in older adults.[22][23] 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 nine 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 four 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.[24][25]

The incidence peaks between the fourth and the seventh decades of life and 80% of patients have a history of hypertension.

See also

References

  1. ↑ MedlinePlus Encyclopedia Multi-infarct dementia
  2. ↑ Cunningham, EL; McGuinness, B; Herron, B; Passmore, AP (May 2015). "Dementia.". The Ulster medical journal 84 (2): 79–87. PMID 26170481.
  3. ↑ Karantzoulis, S; Galvin, JE (November 2011). "Distinguishing Alzheimer's disease from other major forms of dementia.". Expert review of neurotherapeutics 11 (11): 1579–91. PMID 22014137.
  4. ↑ Office of Communications and Public Liaison. "NINDS Multi-Infarct Dementia Information Page". Retrieved 6 December 2011.
  5. ↑ . "Dementia associated with depression". Encyclopedia of the Human Brain. Oxford: Elsevier Science & Technology, 2002. Credo Reference. 19 May 2010. Web. 20 Sept. 2012. <http://www.credoreference.com/entry/esthumanbrain/vi_dementia_associated_with_depression>.
  6. ↑ Love, S (1 December 2005). "Neuropathological investigation of dementia: a guide for neurologists". Journal of Neurology, Neurosurgery & Psychiatry 76 (suppl_5): v8–v14. doi:10.1136/jnnp.2005.080754.
  7. ↑ Arvanitakis, Zoe. "Dementia And Vascular Disease".
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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. July 2006;31(7):376–8. doi:10.1097/01.rlu.0000222736.81365.63. PMID 16785801.
  12. ↑ 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.
  13. ↑ Waldemar G. Recommendations for the diagnosis and management of Alzheimer's disease and other disorders associated with dementia: EFNS guideline. Eur J Neurol. January 2007;14(1):e1–26. doi:10.1111/j.1468-1331.2006.01605.x. PMID 17222085.
  14. ↑ 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.
  15. ↑ Erkinjuntti, Timo (Feb 2012). New Oxford textbook of psychiatry. (2 ed.). Oxford: Oxford University Press. ISBN 9780199696758. Retrieved 7 November 2015.
  16. 1 2 3 4 5 Baskys, A; Cheng, JX (November 2012). "Pharmacological prevention and treatment of vascular dementia: approaches and perspectives.". Experimental gerontology 47 (11): 887–91. PMID 22796225.
  17. 1 2 van de Vorst, Irene E; Vaartjes, Ilonca; Geerlings, Mirjam I; Bots, Michael L; Koek, Huiberdina L (28 October 2015). "Prognosis of patients with dementia: results from a prospective nationwide registry linkage study in the Netherlands". BMJ Open 5 (10): e008897. doi:10.1136/bmjopen-2015-008897.
  18. ↑ Guehne, U; Riedel-Heller, S; Angermeyer, MC (2005). "Mortality in dementia.". Neuroepidemiology 25 (3): 153–62. PMID 15990446.
  19. ↑ Bruandet, A; Richard, F; Bombois, S; Maurage, C A; Deramecourt, V; Lebert, F; Amouyel, P; Pasquier, F (1 February 2009). "Alzheimer disease with cerebrovascular disease and vascular dementia: clinical features and course compared with Alzheimer disease". Journal of Neurology, Neurosurgery & Psychiatry 80 (2): 133–139. doi:10.1136/jnnp.2007.137851.
  20. ↑ Villarejo, A; Benito-León, J; Trincado, R; Posada, IJ; Puertas-Martín, V; Boix, R; Medrano, MR; Bermejo-Pareja, F (2011). "Dementia-associated mortality at thirteen years in the NEDICES Cohort Study.". Journal of Alzheimer's disease : JAD 26 (3): 543–51. doi:10.3233/JAD-2011-110443. PMID 21694455.
  21. ↑ Garcia-Ptacek, S; Farahmand, B; Kåreholt, I; Religa, D; Cuadrado, ML; Eriksdotter, M (2014). "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 : JAD 41 (2): 467–77. PMID 24625796.
  22. ↑ 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.
  23. ↑ "Vascular Dementia: A Resource List".
  24. ↑ 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.
  25. ↑ 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.

External links

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