Parkinson's Disease: The Basics

first of all I just want to thank Laura Laura zeglen was the one who was just up here she is our education and outreach core coordinator for the Udall Center and without her none of this would be possible so thanks Laura I see some familiar faces in the audience thank you for coming back and for all of you who are new welcome the PD a new symposium that we do has been going on since 2009 so this is our 8th year usually I'm the one who is standing behind and and then introducing all of the speakers and not the one who's speaking or at least I haven't done so for the last few years or so a lower insisted that I had to speak this year because people want to listen to me is what she said if that's true I want to take you home with me to show my family that people actually do want to listen to me especially my two and a half year old he just doesn't really want to hear anything that I have to say so well anyway um every year for the PD a new lecture we always start with a what we call the Parkinson's disease one-on-one talk this is the basic talk it's an introduction and partly it's for those of you who are new who may be newly diagnosed who may not know a whole lot some of you veterans who have been through a lot of these you'll know a lot of the information so I'm sorry to repeat some of this I've tried to include a couple of different things this year so that you can be engaged and listen to it and and the thing that I've decided to do this year in my talk is to include five Parkinson's disease myths that I'm going to debunk for you so let's get started first of all what's Parkinson's disease it's a progressive neurodegenerative disorder that means is there are nerve cells in the brain that slowly die off over time was first described by dr. James Parkinson and is the second most common neurodegenerative disease the first one being Alzheimer's disease and it's estimated that if you take a population of people over the age of 60 about one in every 100 patients will have Parkinson's disease that's pretty common and so if you look at the census data that comes out to be about thirty-five thousand people in the state of Michigan with Parkinson's disease and about one to one and a half million people in the United States with Parkinson's a little bit of a history lesson here James Parkinson is an English family physician and who practiced in London naturally during the time that he practice he wasn't really all that well-known but he described the symptoms of Parkinson's disease actually very clearly in a pamphlet a book called the essay on the shaking palsy in 1817 so this year is the 200th anniversary of the SEM shaking palsy and he called it the shaking palsy but john martine Charcot who was actually a famous french neurologist was the one who decided to name this disorder after James Parkinson all right who gets Parkinson's disease do any of you know who these people are well let's see so upper left corner Michael J Fox below him Muhammad Ali blow him Johnny Cash upper right corner Kirk Gibson me and Janet Reno and then the bottom right may not know now it's actually Maurice white who's the founder of Earth Wind and Fire so all these people have had or have Parkinson's disease and gives you kind of a an idea it's a good range of people the mean age of diagnosis is in the seventh decade so between the ages of 60 and 70 and age is really the most common and most consistent risk factor for Parkinson's disease so as you get older you're much more likely yet Parkinson's there's slight male to female predominance some men are slightly more likely to get parking diseases on women or actually I should take that back it's when you take everyone with Parkinson's ease there's more slightly more men with it than women and there's a lot of studies out there looking at risks for Parkinson's disease and in terms of just demographic factors age gender race age is the only one that's very consistent and but there are some studies are showing that certain populations racial populations may have a lower risk and that's the African American population all right so here's the first myth I don't know if how many of you have thought this or think this but I saw someone actually a couple people in clinic this week who came in one I'd been following for at least a few years came with her son who basically says you know me and my brother don't believe that our mom has Parkinson's disease because she doesn't shake so I'm any of you think this heard this it's actually fairly common and that's not true it's actually up to about 20% of patients with Parkinson's disease do not have a tremor or shaking and so you don't have to have tremor in order to have Parkinson's disease so what are the main motor symptoms of Parkinson's disease a lot of the books that you will look at will name four cardinal symptoms is what they call it motor symptoms but they're basically four of them tremor is always one of them the second one is rigidity or stiffness of the limbs the rigidity itself people may not necessarily feel or experience early on in the course but it may be present on examination if you go to your physician or ologist they might kind of take your hand and move it around a little bit or leg and move it around a little bit that's testing for rigidity or stiffness a lot of people noticed that much more as the disease progresses when medications wear off then they may notice that they're much more stiff so that's one of the main symptoms slowness or absence of movement is probably the defining feature of Parkinson's and I'm gonna go into this in a little bit more detail on a couple more slides but this is called bradykinesia that's what we call it in the medical literature and then the final one is poor balance what we call postural instability and that's when I don't know some of your physicians or neurologists they'll test it by having you stand standing behind you giving a pull backwards on your shoulders and seeing how many steps it takes for you to regain your balance normal would be two steps or less abnormal would be if you fall down of course and hopefully that that's never happened but postural instability I don't necessarily consider it as as a cardinal symptom not because it doesn't happen but because when you're making the diagnosis early on in the course of Parkinson's disease this feature usually is not present it's not it doesn't seem to come on until a little bit later in the course of the disease so while it is something that happens to many people with Parkinson's disease a lot of times at the time of diagnosis it really shouldn't be present so I really talked mostly about the first three as Cardinal symptoms for that reason I'm just gonna take a couple slides and go into tremor and bradykinesia in just a little bit more detail the tremor itself occurs in only certain body parts so the hands the legs and the chin are probably the most common head and voice are actually rarely involved so if you see someone who has a head tremor it's probably not Parkinson's disease odds are it's more likely a different condition called a central tremor same thing with the voice and the tremor in Parkinson's disease is what's called a rest tremor and what we mean by that is when the limb that's involved by the arm or the leg is at rest supported by gravity so we usually test us with the hand resting or the arm resting on the arm of the chair or in the lap that's when the tremor seems to be most prominent and then when the limb is in use so if it's in the hand when the limb is being used to write or eat or do something else that's when the tremor lessens many times it goes away with action in the leg it would be presence sitting down and then going away when walking and so this rest tremor is is very characteristic of Parkinson's disease there are many patients who have a tremor that's kind of opposite where the tremor say in the hands is worse when using the hands and then gets better or goes away at rest that usually is more common with essential tremor a different condition but when tremor is very severe it can be present both at rest and with action so even though I'm telling you about these rules this is more a general phenomenon doesn't mean that you if you have it with action that you don't have Parkinson's disease it's it's just that in most cases it's more prominent at rest the other thing with tremor and at least symptoms of Parkinson's disease it's starts on one side and then tends to spread over the to the other side after a few years and the side that's affected later is usually continues to be much less affected throughout the course of the disease so there's this asymmetry where one side is much worse than the other and people always say yeah this my left sides always been my worst side you get that in the history very often the slowness of movement or the bradykinesia which is the the fancy term that that we used to make ourselves look smart is