For anyone diagnosed with ADHD, taking stimulants is associated with 8+x increase of being diagnosed with a basal ganglia and cerebellum disease later in life.
I believe this is NOT causative, but is instead a correlation between other diseases associated with Dopamine production and ADHD. I take and have continued to take stimulants for ADHD.
In my family's case, we likely have something called Dopa Responsive Dystonia (DRD), and what the author is describing sounds to me like what I experienced prior to being diagnosed with ADHD, and later with DRD.
Having said that, I'm not a doctor, so please go see an experienced movement disorder specialist if you are reading this and have any concerns.
DRD is very hard to diagnose, but easy to treat. Because the stimulants (Adderall and Ritalin) made the DRD symptoms worse, my mother happened to get early onset Parkinson's, and my grandmother also responded to carbodopa/levodopa (carbo/levo), it was fairly obvious in retrospect, but if we didn't have a family member with early onset Parkinson's I doubt it would have been picked up.
My sense is that anyone with ADHD who uses stimulants should see an experienced movement disorder neurologist or few about basal ganglia and cerebellum diseases and try out medications based on their assessment. From personal experience, it became extremely clear I had DRD after taking carbo/levo, but there's no way I would have really known without trying it. It also helps with some of the stimulant side effects, which I still continue to take because they are very effective.
My family has seen maybe six neurologists total, and only one really knew about DRD. The Dystonia Foundation has a decent doctor locator.
Segawa's is completely irrelevant in this case and not supported by any symptoms the author reports in the original article. I have diagnosed Segawa's. It is quite irresponsible to wave people off of successful treatments of ADHD, as you're doing here, because of your family's (unfortunate) history with a genetic disease. I apologize that we know little about Segawa's and you've had a journey to understand it, but there is approximately zero overlap between common ADHD symptoms and the presentation of Segawa's, which is primarily motor-related.
Please, don't read comments like these and distance yourself from treatment. There is always more to a study.
What is your take on link to Parkinsons and Alzheimers from therapeutic doses of amphetamines 60mg and below daily?
Am I trading my future brain function for quality of life improvements in the current?
The thought of irreversibly damaging my dopamine transport system later on in life feels like I am making a deal with the devil every time I take a dose of stimulants to correct my dopamine imbalance and cognitive deficits to feel neurotypical for a fleeting period of time soon after ingestion.
Any link to hemorrhagic stroke later in life as well? Thanks for you time.
Thoughts on any neuroprotective measures I can take now like memantine or bromocriptine(sp?)?
I think you're misinterpreting my post based on some of the other responses. I will update it to unambiguously state that people taking stimulants for ADHD should continue to take them, just like I have continued to.
I'm not misinterpreting your post. You diagnosed the author with Segawa's based on your experiences by pointing out you wouldn't be surprised if he "had something similar". He does not, with certainty. You're also warning folks that the only consistently successful treatments we have for this (much, much more common) hyperactivity disorder are associated with unlikely neurological outcomes. Sure, an 8x increase sounds high, until you realize that it's multiplying a mere fraction, context you do not include.
I'm sorry to appeal to authority here, but comments like these do actually harm people by shying them away from treatment (just look at your replies), and please don't write them. Again, I'm sorry you're dealing with Segawa's, but even your edits in response to my comment are making your statement more harmful because they're based in pure speculation.
Hate to break it to you, but the OP's edited comment is far less harmful than yours.
I've been suffering from a myriad of symptoms that happen to match up with Segawa's... a disease I learned about less than ten minutes ago.
> please don't write them
Please don't make statements requesting that other's don't share their experiences with misdiagnosis and rare conditions. It's rude and furthers the stigma that some conditions are too rare for their sufferers to discuss.
> Hate to break it to you, but the OP's edited comment is far less harmful than yours.
It has been significantly, damned near whole cloth, edited in several ways since I said something, so I'd ask a little consideration that I'm coming from a good place. I'm not asking for anyone to avoid discussing Segawa's; I'm specifically responding to the speculation, across multiple comments, that the common element of dopamine as a neurotransmitter makes them related diseases. Given that people attack doctors when they try to arrest harmful discussion like this, I'm taking great pains to not be rude, so I apologize for coming across that way.
