Movement disorders are common in patients with autoimmune disorders - affecting the central (brain) and peripheral (body) nervous system. They may be seen in autoimmune disorders triggered by an infectious or toxic agent, as in basal ganglia encephalitis with antibodies against the dopamine-D2 receptors.
Is Parkinson's disease really a deficiency of dopamine or is it an inability to utilize the dopamine hormone? Similar to hypothyroidism or T2 diabetes? We have the hormone but can't metabolize it, so doctors flood our endocrine system with a synthetic hormone to ease symptoms and never treat the underlying cause of hormone resistance.
[For example: when I treated my central (brain) hypothyroidism with natural desiccated thyroid hormone my thyroid gland atrophied because I have hormone resistance not related to thyroiditis from Hashimoto's antibodies, it is caused by injury to the hypothalamic/pituitary/adrenal (HPA) axis. The root cause of my central hypothyroidism is environmental exposure to chemical toxins. The same is true for my central Diabetes Insipidus, I have excess insulin in my blood that my body can't use because the vasopressin/antidiuretic hormone (ADH) receptors are blocked by antibodies. Again, this can been traced upstream to HPA axis injury.]
Chorea or dystonia are usually the most prominent movement disorders in patients with dopamine-D2 receptor antibodies. Movement disorders are also observed in patients with diffuse or limbic encephalitis (brain inflammation) with antibodies directed against neuronal cell-surface antigens. Anti-NMDA receptor encephalitis is on of the most common and may present with a variety of movement disorders, including: chorea, dystonia, myorhythmia and stereotypies. Chorea is also seen in rheumatic disorders such as SLE (Lupus) or antiphospholipid syndrome.
Other motor abnormalities such as faciobrachial dystonic seizure and neuromyotonia (paraneoplastic Isaacs's syndrome which looks a helluv a lot like ALS) are see in LGI1 and Caspr-2 antibodies and Voltage Gated Potassium Channel antibodies (VGKC channelopathy), this is important because they may be a harbinger for the onset of overt limbic encephalitis.
Autoimmunity against the enzyme glutamic acid decarboxylase (GAD) usually presents with movement disorders, most commonly stiff-person syndrome (can also paraneoplastic) or cerebellar ataxia.
Disorders with uncertain autoimmune mechanisms such as Hashimoto's encephalitis and idiopathic opsoclonus-myoclonus syndrome (neuroblastoma) commonly present with tremor, myoclonus and ataxia.
Autoimmune dysautonomia, also know as autoimmune autonomic ganglionopathy (AAG) is a condition in which the body's immune system mistakenly attacks and damages parts of the autonomic nervous system. Symptoms may include severe orthostatic hypertension, fainting, dilated pupils, urinary retention, and dry mouth and eyes. Treatment options include plasmapheresis, IV immunoglobulin, corticosteroids or immunosuppressive drugs.
Antibodies are common in patients with: epilepsy, encephalitis, cerebellar ataxia, SLE/Lupus, Sjogren's syndrome, schizophrenia, mania or stroke. These autoimmune anti-receptor antibodies can bind neurons in a few brain regions, activate glutamate receptors, decrease glutamate receptor expression, impair glutamate-induced signaling and function (glutamate excitotoxicity), activate blood brain barrier endothelial cells, kill neurons, damage the brain, induce behavioral/psychiatric/cognitive abnormalities and ataxia and can be removed or silenced in some patients by immunotherapy.
Tremors have been well described in association with monoclonal gammopathy (a disease that affects the production of gamma globulin and related immunoglobulins). Gammopathy is one of the well-known causes of tremors in the adult population. It can cause both resting and kinetic tremors in the upper extremities. It is supposed that peripheral neuropathy associated with gammopathy is the main underlying cause of tremors in these groups of patients. However, central (brain)causes are also suggested. In this case, we are led to conclude that our patient's tremor was centrally mediated since it responded well to dopamine replacement therapy. Further study is needed to elucidate the role of dopamine depletion in tremors associated with gammopathies. pubmed.ncbi.nlm.nih.gov/349...
