Tag Archives: Science

A Good Life With Parkinson’s

“I choose to make the rest of my life the best of my life.” Louise Hay

“Avoiding problems you need to face is avoiding the life you need to live.” Paulo Coelho

Try to live following the advice of the opening quotes: Today renews your lease on the rest of your life, enjoy it (get up, get out, get going). Today acknowledge your Parkinson’s; give it a nudge, because you are ready for the battle and for life.


Live a better and healthier life by following this circle of words [yes, they all begin with the letter ‘F’ (click here to download the schematic above)]:
Exercise as much as your body can take, then do some more. Getting/staying fit really matters in your battle with Parkinson’s.

Stay strong in your effort with your adversity.

Food- Feed your brain properly, fuel your body well; it will make a difference.

Flexible (two definitions)-
Stay flexible by frequent (I mean really often) stretching; you’ve got a life-altering disorder, stay flexible and let your life follow what happens because it’ll be okay.

Fulltime– It takes time and effort to manage your life. You can find the time because managing your life well from this minute on will matter later in your life;

Faith (multiple definitions)– Believe in your ability to successfully navigate your life; trust in your loved ones to support your journey; believe that a higher entity truly loves you and acknowledges your strength and passion for life.

Forty-winks and sleep some more- The brain is like a sponge that fills up all day with fluid; sleep allows the brain to drain, to renew, to fire-up strong upon waking; sleep is a very good thing.

A Good Life With Parkinson’s: Our Common Bond and Hope
I feel your stiffness; I know it well.

I sense your troubled thoughts; my mind also has questions.
I notice your tremor; mine can act up too.
I perceive your frustation; life with Parkinson’s can be problematic.
I see your shuffle; my right leg drags when I’m tired.
I admire your strength; I’ve got it too.
I acknowledge your life-accomplishments; we are still the same person as before Parkinson’s.
I see your honor; our work our living makes a difference.
I see your smile; those around us still care for us, no matter what.
I feel your effort; like you, I’ll never give up.

“Life is an opportunity, benefit from it. Life is beauty, admire it. Life is a dream, realize it. Life is a challenge, meet it. Life is a duty, complete it. Life is a game, play it. Life is a promise, fulfill it. Life is sorrow, overcome it. Life is a song, sing it. Life is a struggle, accept it. Life is a tragedy, confront it. Life is an adventure, dare it. Life is luck, make it. Life is too precious, do not destroy it. Life is life, fight for it.” Mother Teresa

Cover photo credit: http://ognature.com/path-snow-winter-mist-sunset-sun-trees-wallpaper-iphone-6/


Dopamine Agonist Withdrawal Syndrome (DAWS) in Parkinson’s

“Some remedies are worse than the disease.” Publilius Syrus

“Each patient carries his own doctor inside him.” Norman Cousins

Summary: Dopamine agonists are widely used in the treatment of Parkinson’s, especially as a first-line therapy. Some patients on a dopamine agonist experience side-effects that require either tapering or discontinuation of the drug.  First described in 2010, dopamine agonist withdrawal syndrome (DAWS) is a complication of ~20% of Parkinson’s patients who are either lowering or stopping the dopamine agonist.  DAWS presents as a cluster of physical and behavioral symptoms [e.g., agitation, depression, drug craving, and panic attacks (to give a few possible symptoms)]. There is no known standard-of-care in dealing with DAWS in Parkinson’s. Presented here is a brief overview of DAWS in Parkinson’s including dopamine agonists, clinical description, risk factors and prevalence, mechanism of action, treatment/management, and key publications.

“To heal illness, begin by restoring balance.” Caroline Myss

Dopamine agonists (DA): Dopamine agonists are ‘mimics’ of dopamine that pass through the blood brain barrier to interact with target dopamine receptors. Symptomatic treatment of Parkinson’s remains dopamine replacement, including the DA’s.  Dopamine agonists are frequently the first line of choice for therapy for the just diagnosed Parkinson’s patient. Dopamine agonists do help control motor symptoms in Parkinson’s although there can be significant side-effects (see Table below). Also below is a Table describing DA’s. The DA side effects can become intolerable for some people-with-Parkinson’s, and the decision to taper or withdraw the DA is made. Or maybe you’re a candidate for deep-brain stimulation (DBS) surgery and to calibrate the device you’ll be asked to stop your Parkinson’s medication for a short period of time.



“I enjoy convalescence. It is the part that makes the illness worth while.” George Bernard Shaw

First report of dopamine agonist withdrawal syndrome (DAWS): Dopamine agonist withdrawal syndrome (DAWS) was first described in 2010 by Rabinak and Nirenberg on five of their patients with non-motor impulse control behavioral disorders (ICD) caused by the DA; thus, they were tapered. Two patients were further described in this publication. The first patient was a 67-year-old woman with a six year history of Parkinson’s, and she had been taking various drugs including a DA. She had developed a difficult ICD, and they elected to taper the DA; unexpectedly, she then had severe anxiety and dysphoria. They tried an increase in carbidopa/levodopa and they used other therapy for cognitive behavior control; to no benefit to the patient. They changed her back to the original DA dose and she had a rapid and dramatic improvement in all of her symptoms. This patient continues to use the DA and remains with the difficult ICD.

Patient #2 was a 61-year-old woman with a six-year history of Parkinson’s and likewise an ICD prompted by the DA; she began a DA tapering with increased carbidopa/levodopa medication.  During the DA taper, she developed depression and severe anxiety and became agitated; she also had fatigue and insomnia.  As with Patient #1, adding back the DA improved all of her non-motor symptoms. It took several years for her to successfully reduce her DA doseage. The figure below visually highlights some of the key symptoms of DAWS.


What both cases shared were prominent psychiatric symptoms, poor response to both additional carbidopa/levodopa (to take the place of the DA) and psychiatric medication; however, both had rapid improvement in their ‘new symptoms’ when placed back on the DA. The majority of DAWS symptoms are presented in the the Table below.Document5“The secret of learning to be sick is this: Illness doesn’t make you less of what you were. You are still you.” Tony Snow

Risk-factors and prevalence of DAWS: Since the original study in 2010, there have been several follow-up studies on DAWS. Some of the studies speculated that a large DA dose in the presence of pre-existing ICD are the most important risk factors for DAWS. The ‘number’ talked about frequently is something called the ‘levodopa equivalent daily dose’ (LEDD) of the dopamine agonist, where it has been suggested that >150 mg was linked to an increased risk of DAWS. Use this on-line program to calculate your LEDD (click here).  Here is an LEDD example: someone taking 14 mg ropinirole/day (with the online algorithm), the LEDD would be 280 mg daily.  What? OK, so what did you say?  This means if you wanted to replace the 14 mg/day ropinirole with carbidopa/levodopa you would need about 300 mg per day of levodopa based on this calculation.  I refer you to do the papers cited at the end of the blog post for more details about LEDD. What is interesting is several of the studies have compared the taper versus total withdrawal of the DA; it does not seem to alter the risk of DAWS.  Good news is if you’re not having any detrimental side effects from the DA, just continue on and you’re good to go. The bad news is if you are having some side effects and you want to try and eliminate them by tapering down need to carefully consult with your neurologist and work up a feasible plan.  Please remember I’m a biochemist, not a physician, and I just am interpreting data from publications.

The prevalence of DAWS has been reported to be between 15 and 19% in patients with Parkinson’s; it seems to be consistently about one-in-five.  As mentioned previously, there appears to be no difference in relative risk of DAWS comparing patients that discontinue DA completely or those that reduce the DA by taper. Based on the percentage mentioned above, this says ~4 out of 5 people-with-Parkinson’s can DA taper without any problems.

