Bob  Lane Reviews the first two chapters of Navigating Life with Parkinson's Disease  (from June 2014 Newsletter)

 

- Parkinson's Disease (PD) is neurodegenerative, associated with premature death of neurons in the substantia nigra region of the brain.

- There are four cardinal symptoms: tremor, slow movement, rigidity, and postural instability. At least two of these symptoms must be present for
a PD diagnosis.

- Secondary symptoms include tiny cramped handwriting, soft voice, “masking” (reduced facial expression), slowness of movement, stooped posture, “freezing”, tremor, shuffling, loss of sense of smell, loss of repartee (or, loss of conversation consisting of witty remarks), drooling, no arm swing,…the list is long.

- Unlike other cells, nerve cells don’t reproduce to replace dying cells. In PD, dopaminergic cells are dying off at a higher rate than normal; when a certain proportion of the cells are dead, PD symptoms set in.

- PD is highly individualized, each person having a different combo of symptoms, and progresses at widely varying rates from person to person.

- The cause of PD is not known (pesticides are suspected, and genetics seems to play a role), and there is no cure. All current treatments are symptom management.

- Two of the scales for measuring the stages of PD progression are Unified Parkinson's Disease Rating Scale (UPDRS) and Hoehn and Yahr.

 

Placebo, nocebo by Billy Ray Boyd (from July-August Newsletter)

In a clinical trial, one group of subjects is typically given the drug, surgery, etc. being tested, while the control group is given a sugar pill or sham surgery—the placebo. It’s common for the placebo group to show improvement simply because they think they’re getting the ‘real’ treatment and expect improvement. That’s the placebo effect. Researchers subtract the placebo group’s improvement from the real-treatment group’s results to determine the effectiveness of the treatment under study. For example, if the group given the treatment under study shows a 70% improvement and the placebo group shows a 40% improvement, then the difference—70% minus 40% = 30%—is attributed to the treatment itself.

The implication is that the placebo effect isn’t just a complication that has to be accounted for in scientific studies; rather, the expectation of a positive effect is, in and of itself, a healing force—if we can but harness it somehow.

The opposite of the placebo effect is the nocebo effect, e.g., if doctors tell you solemnly that you have a fatal condition and only weeks to live, your
chances of dying soon can be greater than if you hadn’t been subjected to predictions of doom.

Some conditions (e.g., asthma) are more susceptible to the placebo effect than others (e.g., abroken arm). As I understand it, the placbo effect in PD is quite strong, though not necessarily longlasting, and its strength varies from person to person.

And it’s not a simple either/or; positive motor expectations of deep brain stimulation (DBS) seem to have positive (placebo) effect on motor
symptoms while simultaneously exerting a negative (nocebo) effect on cognitive/verbal functions.

(http://www.sciencedirect.com/science/article/pii/S0166432813002593)

I wonder what the nocebo effect is of subjecting ourselves to dire predictions about what’s likely in store for us down the line—does that become at
least in part a self-fulfilling prophesy?

How might we be able to harness the placebo effect? When might it be ethical for a healthcare provider to deceive a patient by prescribing a placebo? Is there a danger of falling into ungrounded, wishful-thinking denial about the realities of the condition? How do we keep ourselves informed about the realities of our condition without the nocebo effect kicking in?

Research in this area is limited, perhaps because there’s more money to be made from surgeries and pharmaceuticals than from understanding the
power (and limitations) of expectations. In any case, you can find more info on the placebo effect as a healing modality by googling “harness
placebo parkinson” and on the power of negative expectations by googling “parkinson nocebo”.

 

“The medicine in our minds,” about the potential of the placebo effect as a treatment modality.
http://www.bbc.com/news/health-26191713

“‘Most family doctors’ have given a patient a placebo drug.” Results of a survey of family doctors (GP’s or General Practitioners) in the UK. http://www.bbc.com/news/health-21834440

“The Nocebo Effect Can Harm Your Health,”

http://www.psychologytoday.com/blog/owningpink/201308/the-nocebo-effect-negative-thoughtscan-harm-your-health

 

Singh at Enloe (from September 2014 Newsletter)

On July 17, 2014, at the Enloe Conference Center in Chico, local neurologist Paramjit Singh, MD, presented an overview of Parkinson’s disease and
fielded questions. The following is a summary of notes taken by Bob Lane, co-facilitator of our support group.

Parkinson’s is a disease of aging in which dopamine production declines at a faster rate than for most people. 1400 are affected out of every 100,000 by age 55 to 64, but by age 85 to 94 this ratio increases to 4,300 out of every 100,000.

 

To determine if a person has Parkinson’s disease, a neurologist must evaluate the whole person. Dr. Singh starts his evaluation by greeting a new patient in the waiting room where he can observe how they get up out of the chair, because posture is affected. The four principle motor symptoms can be remembered by the acronym “TRAP”:
1) Tremor
2) Rigidity
3) Akinesia/bradykinesia (slow movement)
4) Postural instability

The Parkinson’s disease patient’s body is flexed and has balance issues. Their movements are affected including smaller steps, fewer eye blinks,
and less facial expression.

Tremor begins on one side as a “pill-rolling” tremor, which subsides during sleep. Sometimes the tremor affects the jaw.

Rigidity means less flexibility, and implies more difficulty in getting around.

Akinesia/bradykinesia indicates the body’s spontaneous reactions are slowing. The patient doesn’t spontaneously swallow, which can result
in drooling. Later it can lead to difficulty in opening the eyes. There is difficulty in managing the inertia of the body. Other symptoms include
facial expression becoming a blank stare, smaller handwriting, arms that don’t swing when walking, softer voice, and dandruff. In some cases
“freezing-up” occurs, in which the person is unable to move from the spot where they’re standing.

Postural instability refers to general stiffness and weakness.

In addition to the motor symptoms (TRAP), nonmotor symptoms are also possible. For example, a patient may lose their olfactory sense, or have
mood problems including depression and apathy.

When there’s no known cause for the disease, it’s said to be idiopathic. If the cause is known, it’s called “secondary Parkinson’s,” e.g., stroke in the
basal ganglia (dopamine-producing part of the brain), drugs or other toxins, trauma, head injury, MPTP (a neurotoxin precursor), or genetic factors
(familial varieties are very rare).

By the time the Parkinson’s disease patient shows symptoms, dopamine production in the brain has already declined by approximately 70%. It is
possible that stem cells will be able to replace the dead or damaged dopamine-producing cells.

In the early stage of treatment, the symptoms are mild. Everyday activities can continue. In the next stage, the response to treatment is fluctuating.

The early treatment is to have dopamine agonists stimulate the remaining cells to produce MAO type B inhibitors to stop production of dopamine. [When these drugs lose effectiveness, Levodopa is usually prescribed.] As the disease progresses, the patient must take more and more medicine and the frequency of side effects increases, e.g., Levodopa-induced Dyskinesia (involuntary movements).

As the disease progresses further, deep brain stimulation (DBS) becomes the mainstay of treatment. A good candidate for DBS is under 75 and has idiopathic Parkinson’s disease. They should have good cognitive function and motor improvement with levodopa. There should also be no heart or lung disease.

The candidate should have a normal MRI and be able to remain calm during surgery, during which they are awake. One must also be able and willing
to follow up with their programmer.

 

Parkinson’s disease patients should exercise and stretch regularly. Tai Chi is a good exercise for PD, as is walking and bicycling.