I’m confused. I’ve been clinically diagnosed with Parkinson’s with a DatScan performed in Dec. 2018. 4 months prior to my DatScan raised my antidepressant to max levels from the lowest level I had been taking for about 6 years prior. My symptoms got worse overnight. Looking back, my symptoms started the same as the time as started the antidepressants. They never were very bad until I raised my antiDepressant. My first neurologist said I did not have parkinsons. (It
Was Prior to raising my antidepressants) I assumed the worsening of symptoms was the progression of the disease,not the raising of the antidepressants. as soon as I cut back on my antidepressants, my symptoms improved immediately. I am actually off antidepressants 2 months and my symptoms are improving and some are disappearing.
I have a perfect sense of smell, and do not respond to C/L. Never had sleep issues or constipation. My symptoms actually get worse on C/L. 10mg of The anti-depressant I was on raises gaba levels 35%. I was on 40mg. New studies show how high GABA levels Suppress your neurons producing dopamine.
My symptoms are asymmetrical. Previous studies show that only 4% of drug induced Parkinson’s was a asymmetrical. New studies that came out less than five years ago debunk that study. They studied people in psychiatric wards that’s been a long term Antipsychotic drugs. It says anywhere from 40 to 50% can be asymmetrical.
Dat scans are used to differentiate between drug-induced Parkinson’s and regular Parkinson’s. However also did another study with Parkinson’s patients and effect of two different antidepressants on DatScan’s and compared them to healthy subjects and antidepressant less Parkinson’s patients. Both antidepressants lowered DatScan results, Especially citalopram The anti-depressant I was taking.
I’m probably grasping at straws. If you could please respond.
1. Have you lost your sense of smell? If so when?
2. Have u taken c/l? If yes, did u respond?
3. Any sleep issues? Acting out your dreams?
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38yroldmale
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I suggest you seek another medical opinion once you know you are clear of the antidepressant. I believe there is research out there that some antidepressants inhibit dopamine production so the increased symptoms you experienced could be a result.
My sense of smell has gradually decreased, 11 years since the onset of symptoms, although it is not gone. I am very responsive to c/l and I have never had any dream issues, I just don't sleep very well.
Everything you have written indicates a drug-induced parkinsonism. Personally I never lost my sense of smell. I do respond to carbidopa levodopa. I did have insomnia for a while. No question about PD in my case.
What I failed to mention is my father had Parkinson’s? Possibly my grandfather? It could be the fact that I unmask Parkinson’s early? Or maybe I have done irreversible damage and may not progress?
Those are also possibilities I read up about. If that’s the case it’s highly likely that I would get Parkinson’s later on? my symptoms are not disappearing very quickly. My gait is still quite weird. Arm swing Comes and goes. My right arm still doesn’t feel quite my own. What’s unusual is that you’d think that symptoms are getting better would be linear, But I still have lots of bad days. If I had to guess I am making 3 steps in the right direction, Then two back. It took me so long to come to terms with the diagnosis, I can’t believe it till I get better, if I get better.
Thanks Park-bear. I really value your opinion. You seem to be one of the smartest people I know with Parkinson’s.
Given your family history I recommend getting your genome checked by 23 and me to see if you have Parkinson's prone mutations. If so I suggest taking thiamine to halt or slow progression.
Also consider drug induced dystonia. Dystonia is very similar to P,D but with the exception of dopa responsive dystonia (which is usually a childhood onset), does not respond to C/L and sense of smell is normal. To answer your questions my smell was normal for the first four years I had PD and is only slightly impaired now. I have a minimal response to C/L and it actually makes my secondary dystonia worse, my sleep is fairly normal. I was diagnosed with primary hemidystonia before it being changed to PD when I had a datscan. I'm 46, had PD since 41.
My husband was about your age when he was diagnosed last year. He is not taking any drug for it but recently his leg started having tremors as well. His sense of smell is different now. How was the progression for you? The reason of my question is just because of age similarities. Thanks
I developed severe dyskinesia from meds 1.5 years ago that lead me to have brain surgery in April. Life is good again! So hard to say on progression - dyskinesia came on less than two years into low dose meds.
As far as I know the SSRIs reduce the amount of dopamin secretion.If you have had a positive DatScan then the PD diagnosis is almost confirmed unless the scan was misinterpreted.