“It is in moments of illness that we are compelled to recognize that we live not alone but chained to a creature of a different kingdom, whole worlds apart, who has no knowledge of us and by whom it is impossible to make ourselves understood: our body.” Marcel Proust

DA mechanism of action to cause DAWS:  To recap, DAWS occurs in a subset of patients with Parkinson’s that have had difficulties managing the side effects of a DA, and the decision has been made to remove that DA from the patient’s regimen.  The simplest notion is that you would then replace the DA with an increased dose of carbidopa/levodopa (using the LEDD); however, this is Parkinson’s and this is the brain and it’s just not going to be that easy. The diagram below summarizes a very simplistic view of dopamine and DA’s in their interactions with motor and reward pathways.  There is no doubt that in treating Parkinson’s, the replacement of dopamine is crucial for many different physiological functions in the human body. Dopamine agonists and dopamine share similar binding properties to dopamine receptors. They are very important in improving motor symptoms (through the nigrostriatal pathway) but there is also some potential detrimental crossover to the reward center (through the mesocorticolimbic pathway).  It is this minor pathway that is linked to the increased risk of ICD in some patients being treated with a DA. It is not clear, however from the data published so far that there is a difference in this 20% of the patient population in their mesocorticolimbic circuitry system with the DA in comparison to the other 80% of the population.  In summary, what causes DAWS during DA tapering is not well understood.18.01.07.Dopamine_Motor_Reward“Medicine is intention. Those who are proficient at using intention are good doctors.” Sun Simiao

Treatment/management of DAWS during DA taper:  DAWS is a relatively recent phenomena related to DA withdrawal.  Patients with (i) a predisposition to ICD and (ii) a larger dose of DA are apparently at increased risk of developing DAWS. There is no well-delineated treatment plan that the neurologist can follow; best recommendation (from the papers cited below) is the patient should be tapered at a very slow dose reduction over a long period of time, and see what happens. Clearly, it is crucial that the patient and the neurologist carefully evaluate signs of ICD and DAWS at every visit, especially for patients at high risk.

“The treatments themselves do not ‘cure’ the condition, they simply restore the body’s self-healing ability.” Leon Chaitow

 Summary: As someone with Parkinson’s, I’ve done a lot of reading about treatment strategies (what’s good and what’s not so good). For someone my age there would almost always be a recommendation to begin the DA (the so-called sparing one of levodopa until it’s absolutely needed) and then as symptoms progressed, you would switch over and combine the DA with carbodipa/levodopa.  Had I read the opinions of Dr. Ahlskog in the beginning, I might have opted to start with carbidopa/levodopa without the DA (Ahlskog JE. Cheaper, Simpler, and Better: Tips for Treating Seniors With Parkinson Disease. Mayo Clinic Proceedings. 2011;86(12):1211-6. doi: https://doi.org/10.4065/mcp.2011.0443). Biochemically, DAWS is an interesting problem but there needs to be additional studies to delineate the mechanism of action. Finally  DAWS clinically is worrisome and definitely not well-understood; and likely, the scope of DAWS is under-recognized.

Key References:

  1. Rabinak CA, Nirenberg MJ. Dopamine agonist withdrawal syndrome in Parkinson disease. Arch Neurol. 2010;67(1):58-63. doi: 10.1001/archneurol.2009.294. PubMed PMID: 20065130.
  2. Nirenberg MJ. Dopamine agonist withdrawal syndrome and non-motor symptoms after Parkinson’s disease surgery. Brain. 2010;133(11):e155; author reply e6. doi: 10.1093/brain/awq165. PubMed PMID: 20659959.
  3. Cunnington AL, White L, Hood K. Identification of possible risk factors for the development of dopamine agonist withdrawal syndrome in Parkinson’s disease. Parkinsonism Relat Disord. 2012;18(9):1051-2. doi: 10.1016/j.parkreldis.2012.05.012. PubMed PMID: 22677468.
  4. Pondal M, Marras C, Miyasaki J, Moro E, Armstrong MJ, Strafella AP, Shah BB, Fox S, Prashanth LK, Phielipp N, Lang AE. Clinical features of dopamine agonist withdrawal syndrome in a movement disorders clinic. J Neurol Neurosurg Psychiatry. 2013;84(2):130-5. doi: 10.1136/jnnp-2012-302684. PubMed PMID: 22933817.
  5. Edwards MJ. Dopamine agonist withdrawal syndrome (DAWS): perils of flicking the dopamine ‘switch’. J Neurol Neurosurg Psychiatry. 2013;84(2):120. doi: 10.1136/jnnp-2012-303570. PubMed PMID: 22993451.
  6. Nirenberg MJ. Dopamine agonist withdrawal syndrome: implications for patient care. Drugs Aging. 2013;30(8):587-92. doi: 10.1007/s40266-013-0090-z. PubMed PMID: 23686524.1.
  7. Nirenberg MJ. Dopamine agonist withdrawal syndrome: implications for patient care. Drugs Aging. 2013;30(8):587-92. doi: 10.1007/s40266-013-0090-z. PubMed PMID: 23686524.
  8. Solla P, Fasano A, Cannas A, Mulas CS, Marrosu MG, Lang AE, Marrosu F. Dopamine agonist withdrawal syndrome (DAWS) symptoms in Parkinson’s disease patients treated with levodopa-carbidopa intestinal gel infusion. Parkinsonism Relat Disord. 2015;21(8):968-71. doi: 10.1016/j.parkreldis.2015.05.018. PubMed PMID: 26071817.
  9. Huynh NT, Sid-Otmane L, Panisset M, Huot P. A Man With Persistent Dopamine Agonist Withdrawal Syndrome After 7 Years Being Off Dopamine Agonists. Can J Neurol Sci. 2016;43(6):859-60. doi: 10.1017/cjn.2015.389. PubMed PMID: 26842385.
  10. Patel S, Garcia X, Mohammad ME, Yu XX, Vlastaris K, O’Donnell K, Sutton K, Fernandez HH. Dopamine agonist withdrawal syndrome (DAWS) in a tertiary Parkinson disease treatment center. J Neurol Sci. 2017;379:308-11. doi: 10.1016/j.jns.2017.06.022. PubMed PMID: 28716269.
  11. Yu XX, Fernandez HH. Dopamine agonist withdrawal syndrome: A comprehensive review. J Neurol Sci. 2017;374:53-5. doi: 10.1016/j.jns.2016.12.070. PubMed PMID: 28104232.
  12. Solla P, Fasano A, Cannas A, Marrosu F. Dopamine agonist withdrawal syndrome in Parkinson’s disease. J Neurol Sci. 2017;382:47-8. doi: 10.1016/j.jns.2017.08.3263. PubMed PMID: 29111017.

“Life always gives us exactly the teacher we need at every moment. This includes every mosquito, every misfortune, every red light, every traffic jam, every obnoxious supervisor (or employee), every illness, every loss, every moment of joy or depression, every addiction, every piece of garbage, every breath. Every moment is the guru.” Joko Beck

Cover photo credit: f.fwallpapers.com/images/sun-peeking-through-snow-covered-trees.jpg

Agitation- img.aws.livestrongcdn.com/ls-article-image-400/cme/cme_public_images/www_livestrong_com/photos.demandstudios.com/49/85/fotolia_4199215_XS.jpg
Depression- http://www.scientificamerican.com/sciam/cache/file/FCD288AE-5C2E-49F2-85858FA255A8034B_source.jpg
Fatigued- www.belmarrahealth.com/wp-content/uploads/2017/03/fatigue-in-the-elderly-300×200.jpg
Panic attack- lifetimewoman.com/wp-content/uploads/2016/09/panica-1.jpg

Complementary and Alternative Medicine (CAM) and Over-the-Counter Therapies in Parkinson’s

With Parkinson’s, exercise is better than taking a bottle of pills. If you don’t do anything you’ll just stagnate.” Brian Lambert

“With Parkinson’s you have two choices: You can let it control you, or you can control it. And I’ve chosen to control it.” US Senator Isakson

Introduction: Having one of the numerous neurodegenerative disorders can be disheartening, difficult and life-threatening/ending; however, Parkinson’s remains in the forefront of treatment schemes and therapeutic options.  We may have a slowly evolving disorder, yet I remain firmly entrenched both in striking back to try-to-slow its progression and in remaining hopeful that new advances are on the horizon to throttle-back its progression.  Recently, several people have asked for an update on my strategy for treating Parkinson’s.  My plan consists of (i) traditional Parkinson’s medication,  (ii) supplemented by a complementary and alternative medicine (CAM) approach, and (iii) fueled by exercise. My philosophy is simple because I truly believe there are steps I can follow to remain as healthy as possible, which include having a positive mindset to support this effort, and to accept the axiom of the harder I try the better I’ll be.

“Life is to be lived even if we are not healthy.” David Blatt

Complementary and Alternative Medicine (CAM):The National Institutes of Health defines CAM as follows: “Complementary and alternative medicine (CAM) is the term for medical products and practices that are not part of standard medical care. ‘Complementary medicine’ refers to treatments that are used with standard treatment. ‘Alternative medicine’ refers to treatments that are used instead of standard treatment.”  Here is a nice overview of CAM (click here). The National Center for CAM (click here for NCCAM) gives five categories to broadly describe CAM (see below, and followed by some representative components for each of the 5 categories):


(1) Alternative medical systems include treatment by traditional Chinese medicine, Ayurveda and naturopathic medicine;
(2) Mind-body interventions like mindfulness meditation;
(3) Biologically-based therapies include over-the-counter natural products and herbal therapies;
(4) Manipulative and body-based methods describe chiropractic and massage therapies;
(5) Energy therapies include techniques such as Reiki and therapeutic touch.

