Dementia medical therapy: Difference between revisions

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{{Template:Dementia}}
{{Template:Dementia}}
{{CMG}}
{{CMG}}
==Overview==
The mainstay of management is symptomatic: treatment of behavioral disturbances, environmental manipulations to support function, and counseling with respect to safety issues. Treatment of behavioral and sleep problems is an important aspect of the care of patients with dementia.<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> A close discussion with the patient's caregiver is essential.<ref name="pmid8543219">{{cite journal |vauthors=Pruchno RA, Smyer MA, Rose MS, Hartman-Stein PE, Henderson-Laribee DL |title=Competence of long-term care residents to participate in decisions about their medical care: a brief, objective assessment |journal=Gerontologist |volume=35 |issue=5 |pages=622–9 |date=October 1995 |pmid=8543219 |doi=10.1093/geront/35.5.622 |url=}}</ref><br />Mostly dementia is because of irreversible causes and in those cases treatment goal is to improve patient care and delay in disease progression and improvement in quality of life.
==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 :
 
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>
 
*Treat all reversible causes
*Identify and treat nonreversibly disease etiologies
*Treat risk factors for those patients with vascular dementia
 
===Pharmacotherapy===
 
[[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.
 
===Medications===
 
*[[Acetylcholinesterase inhibitor]]s
 
[[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.  
 
*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>
 
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
 
====Acute Pharmacotherapies====


*'''Alzheimer's Disease'''
*Symptomatic
*:*[[Alpha-tocopherol]]
*Treatment of behavioral disturbances
*:*[[Anticholinesterase]]s
*Environmental manipulations to support function
*:*Selegiline
*'''Parkinson's Disease'''
*:*[[Anticholinergic]]s
*:*[[Dopamine]]
*:*Dopamine agonists
*:*Selegiline


====Off Label====
*Counseling with respect to safety issues.


*Amyloid deposit inhibitors
More precise diagnosis is required for effective management and accurate prognosis. Medical therapy for dementia include:


[[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>
*[[Cholinesterase inhibitors]] ( [[Donepezil]] , [[Rivastigmine]] , [[Galantamine]] )<ref name="pmid7902967">{{cite journal |vauthors=Orrego F, Villanueva S |title=The chemical nature of the main central excitatory transmitter: a critical appraisal based upon release studies and synaptic vesicle localization |journal=Neuroscience |volume=56 |issue=3 |pages=539–55 |date=October 1993 |pmid=7902967 |doi=10.1016/0306-4522(93)90355-j |url=}}</ref>


*Antipsychotic drugs
They increase cholinergic transmission by inhibiting cholinesterase at the synaptic cleft and provide modest symptomatic benefit in some patients with dementia. Studies show benefit of cholinesterase inhibitors in patients with mild to moderate dementia (eg, MMSE 10 to 26) is a small improvement in cognition, neuropsychiatric symptoms, and activities of daily living. However, in patients with advanced dementia,  absolute effects may be less clinically significant than those seen in patients with mild to moderate dementia. These enhance vagal tone and are contraindicated in patients with baseline bradycardia or known cardiac conduction system disease (eg, sick sinus syndrome, incomplete heart block) due to risk of syncope, falls, and fractures. Gastrointestinal symptoms (upset stomach, nausea, diarrhea, anorexia) are the most common side effects with prolonged use [[Donepezil]] and [[Galantamine]]. Patients on a stable dose of these drugs are then seen every 6 to 12 months thereafter. Routine laboratory monitoring is not required for any of the cholinesterase inhibitors.


[[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> 
*[[Memantine]]


*[[Antidepressant]] drugs
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. They have modest benefits in patients with moderate to severe dementia.<ref name="pmid12672860">{{cite journal |vauthors=Reisberg B, Doody R, Stöffler A, Schmitt F, Ferris S, Möbius HJ |title=Memantine in moderate-to-severe Alzheimer's disease |journal=N Engl J Med |volume=348 |issue=14 |pages=1333–41 |date=April 2003 |pmid=12672860 |doi=10.1056/NEJMoa013128 |url=}}</ref>Dizziness is the most common side effect. Confusion and hallucinations also occur at a low frequency, but its use increase agitation and delusional behaviors in some patients.<ref name="pmid16087923">{{cite journal |vauthors=Ridha BH, Josephs KA, Rossor MN |title=Delusions and hallucinations in dementia with Lewy bodies: worsening with memantine |journal=Neurology |volume=65 |issue=3 |pages=481–2 |date=August 2005 |pmid=16087923 |doi=10.1212/01.wnl.0000172351.95783.8e |url=}}</ref> Memantine use improve cognition and global assessment of dementia. Its use in combination with a cholinesterase inhibitor in patients with advanced disease is recommended. As it is disease modifying, continue memantine even if no clinical improvement.