is really its slowness so on history when when we ask about it people will say or will ask whether or not takes you longer time to do things say in the morning to brush your teeth to get ready do you slow down in terms of your walking some people may say that's more weakness so my left side is is weaker and that's because the side is not moving quite as quickly or quite as in a coordinated fashion as it should be but when you test strength it's usually not a weakness not a muscle weakness it's just that it's not moving quite as well so in coordination sometimes is a term that's used to describe the brady kinesia on walking people might say that legs are dragging there's a loss in the swing of the arms of course the walking may be slowed and in addition to motor symptoms meaning problems with movements there can be slowness of other things as well so if there's gonna be slowness of thought sometimes there can be slowness of swallowing structures so that you have difficulty swallowing or choking there can be slowness of the bowels and so you can have constipation so there's slowness throughout the body and here's a list of other signs and symptoms usually related to a combination of the brady kinesia the slowness and the rigidity so a handwriting you may we may talk about what's called micrographia which is the handwriting starts out big and the more you write it gets smaller and smaller some people may have a more serious stoic expression on their face what we call a poker face but gait or the walking may be more shuffling so smaller steps smaller arm swing the posture may become a little bit more stooped where the head is a little bit more drooped shoulders are kind of slumped forward leg cramps are actually fairly common symptom where and then usually is most common at nighttime or early in the morning and that's probably some of the stiffness coming back when the medications are wearing off causing cramps and then other activities like standing from a low chair or a low car seat difficulty turning over in bed these are a lot of the things that people may experience alright the second myth Parkinson's disease only affects movement I had a patient last week who actually was having a lot of pain in the arm and the leg and the pain in the arm leg actually would occur when the medication would wear off so right before they're due for their next dose that's kind of when they would have it and it would actually go away with medication and they went to their family doctor first the family doctor said now that can't be Parkinson's disease doesn't cause pain it only causes problem with movements so I want to let you know that's not the case and I'm sure most of you realize this so there are what we call a lot of non-motor symptoms so on the top is kind of the tip of the iceberg that's the motor symptoms that we've been talking about that's what James Parkinson described it's what we've known about for 200 years but underneath there is this whole host of symptoms which we're now calling non-motor symptoms that have gotten a lot of attention over the past 20 years or so and these are symptoms that really are very common in patients with parkinson's disease and non-motor symptoms can be categorized into into three categories first is cognitive psychiatric on the left side and that encompasses some psychiatric problems like anxiety depression these mood disorders you can get dementia fatigue psychosis which manifests most commonly as hallucinations where are you and their visual hallucinations where you see things that other people may not see and it's sleep problems are very common over the next couple of slides I'm going to talk a little bit about dementia fatigue and sleep disorders in Parkinson's disease autonomic symptoms are the second category and today as you can see actually our program is a lot there are a lot of topics that are being covered in this category like sexual dysfunction and urinary difficulties you can also get sweats Disney a– is a term meaning shortness of breath that's usually much more common when people have dyskinesias these are extra and voluntary fidgety restless kind of type movements that can cause problems with with breeding suburi is is really where you get these kind of sweat glands that these oil expect plans that and tends to be on the face and then constipation which i mentioned a little bit earlier and then sensory deficits tingling sensations the pain that I mentioned in the example that I gave a little bit earlier there is olfactory problems olfaction is the sense of smell and that's almost decreased or gone in most patients with Parkinson's disease I have a slide on that and a little bit and then of course pain which is usually but not always connected to the stiffness or the rigidity how often are non-motor symptoms occurring there was this nice study here back in 2009 it was an Italian study so they called it pre amo which is Parkinson's disease and non-motor symptoms and really the upshot of the study was that virtually every patient with Parkinson's disease has some non-motor symptoms and the average patient had at least eight different non-motor symptoms most frequently these were mood problems so anxiety or depression and the frequency of these non-motor symptoms increases as the disease progresses so the longer you've had the more likely or to have some of these non-motor symptoms in addition non-motor symptoms are not only frequent but they can be very disabling as well so this is what's called the Sydney multicenter study and it started back in the mid 1980s it was basically a drug study looking at our comparing levodopa to bromocriptine if I remember correctly bromocriptine is a very old dopamine agonist that's no longer on the market and it was basically designed to just look at the effects of these drugs but they were able to get these subjects to follow up 15 years later and then 20 years later so you can see out of the hundred thirty six patient's enrolled 52 were available for 15 year follow-up 36 patients were available for 20 year follow-up and what was really interesting is that many of these patients had motor fluctuations actually almost all of them had motor fluctuations so motor fluctuations is a term that we use to describe wearing off in dyskinesias wearing off is the phenomenon where you take your medications your symptoms are fairly well controlled but before you're due for the next dose you have a recurrence of Parkinson's symptoms this can be a variety of things it could be tremor coming back it could be slowness gait difficulty stiffness of the limbs it could be pain could be anxiety or depression could be problems with thinking or memory when the medications are wearing off but then these symptoms go away or get better when you take your next dose of medications that's wearing off this can uses again are these extra fidgety restless kind of tight movements that usually occur at the peak of the levodopa dose and a lot of people kind of fluctuate between feeling good with dyskinesias and then the medication wearing off and feeling slow and stiff so all of these patients in the study at 15 and 20 years had a lot of motor fluctuations but that's actually not what they say were the disabling symptoms the disabling symptoms were some of these non-motor symptoms that's why I'm spending a fair amount of time on these non-motor symptoms so we're gonna talk about a few of these just a little bit more detail first one is dementia in Parkinson's disease and there is actually a very good talk on the web about cognitive impairment which is an impairment in thinking in memory and dementia if you want to go onto the web and look at it later dementia risk is increase with Parkinson's disease it's about two two to six times higher than the general population and risk factors so if you have Parkinson's disease risk factors are age which you can't really do anything about the severity of Parkinson's disease meaning as Parkinson's disease becomes more severe you're more likely to get it which is difficult to do something about also and there and then there are a bunch of risk factors that aren't as strong they are mentioned in some studies and maybe not in other studies so we're not clear how strong these risk factors are and that's the presence of hallucinations mostly visual seeing things that aren't there male gender and then depression now I just want to make sure just because something is a risk factor doesn't mean you're going to get it it just means it puts you at slightly higher risk but again the bottom three are not as strong as just age or the severity of Parkinson's how do we make a diagnosis so the diagnosis of Parkinson's disease dementia has to occur when you've had Parkinson's disease for a number of years so you have to have a diagnosis of Parkinson's disease first and then you start having problems with thinking processes or memory that really impact your ability to do the things that you want