Please Read!!! I’d like for everyone to respond. Yes or No, how many of you have been on antidepressants before being diagnosed with PD?
If yes, how long? I had some struggles in my life in my early 20’s got on SSRI anti depressants and then never got off them. Have I been destroying my brain for nearly 20 yrs? About 1 year ago my depression was out of control while testing for Parkinson’s and I raised my dosage. My symptoms got much worse almost overnight. My mental health was bad I did dare to come down . Now about 2 weeks ago I started to taper down and my symptoms improved immediately. I’m going to taper down and remove them completely.
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38yroldmale
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I was taking paxil before PD I continued to take it because I have a son that likes to ague with me. A couple of weeks ago after reading here about anti-depression pills I decided to go off of them. That lasted about 2 weeks. Everything bothered me. I am now back on them (10mg/a day) and I feel much better. I think my system got used to them.I used them for about 3 years. When I stopped, my system did not like that.... Now with the arguments. I just wave my hand!
No.
Please don’t do anything without consulting with your doctor.
If it were me and I was taking a pharmaceutical that worsened my symptoms when I increased the dose and improved my symptoms when I decreased the dose, I would consider that reason enough to keep reducing the dose and more important than a doctor's opinion.
This article says SSRIs may worsen symptoms in Parkinson's, so I don't think it a stretch to believe that 20 years of it could cause Parkinson's.
"This article says SSRIs may worsen symptoms in Parkinson's, so I don't think it a stretch to believe that 20 years of it could cause Parkinson's."
As a general rule, this isn't particularly logical. Alcohol may worsen symptoms in Parkinson's but if 20 years of it was enough to cause it, PD would be everywhere.
In particular, elevated serotonin levels trigger a compensatory drop in dopamine. The relationship between serotonin and dopamine can be visualized as a seesaw: When serotonin goes up, dopamine goes down. And it is dopamine suppression that has long been associated with this loss of motor control.
In a particularly relevant study published in the July 1988 issue of Biological Psychiatry, Dr. Marc Laruelle used one of the serotonin boosters (Paxil) with a radioactive tag on it to study what locations in the human brain are especially targeted by the drug. Laruelle found some of the highest concentrations of the drug's target cells in the involuntary motor system. Indeed, the highest concentration was found in the specific location (called the substantia nigra) known to be involved in Parkinson's disease.
Because of growing concern about these side effects, in recent years the serotonin-dopamine connection has become an area of active research. Neuroscientists have specifically designed experiments to test whether or not serotonin boosters are associated with a dopamine drop in the involuntary motor system. Dr. Junji Ichikawa at Case Western Reserve University School of Medicine measured dopamine levels in rats before and after administration of Prozac. In the August 1995 issue of the European Journal of Pharmacology, Ichikawa reported Prozac produced a 57% drop in dopamine in the involuntary motor system. By contrast, older antidepressants did not produce a drop in dopamine.
Another quote
n the case of Parkinson's disease, we know the group of cells in the brain that are destroyed. The cells are believed to be weak links in neural circuitry particularly vulnerable to damage. Autopsy studies have shown that by age sixty individuals who do not have Parkinson's disease have lost about 40% of cells in this region as a result of normal aging. By contrast, patients with Parkinson's disease have lost 80% or more of the cells in this region. If normal aging claims 40% of the cells and patients with Parkinson's disease have lost 80%, this normally leaves a comfortable reserve of 40% offering protection against the disease.
We know a great deal about Parkinson's disease because this is such a well-studied entity, but this model of a comfortable reserve that can be eroded may well apply to other areas of the brain and symptoms that are less well understood. What if being on a serotonin booster for a decade damages a quarter or a third of the cells in a particular region of the brain? This might not be sufficient to produce symptoms in a young patient, but would dangerously narrow the margin of safety later in life. Will someone who has been on a serotonin booster for a decade in her twenties be prone to prematurely develop neurological conditions — senile tics, gait disturbances, memory loss, personality changes, or dementia — because of silent damage sustained years earlier while on the drug?
