[Anesthesia of the glossopharyngeal nerve, vagus nerve and cervical cranial ganglion at the base of the skull].
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PURPOSE: To define the variations of the courses of the cranial nerves and the inferior petrosal sinuses as they enter and traverse the jugular foramen. METHODS: Thirty-nine cadaveric specimens containing the jugular foramen were scanned with 1-mm contiguous axial and coronal CT sections. Each specimen was dissected to evaluate the position of the cranial nerves and inferior petrosal sinus as they entered the jugular foramen. RESULTS: The glossopharyngeal nerve entered the most superior, anterior, and medial aspect of the jugular foramen and descended in the anterior portion of the jugular foramen, often within a groove. The vagus and accessory nerves could not be separated by CT. They entered the jugular foramen most often anterior or anterior and inferior to the jugular spine of the temporal bone and descended in a position ranging from medial to anterior to the jugular vein. The inferior petrosal sinus most often coursed inferior to the horizontal portion of the glossopharyngeal nerve and entered the jugular system in the jugular foramen, at the exocranial opening or below the skull base. A pars nervosa and pars venosa could be identified only at the endocranial opening, where the jugular spine separated the pars nervosa containing the inferior petrosal sinus and three cranial nerves from the pars venosa containing the jugular vein. CONCLUSION: Our evaluation demonstrated anatomic variation in the area of the jugular foramen.
Seven heads and necks of Bactrian camels were dissected to investigate the origin, course, branches and distribution of the accessory nerve and vagus nerve in the cranial cervical region. The spinal root and external branch of the accessory nerve were not present, but there was a delicate communicating branch between the dorsal root of the first cervical nerve and the root of the vagus nerve. The sternocephalic muscle was innervated by the second cervical nerve while the brachiocephalic and trapezius muscles were supplied by the sixth and seventh cervical nerves. In the head and cranial cervical region of the Bactrian camel the vagus nerve gave off the auricular branch, pharyngeal branch, cranial laryngeal nerve, a common trunk to the larynx, oesophagus and trachea, and some communicating branches connecting with the glossopharyngeal, hypoglossal, first cervical nerves and the cranial cervical ganglion.
Action potentials evoked by the stimulation of the hepatic branch of the splanchnic nerve were recorded from the peripheral cut end of the dorsal celiac branch of the vagus nerve in the rat. Action potentials were clearly demonstrated after averaging over 100 times by a computer. The observations indicate the existence of a nervous pathway from the hepatic branch of the splanchnic nerve to the dorsal celiac branch of the vagus nerve in the rat.
The authors studied human vagus nerve electrophysiology intraoperatively on 21 patients (age range: 4 to 31 years) during implantation of a vagus nerve stimulator for seizure control. The study was performed with direct electrical stimulation of the vagus nerve with various stimulation parameters resembling those employed by the Cyberonics NeuroCybernetic Prosthesis System (Houston, TX), which is used clinically for vagus nerve stimulation for treatment of seizures. Recordings were made directly from the rostral end of the vagus nerve. The response of the vagus nerve to various stimulus parameters in patients of different ages was studied. Based on the vagus nerve characteristics, age-related adjustments for stimulus parameters were recommended.
OBJECTIVE: To locate the recurrent laryngeal nerve fascicles in vagus and investigate the effect of latero-terminal neurorrhaphy to repair recurrent laryngeal nerve. METHOD: The method of dissection and acetylcholinesterase histochemical staining of neural fibers were used to locate the recurrent laryngeal nerve fascicles in vagus. Then 60 SD rats were divided into three groups. In experimental group right recurrent laryngeal nerve were incised and anastomosed to recurrent laryngeal nerve fascicles in vagus by means of latero-terminal neurorrhaphy. In control group right recurrent laryngeal were incised and sutured immediately by means of end-to-end nerve anastomosis. In normal group rats were not treated by any elements. One to three months later, 10 rats from each group were examined for vocal cord movement and nerve regeneration by using fibrolaryngscope and nerve electrormyography. RESULT: The recurrent laryngeal nerve fascicles is in the medial-front segment of the vagus and its diameter is about one-fourth as large as the vagus. One months after operation, This effect of latero-terminal neurorrhaphy had significant difference compared with the control group (P < 0.05). Three months after operation, This effect of latero-terminal neurorrhaphy had not significant difference compared with the control group (P > 0.05). CONCLUSION: The location of the recurrent laryngeal nerve fascicles in vagus provids important anatomical guideline for surgery. The latero-teminal neurorrhaphy has a similiar treatment effect compared with end-to-end nerve anastomosis. This microsurgical technique provides a new method for repairing recurrent laryngeal nerve.
