Search

The carotid sinus nerve branches off the glossopharyngeal nerve just after its appearance from the jugular foramen, descends along the internal carotid artery, and enters the carotid sinus. There have been many studies of the pathway and the course of the carotid sinus nerve and its communications with surrounding nerves. The intercommunication is exceedingly complicated. Acknowledgment of its anatomic diversity can be important in specific operations dealing with this area. Herein we review the anatomy, variations, pathology, and clinical applications of the carotid sinus nerve., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Objective: This 3-dimensional histologic study aimed to provide a precise description of the meningeal structures in the jugular foramen., Methods: 22 posterior skull base tissue blocks containing the jugular foramen region were obtained from 11 human cadaveric heads. These blocks were plastinated and cut into serial sections. After staining, these sections were examined under an optical microscope and used to reconstruct a 3-dimensional visualization model., Results: At the intracranial orifice of the jugular foramen, the meningeal dura formed 2 separate dural perforations: the glossopharyngeal meatus and the vagal meatus. The arachnoid extended into 2 dural meatuses and terminated at the inferior ganglion of the glossopharyngeal nerve in the glossopharyngeal meatus and the superior ganglion of the vagus nerve in the vagal meatus. At the intraforaminal part of the jugular foramen, the meningeal dura encased the glossopharyngeal nerve to form a dural sheath while encasing the vagus and accessory nerves to form a dural network. At the extracranial orifice of the jugular foramen, the dural wall of the jugular bulb extended downward to form a dense connective tissue sheath. The initial end of the internal jugular vein invaginated into this sheath and fused with the jugular bulb., Conclusions: Knowledge of the anatomy of the meningeal architecture of the jugular foramen can be helpful in avoiding surgical complications of the lower cranial nerves when this complex area is approached., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Objective: The chemoreceptor network, consisting of the glossopharyngeal nerve and carotid body (GPN-CB), is essential for the regulation of blood pH. Its ischemic insults after subarachnoid hemorrhage (SAH), which may contribute to acidosis, have not been investigated., Methods: Twenty-three hybrid rabbits were used. They were divided into 3 groups: 5 as a control group, 5 as a sham group, and the remaining 13 as the study group. Injections included 1 cm 3 serum saline and 1 cm 3 autolog arterial blood into the cisterna magna in the sham and study group, respectively. Blood pH values of all animals were recorded. After 2 weeks, animals were euthanized. The number of normal and degenerated neurons of the carotid bodies (CBs) was counted by stereologic methods and analyzed statistically., Results: Two of 13 rabbits died within the second week. The mean blood pH values were measured as 7.35 ± 0.07 in the control group (n = 5), 7.33 ± 0.06 in the sham group (n = 5), 7.29 ± 0.05 in rabbits with slight acidosis (n = 6), and 7.23 ± 0.02 in rabbits with prominent acidosis (n = 7). In the control group, the average normal neuronal density of the CBs was 6432 ± 790/mm 3 and the degenerated neuron density was 11 ± 3/mm 3 , whereas the degenerated neuronal density in CBs was 35 ± 8/mm 3 in the sham group and 1034 ± 112/mm 3 in the slight acidosis-developed group (n = 6; P < 0.05). Conversely, degenerated neuron density of CBs was 2134 ± 251/mm 3 in the prominent acidosis-developed animals (n = 7; P < 0.005). Interestingly, in the rabbits who died, the degenerated neuron density of the CB was 3160 ± 840/mm 3 ., Conclusion: An inverse relationship between neurodegeneration in the CB and pH values secondary to the disruption of the GPN-CB network after SAH was found, which may contribute to developing acidosis., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Object: The glossopharyngeal nerves (GPNs) and carotid bodies (CBs) have an important role in the continuation of the cerebral autoregulation and cardiorespiratory functions. The relationship between degenerative injury of CB and the GPN in subarachnoid hemorrhage (SAH) was studied., Methods: Twenty rabbits were included in this study. Five of them (n=5) were used as control group. The remaining animals (n=15) were exposed to experimental SAH. In the six animals of the SAH group, severe signs of illness were observed, and these six animals were killed in the first week after SAH. Others animals (n=9) were followed for 20 days and then sacrificed. GPNs and CBs were examined and, the live and degenerated GPN axon number, and of CB neuron numbers were stereologically estimated., Results: The mean number of live neurons in CBs was 4206.67±148.35 and live axons of GPNs were 1211.66±14.29 in the animals of the control group. The number of degenerated neurons of CBs was 2065±110.27 and the number of degenerated axons of GPNs was 530.83±43.48 in early killed animals with SAH. The number of degenerated neurons of CBs and the number of degenerated axons of GPNs were found as 1013.89±4184 and 2270.5±134.38 in the living animals with SAH, respectively., Conclusions: High number of degenerated axons of GPN and neurons of CBs of the early killed animals suggest that the mortality in early SAH might be due to GPNs injury secondary to compression of their axons or supplying vessels by the probably herniated brainstem, and secondary denervation injury of CBs, and lung., (Crown Copyright © 2013. Published by Elsevier B.V. All rights reserved.)