“My way of dealing with Parkinson’s is to keep myself busy and ensure my mind is always occupied.” David Riley

CAM and Parkinson’s: Published CAM clinical trial studies have yielded only a sliver of positive response to slowing the progression of Parkinson’s, several were halted due to no change compared to the placebo-control group. Regardless of these ‘failed’ studies, many have embraced a CAM-based approach to managing their disorder, including me. Please remember that I’m not a clinician, and I’m not trying to convince you to adopt my strategy.  I am a biochemist trained in Hematology but I do read and ponder a lot, especially about Parkinson’s.  We know a lot about Parkinson’s and we’re learning a lot about the molecular details to how it promotes the disease.  There is not a cure although we have a growing array of drugs for therapeutic intervention.  Without a  cure, we look at the causes of Parkinson’s (see schematic below), we consider various CAM options, and we go from there (see schematic below). If you venture into adding to your portfolio of therapy, it is imperative you consult with your Neurologist/family medicine physician beforehand.  Your combined new knowledge with their experience can team-up to make an informed decision about your herb, over-the-counter compound use and its potential benefit/risk ratio.

17.12.31.PD_Cause.CAM“I discovered that I was part of a Parkinson’s community with similar experiences and similar questions that I’d been dealing with alone.”Michael J. Fox

A strategy for treating Parkinson’s: The treatment plan I follow uses traditional medical therapy, CAM (several mind-body/manual practices and numerous natural products) and the glue that ties it all together is exercise.  Presented here is an overview of my medical therapy and CAM natural products. I only list the exercises I am using, not describe or defend them.  Due to my own personal preference for the length of a blog post, I will return to them later this year and include an update of the mind-body/manual practices that I’m currently using. Please note that these views and opinions expressed here are my own. Content presented here is not meant as medical advice. Definitely consult with your physician before taking any type of supplements.   The schematic below gives a ‘big-picture’ view of my treatment strategy.

18.01.01.Daily_Take. brain.druge.CAM.Exercise

To some, my treatment plan may seem relatively conservative. It has been developed through conversations with my Neurologist and Internist.  This was followed by studying the medical literature on what has worked in Parkinson’s treatment, the list of compounds to consider was defined/refined (actually, my choice of OTC compounds has been trimmed from several years ago).  My CAM drug/vitamin/natural products strategy for treating Parkinson’s goes as follows: a) compounds (reportedly) able to penetrate the blood brain barrier; b) compounds (possibly) able to slow progression of the disorder; c) compounds that either are anti-oxidative or are anti-inflammatory; d) compounds that don’t adversely alter existing dopamine synthesis/activity; e) compounds that support overall body well-being; and f) compounds that support specific brain/nervous system health/nutrition. [Please consult with your physician before taking any type of supplements.] The Table below presents a detailed overview of my strategy for treating Parkinson’s.

18.01.01.DailyTherapy4Note of caution: Most herbs and supplements have not been rigorously studied as safe and effective treatments for PD. The U.S. Food and Drug Administration (FDA) does not strictly regulate herbs and supplements; therefore, there is no guarantee of safety, strength or purity of supplements.

On a daily basis, I use a combination of Carbidopa/Levodopa (25 mg/100 mg tablet x 4 daily, every 5 h on an empty stomach if possible, typically 6AM, 11AM, 4PM, 9PM) and a dopamine agonist Requip XL [Ropinirole 6 mg total (3 x 2 mg tablets) x 3 daily, every 6 h, typically 6AM, noon, 6PM).  This treatment strategy and amount combining Carbidopa/Levodopa and Ropinirole has been in place for the past 18 months (NOTE: I stopped using the additional dopamine agonist Neupro transdermal patch Rotigotine). For an overview on Carbidopa/Levodopa, I highly recommend the following 2 papers:
[1.] Ahlskog JE. Cheaper, Simpler, and Better: Tips for Treating Seniors With Parkinson Disease. Mayo Clinic Proceedings. 2011;86(12):1211-6. doi: https://doi.org/10.4065/mcp.2011.0443.
[2.] 1. Espay AJ, Lang AE. Common Myths in the Use of Levodopa in Parkinson Disease: When Clinical Trials Misinform Clinical Practice. JAMA Neurol. 2017. doi: 10.1001/jamaneurol.2017.0348. PubMed PMID: 28459962.

An FDA-approved calcium-channel blocker (CCB) named Isradipine penetrates the blood brain barrier to block calcium channels and potentially preserve dopamine-making cells. Isradipine may slow the progression of Parkinson’s. The primary use of Isradipine is in hypertension; thus, to treat my pre-hypertension I switched from the diuretic Hydrochlorothiazide to the CCB Isradipine.  A CCB is a more potent drug than a diuretic; importantly, my blood pressure is quite normal now and maybe I’m slowing the progression of my Parkinson’s. Please see this blog post for a review of Isradipine (click here). [Please consult with your physician before taking any type of new medication.

N-Acetyl-Cysteine (NAC; 600 mg x 3 daily) is a precursor to glutathione, a powerful anti-oxidant. In several studies, NAC has been shown to be neuroprotective in Parkinson’s (click here).  I have recently posted an overview of NAC (click here). Furthermore, the ‘Science of Parkinson’s disease’ has presented their usual outstanding quality in a blog post on NAC in PD (click here);
trans-Resveratrol (200 mg daily) is an antioxidant that crosses the blood-brain barrier, which could reduce both free-radical damage and inflammation in Parkinson’s. If you decide to purchase this compound, the biologically-active form is trans-Resveratrol. The ‘Science of Parkinson’s disease’ has an excellent blog post on Resveratrol in PD (click here);
Grape Seed (100 mg polyphenols, daily) is an antioxidant that crosses the blood-brain barrier, which could reduce both free-radical damage and inflammation in Parkinson’s;
Milk Thistle (Silybum Marianum, 300 mg daily) and its active substance Silymarin protects the liver.  Dr. Jay Lombard in his book, The Brain Wellness Plan, recommends people with PD who take anti-Parkinson’s drugs (metabolized through the liver) to add 300 mg of Silymarin (standardized milk thistle extract) to their daily medication regime.
Melatonin (3 mg 1 hr before sleep) Melatonin is a hormone that promotes sustained sleep. Melatonin is also thought to be neuroprotective (click here);
Probiotic Complex with Acidophilus is a source of ‘friendly’ bacteria to contribute to a healthy GI tract.
Vitamin (daily multiple)
A high-potency multivitamin with minerals to meet requirements of essential nutrients, see label for content [I only take 1 serving instead  of the suggested 2 gummies due to my concern about taking a large amount of Vitamin B6 as described in a recent blog (click here)]:
IMG_2059 copyVitamin D3 (5000 IU 3 times/week) is important for building strong bones. Now we also know that vitamin D3 is almost like ‘brain candy’ because it stimulates hundreds of brain genes, some of which are anti-inflammatory and some support nerve health (click here). Supplementation with vitamin D3 (1200 IU/day) for a year slowed the progression of a certain type of Parkinson’s (click here). Furthermore, augmentation with vitamin D3 was recently shown to slow cognitive issues in Parkinson’s (click here).

NO LONGER TAKE Coenzyme Q10 (CoQ10), Creatine and Vitamin E because they did not delay the progression of Parkinson’s or they were harmful.
NO LONGER TAKE a high potency Vitamin B Complex (see label below) due to my concern that a large excess vitamin B6 could be detrimental to Carbidopa/Levodopa (click here for blog post):
Screen Shot 2018-01-02 at 11.39.56 PM
List of several recent PubMed peer-reviewed CAM reviews (includes a more comprehensive overview of all areas of CAM in treating Parkinson’s):
Bega D, Zadikoff C. Complementary & alternative management of Parkinson’s disease: an evidence-based review of eastern influenced practices. J Mov Disord. 2014;7(2):57-66. doi: 10.14802/jmd.14009. PubMed PMID: 25360229; PMCID: PMC4213533.

