Dementia: Difference between revisions

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'''Dementia''' is "progressive decline in two or more cognitive domains that is severe enough to interfere with the performance of everyday activities."<ref name="pmid12614094">{{cite journal |author=Karlawish, J. & Clark, C. |title=Diagnostic evaluation of elderly patients with mild memory problems |journal=Ann Intern Med |volume=138 |issue=5 |pages=411-9 |year=2003 |pmid=12614094 | url=http://www.annals.org/cgi/content/full/138/5/411}}</ref>
Deficits in cognitive function contribute to impaired functional status.<ref name="pmid17827410">{{cite journal |author=Royall DR, Lauterbach EC, Kaufer D, Malloy P, Coburn KL, Black KJ |title=The cognitive correlates of functional status: a review from the Committee on Research of the American Neuropsychiatric Association |journal=The Journal of neuropsychiatry and clinical neurosciences |volume=19 |issue=3 |pages=249–65 |year=2007 |pmid=17827410 |doi=10.1176/appi.neuropsych.19.3.249}}</ref> The deficits in the domains of cognitive function are<ref name="pmid17551132">{{cite journal |author=Holsinger T, Deveau J, Boustani M, Williams JW |title=Does this patient have dementia? |journal=JAMA |volume=297 |issue=21 |pages=2391–404 |year=2007 |pmid=17551132 |doi=10.1001/jama.297.21.2391}}</ref>:
* Agnosia - "Failure to recognize or identify objects despite intact sensory function"<ref name="pmid17551132"/>
* Aphasia - "Deterioration of language function"<ref name="pmid17551132"/>
* Apraxia - "Impaired ability to execute motor activities despite intact motor abilities, sensory function, and comprehension of the required task"<ref name="pmid17551132"/>
* Disturbance in executive functioning - "The ability to think abstractly and to plan, initiate, sequence, monitor, and stop complex behavior"<ref name="pmid17551132"/>
==Classification==
Vascular dementia can affect both cortical and subcortial locations.
===Cortical dementias===
Among the many causes of cortical dementia, common causes are:
* [[Alzheimer's disease]] which usually affects posterior cortical regions before progressing to the frontal cortex.
* [[Frontotemporal lobar degeneration]] (Pick's Disease)
* Dementia with Lewy bodies<ref name="pmid7994501">{{cite journal |author=McKeith IG, Fairbairn AF, Perry RH, Thompson P |title=The clinical diagnosis and misdiagnosis of senile dementia of Lewy body type (SDLT) |journal=Br J Psychiatry |volume=165 |issue=3 |pages=324–32 |year=1994 |month=September |pmid=7994501 |doi= |url= |issn=}}</ref>
===Subcortical dementias===
Among the many causes of subcortical dementia, common causes are:
* [[Parkinson's disease]]
* [[Vitamin B12 deficiency]]
* Some [[vascular dementia]]s
==Epidemiology==
22.2% of individuals in the United States age 71 years or older have cognitive impairment without dementia (Dementia Severity Rating Scale score of 6 to 11). 12% of these patients progress to dementia annually. Progression is more common among patients with subtypes of prodromal Alzheimer disease and cerebrovascular disease.<ref name="pmid18347351">{{cite journal |author=Plassman BL, Langa KM, Fisher GG, ''et al'' |title=Prevalence of cognitive impairment without dementia in the United States |journal=Ann. Intern. Med. |volume=148 |issue=6 |pages=427–34 |year=2008 |month=March |pmid=18347351 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=18347351 |issn=}}</ref>
