Because controversy exists regarding continued use of the seated position for neurosurgical procedures, this prospective (1981-1983) and retrospective (1972-1981) analysis of 554 seated patients was done to establish the incidence and severity of venous air embolism (VAE) related to type of surgical procedure and anesthetic technique; to examine the impact of specific monitoring practices on detection, morbidity, and mortality; and to establish the incidence of other complications related to the seated position (hypotension, quadriplegia, and arterial air embolism (AAE)). The overall morbidity and mortality related to the seated position was 1% (2 VAE, 1 AAE, 2 hypotension, 1 myocardial infarction) and 0.9% (1 VAE, 1 AAE, 2 hypotension, 1 quadriplegia), respectively. There has been no mortality since 1975. N2O did not seem to increase the incidence or severity of VAE. The seated position is safe in experienced hands if appropriate surgical and anesthetic skills are exercised in patient selection and management. Caution is advised in patients with atherosclerotic cardiovascular disease, severe hypertension, cervical stenosis, and right to left intracardiac shunts.

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Acute insulin-induced hypoglycemia provokes changes in central nervous system activity and release of counterregulatory hormones. The clinical relationship between central nervous system activity, hormone secretion, and vital signs has not to our knowledge been previously reported. We used computerized electroencephalographic (CEEG) analysis to monitor 5 nondiabetic subjects during acute insulin-induced hypoglycemia (0.75 U/kg intravenous push). Their glucose nadir was 38 +/- 6 mg/dl (mean +/- 1 SD). A three-phase pattern of change in CEEG power in response to hypoglycemia was observed: phase 1 was characterized by an increase in total CEEG power (natural log of activity = 9.1 +/- 1.3 microV2) over baseline (8.7 +/- 1.2 microV2) in the theta, delta, and beta frequency bands. This phase preceded and coincided with the glucose nadir. During phase 2, power in all frequency bands fell significantly below baseline. A nadir in CEEG power (8.0 +/- 1.6 microV2) occurred 40 to 55 minutes after insulin injection as glucose levels were rising. During phase 3 there was a return to baseline in CEEG power and frequency spectra. Heart rate increase just before phase 1; peak heart rate (91 +/- 8 beats/min) coincided with peak CEEG power and was significantly higher than basal rate (71 +/- 11, P less than 0.05). A significant increase in respiratory rate occurred during phase 1 of the CEEG and persisted through phase 2. A significant decrease in mean blood pressure (nadir = 73 +/- 6 mm Hg) below preinsulin blood pressure (81 +/- 8 mm Hg, P less than 0.05) coincided with the nadir of CEEG power in phase 2.(ABSTRACT TRUNCATED AT 250 WORDS)

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The clinical and electrophysiological observations in two cases of distal ulnar neuropathy from carpal ganglia are reported. In the first case, the ganglion was compressing the ulnar nerve just proximal to its division; in the second case, the ganglion was compressing the deep branch of the ulnar nerve just at its origin. In both cases, both axonal degeneration and segmental demyelination were present. A clinical classification of the compression syndromes of the deep ulnar branch is proposed.