What I didn’t find here is about polymorphism in MAO and COMT genes. We must understand that we are different in our genetic makeup. I donot think SSRIs make any problem with people having fast MAO or COMT but of course it can act as predisposing factor to PD for people with slow MAO and COMT enzymes.
In this case Dopamine and Seretonin degradation becomes slow and Dopamine turn into a dangerous compound called Dopamine-quinone which triggers neurodegeneration.
I don't think it a stretch to imagine the possibility that 20 years of alcoholism or 20 years of some pharmaceuticals may cause Parkinson's in some people.
Parkinson's may have a dozen causes. It may have 2 dozen causes.
"I don't think it a stretch to imagine the possibility that 20 years of alcoholism or 20 years of some pharmaceuticals may cause Parkinson's in some people."
I was very clear about what I was responding to. I literally quoted it. You were presumably implying that exacerbation increases materially the risk that the factor was a contributing cause. If you werent doing that, I'm afraid your writing is unclear (which might explain your complaint that this is getting all too common - perhaps look internally), because that's how native English speakers interpret 'so' in the context in which you used it.
I dont think you can draw any great inferences from exacerbation. The medical world is full of stuff that is likely to exacerbate yet is not considered a materially likely cause.
If you are now reducing your remarks to "for all we know, pretty much anything may cause PD" then yeah, no kidding.
Yes, MBA. Neurogist, Dr Dale Bredesen has found 30 different possible causes of Alzheimer's, so there are, very likely, several different possible causes of Parkinson's. This would explain why medication has different effects on PwP.
I have just read the article on management of depression in PD and didn't see the reference to SSRIs worsening symptoms. I must have missed it. Could you quote it please.
Above, I said, "... This article says SSRIs may worsen Parkinson's symptoms ..."
From the link;
" ... there is concern that SSRIs may aggravate motor symptoms in patients with Parkinson’s disease. However, clinical experience and open-label studies have suggested relatively good tolerability of SSRIs with low incidence of worsening motor symptoms in this patient population (1, 4).”
"Our study shows that the risk of PD increases during the first two years of use of antidepressants, whether they are tricyclic antidepressants or SSRIs.”
Re the other matter. A PWP cannot experience an improved quality of life without a relief of symptoms.
Slowing progression means quality of life continues to deteriorate, albeit slowly. Improving quality of life means a reversal of symptoms.
One follows the other. They are the same thing.
As per the Michael J Fox Foundation;
"Preventing or slowing progression: Studies have linked exercise to reduced risk of Parkinson's and slower progression."
As per the Mayo Clinic
"However, evidence from many avenues of scientific investigation argues for ongoing aerobic exercise as a means to slow PD progression. This should be routine advice to patients with PD.
Depression, disability, postural instability, and cognitive impairment have the greatest influence on QoL in Parkinson's disease. The improvement of these features should therefore become an important target in the treatment of the disease.
I hereby announce 3 proclamations which shall go forth across the land. 1) the earth is round, 2) exercise slows progression, and, 3) SSRIs have induced PD in some people.
Ah well now you are referencing Simon, my fellow countryman (along with Jacinda Ardern and Ed Hillary) who talks common sense not conspiracy stuff so i have to believe him.j I await news of whether the benefits gained at 6 months is sustained.
(And now your may is not a may but a does - tricky)
This is interesting. My husband has initial appt with neurologist in a few days. ( had to pay privately as cannot wait until Feb for a so called expidited appt on NHS....). He has suspected Parkinson's and has been SSRI for a very long time
Be careful. My husband very slowly came off mirtazapine over 3 months which isn’t an ssri but after a couple of months he had a huge crash and became seriously suicidal. He had been on Fluoxetine before that which is an ssri and this made him suicidal too.
It’s hard to know which comes first. Does PD lead to depression or ssri lead to PD.?
I think mirtazapine definitely caused some PD like symptoms like wooden face , apathy, lethargy and wanting to sleep all day. That lead to not much exercise, people interacting with him differently due to no expressions so he socially withdrew because of their reactions to him which probably made his depression worse. Now his mirtazapine is at only 10% the level he was on at its height (only 3 mg instead of 30) and his above symptoms have improved, but it will take a year to get off completely, if at all. He is still on sertraline and any attempt to decrease this by even 10% gives him nausea.