==Diagnosis==
Studies on diagnosing dementia are compromised by the lack of a true reference standard for comparison.<ref name="pmid9385127">{{cite journal |author=Erkinjuntti T, Ostbye T, Steenhuis R, Hachinski V |title=The effect of different diagnostic criteria on the prevalence of dementia |journal=N. Engl. J. Med. |volume=337 |issue=23 |pages=1667–74 |year=1997 |month=December |pmid=9385127 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=9385127&promo=ONFLNS19 |issn=}}</ref><ref>
Rockwood K et al. [http://dx.doi.org/10.1016/j.jalz.2007.07.014 Toward a revision of criteria for the dementias]. Alzheimer's and Dementia 3 (4), 428 (2007)
{{doi|10.1016/j.jalz.2007.07.014}}</ref>
A number of [[systematic review]]s, including ones by the [http://www.ahrq.gov/clinic/uspstfix.htm U.S. Preventive Services Task Force (USPSTF)]<ref name="pmid12779304">{{cite journal |author=Boustani, M.; Peterson, B.; Hanson, L.; Harris, R.; & Lohr, K. |title=Screening for dementia in primary care: a summary of the evidence for the U.S. Preventive Services Task Force |journal=Ann Intern Med |volume=138 |issue=11 |pages=927-37 |year=2003 |pmid=12779304 | url=http://www.annals.org/cgi/content/full/138/11/927}}</ref>, [http://www.sgim.org/clinexam-rce.cfm Rational Clinical Examination]<ref name="pmid17551132">{{cite journal |author=Holsinger T, Deveau J, Boustani M, Williams JW |title=Does this patient have dementia? |journal=JAMA |volume=297 |issue=21 |pages=2391–404 |year=2007 |pmid=17551132 |doi=10.1001/jama.297.21.2391}}</ref>, and others<ref name="pmid17178826">{{cite journal |author=Cullen B, O'Neill B, Evans JJ, Coen RF, Lawlor BA |title=A review of screening tests for cognitive impairment |journal=J. Neurol. Neurosurg. Psychiatr. |volume=78 |issue=8 |pages=790–9 |year=2007 |pmid=17178826 |doi=10.1136/jnnp.2006.095414}}</ref>, have summarized the diagnostic accuracy of screening tests.
===Consequences of labeling===
In one study, learning of having ''mild'' cognitive impairment reduced stress.<ref> Carpenter, B. D., Xiong, C., Porensky, E. K., Lee, M. M., Brown, P. J., Coats, M., et al. (2008). Reaction to a dementia diagnosis in individuals with alzheimer's disease and mild cognitive impairment, Journal of the American Geriatrics Society, 56(3), 405-412. {{doi| doi:10.1111/j.1532-5415.2007.01600.x.}}</ref>
===Neuropsychiatric testing===
====Mini-mental state examination====
The Mini-mental state examination (MMSE) is the most studied test.<ref name="pmid17551132"/> A [[systematic review]] concluded that the accuracy of the MMSE is:<ref name="pmid12779304"/>:
* [[sensitivity (tests)|sensitivity]] 71% to 92%
* [[specificity (tests)|specificity]] 56% to 96%
A copy of the Mini-mental state examination can be found in the appendix of the original publication.<ref name="pmid1202204">{{cite journal |author=Folstein MF, Folstein SE, McHugh PR |title="Mini-mental state". A practical method for grading the cognitive state of patients for the clinician |journal=Journal of psychiatric research |volume=12 |issue=3 |pages=189-98 |year=1975 |pmid=1202204 |doi=10.1016/0022-3956(75)90026-6}}</ref>
====Modified Mini-Mental State examination (3MS)====
A [[meta-analysis]] concluded that the Modified Mini-Mental State (3MS) examination has:<ref name="pmid17178826"/>
* [[sensitivity (tests)|sensitivity]] 83% to 94%
