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Dementia
ICD-10 F00-F07
ICD-9 290-294
OMIM [1]
DiseasesDB 29283
MedlinePlus 000739
eMedicine /
MeSH {{{MeshNumber}}}


Senile dementia (from Latin de- "apart, away" + mens (genitive mentis) "mind") is the progressive decline in cognitive function due to damage or disease in the brain beyond what might be expected from normal aging. Although dementia is far more common in the geriatric population, it may occur in any stage of adulthood. This age cutoff is defining, as similar sets of symptoms due to organic brain dysfunction are given different names in populations younger than adulthood (see, for instance, developmental disorders).

In dementia, affected areas in cognition may be memory, attention, language, and problem solving. Higher mental functions are affected first in the process. Especially in the later stages of the condition, affected persons may be disoriented in time (not knowing what day of the week, day of the month, month, or even what year it is), in place (not knowing where they are), and in person (not knowing who they are).

Symptoms of dementia can be classified as either reversible or irreversible depending upon the etiology of the disease. Less than 10 percent of cases of dementia are due to causes which may presently be reversed with treatment. Of these cases almost 100% are elderly people. Dementia is a term for a non-specific illness syndrome (set of symptoms) which is caused by many different specific disease processes, in the same way that symptoms of organ dysfunction such as shortness of breath, jaundice, or pain are attributable to many etiologies.

Without careful assessment of history, the short-term syndrome of delirium can easily be confused with dementia, because many of the symptoms of these are also present in dementia. Some mental illnesses including depression and psychosis may also produce symptoms which must be differentiated from both delirium and dementia.[1]

EpidemiologyEdit

The prevalence of dementia is rising as the global life expectancy is rising. Particularly in Western countries, there is an increasing concern about the economic impact that dementia will have in future, older populaces. In Australia, the 2006 estimated prevalence of dementia is 1.03% of the population as a whole. Though reports of some of the longest living people claim them to be free of it (e.g. Yone Minagawa), it is a disease which is strongly associated with age; 1% of those aged 60-65, 6% of those aged 75-79, and 45% of those aged 95 or older suffer from the syndrome.[2]

DiagnosisEdit

Proper differential diagnosis between the types of dementia (see below) will require, at the least, referral to a specialist, e.g. a geriatric internist, geriatric psychiatrist, neurologist, neuropsychologist or geropsychologist. However, there exist some brief tests (5-15 minutes) that have reasonable reliability and can be used in the office or other setting to screen cognitive status for deficits which are considered pathological. Examples of such tests include the abbreviated mental test score (AMTS), the mini mental state examination (MMSE), Modified Mini-Mental State Examination (3MS),[3] the Cognitive Abilities Screening Instrument (CASI),[4] and the clock drawing test.[5]

An AMTS score of less than six (out of a possible score of ten) and an MMSE score under 24 (out of a possible score of 30) suggests a need for further evaluation. Scores must be interpreted in the context of the person's educational and other background, and the particular circumstances; for example, a person highly depressed or in great pain will not be expected to do well on many tests of mental ability.

Mini-mental state examinationEdit

Main article: Mini-mental state examination

The U.S. Preventive Services Task Force (USPSTF) reviewed tests for cognitive impairment and concluded:[6]

sensitivity 71% to 92%
specificity 56% to 96%

A copy of the MMSE can be found in the appendix of the original publication.[7]

Modified Mini-Mental State examination (3MS)Edit

A copy of the 3MS is online.[8] A meta-analysis concluded that the Modified Mini-Mental State (3MS) examination has:[9]

sensitivity 83% to 94%
specificity 85% to 90%

Abbreviated mental test scoreEdit

Main article: abbreviated mental test score

A meta-analysis concluded:[9]

sensitivity 73% to 100%
specificity 71% to 100%

Other examinationsEdit

Many other tests have been studied[10][11][12] including the clock-drawing test example form). Although some may emerge as better alternatives to the MMSE, presently the MMSE is the best studied. However, access to the MMSE is now limited by enforcement of its copyright (details).

