"They created a kind of wiring map of the brain and found that those who had negative behavioural reactions to the medication had one of two things in common.
'We took circuits in the brain that we know have underlying important behaviours and two of those behaviours are choosing and stopping', Dr Mosley said.
People who had stronger choosing circuits or weaker stopping circuits were more likely to be impulsive."
It would be nice if the procedure suggested in the report could actually determine which patients are vulnerable to impulse control disorder arising from dopamine agonists. However, as far as I know most doctors do not even bother to warn patients or their caregivers about potential personality changes when prescribing these medications, much less bother to check for orthostatic hypotension as a result. So even if this procedure is valid I doubt it will ever be used.
Dopamine agonists have a place as a last resort therapy. But those who irresponsibly push this treatment without regard for the adverse effects will have their fair share of bad karma to answer for. Case in point from the article:
"I put her [my wife] through hell — the doctor says it's through no fault of my own — it's just the drugs, but it's probably a lot harder [for her] to live with," Mr Stephens said.
"[With] my mood swings and what-not … my wife said 'I can't take it anymore' and she walked out on Tuesday. "
It seems they are on the verge of being able to tell--the brain scan can detect those with stronger choosing circuits or weaker stopping circuits in their brains. It is now only a matter of quantifying it. But MRIs are not cheap so scanning all parkinson patients to identify the one in six who has the compulsive syndrome would be absurd.
This is only the tip of an icesberg, there are drugs, not of PD,that have far more destructive impulses as a side effect.
Hi park_bear. I ask you, if a specialist puts a patient on this drug (for PD or Restless Legs) surely he should monitor it for addictive behaviour. The Neupro Patch turned my husband’s life around. The diagnosis changed from LBD to PD.
There was a court case a few years ago (can’t remember the location) where a patient developed a gambling addiction and lost his house. He wasn’t monitored and he won the case, and so he should. Our neurologist monitors his patients very closely and has taken patients off the drug. His patients are fully informed. His attitude to B1 was ... “try it, you won’t find anyone doing research into it, as you can’t patent a vitamin”. We love him to bits.
My husband’s personality probably fits with the research. He is very disciplined and has a business and accounting background. I must ask our neurologist about this theory. It makes sense. He’s always interested in my research (mostly from this site and links). Keep up the good work.
My husband had that sort of reaction to mirtazapine / fluoxetine combo to start with. He started gambling , without me knowing, buying lots of everything and eating continually, and non stop talking. And speeding in the car getting tickets. It was awful. It stopped when the fluoxetine stopped. Sertraline(Zoloft) also has a similar effect but to a lesser degree. I am now learning how to balance it by reducing the dose a fraction if he starts speeding and over eating and searching for stuff to buy on line that we don’t need. I know he needs a little extra when he isn’t hungry, and he hides in his bedroom and won’t come out or talk to anyone. Winter also has this effect so I’m pretty sure it’s seratonin fluctuations.
I very much like your adaptation to the individual situation, it is exactly what a good (well, these days, 'very' good) clinician would do.
Also your interpretation of "serotonin fluctuations" is spot on. SPOT ON.
You are on the right track, because it does not matter knowing whether you are a stronger chooser or a weaker resistor, you still must "titrate" to your individual situation and where that is, by CLINICAL INDIVIDUAL FREQUENT ONGOING ADJUSTMENTS using your intuitive scientific method...
Which is in fact the distinction some people need 8 or 9 years of study to realize, which is the difference between group statistics and the individual within those statistics (the individual is uniquely unpredictable) even though part of a large collective that collectively can be described as average, or "curvilinear," or modal, or leveled (inside a particular tenth, or quarter, or fifth, or half (average) or median (half above, half below)) members of a population. Fine for research, but still does not get you to the individual, who may be scaled high on the scale, low on the scale, or way out on the tails of the scales, plus or minus. Big big difference in effect, and response, and outcome in that case, and can't be predicted for any individual using group statistics. At all.
You couldn't trust any sort of surgery with statistically numb levels of specificity, say for example, eye surgery, or slicing out a cancer tumor while preventing a few cells popping out and "seeding" into metastatic translocation (turning into new tumors all across the body), no different than being a single member of a large population of subjects, because to get the reliability level trustworthy enough, say 95% or 99%, as must be done with statistics describing GROUPS of patients, you must by the same mathematics sacrifice confidence in the INDIVIDUAL's case...which basically means that even though predicting a score with confidence about a group of people means that the individual probability of a single individual person's score is statistically zero. ZERO. I SAID ZERO.
So you still have to very carefully experiment, and thereafter very frequently abd sensitively observe, then "titrate," on a sample size (of 'n') of 1...your husband. Which is exactly what you have been doing. So bravo.
Thanks Marion. It’s nice to have validation of my methods as doctors frown on me. They don’t have to live with the ups and downs though!
Meanwhile as I write he is busy buying a big stack of bridge books , singing and playing musics indicating we are on an up again!
Actually it is not so much the substance that is addictive, it is actually the adaptive nature and somewhat complex nature of that adaptation of our own brains that is the addictively active entity. And it really helps to think like that, that it is not the substance, but our own brains are the "addictors," not the chemicals themselves.
Addiction does not require a "high," for example, nicotine, amphetamines, codeine, caffiene, theobromine (in black tea), antihistamines. Energized feeling, or agitation, or itching, can be the response and experience. Or violent retching, nausea and throwing up, bigtime sweathing and feverishness if the mu-opioid or sigma receptors are involved, as they often are...So then, rather, it's our RESPONSE to the nicotine...whether the feeling is good, bad, or returning from bad to just plain normal (depending on the stage of the addiction)...our brain addicts ITSELF to the chemical.
And that is, as it turns out, the nature of nerve cells. Cannabis can give you a high, and it can addict you too. But not all addiction experiences are "high." So this story, in itself, is really kind of old news.
As to the original term for opiate class addictives, which was "alkaloids" including morphine, heroin, nicotine (a stimulant, ie cigarettes, chew, vaping), they don't produce "high," they produce energy, agitation, irritation, as the subjective experience..."turned on...")...extreme disorientation, inability to hold your head up or steady and endlessly dizzy into the bargain, again with heavy doses of antihistamines...but yet, still addictive. Very addictive, as a matter of fact in some cases, like nicotine (especially if inhaled) and opioids. And similarly, so addictive also are antidepressants that work on the tryptamine (5HT, serotonin) side of the stimulation/mood activating side of the chemistry).
It's just the way we are built, as we are learning (actually we were learning this in the late 70s/early 80s, it's not that new anymore...but we didn't for a fair time realize just how extensive it was, nor how yet to deal with it (though some were even back then speculating that it might be very widespread as a more general tendency underlying a very large swath of human learning mechanism, but it was still an infancy research topic in experimental psychology, because the original demonstrations were from psychology research into, if you will believe it, color vision in cats...(how about that for a left field example of basic research migrating into new science directions?!!!), and so yet to be tested and then eventually shown for real and justified to publicize as more widely spread than just "substance abuse addictions").
There is now a PNT article about this research (including a link to the abstract of the research paper).
NEUROSCIENTIST SHOWS WHAT FASTING DOES TO YOUR BRAIN & WHY BIG PHARMA WON’T STUDY IT
Trials coming from Zhittya 
Influence of sunlight on dopamine transporters.
I wonder
GREAT NEWS! Intra-Nasal FGF-1 Human Trials have started! WATCH video! Tremor reduced!