* [[specificity (tests)|specificity]] 85% to 90%
A copy of the 3MS is online.<ref name="pmid10676583">{{cite journal |author=Hogan DB, Ebly EM |title=Predicting who will develop dementia in a cohort of Canadian seniors |journal=The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques |volume=27 |issue=1 |pages=18–24 |year=2000 |pmid=10676583 |doi=}} [[http://www.cjns.org/27febtoc/predicting_appendix_.html Appendix: The Modified Mini-Mental State (3MS)]]</ref>
====Abbreviated mental test score====
A [[meta-analysis]] concluded:<ref name="pmid17178826"/>
: [[sensitivity (tests)|sensitivity]] 73% to 100%
: [[specificity (tests)|specificity]] 71% to 100%
====Clock drawing task====
{| class="wikitable" align="center"
|-
! Dementia type
! CLOX1<br>(Executive control)
! CLOX2<br>(Posterior cortical)
! Pentagons copying<br>on MMSE
!Total MMSE score
|-
| Posterior cortical and<br>diffuse cortical<br>dementias
| Abnormal
| Abnormal
| Abnormal
| Abnormal
|-
| Subcortical and<br>frontal cortical<br>dementias
| ''Abnormal''
| Normal
| Normal
| Normal
|}
The Clock drawing task (CLOX) consists of two tests and is available online at PubMed Central.<ref name="pmid9598672">{{cite journal |author=Royall, D.; Cordes J.; & Polk M. |title=CLOX: an executive clock drawing task |journal=J Neurol Neurosurg Psychiatry |volume=64 |issue=5 |pages=588-94 |year=1998 |pmid=9598672 | url=http://jnnp.bmj.com/cgi/content/full/64/5/588}} [http://www.pubmedcentral.nih.gov/articlerender.fcgi?pubmedid=9598672 Full text at PubMed Central]  [http://jnnp.bmj.com/cgi/content/full/64/5/588/F3 Example form]</ref> The CLOX1 task has the subject draw a clock face without any prompting other than the instructions "Draw me a clock that says 1:45. Set the hands and numbers on the face so that a child could read them". The CLOX1 is tests executive function and correlates with the EXIT25 test of executive function. The CLOX2 task has the subject copy a clock face from an example, does not test executive function and correlates with the MMSE.
The CLOX may avoid the bias of the MMSE toward cortical dementias.<ref name="pmid9598672"/> In addition, "as Alzheimer’s disease affects posterior cortical regions before invading the frontal cortex, isolated ECF impairment (CLOX1) is not likely to represent early Alzheimer’s disease."<ref name="pmid9598672"/> Thus, isolated abnormalities of the CLOX1 may be able to detect reversible dementias such as subcortical [[stroke]], [[depression]], [[vitamin B12 deficiency]], [[polypharmacy]], and [[hypothyroidism]].<ref name="pmid9598672"/>
====Other examinations====
Many other tests have been studied <ref name="pmid17163083">{{cite journal |author=Sager, M.; Hermann, B.; La Rue, A.; & Woodard, J. |title=Screening for dementia in community-based memory clinics |journal=WMJ |volume=105 |issue=7 |pages=25-9 |year=2006 |pmid=17163083}}</ref><ref name="pmid17287448">{{cite journal |author=Fleisher, A.; Sowell B.; Taylor C.; Gamst A.; Petersen R.; & Thal L. |title=Clinical predictors of progression to Alzheimer disease in amnestic mild cognitive impairment |journal=Neurology |volume=68 |issue=19 |pages=1588-95 |year=2007 |pmid=17287448}}</ref><ref name="pmid12614094"/> including the Executive Interview (EXIT)<ref>Royall DR, Mahurin RK, Gray KF. Bedside assessment of executive cognitive impairment: the executive interview. J Am Geriatr Soc. 1992;40:1221-6. PMID 1447438</ref>.
