Parkinson’s and depression
Robin Williams’s widow has announced that he had recently been diagnosed as having Parkinson’s, although the disease was in its early stages.
Parkinson’s is a nasty progressive illness with many many manifestations. It can be treated, but it can’t be cured, and it tends to worsen over time even with treatment, although there’s a lot of variation in severity. Bu think Michael J. Fox, whose attitude can’t be beat but who has become more symptomatic as time has passed.
One of the little known manifestations of Parkinson’s is that patients are commonly depressed, and it is generally thought that much of the depression is the result of the brain changes of Parkinson’s, although it’s hard to know for sure:
For people with depression and Parkinson’s disease, each illness can make symptoms of the other worse. For example, people with both illnesses tend to have more movement problems and greater levels of anxiety than those who have just depression or Parkinson’s disease. Compared with people who are depressed but do not have Parkinson’s, people who have both illnesses may have lower rates of sadness and guilt, but greater problems with concentration. One recent brain imaging study also suggests that people with Parkinson’s disease may have an unusually high number of reuptake pumps for the brain chemical messenger serotonin. Serotonin helps regulate mood, but overactive pumps reduce serotonin levels, possibly leading to depressive symptoms in some people with Parkinson’s disease.
Although people can react to a diagnosis by becoming depressed, the depression in Parkinson’s often appears to precede the diagnosis of the neurological disorder:
The relation between depression and the temporal course of the motor symptoms of PD has been studied in different ways. Two well conducted studies have addressed the idea that psychiatric symptoms (particularly depression and anxiety) may precede motor symptoms of PD by a number of years (as often they do in Huntington’s disease). These studies used a case”“control methodology and found that the odds ratio for a previous history of depression in the PD cases was around 2 compared to controls. The average time between onset of depressive symptoms and motor symptoms was around six years, which correlates well with positron emission tomography (PET) studies suggesting that the onset of the disease process may predate motor symptoms by the same time period.
To me that indicates a physiological basis for many cases of depression in Parkinson’s patients. There’s really no way to tell about Robin Williams, of course. But it definitely could have been a factor.
Addiction, depression, and Parkinson’s. Any one of those I can’t imagine handling.
Parkinson goes from bad to worse. If I still had insurance, I might kill myself if I Parkinson’s just so my family could benefit from it
I respectfully disagree there is a linkage.
For a variety of anatomic and physiologic reasons.
There have been a number of similar linkages. In the pre-CT era, it was held that depression could precede any regional symptoms of pancreatic cancer (pain, loss of appetite, N+V).
In the era of “modern” medicine it was held that peptic ulcer disease and ulcerative colitis were psychosomatic diseases—psychologic diseases with serious organic expressions, able to cause death due to infection, blood loss,etc.. Totally wrong.
More recently it was held that the course of breast cancer was worse in depressed patients.
Almost all of the attempts to link mental illnesses to physical causes and ills (imbalances, Parkinson’s, whatever) have in the end been false. I say almost because I do not claim to have done an exhaustive search. Skepticism is however appropriate.
I would also caution against acceptance of data as “good’ data.For example, why were PET studies done instead of MRIs? Or why not both? What are their diagnostic utilities and differences in the context of depression and basal ganglia disease?
That PET scans “may” show some things does not by itself mean much. Not to me at least.
Don Carlos:
Neither ulcers nor breast cancer nor peptic ulcer disease nor ulcerative colitis are brain diseases, so it is not surprising that the links are tenuous.
Parkinson’s, on the other hand, is a disease that directly affects the brain:
So your analogies are not good ones.
MS, a disease that affects the nervous system including the brain in many cases, also has a higher incidence of depression, much like Parkinson’s.
I have been savaged before by commenters here with medical degrees for speaking anecdotally about my father’s experience with Parkinson’s — apparently because I said things about his experience that contradicted their professional opinions and therefore should not have been uttered by a layperson whose observations of a real and suffering person could not possibly have value — so I’ll be cautious. Anecdote, of course, means nothing. What happened to one person means nothing much about what happens to other people with the same diagnosis. I am speaking only of one person and not pronouncng anything about the disease in general — though honestly, after decades of helping my parents battle it, I do feel that I know a little bit about it.
That said, my father was deeply depressed for many years before he was diagnosed with Parkinson’s. He refused any treatment for the depression, denied its existence and grew worse and worse for maybe a decade, maybe more — it’s hard to pinpoint when these things begin. However, following a belated Parkinson’s diagnosis (his was atypical in some ways at first and took a while to identify), he was placed on medication targeted at the disease while continuing to refuse antidepressants. His bodily deterioration slowed, but of course did not improve, in response to the meds — and the depression steadily lifted. Just when you would think he would have every reason on earth to be depressed, as he slowly, inexorably lost control over his body and speech and gave up, little by little, all of his independence, bodily comfort and pleasures, he became more cheerful and optimistic than any of his children could remember that he had ever been, and continued that way in the face of utter adversity until the last few awful months when only a saint — which he assuredly was not — could have remained positive. Of course I don’t know, and there are many potential explanations, so hold off your dogs if you have a fancy degree of one sort or another and are tempted to loose them on me, please. But it certainly appeared possible to me that his depression was organically related to his disease, rather than an independent phenomenon or a reaction to the devastation that it wrought. His neurologist thought so. It looked that way to most people who knew him. I’ll never know, but I would not be at all surprised to learn that it was so.