Some people will respond well to levodopa-carbidopa treatment. In this case report, the man had a primary diagnosis of Parkinson's disease and started on l-c with significant improvement of his tremors. Blood work showed a significant increase in lambda light chain levels and the presence of an M spike in serum protein electrophoresis. He was found to have multiple myeloma and Waldenstrom's macroglobulinemia - a type of non-Hodgkin's lymphoma. The underlying malignancy was treated with chemotherapy and immunotherapy and the tremor did not recur in the one year follow-up.
The process of paraneoplastic neurological syndromes is presumed to result from an immune attack on the underlying cancer. The different types of cancer antibodies occur in different tumors and lead to different clinical symptoms. A PET/CT using [18F]FDG tracer can help detect tumors in patients with paraneoplastic disease where conventional imaging misses them.
There is an intimate link between Neurodegenerative disorders (Parkinson's/Dementia/ALS), autoimmune disorders and cancer. This isn't new information for neurologists, oncologists and immunologists or even general practitioners.
If movement disorders are common in patients with autoimmune disorders - then isn't the reverse also true? Why aren't people who've been diagnosed with NDD routinely screened for autoimmune/paraneoplastic disease? If you've been diagnosed with PD and an autoimmune disease or cancer - have you been treated with IVIG and plasmapheresis or steroids?
**This blew me away - 1% of people with a Huntington's disease phenotype (trait) do not have the Huntington gene mutation. WTF. Now we have Huntington's Disease-Like syndromes too? The environmental toxins and poisons are becoming more complex.
Treatable conditions should be treated. This is a battle I fight every. single. day. I'd love for people to weigh in and tell their story of cancer/autoimmune/neurological co-diagnosis so that we can shine a light on the complexity and intimacy of these related diagnoses.
Peace,
SE
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This is some deep thinking, that I had not known much about, before. Each day, for me, become quite a challenge, just having PD, and Cerebellar Ataxia, let alone thinking of autoimmune ailments! Ironically, my neurologist is now thinking I may have the auto-immune disorder Myasthenia Gravis, and I’m going through testing on that! Theoretically, this article, and way of thinking, and bringing cancer diagnostics into the picture, does seem logical, and possible, in some individual cases! Further research, an studies, should reflect more info. about autoimmunity and neurological degeneration diseases, such as PD!
I didn't do this before writing my post - I searched the term "is Parkinson's an autoimmune disease" and found this published paper: Parkinson's disease is an autoimmune disease: A reappraisal
I have not been diagnosed with PD (Marc withdrew his diagnosis), but whatever it is that is wrong with me, I believe it is connected to my Hashimoto's.
I am off gluten and off lectins. I do have a bad Pepsi habit, but it is real sugar Pepsi (corn syrup has lectins [I think]).
Hello SE, I am slowly feeling more normal. Less twitching. I have gone back to being left handed on the mouse. But I do a lot of things. I don't mind being Lectin free. Today I created a lectin free BBQ sauce: Strawberry jam (basically sugar and strawberries), and equal amount of minced garlic (from a jar), some apple cider vinegar, a tablespoon of regular cinnamon (not ceylone), and some salt and some garlic powder. It's good.
My husband has had RA for a long time. Then in 2019 had cholangitis, an infection sitting inside his common bile duct. It resulted in sepsis, with later some small cerebellar TIA's. Then he developed Parkinson's symptoms, almost like speed dating. His pelvic stability went, he can hardly hold himself upright sitting. His posture started to get stooped, his gait slow, then came the initiating problems and later the freezing . Drooling started to follow, coughing and almost choking in bed, but unable to turn himself onto the side. Now a bit of a tremor at the end. It'd almost like PD in reverse order.
He has also a rare genetic optic atrophy disorder, so he sees a professor at the Lions Eye Institute every year and genetic testing showed a pathological allele in his OPA1 gene. When his professor saw him in 2019, he immediately made us aware that this genetic mutation can affect other tissues as well in a small selection of patients and present as Parkinsonism. It affects mitochondria, so the optic nerve is the most affected, but brain and muscles also have a lot of mitochondria.
It is a rare condition (only about 5000-10000 cases in the Western world), but it is also a condition, that many more may have, but it never presents as a problem. The condition is called ADOA (autosomal dominant optic atrophy), but for those unfortunate as my husband, it's ADOA+ or ADOA plus, meaning they have more symptoms, which can be Parkinson's like or even MS like.