===Laboratory tests===
====Apolipoprotein E4====
Although [[apolipoprotein E4]] is an important susceptibility gene for [[Alzheimer's disease]]<ref name="pmid10944568">{{cite journal |author=Skoog I |title=Detection of preclinical Alzheimer's disease |journal=N. Engl. J. Med. |volume=343 |issue=7 |pages=502–3 |year=2000 |month=August |pmid=10944568 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=10944568&promo=ONFLNS19 |issn= |quote=The APOE 4 allele is a susceptibility gene for Alzheimer's disease and seems to affect the age of onset of the disease. However, the presence of this allele alone is not sufficient to predict which asymptomatic subjects will ultimately have Alzheimer's disease, and the disease never develops in many subjects with this genotype}}</ref>, its [[sensitivity and specificity]] are insufficient (65 and 68 percent, respectively) to be used as a diagnostic test.<ref name="pmid12160362">{{cite journal |author=Kivipelto M, Helkala EL, Laakso MP, ''et al'' |title=Apolipoprotein E epsilon4 allele, elevated midlife total cholesterol level, and high midlife systolic blood pressure are independent risk factors for late-life Alzheimer disease |journal=Ann. Intern. Med. |volume=137 |issue=3 |pages=149–55 |year=2002 |month=August |pmid=12160362 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=reprint&pmid=12160362 |issn=}}</ref>
[[Apolipoprotein E4]] does not added to other tests in predicting who will develop Alzheimer's.<ref name="pmid18723162">{{cite journal |author=Devanand DP, Liu X, Tabert MH, ''et al'' |title=Combining early markers strongly predicts conversion from mild cognitive impairment to Alzheimer's disease |journal=Biol. Psychiatry |volume=64 |issue=10 |pages=871–9 |year=2008 |month=November |pmid=18723162 |doi=10.1016/j.biopsych.2008.06.020 |url=http://linkinghub.elsevier.com/retrieve/pii/S0006-3223(08)00788-9 |issn=}}</ref>
==Treatment==
===Approaches to treatment===
"Actively involving caregivers in making choices about treatments" my be the most important way to delay institutionalization of patients with dementia.<ref>Spijker A et al. Effectiveness of Nonpharmacological Interventions in Delaying the Institutionalization of Patients with Dementia: A Meta-Analysis.J Am Geriatr Soc. 2008 Apr 11. PMID 18410323</ref>
The use of care managers may help.<ref name="pmid17101935"/><ref name="pmid17116916">{{cite journal |author=Vickrey BG, Mittman BS, Connor KI, ''et al'' |title=The effect of a disease management intervention on quality and outcomes of dementia care: a randomized, controlled trial |journal=Ann. Intern. Med. |volume=145 |issue=10 |pages=713–26 |year=2006 |pmid=17116916 |doi=}}</ref>
===Non drug treatments===
====Behavior management techniques (BMT)====
Behavior management techniques (BMT) might help.<ref name="pmid14559955">{{cite journal |author=Teri L, Gibbons LE, McCurry SM, ''et al'' |title=Exercise plus behavioral management in patients with Alzheimer disease: a randomized controlled trial |journal=JAMA |volume=290 |issue=15 |pages=2015–22 |year=2003 |pmid=14559955 |doi=10.1001/jama.290.15.2015}}</ref> More specifically, " interventions that address behavioral issues and unmet needs" may help.<ref name="pmid17101935">{{cite journal |author=Ayalon L, Gum AM, Feliciano L, Areán PA |title=Effectiveness of nonpharmacological interventions for the management of neuropsychiatric symptoms in patients with dementia: a systematic review |journal=Arch. Intern. Med. |volume=166 |issue=20 |pages=2182–8 |year=2006 |pmid=17101935 |doi=10.1001/archinte.166.20.2182}}</ref>
====Exercise====
Home-based program of physical activity might benefit according to a [[randomized controlled trial]].<ref>Lautenschlager NT, Cox KL, Flicker L, Foster JK, van Bockxmeer FM, Xiao J, et al. [http://jama.ama-assn.org/cgi/content/full/300/9/1027 Effect of Physical Activity on Cognitive Function in Older Adults at Risk for Alzheimer Disease: A Randomized Trial]. JAMA. 2008 Sep 3;300(9):1027-1037.</ref>
====Bright lights====
Any initial randomized controlled trial suggests that bright light helps.<ref name="pmid18544724">{{cite journal |author=Riemersma-van der Lek RF, Swaab DF, Twisk J, Hol EM, Hoogendijk WJ, Van Someren EJ |title=Effect of bright light and melatonin on cognitive and noncognitive function in elderly residents of group care facilities: a randomized controlled trial |journal=JAMA |volume=299 |issue=22 |pages=2642–55 |year=2008 |month=June |pmid=18544724 |doi=10.1001/jama.299.22.2642 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18544724 |issn=}}</ref>
===Medications===
According to the [[clinical practice guideline]] by the [[American College of Physicians]], "the evidence is insufficient to compare the effectiveness of different pharmacologic agents for the treatment of dementia."<ref name="pmid18316755">{{cite journal |author=Qaseem A, Snow V, Cross JT, ''et al'' |title=Current pharmacologic treatment of dementia: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians |journal=Ann. Intern. Med. |volume=148 |issue=5 |pages=370–8 |year=2008 |month=March |pmid=18316755 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=18316755 |issn=}}</ref>
"Treatment of dementia with cholinesterase inhibitors and memantine can result in statistically significant but clinically marginal improvement in measures of cognition and global assessment of dementia" according to a [[systematic review]] for the [[clinical practice guideline]].<ref name="pmid18316756">{{cite journal |author=Raina P, Santaguida P, Ismaila A, ''et al'' |title=Effectiveness of cholinesterase inhibitors and memantine for treating dementia: evidence review for a clinical practice guideline |journal=Ann. Intern. Med. |volume=148 |issue=5 |pages=379–97 |year=2008 |month=March |pmid=18316756 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=18316756 |issn=}}</ref>
====Cholinesterase inhibitors====
Available cholinesterase inhibitors drugs are donepezil, galantamine, rivastigmine, and tacrine.
