Hello Joeaverage,
The first step is to be evaluated by a physician, to determine if
the patient has ARBD (Alcohol related brain damage) and/or Alzheimers.
?There are many different ways in which alcohol can be tied to dementia:
- Some people who have had a history of alcohol abuse may develop
alcohol related dementia (Alcohol leading to dementia).
- Some people who have Alzheimer disease or another dementia may also
have an alcohol problem (Alcohol + dementia)
- Some people who are developing Alzheimer disease or other dementia,
in the early stages may turn to alcohol as their way of dealing with
what can be frightening changes in their memory. (Dementia may lead to
increased alcohol use by some people to cope).?
http://www.agingincanada.ca/Seniors%20Alcohol/1e3-1.htm
?ARBD has a better prognosis than other types of dementia (Smith and
Atkinson 1995). In general one quarter of people with ARBD experience a full
recovery, one quarter experience significant recovery, one quarter experience
slight recovery and one quarter no recovery (Smith and Hillman 1999). The
degree of cognitive recovery varies between individuals and depends on
various factors relating to the extent of brain damage. Recovery also
depends on the cause of brain damage. This fact emphasises the need for
knowledge and awareness of the effects of alcohol misuse.
Abstinence from alcohol halts the progression of the condition and recovery
may be seen. Acute episodes of Wernicke?s encephalopathy can be treated
with high doses of thiamine (vitamin B12) and the persistent effects of
Korsakoff?s syndrome can be prevented or reduced with abstinence and
continued vitamin supplements and recovery can continue for up to two years
(Elleswei 2000; Lishman 1990). Other types of ARBD respond to abstinence
from alcohol (Elleswei 2000; Lishman 1990; Oslin et al. 1998).? Page 8
http://www.aerc.org.uk/documents/pdf/finalReports/AERC%20report%20Mcabe.pdf
?In older patients with alcohol intoxication, the possibility of
mixed intoxication, frequently with benzodiazepines, should also be
considered. Finlayson et al31 found that 14% of elderly inpatients in
an alcohol treatment unit were also abusing prescription medications.
The elderly have increased biological sensitivity to alcohol, and
intoxication may occur at lower dosage levels.32 Aging processes,
reduced brain reserve, physical illness, and impairment of hearing and
vision predispose the elderly to delirium.26 A history of alcohol use,
the smell of alcohol, and features of intoxication help differentiate
alcohol intoxication delirium from other causes of delirium in the
elderly. Alcohol intoxication is a time-limited condition, and the
delirium usually resolves as intoxication ends or within hours to days
thereafter. Antipsychotics are occasionally necessary for psychotic
symptoms and associated combative behavior. Treatment with thiamine
50-100 mg intramuscularly for 3 days is advisable.?
http://www.naccme.com/cg/displayArticle.cfm?articleID=cgac1984
?There is a need for specialist psychiatric expertise in
prescribing and monitoring psychotropic
medication, since people with ARBD may be particularly vulnerable to
side effects: GPs, service
users, carers and service providers need to be aware of this possibility.?
http://www.alcoholinformation.isdscotland.org/alcohol_misuse/files/ARBD_afullerlife.pdf
Drugs used to treat alcoholic dementia
======================================
Rivastigmine (Exelon®)
?A case of Alcohol-Induced Persisting Dementia (AIPD) in a 62-year-old
man is presented. His progress on treatment with the
acetylcholinesterase inhibitor, rivastigmine, is followed. The
significant improvement observed suggests that AIPD may be a new
indication for this class of drug.?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12806761&dopt=Abstract
Memantine - ?Neuronal loss is associated with alcohol dementia too,
apparently through excitotoxicity during repeated alcohol withdrawal.
