This clinical report represents the first English-language recommendations for the management of pediatric AP. Future aims should include prospective multicenter pediatric studies to further validate these recommendations and optimize care for children with AP.

Background and Objectives:Duplications of the alimentary tract are rare anomalies. We report our experience with foregut duplication cysts including their clinical presentation, diagnostic modalities, and surgical management.Methods:We report a 20-year retrospective review of all foregut duplication cysts managed at our institution.Results:Twelve patients with 13 foregut duplication cysts were identified. The ages of the children at the time of surgery ranged from infancy to adolescence, with a mean age of 7.2 years. Half of the patients presented with abdominal pain and vomiting, and the remaining either had respiratory distress or were asymptomatic. All resections were performed electively. Two of the 11 patients had other congenital anomalies, including a congenital pulmonary airway malformation and coarctation of the aorta. One patient had prenatal diagnosis by ultrasonography. Nine patients underwent complete successful excision with no complications. Three patients whose symptoms resolved during hospitalization remained under observation because of parental preference.Conclusions:Foregut malformation in children may present with a variety of symptoms or can be found incidentally. The decision and timing of surgery is based on the clinical presentation. Surgical intervention in asymptomatic patients should be based on a thorough discussion with the parents.

Neurovascular coupling refers to the link between an increase in neural activity in response to a task and an increase in cerebral blood flow denoted "functional hyperemia." Recent work on postural tachycardia syndrome indicated that increased oscillatory cerebral blood flow velocity (CBFv) was associated with reduced functional hyperemia. We hypothesized that a reduction in functional hyperemia could be causally produced in healthy volunteers by using oscillations in lower body negative pressure (OLBNP) to force oscillations in CBFv. CBFv was measured by transcranial Doppler ultrasound of the left middle cerebral artery. We used passive arm flexion applied during eight periodic 60-s flexion/60-s relaxation epochs to produce 120-s periodic changes in functional hyperemia (at 0.0083 Hz). We used -30 mmHg of OLBNP at 0.03, 0.05, and 0.10 Hz, the range for cerebral autoregulation, and measured spectral power of CBFv at all frequencies. Arm flexion power performed without OLBNP was compared with arm flexion power during OLBNP. OLBNP power performed in isolation was compared with power during OLBNP plus arm flexion. Cerebral flow velocity oscillations at 0.05 Hz reduced and at 0.10 Hz eliminated functional hyperemia, while 0.03 Hz did not reach significance. In contrast, arm flexion reduced OLBNP-induced oscillatory power at all frequencies. The interactions between OLBNP-driven CBFv oscillations and arm flexion-driven CBFv oscillations are reciprocal. Thus induced cerebral blood flow oscillations suppress functional hyperemia, and functional hyperemia suppresses cerebral blood flow oscillations. We conclude that oscillatory cerebral blood flow produces a causal reduction of functional hyperemia.

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