Do not attempt to come off the SSRIs without the doctors support especially if you don’t have a support person in the know about what you are doing as if you become suicidal you will have no one to monitor you or save you. Having said that our doctor just said halve it each week then stop completely over a month. I would not recommend doing it that fast. You’ll have much more success if you do it over a very long time a tiny bit at a time, then if you start feeling a bit worse stay at that level for a bit until you feel better, or if you feel worse get straight back to the doctor. After this long time I can’t see there is any rush to stop cold turkey.
"It’s hard to know which comes first. Does PD lead to depression or ssri lead to PD.?"
Depression, apathy and anxiety are definitely PD symptoms. Im not sure if the mechanism is well understood (and if it is, not by me). It makes sense that a screwed up dopamine system could lead to mood issues, though there is likely more to it than that.
Whether SSRIs lead to PD is probably a seperate question, and one that might only be answerable in a couple of decades when the first generation of long term SSRI users hit their 60s. They are only 20 to 30 years old now (SSRIs, I mean).
"University found that the antidepressant drug "nortiptyline" stopped the growth of a protein that builds up in the brains of people With Parkinson's. When researchers examined medical records of people with both depression and Parkinson's, they found that those who took nortriptyline delayed starting standard medications for Parkinson's compared to people who took a different antidepressant or none at all." Sonya Collins - WebMed.com."
Having found this article, I still believe that all antidepressant meds are bad for Parkinson's. My husband never took any SSRI not does he intent to. There are a lot of natural antidepressant supplements that outperform synthetic ones.
Same edition of WebMed. com: "Columbia University study found that . . . .immune-suppressing medications might one day protect these (dopamine) brain cells."
Also, "Oxidized or Corroded dopamine could also be part of the problem. Northwestern University researchers found that oxidized dopamine accumulates in the brains of people with Parkinson's slows down some brain activity, and leads to the death of brain cells, which causes more oxidation. When the researchers treated brain cells with antioxidants, it stopped the process that led to cell death and oxidation."
I don't know about leading to PD. But I can say that much is conceivably possible, sure. Certainly the circuitry is shared, but developmentally we do have links between Tryptophan groupings of molecules and Dopamine functions, but that is so so simplistic and early to use to explain something on either an individual level or a congregate one. So much is influenced by the individual situation, as well. These neurotransmitters, and the periodic partial picture intervention molecules that drugs represent, have many functions and chemically they are very complex, and operate in many theatres and they are none of them simple, many of them chemically and mechanistically highly complex, highly complex. That happens in neurobiology AND neuroanatomy, and then neurochemistry...which are also all moving feasts might I add...when a certain chemical serves 20 or so different functions, all differing in location, location on the cell, location in the cell (which is different), migration of each from one location to another in or on or between the cells...and let's not forget that the shape of the molecule matters greatly, the angle of this carbon to that aldehyde, this nitrogen, that flourine, this hydroxide, that benzene ring, that place on the chain, that place on the chain...and the distance between them...and the specific angles of this or that fucntional group...location and function in the mechanisms of the various parts of the body and organs, all differing in hundreds of different ways, all working off the same chemical. Has it occurred to anyone that just in the basics of "chemists" as we say in Britain, and "pharmacy," as we say in the US, that any particular chemical can and generally does go through, in some cases, reaction mechanism transactions of over 100 steps...I knew that because one of my roommates, who was in chemistry school, complained that he had all these chemical reaction mechanisms they were forced to memorize that were over 100 steps, TYPICALLY... once complained that is, my friends in the pharmacy industry have to memorize reaction mechanisms that occur in set sequences of 100 steps and sometimes more...this is the nature of human chemistry.
Took Prozac and Clozapine in my early 50's for about two years. Diagnosed with PD at 65. Should never have been on Clozapine...bad drug given my moderate symptoms, but I would stay awake for days without it. Interesting discussion. I would not have put these two facts together. My insomnia now does mirror what I experienced then. Serotonin up, dopamine down.
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