Gastric emptying and vagus nerve function after laparoscopic partial fundoplication. (1/11)

OBJECTIVE: To establish the relation between vagus nerve dysfunction, gastric emptying, and antireflux surgery. SUMMARY BACKGROUND DATA: Delayed gastric emptying occurs in up to 40% of reflux patients. After antireflux surgery, gastric emptying becomes normal or is even accelerated. Occasionally, severe gastric stasis is found and is associated with a negative outcome of the antireflux procedure. It has been suggested that injury to the vagus nerve could be the cause of this delayed emptying. METHODS: We evaluated in a prospective study gastric emptying of solids and vagus nerve function (pancreatic polypeptide response to hypoglycemia) before and after surgery in 41 patients (22 women; age 43 +/- 1.6 years) who underwent laparoscopic hemifundoplication. RESULTS: All patients had relief of reflux symptoms varying from adequate (n = 8) to complete relief (n = 33). Gastric emptying of solids increased significantly (P < 0.001) after operation: lag phase from 19 +/- 2 to 10 +/- 1 minute, emptying rate (%/h) from 37 +/- 2 to 48 +/- 5 and half emptying time from 110 +/- 8 to 81 +/- 4 minutes. Gastric emptying improved to a similar extent in patients with delayed and normal preoperative gastric emptying. Postoperative signs of vagus nerve damage (PP peak < 47pmol/L) were present in 4 patients (10%). In these 4 patients gastric emptying both before and after operation did not differ from patients with normal vagus nerve function. In fact, none of the 41 patients had severely delayed emptying after laparoscopic hemifundoplication. CONCLUSIONS: Laparoscopic hemifundoplication affects vagus nerve integrity in 10% of patients, but this does not lead to a delay in gastric emptying. In fact, gastric emptying improved significantly after fundoplication.  (+info)

Novel role of neuronal Ca2+ sensor-1 as a survival factor up-regulated in injured neurons. (2/11)

A molecular basis of survival from neuronal injury is essential for the development of therapeutic strategy to remedy neurodegenerative disorders. In this study, we demonstrate that an EF-hand Ca2+-binding protein neuronal Ca2+ sensor-1 (NCS-1), one of the key proteins for various neuronal functions, also acts as an important survival factor. Overexpression of NCS-1 rendered cultured neurons more tolerant to cell death caused by several kinds of stressors, whereas the dominant-negative mutant (E120Q) accelerated it. In addition, NCS-1 proteins increased upon treatment with glial cell line-derived neurotrophic factor (GDNF) and mediated GDNF survival signal in an Akt (but not MAPK)-dependent manner. Furthermore, NCS-1 is significantly up-regulated in response to axotomy-induced injury in the dorsal motor nucleus of the vagus neurons of adult rats in vivo, and adenoviral overexpression of E120Q resulted in a significant loss of surviving neurons, suggesting that NCS-1 is involved in an antiapoptotic mechanism in adult motor neurons. We propose that NCS-1 is a novel survival-promoting factor up-regulated in injured neurons that mediates the GDNF survival signal via the phosphatidylinositol 3-kinase-Akt pathway.  (+info)

Calcium-fluxing glutamate receptors associated with primary gustatory afferent terminals in goldfish (Carassius auratus). (3/11)

Presynaptic ionotropic glutamate receptors modulate transmission at primary afferent synapses in several glutamatergic systems. To test whether primary gustatory afferent fibers express Ca(2+)-permeable AMPA/kainate receptors, we utilized kainate-stimulated uptake of Co(2+) along with immunocytochemistry for the Ca(2+)-binding proteins (CaBPs) calbindin and calretinin to investigate the primary gustatory afferents in goldfish (Carassius auratus). In goldfish, the primary gustatory nucleus (equivalent to the gustatory portion of the nucleus of the solitary tract) includes the vagal lobe, which is a large, laminated structure protruding dorsally from the medulla. Kainate-stimulated uptake of Co(2+) (a measure of Ca(2+)-fluxing glutamate receptors) shows punctate staining distributed in the distinct laminar pattern matching the layers of termination of the primary gustatory afferent fibers. In addition, CaBP immunocytochemistry, which correlates highly with expression of Ca(2+)-permeable AMPA/kainate receptors, shows a laminar pattern of distribution similar to that found with kainate-stimulated cobalt uptake. Nearly all neurons of the vagal gustatory ganglion show Co(2+) uptake and are immunopositive for CaBPs. Transection of the vagus nerve proximal to the ganglion results in loss of such punctate Co(2+) uptake and of punctate CaBP staining as soon as 4 days postlesion. These results are consonant with the presence of Ca(2+)-fluxing glutamate receptors on the presynaptic terminals of primary gustatory terminals, providing an avenue for modulation of primary gustatory input.  (+info)

Traumatic retroclival epidural hematoma in a child: case report. (4/11)

An 11-year-old girl presented with a very rare traumatic retroclival epidural hematoma manifesting as bilateral abducens nerve palsy, deviation of the uvula to the left, and weakened movement of tongue, which developed after a motor vehicle accident. The patient was treated conservatively and showed good outcome. Retroclival hematoma is a mainly pediatric entity usually associated with ligamentous injury at the craniocervical junction, and can be treated conservatively with good outcome.  (+info)

Carotid body tumour resection with LigaSure device. (5/11)

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Vernet's syndrome caused by large mycotic aneurysm of the extracranial internal carotid artery after acute otitis media--case report. (6/11)

An 85-year-old man presented with a rare large aneurysm of the extracranial internal carotid artery (ICA) due to acute otitis media manifesting as Vernet's syndrome 2 weeks after the diagnosis of right acute otitis media. Angiography of the right extracranial ICA demonstrated an irregularly shaped large aneurysm with partial thrombosis. The aneurysm was treated by proximal ICA occlusion using endovascular coils. The ICA mycotic aneurysm was triggered by acute otitis media, and induced Vernet's syndrome as a result of direct compression to the jugular foramen. Extracranial ICA aneurysms due to focal infection should be considered in the differential diagnosis of lower cranial nerve palsy, although the incidence is thought to be very low.  (+info)

Usefulness of neuromonitoring in thyroid surgery. (7/11)

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Injury of the peripheral cranial nerves during carotid endarterectomy. (8/11)

The incidence of local nerve injury among 192 consecutive carotid endarterectomies in 162 patients between 1977-1983 was determined from review of the medical records. Two facial nerve, 5 hypoglossal nerve, and 2 vagus nerve injuries were discovered for a total incidence of 4.7%. Only the 2 facial nerve injuries failed to improve over 2 years. Followup ranged from 1 to 60 months in this group of patients. Careful attention to details of tissue dissection at surgery should lower the incidence of nerve injury during carotid endarterectomy.  (+info)