to do in daily life no and this could be being just shopping encounters at the grocery store with cashiers figuring out change dressing bathing driving all of these types of issues and so you have to have problems in two of these areas one is attention so you can have inattention where you're slower doing more errors executive dysfunction which is what we talked about excuse me when you have difficulty shifting from one task to the other the so called multitasking you patients with Parkinsons have difficulty with us actually most people have difficulty with this even if we don't think we do but if you're focusing on one task and then someone comes and interrupts you people with Parkinson's in general have a tendency to kind of forget what they were working on or not pay that much attention to the person that are interrupting them and so that may come out as as as forgetfulness or memory loss so example it'd be you know you're working at your computer your wife comes in says go take out the trash you're concentrating on and saying yeah yeah yeah whatever I'll take it out later and then later on it doesn't get taken out and then the your wife says you know why didn't you take it out I told you we said no you didn't and that's not a memory problem that's just an attention problem you weren't paying attention to her saying that visual spatial impairment which is a problem with you know judging spaces in between things that you know where you are in relationship to your environment where environment is in relationship to you and so problems with judging distances can manifest as driving problems potentially or if you are walking around with a walker or a cane you know bumping into things these types of problems and then of course memory loss and I just want to take a couple of minutes to discuss the difference between Parkinson's disease dementia and Lewy body dementia or dementia with Lewy bodies or Lewy body disorders which you may have heard about actually when you look at Lewy body disease or Lewy body disorders and Parkinson's disease dementia under a microscope during autopsy they actually look very similar clinically what happens is Parkinson's disease with dementia happens when you have Parkinson's disease first and then the dementia too develops a little bit later dementia with Lewy bodies or Lewy body dementia the dementia or this problems with thinking and memory happen either before the onset of the Parkinson's disease or around the same time or shortly thereafter and so it's really some people think that they're the pretty much the same thing it's just the timing of when you get a lot of the symptoms but I wanted to point out those terms just in case you've heard about it and are wondering moving on to fatigue fatigue is actually a very common symptom it probably occurs in about 40 or 50 percent of patients with Parkinson's disease and this is often described as a lack of energy feeling drained and the fatigue tends to be fairly extreme as well and it's different or differentiated from sleepiness so sometimes people can be sleepy and want to go take a nap and they'll say it's fatigue but this kind of fatigue is a little bit different it's just a feeling like you physically can't do anything because you don't have the energy now the patients who have fatigue it over half and consider it to be the most or at least one of the top three most disabling symptoms for that and more so than motor symptoms unfortunately we don't have really great treatments for fatigue fatigue is associated with depression and is associated with sleep problems so a lot of times we try and address that maybe try medication for depression try and help with the sleep and hoping that treating that the fatigue will become better and that works sometimes but not all the time and then exercise is something that's going to be really helpful for fatigue it doesn't seem like it because at the time you're feeling drained and don't want to do it but over I exercise is very helpful for fatigue because sleep disorders are connected to fatigue I thought I'd spend some time talking about this this is also very common if you see occurs in 49 to 81 percent of the patients so it's a majority of patients have some sort of sleep problem the most common is what we call sleep fragmentation which is you can fall asleep but you wake up multiple times at night and when you wake up then you're unable to fall asleep or have more difficulty falling asleep and this can be due to a number of different reasons for example frequent urination you got to get up and go three times a night four times a night on that disrupts your sleep many patients overnight is the time when they're not taking their medications quite as frequently or as often so a lot of the Parkinson's Parkinson's symptoms can come back like pain rigidity stiffness so this can cause problems with turning over in bed and getting comfortable in the bed and in some patients the tremor may come back and wake you up so these are problems that can actually impact the sleep what we do with frequent urination i I often send people to the urologist so there'll be someone talking about that later today I'm sorry about that when the symptoms of Parkinson's disease come back a lot of times we can do what's called a controlled release of cinema which is carbidopa levodopa explain that a little bit later but that kind of kicks in a little bit later and then and kicks in so that in the latter half of the night you have some medication on board some people might wait when they wake up take an extra dose overnight to help those kinds of symptoms so they can get comfortable and fall back asleep Rambis REM sleep behavior disorders probably the other very common sleep disorder in Parkinson's disease this is something where when you're sleeping and you're active dream phase you start acting out the dreams so talking and sleep screaming thank you yelling and then and then moving around in bed and normally during that dream state the brain sends signals to the body to kind of paralyze us you're not doing this in dream state and that ability some somehow is lost in Parkinson's disease and so when things are very severe you can injure yourself you can injure your bed partner you hear stories of people falling out of bed you know tackling the dresser because it's an intruder in the house and injuring themselves bedside lamps being on the floor when they wake up so this can be fairly you know it can range from just benign and just screaming to something where you can actually injure yourself the important thing about this that I want to point out is this is something that could happen before the onset of Parkinson's disease so it may happen many many years before you actually even get the motor symptoms of Parkinson's disease and it's actually estimated that most people with this condition even before you have Parkinson's will develop probably a Parkinson's like condition over time so that's something to be aware of and the treatment for this is there are two medications out there Clinton as a Pam which is klonopin it's a I think of it as a different version of xanax or ativan which are used for anxiety and that can help calm down these movements and melatonin and actually which is available over-the-counter can be an effective treatment as well or the static hypotension is another non-motor symptoms I just wanted to cover basically because it's very this is where you get lightheadedness or dizziness when you stand up suddenly from a sitting down or a lying down position and this is due to the fact that when you stand out blood pressure drops so not enough blood goes to the brain and it can lead to increased Falls when you're when you're dizzy for most people it lasts for a few seconds 30 seconds and then kind of goes away and then you can start walking and doing things and others lightheadedness can last for a fair amount of time the Parkinson's disease by itself causes it but the medications that you take for your Parkinson's disease can worsen it so it is something that to be aware of there are medications too to increase the blood pressure if needed there are other tactics to kind of help increase blood flow to the regulate when you stand up so when you're sitting down crossing your legs or crossing your legs when you stand up it kind of helps bring the blood back to the brain there are other things like support hose abdominal binders that people can use and if you're on blood pressure medications that drop is sometimes coming off or reducing that can help with this problem as well and then finally the the easiest thing I think is the easiest thing but it seems to be very difficult for many people is just drinking more water so a factory dysfunction I think this is the last was the last non-motor since i'm going to talk about this is where you have a decreased or a loss of the sense of smell the reason I point this out is because for the majority of people with