Knowledge is power ....learn about your disease.
Shortness of breath, a 'wearing-off' symptom in Parkinson's disease.
Khan W, Naz S, Rana AQ.
Clin Drug Investig. 2009;29(10):689-91. doi: 10.2165/11315290-000000000-00000.
PMID: 19715385
Respiratory function in Parkinson's disease.
Shill H, Stacy M.
Clin Neurosci. 1998;5(2):131-5.
PMID: 10785839 Review.
Upper airway muscles dysfunction and levodopa responsiveness in Parkinson's disease.
Brescia Morra V, Polverino M, De Luca G, Landi P, Galdi A, Campanella G.
Acta Neurol (Napoli). 1992 Aug-Dec;14(4-6):512-8.
PMID: 1293993
Respiratory dysfunction in Parkinson's disease.
Brown LK.
Clin Chest Med. 1994 Dec;15(4):715-27.
PMID: 7867286 Review.
Obstructive and restrictive pulmonary dysfunction increases disability in Parkinson disease.
Sabaté M, Rodríguez M, Méndez E, Enríquez E, González I.
Arch Phys Med Rehabil. 1996 Jan;77(1):29-34. doi: 10.1016/s0003-9993(96)90216-6.
PMID: 8554470
Here's a review just published last month:
ncbi.nlm.nih.gov/pmc/articl...
"The presence of respiratory symptoms in Parkinson's disease (PD) has
been known since the first description of the disease, even though the
prevalence and incidence of these disturbances are not well defined.
Several causes have been reported, comprising obstructive and
restrictive pulmonary disease and changes in the central ventilatory
control, and different pathogenetic mechanisms have been postulated
accordingly. In our review, we encompass the current knowledge about
respiratory abnormalities in PD, as well as the impact of
anti-Parkinsonian drugs as either risk or protective factors. A
description of putative pathogenetic mechanisms is also provided, and
possible treatments are discussed, focusing on the importance of
recognising and treating respiratory symptoms as a key manifestation of
the disease itself. A brief description of respiratory dysfunctions in
atypical Parkinsonism, especially α-synucleinopathies, is also provided."
It's a good review, but I don't think it goes far enough - I don't think the authors have fully explored all the possible mechanisms involved in respiratory dysfunction in PD. OTOH, I am gratified to see they drew parallels between NMLS and NMS:
" a significant reduction of anti-Parkinsonian drugs are risk factors for
the so-called neuroleptic malignant-like syndrome (NMLS), a rare but
severe clinical condition, resembling the well-known neuroleptic
malignant syndrome, characterised by hyperthermia, impaired
consciousness, autonomic dysfunction (e.g. respiratory failure) and elevated serum creatine kinase levels."
I suspect there are similar mechanisms involved in SUDPAR.
Some possible avenues for discussion and research:
- autonomic nervous system dysfunction leading to immune dysregulation which could cause chronic inflammation and increased vulnerability to infection
- direct effects of a-syn pathology on immune cell function
ncbi.nlm.nih.gov/pmc/articl...
- peripheral dopamine and its effects on the Na/K ATPase in lung epithelium
ncbi.nlm.nih.gov/pmc/articl...
- role of serotonergic system (it's implicated in sudden death in PD and MSA as well as SIDS, and is involved in ventilatory response generally)
pubmed.ncbi.nlm.nih.gov/194...
Very Nice! Ta for that! cheers!
more speculative - just want to add this in case I forget about it - the role of paraoxonase in oxygen sensing in the periphery. There is evidence for AMPK's role in peripheral oxygen sensing with feedback to ventilatory control in brainstem; it might act through the AMPK/PON1 signalling axis (the latter statement is just speculation).
PON1 gene variants are associated with PD, and it is thought that these variants increase susceptibility to damage from environmental toxicants such as organophosphate pesticides which could initiate the disease process. I don't know if PON1 has a role in the ongoing PD disease process. I'm also very interested in PON2 as it is expressed much more highly in females than males; it is localized in mitochondria and is probably not directly involved in response to pesticide exposure; it interacts with coenzyme Q10.
There was a medical hypothesis-type article that suggests flavonoids for prevention of SUDPAR; I like the idea but have to admit that not much evidence was presented:
kenkyugroup.org/article/9/1...
High flavonoid foods like blueberries and acai unpregulate PON1 expression. Acai also increases erythropoietin production - perhaps by acting as a hormetic effector, mimicking hypoxia:
ncbi.nlm.nih.gov/pmc/articl...
An interesting sort of related factoid is that cetaceans (whales and dolphins) have evolved to lack PON1 activity. It may have something to do with adaptations diving; type of dietary fat intake is another possibility:
youtu.be/S36zqLDrecI?t=200
{ sorry I'm blathering on about this stuff; it keeps my mind off of other things... }
thanks! ive been more or less aware of this data or lack thereof but i eat the rainbow because of the role of flavonoids , like berries. Im pretty concerned of SUDPAR. Thank you!