Another approach to screening for dementia is to ask an informant (relative or other supporter) to fill out a questionnaire about the person's everyday cognitive functioning. Informant questionnaires provide complementary information to brief cognitive tests. Probably the best known questionnaire of this sort is the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE).[13]

Further evaluation includes retesting at another date, and administration of other (and sometimes more complex) tests of mental function, such as formal neuropsychological testing.

Laboratory testsEdit

Routine blood tests are also usually performed to rule out treatable causes. These tests include vitamin B12, folic acid, thyroid-stimulating hormone (TSH), C-reactive protein, full blood count, electrolytes, calcium, renal function and liver enzymes. Abnormalities may suggest vitamin deficiency, infection or other problems that commonly cause confusion or disorientation in the elderly. The problem is complicated by the fact that these cause confusion more often in persons who have early dementia, so that "reversal" of such problems may ultimately only be temporary.

Chronic use of substances such as alcohol can also predispose the patient to cognitive changes suggestive of dementia.

ImagingEdit

A CT scan or magnetic resonance imaging (MRI scan) is commonly performed, although these modalities (as is noted below) do not have optimal sensitivity for the diffuse metabolic changes associated with dementia in a patient who shows no gross neurological problems (such as paralysis or weakness) on neurological exam. CT or MRI may suggest normal pressure hydrocephalus, a potentially reversible cause of dementia, and can yield information relevant to other types of dementia, such as infarction (stroke) that would point at a vascular type of dementia. However, the functional neuroimaging modalities of SPECT and PET have shown similar ability to diagnose dementia as clinical exam.[14] The ability of SPECT to differentiate the vascular cause from the Alzheimer disease cause of dementias, appears to be superior to differentiation by clinical exam.[15]

TypesEdit

Cortical dementiasEdit

Subcortical dementiasEdit

  • Dementia not otherwise specified (used in cases where no specific criteria is met)

Dementia and early onset dementia have been associated with neurovisceral porphyrias. Porphyria is listed in textbooks in the differential diagnosis of dementia. Because acute intermittent porphyria, hereditary coproporphyria and variegate porphyria are aggravated by environmental toxins and drugs the disorders should be ruled out when these etiologies are raised.


TreatmentEdit

Except for the treatable types listed above, there is no cure to this illness, although scientists are progressing in making a type of medication that will slow down the process. Cholinesterase inhibitors are often used early in the disease course. Cognitive and behavioral interventions may also be appropriate. Educating and providing emotional support to the caregiver (or carer) is of importance as well (see also elderly care).

A Canadian study found that a lifetime of bilingualism has a marked influence on delaying the onset of dementia by an average of four years when compared to monolingual patients. The researchers determined that the onset of dementia symptoms in the monolingual group occurred at the mean age of 71.4, while the bilingual group was 75.5 years. The difference remained even after considering the possible effect of cultural differences, immigration, formal education, employment and even gender as influences in the results.[16]

MedicationsEdit

Tacrine (Cognex), donepezil (Aricept), galantamine (Reminyl), and rivastigmine (Exelon) are approved by the United States Food and Drug Administration (FDA) for treatment of dementia induced by Alzheimer disease. They may be useful for other similar diseases causing dementia such as Parkinsons or vascular dementia.[17]

  • N-methyl-D-aspartate Blockers

Drugs within the class known as N-methyl-D-aspartate (NMDA) blockers include memantine (Namenda), which has been approved by the FDA for the treatment of moderate-to-severe dementia.

Off labelEdit

  • Amyloid deposit inhibitors

Minocycline and Clioquinoline, antibiotics, may help reduce amyloid deposits in the brains of persons with Alzheimer disease.[18]

  • Antipsychotic drugs

Haloperidol (Haldol), risperidone (Risperdal), olanzapine (Zyprexa), and quetiapine (Seroquel) are frequently prescribed to help manage psychosis and agitation. Treatment of dementia-associated psychosis or agitation is intended to decrease psychotic symptoms (for example, paranoia, delusions, hallucinations), screaming, combativeness, and/or violence.[19][20]

Depression is frequently associated with dementia and generally worsens the degree of cognitive and behavioral impairment. Antidepressants may be helpful in alleviating cognitive and behavior symptoms by reuptaking neurotransmitter regulation through reuptake of serotonin, noradrenaline and dopamine.

