For those who care for someone with Parkinson's disease
[Home] [Forum] [Help] [Search] [Register] [Login] [Donate]
You are not logged in


Topic Sinemet reduction for help with dementia Go to previous topic Go to next topic Go to higher level

By chroop67 On 2013.07.04 21:51
I would like to know what your experiences have been with regard to sinemet reduction for help with dementia. I know that the trade off is less mobility but i am wondering if anyone has felt that the regained cognitive ability has been worth it?

By LOHENGR1N On 2013.07.05 00:13
Sinemet reduction may help with Delirium....Not Dementia. Dementia is a steady decline different from Delirium if it is Delirium then reducing a drug like Sinemet might help if it truely is Dementia there is no know treatment proven to regain functions lost.

I posted this before but it's no trouble to post again for those newer to the forum I hope it answers some questions and gives some information to help understand these puzzling conditions. I cut and pasted from http://www.hopkinsmedicine.org/gec/series/dementia.html

Dementia is a progressive decline in memory and at least one other cognitive area in an alert person. These cognitive areas include attention, orientation, judgment, abstract thinking and personality. Dementia is rare in under 50 years of age and the incidence increases with age; 8% in >65 and 30% in >85 years of age.

Dementia results from brain damage. The causes include the following; Alzheimer’s Disease, Stroke, Pick’s disease, Huntington’s, Downs Syndrome, Creutzfeldt-Jacob, AIDS, alcoholism, Parkinson’s disease and other neurodegenerations.

Diagnosis
There are three purposes why diagnosing dementia is essential.

By determining the probable cause, treatable disorders can be identified, such as medication toxicity (benzos, H2 blockers and anticholinergics), and thyroid disease.
There are symptoms and comorbidities that are treatable, such as depression, delirium (see below), delusions, hallucinations, and agitation.
Caregivers must be identified and environmental issues taken into consideration.

A diagnosis of dementia is based on:
memory loss - both in short and long-term, plus one or more of the following:

aphasia – language problems
apraxia – organizational problems
agnosia – unable to recognize objects or tell their purpose
disturbed executive function – personality and inhibition

Dementia vs Delirium
In order to make a diagnosis of dementia, delirium must be ruled out. However, patients with dementia are at increased risk of delirium and may have both. Delirium is an acute disorder of attention and global cognition (memory and perception) and is treatable. The diagnosis is missed in more than 50% of cases. The risk factors for delirium include age, pre-existing brain disease, and medications. There are many causes, the most common are:

D Dementia
E Electrolyte disorders
L Lung, liver, heart, kidney, brain
I Infection
R Rx Drugs
I Injury, Pain, Stress
U Unfamiliar enviroment
M Metobolic

Prevention of delirium includes the avoidance of psychoactive drugs, quiet environment, daytime activity, dark and quiet at night, visual and hearing assistive devices, orientation devices, and avoidance of restraints.

Diagnosis of delirium is based on clinical observation; no diagnostic tests are available. The essestial features of delirium include:

Acute onset (hours/days) and a fluctuating course
Inattention or distraction
Disorganized thinking or a altered level of consciousness
Treatment of delirium, like dementia, is managed both pharmacologically and non-pharmacologically.

By chroop67 On 2013.07.05 22:15
Thanx, your response offers clarity. Why then in a lot of the literature do they suggest reduction of sinemet for dementia. I have read much and they all say that you have to balance the loss of mobility that the reduction may cause and the lessening of the dementia symptoms. They never say delerium always dementia with hallucinations, paranoia and altered personality. Those are exactly what my mom is experiencing, not sudden onset but a gradual ramping up of the above symptoms.

By chroop67 On 2013.07.05 22:29
Here is an excerpt regarding the above.

4.1. Dementia

Community-based studies of dementia in patients with PD have reported a prevalence between 28% and 44%, with longitudinal studies estimating that dementia occurs in up to 75% of patients The pattern of deficits is similar to dementia with Lewy bodies and differs from that in Alzheimer's disease for the predominant involvement of executive, visuospatial, and attention dysfunction and for the presence of cognitive fluctuations

The cognitive symptoms are a consequence of dopaminergic depletion
Dopaminergic replacement does not lead to cognitive improvement or may even worsen it, but cholinergic enhancement can instead be helpful. Cholinesterase inhibitors, in fact, may be effective in ameliorating cognition, but their tolerability seems variable due to peripheral cholinergic adverse effects and in some case can worsen motor functions. Rivastigmine seems the most useful agent
Avoiding the medications that can possibly worsen dementia, like anticholinergics and DA-agonists, as well as maintaining L-Dopa at the lowest effective doses, is certainly a key strategy to contain confusion, hallucinations, and psychosis in advanced patients
4.2. Hallucinations and Psychosis

Behavioral disorders, and especially hallucinations, illusions, and other psychotic symptoms, are also frequent in advanced PD with frequency rates ranging from 25 to 30%. Resembling very closely those seen in dementia with Lewy bodies, psychotic symptoms in PD are represented by delusions (false and fixed beliefs maintained despite evidence to the contrary) and, particular, hallucinations (abnormal perceptions that can involve any sensory modality in the absence of a physical stimulus). Visual hallucinations, simple or complex in form, are the most common psychotic symptom in advanced PD patients, typically occurring in dim surrounding, but often occurring through the entire day in late-stage patients

A range of factors contributes to the development of hallucinations and psychosis in PD, including intrinsic pathology and dopaminergic replacement therapy.

