Parkinson’s disease is the most common movement disorder in developed countries. Even with levodopa therapy the cause of death in such patients is commonly respiratory. Characteristic findings in such patients are a reduction in both maximal static inspiratory and expiratory pressures as well as maximal inspiratory and expiratory flows. Moreover, such patients are unable to generate a rapid rise in peak expiratory flow which may be important for a maximally effective cough, a finding consistent with the hypokinesia typical of the condition. These abnormalities were shown to be correctable in a substantial proportion of patients by the administration of apomorphine. Interestingly, patients with early Parkinson’s disease and normal respiratory muscle strength are markedly less able to perform repetitive bursts of respiratory muscle work than age matched controls. Problems in the coordination of activation of respiratory muscle also seem to be responsible for the dyspnoea which can occur in patients with dystonia.

Upper airway flutter is sometimes found on the flow volume loops of parkinsonian patients; this indicates upper airway dysfunction and sleep abnormalities might therefore be expected. Obstructive apnoeas are more common in parkinsonian patients, but a range of other abnormalities are also found which result in fragmented sleep architecture. In the related condition of multisystem atrophy, glottic narrowing during sleep has been suggested as a possible cause of sudden nocturnal death. This is not always detectable by fibreoptic examinations conducted while the patient was awake, and polysomnography may therefore be indicated in symptomatic patients. However, in another study of patients with progressive supranuclear palsy, frequent desaturations were not found.

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12 Replies

  • Just when I thought I heard it all...

    Something else to look forward to. Does that happen to everybody with Parkinson's if you live long enough?

  • unknown the frequency but now we know what to watch for as our PD experience/symptoms list grows

  • I take amantadine alone. Is it a neurotoxic drug one may ask. I am trying to discover if that is the cause of my unilateral lung diaphragm paralysis.

    ref. so far:

    A common-sense approach to treatment of diaphragmatic paralysis can include:

    •Remove/treat any obvious contributing factors (hypokalemia, hypophosphatemia, high-dose steroids, neurotoxic drugs, neuromuscular blockers).

  • Roy did you stop taking Sinemet? And know only Amantadin which my nero px for stiffnes reply to this issue please

  • I stopped, one by one, sinemet, ropinirole and neupro. I use amantadine, 2x / day. Still tremor my most irritating symptom. What next!

  • RoyProp

    Does amantadine helps with stiffness? if you have that symptom?

  • I am not stiff. Cannot say it is the amantadine.

    I am still "fluid" in my choice of medication. Now will see about moving back to C/L after viewing Doc Fahn on this video >

    Doc. Stanley Fahn

    World-famous leader in movement disorders, Dr. Stanley Fahn was the keynote speaker discussing myths and misconceptions in PD, and several members of the University of Florida Center for Movement Disorders and Neurorestoration also spoke and participated.



    Myth 4. “No response to Sinemet 25/100 three times a day is considered a non-responder.”

    a.Each person should be treated individually and each may require a different dosage of Sinemet to get a response.

    b.Some physicians fail to push the dose after it reaches 300 or 600 mg/day.

    c.My “limit” is 2,000 mg/day.

    Parkinson’s disease (PD) is explained through animation. The video focuses on five main factors: causes, symptoms, diagnosis, treatment and the pathology of Parkinson’s disease.

    7:28 Benztropine helps w/ tremors

  • RoyProp

    What is Diaphragmatic Paralysis?

  • paralysis of one or both diaphragms located below the lungs and controlled by two, phrenic nerves. Diaphragms move the lungs to inhale or exhale air.

  • Is this a by product of the disease or a side effect of the meds (sinemet, amantadine etc) - I notice my mom has shallow breathing, and I always tell her to take deep breaths all the time ...

  • I have no answer. In the meantime, thiamine (Vit B1) therapy is my interest in asking why is it not getting more attention?

    Recently a considerable improvement of motor and non-motor symptoms in patients affected by PD was observed with intramuscular daily doses of 100–200 mg of thiamine.

    In this report we describe the results obtained from three patients with newly diagnosed PD. We have decided to treat the patients with high doses of thiamine in order to clarify the potential effect of vitamin B1 alone in the initial therapy of the disease.

  • All muscles need dopamine to work i thought.. Diaphragm is a muscle isnt it? Pre. Drug treatment llife span. About 10 yrs.

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