What I didn’t know about Parkinson’s Disease
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I thought my knowledge of Parkinson’s disease (PD) was adequate for primary care. I had been taught that Parkinson’s disease is a movement disorder caused by the loss of dopamine-producing cells in the substantia nigra of the brain. Not uncommon, particularly in older men, it generally presents with motor symptoms like asymmetric tremor, “festinating” gait, stooped posture, lack of facial expression, and micrographia. The disease progresses leading to disability and possibly dementia but generally responds to dopaminergic medication, although often requiring complex regimens, or possibly deep brain stimulation. I have been to CME’s on movement disorders given by university neurologists and neurosurgeons in which they showed videos of patients with their deep brain stimulator turned off and on. The case examples of Parkinson’s disease were always classic and full blown.
As usual, patients teach us more about diseases than professors do. Let me tell you what I have learned about Parkinson’s disease since my wife Connie was diagnosed two years ago.
Connie was far more athletic than I; she competed every year in the annual Labor Day swim across the lake in our community and she jested that she always came in last, but she always made it across. When she started complaining of decreased exercise tolerance about ten years ago, we both focused on cardiac disease because her mother had a sudden cardiac death after swimming at age 77 in 1989 – ironically the very year in which Bernadine Healy, as president of the American Heart Association, began the educational campaign about the prevalence and atypical presentation of coronary disease in women.
Our primary care physician immediately ordered a treadmill stress EKG for Connie which was normal and an echocardiogram which showed hemodynamically insignificant aortic valvular sclerosis and mild mitral regurgitation. She complained of muscle aches which we attributed to statin therapy. Connie did fatigue easily, but she continued to ski every year even though she could no longer keep up with me, especially when we were at high altitude. We also noticed that she was having difficulty making right turns on skis. She developed bursitis in her left hip which in retrospect was probably due to asymmetric muscle tone. When she was no longer able to climb up the almost always non-functioning escalator from the Washington subway (the equivalent of four or more flights of steps, depending on the station), she began driving instead.
When standing, she tired easily and felt faint. We ruled out Addison’s, hypothyroidism, and even tested for Lyme antibodies. She had problems with typing and with her voice which we attributed to overuse from a lifetime of broadcast journalism. An astute physiatrist friend of ours at a social function noticed that she was unable to rapidly oppose her left thumb and fingers. That gave us the clue that we needed a neurologic evaluation which we finally got around Labor Day of 2010. That was the first year that she did not do the Labor Day swim across the lake. She took her first dose of levodopa before we left the pharmacy and she said it felt immediately that the molasses around her legs suddenly melted and she could walk again. Unfortunately dopaminergics soon lost their benefit and she switched to selegiline which has also had minimal effect but at least the side effects are more tolerable to her.
What I did not know about Parkinson’s disease is that non-motor symptoms are common and may even be the predominant features in the early stage of the disease. Common non-motor symptoms include constipation, aches and pains, urinary frequency, dizziness, anxiety, depression, sleep disorders, and postural hypotension – all of which I see regularly in primary care and never considered as possible manifestations of Parkinsonism. In retrospect, Connie had ALL these symptoms which we had previously attributed to too much caffeine, too little exercise, etc.
What we have also discovered is that exercise, especially for Parkinsonism in which rigidity predominates, may be more effective than medication. Parkinsonism is a clinical diagnosis, although the presence of alpha-synuclein in salivary gland biopsy offers a promising although invasive diagnostic method.[3,4] A PET scan compound to measure dopamine transport activity was recently FDA approved and is under investigation as a clinical tool. An exciting approach to screening for PD using voice patterns in telephone interviews was described at the Technology-Education-Development (TED) conference last year in Edinburgh. We are exploring the potential of transcranial magnetic stimulation (TMS) to predict the effect of deep brain stimulation in clinical trials of TMS as a possible therapy for Parkinson’s.[7,8] Connie is excited about the possibility of participating in medical research and plans to contribute to a brain bank at death.