Parkinson's disease this is something that is lost or is noticed before the onset of the motor symptoms and so pretty much everyone has this even if you don't perceive this when we do formal testing there is usually some loss of sense of smell and unfortunately it's not there's not a whole lot that we can do about it it doesn't seem to be related to the length of Parkinson's disease doesn't seem to be related to treatment but I pointed out because this is an area of research where people are trying to identify patients who might develop Parkinson's disease so that if we have medications that can slow down the progression we can potentially try them and people who are at higher higher risk of Parkinson's disease and that's someone with a loss of sense of smell and maybe someone with the REM behavior disorder all right Parkinson's disease myth I think this is the third one my doctor ruled out Parkinson's with an MRI and I see this a lot so people who come to me for the first time and to me they I think they have Parkinson's disease and they said well my other neurologists are actually my family doctor said it couldn't be because my MRI looks normal and the truth is is that for the majority of patients with parkinson's disease their MRI is normal or what we say normal for age so there may be some little things that you see with aging but it's not there's not something there that's causative of Parkinson's disease and really there is unfortunately I guess still at this time no definitive tests for Parkinson's disease other than autopsy but no one has really asked for it so we don't really use it there is one test though that I want to point out and this is something called a DAT scan some people have heard of it as a test for Parkinson's disease and that's not really accurate and so I just want to go over it what a Dan scan is it's a suspect scan what that means is you get injected with the radio labeled dye this dye travels to the brain and binds to the dopamine cells in the brain and so what you can see is in the middle there if you see under normal that's what a normal SPECT scan looks like so meaning if you have an abundance of dopamine cells in the brain you get a that looks like this very that's what we call a very robust uptake of the dye now if you have a loss of dopamine which is what you see in Parkinson's disease it looks kind of like the picture on the left where there's not as much uptake the problem is is does that mean you have Parkinson's disease and that's not necessarily the case because there are a couple of different other conditions that can cause loss of dopamine in the brain besides Parkinson's disease these are what we call the atypical Parkinson's syndromes they go by the names of multiple system atrophy progressive supranuclear palsy the dementia with Lewy bodies is another and then corticobasal degeneration so all this test can say is that you actually have loss of dopamine in the brain it doesn't make the diagnosis of Parkinson's disease some of the indications in which we might consider using it to be honest with you I don't use it all that often because for many people the examination you is it's pretty clear whether or not there is at least Parkinson's symptoms and you don't need this test to kind of tell you but in someone with a very severe tremor and you're not clear if it's a rest tremor or an action tremor it looks fairly similar this is a test that might allow you to say could it be essential tremor could it be more potentially Parkinson's disease sometimes there are people who come in on drugs that block dopamine receptors and when that happens they can develop the symptoms of Parkinson's and you're not quite sure or you stop the drug that caused it and they're not getting better sometimes you can get this test to see well if they're not getting better is it because there is a loss of dopamine cells in the brain and then the medication just kind of unmasked it and but if it looks normal that means there probably could be a good chance that's the person will recover some of the the symptoms so that's the dad skin so because there's no test how do we make the diagnosis of Parkinson's disease it's clinical meaning it's based on what you tell me and then your examination broadly speaking we want you to have at least two out of the three motor symptoms and these three motor symptoms are the tremor the rigidity and the brady kinesia which is the slowness of movement you really should have the slowness of movements in order to make this diagnosis and then usually we're not as sure of the diagnosis until you start medications and then when you start medications and there's a very good response to the medications that's when we're more confident of the diagnosis of Parkinson's disease why is it still difficult for many people to diagnose Parkinson's disease well if you think about it aside from there being no definitive test a lot of the symptoms of Parkinson's disease can overlap with a lot of things that happen as you age so a slowness that's I've told you that's one of the defining features of Parkinson's disease but people can slow down for various reasons as actually as you get older you do slow down as you get older you're more likely to get our arthritis and that can cause stiffness slowness difficulty walking all of these things are kind of the motor symptoms and tremor sometimes can be caused by nerves or at least that's what a lot of the family physicians will will kind of tell you that the tremors from nerves and let's just wait and see so early on when the symptoms aren't as pronounced people you know you might get confused not confused actually I shouldn't say but you might suspect that there are other common causes like the arthritis or nerves that might be responsible for it and it's not until symptoms get a little bit more severe that you're able to put it all together and say maybe this is more Parkinson's disease so those aren't results I think that if you have Parkinson's disease or if you have a suspicion of Parkinson's disease you go see a specialist and what do I mean by that I guess there are two types of specialists specifically one is a neurologist so neurologist is someone who has graduated medical school and then has completed a residency which is training in Neurology so neurology is the specialization of nervous system disorders of which Parkinson's disease is one and so there are a lot of neurologists out there general neurologists and they would know more about Parkinson's disease hopefully then your family doctor and then there's what's called the movement disorders neurologists so this is someone who's a neurologist meaning they graduated Medical School completed neurology residency and then has done an extra year or two just seeing patients with movement disorders of which Parkinson's disease comprises about 80% of all types of movement disorders in a movement disorders clinic so they're moving disorder specialists someone who has completed fellowship and movement disorders has probably seen more Parkinson's disease patients than a general neurologist so who should you see well being a movement disorders neurologist I'm gonna say that you're gonna want to see movement disorders from ologist it's like going to to a car salesman and asking if you should buy from him or someone else it you know that's just the natural bias but I do want to point out that that doesn't mean general neurologists are bad or poor they're very good general Rawls who know how to manage Parkinson's disease so whoever you have is is fine but I think I will I'd like to make a point that you should see at least a neurologist and not have your Parkinson's disease managed by your primary care physician and the reason for this is there is this paper in neurology neurology is the is basically one of the top clinical journals in our specialty and this was a study which looked at the Medicare database population and they separated patients who were actually who had seen a neurologist recently who had not and it sounds like they're Parkinson's disease was managed by the primary care physician and then looked and those who are managed by a neurologist had a reduced risk of being hospitalized for certain conditions so reduced risk of being hospitalized for hallucinations reduce risk of being hospitalized for a urinary tract infection and reduced risk of being hospitalized for fall and a traumatic fall so I think there's something that a neurologist is doing the guess is that neurologists are much more familiar with all the different medications for managing Parkinson's disease and also more familiar with some of the complications and the different symptoms like non-motor symptoms that can occur and that's why there is this reduction in hospitalizations related to Parkinson's disease we're gonna talk about treatment now and the first thing I'm like to say is that just because someone has diagnosed with you diagnosed you with Parkinson's