Biomedical subjects
Publications and source records attributed to J Cummiskey.
A 34-year-old woman with a history of chronic nephropathy, kidney transplant rejections, and repeated hemodialysis developed symptoms of automatic respiratory failure during all states of sleep. The neuropathologic examination revealed symmetric brainstem lesions, explaining the sleep-related respiratory failure. Histology affirmed the diagnosis of Leigh's disease.
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The disease activity in five patients with sarcoidosis were studied by "conventional" tests over a period of 1 to 3 years. The value of bronchoalveolar lavage (BAL) angiotensin converting enzyme (ACE) activity was examined for its usefulness in predicting disease activity. Gallium scans were positive in 4 of the 5 patients, serum lysozyme in three patients, bronchoalveolar lavage (BAL) lymphocytes were elevated in five patients (three greater than 27%), serum ACE was elevated in one patient and the chest roentgenogram had deteriorated in one patient. Pulmonary function tests were unchanged in all five patients. Patients were ranked in order of activity based on these "conventional" tests. The ranking of activity correlated with the ACE activity in the bronchoalveolar lavage when expressed per micrograms lavage protein. Control subjects had a BAL ACE activity of 7.8 +/- 4.5 units/micrograms protein (p less than 0.05). There was no significant difference in the lavage protein in the control (29 +/- 24 micrograms/ml) compared to the sarcoidosis patients (31 +/- 6 micrograms/ml). We concluded that: (1) the changes in ACE activity in bronchoalveolar lavage represents a real increase in production or decreased clearance of ACE by the lung; (2) BAL ACE is not elevated due to increased permeability of pulmonary capillaries; (3) BAL ACE is a useful measure of disease activity in sarcoidosis patients.
We studied five male nonobese patients (mean age, 61 years) who had moderate chronic obstructive pulmonary disease (COPD). Each patient underwent three successive nights of systematic monitoring of sleep variables. On nights 2 and 3, patients received placebo and flurazepam (30 mg). Patients were also given flurazepam (15 mg) for seven consecutive nights and underwent sleep monitoring on nights 1 and 7. Two patients exhibited oxygen desaturation during rapid-eye-movement (REM) sleep, both spontaneously and after administration of flurazepam. The three other patients had no nocturnal oxygen desaturation, either spontaneously or after ingestion of flurazepam. We concluded that sleep-induced respiratory abnormalities are not systematically worsened by flurazepam. Flurazepam (15 mg) had no effect on the sleep disturbances of our patients with COPD after seven nights of administration.
In order to determine whether reversible alterations in ventilatory control are found in obstructive sleep apnea syndromes, 5 male patients 31 to 57 yr of age presenting with the syndrome were polygraphically monitored before and several times during the 6 months after tracheostomy. They also had a hypercapnic ventilatory response study before surgery and again 3 months after surgery during the daytime. A dramatic decrease in overall apnea index was seen immediately after surgery, but the number of central apneas and the central apnea index did not reach low values until several months after tracheostomy. Ventilatory response to CO2 improved in all cases after surgery.
Tracheal sound recordings and O2 saturation were compared with conventional recordings of respiratory events (thermistors, strain gauges, and O2 saturation) in 14 patients referred for assessment of sleep apnea syndrome. There was no significant difference in the number of respiratory events associated with desaturation recorded during the sleep by the two methods. Tracheal sound recordings were more useful in analyzing the cause of the respiratory event. Hypopnea without desaturation was seen more often with tracheal sound recordings than with the conventional methods. The durations of apneic and hypopneic events were significantly longer when recorded by thermistors and strain gauges than by breath sounds.
Obstructive sleep apnea syndrome (OSAS), a disabling disorder that leads to life-threatening cardiorespiratory events during sleep, has been treated by tracheostomy. This article reports long-term follow-up data of 50 patients who have undergone this procedure, and the indications for surgery are summarized. Surgery may result in secondary local and general acute and subacute complications, but, on a long-term basis, patients were completely relieved of clinical symptoms, returned to full activity, and adapted normally to social and familial life. Temporary closure of the tracheostomy during sleep led to recurrence of obstructive sleep apnea.
Twenty-six patients with chronic obstructive airflow disease (23 also complained of excessive daytime somnolence) were monitored during sleep, using noninvasive techniques, for evaluation of respiratory and sleep variables. Ten of the 26 had a second more extensive evaluation, including measurement of endoesphageal pressure; 5 underwent a study of nocturnal hemodynamics, with measurement of systemic and pulmonary pressures; 5 received O2 in air during sleep under controlled conditions. Eight of the studied patients underwent tracheostomy and were restudied postoperatively. Both sleep stage and type of abnormal respiratory event during sleep affected oxygenation levels. A mean of 92% of all abnormal respiratory events during sleep contained an obstructive component. Apneic events may affect systemic and pulmonary arterial pressures during sleep. Administration of O2 in air may, in some cases, be detrimental to the sleeping patient. Tracheostomy unexpectedly improved the daytime, awake blood gas readings of somee patients. The mechanism of daytime somnolence was not elucidated in all cases.
To determine if a familial abnormality in the control of breathing might explain the reasons for the sudden infant death syndrome (SIDS), three groups of parents were studied. The first (N = 8 sets of parents) had one infant die of SIDS (one SIDS), whereas the second (N = 6) had a SIDS victim plus a second child with a "near-miss" occurrence (two SIDS). When compared to the third group (controls), these parents demonstrated no abnormality in the ventilatory response to hypoxia or hypercapnia. Similarly, they had normal respiratory frequency, tidal volume, inspiratory time, and arterial blood gas tensions. We conclude that a familial abnormality in breathing control measured during wakefulness is not the basis for SIDS.
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Six young male patients with grade I (mild) myotonic dystrophy and a complaint of excessive daytime sleepiness were studied during wakefulness and sleep. Pulmonary function tests during wakefulness showed evidence of mild abnormality related to respiratory muscle weakness. During sleep, some patients developed a sleep apnea syndrome with high sleep Apnea Indices. There was no relation between hypoxic and hypercapnic ventilatory responses during wakefulness and sleep Apnea Indices. But hypoxemia and hypercapnia worsened considerably during REM sleep. Myotonic dystrophy patients with sleep apnea presented increased pulmonary and systemic arterial pressures during sleep. It was also during sleep that arrhythmias were observed.
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