Bega D, Gonzalez-Latapi P, Zadikoff C, Simuni T. A Review of the Clinical Evidence for Complementary and Alternative Therapies in Parkinson’s Disease. Current Treatment Options in Neurology. 2014;16(10):314. doi: 10.1007/s11940-014-0314-5.

Ghaffari BD, Kluger B. Mechanisms for alternative treatments in Parkinson’s disease: acupuncture, tai chi, and other treatments. Curr Neurol Neurosci Rep. 2014;14(6):451. doi: 10.1007/s11910-014-0451-y. PubMed PMID: 24760476.

Kim HJ, Jeon B, Chung SJ. Professional ethics in complementary and alternative medicines in management of Parkinson’s disease. J Parkinsons Dis. 2016;6(4):675-83. doi: 10.3233/JPD-160890. PubMed PMID: 27589539; PMCID: PMC5088405.

Kim TH, Cho KH, Jung WS, Lee MS. Herbal medicines for Parkinson’s disease: a systematic review of randomized controlled trials. PLoS One. 2012;7(5):e35695. doi: 10.1371/journal.pone.0035695. PubMed PMID: 22615738; PMCID: PMC3352906.

Wang Y, Xie CL, Wang WW, Lu L, Fu DL, Wang XT, Zheng GQ. Epidemiology of complementary and alternative medicine use in patients with Parkinson’s disease. J Clin Neurosci. 2013;20(8):1062-7. doi: 10.1016/j.jocn.2012.10.022. PubMed PMID: 23815871. 

Today we take control over our Parkinson’s:
Please stay focused on dealing with your disorder.
Please learn as much as you can about Parkinson’s.
Please work with your neurologist to devise your own treatment strategy.
Please stretch and exercise on a daily basis, it will make a difference.
Please be involved in your own disorder; it matters that you are proactive for you.
Please stay positive and focused as you deal with this slowly evolving disease.
Please stay hopeful you can mount a challenge to slow the progression.
Please remain persistent; every morning your battle renews and you must be prepared.


In the midst of winter, I found there was, within me, an invincible summer.  And that makes me happy. For it says that no matter how hard the world pushes against me, within me, there’s something stronger – something better, pushing right back.” Albert Camus

Cover photo credit: news.nowmedia.co.za/medialibrary/Article/109153/Wine-grape-crop-6-7-down-in-2016-800×400.jpg


The Yack on NAC (N-Acetyl-Cysteine) and Parkinson’s

“Once you choose hope, anything’s possible.” Christopher Reeve

“Hope is like a road in the country; there was never a road, but when many people walk on it, the road comes into existence.” Lin Yutang

Introduction: N-Acetyl-Cysteine (or N-acetylcysteine, usually abbreviated NAC and frequently pronounced like the word ‘knack’) is an altered (modified by an N-acetyl-group) form of the sulfur-containing amino acid cysteine (Cys).  NAC is one of the building blocks for the all important antioxidant substance glutathione (GSH).   GSH is a powerful reagent that helps cells fight oxidative stress.  One of the putative causes of Parkinson’s is oxidative stress on dopamine-producing neurons (see figure below). This post summarizes some of the biochemistry of NAC and GSH.  Furthermore, NAC may provide some neuroprotective benefit as a complementary and alternative medicine (CAM) approach to treating Parkinson’s.

“Losing the possibility of something is the exact same thing as losing hope and without hope nothing can survive.” Mark Z. Danielewski


 Glutathione (GSH):  GSH is a 3-amino acid substance (tripeptide) composed of Cys linked to glutamate (Glu) and followed by glycine (Gly). NAC would need to be de-acetylated to provide Cys and that would feed in to the reaction synthesis. Importantly, Cys is the rate limiting reactant, which means without adequate amounts of Cys you do not make GSH.   The schematic below gives the orientation and order of addition of the three amino acid components to give you GSH.


There are two advantages of NAC over Cys for making GSH: (i) the sulfhydryl group of NAC remains reduced (that is as an SH group) more so than the SH group of Cys; and (ii) the NAC molecule appears to transport itself through cell membranes much more easily than Cys.  The reduced (i.e.,  free SH group) form of GSH, once synthesized within the cell, has several key functions that range from antioxidant protection to protein thiolation to drug detoxification in many different tissues.   The key function of GSH is to provide what is known as “reducing equivalents” to the cell, which implies an overall key antioxidant effect.

The schematic below shows NAC transport from extracellular to intracellular (inside the cell), and the primary reactions for detoxification and thiolation from GSH. Implied by this figure below is that GSH is not easily transported into the cell. Furthermore, in a more toxic/hostile environment outside of the cell, you can easily oxidize 2 GSH molecules to become GSSG (the reduced SH group gets oxidized to form an S-S disulfide bond) and GSSG does not have the antioxidant effect of GSH.   However, inside the cell, GSH is a very potent antioxidant/detoxifying substance. And the beauty of being inside the cell, there is an enzyme called GSH-reductase that regenerates GSH from GSSG.


To recap and attempt to simplify what I just said, NAC gets delivered into a cell, which then allows the cell to generate intracellular GSH.  The presence of intracellular GSH gives a cell an enormous advantage to resist potentially toxic oxidative agents. By contrast, extracellular GSH has a difficult path into the cell; and is likely to be oxidized to GSSG and rendered useless to help the cell.

“Just remember, you can do anything you set your mind to, but it takes action, perseverance, and facing your fears.”  Gillian Anderson

One of many biological functions of NAC:   Perhaps the most important medical use of NAC is to help save lives in people with acetaminophen toxicity, in which the liver is failing.  How does NAC do this?  Acetaminophen is sold as Tylenol.  It is also added to compounds that are very important for pain management ()analgesics), including Vicodin and Percocet. Acetaminophen overdose is the leading cause of acute liver failure in the USA.   This excess of acetaminophen rapidly consumes the GSH in the liver, which then promotes liver death.  NAC quickly restores protective levels of GSH  to the liver, which hopefully reverses catastrophic liver failure to prevent death.

Systemically, when taken either orally or by IV injection, NAC would have 2 functions.  First, NAC replenishes levels of Cys to generate the intracellular antioxidant GSH (see schemes above).  Second, NAC has been shown to regulate gene expression of several pathways that link oxidative stress to inflammation.  Since the primary goal of this post relates to NAC as a CAM in Parkinson’s, I will not expand further on the many uses of NAC in other disease processes.  However, listed at the end are several review articles detailing the numerous medicinal roles of NAC.

“Love, we say, is life; but love without hope and faith is agonizing death.” Elbert Hubbard

Use of NAC as a CAM in Parkinson’s:   This is what we know about oxidative stress in Parkinson’s and the potential reasons why NAC could be used as a CAM in this disorder, it goes as follows  (it’s also conveniently shown in the figure at the bottom):

1. Substantia nigra dopamine-producing neurons die from oxidative stress, which can lead to Parkinson’s.

2.What is oxidative stress? Oxidative stress happens when your cells in your body do not make/have enough antioxidants to reduce pro-oxidants like free radicals. Free radicals cause cell damage/death when they attack proteins/cell membranes.

3.We speak of oxidative stress in terms of redox imbalance (which means the balance between increased amounts of oxidants or  decreased amounts of antioxidants).

4.Glutathione (GSH) is a key substance used by cells to repair/resist oxidatively damaged cells/proteins.

5.”Forces of evil” in the brain that make it difficult to resist oxidative stress:  decreased levels of GSH,  increased levels of iron and  increased polyunsaturated fatty acids.

6.Extracellar GSH cannot be transported easily into neurons, although there is evidence GSH gets past the blood brain barrier;

7.N-acetyl Cysteine (NAC), is an anti-oxidant and a precursor to GSH.  NAC gets through the blood brain barrier and can also be transported into neurons.

8.Cysteine is the rate-limiting step for GSH synthesis (NAC would provide the cysteine and favor synthesis of GSH).

9.Animal model studies have shown NAC to be neuroprotective.

10. Recent studies have shown NAC crosses the human blood brain barrier and may be a useful PD-modifying therapy.



“You cannot tailor-make the situations in life but you can tailor-make the attitudes to fit those situations.”  Zig Ziglar

Scientific and clinical support for NAC in treating Parkinson’s: Content presented here is meant for informational purposes only and not as medical advice.  Please remember that I am a basic scientist, not a neurologist, and any use of these compounds should be thoroughly discussed with your own personal physician. This is not meant to be an endorsement  because it would be more valuable and important for your neurologist to be in agreement with the interpretation of these papers.