disease or thinks that you might have Parkinson's disease does not mean that you need to start medications for it okay right now we don't have a medication that can slow down the progression of Parkinson's disease at least not one that is conclusively proven to do so so the decision to start treatment with medications is based on your symptoms and how those symptoms affect the quality of your life and if they don't seem to affect the quality of your life it is reasonable to not star medications because medications have side effects but if it does affect the quality of your life then it would be reasonable to maybe start a medication to see if you can make those symptoms a little bit better so that you can do the things that you want to do regardless of whether or not you decide to start medications there are a lot of non pharmacologic meaning non-medication therapies and treatments tell Parkinson's disease and first of all there is physical therapy occupational therapy speech therapy this can help your movements your ability to do your activities of daily living and your speech as well and the next talk is going to be on exercise in Parkinson's disease given by just some physical therapists and so I'm not going to delve too much into this but keep in mind that these are ways to help your mobility to better your activities or your ability to do activities and better your ability to communicate as well I always get asked whether there is some special diet some nutritional supplements something else that can help with my Parkinson's disease besides the drugs and unfortunately right now nothing has been shown to conclusively improve the symptoms of Parkinson's disease doesn't mean that they can't they just haven't necessarily been tried in the rigorous clinical trial format that we are used to for our medications something on exercise I firmly believe that everyone with Parkinson's disease should be exercising my recommendation is usually thirty minutes five times a week so a total of 150 minutes a week a moderate intensity what does that mean the way I see it it's usually exercise that's rigorous enough to cause you to be a little bit short of breath meaning that you you couldn't hold a normal conversation easily while exercising and something that increases your heart rate so and that's gonna be a different for different people depending on your condition so if you're not in very good shape just even walking once around the block may be a moderate intensity for you if you are a marathon runner just welcome them around the block is probably not going to be moderate intensity there are a number of different types of exercises that have actually been proven to improve symptoms of Parkinson's disease whether it's balance strength movements and includes biking boxing Tai Chi you name it it's it's probably out there the problem is is not one exercise modality has been compared to another one so we can't say that one is better than the other but the fact that so many different exercise options have been proven as shown have been shown to be effective for at least some aspect of Parkinson's disease it really makes me think that's just exercise in general more activity is better than nothing so I always say pick the activity that you like that you're gonna stick to and then go for it I mean it's no use to to go bicycling even though it's been proven to be helpful for Parkinson's disease it's no use to do it if if you actually can't and go out and do it right so if you know in Michigan sometimes it's harder to do that in the wintertime you know so if there's gonna be half the year that you can't do it maybe it's not the best one for you but if you're a bicycling fanatic and you will do it in the winter time or you have a stationary bike that you can do during the winter time then maybe that's a good thing for you talking about medications now and before I go into all the medications you're gonna see I've actually there's a slide on each of the different forms of medications some of them have pictures of what the pills look like I'm not actually necessarily going to talk about what pill is right for you what pill is right at which stage because really this is an individual decision it depends on what symptoms you have and it's a discussion that you should be having with your neurologist my goal here is to really just tell you all the different options out there so if you haven't been tried on it or if you've not familiar with it your physician has never brought it up to you it might be worthwhile to say hey you know I went to this talk that all these medications are out there could any of them be appropriate for me and they may not be depending on your situation but at least you should be aware of them all all of the medications are virtually all of them have to do with dopamine in some respects so what I'm showing here is this is a cut through the midbrain the midbrain kind of resides between your brain and the spinal cord and so if you cut through there that's the area where there's a structure called the substantia nigra and the substantia nigra is where there are a lot of dopamine producing cells and you can see on the stain the this section the substantia nigra stains dark and so you can see there's there dark lines in someone without Parkinson's disease in Parkinson's you can see that there's less staining so what that does is shows you that there's less dopamine producing cells in the brain and so all of the medications that we have are aimed at trying to replenish the dopamine or act on the dopamine system in some way to restore movement here's the the list of I think the current medications that we have for treating Parkinson's disease that are approved in the United States and so we'll go into into each of these in a little bit more detail first one is carbidopa levodopa this is known by the brand name of Sinemet it's combination of two medications levodopa is actually changed in the brain to dopamine so you're really kind of replacing dopamine itself carbidopa is a medication that prevents the breakdown of the levodopa in the stomach so if you just give levodopa most of it gets broken down in the stomach causes a lot of nausea and not enough gets into the brain so when you couple them together it doesn't get broken down more gets into the body it is the most effective medication for the motor symptoms of Parkinson's disease it's been around a long time it's available in generic form and it is it is very very effective which is why most people at some point will be on this medication it is interfered or at least protein interferes with the absorption of cinema so a lot of times you'll see advice on telling you to take it on an empty stomach and what that means is 30 minutes before a meal or 1 hour it's not necessary though to take it on an empty stomach a lot of people will take it with food and still get a good effect but there are people out there who will notice that when they take it with meals that particular dose doesn't seem to have enough effect or at least not as much effect as it when they take it on an empty stomach so only you will know but nausea is one of the most common side effects of cinema so if you do that taking it with meals actually cuts down or can cut down on the nausea so depending on your situation you might want to take it with meals you might want to take it on an empty stomach other side effects are lightheadedness sleepiness overtime it can contribute to the dyskinesias that I talked about earlier and then sometimes it can cause hallucinations or vivid dreams as well so that brings me to this number four which is the sentiment that levodopa I heard that levodopa will only work for about five years and then stop working so I want to save my levodopa my Sinemet for when I get really bad because then it'll only work for those five years and then and then so I want to save her for that and that this is a complete myth actually this is not true if you've heard it still out there for some reason and this it was kind of taken from there's this old study where from the Mayo Clinic where they were estimating how many people would have dyskinesias and wearing off by what time and the point of this study or the the main point was that about 50% of patients would have dyskinesias at around five years and that somehow we think led to this myth being perpetuated that it only works for five years and again that's not true what does happen with progression of Parkinson's disease what you can see here is there's a slide on the left is early disease and the curve is the level of liebe oppan in the body so you take it and there's this window therapeutic window it's a wide therapeutic window meaning you take it the levodopa level rises and then it kind of decreases and if you're in that green window things are good you're on symptoms are helped as Parkinson's disease progresses what you see is this that window kind of narrows so that advanced