====Neuropeptide-modifier====
Memantine is a neuropeptide-modifier that acts on the N-Methyl-D-Aspartate (NMDA) [[cell surface receptor]]s for the [[neurotransmitter]] [[glutamate]].
====Anti-psychotics====
The newer, atypical [[antipsychotic agent]]s (olanzapine, quetiapine, risperidone), were found to have "adverse effects offset advantages in the efficacy of atypical antipsychotic drugs for the treatment of psychosis, aggression, or agitation in patients with Alzheimer's disease."<ref name="pmid17035647">{{cite journal |author=Schneider LS, Tariot PN, Dagerman KS, ''et al'' |title=Effectiveness of atypical antipsychotic drugs in patients with Alzheimer's disease |journal=N. Engl. J. Med. |volume=355 |issue=15 |pages=1525–38 |year=2006 |pmid=17035647 |doi=10.1056/NEJMoa061240|url=http://content.nejm.org/cgi/content/full/355/15/1525}}</ref>
Withdrawing psychotropics mediations may prevent falls.<ref name="pmid10404930">{{cite journal |author=Campbell AJ, Robertson MC, Gardner MM, Norton RN, Buchner DM |title=Psychotropic medication withdrawal and a home-based exercise program to prevent falls: a randomized, controlled trial |journal=J Am Geriatr Soc |volume=47 |issue=7 |pages=850–3 |year=1999 |pmid=10404930 |doi=}}</ref>
====Dietary supplements====
[[Ginkgo biloba]] has conflicting evidence regarding its efficacy.<ref name="pmid12186600">{{cite journal |author=Solomon PR, Adams F, Silver A, Zimmer J, DeVeaux R |title=Ginkgo for memory enhancement: a randomized controlled trial |journal=JAMA |volume=288 |issue=7 |pages=835–40 |year=2002 |pmid=12186600 |doi=}}</ref><ref name="pmid9343463">{{cite journal |author=Le Bars PL, Katz MM, Berman N, Itil TM, Freedman AM, Schatzberg AF |title=A placebo-controlled, double-blind, randomized trial of an extract of Ginkgo biloba for dementia. North American EGb Study Group |journal=JAMA |volume=278 |issue=16 |pages=1327–32 |year=1997 |pmid=9343463 |doi=}}</ref><ref name="pmid19160216">{{cite journal |author=Birks J, Grimley Evans J |title=Ginkgo biloba for cognitive impairment and dementia |journal=Cochrane Database Syst Rev |volume= |issue=1 |pages=CD003120 |year=2009 |pmid=19160216 |doi=10.1002/14651858.CD003120.pub3 |url=http://dx.doi.org/10.1002/14651858.CD003120.pub3 |issn=}}</ref>
==Prevention==
===Physical activity===
Most<ref name="pmid8768414">{{cite journal |author=Byles JE, Sanson-Fisher RW |title=Mass mailing campaigns to promote screening for cervical cancer: do they work, and do they continue to work? |journal=Aust N Z J Public Health |volume=20 |issue=3 |pages=254–60 |year=1996 |month=June |pmid=8768414 |doi= |url= |issn=}}</ref><ref name="pmid18094335">{{cite journal |author=Ravaglia G, Forti P, Lucicesare A, ''et al'' |title=Physical activity and dementia risk in the elderly. Findings from a prospective Italian study |journal=Neurology |volume= |issue= |pages= |year=2007 |pmid=18094335 |doi=10.1212/01.wnl.0000296276.50595.86 |issn=}}</ref><ref name="pmid16418406">{{cite journal |author=Larson EB, Wang L, Bowen JD, ''et al'' |title=Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older |journal=Ann. Intern. Med. |volume=144 |issue=2 |pages=73–81 |year=2006 |pmid=16418406 |doi= |issn=}}</ref><ref name="pmid15383515">{{cite journal |author=Abbott RD, White LR, Ross GW, Masaki KH, Curb JD, Petrovitch H |title=Walking and dementia in physically capable elderly men |journal=JAMA |volume=292 |issue=12 |pages=1447–53 |year=2004 |pmid=15383515 |doi=10.1001/jama.292.12.1447 |issn=}}</ref>, but not all<ref name="pmid12815136">{{cite journal |author=Verghese J, Lipton RB, Katz MJ, ''et al'' |title=Leisure activities and the risk of dementia in the elderly |journal=N. Engl. J. Med. |volume=348 |issue=25 |pages=2508–16 |year=2003 |pmid=12815136 |doi=10.1056/NEJMoa022252 |issn=}}</ref> studies find that physical activity is associated with reduced risk of dementia. These observational studies cannot prove cause and effect.