We now study Connie’s disease — not Parkinson’s disease. She has discovered that dancing is easier than walking, so she dances down the street. We have found the Parkinson’s Disease Foundation website (http://www.pdf.org) and the Michael J. Fox Foundation (http://michaeljfox.org) helpful sources of information and links to online and local support groups. There are many exercise programs and speech therapies specifically for people with Parkinsonism and we are exploring what is available to us in the Washington area. We are fortunate that the Capital Area Permanente Medical Group now has a neurologist who specializes in movement disorders and he has been extremely helpful as has our primary care physician.
Because Connie gets her best relief from exercise, she stretches and swims regularly. Although cold weather exacerbates her stiffness, she continues to ski. We stick to the easier groomed trails and spend much of our time working with adaptive snowsports programs. The participants remind us that all of us are only temporarily able-bodied at best. One of the only good results of our nation’s decade of war is that the US has the best Paralympic athletes ever.
I have been a physician for nearly forty years now, over half my life, and I strongly believe the adage that the secret of caring for the patient is caring about the patient. I deliberately choose to blur the boundaries of “clinical detachment” and it has almost always been mutually beneficial. The most rewarding thing I have done in my life was being primary care giver for both of my parents in the final years of their lives. I know that being involved in the clinical care of family members is controversial. I always sought the consultation of my parents’ doctors, but I do not regret taking an active role in their care. They had formalized the relationship by naming me durable power of attorney for healthcare and I am sure I knew both their health and their preferences better than anyone else.
Connie and I have formalized this arrangement in living trusts and we continue to discuss our options and preferences as we age. It is different having a spouse with a degenerative neurologic illness; when I agreed to marry Connie we were both in our 50s and we had both seen firsthand the effect of progressive disability on couples. She knew that my father had Alzheimer’s disease and my mother was overwhelmed caring for him and maintaining their home.
When we married, my parents were already in their 90s. I made it clear that my relationship with them would be a priority for me just as her priority was her relationship with her two sons, then in college. Although my father was dependent because of almost total short-term memory loss, he was physically strong and was ambulatory until the last month of his life. In fact, he pushed my mother’s wheelchair after she was incapacitated by neuropathic pain secondary to osteoporotic spinal fractures and they had to move into assisted living.
I assumed that I would more likely be getting assistance than giving it in my marriage. My “retirement” has not turned out to be a life of leisure and that is a mixed blessing. Every day we are both frantically trying to get our professional work and domestic chores done. I get irrationally irritated when Connie asks me to do something for her that she is usually able to do for herself. The fact that I am not as quick, strong, or energetic as I used to be adds to that frustration. I have to take a deep breath literally and count our blessings. Getting outdoors in the sunshine helps too.
Charles Sneiderman MD PhD DABFP
Family Physician and Medical Director
Culmore Clinic, Falls Church, VA
Published March 12, 2013
- Khoo TK, Yarnall AJ, Duncan GW, et al. The spectrum of nonmotor symptoms in early Parkinson Disease. Neurology. 2013. 80:276-281.
- Tomlinson CL, Patel S, Meek C, et al. Physiotherapy versus placebo or no intervention in Parkinson’s disease. Cochrane Database Syst Rev. 2012 Aug 15;8:CD002817.
- Cersosimo MG, Benarroch EE. Autonomic involvement in Parkinson’s disease: pathology, pathophysiology, clinical features and possible peripheral biomarkers. J Neurol Sci. 2012 Feb 15;313(1-2):57-63.
- Gibbons CH, Wang N, Lafo J, Freeman R. Alpha-synuclein as a cutaneous biomarker of Parkinson disease. Oral poster presented at the 23rd International Symposium on the Autonomic Nervous System. Oct 31, 2012, Paradise Island, Bahamas.
- Shtilbans A, Henchcliffe C. Biomarkers in Parkinson’s disease: an update. Curr Opin Neurol. 2012. 25(4):460-465.
- Technology, Entertainment, Design (TED). TED Fellows Network -Max Little. http://fellows.ted.com/profiles/max-little
- Berardelli A, Conte A, Fabbrini G, et al. Pathophysiology of pain and fatigue in Parkinson’s disease. Parkinsonism Relat Disord. 2012. Jan; 18 Suppl 1:S226-S228.
- Yang YR, Tseng CY, Chiou SY, et al, Combination of rTMS and treadmill training modulates corticomotor inhibition and improves walking in Parkinson disease: a randomized trial. Neurorehabil Neural Repair. 2013. 27(1):79-86.