disease when the peak of the medication goes up when you're at the top that's when you're getting dyskinesias and then it kind of goes down and you have a good time and then it's wearing off much sooner than before and when you get these discs and users in this wearing off I think that's what the point of the article was that you can start getting this doesn't mean that the levodopa doesn't work or stops working it's just not working as well you still get a good effect it's just the effects the lasts for a shorter period of time so there are ways of trying to increase the effect of levodopa and that's what a lot of the additional medications out there are for levodopa comes in a lot of different formulations there's a standard or regular there's a controlled release formulation which personally I use only as a bedtime dose to kind of kick in a little bit later in the night so that there might be some on board later in the night and in the morning there's a newer medication called right tari which is an extended release capsule it actually is a capsule with beads of immediate release and then more extended release and the thought is that it lasts a little bit longer so you don't have that wearing off it unfortunately is not available in a generic formulation so my experience so far there have been a lot of people who have been unable to get it because they're pharmaceutical Benefits don't pay for it and then there is Parc Oppo which is actually a dissolvable form levodopa you put it on your tongue you swallow it it kicks in maybe a little bit sooner but it's good for people with maybe swallowing problems there's also another formulation of levodopa that just came out not too long ago at least in the United States it's been around in Europe for many years that's called the duopa intestinal gel it's basically carbidopa levodopa that's in a gel form it gets infused into the duodenum which is a portion of the intestine where levodopa gets absorbed so you have to get a what's called a GJ tube it's basically a feeding to that where the tip of that tube goes directly into the intestine you then have this cartridge free-standing cartridge that then infuses the gel into the intestine and because it's being continuously infused there's a smoother motor function throughout the day there's less off time and it's relatively safe in terms of the surgery itself but sometimes you know the the cartridge delivery depends on the tube going into the intestine sometimes potentially if you're active there can be issues with dislodging of the tube malfunctioning of the pump so those are the the potential side effects doesn't happen with everyone obviously but those are the things that you need to know about so dopamine agonists are another class of medications these are medications are really the way I explain it is it's there they actually look like dopamine chemically usually one of the groups has changed a little bit so it's not quite dopamine but it acts on the dopamine receptors in the brain and there are a lot of different formula different brands of dopamine agonists you might know them as repenter all which is Requip pramipexole which is mirror packs we're ticketing which is a patch formulation of a dopamine agonist it's also known as new Pro and then April morphine which you may not be as familiar with it's actually an injectable form of dopamine agnus the benefit of that is it kicks in really quickly within 5 minutes or 10 minutes but only lasts about our so it's good for people who might were off very suddenly and then be stuck and have no way of getting to you know their next dose of medication but if it's on you can inject yourself it can kick in much more quickly that way compared to levodopa on the motor symptoms these are more moderately effective and they're typically associated with more side effects so more nausea than leave it open more sleepiness even lower extremity swelling and then the impulse control disorders which if you don't know what they are there are disorders where you have an urge to do things that you can't control and this would be gambling some people have compulsive shopping or binge eating some people have what's called hobby ISM where they do whatever hobbies they want and they're not but or a hobby that they want and just do it obsessively and then it can cause psychosis in some patients so that's again hallucinations delusions comt inhibitors are something that are a medication that we use more for wearing off seoane comt is an enzyme in the brain that breaks down dopamine so if you inhibit it you're basically blocking the enzyme dopamine hangs around a little bit longer and so you get more effect from your cinema dosing calm tan or intact bone is the most common one there's also another one called tilt Capone or it's has more we don't really use it because of liver function problems and so again it helps wearing off and then there's a formulation called still Evo which you may have heard about some of you may be on it what still Evo is is a combination of cinnamon and ant a Capone or content just in one pill to make it easier there's also an Emmy Obie inhibitor this again is a another medication that prevents the breakdown of dopamine in the brain this is actually I'm sorry I didn't update the slide but they're actually three mao-b inhibitors on the market now saline Andrus athlean are the ones that are available in generic form there's a new one that was just approved by the FDA called Sadako xad heo and it's in my mind it's it's similar to these medications it's just because it's not available in generics and be available in brand name only so it's a little bit more expensive compared to levodopa these medications have a mild symptomatic effect and one of them were saddling there was one study of rescheduling where they thought where we thought that it might slow down the progression of Parkinson's disease it's a very controversial study so we are not necessarily recommending this as a possible medication to slow down the progression of Parkinson's disease all right going into the last part of my talk here the final PD myth surgical treatments such as deep brain stimulation should only be considered as a last resort that's no longer the case maybe about 10 years ago people would just hold off on it and wait until they're really bad but nowadays we're recommending a little bit earlier what is deep brain stimulation it's a surgical procedure where you have an electro that's placed specifically in a part of the brain connected by wires to a pacemaker in the chest when you turn on the stimulation it delivers electrical stimulation to the brain and we think it overrides abnormal brain activity and helps the symptoms of Parkinson's disease so if you have tremor it can make the tremor go away but what it's really good at is making the off time more like the on time so people who are good candidates are obviously if they have Parkinson's disease if you have the tremor that's interfering with the quality of life despite anything that your neurologist can do with medications you might be a good candidate and then the other person is someone who has these motor fluctuations so particular medications are good they wear off on they fluctuate throughout the day and we can't adjust the medications to make that smoother that's where you might be a good candidate there are limitations for this obviously it's a brain surgery so there are risks of bleeding and stroke it also only works on the symptoms that are helped by levodopa so when you take your medications and you feel good but you still have some symptoms maybe speech or something like that that's affected despite treatment with levodopa that's still gonna be present with the deep brain stimulation so speech is one example that deep brain stimulation doesn't help this gait instability postural instability that people develop is also not helped by deep brain stimulation and actually if you're interested in more information on deep brain stimulation dr. Emily Levin last year gave a dedicated talk to deep brain stimulation so you can look at that for a little bit more detailed information so these are kind of the the five myths first of all the main motor symptoms are tremor rigidity and slowness but tremor does not have to be present in order to diagnose Parkinson's disease Parkinson's disease is not just about movement there are a lot of different non-motor symptoms that I covered earlier today the diagnosis can be difficult so I my recommendation is to have it managed and diagnosed by a neurologist number four levodopa is the best medication that we have it works well for a long time there are other medications that can be helpful but most people at some point will be on levodopa and then i'll last you know when medications aren't perfect now they can't control everything and at some point deep brain stimulation could be considered and that's something that you should at least know about