He is on Madopar, twice daily (morning and mid-afternoon), but not sure whether it helps or not. Probably not, because his best time is always in the mornings, that's far away from his last medication. But we have stopped twice and after a few weeks we panicked when he got worse, so we restarted. It may only have been one of his many downs & ups, we didn't know. He has seen a neuro (said if it looks like PD it's PD), then has seen a movement specialist, who said he thinks it's not PD (he had not so many symptoms then), but didn't offer any further help, was arrogant and and offered no interest in finding someone to refer him on. Our next neuro appointment is in 2023 with a younger PHD neurologist recommended by his Lions Eye institute professor. It's hard having to guess what to do without any guidance, but there is also some hope. Kurt's cells from the rare disease database are with a biotech company in Perth, who are working with his cells to develop a drug candidate. If he gets into a trial that could help to stop or even slightly reverse some of his symptoms. But it's a race against time as his PD symptoms are fast progressing. Vision loss is also progressing, but much more moderately than his PD.
Anyway, the short of this long post is... if there's anyone out there with atypical symptoms and responses to medications and has some vision loss that has been attributed to "a weak optic nerve" then this might be helpful. Just remember, it is rather rare and it has nothing to do with age related macular degeneration or myopia/presbyopia. But I did see a post of someone who said he/she was blind, so if you're reading this or know the person, then this would definitely be something to consider.
Does your husband have vascular PD? I wrote another post about neuroinflammation and the production of reactive oxygen species that might be informative for you.
No, not vascular in this case, the brain vessels appeared normal. But he has RA, which is an auto-immune disease. But you mention that you think that underlying PD is a mitrochondrial defect. In my husband's case ADOA is a defect in the mitochondrial OPA1 gene. It doesn't produce enough of a dynamin-like protein that gives mitochondria stability.
RA has also caused some brain inflammation as seen in white matter on MRI.
Have you looked into the effects of melatonin on optic neuritis? Melatonin has also shown benefit in human PD studies. Melatonin is produced in every mitochondria in the body and acts as a protectant of the mitochondria by neutralizing ROS and RNS rapidly, but by age 50, melatonin production has declined very significantly where it is no longer able to act as effectively to neutralize oxidative stress in the mitochondria allowing the mitochondria to suffer increasing damage from ROS, RNS, apoptosis and inflammation. Melatonin also has antiapoptotic effects as well as anti inflammatory effects. Melatonin is protective of the eyes in general.
If by RA, you mean rheumatoid arthritis, you might do research on borax/boron as a remedy. It is extremely effective for my type of severe arthritis as in no symptoms for well over a decade.
Thanks for that melatonin info. We only tried small dosages (3mg) and only for a short period. Your research sounds very interesting, but my husband is on two blood thinners, so it may not be safe for him. But I also read somewhere that melatonin is also produced during the day and it's activated in your retina, specifically the top half. The article said that this was so that when we spend time outdoors during the sunlight hour, we would get it from above, but also that during dark hours sitting in front of a fire (red light, from below) it would not turn off melatonin production at night. It was also hinted, that Vit D from sunlight is maybe more important than from a supplement.
You get melatonin from the morning and afternoon sun, but it gets a little difficult come winter time or extreme hot summers. Vitamin D you get more from midday sun. I wrote the following about how to get melatonin without supplementing as some people find that melatonin supplements make them too sleepy the next day or otherwise makes them feel off and melatonin obtained naturally does not have these effects. Melatonin and vitamin D seem to have synergy together :
If you are concerned about the blood thinning effect, you might ask his doctor if you can drop one of his blood thinners while you test melatonin. Blood thinners can have unwanted side effects :
Don't forget the borax/boron for different types of arthritis. It works for many people and it also helps to prevent osteopenia and osteoporosis among other things.
First, thank you for sharing your story. Hopefully it can help someone else struggling to find answers. This is so far out of my lane, but I did read that people treated for RA had lower incidence of Parkinson's. Have you considered functional medicine to help rebalance his gut after sepsis? There is a lot of emerging research on the gut/brain connection.
Thank you SE. Unfortunately functional medical practitioners are not so common in my area (Western Australia). Naturopaths are around, but hard to know which ones are good and worth it. Would be great if someone in the forum from Perth has found good practitioners. We just joined Parkinsons WA and hope to get some tips from some of their meetings.
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