  • Antianxiety drugs

Many patients with dementia experience anxiety symptoms. Although benzodiazepines like diazepam (Valium) have been used for treating anxiety in other situations, they are often avoided because they may increase agitation in persons with dementia or are too sedating. Buspirone (Buspar) is often initially tried for mild-to-moderate anxiety.

Selegiline, a drug used primarily in the treatment of Parkinson's disease, appears to slow the development of dementia. Selegiline is thought to act as an antioxidant, preventing free radical damage. However, it also acts as a stimulant, making it difficult to determine whether the delay in onset of dementia symptoms is due to protection from free radicals or to the general elevation of brain activity from the stimulant effect.

PreventionEdit

Main article: Prevention of dementia

Since there is no cure for dementia, the best an individual can do is to prevent it from developing in the first place.

The main method to prevent dementia is to live an active life, both mentally and physically. It appears that the regular moderate consumption of alcohol (beer, wine or distilled spirits) may reduce risk.[21]

Furthermore, there are medications which might contribute to prevent the onset of dementia, including hypertension medications, anti-diabetic drugs and NSAIDs.[22]

Studies published in US journals suggested that a Mediterranean diet or long-term beta-carotene supplements could ward off dementia. [2]

Risk to self & othersEdit

Driving with Dementia could lead to severe injury or even death to self and others. Doctors should advise appropriate testing on when to quit driving.[23]

Florida's Baker Act allows law enforcement and the judiciary to force mental evaluation for those suspected of suffering from Dementia or other mental incapacities.

ServicesEdit

Adult daycare centers as well as special care units in nursing homes often provide specialized care for dementia patients. Adult daycare centers offer supervision, recreation, meals, and limited health care to participants, as well as providing respite for caregivers.