[[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]].
*[[Antioxidants]]


*Antianxiety drugs
This category includes [[vitamin E]] and [[selegiline]] <ref name="pmid9110909">{{cite journal |vauthors=Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, Woodbury P, Growdon J, Cotman CW, Pfeiffer E, Schneider LS, Thal LJ |title=A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study |journal=N Engl J Med |volume=336 |issue=17 |pages=1216–22 |date=April 1997 |pmid=9110909 |doi=10.1056/NEJM199704243361704 |url=}}</ref>


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.  
They have modest benefit in delaying functional progression in patients with mild to moderate Alzheimer Disease. Vitamin E at a dose of 2000 international units per day confers a modest benefit in delaying functional progression in patients with mild to moderate disease, with no  effect on cognitive performance. High dose Vitamin E is associated with an increase in all-cause mortality and also with heart failure in patients with cardiovascular disease.<ref name="pmid24381967">{{cite journal |vauthors=Dysken MW, Sano M, Asthana S, Vertrees JE, Pallaki M, Llorente M, Love S, Schellenberg GD, McCarten JR, Malphurs J, Prieto S, Chen P, Loreck DJ, Trapp G, Bakshi RS, Mintzer JE, Heidebrink JL, Vidal-Cardona A, Arroyo LM, Cruz AR, Zachariah S, Kowall NW, Chopra MP, Craft S, Thielke S, Turvey CL, Woodman C, Monnell KA, Gordon K, Tomaska J, Segal Y, Peduzzi PN, Guarino PD |title=Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial |journal=JAMA |volume=311 |issue=1 |pages=33–44 |date=January 2014 |pmid=24381967 |pmc=4109898 |doi=10.1001/jama.2013.282834 |url=}}</ref> 


[[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
There is some beneficial effect of [[selegiline]] in the treatment of cognitive benefits and in the treatment of behavior and mood in some studies.<ref name="pmid9110909">{{cite journal |vauthors=Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, Woodbury P, Growdon J, Cotman CW, Pfeiffer E, Schneider LS, Thal LJ |title=A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study |journal=N Engl J Med |volume=336 |issue=17 |pages=1216–22 |date=April 1997 |pmid=9110909 |doi=10.1056/NEJM199704243361704 |url=}}</ref> <ref name="pmid7700465">{{cite journal |vauthors=Potter LT |title=Discovery of treatments for Alzheimer's disease |journal=Neurobiol Aging |volume=15 Suppl 2 |issue= |pages=S67–9 |date=1994 |pmid=7700465 |doi=10.1016/0197-4580(94)90173-2 |url=}}</ref> <ref name="pmid8227897">{{cite journal |vauthors=Burke WJ, Roccaforte WH, Wengel SP, Bayer BL, Ranno AE, Willcockson NK |title=L-deprenyl in the treatment of mild dementia of the Alzheimer type: results of a 15-month trial |journal=J Am Geriatr Soc |volume=41 |issue=11 |pages=1219–25 |date=November 1993 |pmid=8227897 |doi=10.1111/j.1532-5415.1993.tb07306.x |url=}}</ref>  Studies also showed significant delays in time to the primary outcome (death, institutionalization, loss of ability to perform ADLs, or severe dementia)<ref name="pmid91109092">{{cite journal |vauthors=Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, Woodbury P, Growdon J, Cotman CW, Pfeiffer E, Schneider LS, Thal LJ |title=A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study |journal=N Engl J Med |volume=336 |issue=17 |pages=1216–22 |date=April 1997 |pmid=9110909 |doi=10.1056/NEJM199704243361704 |url=}}</ref><ref name="pmid77004652">{{cite journal |vauthors=Potter LT |title=Discovery of treatments for Alzheimer's disease |journal=Neurobiol Aging |volume=15 Suppl 2 |issue= |pages=S67–9 |date=1994 |pmid=7700465 |doi=10.1016/0197-4580(94)90173-2 |url=}}</ref>


==References==
==References==

Latest revision as of 18:39, 9 October 2020

Dementia Microchapters

Patient Information

Overview

Classification

Causes

Differential Diagnosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The mainstay of management is symptomatic: treatment of behavioral disturbances, environmental manipulations to support function, and counseling with respect to safety issues. Treatment of behavioral and sleep problems is an important aspect of the care of patients with dementia.[1] A close discussion with the patient's caregiver is essential.[2]
Mostly dementia is because of irreversible causes and in those cases treatment goal is to improve patient care and delay in disease progression and improvement in quality of life.

Medical Therapy

The mainstay of management of dementia is :

  • Symptomatic
  • Treatment of behavioral disturbances
  • Environmental manipulations to support function
  • Counseling with respect to safety issues.

More precise diagnosis is required for effective management and accurate prognosis. Medical therapy for dementia include:

They increase cholinergic transmission by inhibiting cholinesterase at the synaptic cleft and provide modest symptomatic benefit in some patients with dementia. Studies show benefit of cholinesterase inhibitors in patients with mild to moderate dementia (eg, MMSE 10 to 26) is a small improvement in cognition, neuropsychiatric symptoms, and activities of daily living. However, in patients with advanced dementia, absolute effects may be less clinically significant than those seen in patients with mild to moderate dementia. These enhance vagal tone and are contraindicated in patients with baseline bradycardia or known cardiac conduction system disease (eg, sick sinus syndrome, incomplete heart block) due to risk of syncope, falls, and fractures. Gastrointestinal symptoms (upset stomach, nausea, diarrhea, anorexia) are the most common side effects with prolonged use Donepezil and Galantamine. Patients on a stable dose of these drugs are then seen every 6 to 12 months thereafter. Routine laboratory monitoring is not required for any of the cholinesterase inhibitors.

