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Biomedical subjects

D S Sax

Publications and source records attributed to D S Sax.

At least 37 records · Page 2Linked to original sources
PubMed1979

Sacral signal tracing: the electrophysiology of the bulbocavernosus reflex.

We studied 52 men with electrophysiologic testing of the bulbocavernosus reflex to determine reflex latency. The bulbocavernosus reflex was demonstrated to be a segmental polysynaptic reflex with cross-over in the sacral spinal cord. Excellent correlation was obtained between prolonged latency and clinical evidence of neuropathy. The examination may be useful clinically to evaluate patients suspected to have sacral cord lesions or pudendal neuropathy (for example impotence, chronic back pain and lesions of the cauda equina and peripheral nerves).

Adult↗
PubMed1979

Peripheral neuropathy in arsenic smelter workers.

We conducted a double-blind controlled study of individuals exposed to arsenic trioxide in a copper-smelting factory. Subjects fell into three categories of peripheral neuropathy: none, subclinical, and clinical. The subclinical group had no symptoms or signs of numbness or reduced reflexes, but did have reduced nerve conduction velocity and amplitude measurements. Clinical neuropathy groups had signs and symptoms of neuropathy and electrophysiologic abnormalities. The clinical and subclinical groups correlated with increased content of arsenic in urine, hair and nails. The incidence of subclinical and clinical neuropathy was greater in arsenic workers than in unexposed controls.

Adult↗
PubMed1978

Cyclic alterations of blink reflexes: an EEG and EMG study during wakefulness and sleep.

Studies of the blink reflex were undertaken in twelve normal subjects during wakefulness and different sleep stages. The early R1 and the late R2 components of the reflex were analyzed. R1 was present in only one subject during stage I sleep and subsequently disappeared in stage II to IV. In all subjects, R2 was gradually diminished and totally disappeared during stage IV. During the REM stage, R1 was seen in only four-out-of-twelve subjects but all R2 returned. Alterations of R1 and R2 of the blink reflex during different sleep stages suggest that the underlying mechanism includes both supranuclear and infranuclear activities. Our finding strengthens further the notion of dual hyponogenic mechanisms for sleep.

Adult↗
PubMed1975

Arterial blood gases and pH during sleep in chronic obstructive pulmonary disease.

Arterial blood gases were measured during 7 hours of sleep in 15 patients with severe stable chronic obstructive pulmonary discrease (COPD); 6 awake patients with COPD studies in recumbency for an average of 5 hours served as controls. Mean maximal decrease in arterial oxygen partial pressure (PaO2) (plus or minus SD) was 13.5 plus or minus 3.9 mm Hg for sleeping patients (p less than 0.005) and 5.5 plus or minus 1.7 mm Hg for controls (p less than 0.1), respectively. Changes in pH during sleep were of the magnitude expected with acute changes in arterial carbon dioxide partial pressure (PaCO2) in patients with chronic hypercapnia. Consistent changes in heart rate, respiratory frequency or cardiac rhythm were not observed during sleep. Nocturnal worsening of hypoxemia could be explained by alveolar hypoventilation in six sleeping patients and in five controls; in nine sleeping patients, further impariment of ventilation-perfusion mismatch also contributed to worsening of hypoxemia. There was no relationship between the decrease in PaO2 during sleep and the degree of airways obstruction or the PaO2 level when awake. Because of low PaO2, when awake, a fall in PaO2 during sleep brings values into the steep part of the oxyhemoglobin dissociation curve where slight changes in PaO2 result in marked changes in oxygen content. All patients with COPD whose waking PaO2 was below 60 mm Hg had PaO2 below 50 mm Hg during sleep; nocturnal oxygen therapy should be considered in such patients, particularly in the presence of polycythemia or troublesome right-sided heart failure.

Adult↗
PubMed1975

Effects of levodopa on the bladder outlet.

Lower urinary tract function was studied in patients with Parkinson's disease. A significant proportion of patients receiving levodopa manifested clinical and radiological evidence of bladder outlet obstruction. We believe that neuropharmacologic bladder neck obstruction may be caused by the alpha-adrenergic properties of the metabolites of levodopa.

3,4-Dihydroxyphenylacetic Acid↗