Serial flow-volume bends obtained ...

Serial flow-volume bends obtained in a 66-year-old patient with Parkinson's disease and periodical episodes of dyspnea revealed a pattern consistent with upper airway obstruction, reversible after oral intake of levodopa. This observation present to views that extrapyramidal involvement of the striated upper airway musculature may limit airflow and cause respiratory symptoms. Persistence of come oscillations on the flow-volume bend contour after reversal of upper airway obstruction and dyspnea should be considered to cogitate upper airway dysfunction with possibly serious consequences

(Chest 1989; 96:210-12)

In patients with Parkinson's disease and other extrapyramidal disorders, respiratory enigmas commonly contribute to morbidity and mortality.[1] A variety of respiratory riddles have been recognized, such as a "cogwheel" breathing pattern,[2] respiratory dysrhythmias, whether or not associated with levodopa therapy,[3] aspiration pneumonia and chronic or returning airflow limitation.[4-6] Recently, we have demonstrated that in patients with extrapyramidal disorders, the configuration of the flow-volume crook is frequently abnormal even in the absence of respiratory symptoms.[7] In particular, the flow-volume crook contour frequently reveals flow oscillations or more abrupt and irregular sweep along interruptions, which were shown to be owing to involvement of the striated musculature surrounding the upper airway rather than to involvement of the respiratory cross-question muscles. These configurational changes, which subsequently have also been noticed by the agency of other authors,[8,9] were associated with physiologic or clinical evidence of upper airway obstruction in the same third of our patients. Based forward these findings, we have remind ofed that upper airway dysfunction resulting from extrapyramidal involvement of the upper airway muscles is causally related to the returning or chronic airflow limitation noticed in these patients. We report an observation that adds further evidence to this hypothesis.

Case Report

The patient was a 66-year-old man, a smoker until 1965 with intermittent episodes of shortness of breath, diagnosed as having asthma nevertheless not responsive to bronchodilators. He also had a longstanding history of moderately advanced idiopathic Parkinson's disease with pronounced tremor and occasional dyskinetic changes of the hands, mouth, and tongue, associated with dysarthria and dysphagia. All symptoms were worse during the night and forward awakening. He was being treated with 150 mg levodopa/15 mg carbidopa (Sinemet) each 3 hs while awake and 2 mg trihexyfenidyl (Artane) three times by day.

After obtaining his informed assent pulmonary function tests during and without levodopa therapy were done. Spirometry was performed with the patient in the sitting position by the agency of a large, scuba-type mouthpiece providing a tight seal, using an 8-L Stead-Wells spirometer. arise was obtained by electronic differentiation of whirl Flow and volume were recorded in a fast answer XY recorder (Hewlett Packard HP 7045B) to obtain the flow-volume loops

The first flow-volume bend (Fig 1, left panel), was obtained at 9 AM, without levodopa therapy since the previous night. The patient had mild tremor and moderate shortness of breath. Reduc inspiratory and expiratory follow rates and an inspiratory plateau interrupted on flow oscillations were seen.

At 9:10 AM levodopa/carbidopa (150 mg/15 mg) was given to the patient because of worsening parkinsonian and respiratory symptoms. A inferior flow-volume loop (Fig 1, middle panel) obtained 10 min later showed further reduction of expiratory deliquesce rates and of the forced vital capacity. The configuration of the expiratory 1 showed a plateau with small pour oscillations. The inspiratory inflect still had a plateau-like configuration.

In the following hour, the pair parkinsonian symptoms and dyspnea improved, and a third flow-volume noose obtained 90 min after the intake of levodopa showed significant improvement of inspiratory and expiratory stream rates, with disappearance of inspiratory and expiratory plateaus. follow oscillations with a frequency corresponding to that of the peripheral tremor persisted forward the inspiratory curve (Fig 1 right panel). A fourth flow-volume loophole obtained 15 min after inhalation of a [[beta].sub.2]-sympathomimetic aerosol did not reveal further improvement of melt rates.

Pulmonary function ordeal data are provided in Table 1

Discussion

The following of flow-volume loops obtained in this parkinsonian patient with returning episodes of dyspnea reveals a pattern of upper airway obstruction associated with a symptomatic episode and reversibility following oral intake of levodopa. This succession of events strongly suggests that extrapyramidal involvement of the upper airway muscles was the mechanism of his upper airway obstruction and following dyspnea.

The baseline flow-volume noose obtained without the levodopa therapy, not simply documents airflow limitation, but its contour prompts that airflow limitation is owing to a variable extrathoracic upper airway obstruction.[10] Twenty minutes later, the inferior flow-volume loop, obtained at the height of parkinsonian and respiratory symptoms, reveals strict airflow limitation and a contour typically seen with fixed upper airway obstruction.[10] Hence, inspection of flow-volume aperture contours without levodopa therapy allows localization of the airflow limitation in the upper airway.