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| ==Medical Therapy== | | ==Medical Therapy== |
| 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. [[Acetylcholinesterase inhibitor|Cholinesterase inhibitor]]s 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 career) is of importance as well (''see also [[Elderly care|elderly care]]'').
| | The mainstay of management of dementia is : |
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| 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. <ref>{{cite web | url=http://www.medicalnewstoday.com/medicalnews.php?newsid=60646 | title=Bilingualism Has Protective Effect In Delaying Onset Of Dementia By Four Years, Canadian Study Shows | publisher=Medical News Today | date=[[2007-01-11]] |accessdate=2007-01-16}}</ref>
| | * Symptomatic |
| | * Treatment of behavioral disturbances |
| | * Environmental manipulations to support function |
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| *Treat all reversible causes | | * Counseling with respect to safety issues. |
| *Identify and treat nonreversibly disease etiologies
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| *Treat risk factors for those patients with vascular dementia
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| ===Pharmacotherapy===
| | More precise diagnosis is required for effective management and accurate prognosis. Medical therapy for dementia include: |
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| [[Snoezelen|Snoezelen rooms]] that provide patients with a soothing and stimulating environment of light, color, music and scent have been used in the therapy of dementia patients. | | * [[Cholinesterase inhibitors]] ( [[Donepezil]] , [[Rivastigmine]] , [[Galantamine]] ) |
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| ===Medications===
| | They increase cholinergic transmission by inhibiting cholinesterase at the synaptic cleft and provide modest symptomatic benefit in some patients with dementia. |
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| *[[Acetylcholinesterase inhibitor]]s | | * [[Memantine]] |
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| [[Tacrine]] (Cognex), [[donepezil]] (Aricept), [[galantamine]] (Reminyl), and [[rivastigmine]] (Exelon) <ref name="pmid9932386">{{cite journal |vauthors=Lancelot E, Beal MF |title=Glutamate toxicity in chronic neurodegenerative disease |journal=Prog. Brain Res. |volume=116 |issue= |pages=331–47 |date=1998 |pmid=9932386 |doi=10.1016/s0079-6123(08)60446-x |url=}}</ref>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.<ref>Lleo A, Greenberg SM, Growdon JH. Current pharmacotherapy for Alzheimer's disease. Annu Rev Med. 2006;57:513-33. Review. PMID 16409164</ref> They increase cholinergic transmission by inhibiting cholinesterase at the synaptic cleft and provide modest symptomatic benefit in some patients with dementia.
| | Excessive NMDA stimulation can be induced by ischemia and lead to excitotoxicity, suggesting that agents that block pathologic stimulation of NMDA receptors may protect against further damage in patients with vascular dementia. |
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| *N-methyl-D-aspartate Blockers<ref name="pmid9860805">{{cite journal |vauthors=Danysz W, Parsons CG |title=Glycine and N-methyl-D-aspartate receptors: physiological significance and possible therapeutic applications |journal=Pharmacol. Rev. |volume=50 |issue=4 |pages=597–664 |date=December 1998 |pmid=9860805 |doi= |url=}}</ref>
| | They have modest benefits in patients with moderate to severe AD |
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| 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. The mechanism of action of memantine is distinct from those of the cholinergic agents; it is neuroprotective. Glutamate is the principal excitatory amino acid neurotransmitter in cortical and hippocampal neurons
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| ====Acute Pharmacotherapies====
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| *'''Alzheimer's Disease'''
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| *:*[[Alpha-tocopherol]]
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| *:*[[Anticholinesterase]]s
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| *:*Selegiline
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| *'''Parkinson's Disease'''
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| *:*[[Anticholinergic]]s
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| *:*[[Dopamine]]
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| *:*Dopamine agonists
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| *:*Selegiline
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| ====Off Label====
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| *Amyloid deposit inhibitors
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| [[Minocycline]] and Clioquinoline, antibiotics, may help reduce [[amyloid]] deposits in the brains of persons with Alzheimer disease.<ref>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</ref>
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| *Antipsychotic drugs
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| [[Haloperidol]] (Haldol)<ref name="pmid1356550">{{cite journal |vauthors=McKeith I, Fairbairn A, Perry R, Thompson P, Perry E |title=Neuroleptic sensitivity in patients with senile dementia of Lewy body type |journal=BMJ |volume=305 |issue=6855 |pages=673–8 |date=September 1992 |pmid=1356550 |pmc=1882909 |doi=10.1136/bmj.305.6855.673 |url=}}</ref>, [[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.<ref>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</ref><ref>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</ref>
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| *[[Antidepressant]] drugs
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| [[Clinical depression|Depression]] is frequently associated with dementia and generally worsens the degree of [[cognitive]] and [[behavioral]] impairment. [[Antidepressant]]s may be helpful in alleviating cognitive and behavior symptoms by reuptaking [[neurotransmitter]] regulation through reuptake of [[serotonin]], [[noradrenaline]] and [[dopamine]].
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| *Antianxiety drugs
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| 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.
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| [[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. A meta-analysis of 12 trials found that 8 of the studies suggested some beneficial effect of selegiline in the treatment of cognitive benefits and, in three trials, in the treatment of behavior and mood
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| ==References== | | ==References== |