Screen Shot 2017-05-25 at 3.43.19 PM

To evaluate the use of NAC in Parkinson’s, Katz et al. treated 12 patients with Parkinson’s with oral doses of NAC twice a day for two days.   They studied three different doses of 7, 35, and 70 mg per kilogram. For example, in a person weighing 170 pounds, from a Weight Based Divided Dose Calculator (click here), this would be 540, 2700, and 5400 mg/day of NAC for 7, 35, and 70 mg/kg, respectively. Using cerebral spinal fluid (CSF), they measured levels of  NAC, Cys, and GSH at baseline and 90 minutes after the last dose. Their results showed that there was a dose-dependent range of NAC as detected by CSF. And they concluded that oral administration of NAC produce biologically relevant CSF levels of NAC at the three doses examined; the doses of oral NAC were also well-tolerated.  Furthermore, the patients treated with NAC had no change in either motor or cognitive function. Their conclusions support the feasibility of using oral NAC as a CAM therapy for treatment of Parkinson’s.

Screen Shot 2017-05-25 at 3.47.06 PM

In a separate study, Monti at al  presented some preliminary evidence for the use of NAC in Parkinson’s. The first part of their study consisted of a neuronal cell system that was pre-treated with NAC in the presence of the pesticide rotenone as a model of Parkinson’s.   These results showed that with NAC there was more neuronal cell survival after exposure to rotenone compared to the rotenone-treated cells without NAC. The second part of the study was a small scale clinical evaluation using NAC in Parkinson’s. These patients were randomized and given either NAC or nothing and continued to use their traditional medical care. The patients were evaluated at the start and after three months of receiving NAC; they measured dopamine transporter binding and  performed the unified Parkinson’s disease rating scale  (UPDRS) to measure clinical symptoms. The clinical study revealed an increase in dopamine transporter binding in the NAC treatment group and no measurable changes in the control group. Furthermore UPDRS scores were significantly improved in the NAC treatment group compared to the control patient group.   An interesting feature of this study was the use of pharmaceutical NAC, which is an intravenous (IV) medication and they also used 600 mg NAC tablets. The dose used was 50 mg per kg mixed into sterile buffer and infused over one hour one time per week. In the days they were not getting the IV NAC treatment, subjects took 600 mg NAC tablets twice per day.

 Okay, what did I just say? I will try to summarize both of these studies in a more straightforward manner.   The results above suggest that NAC crosses the blood brain barrier and does offer some anti-oxidative protection. In one study, this was shown by increased levels of both GSH and Cys dependent on the NAC dose. In another study, they directly measured dopamine transporter binding, which was increased in the presence of NAC. In the second study using a three month treatment strategy with NAC, there was a measurable positive effect on disease progression as measured by UPDRS scores.  

“Our greatest weakness lies in giving up. The most certain way to succeed is always to try just one more time.” Thomas A. Edison

Potential for NAC in treating Parkinson’s: Overall, both studies described above suggest the possibility that NAC may be useful in treating Parkinson’s. However, in both cases these were preliminary studies that would require much larger randomized double-blind placebo-controlled trials to definitively show a benefit for using NAC in treating Parkinson’s. On a personal note, I have been taking 600 mg capsules of NAC three times a day for the past year with the hope that it is performing the task as outlined in this post. Using information from the first study that would be a NAC dose of 24 mg per kilogram body weight. In conclusion, the information described above suggests that NAC may be useful in regulating oxidative stress, one of the putative causes of Parkinson’s. As with all studies, time will tell if ultimately there is a benefit for using NAC in Parkinson’s.

“I am not an optimist, because I am not sure that everything ends well. Nor am I a pessimist, because I am not sure that everything ends badly. I just carry hope in my heart. Hope is the feeling that life and work have a meaning. You either have it or you don’t, regardless of the state of the world that surrounds you. Life without hope is an empty, boring, and useless life. I cannot imagine that I could strive for something if I did not carry hope in me. I am thankful to God for this gift. It is as big as life itself.” Vaclav Havel

References Used:
Katz M, Won SJ, Park Y, Orr A, Jones DP, Swanson RA, Glass GA. Cerebrospinal fluid concentrations of N-acetylcysteine after oral administration in Parkinson’s disease. Parkinsonism Relat Disord. 2015;21(5):500-3. doi: 10.1016/j.parkreldis.2015.02.020. PubMed PMID: 25765302.

Martinez-Banaclocha MA. N-acetyl-cysteine in the treatment of Parkinson’s disease. What are we waiting for? Med Hypotheses. 2012;79(1):8-12. doi: 10.1016/j.mehy.2012.03.021. PubMed PMID: 22546753.

Monti DA, Zabrecky G, Kremens D, Liang TW, Wintering NA, Cai J, Wei X, Bazzan AJ, Zhong L, Bowen B, Intenzo CM, Iacovitti L, Newberg AB. N-Acetyl Cysteine May Support Dopamine Neurons in Parkinson’s Disease: Preliminary Clinical and Cell Line Data. PLoS One. 2016;11(6):e0157602. doi: 10.1371/journal.pone.0157602. PubMed PMID: 27309537; PMCID: PMC4911055.

Mosley RL, Benner EJ, Kadiu I, Thomas M, Boska MD, Hasan K, Laurie C, Gendelman HE. Neuroinflammation, Oxidative Stress and the Pathogenesis of Parkinson’s Disease. Clin Neurosci Res. 2006;6(5):261-81. doi: 10.1016/j.cnr.2006.09.006. PubMed PMID: 18060039; PMCID: PMC1831679.

Nolan YM, Sullivan AM, Toulouse A. Parkinson’s disease in the nuclear age of neuroinflammation. Trends Mol Med. 2013;19(3):187-96. doi: 10.1016/j.molmed.2012.12.003. PubMed PMID: 23318001.

Rushworth GF, Megson IL. Existing and potential therapeutic uses for N-acetylcysteine: the need for conversion to intracellular glutathione for antioxidant benefits. Pharmacol Ther. 2014;141(2):150-9. doi: 10.1016/j.pharmthera.2013.09.006. PubMed PMID: 24080471.

Taylor JM, Main BS, Crack PJ. Neuroinflammation and oxidative stress: co-conspirators in the pathology of Parkinson’s disease. Neurochem Int. 2013;62(5):803-19. doi: 10.1016/j.neuint.2012.12.016. PubMed PMID: 23291248.

Cover photo credit: https://s-media-cache-ak0.pinimg.com/originals/e8/33/ae/e833aeb408a432d419628c803bf14498.jpg


Parkinson’s Disease Research: A Commentary from the Stands and the Playing Field

“You can have a very bad end with Parkinson’s, but on the other hand, you can be like me, because I’m lucky. I’m not having a bad end.” Margo MacDonald

“My age makes me think how valuable life is. How bad is something like Parkinson’s in relation to not having life at all?” Michael J. Fox

Introduction: Last month, together with Dr. Simon Stott and his team of scientists (The Science of Parkinson’s Disease), we co-published a historical timeline of Parkinson’s disease beginning with the description of the ‘shaking palsy’ from James Parkinson in 1817. My post entitled “Milestones in Parkinson’s Disease Research and Discovery” can be read here (click this link). The Science of Parkinson’s Disease post entitled “Milestones in Parkinson’s Disease Research and Discovery” can be read here (click this link).

We spent a lot of time compiling and describing what we felt were some of the most substantial findings during the past 200 years regarding Parkinson’s disease.  I learned a lot; truly amazing what has been accomplished in our understanding of  such a complex and unique disorder.  Simon posted a follow-up note entitled “Editorial: Putting 200 years into context” (click this link). I have decided to also post a commentary from the standpoint of (i) being someone with Parkinson’s and (ii) being a research scientist.

“Every strike brings me closer to the next home run.” Babe Ruth

Baseball: I want to use the analogy of a baseball game to help organize my commentary. Baseball fans sit in the stands and have fun watching the game, thinking about the strategy behind the game, eating/drinking, and sharing the experience with family/friends/colleagues.   Most baseball players begin playing early in life and the ultimate achievement would be to reach the major leagues. And this would usually have taken many years of advancing through different levels of experience on the part of the ballplayer. How does how this analogy work for me in this blog? Stands: I am a person-with-Parkinson’s watching the progress to treat and/or cure this disorder. Playing field: I am a research scientist in a medical school (click here to view my training/credentials).