A brief anecdotal report suggests that memantine may have some role in
treating alcohol dementia.(14) Memantine appeared to help in terms of
improved mental state, verbal fluency, word recall, drawing and
general intellectual capacity. In addition, PET scans demonstrated a
renormalization of glucose metabolism and an increase in cerebral
blood flow. Such a case report is often the first step to a clinical
trial, but the isolated findings should not be generalized until a
controlled trials, since alcohol dementia can spontaneously improve.?
http://www.lef.org/magazine/mag2001/july2001_report_brain_01.html
Donepezil (Aricept®) - ?The patient had no family history of
Alzheimer's disease, no history of head injury, and single-photon
emission computed tomography showed no typical findings of Alzheimer's
disease. His cognitive function was impaired. He was treated with
donepezil for alcohol-related dementia, and 3 months later, his
cognitive function had improved. More research is needed to confirm
donepezil's role in treating alcohol-related dementia.?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15040658&dopt=Abstract
?Donepezil has two advantages over tacrine: It has fewer side
effects, and it can be given once daily rather than three times daily.
Donepezil does not appear to affect liver enzymes, and therefore does
not require weekly blood tests. The frequency of abdominal side
effects is also lower. The monthly cost is approximately the same.?
http://neurology.health-cares.net/alzheimers-disease-medications.php
These drugs are used to treat dementias in general, but the
patient?s doctor can prescribe medications appropriate for the
patient. Alzheimers dementia is not the same as alcoholic dementia,
although some Alzheimer?s drugs may be used.
Antipsychotic drugs, such as haloperidolSome Trade Names
HALDOL
, olanzapineSome Trade Names
ZYPREXA
, and risperidoneSome Trade Names
RISPERDAL
(see Antipsychotic Drugs ), are often used to control the agitation
and outbursts that may accompany advanced dementia. However, these
drugs are not very effective for this purpose, and they can cause
serious side effects. Antipsychotic drugs are most effective in people
who have hallucinations, delusions, or paranoia in addition to
dementia.?
http://www.merck.com/mmhe/sec06/ch083/ch083c.html
Alcoholic dementia can be slowed or arrested with alcohol abstinence.
http://members.aapa.org/aapaconf2005/syllabus/5018StewartDementia.pdf
?Nutritional problems, which often accompany consistent or episodic
heavy use of alcohol, are thought to be contributing factors. Key
parts of the brain may suffer damage through vitamin deficiencies,
particularly marked levels of thiamine deficiency and the direct
effect that alcohol has on the absorption and use of thiamine. Anyone
who drinks excessive amounts of alcohol over a period of years may get
alcohol related dementia. Males who drink more than six standard
alcoholic drinks a day, and women who drink more than four alcoholic
drinks a day seem to be at increased risk of developing alcohol
related dementia. The risk clearly increases for people who drink high
levels of alcohol on a regular basis.?
?At an early stage of the disease, problems may be reduced or
reversed if the person abstains from alcohol, their diet is improved
and vitamins, especially thiamine, vitamin B1, replaced.Thiamine is
important to limit some of the toxic effects of alcohol, and is an
important supplement for heavy drinkers. Community support is
available for the person with dementia, their families and carers.
This support can make a positive difference to managing dementia.?
http://neurology.health-cares.net/alcohol-related-dementia.php
?A deficiency of thiamine (vitamin B-1) is responsible for the
symptom complex manifested in Wernicke-Korsakoff syndrome, and any
condition resulting in a poor nutritional state places patients at
risk. Heavy, long-term alcohol use is the most common association with
Wernicke-Korsakoff syndrome. Alcohol interferes with active
gastrointestinal transport, and chronic liver disease leads to
decreased activation of thiamine pyrophosphate from thiamine, as well
as a decreased capacity of the liver to store thiamine. Thiamine is
converted to thiamine pyrophosphate, which serves as a cofactor for
several enzymes that function in glucose utilization. These enzymes
include transketolase, pyruvate dehydrogenase, and alpha
ketoglutarate.
Thiamine deficiency results in a diffuse decrease in cerebral
glucose utilization. However, symptoms are attributed to focal areas
of damage. Ocular motor signs are attributable to lesions in the
brainstem affecting the abducens nuclei and eye movement centers in
the pons and midbrain. These lesions are characterized by a lack of
significant destruction to nerve cells, which accounts for the rapid
improvement and degree of recovery observed with thiamine repletion.