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Vagus nerve stimulation is a progressive therapy for intractable epilepsy. Variations in cervical anatomy can complicate localization of the vagus nerve and may lead to inappropriate placement of the stimulator leads. We have developed two intraoperative techniques that improve correct identification of the vagus nerve. Both of these techniques utilize the co-localization of the recurrent laryngeal nerve with the vagus nerve. For patients undergoing stimulator placement with regional and local anesthesia, the stimulator current intensity is increased until alteration of voice can be confirmed with a voice test. Patients undergoing general anesthesia can also be tested by direct stimulation of the isolated vagus nerve. Utilizing visualization of the larynx and vocal cords via fiberoptic endoscopy, direct stimulation of the vagus nerve will produce a contraction of the left lateral wall of the larynx and tightening of the left vocal cord. Neither of these procedures produce any untoward effects for the patients. We have found these methods improve our ability to confirm correct placement of the stimulator with minimal increase in operative time (with Video).
Vagus nerve stimulation (VNS) was first tried as a treatment for seizure patients in 1988. The idea to stimulate the vagus nerve and disrupt or prevent seizures was proposed by Jacob Zabarra. He observed a consistent finding among several animal studies which indicated that stimulation of the vagus nerve could alter the brain wave patterns of the animals under study. His hypothesis formed the basis for the development of the vagus nerve stimulator, an implantable device similar to a pacemaker, which is implanted in the left chest and attached to the left vagus nerve via a stimulating lead. Once implanted, the stimulator is programmed by a physician to deliver regular stimulation 24 hours a day regardless of seizure activity. Patients can also activate extra 'on-demand' stimulation with a handheld magnet. Clinical studies have demonstrated VNS therapy to be a safe and effective mode of treatment when added to the existing regimen of severe, refractory patients with epilepsy. Efficacy ranges from seizure free to no response with the majority of patients (> 50%) reporting at least a 50% improvement in number of seizures after 1.5 years of treatment. The side-effect profile is unique and mostly includes stimulation-related sensations in the neck and throat. The mechanism of action for VNS is not clearly understood although two theories have emerged. First, the direct connection theory hypothesizes that the anticonvulsant action of VNS is caused by a threshold raising effect of the connections to the nucleus of the solitary tract and on to other structures. The second is the concept that chronic stimulation of the vagus nerve increases the amount of inhibitory neurotransmitters and decreases the amount of excitatory neurotransmitters. Additional research into the optimal use of VNS is ongoing. Animal and clinical research have produced some interesting new data suggesting there are numerous ways to improve the clinical performance of vagus nerve stimulation as a treatment for refractory patients.
The course of the right recurrent laryngeal nerve (RLN) within the vagus nerve was examined under the light microscope, using horseradish peroxidase. In the higher cervical vagus, i.e. from the base of the skull to the level of the carotid bifurcation, the recurrent laryngeal nerve fibres formed on average 5-6 small separate bundles (15-40 microns in diameter); in the middle cervical vagus, on average from the level of 8-14 mm caudally from the bifurcation, there were fewer bundles with a diameter range of 10-50 microns; in the lower cervical vagus, indicated as being from 14-26 mm caudally from the middle cervical vagus, the bundles merged into a single larger bundle (50-70 microns).
The efferent connections of two types neurons in the dorsal motor nucleus of the vagus nerve (DMV) were studied in the cat by light and electron microscopy following horseradish peroxidase (HRP) injections into the cervical vagus nerve or brainstem. After injections of HRP into the vagus nerve, up to 80% of medium-sized neurons averaging 26 x 20 micrometers in 1-micrometer-thick sections were retrogradely labeled while no small neurons were labeled in the DMV. Incubation with either diaminobenzidene (DAB) or p-phenylenediamine-pyrocatechol (PPD-PC) chromogens yielded electron-dense reaction products localized mainly in lysosomes. Identification of label at the ultrastructural level was facilitated by omitting lead citrate staining and by counting numbers of lysosomes, which were higher in labeled neurons. Quantitative comparisons of the dimensions of labeled and unlabeled somata demonstrated that retrograde transport and incorporation of HRP had no effect on cell size within the 2-3-day survival times used in this study. In order to determine whether neurons in the DMV project to higher levels of the brain stem, large injections of HRP (1-3 microliters) were made into the pons, mesencephalon, hypothalamus, and amygdala. After injections of HRP into the brainstem, only small neurons, measuring 17 x 10 micrometers, were retrogradely labeled. Approximately 90% of the small neurons remained unlabeled following the HRP injections. The ultrastructural features of the labeled small neurons included an invaginated nucleus, low cytoplasmic/nuclear ratio, and relatively fewer organelles than the medium-sized neurons. A quantitative analysis of labeled and unlabeled small neurons demonstrated that the labeled neurons were significantly larger than the unlabeled small neurons. Thus, two populations of small neurons may exist in the DMV. One population appears to have ascending projections to higher levels of the brainstem while the other more numerous population may be interneurons or project for only short distances.