If you diagnosed yourself with Segawa's based on Wikipedia, please bear in mind that my single diagnosis across my entire career involved four months of differential diagnosis and observation, and led to a publication. It's simply that rare. There are several much more common possibilities, and I'd ask you to talk with your neurologist with an open mind rather than assuming the Internet has steered you correctly. That's also part of the reason I've responded as I have, exactly due to what you're saying.
It has not been edited near whole cloth. I added two sentences and modified two others. I think I've been very understanding of your skepticism, but at this point you're literally making stuff up.
Appreciate the comment and was unaware that it had been edited after your second comment.
I won't be diagnosing myself off of Wikipedia, next to no one in my family has the symptoms that I do so I doubt it's something like Segawa's.
I appreciate the apology and hope my reply didn't come off as too aggressive. Part of my tone comes from personal experience: doctors stating that I don't have a condition because it would be "statistically unlikely"... all without running a single test.
It was edited after their second comment, but they are exaggerating how much it was edited.
I added the first italicized sentence after their first comment, and after their second comment added the second italicized sentence and modified two other non-italicized sentences. I think... I may have just modified one non-italicized sentence after their second comment.
I am not a doctor and I did not diagnose them with anything. I stated that what they described sounded very similar (nearly identical) to my experience, initially with ADHD and then with DRD. I have updated the initial post with clarifying statements.
I don't intend to mislead anyone. However, I do want people to be aware of possible links between ADHD and other disorders so that they can evaluate their own situation and seek medical care if they would like to.
More to the point, my family has been misdiagnosed for decades, and this likely would have been avoided if we were more aware of other possible diagnoses.
My answer to that question will come across snarky or "the medical profession appealing to authority," I'm afraid, because I'd like to see your remarks entirely removed as medically harmful. Your purpose is clear from your other, more to the point remark: if only it had been for a random HN commenter who's never been to medical school speculating about two entirely unrelated diseases based on the presence of a common hormone, you might have avoided the diagnostic history and pain in your family that you report. That's a ridiculous position, both interpersonally as well as scientifically, but I know that engaging on it with you will look like I'm trying to steer people to my field rather than encouraging independent research of our discipline.
I'm here because I'm learning to write software, but I wouldn't pretend to understand the paper or mathematic theory behind, say, Paxos because I recognize some terms in it. I know my limitations, and all I ask is that you consider them, as well. The problem with raising awareness as you are is that it's difficult to objectively remove yourself: Segawa's is _incredibly_ rare, making all of the events in your family difficult to explain. Scientifically, transferring your experiences to others is a very tall order without much further study (and I hope you, and your family, are being studied, specifically because the genetics of Segawa's are poorly understood). What people portray as medical professionals swinging the hammer on "the information that could make us irrelevant" is actually trying to stand fast to the exact same scientific discipline that you, and every member of this audience, does in _every single other context_.
Your speculation about the relationship between ADHD and Segawa's is so far off base that a second-year medical student could probably explain why; you just happen to have been diagnosed with both. Left unspoken: it is quite possible to have both, because they present and manifest in different ways.
I'm happy to modify the portions of my post you think are medically harmful. I could be wrong, and I've been wrong before. But at the same time you could be wrong, and I think you are relying a bit much on appeals to authority. Just my opinion of course. I also wouldn't sell yourself short about making contributions to other fields. If you're wrong, you're wrong, but let someone else tell you that. I had to dig around and look real hard to even begin to figure out what was going on with my grandmother and ultimately my family. I was wrong a few times along the way, but we were able to figure it out.
My guess is that DRD is under diagnosed because of reduced or low penetrance in some cases. As far as I can tell, for the majority of our lives, no single person in my immediate family would fit the diagnoses, but as a family, we apparently do, especially if someone knows where to look and what to look for. I suspect my extended family on my grandma's side has it as well, but I doubt any family with it would be diagnosed unless they happened to have someone who presented with it in an obvious way.
The urgency you're detecting in my posts is because in my experience, 10+ doctors and 4 neurologists missed it and/or mistook it for other diseases. It was especially hazardous for my grandmother because they were insisting on doing the medical version of taking her out back and shooting her even though their treatment of her in medical and custodial care settings was causing the very symptoms they claimed were due to other disorders. And yes, I do not want someone else to go through that, especially since having other relatives who also respond to carbo/levo seems to be critical in helping establish a diagnosis when there isn't someone in the family who presents in a typical way.