“Never allow the fear of striking out keep you from playing the game!”  Babe Ruth

Observation from the stands:
I am a spectator like everyone else with Parkinson’s. I read much of the literature available online.  Like you, I think about my disorder; I think about how it’s affecting me every day of my life. Yes, I want a cure for this disease.  Yes, I’m rather impatient too.  I understand the angst and anxiety out there with many of the people with Parkinson’s. In reality, I would not be writing this blog if I didn’t have Parkinson’s. Therefore, I truly sense your frustration that you feel in the presence of Parkinson’s, I do understand.  Given below are examples of various organizations and ads and billboards in support of finding a cure for Parkinson’s.  Some even suggest that a cure must come soon.   However, the rest of my post is going to be dedicated to trying to explain why it’s taking so long; why I am optimistic and positive a cure and better treatment options are going to happen.  And it is partly based on the fact that there really are some amazing people working to cure Parkinson’s and to advance our understanding of this disorder.

“When you come to a fork in the road take it.” Yogi Berra

Observations from the playing field (NIH, war on cancer, research lab, and advancing to a cure for Parkinson’s):

National Institutes of Health (NIH) and biomedical research in the USA: Part of what you have to understand, in the United States at least, is that a large portion of biomedical research is funded by the NIH (and other federally-dependent organizations), which receives a budget from Congress (and the taxpayers). What does it mean for someone with Parkinson’s compared to someone with cancer or diabetes? The amount of federal funds committed to the many diseases studied by NIH-funded-researchers are partly divvied up by the number of people affected. I have prepared a table from the NIH giving the amount of money over the past few years for the top four neurodegenerative disorders, Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis (ALS), and Huntington’s Disease, respectively [taken from “Estimates of Funding for Various Research, Condition, and Disease Categories” (click here)]. And this is compared to cancer and coronary arterial disease and a few other major diseases. Without going into the private organizations that fund research, a large amount of money comes from the NIH. Unfortunately, from 2003-2015, the NIH lost >20% of its budget for funding research (due to budget cuts, sequestration, and inflationary losses; click here to read further).   Therefore,  it is not an overstatement to say getting  funded today by the NIH is fiercely competitive.  From 1986 to 2015, my lab group was supported by several NIH grants and fellowships  (and we also received funding from the American Heart Association and Komen for the Cure).


“In theory, there is no difference between theory and practice. But in practice, there is.” Yogi Berra

War against cancer: In 1971, Pres. Richard Nixon declared war against cancer and Congress passed the National Cancer Act.  This created a new national mandate “to support research and application of the results of research to reduce the incident, morbidity, and mortality from cancer.” Today, cancer is still the second leading cause of death in the USA; however, we’ve come such a long way to improving this statistic from when the Cancer Act was initiated.

Scientifically, in the 1970’s, we were just learning about oncogenes and the whole field of molecular biology was really in its infancy. We had not even started sequencing the human genome, or even of any organism.  We discovered genes that could either promote or suppress cellular growth.   We began to delineate the whole system of cell signaling and communications with both normal and malignant cells. We now know there are certain risk factors that allow us to identify people that may have increased risk for certain cancers. Importantly,  we came to realize that not all cancers were alike,  and it offered the notion to design treatment strategies for each individual cancer.  For example,  we now have very high cure rates for childhood acute leukemia and Hodgkin’s lymphoma and we have significantly improved survival statistics for women with breast cancer. Many might say this was a boondoggle and that we wasted billions of dollars  funding basic biomedical research on cancer; however, basic  biomedical research is expensive and translating that into clinical applications is even more expensive.  [ For a  very nice short review on cancer research please see the following article, it may be freely accessible by now: DeVita Jr, Vincent T., and Steven A. Rosenberg. “Two hundred years of cancer research.” New England Journal of Medicine 366.23 (2012): 2207-2214.]

“One of the beautiful things about baseball is that every once in a while you come into a situation where you want to, and where you have to, reach down and prove something.” Nolan Ryan

The biomedical research laboratory environment:  A typical laboratory group setting is depicted in the drawing below. The research lab usually consists of the lead scientist who has the idea to study a research topic, getting grants funded and in recruiting a lab group to fulfill the goals of the project.  Depending on the philosophy of the project leader the lab may resemble very much like the schematic below or may be altered to have primarily technicians or senior postdoctoral fellows working in the lab  (as two alternative formats). A big part of academic research laboratories is education and training the students and postdocs to go on to advance their own careers; then you replace the people that have left and you continue your own research.  Since forming my own lab group in 1986, I have helped train over 100 scientists in the research laboratory: 17 graduate students, 12 postdoctoral fellows, 17 medical students, and 64 undergraduates. The lab has been as large as 10 people and a small as it is currently is now with two people. People come to your lab group because they like what you’re doing scientifically and this is where they want to belong for their own further training and advancement.  This description is for an academic research  laboratory; and  I should also emphasize that many people get trained in federal government-supported organizations, private Pharma and other types of research environments that may differ in their laboratory structure and organizational format.


“Hitting is 50% above the shoulders.” Ted Williams

 In search of the cure for Parkinson’s:    First, I understand the situation you’re in with Parkinson’s because I’m living through the same situation.   But when people find out I’m a research scientist they always wonder why aren’t we doing more to find a cure, and I  hear the sighs of frustration and I see the anxiety in their faces. Second, the previous three sections are not meant to be an excuse for why there is still no cure for Parkinson’s. It is presented in the reality of what biomedical research scientists must undergo to study a topic.  Third, the experiments that take place in basic biomedical research laboratory may happen over weeks to months if successful. Taking that laboratory data to the clinic and further takes months and years to succeed if at all.   The section on cancer reminds me a lot of where we are going with Parkinson’s and trying to advance new paradigms in the treatment and curative strategies.  Professionally, I have even decided  to pursue research funding in the area of Parkinson’s disease.   Why not spend the rest of my academic career studying my own disease; in the least I can help educate others about this disorder. Furthermore, I can assure you from my reading and meeting people over the last couple of years, there are many hundreds of scientists and clinicians throughout this world studying Parkinson’s and trying to advance our understanding and derive a cure.  I see their devotion, I see their commitment to helping cure our disorder.

The science behind Parkinson’s is quite complicated. These complications suggest that Parkinson’s may be more of a syndrome rather than a disease. Instead of a one-size-fits-all like a disease would be classified; Parkinson’s as a syndrome would be a group of symptoms which consistently occur together.  What this might imply is that some treatment strategy might work remarkably well on some patients but have no effect on others. However, without a detailed understanding and advancement of what Parkinson’s really is we will never reach the stage where we can cure this disorder.

In a recent blog from the Science of Parkinson’s disease, Simon nicely summarized all the current research in 2017 in Parkinson’s disease (click here to read this post). To briefly summarize what he said is that there are multiple big Pharma collaborations occurring to study Parkinson’s.  There are more than 20 clinical trials currently being done in various stages of completion to prevent disease progression but also to try to cure the disorder.  From a search of the literature, there are literally hundreds of research projects going on that promise to advance our understanding of this disorder. With the last point, it still will take time to happen. Finally, I am a realist but I’m also optimistic and positive that we’re making incredible movement toward much better therapies, which will eventually lead to curative options for Parkinson’s.

And a final analogy to baseball and Parkinson’s, as Tommy Lasorda said “There are three types of baseball players: those who make it happen, those who watch it happen, and those who wonder what happens.”  I really want to be one of those scientists that help make it happen (or at least to help advance our understanding of the disorder).

“You can’t expect life to play fair with your heart or your brain or your health. That’s not the nature of the game we call life. You have to recognize the nature of the game and know that you can do your best to make the right choices, but life if going to do whatever the hell it pleases to you anyway. All you can control is how you react to whatever life throws at you. You can shut down or you can soar.” Holly Nicole Hoxter

Cover photo credit: PNC Park photo: i.imgur.com/32RWncK

Sign post scienceofparkinsons.com/

Building Empathy for Parkinson’s

“When people talk, listen completely. Most people never listen.”  Ernest Hemingway

“To perceive is to suffer.”  Aristotle

Introduction: The loss of dopamine-producing neurons in the mid-brain leads to Parkinson’s disease, which usually presents with motor dysfunction of different degrees of progression from person-to-person.  This post explores the differences between empathy and sympathy, and describes a new device that allows one to actually experience a person-with-Parkinson’s tremor; surely providing much empathy from the experience.