OBJECT: The authors describe a technique in which the cervical portion of the vagus nerve is exposed during procedures such as neuroma resection or, more commonly, during the placement of a vagus nerve stimulator. METHODS: To test their hypothesis that a posterolateral approach to the vagus nerve may be feasible and efficacious, the authors performed dissection of the left-sided vagus nerve in 13 adult cadavers. The carotid sheath was exposed via the posterior cervical triangle, and the vagus nerve was identified posterolaterally. Measurements were made of the length of available nerve, and the anatomical approach was documented. As part of a comparison study regarding the available length of nerve, the authors exposed the left vagus nerve in five additional adult cadavers via a standard anterior approach to the carotid sheath, and compared the results obtained with each technique. A mean length of 12 cm of the vagus nerve was isolated when using the posterior approach to the carotid sheath, whereas a mean length of 11 cm of the nerve was documented when using the anterior approach. With the aforementioned posterior approach, no obvious injury occurred to the vagus nerve or other local neurovascular structures such as the spinal accessory nerve. CONCLUSIONS: Evaluation of the findings obtained in the present cadaveric study showed that a posterior approach to the vagus nerve is feasible. The technique for posterior exposure of the carotid sheath may prove useful in surgical exposures of the vagus nerve when a standard anterior method is not possible.
OBJECTIVE: To perform an open-label, long-term efficacy and safety/tolerability study of vagus nerve stimulation (VNS) of 454 patients with refractory epilepsy. METHODS: Subjects were enrolled from five clinical trials of VNS between 1988 and 1995 after undergoing an implantation of a pulse generator in the chest and a left cervical vagus nerve-stimulating lead coil. Patients were assessed at 6-month intervals until device approval. Seizure frequencies, medication treatment, and adverse events (AEs) were recorded and entered into a database. RESULTS: A total of 454 patients were implanted, and 440 patients yielded assessable data. A > or =50% seizure reduction postimplantation occurred in 36.8% of patients at 1 year, in 43.2% at 2 years, and in 42.7% at 3 years. Median seizure reductions compared with baseline were 35% at 1 year, 44.3% at 2 years, and 44.1% at 3 years. Most common AEs postimplantation at 1 year were hoarseness (28%) and paraesthesias (12%), at 2 years were hoarseness (19.8%) and headache (4.5%), and at 3 years was shortness of breath (3.2%). Continuation rates were 96.7% at 1 year, 84.7% at 2 years, and 72.1% at 3 years. CONCLUSION: Long-term, open-label vagus nerve stimulation (VNS) provided seizure reduction similar to or greater than acute studies, for median reductions and for those reaching a > or =50% seizure reduction. VNS remained safe and well tolerated, with nearly three-quarters of the patients choosing to continue therapy.
The aim of this study was to find out whether dysglycaemia causes neuropathy in the vagus nerve of insulin-treated diabetic BB/Wor rats. Specimens were collected from the left vagus nerve proximal and distal to the level of recurrent laryngeal branch and from the recurrent branch itself in control rats and diabetic BB/Wor rats subjected to hyper- or hypoglycaemia. Myelinated and unmyelinated axons were counted and myelinated axon diameters were measured by electron microscopy. In controls, the vagus nerve proximal to the recurrent branch exhibited three regions in terms of fibre composition: part A was mainly composed of large myelinated axons, part B contained small myelinated and unmyelinated axons, and part C contained mainly unmyelinated axons. The distal level resembled part C at the proximal level and the recurrent branch resembled parts A and B. In hyperglycaemic rats, a normal picture was found at the proximal and distal levels of the vagus nerve and in the recurrent branch. In hypoglycaemic rats, signs of past and ongoing degeneration and regeneration of large myelinated axons were found at the proximal and distal levels and in the recurrent branch. We conclude that hypoglycaemia elicits degenerative alterations in large myelinated axons in the vagus and recurrent laryngeal nerves in diabetic BB/Wor rats. The absence of signs of neuropathy in unmyelinated and small myelinated axons suggests that the sensory and autonomic components of the nerve are less affected. In contrast, the hyperglycaemic rats examined here did not show obvious degenerative alterations.
