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Dementia medical therapy

From Wikidoc - Reading time: 4 min

Dementia Microchapters

Patient Information

Overview

Classification

Causes

Differential Diagnosis

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

Overview[edit | edit source]

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[edit | edit source]

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[edit | edit source]

  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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