The brain has its own regions, just like the brain is a region of the body. One overlooks neuroanatomy and physiology in linking Parkinson’s and depression just because both must originate in the region of the brain.
You may not find my analogies to be good, Neo, but I do not find your “They both occur in the brain” logic to be good either.
and what about conditions where the best “cure” is if people were not so mean, sadistic, and ill informed? wait till the world gets better?
The link between Parkinsonism and depression is not surprising since Parkinsonism is frequently a disease affecting much more than the substantia nigra. For example, many patients with Parkinsonism also suffer with dementia.
The brain does have “regions” but the environmental factors or genetic factors which predispose people to Parkinsonism are not always confined to those “regions” but damage other “regions” of the brain as well.
Well, that’s sad that Williams’ recent diagnosis of Parkinson’s may have factored into his suicide. Learning you have such a debilitating disease (or a disease with a high mortality rate) can be overwhelming. Wish he had given himself to to adjust to the news if this was one of the deciders for his suicide.
On a side note: IIRC, the majority of Jack Kevorkian’s “patients” did not have a terminal disease, they were suffering from depression.
Thanks for addressing this in today’s post. I find the link interesting. My father was not depressed but he was a former alcoholic and a former smoker. The relationship of smoking and Parkinson’s has been addressed by research and it seems to be the nicotine in it.
http://aje.oxfordjournals.org/content/155/8/732.full
and http://www.haaretz.com/news/national/israeli-discovery-explains-why-smoking-slows-down-development-of-parkinson-s-1.459535
I am still interested in finding any research concerning the drugs for Parkinson’s and depression.
BTW Amantadine, another drug used for Parkinson’s is also effective in staving off the flu if you know you have been exposed to it. While my father was ill, everyone in close contact with him came down with the flu. He needed someone who had not been exposed to care for him. I lived in another state, so I contacted my doctor to see what I could do to keep from getting the flu. He gave me a prescription for amantadine and told me it has been shown to either keep one from coming down with the flu or make it a lighter case. I did not get the flu and kept the drug on hand until flu vaccine was available.
Don Carlos…
your not very good are you?
here: Depression in Parkinson’s disease: Convergence from voxel-based morphometry and functional magnetic resonance imaging in the limbic thalamus
Our results showed decreased activation in the left mediodorsal (MD) thalamus and in medial prefrontal cortex in PD patients with depression compared to those without depression. Based upon these results and the increased neuron count in MD thalamus found in previous studies, we conducted a region of interest (ROI) guided voxel-based morphometry (VBM) study comparing the thalamic volume. Our results showed an increased volume in mediodorsal thalamic nuclei bilaterally. Converging morphological changes and functional emotional processing in mediodorsal thalamus highlight the importance of limbic thalamus in PD depression. In addition this data supports the link between neurodegenerative alterations and mood regulation.
i work in one of the worlds top medical schools
we do a lot of research here, and i read an aweful lot of it… and i have a memory similar to rain mans…
[in fact, its something that those who use me for my talents are always amazed at, and the speed of recal and ability to go find the papers to prove my point]
Depression is the most common psychiatric disease in Parkinson disease (PD) occurring in approximately half of patients.
PD patients have more depressive symptoms than other comparable chronic disabling diseases (Cole et al., 1996 and Nuti et al., 2004)
Depressive symptoms are seen before motor symptoms in 12—37% of PD patients (Taylor et al., 1986)
patients with depression and PD fail to produce a euphoric response after administration of methylphenidate. The effect produced by this agent depends on the integrity of dopamine mesolimbic pathways, implying that degeneration of dopamine neurons is probably involved in the mechanisms leading to depression in PD (Cantello et al., 1989).
if you want i can pull lots and lots of stuff for you so you can stop going around spouting old data if it even was data…
Dopamine Modulates the Response of the Human Amygdala: A Study in Parkinson’s Disease
Transient Acute Depression Induced by High-Frequency Deep-Brain Stimulation (jama)
Negative symptoms: A review of schizophrenia, melancholic depression and Parkinson’s disease
Deep brain stimulation for Parkinson’s disease dissociates mood and motor circuits: A functional MRI case study
time to go back to school and update your knowlege as a lot has changed since we called docs sawbones..
[and thats a jibe, not a insult… take it as such]
Art castigates me for using old data, which I did not do. I cited historical examples of erroneous associations. And then he cites a 1986 reference. But I appreciate the literature search, Art, even though I am not sure you know what this stuff really means.
So what are you all going to say about the high incidence of psychosis in cases of Parkinson’s? You didn’t cite that (see uptodate.com)
Anecdote means “magic” to the empirically trained scientist. His own observation, however, is “data” because the scientist filters the observation through tests, which were designed (until PC set in) on past findings and conclusions of science and a dedication to find the truth. Still, the “layman,” lacking the Tests, sometimes (not often, but sometimes) advances more quickly than the scientist, who, due to the Tests, doesn’t know how to see. In fact, most “HUGE” scientific discoveries fit this model where the scientist with the new theory or discovery is analogous to the layman with his/her magical anecdotes.