Further readingEdit

ReferencesEdit

  1. American Family Physician, March 1, 2003 Delirium
  2. Dementia Estimates and Projections: Australian States and Territories. Alzheimer's Australia. URL accessed on 2006-10-04.
  3. Teng E L, Chui H C. The Modified Mini-Mental State (3MS) examination. J Clin Psychiatry 1987;48:314–18. PMID 3611032
  4. Teng E L, Hasegawa K, Homma A, et al. The Cognitive Abilities Screening Instrument (CASI): a practical test for cross-cultural epidemiological studies of dementia. Int Psychogeriatr 1994;6:45–58. PMID 8054493
  5. Royall, D.; Cordes J.; & Polk M. (1998). CLOX: an executive clock drawing task. J Neurol Neurosurg Psychiatry 64 (5): 588-94.
  6. Boustani, M.; Peterson, B.; Hanson, L.; Harris, R.; & Lohr, K. (2003). Screening for dementia in primary care: a summary of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med 138 (11): 927-37.
  7. Folstein MF, Folstein SE, McHugh PR (1975). "Mini-mental state". A practical method for grading the cognitive state of patients for the clinician. Journal of psychiatric research 12 (3): 189-98.
  8. Appendix: The Modified Mini-Mental State (3MS). URL accessed on 2007-09-06.
  9. 9.0 9.1 Cullen B, O'Neill B, Evans JJ, Coen RF, Lawlor BA. A review of screening tests for cognitive impairment. J Neurol Neurosurg Psychiatry. 2007 Aug;78(8):790-9. Epub 2006 Dec 18. PMID 17178826
  10. Sager, M.; Hermann, B.; La Rue, A.; & Woodard, J. (2006). Screening for dementia in community-based memory clinics. WMJ 105 (7): 25-9.
  11. Fleisher, A.; Sowell B.; Taylor C.; Gamst A.; Petersen R.; & Thal L.. Clinical predictors of progression to Alzheimer disease in amnestic mild cognitive impairment. Neurology.
  12. Karlawish, J. & Clark, C. (2003). Diagnostic evaluation of elderly patients with mild memory problems. Ann Intern Med 138 (5): 411-9.
  13. Jorm, A.F. (2004). The Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE): A review. International Psychogeriatrics, 16, 1-19.
  14. Bonte, FJ, Harris TS, Hynan LS, Bigio EH, White CL 3rd (July 2006). Tc-99m HMPAO SPECT in the differential diagnosis of the dementias with histopathologic confirmation. Clinical Nuclear Medicine 31 (7): 376-8.
  15. Dougall, NJ, Bruggink S, Ebmeier KP (Nov-Dec 2004). Systematic review of the diagnostic accuracy of 99mTc-HMPAO-SPECT in dementia. The American Journal of Geriatric Psychiatry 12 (6): 554-70.
  16. Bilingualism Has Protective Effect In Delaying Onset Of Dementia By Four Years, Canadian Study Shows. Medical News Today. URL accessed on 2007-01-16.
  17. Lleo A, Greenberg SM, Growdon JH. Current pharmacotherapy for Alzheimer's disease. Annu Rev Med. 2006;57:513-33. Review. PMID 16409164
  18. Choi, Y., Kim, H.S., Shin, K.Y., Kim, E.M., Kim, M., Kim, H.S., Park, C.H., Jeong, Y.H., Yoo, J., Lee, J.P., Chang K.A., Kim S., & Suh, Y.H. Related Minocycline Attenuates Neuronal Cell Death and Improves Cognitive Impairment in Alzheimer's Disease Models. Neuropsychopharmacology. 2007 Apr 4; PMID 17406652
  19. Wei, Z., Mousseau, D.D., Dai, Y., Cao, X., Li, X.M. (2006). Haloperidol induces apoptosis via the sigma2 receptor system and Bcl-XS. Pharmacogenomics J. 6(4):279-88. Epub 2006 Feb 7. PMID 16462815
  20. Wang, H., Xu, H., Dyck, L.E., & Li, X.M. (2005). Olanzapine and quetiapine protect PC12 cells from beta-amyloid peptide(25-35)-induced oxidative stress and the ensuing apoptosis. Journal Neuroscience Res, 81(4):572-80. PMID 15948179
  21. Mulkamal, K.J., et al. Prospective study of alcohol consumption and risk of dementia in older adults. Journal of the American Medical Association, 2003 (March 19), 289, 1405-1413; Ganguli, M., et al. Alcohol consumption and cognitive function in late life: A longitudinal community study. Neurology, 2005, 65, 1210-12-17; Huang, W., et al. Alcohol consumption and incidence of dementia in a community sample aged 75 years and older. Journal of Clinical Epidemiology, 2002, 55(10), 959-964; Rodgers, B., et al. Non-linear relationships between cognitive function and alcohol consumption in young, middle-aged and older adults: The PATH Through Life Project. Addiction, 2005, 100(9), 1280-1290; Anstey, K. J., et al. Lower cognitive test scores observed in alcohol are associated with demographic, personality, and biological factors: The PATH Through Life Project. Addiction, 2005, 100(9), 1291-1301; Espeland, M., et al. Association between alcohol intake and domain-specific cognitive function in older women. Neuroepidemiology, 2006, 1(27), 1-12; Stampfer, M.J., et al'. Effects of moderate alcohol consumption on cognitive function in women. New England Journal of Medicine, 2005, 352, 245-253; Ruitenberg, A., et al. Alcohol consumption and risk of dementia: the Rotterdam Study. Lancet, 2002, 359(9303), 281-286; Scarmeas, N., et al. Mediterranean diet and risk for Alzheimer’s disease. Annals of Neurology, 2006 (published online April 18, 2006).
  22. West Virginia Department of Health and Human Resources (with further links to experiments respectively)
  23. Drivers with dementia a growing problem, MDs warn, CBC News, Canada, September 19, 2007

External linksEdit



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