“No one cares how much you know, until they know how much you care”  Theodore Roosevelt

A lesson learned from the classic rock opera “Tommy” by The Who: The plot of the 1969 rock opera “Tommy” begins with Tommy’s parents.  His father, Captain Walker, fought in World War II but it is assumed he died. However, Captain Walker is alive and returns home to his wife and Tommy. Believing her husband to be dead, Mrs. Walker has a new lover.  Captain Walker accidentally kills the lover, in the presence of Tommy. Tommy is traumatized by what he witnessed; he becomes catatonic.  Three musical examples: Go to the Mirror (listen here) Tommy sings “See me, me, feel me, touch me, heal me / See me, feel me, touch me, heal me.” Tommy’s father sings “I often wonder what he is feeling / Has he ever heard a word I’ve said? / Look at him in the mirror dreaming / What is happening in his head?” In Tommy Can You See Me? (listen here)  his mother sings “Tommy can you hear me? / Can you feel me near you? /  Tommy can you feel me / Can I help to cheer you.” In See Me, Feel Me (listen here) Tommy sings “See me, feel me, touch me, heal me / See me, feel me, touch me, heal me / See me, feel me, touch me, heal me / See me, feel me, touch me, heal me / Listening to you, I get the music / Gazing at you, I get the heat / Following you, I climb the mountain / I get excitement at your feet.” Hopefully, you can empathize, not sympathize, with Tommy and the life-struggles he encounters and overcomes in this rock opera.

“for there is nothing heavier than compassion. Not even one’s own pain weighs so heavy as the pain one feels with someone, for someone, a pain intensified by the imagination and prolonged by a hundred echoes.” Milan Kundera

*Empathy vs. sympathy: Empathy means you have the ability to understand and share the feelings of another.  By contrast, sympathy means feelings of pity and sorrow for someone else’s misfortune (https://en.oxforddictionaries.com/definition/empathy). Yes, it sucks to have a chronically-progressing neurodegenerative disorder like Parkinson’s. But it could be worse, really.

Empathy.  What a great word.  Try to be empathetic to me; you don’t have to become one with me, just strive to understand how I’m feeling.  Our bond will surely strengthen.  You may not be able to exactly feel what I’m feeling, but just trying says much to you, your inner processing, the soul of your humanity.

Please don’t pity me, that reduces the feelings between us.  Please don’t have sorrow or sadness for me, it weakens our ties. If you give me sympathy, you’ll never truly be able to grasp the extent and meaning of my Parkinson’s.  Parkinson’s is not my friend; however, having your friendship and understanding (empathy) instead of your pity (sympathy) will give me strength and help me deal on a more positive-front with this unrelenting disorder.

*This post is dedicated to the first-year medical students at the UNC School of Medicine. On Friday, May 5, I had the privilege and honor of being presented as a person-with-Parkinson’s in our Neurologic Block. They asked very specific questions in their attempt to understand Parkinson’s and to learn how I am living with this disorder. It was clear that they were trying to follow the advice of Dr. William Osler who said “It is much more important to know what sort of a patient has a disease than what sort of a disease a patient has.”

“Some people think only intellect counts: knowing how to solve problems, knowing how to get by, knowing how to identify an advantage and seize it. But the functions of intellect are insufficient without courage, love, friendship, compassion, and empathy.”  Dean Koontz

What is the life expectancy of someone diagnosed with Alzheimer’s, Parkinson’s, Amyotrophic Lateral Sclerosis (ALS), and Huntington’s disease? These neurodegenerative disorders are listed in ranked order of how many people are affected from most to least, respectively. Alzheimer’s typically progress over 2 to 20 years, and individuals live for 8 to 10 years after the diagnosis.  People who have Parkinson’s usually have the same average life expectancy as people without the disease.  Life expectancy from ALS is usually at least 3-4 years. The time from diagnosis  of Huntington’s to death is about 10 to 30 years.  Each of these disorders is uniquely different and unsettling to me; but your empathy, not your sympathy, will truly help me sail my boat along the shoreline for many more years.  Accept me with ‘my unique medical issues’, try to understand it. Your empathy will add stability to my battle; just watch.

“Resolve to be tender with the young, compassionate with the aged, sympathetic with the striving, and tolerant of the weak and the wrong. Sometime in life you will have been all of these.” Lloyd Shearer

A novel engineering device is empathy-producing to someone with Parkinson’s: The whole story is revealed from watching this video (click here). Klick Labs in Toronto, Canada, has created the SymPulse Tele-Empathy Device. This device is capable of mimicking and producing the tremors and involuntary movements of someone with Parkinson’s in people without Parkinson’s. The video is quite powerful, you immediately sense the empathy.

The SymPulse Tele-Empathy Device is based on digitized muscle activity from electromyograms of Parkinson’s patients. The signal is unique for each person with Parkinson’s. When the person without Parkinson’s receives this novel voltage pattern, their muscles will contract exactly as found in the person with Parkinson’s. Developing such a device shows the deviant nature of Parkinson’s to disrupt/distort normal neuro-muscular circuitry.

This device could be used to increase empathy in doctors and other caregivers. And it could enable family members and loved-ones the unique opportunity to experience the actual tremor/involuntary movements of their special person with Parkinson’s. Company officials note that most people wear the device for at most a couple of minutes; turn off the device and they return to normal. Remember, there is no off-on switch for the person with Parkinson’s.  I can only imagine empathy evolving from this device when used on someone without Parkinson’s.

“When we honestly ask ourselves which person in our lives mean the most to us, we often find that it is those who, instead of giving advice, solutions, or cures, have chosen rather to share our pain and touch our wounds with a warm and tender hand. The friend who can be silent with us in a moment of despair or confusion, who can stay with us in an hour of grief and bereavement, who can tolerate not knowing, not curing, not healing and face with us the reality of our powerlessness, that is a friend who cares.” Henri J.M. Nouwen

Cover photo credit: gsmnp.com/wp-content/uploads/View-of-Smoky-Mountains-from-Oconaluftee.jpg

Life-Journey with Parkinson’s Blog (2016-2017): Recap of Quotes, Service, and Research

“Give your life a destination.” Debasish Mridha

“We’re all a beautiful, wonderful work in progress….Embrace the process!” Nanette Mathews

Précis: This post is a review of my public journey and life-steps with Parkinson’s in the 2nd year of the blog: i) rationale for the blog; ii) quotes/highlights from selected posts between March 2016-March 2017; iii) overview of service activities/events; iv) research and the 4th World Parkinson Congress; v) some of the people that make a difference in my life, and vi) six favorite cover photos from the past year.

Update on I’m Still Here: Journey and Life with Parkinson’s

A thought from Day 01: On March 9, 2015, I began my journey and Parkinson’s-life-story with this blog.  The first blog post ended with the following comment: “I am trying to live life well and authentically, and not be defined by my PD. With the help of family, friends, colleagues, and personal physicians, my goals are to stay positive and strive to keep focused on what matters the most…I am still here!”

Foundational themes of the blog:  The overall goal of the blog is divided between these topics: (a) to describe living with Parkinson’s (“Life Lessons”); (b) to present emerging medical strategies for dealing with Parkinson’s (“Medical Education”); (c) to provide a support mechanism for anyone with Parkinson’s or another neurodegenerative disorder (“Strategy for Living”); and (d) to give an overview of the scientific aspects of Parkinson’s (“Translating Science”).  I really appreciate your continual support, feedback, critiques, and suggestions for future topics (here’s an example): “I enjoy reading your informative blog posts. I believe that addressing the many frustrations of living with Parkinson’s as you are doing with such “matter of factness” and then with a plan of action, must be inspiring to others dealing with the same.  All the while working so hard to maintain your positive outlook…the mental exercise! The other side of the overall challenge in this competition with Parkinson’s Disease to live your present life fully.” If there are some specific topics/life aspects of Parkinson’s you’d like for me to research and present here, please send me the topic(s).  If there is some format change in presentation you’d like to see to improve the readability of future posts, please send me a suggestion.