In the treatment of these complications the first step should always be to evaluate the role of drugs that can potentially induce or worsen psychosis, such as amantadine, anticholinergics, COMT-inhibitors, and DA-agonists. These drugs should be tapered off, balancing the effect on psychosis with worsening of motor function.

All precipitating events, like urinary and pulmonary infections, cerebrovascular events, and metabolic dysfunctions, should be also carefully investigated and treated if possible, as even mild metabolic imbalance or infection can profoundly affect the development of psychotic symptoms.

Decreasing the dose of L-Dopa should also be considered when severe psychosis persists, even though this action could worsen parkinsonim.

All traditional antipsychotic drugs, such as haloperidol, aripriprazole, and chlorpromazine, should be avoided because of the high sensitivity of PD patients to the motor adverse effects induced through potent antagonisms of D2 receptors.

Clozapine and quetiapine are the only two newest antipsychotic that should be considered atypical, thus safe in PD, due to their predominant affinity for D1 and D4 receptor and low affinity for D2 receptors.

There is a wealth of evidence demonstrating the efficacy and tolerability of clozapine in PD, but its use is limited by the need of weekly blood testing for the initial 6 months of treatment A more practical alternative is represented by quetiapine. Unlike clozapine, quetiapine does not require monitoring of blood cell counts and it is effective in suppressing hallucinations and psychosis in the majority of patients at relatively low doses, ranging from 12.5mg to 100mg.

Main side effects of quetiapine and clozapine are sedation and postural hypotension.

By LOHENGR1N On 2013.07.06 00:47
Okay, I'll try to explain this getting rid of the medical mumbo jumbo. As I've always said our medications are mind altering drugs. Sinemet is made from ergot as are other medications however so is Lysergic Acid from which LSD is synthesized. Most of Our hallucinations are not like the 60's opt art psychedelic posters. More along the line of say you're driving at night and up ahead at the edge of where your headlights shine you see something ..a person? As you get there nope a mail box on a post along the road side. We see something at the edge of our vision we think one thing only to have it be something else. However over time increasing our medication we can for lack of a better term tip over that fine line and with too much Sinemet have more vivid hallucinations. Which is why it is important for Neurologists to monitor our increases and to make those increases slowly not large increases all at once. It's still the best medicine we have to help us Parkinson's patients.

Many Doctors know dementia can come with Parkinson's and some probably don't even take time to consider delirium from medication. In fact years ago P.D. was a disease of the elderly and elderly could expect dementia to some degree so it really wasn't that alarming a development. Things have changed and now answers are needed and some even demanded We can expect like from congress the medical field to spout off ideas as facts and revamp the evidence to fit the proposed solutions.

As for articles on decreasing dopamine to help dementia? The Doctors got it wrong. The wrong diagnosis. Did you ever try to have a doctor say they were wrong? Most won't they'll drop you as a patient and go to their grave never admitting it. Think about cholesterol and you can't eat eggs so the Doctors said then found still high readings, then they found out our bodies make it. So it's okay to eat eggs but don't over do it? They were wrong, proved themselves wrong and still deny it. So while the diagnosis was wrong it is easier to say cutting back on a drug like Sinemet. Change the disease not the diagnosis. Both Dementia like Delirium are judgment calls made upon doctors visits, observation and symptoms. Like Parkinson's Disease there are currently no medical tests per sae to diagnose them. The cat scans, mri's and such can show damage or even lack of neurotransmitters however they don't contribute to the diagnosis. They can rule out tumor or traumatic brain injury but other than that they run the costs up for insurance and co-pays. So it comes down to the fraternity of doctors never admitting mistaken diagnosis or another doctor being wrong to the public. Just change the parameters of a disease. As it says in the post above the first step should be investigate the roll of drugs (medication) in these problems.

By parkinit On 2013.07.19 16:17
chroop -

Can you share your resource for your excerpt?

Thanks!

By Mary556 On 2014.06.22 06:01
searching for an answer about Sinemet and delerium, I found this info in the archives today. It is very helpful. Thank you, Lohengr1n and chroop67. Thank you, Jim, for giving us this site.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3038575/


© 2003-2017 MyParkinsons.org · Privacy Policy & Terms of Use
Published by jAess Media. This website and Forum is sponsorsed by people like you