My husband is 80 with his PD diagnosed about 7 years go. He lost his sense of smell before his diagnosis. He doesn't do well with out his Rytary.(dopamine) He has always acted out his dreams, even when he was 20. He is taking melatonin at 4 pm now, and at bedtime. This has stopped his sundowning. He took citaloprom for awhile, but went off it when he went on drugs for psychosis.
The dat scan confirms whether one has Parkinson's or not. The scan clearly depicts the dead cells or calcific deposits on either side of globus Padilli and cerebral atrophy.
Yes, the sense of smell diminishes with time and cannot be restored.
Useless dreams throughout the night also happened with me. I controlled them by skipping dinner and having only vegetables soup or warm milk. Keep yourself light in the night.
Deep breath for 10 minutes before sleeping gives a miraculous relief. Pl try this
Your problem definitely could be drug induced from SSRIs, which are known to cause dopmine-relsted problems due to their stimulant-side action (epinephrine and norepinephrine), which when combined with their direct serotonin action causes side effect problems in sensitive individuals. I don't know that they kill off dopamine producing substanta nigra cells, so if not too far along they might rebound production or their dopamine production might no longer be blocked, emphasis on "might" though.
Does not preclude the possibility you are eventually to develop actual PD though, nothing says a person can't have "co-occurring" disorders, and problems in the serotonin side of the complex of mechanisms seems lately to be associated with decades-later appearance of PD. That's where the common assocition beteen depression and PD comes from, for dopamine is an important factor in both.
However the good news is that this mechanism is not exacerbated by all anti depressants, only the ones on the stimulant serotonin "uptake-supressing" group known as SSRI. There are other froups of anti depressants that bypass this stimulant-side issue: SNRIs (e.g., duloxetine), the older group of original anti depressants known as "tricyclics" (though they come with some of their own side effects), and perhaps the best of the anti depressants, the MAO inhibitors, particulary the MAO-B inhibitors, which have both anti depressant action and are helpful in PD, which could mean that it might (MIGHT) be helpful if you turn out to have early PD or eventually develop "real" PD. Don't know enough to say what the GABA role might be, but perhaps these alternative anti depressant groups are worth looking into.
Tiny comment about GABA, since you mention it. I don't know what it really has to do with PD (that is, if you actually HAVE PD), others may know something definitive. But gaba is your nerve system and brain's natural braking system, it slows you down, especially if you are highly anxious...which is why drugs that specifically enhance your gaba are listed within the group of medications intentionally referred to as anti-anxiety meds, or "anxiolytics." They differ in the degree each has in some forms of skeletal-muscle relaxation, and consciousness (often inducing tiredness and sleepiness, or just relieve the anxiety (and-or it's experience of stress) at the lower doses), sometimes used temporarily to induce sleep. There are a couple of classes of anxiety meds and supplements. Sometimes used in combination with depression meds. You can take it from there in pursuing your general understanding.
Ok, I was half expecting you to say acetylcholine, which tricyclic antidepressants interrupt by the way. I'll look into it. It's good to learn something new every day.
1. I started to notice I had lost some sense of smell about a year before PD diagnosis (2017). I notice some smells (perfumes, air freshener etc.) but less so unpleasant odours.
2. I currently take a lowish dose of C/L (Sinimet) 4*12.5/50mg tablets a day. I have stopped taking C/L in the past for several weeks without much effect on PD symptoms and I'm not convinced that there has ever been a really noticeable effect on me. The reason I stopped in the past was because I had experienced unpleasant symptoms (severe anxiety and palpitations) that went away when I stopped C/L altogether. I have since seen a Professor of Neuropsychiatry who has put me on Duloxetine (promotes Serotonin and Noradrenaline) and I self administer a GABA supplement. Since then I have been OK with a gradual increase in C/L and seeing whether I feel any positive effects. The neuro said that it is not unusual for other neurotransmitters to be depleted, as well as dopamine, and maintaining a balance is important. The anxiety (which can be driven by dopamine) was severe enough that I would rather have movement problems than that again.
3. Unless someone wakes me I sleep for 9 to 10 hours a night. I have vivid dreams almost every night. I hardly ever act them out.
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Mannitol and sense of Taste/Smell
Can moderating meds forestall diskinesia side effects?
Has anyone been able to reduce their C/L dose once they started on High Dose Therapy B-1? If so, how and why did you decide to reduce C/L? 
Gou Teng helps with my tremors . 
