Karl, I wouldn't worry about the machine making your PD worse. Possibly, the dopamine reuptake mechanism is temporarily affected, but this doesn't mean your PD is getting worse because of it. Also:

"Effects of the Obstructive Sleep Apnea Syndrome (OSAS): Patients with obstructive sleep apnea syndrome (OSAS) ( which includes difficulty sleeping, sleep fragmentation and nocturnal hypoxemia) have sown short-term memory and cognitive impairment."

That sounds pretty bad, too, so OSAS should be addressed.

Also, PWPD respond subnormally to hypoxia which can be dangerous, so it should be avoided:

Parkinson's disease and impaired chemosensitivity to hypoxia

Correspondence

Parkinson's disease and impaired chemosensitivity to hypoxia

Hiroshi Onoderaa, Corresponding Author Contact Information, Shinichi Okabeb, Yoshihiro Kikuchib, Takehide Tsudab and Yasuto Itoyamab
aDepartment of Neurology, Tohoku University School of Medicine, Sendai 980-8574, Japan
bFirst Department of Internal Medicine, Sendai, Japan

Available online 1 April 2005.

Refers to: Parkinson's disease and impaired chemosensitivity to hypoxia
The Lancet, Volume 356, Issue 9247, 16 December 2000, Page 2099
Georg Röggla, Wim Weber and Martin Röggla



Authors' reply

Sir—We reported that patients with Parkinson's disease had an impaired hypoxic ventilatory response (HVR) accompanied by blunted perception of dyspnoea, even at an early stage of disease. Since dopamine decreases HVR and dopamine receptor antagonists increase HVR,1 Georg Röggla and colleagues raise an important issue; whether the disease itself or the therapy is causal for impaired HVR. We believe that Parkinson's disease itself impairs the chemosensitivity to hypoxia, as evidenced by the fact that parkinsonian patients taking no drugs that affect dopaminergic functions (levodopa, dopamine-receptor agonists, or both) had a significant reduction of HVR compared with controls.

We compared HVR in patients who had no history of taking dopaminergic drugs (mean age 54ˇ2 years [SD 9ˇ7]) with that in patients taking levodopa, dopamine-receptor agonists, or both (mean age 60ˇ2 years [SD 7ˇ6]). Patients with Parkinson's disease (Hoehn and Yahr stage 2–3) and controls (mean age 53ˇ8 years [9ˇ5]) did not smoke and had no history of respiratory disorders during the previous 6 months. In the hypoxic test, end-tidal carbon dioxide tension (PETCO2) was maintained at the value of each participant's resting PETCO2 during the procedure. The chemosensitivities to hypoxia were expressed as the slope of the regression line relating ventilation to changes in oxygen saturation in arterial blood calculated by least-squares linear regression analysis and measured in L/min, divided by the percentage change in saturation. All patients and controls had normal basic pulmonary functions, such as vital capacity, forced expiratory volume in 1 s, arterial oxygen tension, and arterial carbon dioxide tension.

Chemosensitivity to hypoxia was significantly lower in parkinsonian patients taking dopaminergic medications than in controls. Patients who received no dopaminergic medication had significantly lower HVR than controls. Interestingly, the degree of impairment in HVR of patients without dopaminergic medication was similar to that of patients taking these drugs. These results clearly show that Parkinson's disease itself impairs the chemosensitivity to hypoxia. Dopaminergic drugs at the doses commonly used to treat patients with Parkinson's disease might not, therefore, impair further the HVR in patients with Parkinson's disease. Investigation would be useful of whether dopamine receptor antagonists that do not cross the blood-brain barrier could have a beneficial effect on HVR in patients with Parkinson's disease.2 As Röggla and colleagues mention a study is needed of whether patients with Parkinson's disease have a higher risk of respiratory disorders or sudden death in conditions than non-parkinsonian patients when hypoxia is induced, for example, while flying or at high altitude.

The impaired HVR in Parkinson patients cannot be explained solely by a dysfunction of the dopaminergic system. If only dopaminergic systems in the carotid body were damaged in Parkinson's disease, patients would have higher HVR than controls.1 and 2 We must take into account the possibility that other neurotransmitter systems commonly affected in Parkinson's disease, such as serotonergic or noradrenergic systems, play a critical part in the impaired HVR.3

http://www.sciencedirect.com/science...f66f6aac8aa8d6