Ask The Expert: Answers To Your Questions On Parkinson’s Disease
Is Parkinson’s caused by bacteria? Can you recommend resources for caregivers of Parkinson’s patients? Dr. Zoltan Mari, director of the National Parkinson’s Foundation Center of Excellence at Johns Hopkins School of Medicine, answered these listeners’ questions and more. Some questions have been edited for space and clarity.
Q: Can you discuss the possibility that Parkinson’s is caused by bacterial infections? I’ve read that things like Lyme tick bacteria can cause Parkinson’s. True? – From Jane via Facebook
A: There is no convincing evidence of a bacterial etiology for Parkinson disease. Some infections may produce parkinsonism, with very similar presentation to Parkinson disease. These include viral encephalitides, which are very rare. Between about the two World Wars there was an epidemic called “encephalitis lethargica” (von Economo disease), a suspected viral infection (they never actually managed to isolate the virus) which rendered thousands severely parkinsonian – kindly depicted in the movie “Awakenings.” However, no bacterial infection has been linked to Parkinson disease or parkinsonism. There are hypotheses related to an immune-mediated mechanism that might play a role, but Lyme disease specifically has not been linked to PD with credibility.
Q: Is there a good place to start looking for information so families of Parkinson’s patients can help their loved ones? Also, is there a diet that can help with the symptoms or side effects from the medication? – From Angel via Facebook
A: The NINDS, The MJFF, and the NPF all have significant and highly useful web presence to provide advice on all daily issues relevant to patient’s with PD and their families. For example, the NPF has a great selection of brochures to advise on a number of topics, including nutrition.
Q: I have restless leg syndrome, which is remedied with Vitamin E as opposed to prescription medicines. I’ve heard that RLS is a precursor to Parkinson’s. Is that true and, if so, is there anything that can be done earlier instead of later? – From Crys via Facebook
A: While RLS is related to PD (its prevalence is increased in PD compared to the general population; both PD & RLS can improve with dopamine agonist medications), the relationship is not clear at the moment. RLS does not appear to be a so called “prodromal” condition for PD and as far as we know, having RLS does not significantly increase the risk of PD later on. Another condition, REM Behavior Disorder (or RBD), however, is a well-known risk factor/prodromal condition.
Q: Linda Ronstadt has lost her ability to sing due to Parkinson’s. Do all singers who come down with Parkinson’s lose that ability? – From Kristin via Facebook
A: No. In fact it is somewhat unusual (albeit possible). Interestingly, the opposite situation can sometimes be seen, in which patients who have significant speech impairment can still sing.
Q: What is the latest on studies focused on nicotine, both as a treatment and from diminishing a user’s chance of getting Parkinson’s? – From Eric via website
A: Nicotine does not appear to be a good treatment for the symptoms of PD, the way for example levodopa is. However, it is being looked at as possibly reducing the risk of developing the disease or slowing down progression. Those putative effects (prevention, disease modification) have not yet been conclusively proven, but remain possible. It has been observed that those who smoke cigarette, while increasing their risks for diseases more deadly than PD, have a lower risk of PD than that of nonsmokers. Research is currently under way to investigate this further.
Q: Has there been any research conducted using herbs, vitamins and nutrition to treat and prevent Parkinson’s? – From Valencia via email
A: Unfortunately, research has been rather limited in this area. Therefore, for the most part we don’t really know for certain whether these natural agents may or may not have an impact on PD. It is probable they are not very effective. They may be safe though and usually inexpensive. Since the chances of them being highly effective are low, there remains little scientific or industrial interest in funding such research.
Q: I have a friend who has been diagnosed with something called “essential tremor,” and her doctor tells her that this was caused by a medication she takes for some other condition. However, she also exhibits some of the non-motor symptoms related to Parkinson’s you have discussed. What is the difference between Parkinson’s and “essential tremor?” Are the two easily misdiagnosed? – From Pam via email
A: Essential tremor is another disease, although its definition or even existence have been recently questioned and reviewed. In any case, ET is a disease much different from PD in that it is considered a mainly tremulous disease that does not display the classical parkinsonian motor symptoms besides tremor (slowness, stiffness). Whether imbalance is part of the ET phenotype is questionable, but more than likely yes. The rate of progression and the overall disability in ET is generally far less than PD. The tremor is different in that ET patients shake when they are moving and attempting to use their hands (such as holding a cup of writing), whereas in PD tremor is characteristically “resting”, i.e. worse when the hands are relaxed and tend to reduce when the hands are used in active tasks. Also, ET is often familiar, whereas PD is rarely familiar. ET is more common than PD.
The relationship between ET and PD is not fully known, but we do know that those who have ET are more than 4x greater likelihood of coming down with PD later in life than the general population.
The friend you are describing may or may not have ET, but ET is a primary idiopathic brain disease and is not caused by medications. However, there is another kind of tremor, which is called “exaggerated physiological tremor” and it is even more common than ET. Most tremor that’s seen as a medication side effect is of this variety and it can resemble ET very closely. Another common cause of exaggerated physiological tremor is hyperthyroidism and this is also the kind of tremor we all have if we drink too much coffee.
Q: We know that people who have hyperthyroidism have very little incidence of heart disease. Are there any known medical conditions which seem to confer some similar degree of “immunity” from Parkinson’s? – From Bob via Facebook
A: As mentioned above, it seems that patients who smoke may have a somewhat reduced risk of PD (of course no one should ever smoke thinking this protects them from PD as while that may or may not be true, what’s certain is that the downside from increased cancer risk far outweighs the putative PD protection benefits). Another recent observation is that people who exercise regularly could see their PD progression slow down or even have a slightly reduced PD risk. This is a very active area of research and many other environmental factors and possibly neuroprotective agents are being investigated in this context.
