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The Link Between Sleep Apnea, ADHD and Parkinson's

kkentm

By kkentm
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Diceroll2011 Newbie

Diceroll2011

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One of the most bizarre posts here.

More speculation than science, and I'm not sure why the Neuroscience department would not have just supported you if they found your findings credible.

 

I think your first steps should be to present a more comprehensible proposal, because as it stands, it is all over the place and makes some seriously baseless claims.

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thehumanmacbook Newbie

thehumanmacbook

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Hi there,

 

My name is Kent Mao and I am an undergraduate student at McMaster University. Last week I made a huge discovery linking ADHD to Parkinson’s Disease and I brought my findings to the Department of Neuroscience at my university. All of the professors there believed that this was the biggest breakthrough in Parkinson’s Disease research since its beginning. They told me to bring it to someone or an organization who had the power and influence to do something about it. I decided to send it to the Michael J. Fox Foundation because I believed that they would be the best organization to address this urgent matter. Unfortunately, they replied 3 days later with this message:

 

Dear Kent,

 

Thank you for your email regarding a potential link between ADHD and PD. We certainly agree that identifying early risk factors for PD would be extremely important and MJFF supports a number of projects to identify such risk factors.

 

If you and your professors are interested in pursuing a potential link between ADHD and PD you are welcome to apply to one of our funding programs via the Funding Opportunities section of our website:http://www.michaeljfox.org/research_...ortunities.cfm. As our staff shared and as stated in our RFAs, our funding opportunities are open only to PhD’s and postdoctoral fellows.

 

Sincerely,

MJFF Research

 

They say the goal of medicine is to do whatever it takes to treat and cure the sick. I used to believe in this goal, which is why I decided to study health science in the first place. Now I realize that this goal is tainted with politics and selfish interests. That is why I am posting my findings on the internet and putting the power of medicine into the people themselves. I realize now that us normal civilians are the only ones who truly believe that anything should be done to heal the sick, no matter the political consequences. Feel free to email this or post this anywhere. With every day that passes, hundreds of people are being diagnosed with Parkinson’s Disease. We have all the scientific knowledge and resources to stop this now.

 

Evidence for Link Between ADHD and Parkinson’s Disease

By: Kent Mao

 

Introduction

 

Parkinson’s disease (PD) is a chronic degenerative neurological disorder characterized by neuronal death in the nigro-striatal pathway of the substantia nigra region of the brain. Unfortunately, the administration of treatment and the potential for recovery from PD is strongly hindered by the fact that clinical symptoms are not present until more than 50% of the dopaminergic neurons in the substantia nigra pars compacta are lost (1). Although research has shown that PD symptoms worsen over time due to the steady rate of death of dopaminergic neurons, researchers have failed to realize that the key to understanding the etiology of PD is in identifying the cause of neuronal death prior to the onset of clinical symptoms. This leads us to the idea that our current diagnostic measures for cases of PD are insufficient, as they do not account for the possible presence of clinical symptoms associated with the initiation and progression of neuronal death in the substantia nigra. Unfortunately, a retrospective study on the death of dopaminergic neurons in diagnosed cases of PD is impossible for obvious reasons. However, it is possible to look at the current diagnostically relevant symptoms of PD and link them to another neurological disorder with similar symptoms that are less pronounced.

 

First off, let us investigate the clinical symptoms currently associated with PD. Despite the wide range of symptoms associated with PD, every one of them can be linked to the malfunction of the substantia nigra, which is a structure in the brain that plays an important role in reward, addiction and movement. Therefore, identifying early signs of reward, addiction and movement abnormalities is the key to implementing screening tests for identifying individuals at risk of developing PD before clinical symptoms are apparent.

 

The profoundness of this connection is in the recent overflow of research and studies on another neurological disorder that was previously thought to be unrelated to PD. This disorder is known as Attention Deficit Hyperactivity Disorder (ADHD), a neurological disorder characterized by clinical symptoms that seem to also relate to reward, addiction and movement. More specifically, recent hypotheses suggest that the symptoms of ADHD are caused by an abnormally low level of baseline stimulation in the dopamine reward pathway, resulting in the associated symptoms of substance addiction, thrill-seeking behavior, hyperactivity and attention deficiency. Furthermore, a recent study published in 2010 showed that children with ADHD exhibit a structural abnormality of their substantia nigra (2). Throughout my investigation of this disorder, I was able to identify 4 key symptoms of ADHD that seem to suggest an etiological relationship with PD. These symptoms are abnormalities of: speech, sensory input, fine motor control and resting tremors. I do not believe that mere coincidence can explain the presence of these same abnormalities in cases of PD. In fact, the most biologically plausible explanation is that the neurological symptoms of ADHD worsen with age until clinical symptoms are finally noticed and a diagnosis of PD is given. Although there is very little evidence that the symptoms of ADHD are chronic, this can be easily explained by the development of coping mechanisms by a maturing individual with ADHD. Thus, my hypothesis is that ADHD and PD are two names that have been inaccurately assigned to the same underlying neurological disorder.

