The interdependence of the development of the eye and oculomotor system during embryogenesis is currently unclear. The occurrence of clinical anophthalmia, where the globe fails to develop, permits us to study the effects this has on the development of the complex neuromuscular system controlling eye movements. In this study, we use very high-resolution T2-weighted imaging in five anophthalmic subjects to visualize the extraocular muscles and the cranial nerves that innervate them. The subjects differed in the presence or absence of the optic nerve, the abducens nerve, and the extraocular muscles, reflecting differences in the underlying disruption to the eye’s morphogenetic pathway. The oculomotor nerve was present in all anophthalmic subjects and only slightly reduced in size compared to measurements in sighted controls. As might be expected, the presence of rudimentary eye-like structures in the socket appeared to correlate with development and persistence of the extraocular muscles in some cases. Our study supports in part the concept of an initial independence of muscle development, with its maintenance subject to the presence of these eye-like structures.

The cuffed oropharyngeal airway is a modified Guedel airway and is recommended for anaesthesia in spontaneously breathing patients. To our knowledge this is the first report of transient unilateral lingual nerve palsy after the use of a cuffed oropharyngeal airway to maintain anaesthesia during arthroscopy of an ankle. The aetiology of lingual nerve damage is multi-factorial. The possible mechanisms involved include anterior displacement of the mandible during insertion of the cuffed oropharyngeal airway (as in the jaw hrust manoeuvre), compression of the nerve against the mandible, or stretching of the nerve over the hyoglossus by the cuff of the cuffed oropharyngeal airway. We recommend gentle airway manipulation with the use of the cuffed oropharyngeal airway, avoidance of excessive cuff inflation and early recognition of such a complication if it occurs.

We present a case of a 63-year-old diabetic male who developed malignant otitis externa following mastoidectomy. Extensive skull base osteomyelitis caused thrombosis of the jugular bulb and subsequent paralysis of cranial nerves VII, IX, X and XII. Hewas treated aggressively with intravenous antibiotics and debridement of granulation tissue in the mastoid bowl with full recovery of the cranial nerve palsies associated with recanalization of the jugular bulb. We believe this is the first reported case of malignant otitis externa to occur following mastoidectomy with complete recovery of the cranial nerve paresis.

The facial nerve is monitored intra-operatively using electromyography to identify and prevent damage during the excision of an acoustic neurinoma. In order to determine whether a profound level of peripheral neuromuscular blockade could be achieved without compromising facial electromyographic monitoring, 11 patients undergoing resection of acoustic neuroinoma were studied. After induction of anaesthesia, an infusion of atracurium was administered to reduce the integrated electrically evoked muscle potential (EEMP) of the hypothenar eminence by 70–100%. The facial nerve was directly stimulated in the surgical field and the facial evoked muscle potentials (EMPs) were recorded. Even under complete peripheral neuromuscular blockade (i.e. no electrically evoked muscle potential measurable over the hypothenar eminence, no palpable hypothenar muscle response) it was possible to evoke facial muscle electromyographic responses by stimulation of the facial nerve.

A 53-year-old male patient had been suffering from severe aural symptoms (pulsatile right-sided tinnitus and paroxysmal dizziness attacks with nausea) and right hemifacial spasm. Treatment had involved stellate ganglion block with lignocaine and the injection of intravenous sodium bicarbonate solution for attacks of Meniere's syndrome and facial nerve block with lidocaine for hemi-facial spasm. Despite these treatments, the dizzy attacks became more frequent, developing into the clustering state. Air CT cisternography and vertebral angiography demonstrated an enlarged and curved vertebral artery. Vascular cross-compression of the Vllth and VHIth cranial nerves was therefore suspected. Microvascular decompression was performed. After operation, the pulsatile tinnitus, dizziness and hemifacial spasm disappeared. From the present case and a review of the literature, we conclude that vascular cross-compression of the VHIth cranial nerve should be an indication for microvascular decompression only when symptoms of vascular cross-compression of the Vllth cranial nerve are also seen.