Significant weight loss after laparoscopic Nissen fundoplication.

BACKGROUND: Laparoscopic Nissen fundoplication (LNF) has evolved as a gold standard in antireflux surgery. However, the association between body weight and gastroesophageal reflux disease (GERD) is still unclear, and no data are available concerning the effect of fundoplication on body weight. We present the first report elucidating the impact of LNF on body weight in GERD patients with special emphasis on patients' quality of life. METHODS: From July 2000 to March 2003, LNF was carried out in 213 patients (85 women and 128 men) after thorough preoperative examination including clinical interview with standardized assessment of symptoms and quality of life (QoL), endosocopy, barium swallow, 24-h pH-metry, and manometry. Follow-up investigations were performed 3 and 12 months after LNF obtainable from 209 patients (98.1%) and 154 patients (72.3%), respectively. RESULTS: The mean body mass index (BMI) decreased significantly after LNF (27.6 +/- 5.6 kg/m(2) before LNF vs 26.0 +/- 3.8 kg/m(2) after LNF, p < 0.001). Twelve months after LNF, neither a tendency toward a renewed increase nor a further decrease in BMI was observable. The average body weight loss was 3.9 kg. BMI reduction was higher in women than in men (p < 0.002), and obese patients lost more weight than lean patients (p < 0.001). There was no association between BMI reduction and dysphagia. Plasma cholesterol and triglyceride levels did not change after LNF. The mean general score of the Gastrointestinal Quality of Life Index markedly improved (90.1 +/- 21.3 before LNF vs 118.0 +/- 16.2 after LNF, p < 0.01), as did the GERD-Health Related Quality of Life Index (21.9 +/- 6.4 before LNF vs 3.5 +/- 2.7 after LNF, p < 0.001). However, there was no association between changes in BMI and QoL. CONCLUSION: LNF leads to significant and persistent body weight loss.

Depressive effect of isoflurane on motor evoked potentials in the Nubian goat.

PURPOSE: To determine the effect of isoflurane on motor evoked potentials (MEP) in a new animal model designed to verify the applicability of MEPs in brachial plexus surgery, and to compare the results with previous reports in other animals. METHODS: In seven goats, anesthesia was induced with 3 mg x kg(-1) ketamine i.v. and maintained with nitrous oxide 40% in oxygen and 2 microg x kg(-1) x hr(-1) fentanyl i.v.. The MEP were performed with two subcutaneous needle electrodes placed over the occiput (cathode) and the nasion (anode), with their plugs connected to the power output of a Digitimer D 180 electrical stimulator, connected to the trigger input of an electromyograph (model 8400, Cadwell Laboratories, Inc., Kennwick, Washington). Activation of the Digitimer caused central stimulation of the motor cortex, evoking baseline compound muscle action potentials (CMAPs) which were recorded from the left triceps muscle. Subsequently, isoflurane 2% was administered together with repeated central stimulation at 30 sec intervals. RESULTS: Onset of I- (indirect) waves increased from median 15,8 msec to median 26,8 msec P = 0,018 (latency increase ranged from: 9 to 11.5 msec), while peak-to-peak amplitudes decreased and subsequently disappeared. D- (direct) waves showed no latency increase, and finally disappeared as well. After disappearance of CMAPs, isoflurane administration was stopped and MEP repeated. The CMAPs reappeared (range: 210-360 sec) and regained initial peak-to-peak amplitudes and latencies. CONCLUSION: These animal studies suggest that isoflurane should not be used during the recording of MEPs.

Memantine for prevention of spinal cord injury in a rabbit model.

BACKGROUND: This study was conducted to investigate the effect of memantine, a noncompetitive N-methyl-d-aspartate receptor antagonist, on the neurologic outcome of spinal cord ischemia after aortic occlusion. MATERIALS AND METHODS: New Zealand White rabbits were anesthetized and spinal cord ischemia was induced for 40 minutes by infrarenal aortic occlusion. Animals were randomly allocated to 3 groups. Group 1 (n = 8, control) received no pharmacologic intervention, group 2 (n = 8) received intra-aortic memantine infusion (20 mg/kg) after aortic crossclamping, and group 3 (n = 8) was treated with systemic memantine infusion (20 mg/kg) 45 minutes before aortic occlusion. Neurologic status was scored by the Tarlov system (in which 4 is normal and 0 is paraplegia) at 12, 24, 36, and 48 hours after the operation. Lumbar spinal root stimulation potentials and motor evoked potentials from lower limb muscles were monitored before, during, and after the operation. After the animals were killed, the spinal cords were studied histopathologically. RESULTS: All potentials disappeared shortly after aortic crossclamping. They returned earlier in both memantine-treated groups than in the placebo group. Histologic examination of spinal cords revealed a few abnormal motor neurons in memantine-treated rabbits but found extensive injury in the control group. At 12 hours the median Tarlov scores were 0 in the control group (group 1), 2 in the intra-aortic memantine group (group 2, P =.001 versus control), and 3 in the systemic group (group 3, P =.0002 versus control). At 24 hours median Tarlov scores were 0, 2.5 (P =.0002), and 4 (P =. 0002), respectively. Finally, at both 36 and 48 hours median Tarlov scores were 0, 3 (P =.0006), and 4 (P =.0002), respectively. CONCLUSION: Memantine significantly reduced neurologic injury related to spinal cord ischemia and reperfusion after aortic occlusion.

Leprosy affects facial nerves at the main trunk: neurolysis can possibly avoid transfer procedures.

The predilective sites of lesions in leprous peripheral nerves are well established, and their surgical decompression is common practice when sensorimotor disorders persist after medication. By contrast, the precise localization of leprous facial neuropathy still remains unclear, and musculofascial transfers have been the only type of surgical treatment. The goal of this study was to clarify where leprosy affects facial nerves and to determine whether neurolysis might suffice to restore facial function. In five Indian and two Egyptian patients suffering from leprous facial neuritis, the nerves were stimulated transcranially at the brainstem to evoke efferent motor nerve action potentials, which were recorded from the exposed nerves. Lesions were detected at the main trunk proximally from the first bifurcation in all cases. Epineuriotomy revealed fibrosis of the interfascicular epineurium in all instances, as an indication for interfascicular neurolysis. One patient was able to close his eye and showed a better smile soon after surgery. After 16 and 21 months, respectively, one patient had improved distinctly, two patients slightly, two patients showing no progress, and two patients were lost to follow-up. It is concluded that (1) leprous facial neuropathy is located at the main trunk close to the first bifurcation and not exclusively at the peripheral zygomatic branches, (2) microsurgical neurolysis can be considered in leprous facial neuropathy before transfer procedures as long as voluntary or spontaneous activity is present in the affected muscles, and (3) intraoperative transcranial electrical stimulation is an effective means of localizing the site and proximal extent of leprous facial neuropathy.