Preliminary reports have suggested that chronic, intermittent stimulation of the vagus nerve (VNS) is an alternative treatment for patients with medically refractory seizures. We performed a multicenter, randomized, controlled trial to evaluate the efficacy and safety of adjunctive VNS in patients with poorly controlled partial seizures. An implanted, programmable pacemaker-like device was connected to two stimulating electrodes wrapped around the left vagus nerve. One hundred fourteen patients were randomized to receive 14 weeks of high-level stimulation (presumed therapeutic dose) or low-level stimulation (presumed subtherapeutic dose) using a blinded, parallel study design. Seizure frequency was compared with a 12-week baseline. Mean reduction in seizure frequency was 24.5% for the "high" stimulation group versus 6.1% for the "low" stimulation group (p = 0.01). Thirty-one percent of patients receiving high stimulation had a seizure frequency reduction of > or = 50%, versus 13% of patients in the low group (p = 0.02). Treatment emergent side effects were largely limited to a transient hoarseness occurring during the stimulation train. One patient with no previous history of cardiac disease experienced a myocardial infarction during the third month of vagal stimulation. VNS may be an effective alternative treatment for patients who have failed antiepileptic drug therapy and are not optimal candidates for epilepsy surgery.
Vagus nerve stimulation (VNS) has been shown to induce EEG changes in animals, but human studies have not shown any significant acute EEG changes. This study is to determine the long-term effect of VNS on EEG. Twenty-one patients aged 4 to 31 years (mean: 14.1 +/- 7.0 years) were studied for a mean duration of 16.8 months with serial EEGs performed at baseline and at 3 months, 6 months, and 12 months after receiving a VNS implant. Five patients who showed active spikes/spike and wave activity on baseline EEGs were found to have synchronization of epileptiform activity, progressive increase in duration of spike-free intervals (P < 0.05), and progressive decrease in duration and frequency of spikes/spike and wave activity (P < 0.01) with time. The remaining 16 patients with less active baseline EEGs did not show obvious synchronization or clustering of spikes but also showed a statistically significant progressive decrease in the number of spikes on EEG with time (P < 0.004 at 3 months, P < 0.008 at 6 months, and P < 0.004 at 1 year). Vagus nerve stimulation induces progressive EEG changes in the form of clustering of epileptiform activity followed by progressively increased periods of spike-free intervals. This may reflect the mechanism of action of VNS in achieving seizure control: alternating synchronization and desynchronization of EEG, with the latter being progressively the dominant feature.
It is known that the vagus nerve contains catecholaminergic fibers. However, the origin of these fibers has not been systematically examined. In this study, we addressed this issue using retrograde tracing from the subdiaphragmatic vagus nerve combined with immunocytochemistry. The cervical and thoracic sympathetic trunk ganglia, the nodose ganglia and the dorsal motor nucleus of the vagus nerve were examined following injection of Fluoro-Gold or cholera toxin horseradish peroxidase conjugate into the trunks of the subdiaphragmatic vagus nerve of rats. Numerous retrogradely labeled neurons were seen in the nodose ganglion and the dorsal motor nucleus of the vagus nerve. Very few labeled neurons were found in the sympathetic ganglia (less than 0.06% of the neurons in either superior cervical ganglion or cervicothoracic ganglion were retrogradely labeled). Double labeling with immunofluoresence for catecholamine synthesizing enzymes revealed that: (1) 92% of all Fluoro-Gold retrogradely labeled tyrosine hydroxylase immunoreactive neurons were found in parasympathetic sources (75% in the dorsal motor nucleus of the vagus nerve and 17% in the nodose ganglia), and only 8% in the cervicothoracic sympathetic ganglia; (2) 12% of the retrogradely labeled catecholaminergic neurons in the dorsal motor nucleus of the vagus nerve were also dopamine-beta-hydroxylase immunopositive neurons; (3) 70% of the retrogradely labeled neurons in the sympathetic ganglia were tyrosine hydroxylase immunopositive and 54% of these catecholaminergic neurons contained dopamine-beta-hydroxylase, while 30% of the retrogradely labeled neurons were non-catecholaminergic neurons. These results indicate that catecholaminergic fibers in the abdominal vagus nerve are primarily dopaminergic and of parasympathetic origin, and that only an extremely small number of these fibers, mostly noradrenergic in nature, arise from postganglionic sympathetic neurons.
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