Quotes and highlights from selected posts from March 2016-March 2017:

  1. “As a long-time educator, I feel that my daily lesson plans are partly derived from my life-experiences and that my syllabus is the sum of my life’s journey.”  From Parkinson’s and the Positivity of Michael J. Fox (click here to read post).
  2. “A regular aerobic exercise program likely helps to promote the appropriate conditions for the injured brain to undergo neuroplasticity.”  From Déjà Vu and Neuroplasticity in Parkinson’s (click here to read post).
  3. We are identified by our characteristic symptoms of our unwanted companion named Parkinson’s. We are all in this together, united by our disorder; held together by those who love and care for us.” From Update on I’m Still Here: Life with Parkinson’s (click here to read post).
  4. While we wait for the potion that slows progression, we exercise and remain hopeful. While we live with a neurodegenerative disorder, we strive to remove the label and we stay positive.” From Parkinson’s Treatment With Dopamine Agonist, Complementary and Alternative Medicine (CAM), and Exercise(click here to read post).
  5. Living with Parkinson’s requires you to adapt to its subtle but progressive changes over a long period of time; you need to remain hopeful for many different things.” From Chapter 1: A Parkinson’s Reading Companion on Hope (click here to read post).
  6. “This disorder robs you physically of mobility and flexibility, so maintaining physical strength is really important. This disorder robs you emotionally and this deficit is bigger than the physical defects; thus, to thrive with Parkinson’s demands several character strengths.” From Chapter 3: A Parkinson’s Reading Companion on Strength (click here to read post).
  7. “Life with Parkinson’s is best lived in the current moment without either focusing on the past or dreading the future.”  From Chapter 8: A Parkinson’s Reading Companion on Mindfulness (click here to read post).
  8. “The journey with Parkinson’s requires effort, teamwork, awareness, and a heart-fueled positive attitude to keep going.”  From Chapter 9: A Parkinson’s Reading Companion on Journey (click here to read post).
  9. “Consider your disorder, you must be able to embrace this unexpected turn in your life and manage the best you can. Personalize your disorder and understand its nuances on you; then you will be able to successfully navigate life in its daily presence.” From 9 Life Lessons from 2016 Commencement Speeches (click here to read post).
  10. “I truly believe that the effort most people are using to handle their disorder puts them in a healthier and better lifestyle to manage their symptoms. An emerging predominate picture of Parkinson’s today is a person striving to live strongly.” From The Evolving Portrait of Parkinson’s (click here to read post).
  11. “Believe in Life in the Presence of Parkinson’s”: Every thought expressed here matters to me (click here to read post).
  12. “Your home may change many times over the coming years. Let your heart tell you where your home is.” From 2016 Whitehead Lecture: Advice, Life Stories and the Journey with Parkinson’s (click here to read post).
  13.  “Here’s a simple mindfulness experience/moment: simply be aware of the steam leaving your morning cup of coffee/tea, clear your immediate thoughts, then sip, focus and savor this moment.”  From 7 Healthy Habits For Your Brain (click here to read post).
  14. “You’ve played 17 holes of golf, and you approach the 18th hole to finish the round. This is a long par three with a lake between you on the tee box and the putting surface.  Your three golf buddies have already safely hit their balls over the lake;  you  launch the ball over the water and safely onto the green (this is a big deal).  Without Parkinson’s, your facial expression and your exuberance are so obvious.  With Parkinson’s, your joy and exuberance are still over-flowing inwardly yet it is displayed in a more muted manner.”  From The Mask of Parkinson’s (click here to read post).
  15. “We must remain hopeful that advances in Parkinson’s treatment are being made and that our understanding of the science of Parkinson’s is continuing to evolve.”  From 2016: The Year in Parkinson’s (click here to read post).
  16. “Since receiving my Parkinson’s diagnosis, my opinion of exercise has changed.  With Parkinson’s, I’m now exercising as if my life depends on it.”  From 9 Things to Know About Exercise-induced Neuroplasticity in Human Parkinson’s (click here to read post).

Service and research:
Service- I was most fortunate to be able to participate in 2 ways for the 4th World Parkinson Congress (WPC), first as a member of the Communications Committee, World Parkinson Coalition; second, as the Co-Editor, Daily Parkinson eNewspaper for the 4th WPC.  And it gave me an opportunity to work with the very talented Eli Pollard (Executive Director WPC).  A truly amazing Editorial Board was assembled of PD advocates, researchers, experts, PwP, and just a superb group of people devoted to Parkinson’s (click here to read the Editorial Board Biographical Sketches).   This was a meaningful experience to have worked with the Editorial Board, a real honor.

Being part of the Planning Committee, Moving Day NC Triangle, headed up by Jessica Shurer, was such fun.  This was my first year on the committee; however, it was my second year to organize a team for Moving Day.

PWR!Moves® Instructor Workshop Certificate. Spent a weekend in Greenville, SC to participate and get certified in PWR!Moves (PWR = Parkinson Wellness Recovery).  To sum it up is easy, truly an amazing event.  I was fortunate to have an experienced-talented instructor and a group of personal trainers committed to working with PwP (click here to read the blog post describing the PWR! experience). Although I was happy to contribute as the person-with-Parkinson’s and go through the exercise routines for everyone, it was even more fun getting trained and certified in PWR!Moves.

Research-  One of the new directions in my life is a shift in the focus of my research away from hematology and to Parkinson’s.  I keep asking myself, why? and keep answering why not!  The process is just like everything else related to research and grant applications; you read, plan, write, submit, and wait.  However, I am pleased to say that CJ’s fellowship entitled “Localization of Proteases and their Inhibitors in Parkinson’s Disease” was funded by UNC-CH.  It’s a start…we begin gathering data next month.  And I am so proud of CJ for seeking (and obtaining) funding to get us started in the science of Parkinson’s.

“Life is like a roller-coaster with thrills, chills, and a sigh of relief.” Susan Bennett

The people that make a difference in my life: Collectively, everyone here gives me strength each and every day of my journey with this disorder.


Above- Barbara, the best care-partner/best friend/best everything; I can’t imagine being here and doing all of this without your never-ending love and support.


Top and bottom right panels above- lab/research group [especially important are CJ (currently working in the lab) and Mac (a long-time collaborator) and Chantelle, Savannah, and Jasmine (no longer working in the lab but still are great friends and vital to our success)]; middle panel- nothing more valuable than family, with my sisters (Tina and Kitty), and bottom left panel- my all-important golf buddies [Walter, Kim, Nigel (not pictured) and John].


Panels above- undergraduate classes from SP ’16, FA’ 16 and SP ’17 inspire me every day to keep teaching and fuel my inner-core to keep going another year.

Above panels- medical students (all 180 students/class) enrich my life and challenge me to keep working hard and stay happy.


Besides attending a Parkinson’s Congress, getting certified in PWR!, publishing a book, and walking for Parkinson’s; it was all made easier by my PWR! Physical Therapist and gifted teacher Jennifer (top right panel), expert medical guidance from my Neurologist Dr. Roque (middle panel), Parkinson’s-education-awareness from the best movement disorder center social-worker Jessica (bottom middle panel), perpetual energy and role model of a PwP-advocate Lisa (bottom right panel), and Johanna and Katie (not pictured above) who make my day-job such a joyful experience.  And I apologize to many others who are not pictured here because you do really matter to me.

6 favorite cover photos from the past year (links to photos at the end):


Thank you! Thank you for your support during the second year of my journey with this blog. As always, live decisively, be positive, stay focused, remain persistent and stay you.

“I want to be in the arena. I want to be brave with my life. And when we make the choice to dare greatly, we sign up to get our asses kicked. We can choose courage or we can choose comfort, but we can’t have both. Not at the same time. Vulnerability is not winning or losing; it’s having the courage to show up and be seen when we have no control over the outcome. Vulnerability is not weakness; it’s our greatest measure of courage.”  Brené Brown, Rising Strong

Noted added in proof: For a day or so, a preliminary version of this post appeared in 200 Years Ago James Parkinson published “An Essay On The Shaking Palsy” (click here to view).  Together, this combined post was substantially longer than my usual blog post.  Therefore, I separated them and decided to present this year-end-review in an expanded format.

Cover photo credit: farm4.staticflickr.com/3953/15575910318_ec35ebb523_b.jpg

Photo credits for the 6 favorite cover photos for 2016-2017: top left http://epod.usra.edu/.a/6a0105371bb32c970b015438c5312a970c-pi;  top right: : http://vb3lk7eb4t.search.serialssolutions.com/?V=1.0&L=VB3LK7EB4T&S=JCs&C=TC0001578421&T=marc ; middle left wallpaper-crocus-flower-buds-violet-primrose-snow-spring-flowers.jpg; middle right : http://az616578.vo.msecnd.net/files/2016/03/19/635940149667803087959444186_6359344127228967891155060939_nature-grass-flowers-spring-2780.jpg ; bottom left : http://www.beaconhouseinnb-b.com/wp-content/uploads/dawn-at-spring-lake-beach-bill-mckim.jpg ; bottom right : http://www.rarewallpapers.com/beaches/lifeguard-station-10678