If you want, I can modify my post, but like I said before, I strongly suspect the presentation of ADHD with other characteristics, which are admittedly not symptoms of either disorder, increases the odds that someone has DRD or some other neurological disorder that's also contributing to the presentation of their ADHD.
If you have some compelling evidence that there is no interaction between DRD or similar and ADHD, I'm happy to see it, but from personal experience that is not the case.
I didn't know this, but I take my medication as rarely as possible because I hate the comedown, appetite suppression, and tolerance building that occurs. It sucks, but I had a feeling there was some long-term downside like this. Hopefully lessening frequency to occasional use also lessens the likelihood of what you describe.
I don't think it's a causative relationship. My feeling is that there are a group of disorders related to Dopamine production that overlap with ADHD, for obvious reasons, and if you have one of those you're more likely to get diagnosed with ADHD.
On the flip side, getting treatment for those disorders, provided you have one of them, can also help with some of the ADHD symptoms.
What a beautiful advise, it remembers me of two friends with major depression who stopped taking their meds and thus will not have a bad long term experience with their anti depressants.
One committed suicide last year, one the year before.
Oh, I hear you say that they only should have stopped taking them “if they possibly can”. I’m sure their families now know that they possibly couldn’t.
I would appreciate if you could work that into your future medical horoscopes...
I would really suggest stopping that advise unless you're a medical professional, the long term effects should be considered and attempting to be on a methylphenidate for extended periods of time isn't to be taken lightly due to even obvious and relatively minor effects like increased blood pressure. But, for some people it makes quite a significant and noticeable differences and adding to the stigma of taking a medication by reinforcing that it's non-essential will decrease some folks' quality of life.
Presenting information about the long term effects is good and I, especially, appreciate it - but please don't attempt to judge treatment efficacy when, especially in the realm of neurological disorders, treatment efficacy can vary wildly from case to case.
So please do share your story and invite people to learn, but don't council others.
Just because you don't have anecdotes on your hand doesn't mean that's not the case. I don't know what your definition of "long-term" is, but ultiple specialists I have seen over the years happened to mention that they have patients who have been pretty much on the same stimulant prescription for ADD for 10+ years. I didn't reach that number of years yet, but I am getting close though. Once the specialist finds the drug and dosage that works for you, there should be pretty much no need for any changes to prescription or dosage. That seems to be pretty sustainable to me.
This has always been quite concerning to me as I've had a worsening essential tremor that was slight in my early twenties but is quite observable now that I'm in my thirties. The confounding effect that really hurts me here is that my father has had a benign essential tremor for his whole life - so there's a constant see-saw internally and with medical practitioners about whether my tremor is something to be concerned about or not.
I suspect that my mom developing a tremor is what turned her DRD, which was in retrospect similar to what myself and my grandma have, into Parkinson's. As far as I can tell, for my family anyway, developing the a tremor will rapidly deplete what little Dopamine we can produce and lead to normal'ish looking Parkinson's.
The genetic defects associated with this are I believe a spectrum though, and we happen to be close to one side of it. If you have any symptoms related to DRD, I would see a movement disorder specialist and ask for a trial of carbo/levo. It'll be immediately obvious if it helps, and if you don't have any problems with Dopamine production it won't do anything (except for some mild side effects).
Thanks for the info on ADHD / basal ganglia and cerebellum. I was not aware of this.
It should be noted though that the study authors were pretty clear that the correlation is unclear given that untreated ADHD sufferers had a 2.5-fold increase in the same diseases.
> Researchers postulated that the association between psychostimulant use and BG&C diseases may be a result of a more severe ADHD phenotype, rather than a direct pharmacological effect.
Thank you for citing this article. It is also known that using methamphetamine increases cardiovascular risk. Prescription amphetamines might do the same.
There's no direct link I've read about. From personal experience, having DRD increases the risk of being diagnosed with Alzheimer's, which happened to my grandma about 20 years ago, but that's just because some of the symptoms are very general, and it's especially hard to tease out with co-morbid conditions that may have some overlap.
