Background: Focal congenital hyperinsulinism (CHI) may be cured by resection of the focal, but often non-palpable, pancreatic lesion. The surgical challenge is to minimize removal of normal pancreatic tissue.Aim: To evaluate the results of intraoperative ultrasound-guided, tissue-sparing pancreatic resection in CHI patients at an international expert center.Methods: Retrospective study of CHI patients treated at Odense University Hospital, Denmark, between January 2010 and March 2017.Results: Of 62 consecutive patients with persistent CHI, 24 (39%) had focal CHI by histology after surgery. All patients had a paternal ABCC8 or KCNJ11 mutation and a focal lesion by 18F-DOPA-PET/CT. Intraoperative ultrasound localized the focal lesion in 16/20 patients (sensitivity 0.80), including one ectopic lesion in the duodenal wall. Intraoperative ultrasound showed no focal lesion in 11/11 patients with diffuse CH (specificity 1.0). The positive predictive value for focal histology was 1.0, negative predictive value 0.73.Tissue-sparing pancreatic resection (focal lesion enucleation, local resection of tail or uncinate process) was performed in 67% (n = 16). In 11/12 having tissue-sparing resection and intraoperative ultrasound, the location of the focal lesion was exactly identified. Eight patients had resection of the pancreatic head or head/body, four with Roux-en-Y, three with pancreatico-gastrostomy and one without reconstruction. None had severe complications to surgery. Cure of hypoglycaemia was seen in all patients after one (n = 21) or two (n = 3) pancreatic resections.Conclusion: In focal CHI, tissue-sparing pancreatic resection was possible in 67%. Intraoperative ultrasound was a helpful supplement to the mandatory use of genetics, preoperative 18F-DOPA-PET/CT and intraoperative frozen sections.
The purpose of this study was to investigate the role of reciprocal inhibition in the regulation of antagonistic ankle muscles during bicycling. A total of 20 subjects participated in the study. Reciprocal inhibition was induced by stimulation of the peroneal nerve (PN) at 1.2 times threshold for the M-response in the tibialis anterior muscle (TA) and recorded as a depression of the rectified soleus (SOL) EMG. Recordings were made during tonic plantar flexion and during bicycling on an ergometer bicycle. During tonic contraction, the amount of inhibition in the SOL EMG was linearly correlated to the amount of background EMG. This linear relation was used to calculate the expected amount of reciprocal inhibition at corresponding EMG levels during bicycling. During the early phase of down-stroke of bicycling at 60 revolutions per minute (RPM) and an external load of 1.0 kg, the amount of recorded reciprocal inhibition was significantly smaller than that calculated from the linear relation during tonic contraction. In nine subjects, the SOL H-reflex was used to evaluate the amount of inhibition. At a short conditioning test interval (2-3 ms), the PN stimulation depressed the SOL H-reflex when the subjects were at rest. This short latency inhibition was absent during downstroke, but appeared during upstroke just prior to and during TA activation. A positive linear relation was found between the level of SOL background EMG in early downstroke and the external load (0.5-2.5 kg) as well as the rate of pedaling (30-90 RPM at 1.0 kg external load). The amount of inhibition in the SOL EMG when expressed as a percentage of the background EMG activity decreased significantly with increasing load. During increased pedaling rate, a similar decrease was seen, but it did not reach a statistically significant level. The data illustrate that reciprocal inhibition of the soleus muscle is modulated during bicycling being small in downstroke when the SOL muscle is active and large in upstroke where the muscle is inactive and its antagonist becomes active. The depression of the inhibition in relation to increased load and pedaling rate likely reflects the need of reducing inhibition of the SOL motoneurons to ensure a sufficient activation of the muscle.
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