Q: I once watched a documentary on Lyme disease, and it claimed that upwards of 75 percent of people diagnosed with neurological diseases such as Parkinson’s also tested positive for Lyme disease. Can you elaborate on any connections between Lyme disease and other major neurological disorders such as Parkinson’s? – From Joe via email
A: Unfortunately the possible connection with Lyme disease has been blown out of proportion and this seems to be reflected in public awareness, as Lyme disease almost always comes up in every Parkinson Q&A often at the expense of more important aspects of the disease. There is no compelling evidence of a specific connection between Lyme disease and PD. PD has a specific pathology that is well described and has nothing to do with Lyme disease or the bacteria causing Lyme disease. Lyme disease is due to bacterial infection and can be treated with antibiotics. There have been a growing number of believers in “chronic Lyme”, a vague collection of syndromes attributed to some ongoing chronic pathology that may be responsible a large number of varied and mixed symptoms, but without a clear organic link. I am sorry to say that Lyme titers (serological biomarkers of active or past Lyme infection) have been misused to support these questionable theories. In any case, there are no controlled and high quality research studies to indicate that there’s a true increase in Lyme in PD patients and I doubt much effort will or should be devoted to this as there doesn’t appear to be any specific biological connection between (at least the idiopathic form of) PD & Lyme disease.
Q: I take two medicines that affect dopamine and wonder if taking these for decades could result in a higher likelihood of getting Parkinson’s? I have no family history of Parkinson’s or dementia, and have a healthy diet, exercise and also have (treated) hypothyroidism. – From Jen via email
A: Without the specifics, it is difficult to know. We do know that certain chemicals, such as pesticides & toxins (e.g. rotenone, paraquat, MPTP) can cause parkinsonism. I am not aware of any currently approved medications that also increase that risk. As mentioned before, however, exercise may reduce your chances of coming down with PD (and it is healthy anyway).
Q: My grandfather has Parkinson’s and was diagnosed with Lewy Body Dementia. Could you talk of any correlation and prognosis, and how to help? – From @aswathwood via Twitter
A: Some people believe LBD is a variant of PD. Both are so-called “synucleinopathies”, diseases where there is pathological processing of a protein called alpha-synuclein. When this protein misfolds and then aggregates within the cells it forms “Lewy bodies”, which can be seen both in PD and LBD. Clinically the distinction between LBD and PD is based on the timing of how motor and nonmotor problems appear relative to each other. If significant nonmotor problems (such as dementia or psychosis/hallucinations) appear within 1 year of the onset of motoric parkinsonism (such as slowing, loss of dexterity, imbalance, tremor, stiffness) then by definition the diagnosis is LBD. I don’t know the specifics of your grandfather’s presentation, but if he had classical PD presentation without much nonmotor problems (dementia/psychosis) for years and then started having these, clinically he doesn’t necessarily meet diagnostic criteria for LBD. In terms of how to help, the mainstay of therapy would be symptomatic. If he needs PD medications it is likely he would benefit from levodopa more than dopamine agonists if there is a concern about LBD or nonmotor problems reminiscent of LBD, as dopamine agonists tend to be very poorly tolerated in LBD. If nonmotor symptoms are causing much disability, those can be addressed. There are multiple different medications to enhance memory (such as donepezil) and which one and how much should be used must be highly individualized. Also, the psychosis can be often mitigated by atypical antipsychotics such as quetiapine and clozapine. Please note that other antipsychotics are contraindicated.
Q: Please discuss neuroplasticity and the benefits of exercise for Parkinson patients. – From @DawnDaria via Twitter
A: As I mentioned above, there is increasing interest in the benefits of exercise. It is possible it can reduce the risk of PD and it is even more possible it can slow down the progression of the disease. We do not know why exactly this is. That itself (the putative mechanism of action) is subject of intense speculation and research. There are some theoretical bases to support the idea of enhanced neuronal plasticity in exercise. It is known that neuronal plasticity doesn’t stop in youth, but continues to old age and it is a likely mechanism that is capable of offsetting some of the ongoing pathological damage from PD that destroys cells and networks. I expect that the area of exercise and its effects on PD, PD risk, and PD prognosis/disease course will remain a very hot area of research.
Q: What is hardest for primary caregivers about caring for someone with Parkinson’s, and how can caregivers be best supported by their family and friends? – From Kirsten via Facebook
A: It depends. Some recent research demonstrated that those who see PD patients all the time are more adept in recognizing common warning signs, problems, and more readily able to apply the best treatment options. Treating PD is non-obvious. Rather complex motor and nonmotor problems need to be managed in a constantly changing, dynamic environment throughout the progression of the disease, appearance of new problems, worsening of others, with medications’ side effects changing as well. While early stage and stable PD patients may be well served by regular checkups done at their PCP’s office, it is recommended that a Parkinson specialist (or with another expression “movement disorder neurologist”) evaluate the patient at around the onset of the problem (to ensure that the diagnosis is correct) and intermittently afterwards, especially if new problems emerge. I personally like to work with other providers, including general/community neurologists and PCPs, which may be geographically closer to the patient and can see the patient more often and I am happy to counsel them on PD management when complicated problems are encountered. Another option to help such checkups if there are geographical barriers is an emerging new way of conducting “virtual visits” through telemedicine.