 

Development of Hypothesis

 

In order to evaluate the validity and strength of my hypothesis, we must utilize and integrate the current knowledge we have on ADHD and PD. This knowledge is available in the form of published studies and future implications of my hypothesis depend heavily on the validity of these studies.

 

The development of my hypothesis began after my own clinical diagnosis of ADHD. Naturally, finding out that I had lived 19 years of my life with an undiagnosed neurological disorder made be passionately curious about the subject. Furthermore, the estimated prevalence rate of 5% in North America led me to believe that ADHD was a massively under-diagnosed disorder, which is a common result of a general lack of knowledge on the subject. Furthermore, I concluded that there must be a missing link to another neurological disorder with a similar incidence rate, as neurological disorders do not have a tendency to fix themselves without medical intervention. Studies have shown that PD has a prevalence rate of approximately 1% in seniors over the age of 60 and a prevalence of over 4% in seniors over 80 (3). It seems reasonable to me that a statistical correlation may indeed exist between the prevalence of ADHD and PD if factors resulting in early-aged death are accounted for.

 

Another curious commonality between PD and ADHD is the absence of environmental risk factors. However, genetic risk factors for both PD and ADHD have been identified with a mutation of the DRD4 gene being a common risk factor for both. This common genetic risk factor was of particular interest to me as I had noticed a high number of ADHD-like symptoms in my father as well as ADHD-like symptoms in my grandmother who is currently suffering from clinically diagnosed PD.

 

However, my initial research into PD was not focused on identifying a causal pathway but rather was focused on identifying a better method of treatment for my grandmother’s deteriorating condition. Her case was particularly thought provoking, as her symptoms were much worse than they should have been at her stage of the disease. Despite being treated with l-dopa for her PD and lexapro (an SSRI class drug) for her depression, symptoms of depression and central nerve pain persisted. After suggesting to my father that regular physical activity might help improve her depression as well as delay the progression of PD, he informed me that he had tried his best to encourage this but that my grandmother seemed to have given up mentally and exhibited a severe lack of motivation. Although most doctors would identify lack of motivation as a sign of depression and prescribe SSRIs to increase serotonin levels, I realized that lack of motivation was also indicative of deficient levels of dopamine such as those seen in ADHD.

 

After arriving at this conclusion, I decided to investigate the documented use of amphetamines in treating PD and what I found, or rather was unable to find, was astonishing. To this date, there have been no majorly funded studies conducted on the efficacy of methylphenidate in treating PD. After delving further into this mystery, I stumbled upon a study published in 1975 that reported a drastic reduction in PD symptoms when patients were given a combination of amphetamines and l-dopa in comparison to groups receiving treatment by l-dopa or amphetamines alone (4). However, the incredible significance of this discovery was not realized at the time since ADHD and Ritalin were still foreign terms in the medical community. Although any doctor or researcher can still access this publication, the last time this study was cited was in 1980. Furthermore, I believe the results of this study are still valid due to the replication of similar results in two more recently published but less credible studies, a case study from 2002 (5) and a case series from 2004 (6).

 

Proof

 

Rat models have been used to study the progression of Parkinson’s Disease for many years, most commonly involving 6-OHDA lesions of the nigro-striatial pathway. For those unfamiliar with the significance of rat models, they are used to study every single neurological disorder because of their incredible genetic and physiological similarity to the brains of humans. Thus, anything found in rat models can be safely assumed to be directly applicable to humans. Compensatory responses have been observed and recorded but have hitherto not been linked to ADHD. According to literature, the initiation of dopaminergic neuron degeneration is followed by a brief period of abnormally high dopamine levels resulting in hyperactivity of the rat. As degeneration progresses and dopamine levels decline, compensatory responses present in the form of changes in increased sensitivity/density of post-synaptic dopamine receptors as well as abnormal sprouting of neurons connecting the external capsule to the rostal striatum. The formation of this neuronal connection is not observed in controls and occurs after a significant length of time after initiating degeneration (7). The external capsule is a white matter tract that connects the basal forebrain to the cerebral cortex. The basal forebrain has been implicated in a number of behavioral functions such as arousal, sensory processing, motivation, emotion, learning and memory.

