Atypical Non-tremor Parkinson’s Can Be Confused With PTSD
“You’re a veteran. All Vietnam vets have PTSD.”
This simple statement misses the mark. Prior to my Parkinson’s diagnosis, I was not diagnosed with any of the symptoms attributable to post-traumatic stress disorder (PTSD). Despite having PTSD ruled out by psychologists twice, it still rears its ugly head. Yes, many vets have PTSD. However, I think there are just as many Parkinson’s patients who have acquired similar symptoms, such as in my case, and have atypical non-tremor Parkinson’s — not PTSD.
In my previous columns, I suggested how Parkinson’s may cause PTSD (largely due to the losses and stress involved). With the discovery of a possible atypical non-tremor Parkinson’s associated with a malfunctioning second dopamine center, I have a fresh take on what may be happening to me.
I did not have life-altering anxiety prior to my Parkinson’s diagnosis. For 40 years, I was a fully functioning member of society with decades of successful employment in several highly cognitive professions. It is the atypical non-tremor Parkinson’s that causes symptoms that present like PTSD and confusion in the diagnosis.
The following information is very clinical but worth reading. A 2013 article from the Journal of Depression and Anxiety states:
“The diagnostic criteria for DSM-5 PTSD include symptoms and signs grouped into five main clusters, including exposure to severe stress (Cluster A), intrusion symptoms (Cluster B), persistent avoidance (Cluster C), negative alterations in cognitions and mood associated with the traumatic events (Cluster D), and hyperarousal (Cluster E). In addition, the duration of the disorder must be more than one month (Cluster F), the disturbance must cause clinically significant distress or impairment in social, occupational or other important areas of functioning (Cluster G), and the disturbance must not be attributable to the physiological effects of a substance or another medical condition (Cluster G). The one new diagnostic cluster (Cluster D) in the proposed diagnostic system for PTSD, which was not present in DSM-IV, involves negative alteration in cognition and mood associated with the traumatic event, as evidenced by two or more of seven listed symptoms.”
If you are a combat war vet like me, then the chances are that you fit the first criterion: exposure to extreme stress. But one doesn’t need combat to meet that criterion. Being told you have Parkinson’s and dealing with the progression can cause extreme stress.
With Parkinson’s, there is an added handicap: the malfunctioning second dopamine center. It malfunctions in a way that mimics PTSD, causing many of the symptoms that are diagnostically associated with PTSD. This includes intrusive thoughts, changes in cognitive functioning, changes in mood, hyperarousal, and significant impairment in functioning. In my case, attribution of PTSD continues to be suggested as a stand-alone clinical diagnosis. It serves as a barrier to quality treatment. The most important part of the PTSD criteria is that the symptoms must not be attributable to an organic malfunction. If the practitioner misses the fact that an organic issue is the main source of the problem, then the result will be poor treatment and poor outcomes.
In my story about the untrained dog crashing through my garden, I mention that the brain places a high emotional value on life-threatening situations. It will further enhance the emotive value of those memories. The higher the emotive value, the more likely it is that the memories will become intrusive. This is because the brain is designed to pay attention to memories that have the highest emotion value — those deemed to be most significant to our survival. It is a system that has served our species well over the past millions of years. The problem with atypical non-tremor Parkinson’s is that it comes with its own version of heightened emotional input due to a faulty second dopamine center. It looks like PTSD, but it is not.
Both extreme trauma and the faulty second dopamine center create heightened emotive input. It can be confusing to both patient and practitioner. If the practitioner can take the time to ask the patient about symptoms associated with a faulty second dopamine center, then it may be possible to improve treatment for those Parkinson’s patients who also have PTSD-like symptoms. I propose we develop new diagnostic criteria and add atypical non-tremor Parkinson’s so that a more accurate diagnosis can be made by practitioners.
Maybe next time I see a neurologist, he won’t say, “You don’t show a typical Parkinson’s presentation. And you may have PTSD.” Instead, the doctor will say with confidence, “You are a textbook example of atypical non-tremor Parkinson’s disease with symptoms that look like PTSD.”
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