===Mental activity===
Maintaining activities such as cognitive games and reading, playing musical instruments, and physical activities are associated with reduced the risk of dementia in an observational study.<ref name="pmid12815136">{{cite journal |author=Verghese J, Lipton RB, Katz MJ, ''et al'' |title=Leisure activities and the risk of dementia in the elderly |journal=N. Engl. J. Med. |volume=348 |issue=25 |pages=2508–16 |year=2003 |pmid=12815136 |doi=10.1056/NEJMoa022252 |issn=}}</ref>
===Medications===
===Medications===
Various medications have been associated with progression or prevention ([[cholinesterase inhibitor]]s, [[N-methyl-D-aspartate receptor]] antagonists, [[renin-angiotensin system]] blockers, and [[hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s) of dementia.<ref name="pmid17012333">{{cite journal |author=Ellul J, Archer N, Foy CM, ''et al'' |title=The effects of commonly prescribed drugs in patients with Alzheimer's disease on the rate of deterioration |journal=J. Neurol. Neurosurg. Psychiatr. |volume=78 |issue=3 |pages=233–9 |year=2007 |month=March |pmid=17012333 |doi=10.1136/jnnp.2006.104034 |url=http://jnnp.bmj.com/cgi/pmidlookup?view=long&pmid=17012333 |issn=}}</ref>
Various medications have been associated with progression or prevention ([[cholinesterase inhibitor]]s, [[N-methyl-D-aspartate receptor]] antagonists, [[renin-angiotensin system]] blockers, and [[hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s) of dementia.<ref name="pmid17012333">{{cite journal |author=Ellul J, Archer N, Foy CM, ''et al'' |title=The effects of commonly prescribed drugs in patients with Alzheimer's disease on the rate of deterioration |journal=J. Neurol. Neurosurg. Psychiatr. |volume=78 |issue=3 |pages=233–9 |year=2007 |month=March |pmid=17012333 |doi=10.1136/jnnp.2006.104034 |url=http://jnnp.bmj.com/cgi/pmidlookup?view=long&pmid=17012333 |issn=}}</ref>


Observational, non-ramdomized [[cohort study|cohort studies]] suggest that [[hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s (statins) may<ref name="pmid18663180">{{cite journal |author=Cramer C, Haan MN, Galea S, Langa KM, Kalbfleisch JD |title=Use of statins and incidence of dementia and cognitive impairment without dementia in a cohort study |journal=Neurology |volume=71 |issue=5 |pages=344–50 |year=2008 |month=July |pmid=18663180 |doi=10.1212/01.wnl.0000319647.15752.7b |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=18663180 |issn=}}</ref><ref name="pmid18931004">{{cite journal |author=Haag MD, Hofman A, Koudstaal PJ, Stricker BH, Breteler MM |title=Statins are associated with a reduced risk of Alzheimer disease regardless of lipophilicity. The Rotterdam Study |journal=J. Neurol. Neurosurg. Psychiatr. |volume=80 |issue=1 |pages=13–7 |year=2009 |month=January |pmid=18931004 |doi=10.1136/jnnp.2008.150433 |url=http://jnnp.bmj.com/cgi/pmidlookup?view=long&pmid=18931004 |issn=}}</ref> or may not<ref name="pmid15699299">{{cite journal |author=Zandi PP, Sparks DL, Khachaturian AS, ''et al'' |title=Do statins reduce risk of incident dementia and Alzheimer disease? The Cache County Study |journal=Arch. Gen. Psychiatry |volume=62 |issue=2 |pages=217–24 |year=2005 |month=February |pmid=15699299 |doi=10.1001/archpsyc.62.2.217 |url=http://archpsyc.ama-assn.org/cgi/pmidlookup?view=long&pmid=15699299 |issn=}}</ref><ref name="pmid15534246">{{cite journal |author=Li G, Higdon R, Kukull WA, ''et al'' |title=Statin therapy and risk of dementia in the elderly: a community-based prospective cohort study |journal=Neurology |volume=63 |issue=9 |pages=1624–8 |year=2004 |month=November |pmid=15534246 |doi= |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=15534246 |issn=}}</ref> prevent dementia.
