The effect of call on neurosurgery residents' skills: implications for policy regarding resident call periods.

OBJECT: Although fatigue and its effects on surgical proficiency have been an actively researched area, previous studies have not examined the effect of fatigue on neurosurgery residents specifically. This study aims to quantify the effect of fatigue on the psychomotor and cognitive skills of neurosurgery residents. METHODS: Seven neurosurgery residents performed a minimum of 3 and a maximum of 4 sessions of 6 surgical exercises precall and postcall. The simulation exercises were designed to measure a surgeon's cognitive abilities, such as memory and attention, while performing simulated surgical tasks and exercises that have been previously validated in several studies, including studies measuring the impact of fatigue on general surgery residents. Each exercise measured tool-movement smoothness, time elapsed, and cognitive errors. The change in surgical skills in precall and postcall conditions was assessed by means of an ANOVA, with p < 0.05 considered statistically significant. RESULTS: The neurosurgery residents did not show a statistically significant difference in their surgical skills between the pre- and postcall states (p < 0.3, p < 0.4, and p < 0.2 for movement smoothness, time elapsed, and cognitive errors, respectively). The mean decrement for all residents in the postcall condition was 13.1%. CONCLUSIONS: Postcall fatigue is associated with a marginal decrease in proficiency during simulated surgery in neurosurgery residents. In a similar study, general surgery residents showed a statistically significant decrement of 27.3% in the postcall condition. The impact of fatigue on different specialties should be further investigated prior to implementation of a national physician work-hour policy.

The calcium-sensing receptor (CaSR) defends against hypercalcemia independently of its regulation of parathyroid hormone secretion.

The calcium-sensing receptor (CaSR) controls parathyroid hormone (PTH) secretion, which, in turn, via direct and indirect actions on kidney, bone, and intestine, maintains a normal extracellular ionized calcium concentration (Ca(2+)(o)). There is less understanding of the CaSR's homeostatic importance outside of the parathyroid gland. We have employed single and double knockout mouse models, namely mice lacking PTH alone (CaSR(+/+) PTH(-/-), referred to as C(+)P(-)), lacking both CaSR and PTH (CaSR(-/-) PTH(-/-), C(-)P(-)) or wild-type (CaSR(+/+) PTH(+/+), C(+)P(+)) mice to study CaSR-specific functions without confounding CaSR-mediated changes in PTH. The mice received three hypercalcemic challenges: an oral Ca(2+) load, injection or constant infusion of PTH via osmotic pump, or a phosphate-deficient diet. C(-)P(-) mice show increased susceptibility to developing hypercalcemia with all three challenges compared with the other two genotypes, whereas C(+)P(-) mice defend against hypercalcemia similarly to C(+)P(+) mice. Reduced renal Ca(2+) clearance contributes to the intolerance of the C(-)P(-) mice to Ca(2+) loads, as they excrete less Ca(2+) at any given Ca(2+)(o) than the other two genotypes, confirming the CaSR's direct role in regulating renal Ca(2+) handling. In addition, C(+)P(+) and C(+)P(-), but not C(-)P(-), mice showed increases in serum calcitonin (CT) levels during hypercalcemia. The level of 1,25(OH)(2)D(3) in C(-)P(-) mice, in contrast, was similar to those in C(+)P(-) and C(+)P(+) mice during an oral Ca(2+) load, indicating that increased 1,25(OH)(2)D(3) production cannot account for the oral Ca(2+)-induced hypercalcemia in the C(-)P(-) mice. Thus, CaSR-stimulated PTH release serves as a "floor" to defend against hypocalcemia. In contrast, high-Ca(2+)(o)-induced inhibition of PTH is not required for a robust defense against hypercalcemia, at least in mice, whereas high-Ca(2+)(o)-stimulated, CaSR-mediated CT secretion and renal Ca(2+) excretion, and perhaps other factors, serve as a "ceiling" to limit hypercalcemia resulting from various types of hypercalcemic challenges.