  1. Be sure to read honest and real reviews of Parkinsons Disease Cure on my blog before you buy. Go to gohonestreviews. com/parkinsons-disease-cure-review/ Thanks, Stanley.

  2. Indeed natural herbal medicine are the best,  I was cured by madida herbal supplements of my Parkinson's disease. I am perfectly okay now… Email: [email protected] or visit: for more information and help.

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  5. Here goes,

    Posting this here because I know some of you do research and think I may have stumbled upon a very important insight concerning the etiologies of various neurodegenerative disorders and maybe degenerative disorders in general.

    I’ll cut to the chase and ask the question and then explain how I got to the hypothesis. It is: Is it possible that distinct neurodegenerative and musculoskeletal degenerative disorders are in fact be specific symptom complexes that correspond to dysfunction of specific substructures of the cervical ganglia which subsequently alter certain functionalities of the choroid plexus and have downstream effects on the basal ganglia and spine?

    A recent medical situation in my life prompted me to conduct some personal research to better understand my condition. As a result, I became familiarized with the dynamics of a specific system of structures in the body that, if better understood and regarded as a unified whole, could potentially shed a brighter light in the etiologies of degenerative disorders.

    Essentially, my research led to make connections between three structures in the neck and head: the cervical ganglia, the choroid plexus, and the basal ganglia.

    A few observations became key in developing this idea about cervical ganglia involvement in degenerative disease. The first had to do with the basal ganglia. Basal ganglia dysfunction can cause a dearth of dopamine in the brain and subsequent cluster headaches and Parkinsonism/movement disorder symptomatology. This structure controls voluntary movement in the body and so in the case of movement disorders, it is usually the culprit. The question then becomes what is the fundamental cause of this dysfunction?

    Thinking about a specific syndrome called Eagle’s Syndrome which often presents with symptomatology similar if not identical to that of neurodegenerative/movement disorder. Eagle’s Syndrome is an abnormal ossification and elongation of the styloid process at the base of the skull that interferes with the cervical ganglia and carotid arteries in the neck and creates symptoms.

    I wondered if superior cervical ganglia dysfunction could have downstream effects on the basal ganglia and cause disorder. So I began to attempt to understand the dynamic relationship between the cervical and basal ganglia.

    I began to look more closely at the cervical ganglia, in particular the superior cervical ganglia. This structure innervates the eye, parts of the face, the throat and sinuses, stimulates mucous production, has a part in regulating heartbeat (an aside: the disruption of the cervical ganglia when an Eagle’s Syndrome sufferer turns their head can result in panic symptoms: palpitations, dry mouth, gagging, so this could be a tool when thinking about mental heath physiopathologies as well), and also found that it is the only peripheral structure that sympathetically innervates areas of the head and brain. In particular, it innervates a structure in the brain called the choroid plexus. This was the next bridge on my way to the basal ganglia.

    The choroid plexus and found that it has a few very important functions: 1. To release transferrin that promotes iron homeostasis in the brain 2. Send agents to bind with antibodies to be flushed out of the system when infections are resolved and 3. Stimulate production of cerebrospinal fluid. That all struck me as fairly promising.

    I started with antibodies and found articles about post-infection movement disorders (specifically PANDAS, about which there is now literature about non-pediatric cases) where it is shown that sufferers have anti basal ganglia antibodies.