Observational, non-ramdomized [[cohort study|cohort studies]] suggest that [[hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s (statins) may<ref name="pmid18663180">{{cite journal |author=Cramer C, Haan MN, Galea S, Langa KM, Kalbfleisch JD |title=Use of statins and incidence of dementia and cognitive impairment without dementia in a cohort study |journal=Neurology |volume=71 |issue=5 |pages=344–50 |year=2008 |month=July |pmid=18663180 |doi=10.1212/01.wnl.0000319647.15752.7b |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=18663180 |issn=}}</ref><ref name="pmid18931004">{{cite journal |author=Haag MD, Hofman A, Koudstaal PJ, Stricker BH, Breteler MM |title=Statins are associated with a reduced risk of Alzheimer disease regardless of lipophilicity. The Rotterdam Study |journal=J. Neurol. Neurosurg. Psychiatr. |volume=80 |issue=1 |pages=13–7 |year=2009 |month=January |pmid=18931004 |doi=10.1136/jnnp.2008.150433 |url=http://jnnp.bmj.com/cgi/pmidlookup?view=long&pmid=18931004 |issn=}}</ref> or may not<ref name="pmid15699299">{{cite journal |author=Zandi PP, Sparks DL, Khachaturian AS, ''et al'' |title=Do statins reduce risk of incident dementia and Alzheimer disease? The Cache County Study |journal=Arch. Gen. Psychiatry |volume=62 |issue=2 |pages=217–24 |year=2005 |month=February |pmid=15699299 |doi=10.1001/archpsyc.62.2.217 |url=http://archpsyc.ama-assn.org/cgi/pmidlookup?view=long&pmid=15699299 |issn=}}</ref><ref name="pmid15534246">{{cite journal |author=Li G, Higdon R, Kukull WA, ''et al'' |title=Statin therapy and risk of dementia in the elderly: a community-based prospective cohort study |journal=Neurology |volume=63 |issue=9 |pages=1624–8 |year=2004 |month=November |pmid=15534246 |doi= |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=15534246 |issn=}}</ref> prevent dementia.
===Supplements===
[[Ginkgo biloba]] does not prevent dementia according to a large [[randomized controlled trial]]<ref name="pmid19017911">{{cite journal |author=DeKosky ST, Williamson JD, Fitzpatrick AL, ''et al'' |title=Ginkgo biloba for prevention of dementia: a randomized controlled trial |journal=JAMA |volume=300 |issue=19 |pages=2253–62 |year=2008 |month=November |pmid=19017911 |doi=10.1001/jama.2008.683 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=19017911 |issn=}}</ref> and [[systematic review]]<ref name="pmid19160216">{{cite journal |author=Birks J, Grimley Evans J |title=Ginkgo biloba for cognitive impairment and dementia |journal=Cochrane Database Syst Rev |volume= |issue=1 |pages=CD003120 |year=2009 |pmid=19160216 |doi=10.1002/14651858.CD003120.pub3 |url=http://dx.doi.org/10.1002/14651858.CD003120.pub3 |issn=}}</ref> by the [[Cochrane Collaboration]] in spite of earlier studies that were positive<ref name="pmid12404671">{{cite journal |author=Mix JA, Crews WD |title=A double-blind, placebo-controlled, randomized trial of Ginkgo biloba extract EGb 761 in a sample of cognitively intact older adults: neuropsychological findings |journal=Hum Psychopharmacol |volume=17 |issue=6 |pages=267–77 |year=2002 |month=August |pmid=12404671 |doi=10.1002/hup.412 |url=http://dx.doi.org/10.1002/hup.412 |issn=}}</ref>.