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. They have modest benefits in patients with moderate to severe dementia.[4]Dizziness is the most common side effect. Confusion and hallucinations also occur at a low frequency, but its use increase agitation and delusional behaviors in some patients.[5] Memantine use improve cognition and global assessment of dementia. Its use in combination with a cholinesterase inhibitor in patients with advanced disease is recommended. As it is disease modifying, continue memantine even if no clinical improvement.

This category includes vitamin E and selegiline [6]

They have modest benefit in delaying functional progression in patients with mild to moderate Alzheimer Disease. Vitamin E at a dose of 2000 international units per day confers a modest benefit in delaying functional progression in patients with mild to moderate disease, with no effect on cognitive performance. High dose Vitamin E is associated with an increase in all-cause mortality and also with heart failure in patients with cardiovascular disease.[7]

There is some beneficial effect of selegiline in the treatment of cognitive benefits and in the treatment of behavior and mood in some studies.[6] [8] [9] Studies also showed significant delays in time to the primary outcome (death, institutionalization, loss of ability to perform ADLs, or severe dementia)[10][11]

References

  1. ↑ McKeith I, Fairbairn A, Perry R, Thompson P, Perry E (September 1992). "Neuroleptic sensitivity in patients with senile dementia of Lewy body type". BMJ. 305 (6855): 673–8. doi:10.1136/bmj.305.6855.673. PMC 1882909. PMID 1356550.
  2. ↑ Pruchno RA, Smyer MA, Rose MS, Hartman-Stein PE, Henderson-Laribee DL (October 1995). "Competence of long-term care residents to participate in decisions about their medical care: a brief, objective assessment". Gerontologist. 35 (5): 622–9. doi:10.1093/geront/35.5.622. PMID 8543219.
  3. ↑ Orrego F, Villanueva S (October 1993). "The chemical nature of the main central excitatory transmitter: a critical appraisal based upon release studies and synaptic vesicle localization". Neuroscience. 56 (3): 539–55. doi:10.1016/0306-4522(93)90355-j. PMID 7902967.
  4. ↑ Reisberg B, Doody R, Stöffler A, Schmitt F, Ferris S, Möbius HJ (April 2003). "Memantine in moderate-to-severe Alzheimer's disease". N Engl J Med. 348 (14): 1333–41. doi:10.1056/NEJMoa013128. PMID 12672860.
  5. ↑ Ridha BH, Josephs KA, Rossor MN (August 2005). "Delusions and hallucinations in dementia with Lewy bodies: worsening with memantine". Neurology. 65 (3): 481–2. doi:10.1212/01.wnl.0000172351.95783.8e. PMID 16087923.
  6. ↑ 6.0 6.1 Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, Woodbury P, Growdon J, Cotman CW, Pfeiffer E, Schneider LS, Thal LJ (April 1997). "A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study". N Engl J Med. 336 (17): 1216–22. doi:10.1056/NEJM199704243361704. PMID 9110909.
  7. ↑ Dysken MW, Sano M, Asthana S, Vertrees JE, Pallaki M, Llorente M, Love S, Schellenberg GD, McCarten JR, Malphurs J, Prieto S, Chen P, Loreck DJ, Trapp G, Bakshi RS, Mintzer JE, Heidebrink JL, Vidal-Cardona A, Arroyo LM, Cruz AR, Zachariah S, Kowall NW, Chopra MP, Craft S, Thielke S, Turvey CL, Woodman C, Monnell KA, Gordon K, Tomaska J, Segal Y, Peduzzi PN, Guarino PD (January 2014). "Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial". JAMA. 311 (1): 33–44. doi:10.1001/jama.2013.282834. PMC 4109898. PMID 24381967.
  8. ↑ Potter LT (1994). "Discovery of treatments for Alzheimer's disease". Neurobiol Aging. 15 Suppl 2: S67–9. doi:10.1016/0197-4580(94)90173-2. PMID 7700465.
  9. ↑ Burke WJ, Roccaforte WH, Wengel SP, Bayer BL, Ranno AE, Willcockson NK (November 1993). "L-deprenyl in the treatment of mild dementia of the Alzheimer type: results of a 15-month trial". J Am Geriatr Soc. 41 (11): 1219–25. doi:10.1111/j.1532-5415.1993.tb07306.x. PMID 8227897.
  10. ↑ Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, Woodbury P, Growdon J, Cotman CW, Pfeiffer E, Schneider LS, Thal LJ (April 1997). "A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study". N Engl J Med. 336 (17): 1216–22. doi:10.1056/NEJM199704243361704. PMID 9110909.
  11. ↑ Potter LT (1994). "Discovery of treatments for Alzheimer's disease". Neurobiol Aging. 15 Suppl 2: S67–9. doi:10.1016/0197-4580(94)90173-2. PMID 7700465.

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