Objective: Posteroinferior cerebellar artery (PICA) aneurysms are uncommon and have not been well investigated previously. We report our series of 29 ruptured PICA aneurysms with surgical treatment along with the description of the surgical anatomy of the PICA to the lower cranial nerves in cadaveric specimen., Methods: All patients with ruptured PICA aneurysms who were surgically treated at the First Affiliated Hospital of Soochow University during the period from January 1995 to December 2008 were reviewed retrospectively. Data relating to clinical, radiological, and intraoperative findings were analyzed. Forty formalin-fixed cerebellar hemispheres provided the material for the study of describing the detailed surgical anatomic relationship of the PICA to the lower cranial nerves., Results: In our series, ruptured PICA aneurysms reached an incidence of 2.35% of all ruptured intracranial aneurysms. There were 13 aneurysms (44.8%) located in the proximal segment, and 16 (55.2%) located in the distal segment. Of these, 89.7% were saccular, 6.9% fusiform, and 3.4% dissecting aneurysms. Usually, the surgical outcome was influenced by Poor admission grade, the presence of obstructive hydrocephalus and associated distal AVM. In cadaveric specimen, 17.5% of PICAs passed between the glossopharyngeal and vagus nerves, 7.5% between the vagus and accessory nerves, and 62.5% through the rootlets of the accessory nerve., Conclusion: This report summarizes the presentation and outcome of a large series of 29 patients with ruptured PICA aneurysms, and we conclude that ruptured PICA with surgical treatment usually gets well recovered. The study does, however, also demonstrate that the anatomic relationship of the PICA and lower cranial nerves is somehow variable and irregular. Recognition of the findings in cadaveric dissection is essential in treating lesions of this region., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Background: The lower cranial nerves must be identified to avoid iatrogenic injury during skull base and high cervical approaches. Prompt recognition of these structures using basic landmarks could reduce surgical time and morbidity., Methods: The anterior triangle of the neck was dissected in 30 cadaveric head sides. The most superficial segments of the glossopharyngeal, vagus and its superior laryngeal nerves, accessory, and hypoglossal nerves were exposed and designated into smaller anatomic triangles. The midpoint of each nerve segment inside the triangles was correlated to the angle of the mandible (AM), mastoid tip (MT), and bifurcation of the common carotid artery., Results: A triangle bounded by the styloglossus muscle, external carotid artery, and facial artery housed the glossopharyngeal nerve. This nerve segment was 0.06 ± 0.71 cm posterior to the AM and 2.50 ± 0.59 cm inferior to the MT. The vagus nerve ran inside the carotid sheath posterior to internal carotid artery and common carotid artery bifurcation in 48.3% of specimens. A triangle formed by the posterior belly of digastric muscle, sternocleidomastoid muscle, and internal jugular vein housed the accessory nerve, 1.90 ± 0.60 cm posterior to the AM and 2.30 ± 0.57 cm inferior to the MT. A triangle outlined by the posterior belly of digastric muscle, internal jugular vein, and common facial vein housed the hypoglossal nerve, which was 0.82 ± 0.84 cm posterior to the AM and 3.64 ± 0.70 cm inferior to the MT., Conclusions: Comprehensible landmarks can be defined to help expose the lower cranial nerves to avoid injury to this complex region., (Copyright © 2010 Elsevier Inc. All rights reserved.)

We report a patient with acute cranial polyneuropathy with unilateral involvement of the ninth, tenth, and eleventh cranial nerves. Although this patient lacked a typical cutaneous herpetic manifestation, elevated levels of IgM and IgG antibodies to varicella zoster virus (VZV) in both the serum and cerebrospinal fluid confirmed the clinical diagnosis of VZV infection and zoster sine herpete. Coexisting hypoplasia of the ipsilateral jugular foramen was detected using three-dimensional, surface-rendering displays reconstructed from the cranial helical CT scan. The patient recovered almost completely following treatment with an anti-inflammatory corticosteroid. Anatomical narrowing of the jugular foramen in this patient may have contributed to entrapment of the affected nerves at their passage through the foramen.

Lesions of the brainstem have been associated with obstructive sleep apnea in previous reports. We now report a case in which retromastoid craniectomy with microvascular decompression of the medulla and ninth and tenth cranial nerves resulted in the complete resolution of severe obstructive sleep apnea. Possible mechanisms for this observation are discussed.

The authors report a case of a cervical zoster (C2 - C4) with unilateral involvement of the IXth, Xth, XIth and XIIth cranial nerves. Angiography failed to opacify the ascending pharyngeal artery on the same side, presumably because of a thrombosis secondary to the zoster infection. As the ascending pharyngeal artery is known to supply the last four cranial nerves, this study should be seen as a further example of the varied cranial nerve involvement which may arise on a vascular basis.