    It struck me that if a substructure of the cervical ganglia that innervates parts of the choroid plexus that promote production of antibody binding agents is dysfunctional, an infection could very well trigger an indefinite autoimmune response, attacking the basal ganglia and other systems. Some neurodegenerative and degenerative disorders like MS are thought to be autoimmune, and disruption of the cervical ganglia and subsequent introduction of infection could precipitate an indefinite autoimmune response. Symptom progression might depend on the nature of the ganglia dysfunction (if it is ongoing, say, due to injury and resulting occlusion, or intermittent, say, due to Eagle’s Syndrome, in which turning the head causes ganglia disruption), theoretically accounting for the different subtypes of MS.

    I also had the thought that if iron deregulation in the brain could be caused by dysfunction of a specific substructure of the cervical ganglia and subsequently the choroid plexus, maybe iron irregularities in the basal ganglia would be observed in sufferers of movement disorders, and sure enough, it’s observed in most, if not all of them. At this point I felt like I was really onto something.

    And then a thought occurred to me: what if the first domino to fall in the etiologic chain of ALL of these degenerative disorders begins in the cervical ganglia? This could be why there are peripheral nervous system symptoms that manifest early in diseases like MS (the cervical ganglia innervates the eye and throat and heart, so vision dysfunction, dysphasia, heart rhythm problems etc would be some of the first symptoms you’d expect to see in this etiologic formulation). I’d seen papers talk about a corticothalamic basal ganglia circuit, but not much of anything about the cervical ganglia or choroid plexus, and I thought, “maybe the cervical ganglia is part of that circuit, affecting it indirectly but very profoundly.”

    Not everyone who suffers from degenerative diseases would have Eagle’s Syndrome of course, but maybe there would be occlusion/tortuosity of the ECA or cervical ganglia, or maybe a trauma shifted their positions leaving the cervical ganglia susceptible to injury, or maybe genetic degenerative disorders’ gene expressions simply omit instructions for certain substructures of the cervical ganglia to form and subsequently instruct the choroid plexus.

    So the idea is, if there are three main tasks of the choroid plexus, then there are seven combinations of those tasks (1; 2; 3; 1+2; 2+3; 1+3; and 1+2+3), and there are two ways for each of those tasks to dysfunction (over-firing or under-firing, although I’m not exactly sure about this detail), then each combination of simultaneous or sole dysfunction of cervical ganglia substructures which correspond to areas of the choroid plexus that are involved with completion of one of these three tasks would represent a distinct symptomatology—i.e., a distinct degenerative disorder.

    Important to note is that for antibody binding dysfunction due to lack of transferrin to become part of a neurodegenerative symptom complex, it may require an initial infection of a certain type to kick-start an autoimmune response strong enough to manifest in this way. In my reading about PANDAS I came across mention of “molecular mimicry,” and I thought maybe it was possible in the case of infections that feature such molecules, and in patients that have cervical ganglia dysfunction, that since the infection that the immune system (now totally unchecked by transferrin-aided antibody binding) is targeting resembles healthy structures in the body that all of these factors compounded could lead to ongoing destruction of healthy body tissue.

    It may be the case that I’m off base, or there are ways to easily prove false all that I’ve said, but I don’t know that. That’s why I’m posting, because in the unlikely event that this is not totally crazy, and might actually be plausible, it will be in the hands of people who can do something with it. A theory is judged by its explanatory power, and to me, this one seems to explain a lot. Could it be the skeleton key that unlocks understanding of these diseases and leads to new treatments and potentially cures? Is it simply that the cervical ganglia needs to be attended to more intensively when these disorders manifest?

    According to the literature, somewhere between 80-95% of Eagle’s Syndrome patients who undergo styloidectomies have complete cessation of symptoms. If I am right about the cervical ganglia’s role in degenerative disorders, and some of these patients’ styloid process was in contact with their ECAs and cervical ganglia, the neurological symptomatologies that presented may well have progressed into full-blown neurodegenerative disorder if left unaddressed. It could very well be the case that these successful surgeries represent instances of the curing of previously thought to be incurable neurodegenerative conditions. But again, Eagle’s syndrome merely represents one mechanism of action that could cause cervical ganglia dysfunction.

    I’d appreciate any response, even if it’s to tell me why I’m off base. I hope you’ve read with an open mind, and were willing to ask yourself “what if?” So, the question is: is it possible that superior ganglia dysfunction is the primary etiological feature of a host of neurodegenerative disorders? That this could be a unifying theory?

  6. PD is for a great part mental. It is a brain disease, and the brain controls our movements as well as our thinking and feeling. This man only enumerates physical symptoms. However, it is AS IMPORTANT to talk about the changes in thinking, especially also the difficulty to initiate actions, to DO something. PD patients have great difficulty taking initiative, to just do things. It looks like they don't know or don't want to do something, but they just can't get started. So, many things remain undone, or happen only after the patient is pushed (by herself or other). For this same reason, it seems they do not care anymore about their environment and people. But when pushed a little, their empathy is still there. Etc. — Somehow this is a tabu area, doctors talk about tremor as if that is all.

  7. Great video thanks for your help. Speaking of help it would be helpful if you didn't use the word uh.

  8. 'Parkinson's disease' is a man-made lie. John Parkinson 1567-1650 of London was a chemist and author of some botanical works.

  9. I was diagnosed with Parkinson"s syndrome in may of last year. I had essential tremors since age 55. I have a stooped posture, right arm was not moving. I also have a pulsating feeling in my body. My legs tingle and they were cold.i was advised to give a try on Total cure herbal foundation herbal formula by my doctors which i truly did and the herbal treatment help me get rid Parkinson disease PD within the short period of 15 weeks usage,please do not hesitate to place an order from them at because the herbal products relief me automatically and terminated all the symptoms.

  10. Fàñtastic.explaination abòut Parkinson . It is really very use ful for the people suffering from p.D However the medicines mentioned needs to more information regarding composition as the name of the med icine in U. S may not be the same in other countries particularly in India where i am residing. Overall it is a nice and a valuable information.
    Thanks and regards
    Biswanath Bha ttacharjee

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