 

If Parkinson’s Disease is indeed the result of progressive and chronic ADHD, then observations of rat model behaviour and neurology before 50% of dopaminergic neurons have degenerated should be comparable to clinical symptoms of ADHD. The brief period of abnormally high dopamine levels and hyperactive behaviour is indeed observed in young children with ADHD. As the degeneration progresses and dopamine levels switch from abnormally high to abnormally low, hyperactive behaviour stops. This is also observed in older children and adults with ADHD who do not display the same restlessness and inability to stay still as young children do (8). Lastly, behavioural abnormalities of arousal, sensory processing, motivation, emotion, learning and memory should be observed as the abnormal neuronal connection between the external capsule and rostral striatum is formed. Although such behavioural abnormalities are hard to pinpoint in rat models, they are all characteristic of the clinical symptoms of ADHD.

 

This new knowledge is the key to identifying individuals at high risk of developing Parkinson’s, delaying the onset of the disease, and ultimately finding the cause and cure. Research funding needs to be reallocated to studying the progression of this disease starting from the onset of symptoms that have hitherto been thought to be indicative of a completely unrelated disorder known as ADHD.

 

Sources

 

(1) http://www.jbc.org/content/282/52/37350.full

(2) http://www.behavioralandbrainfunctio...content/2/1/33

(3) http://www.ncbi.nlm.nih.gov/pubmed/1...IT+maintenance.

(4) http://www.sciencedirect.com/science...206704719#sec7

(5) http://www.ncbi.nlm.nih.gov/pmc/arti...491901/?page=1

(6) http://www.sciencedaily.com/releases...0507082157.htm

(7) http://www.ncbi.nlm.nih.gov/pubmed/12061862

(8) http://www.ncbi.nlm.nih.gov/pubmed/11864719

 

Now the last piece of the puzzle: what causes ADHD and how do we cure it? Up until this point, scientists had no idea. What they failed to realize is there is another identified disorder out there that has the same prevalence rate as ADHD as well as the same symptoms. Coincidence? I think not. Having talked to 8 of my friends with ADHD, I have identified a reoccurring set of symptoms in at least one of their parents. Snoring, excessive daytime fatigue and easy irritability. All of which are symptoms of sleep apnea. Furthermore, sleep apnea is a massively under diagnosed disorder that affects 5% of the population including infants and children. Sleep apnea can be caused by an abnormal structure of the airway passage or just by asthma. Either way, these 2 causes of congenital and are very commonly seen in families generation after generation. Unfortunately, they have never been linked to ADHD or Parkinson’s until now. That’s right, Ritalin is not the only option for treating ADHD. Sleep apnea can be treated by surgery or oxygen masks and either treatment has incredibly high success rates with a drastic reduction of symptoms observed within the first few months.

 

Sleep apnea can be easily identified by doctor’s, yet many people live with it unknowingly. Sleep apnea results in the sufferer receiving a lack of oxygen which results in impaired and unrestful sleep. More importantly, a lack of oxygen causes the death of neurons in the brain, which eventually leads to Parkinson’s Disease. If you identify with symptoms of ADHD or sleep apnea, go see your doctor immediately. With the proper treatment, the steady rate of neuronal death can be stopped and Parkinson’s Disease can be eliminated from our society. The power to stop ADHD and Parkinson’s Disease is in your hands!

__________________

Bachelor of Health Sciences 2014

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apache Newbie

apache

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you should read about qEEG and biofeedback... i was screened for sleep apnea, disruptions in normal sleep architecture cause massive changes in prefrontal regulation of and synchronization with other brain regions, add isn't a disorder of lack of attention, it's so heterogeneous, it can include distractibility, which can be highly influenced by the environment in which which you work, which qEEG can confirm... then again most psychiatrists are ridiculous, sleep apnea is one of the most important things to screen for when diagnosing add characteristics, which can be changed and modulated within 3-12 months, lol, no one reads the neurology literature though, there's no money in it when you can sell 200 dollar a month adderall xr.

 

you also way oversimplify lab condition from behavioural add seen in psychiatrists everyday... and we're stuck in the the days of reductionistic bispsychiatry with radioactively labeled glucose and dopaminergic precursors, as thomas kuhn said, what you find is a result of what you are looking for. No one reads research into whole brain functioning, we're all so focussed on reductionistic molecular explanations that we only find synaptic, metabolic, oxidative conclusions.

 

What about MAO-B inhibitors along with L-Dopa, or Memantine to prevent hyper-glutaminergic apoptosis.

 

I don't buy the ADHD, Parkinson's link, your drawing on straws.... but you could certainly be onto something with sleep apnea and ADHD and Parkinsons. You know what else amphetamines do... they increase cerebral blood flow, and oxygen and nutrient delivery, as well as induction of beta wave synchronization for increased cortical regulation of concentration, have you checked out Vinoceptine? PM me about this if you want, I read about this stuff everyday.

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