Mild cognitive impairment

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Mild cognitive impairment
Classification and external resources
ICD-10 F06.7
ICD-9 331.83
Patient UK Mild cognitive impairment
MeSH D060825

Mild cognitive impairment (MCI, also known as incipient dementia, or isolated memory impairment) is a brain function syndrome involving the onset and evolution of cognitive impairments beyond those expected based on the age and education of the individual, but which are not significant enough to interfere with their daily activities.[1] It is often found to be a transitional stage between normal aging and dementia. Although MCI can present with a variety of symptoms, when memory loss is the predominant symptom it is termed "amnestic MCI" and is frequently seen as a prodromal stage of Alzheimer's disease.[2] Studies suggest that these individuals tend to progress to probable Alzheimer’s disease at a rate of approximately 10% to 15% per year.[2]

Additionally, when individuals have impairments in domains other than memory it is classified as nonamnestic single- or multiple-domain MCI and these individuals are believed to be more likely to convert to other dementias (e.g., dementia with Lewy bodies).[3] However, some instances of MCI may simply remain stable over time or even remit. Causation of the syndrome in and of itself remains unknown, as therefore do prevention and treatment.

Diagnosis[edit]

The diagnosis of MCI requires considerable clinical judgement,[2] and as such a comprehensive clinical assessment including clinical observation, neuroimaging, blood tests and neuropsychological testing are best in order to rule out an alternate diagnosis. MCI is diagnosed when there is:[4]

  1. Evidence of memory impairment
  2. Preservation of general cognitive and functional abilities
  3. Absence of diagnosed dementia

Neuropathology[edit]

There is evidence suggesting that although amnestic MCI patients may not meet neuropathologic criteria for Alzheimer's disease, patients may be in a transitional stage of evolving Alzheimer's disease; patients in this hypothesized transitional stage demonstrated diffuse amyloid in the neocortex and frequent neurofibrillary tangles in the medial temporal lobe.[5]

There is emerging evidence that magnetic resonance imaging can observe deterioration, including progressive loss of gray matter in the brain, from mild cognitive impairment to full-blown Alzheimer disease.[6] A technique known as PiB PET imaging is used to clearly show the sites and shapes of beta amyloid deposits in living subjects using a C11 tracer that binds selectively to such deposits.[7] Such tools may help greatly in assisting clinical research for therapies.

Treatment[edit]

There is no proven treatment or therapy for mild cognitive impairment. As MCI may represent a prodromal state to clinical Alzheimer’s disease, treatments proposed for Alzheimer’s disease, such as antioxidants and cholinesterase inhibitors, may be useful. However, several potential treatments are still under investigation.[2] Two drugs used to treat Alzheimer's disease have been assessed for their ability to treat MCI or prevent progression to full Alzheimer's disease. Rivastigmine failed to stop or slow progression to Alzheimer's disease or on cognitive function for individuals with mild cognitive impairment,[8] and donepezil showed only minor, short-term benefits and was associated with significant side effects.[9]

In a two-year randomized trial of 168 people with MCI given either high-dose vitamins or placebo, vitamins cut the rate of brain shrinkage by up to half. The vitamins were the three B vitamins folic acid, vitamin B6, and vitamin B12, which inhibit production of the amino acid homocysteine. High blood levels of homocysteine are associated with increased risk of cognitive decline,[10] dementia, and cardiovascular disease.[11][12][13]

References[edit]

  1. ^ Petersen RC, Smith GE, Waring SC, Ivnik RJ, Tangalos EG, Kokmen E (1999). "Mild cognitive impairment: clinical characterization and outcome". Arch. Neurol. 56 (3): 303–8. doi:10.1001/archneur.56.3.303. PMID 10190820. 
  2. ^ a b c d Grundman M, Petersen RC, Ferris SH, et al. (2004). "Mild cognitive impairment can be distinguished from Alzheimer disease and normal aging for clinical trials". Arch. Neurol. 61 (1): 59–66. doi:10.1001/archneur.61.1.59. PMID 14732621. 
  3. ^ Tabert MH, Manly JJ, Liu X, et al. (2006). "Neuropsychological prediction of conversion to Alzheimer disease in patients with mild cognitive impairment". Arch. Gen. Psychiatry 63 (8): 916–24. doi:10.1001/archpsyc.63.8.916. PMID 16894068. 
  4. ^ Morris, J C., Storandt, M., Miller, J. P., McKeel, D. W., Price, J. L., Rubin, E.H. & Berg, L. (2001). "Mild cognitive impairment represents early-stage Alzheimer disease". Archives of Neurology 58 (3): 387–405. doi:10.1001/archneur.58.3.397. 
  5. ^ Petersen RC, Parisi JE, Dickson DW, et al. (2006). "Neuropathologic features of amnestic mild cognitive impairment". Arch. Neurol. 63 (5): 665–72. doi:10.1001/archneur.63.5.665. PMID 16682536. 
  6. ^ Whitwell JL, Shiung MM, Przybelski SA, et al. (2008). "MRI patterns of atrophy associated with progression to AD in amnestic mild cognitive impairment". Neurology 70 (7): 512–20. doi:10.1212/01.wnl.0000280575.77437.a2. PMC 2734138. PMID 17898323. 
  7. ^ Jack CR, Lowe VJ, Senjem ML, et al. (2008). "11C PiB and structural MRI provide complementary information in imaging of Alzheimer's disease and amnestic mild cognitive impairment" (pdf). Brain 131 (Pt 3): 665–80. doi:10.1093/brain/awm336. PMC 2730157. PMID 18263627. 
  8. ^ Feldman HH, Ferris S, Winblad B, et al. (2007). "Effect of rivastigmine on delay to diagnosis of Alzheimer's disease from mild cognitive impairment: the InDDEx study". Lancet Neurol 6 (6): 501–12. doi:10.1016/S1474-4422(07)70109-6. PMID 17509485. 
  9. ^ Birks J, Flicker L (2006). "Donepezil for mild cognitive impairment". In Birks, Jacqueline. Cochrane Database Syst Rev 3: CD006104. doi:10.1002/14651858.CD006104. PMID 16856114. 
  10. ^ McCaddon,A. et al (2001). "Homocysteine and cognitive decline in healthy elderly". Dement Geriatr Cogn Disord 12 (5): 309–313. doi:10.1159/000051275. PMID 11455131. 
  11. ^ Kelland, K. (2010). B vitamins found to halve aging brain shrinkage. Reuters Health. 
  12. ^ Smith AD, Smith SM, de Jager CA, Whitbread P, Johnston C, Agacinski G, Oulhaj A, Bradley KM, Jacoby R, Refsum H (2010). "Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial". PLoS ONE 5 (9): e12244. doi:10.1371/journal.pone.0012244. PMC 2935890. PMID 20838622. 
  13. ^ Ravaglia, G. Forti, P., Maioli, F., Matelli, M., Servadei, L., Nicoletta, B., Elisa, Porcellini & Licastor, F. (2005). "Homocysteine and folate as risk factors for dementia and Alzheimer disease". the American Journal of Clinical Nutrition 82 (3): 636–643. PMID 16155278. 

External links[edit]