Why Not Use Cholinesterase Inhibitors for Mild Cognitive Impairment?

By Michael Gordon MD; http: //www. annalsoflongtermcare. com; 1/16/2014

For those of us in geriatric, psychogeriatric and adult neurological practice, a substantial percentage of our population will include individuals with dementia of one variety or another, the most typical being a mixture of Alzheimer’s disease with a vascular element. Some of those we see in our practices satisfy the criteria of Mild Cognitive Impairment (MCI) as opposed to dementia, which hinge on a range of medical and neuropsychological standards with no “gold-standard” test that sets apart one part of the cognitive impairment/dementia from another. Contrary to for example thyroid disorder where a basic blood test or two or blood test and scan can determine those individuals with underactive thyroid glands that would profit from replacement therapy, the MRI and neuropsychological and now perhaps genetic and bio-markers may hone on the place in the spectrum of the cognitive impairment diagnosis- but there is often a “fuzzy" analysis halo around the edges.

The reason this is essential for doctors to understand is that the standard therapies for those with a diagnosis of Alzheimer`s, vascular or mixed dementia, the use of cholinesterase inhibitors (donepezil, rivastigmine, galantamine) or NMDA receptor blocker (memantine) would be considered a sensible medicine to use to try and either improve some level of symptoms and- or minimize the rate of acceleration for which there is some proof of advantage. The problem which is often brought up by patients and their families is if there is some evidence of cognitive disadvantages that is grouped as MCI rather than true dementia, “why not make use of those drugs that are utilized to treat dementia in the hope of preventing the transition from MCI to dementia”. It seems very intuitive and the model exists for other conditions, that a drug to treat a condition should be helpful at just about any stage of the affliction, so why wait?

Most people in the field know that many practitioners offer cholinesterase inhibitors to individuals who have what would be likely regarded as as MCI since they have either persuaded themselves that an excess point or 2 can come off the Folstein MMSE or MOCA and place the person in the dementia rather than MCI classification. Obviously this is more likely if the person and their family is extremely insistent that they want to try the drug even if they are advised it is probably not going to be effective. The answer is normally some version of "why wait until things get even worse? " or "isn't prevention much better than cure?"

It was therefore of great curiosity and value to the eldercare health care community to read the study published in the September 16, 2013 Canadian Medical Association Journal that exhibited rather decidedly that as the abstract of the document concludes, "Cognitive enhancers did not enhance cognition or function among sufferers with mild cognitive impairment and were associated with a greater danger of gastrointestinal harms. Our conclusions do not support the use of cognitive enhancers for mild cognitive impairment." As discussed in the Toronto Star article regarding this study which was acquired by all of Canada`s significant newspapers as the analysis was Canadian, "Mild cognitive impairment, or MCI, is marked by memory lapses and problems with language, thinking and decision- making that go over and above what’s anticipated with normal aging, but are not as conspicuous as the changes that would signal the decline of dementia. But... up to 17 per cent of MCI patients do go on in time to develop a dementia such as Alzheimer’s disease.

What exactly does this imply for the eldercare specialist? If after careful investigation it is regarded that the person's cognitive problems are probably within the diagnostic construct of MCI it would be of great benefit following that person on a periodic schedule after determining that there are probably none of the potentially reversible risk components for evident cognitive disadvantages not owing to a dementing illness per se. The typical endocrine, metabolic and prescription medication side effect culprits are usually easily discovered and must be dealt with as part of the monitoring process. If over time, as part of the roughly 17% of MCI patients show evidence of even more cognitive and functional downfall, the use of these medications used in their therapy can be presented with additional overseeing to see their effect.

Having the results of this analysis conveniently accessible can help practitioners explain to their clients and their devoted and anxious family members the reasons why the medications utilized to treat the problem, will not work in its elimination.

 

 

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