The cranial nerves

With the exception of the olfactory and optic nerves, all cranial nerves enter or leave the brain stem. Three of the cranial nerves are purely sensory (I, II and VIII), five are motor (III, IV, VI, XI and XII) and the remaining nerves (V, VII, IX and X) are mixed. The olfactory nerve will be discussed in Chap. 14, the optic nerve in Chap. 8 and the cochlear nerve in Chap. 7. The nuclei of the cranial nerves are arranged in an orderly, more or less columnar fashion in the brain stem: motor nuclei, somatomotor, branchiomotor and visceromotor (parasympathetic), derived from the basal plate, are located medially, whereas sensory nuclei, somatosensory, viscerosensory and vestibulocochlear, derived from the alar plate, are found lateral to the sulcus limitans. The cranial nerves innervate structures in the head and neck as well as visceral organs in the thorax and abdomen. The cranial nerves control eye movements, mastication, vocalization, facial expression, respiration, heart rate and digestion. One or several of the cranial nerves are often involved in lesions of the brain stem, of which the location can usually be determined if the topographical anatomy of the cranial nerves and their nuclei is known. Several examples are shown in Clinical cases. Following a few notes on the development of the brain stem and congenital cranial dysinnervation disorders (Sect. 6.2), the following structures will be discussed: (1) ocular motor nerves and the effects of lesions of individual ocular motor nerves (Sect. 6.3); (2) eye movements and some disorders affecting them (Sect. 6.4); (3) the trigeminal nerve and changes in the blink reflex (Sect. 6.5); (4) the facial nerve and peripheral facial nerve paralysis (Sect. 6.6); (5) the gustatory system (Sect. 6.7); (6) the vestibulocochlear nerve, vestibular control and some peripheral and central vestibular syndromes (Sect. 6.8); and (7) the last four cranial nerves and some disorders affecting them (Sects. 6.9 and 6.10). The English terms of the Terminologia Neuroanatomica are used throughout.</p

Long-term retinal nerve fiber layer changes following nonarteritic anterior ischemic optic neuropathy

Gad Dotan,1 Michaella Goldstein,1 Anat Kesler,1 Barry Skarf21Department of Ophthalmology, Tel Aviv Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; 2Eye Care Services, Henry Ford Hospital, Detroit, MI, USABackground: In cases of nonarteritic anterior ischemic optic neuropathy (NAION), retinal nerve fiber layer (RNFL) thickness changes have been described during the first 12 months following the acute event. The purpose of this study was to report on the long-term RNFL changes in these eyes beyond the first year following onset of NAION.Methods: Fourteen eyes of 13 patients with NAION were analyzed in this retrospective observational case series study. Uninvolved eyes served as controls. All patients underwent a complete neuro-ophthalmological examination and repeat measurements of peripapillary RNFL thickness using Stratus optical coherence tomography.Results: On optical coherence tomography scan performed on average 6 months following onset of NAION, the mean global RNFL thickness (59.8 &plusmn; 11.8 &mu;m) was significantly thinner (P < 0.001) compared with uninvolved eyes (95.1 &plusmn; 13.9 &mu;m). In a second optical coherence tomography scan performed on average 13 (range 12&ndash;23) months later, the mean global RNFL thickness (58.9 &plusmn; 6.5 &mu;m) was not significantly different (P = 0.702) from the first scan.Conclusion: There appears to be no further RNFL loss beyond the first 6 months following an acute event of NAION.Keywords: optical coherence tomography, retinal nerve fiber layer, nonartertic anterior ischemic optic neuropath