>"hyper mobile joints are an uncommon finding in those who do not have attention deficit disorder/attention deficit hyperactivity disorder."
>Differences in the structural integrity of temporal and parietal cortices may underlie wider behavioural phenotypical expression of hypermobility: abnormalities in superior temporal cortex are also seen in autism.11 Inferior parietal cortex can affect proprioceptive awareness and hypermobility is itself linked to dyspraxia.1 Our findings suggest that processes compromising function in neuro-developmental conditions may occur in individuals with hypermobility, putatively enhancing vulnerability to stress and anxiety.
Autism, Joint Hypermobility-Related Disorders and Pain
ASD and HRDs, specially hEDS, are conditions with a strong genetic component, a polymorphic clinical presentation, appearing both in infancy, and sharing several phenotypical features (35). Although existing data does not allow to ascertain increase prevalence of ASD in HRDs, as well as shared underlying patho-mechanisms between both conditions, there is increasing evidence suggesting that these co-occur more often than expected by chance. This requires be confirmed by further investigation which should consider the recent nosological changes both in EDS and the hypermobility spectrum disorders [see (17, 38)], and in ASD (72).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292952
Joint hypermobility and the heritable disorders of connective tissue: clinical and empirical evidence of links with psychiatry
- In 1988, Hofman et al.[58], in a sample of 30 children with MFS,observed that 17% had attention deficit disorder with or without hyperactivity. A decade later, Harris[59] stated, based on his clinical experience with 200 patients with ADHD, that "hyper mobile joints are an uncommon finding in those who do not have attention deficit disorder/attention deficit hyperactivity disorder."
In Sweden,Hollertz[60,61] also pointed out the frequent co-occurrence of ADHD and JH in adults patients. He observed that an orientation to orthopedic and rehabilitation care was common in these patients due to joint problems. Thus, this author speculates about a possible genetic marker com-mon to ADHD and EDS.
Recently, Koldas Dogan et al.[62]explored JH using the Beighton score in 54 children with ADHD compared to 36healthy controls. In this study, JH was significantly more frequentamong patients than among controls (31.5% vs. 13.9%). In accor-dance with these results,
Shiari et al.[63]also found a higher prev-alence of JH, assessed with the same method of the previous study,among Iranian children with ADHD compared to controls (74.4%vs. 12.8%), confirming an association between ADHD and abnormal collagen conditions.
JOINT HYPERMOBILITY AND AUTONOMIC HYPERACTIVITY: RELEVANCE TO NEURODEVELOPMENTAL DISORDERS
> It is likely that the importance of hypermobility and autonomic dysfunction to the generation and maintenance of psychopathology in neurodevelopmental disorders is poorly appreciated. Work underway(autonomic testing, fMRI) will test the hypothesis that autonomic reactivity and interoceptive sensitivity predispose to the expression of psychiatric symptoms, particularly anxiety
- We demonstrate for the first time that rates of hypermobility and symptoms of autonomic dysfunction are particularly high in adults with neurodevelopmental diagnoses. It is likely that the importance of hypermobility and autonomic dysfunction to the generation and maintenance of psychopathology in neurodevelopmental disorders is poorly appreciated. Work underway(autonomic testing, fMRI) will test the hypothesis that autonomic reactivity and interoceptive sensitivity predispose to the expression of psychiatric symptoms, particularly anxiety. It is further hypothesized that inefficient neural co-ordination of efferent autonomic drive with imprecise interoceptive representations may be amplified in hypermobile individuals. In hypermobility, this mechanism might explain increased vulnerability to stress sensitive and developmental neuropsychiatric conditions.
- https://jnnp.bmj.com/content/85/8/e3.40?utm_source=trendmd&u...
[Searching for a biological marker common for both ADHD and EDS].
- https://www.ncbi.nlm.nih.gov/pubmed/22468413
- speculated about a common biological base shared by ADHD and EDS after observing the frequent cooccurrence of both pathologies in a clinical setting.
