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Disorders of the salivary glands
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
Once the facial nerve trunk has been identified, gentle traction anteriorly facilitates further mobilisation. Control of haemorrhage at this stage is vital as bleeding, no matter how minor, significantly impedes visibility for the surgeon. Haemostasis can be achieved with bipolar diathermy, although caution is necessary, particularly as the facial nerve is approached. Damage to the stylomastoid artery, which lies immediately lateral to the nerve, can result in troublesome bleeding immediately prior to identification. Pledget swabs soaked in adrenaline are sometimes helpful in reducing the ooze associated with this phase of the dissection.
The Facial Nerve and its Non-Neoplastic Disorders
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Christopher Skilbeck, Susan Standring, Michael Gleeson
The arterial supply of the segments of the facial nerve is derived from branches of the vertebrobasilar and ECA systems (Figure 112.6).61,62 The labyrinthine artery (internal auditory artery) supplies the cisternal, meatal and labyrinthine segments. It usually arises directly from the AICA as it loops between the cisternal segments of the motor root of the facial nerve, the nervus intermedius and the vestibulocochlear nerves, projecting towards and often into the IAM, but it may arise from the basilar, vertebral or superior cerebellar arteries.63 The greater petrosal nerve is supplied by the petrosal branch of the middle meningeal artery which usually passes through the bone enclosing the geniculate ganglion and tympanic segment of the nerve, less commonly it passes through the hiatus of the greater petrosal nerve: the vessel and nerve are at risk during procedures where the dura is elevated from the floor of the MCF.64 The tympanic and mastoid segments are supplied by the facial arch, an anastomotic network formed by the superficial petrosal branch of the middle meningeal artery and the stylomastoid branch of either the occipital or posterior auricular arteries, which enters the facial canal via the stylomastoid foramen. The lowest branch from the stylomastoid artery to the facial nerve is given off at the level of the origin of the chorda tympani: collaterals of the stylomastoid artery supply the chorda tympani. Branches from the facial arch anastomose with vessels supplying the bone marrow of the facial canal and with anterior and superior tympanic branches of the maxillary artery, the posterior tympanic branch of the posterior auricular artery, and the inferior tympanic branch of the ascending pharyngeal artery.65 The posterior auricular and occipital arteries and their branches, including the stylomastoid artery, supply the facial nerve from the stylomastoid foramen to the parotid gland. The temporofacial and cervicofacial branches that exit the parotid gland are supplied by collaterals of the superficial temporal, transverse facial, facial and maxillary arteries.
3-Tesla magnetic resonance imaging reveals vasculitis-caused otitis media in a patient with giant cell arteritis
Published in Acta Oto-Laryngologica Case Reports, 2021
Natsuki Aoki, Taro Fujikawa, Natsuka Umezawa, Yoshiyuki Kawashima, Taku Ito, Keiji Honda, Takeshi Tsutsumi
Our results suggest that two possible etiopathogenesis of otologic symptoms in GCA. One possibility is small vessel vasculitis in the fallopian canal. Our recent research shows that intense enhancement of the fallopian canal on contrast-enhanced 3 D-GRE imaging acquired at 3-Tesla can be a marker for vasculitis in the temporal bone in ANCA-associated vasculitis with otologic manifestations [8]. Two small arteries inside the fallopian canal, the stylomastoid artery and superficial petrosal artery, are the main blood supply for the tympanic and mastoid cavities, and vasculitis of these arteries leads to otitis media. Small-vessel vasculitis occasionally occurs in association with both clinically diagnosed and biopsy-proven GCA [13,14]. On the other hand, our results did not show any enhanced lesions suggestive of inflammation in the tympanic and mastoid cavities, as was found in ANCA-associated vasculitis [8].
Minimally invasive endoscopic treatment of chronic otitis media with facial nerve palsy- A case report and literature review
Published in Acta Oto-Laryngologica Case Reports, 2021
The two most common surgical approaches as described by Fisch and May in 1972 for facial nerve decompression include the transmastoid approach and the middle fossa craniotomy (MFC). The transmastoid approach has greater access to the tympanic or mastoid segments and can be further subdivided into different approaches, such as the retroauricular or endaural approach. MFC allows good exposure to the labyrinthine segment, geniculate ganglion, and tympanic segment but requires temporal lobe retraction [12]. Surgery dealing with the facial nerve is not exempted without complications. As reported by May and Klein, complications of facial nerve surgery include hearing loss conductive and sensorineural, trauma to the facial nerve itself, tinnitus, labyrinthine injury, dural injury, injury to the middle meningeal artery injury, the sigmoid plate, the superior petrosal vein, the stylomastoid artery, the dura and the brain [14]. Even though there is improvement in the patients undergoing decompression, it is clear that there is always a possible risk of iatrogenic injury to the facial during the surgery [8].
Characteristic manifestation of ocular and cervical vestibular evoked myogenic potentials findings in severe obstructive sleep apnea patients
Published in Acta Oto-Laryngologica, 2021
Hui-Ping Luo, Jing Yu, Xin-Da Xu, Jing Wang, Qing Zhang, Hai-Tao Wu, Fang-Lu Chi
Despite the foregoing findings, no significant differences were found between the study group and the control group in the caloric tests. This indicates that there was no significant functional impairment of the horizontal semicircular canal in the study group. In other words, unlike the otolithic organs, the horizontal semicircular canal and its neural pathway may not be significantly impaired by hypoxemia or by other complications caused by severe OSA. We speculate that we may have obtained a negative result in the caloric tests due to anatomical factors. The blood supply of the inner ear has two main components, one of which is the labyrinthine artery. This artery enters the inner ear through the inner ear canal and then bifurcates into the vestibular artery and the common cochlear artery. The branches of the vestibular artery supply the upper and lateral parts of the utricle and saccule and partially supplement the blood supply of both the superior semicircular canal and the horizontal semicircular canal. The other artery that supplies blood to the semicircular canals is the stylomastoid artery, a branch of the posterior auricular artery. Thus, the blood supply of the semicircular canals may be richer than that of the utricle and saccule, and when hypoxemia and nightly oxygen desaturation caused by severe OSA occurs, the otolithic organs may be more easily influenced than the semicircular canals. We concluded that this might be one of the main reasons that although the VEMP results of patients with severe OSA were worse than those of the healthy controls, no significant difference in the results of the caloric tests was found between the two groups. There are also limits to this study. The sample size could be further improved to eliminate the potential interference in the statistical results. Furthermore, v-HIT could be involved as it becomes a new favorite of clinicians and is widely used in the evaluation of semicircular canal function.