==Screening==
In 2003, a [[clinical practice guideline]] by the [http://www.ahrq.gov/clinic/uspstfix.htm U.S. Preventive Services Task Force (USPSTF)] gave a [http://www.ahrq.gov/clinic/3rduspstf/ratings.htm grade I recommendation], indicating "the evidence is insufficient to recommend for or against routine screening for dementia in older adults".<ref name="pmid12779303">{{cite journal |author=U.S. Preventive Services Task Force |title=Screening for dementia: recommendation and rationale |journal=Ann. Intern. Med. |volume=138 |issue=11 |pages=925–6 |year=2003 |pmid=12779303 |doi=}}</ref>
==Prognosis==
A systematic review of cohort studies concluded that the rate conversion of [[mild cognitive impairment]] to dementia is about 4% per year."<ref name="pmid19010949">{{cite journal |author=Mitchell AJ, Shiri-Feshki M |title=Temporal trends in the long term risk of progression of mild cognitive impairment: a pooled analysis |journal=J. Neurol. Neurosurg. Psychiatr. |volume=79 |issue=12 |pages=1386–91 |year=2008 |month=December |pmid=19010949 |doi=10.1136/jnnp.2007.142679 |url=http://jnnp.bmj.com/cgi/pmidlookup?view=long&pmid=19010949 |issn=}}</ref>
==References==
<references/>

Revision as of 07:27, 10 April 2009

Medications

Various medications have been associated with progression or prevention (cholinesterase inhibitors, N-methyl-D-aspartate receptor antagonists, renin-angiotensin system blockers, and hydroxymethylglutaryl-coenzyme A reductase inhibitors) of dementia.[1]

Observational, non-ramdomized cohort studies suggest that hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins) may[2][3] or may not[4][5] prevent dementia.

  1. Ellul J, Archer N, Foy CM, et al (March 2007). "The effects of commonly prescribed drugs in patients with Alzheimer's disease on the rate of deterioration". J. Neurol. Neurosurg. Psychiatr. 78 (3): 233–9. DOI:10.1136/jnnp.2006.104034. PMID 17012333. Research Blogging.
  2. Cramer C, Haan MN, Galea S, Langa KM, Kalbfleisch JD (July 2008). "Use of statins and incidence of dementia and cognitive impairment without dementia in a cohort study". Neurology 71 (5): 344–50. DOI:10.1212/01.wnl.0000319647.15752.7b. PMID 18663180. Research Blogging.
  3. Haag MD, Hofman A, Koudstaal PJ, Stricker BH, Breteler MM (January 2009). "Statins are associated with a reduced risk of Alzheimer disease regardless of lipophilicity. The Rotterdam Study". J. Neurol. Neurosurg. Psychiatr. 80 (1): 13–7. DOI:10.1136/jnnp.2008.150433. PMID 18931004. Research Blogging.
  4. Zandi PP, Sparks DL, Khachaturian AS, et al (February 2005). "Do statins reduce risk of incident dementia and Alzheimer disease? The Cache County Study". Arch. Gen. Psychiatry 62 (2): 217–24. DOI:10.1001/archpsyc.62.2.217. PMID 15699299. Research Blogging.
  5. Li G, Higdon R, Kukull WA, et al (November 2004). "Statin therapy and risk of dementia in the elderly: a community-based prospective cohort study". Neurology 63 (9): 1624–8. PMID 15534246[e]