Ataxia is a manifestation of damage to the cerebellum, particularly
the superior vermis. The cerebellar changes consist of a degeneration
of all layers of the cortex, particularly the Purkinje cells. The loss
of neurons leads to persistent ataxia of gait and stance. In addition
to cerebellar dysfunction, the vestibular apparatus also is affected.?
?After the initial IV dose, continue daily doses of thiamine
(50-100 mg) as IV, IM, or oral doses depending on patient status.
Supplementation of electrolytes, particularly magnesium and potassium
(often low in people with alcoholism), may be required in addition to
thiamine. In patients who are chronically malnourished, the remainder
of the B vitamins also should be supplemented. Administration of
intravenous glucose to patients who are severely malnourished can
exhaust their supply of thiamine and precipitate Wernicke-Korsakoff
syndrome. Thus, good practice demands administration of thiamine prior
to glucose infusions in patients at high risk for Wernicke-Korsakoff
syndrome.?
http://www.emedicine.com/med/topic2405.htm
?Symptoms of dementia may be treated with a combination of
psychotherapy, environmental modifications, and medication. Drug
therapy can be complicated by forgetfulness, especially if the
prescribed drug must be taken several times daily. Behavioral
approaches may be used to reduce the frequency or severity of problem
behaviors, such as aggression or socially inappropriate conduct.
Problem behavior may be a reaction to frustration or overstimulation;
understanding and modifying the situations which trigger it can be
effective. Strategies may include breaking down complex tasks, such as
dressing or feeding, into simpler steps, or reducing the amount of
activity in the environment to avoid confusion and agitation.
Pleasurable activities, such as crafts, games, and music, can provide
therapeutic stimulation and improve mood.
Modifying the environment can increase safety and comfort while
decreasing agitation. Home modifications for safety include removal or
lock-up of hazards such as sharp knives, dangerous chemicals, and
tools. Child-proof latches or Dutch doors may be used to limit access
as well. Lowering the hot water temperature to 120°F (48.9°C) or less
reduces the risk of scalding. Bed rails and bathroom safety rails can
be important safety measures, as well. Confusion may be reduced with
simpler decorative schemes and presence of familiar objects. Covering
or disguising doors (with a mural, for example) may reduce the
tendency to wander. Positioning the bed in view of the bathroom can
decrease incontinence.?
http://neurology.health-cares.net/dementia-treatments.php
?Treatment - If caught early enough, WKS is a preventable, treatable
disease. Treatment consists of thiamine replacement therapy, sometimes
along with other vitamins. Dosages may vary and should be monitored
closely by a physician. If alcoholic consumption stops and treatment
is properly administered, individuals with early-stage WKS can expect
a marked recovery and may be capable of learning simple, repetitive
tasks.
However, the person's confusion may take some time to subside and even
incomplete recovery of memory can take up to a year. In the later
stages, if damage to the brain is irreversible, individuals are likely
to have lasting problems with memory and gait (for example, lack of
muscle coordination and numbness or weakness in limbs).?
http://www.zarcrom.com/users/alzheimers/odem/al7.html
?The damage sustained can be on a continuum ranging from mild to
very severe. Further brain damage can be avoided if the sufferer
abstains from alcohol and maintains a healthy diet. Recovery outcome
can be split into quarters:
25% make a complete recovery
25% make a significant recovery
25% make a slight recovery
25% make no recovery
Recovery is also dependent on rehabilitative care and a supportive
environment to maintain the required abstinence from alcohol. We need
to look at facilities available and the development of services to
provide the ARBD client with appropriate care during the two-year
window of opportunity they are said to have before they reach their
optimum recovery.?
http://www.carenzacare.co.uk/about.htm#more
Further Information
http://www.carenzacare.co.uk/home.htm
http://www.carenzacare.co.uk/casestudies.htm#dementia
I hope this has helped you out. Please ask for an Answer Clarification
if anything is unclear, and allow me to respond, before you rate this
answer. I will be happy to assist you further, before you rate.
Sincerely, Crabcakes
Search Terms
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ARBD
Korsakoff Syndrome + treatment
Managing alcoholic dementia
Alcohol withdrawal dementia treatment
Alcoholic dementia therapy |