Connective tissue problems and attention deficit and hyperactivity
- To the Editor, The heritable disorders of the connective tissue are a group of genetic disorders affecting connective tissue matrix proteins that classically include Marfan syndrome (MFS), Ehlers–Danlos Syndrome (EDS), benign joint hypermobility syndrome and osteogenesis imperfecta (Grahame 2000). As connective tissue is found throughout the body, the clinical manifestations of these disorders are varied, including disturbances in different systems (skeletal, ocular, cardiovascular, etc.). A common feature of the heritable disorders of the connective tissue is joint hypermobility (JH), which is a highly heritable condition characterized by an increased range of motion of the joints as a consequence of connective tissue involvement.We encountered a 7-year-old boy addressed by teachers due to school problems. His mother suffer from MFS such as his maternal grandmother who died by cardiac complications. Considering familial antecedents, his morphotype (long bone overgrowth), JH and ocular ...
A connective tissue disorder may underlie ESSENCE problems in childhood
Attention-deficit/hyperactivity disorder, joint hypermobility-related disorders and pain: expanding body-mind connections to the developmental age.
>Recent research seems to indicate a degree of co-occurrence of JHS/hEDS and some neuro-developmental disorders including attention-deficit/hyperactivity disorders (ADHD) and developmental coordination disorder (DCD). In the area of ADHD, researchers found that adults with ADHD had higher rates of JH and problems with automatic control of body functions (dysautonomia) compared to healthy controls. Other researchers observed high co-occurrence of JH or EDS with ADHD. Concerning DCD, children with DCD have more symptoms associated with JHS/hEDS compared to typically developing children. The relationship between JH and DCD may be due to poor positional sensing in affected children.
A Cohort Study Comparing Women with Autism Spectrum Disorder with and without Generalized Joint Hypermobility
- This research supports a growing body of literature indicating that immune-mediated disorders are a common comorbid feature in hEDS and GJH. In addition, we have also shown that this dysfunction may be paired with endocrine dysregulation, leading to complex immune and hormonal exophenotypes, such as autoimmune disorders, allergic rhinitis, asthma, endometriosis, and dysmenorrhea. While we have not addressed autism and GJH comorbidity rates in this study, their co-occurrence in the adult ASD female population suggests links between the dysfunction of connective tissue and the immune and endocrine systems in this subpopulation.
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867488/
>ADHD might thus be a (non) allergic hypersensitivity disorder caused by an environmental trigger, based on a non-IgE dependent histamine release from mast cells and basophilic granulocytes, since the histamine H3 receptor is involved in hyperactivity and promotes dopamine release in the frontal cortex. Moreover, polymorphisms in the histamine N-methyl transferase (HNMT) gene, impairing histamine clearance, were found to affect the behavioral responses to food additives, which increase histamine levels #ADHD
I always noticed a pattern of 'see one, and the other is never far behind' with autism and ADHD but I never made the time (irony much) to pin studies to it. Thanks for collecting these.
I believe this is NOT causative, but is instead a correlation between other diseases associated with Dopamine production and ADHD. I take and have continued to take stimulants for ADHD.
https://www.nature.com/articles/s41386-018-0207-5
In my family's case, we likely have something called Dopa Responsive Dystonia (DRD), and what the author is describing sounds to me like what I experienced prior to being diagnosed with ADHD, and later with DRD.
Having said that, I'm not a doctor, so please go see an experienced movement disorder specialist if you are reading this and have any concerns.
DRD is very hard to diagnose, but easy to treat. Because the stimulants (Adderall and Ritalin) made the DRD symptoms worse, my mother happened to get early onset Parkinson's, and my grandmother also responded to carbodopa/levodopa (carbo/levo), it was fairly obvious in retrospect, but if we didn't have a family member with early onset Parkinson's I doubt it would have been picked up.
https://en.wikipedia.org/wiki/Dopamine-responsive_dystonia
My sense is that anyone with ADHD who uses stimulants should see an experienced movement disorder neurologist or few about basal ganglia and cerebellum diseases and try out medications based on their assessment. From personal experience, it became extremely clear I had DRD after taking carbo/levo, but there's no way I would have really known without trying it. It also helps with some of the stimulant side effects, which I still continue to take because they are very effective.
My family has seen maybe six neurologists total, and only one really knew about DRD. The Dystonia Foundation has a decent doctor locator.
https://dystonia-foundation.org/living-dystonia/find-a-docto...