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416 Clinical Pathways in Neuro-Ophthalmology, second edition Figure 18–1. Evaluation of ptosis.
Is the Ptosis Steroid Induced? Topical steroids have been implicated in some cases of ptosis. Discontinuation of the steroids may reverse the ptosis in these cases. Is Aponeurotic Ptosis Present? Levator aponeurosis thinning and=or dehiscence may occur as a result of trauma, surgery, lid swelling, patching, or, most commonly, as an age-related phenomenon (Frueh, 1996; Liu, 1993; Older, 1995). The characteristic features of aponeurotic ptosis are listed in Table 18–8. Patients with aponeurotic ptosis may have significant ptosis in downgaze more than primary position (Dryden, 1992; Wojno, 1993). In the absence of findings to suggest mechanical, neurogenic, myogenic, or neuromuscular etiologies for ptosis, no further evaluation is necessary. Superior visual field loss may occur due to ptosis and may be an indication for surgical correction. The surgical treatment of aponeurotic ptosis is well described in the literature and is not reviewed here (Frueh, 1996; Liu, 1993; Older, 1995). Aponeurotic ptosis does not require any neuroimaging (class III–IV, level B). An approach to the evaluation of ptosis is outlined in Figure 18–1. References Ptosis 417 Abe K, Fujimura H, Tatsumi C, et al. (1995). Eyelid ‘‘apraxia’’ in patients with motor neuron disease. J Neurol Neurosurg Psychiatry 59:629. Adair JC, Williamson DJG, Heilman KM. (1995). Eyelid opening apraxia in focal cortical degeneration. J. Neurol Neurosurg Psychiatry 58:508–509. Afifi AK, Corbett JJ, Thompson HS, Wells KK. (1990). Seizure-induced miosis and ptosis: association with temporal lobe magnetic resonance imaging abnormalities. J Child Neurol 5:142–146. Al-Din AN, Anderson M, Eeg-Olofsson O, et al. (1994). Neuro-ophthalmic manifestations of the syndrome of ophthalmoplegia, ataxia, and areflexia. A review. Acta Neurol Scand 89:157–163. Aramideh M, Ongerboer de Visser BW, Koelman JHTM, Speelman JD. (1995). Motor persistence of orbicularis oculi muscle in eyelid-opening disorders. Neurology 45:897–902. Ashizawa T, Hejtmancki JF, Liu J, Perryman MB, Epstein MF, Koch DD. (1992). Diagnostic value of ophthalmologic findings in myotonic dystrophy: comparison with risks calculated by haplotype analysis of closely linked restriction fragment length polymorphisms. Am J Med Genet 42:55–60. Averbuch-Heller L, Helmchen C, Horn AKE, et al. (1998). Slow vertical saccades in motor neuron disease: correlation of structure and function. Ann Neurol 44:641–648. Averbuch-Heller L, Leigh RJ, Mermelstein V, et al. (2002). Ptosis in patients with hemispheric stroke. Neurology 58:620–624. Averbuch-Heller L, Stahl JS, Remler BR, Leigh RJ. (1996). Bilateral ptosis and upgaze palsy with right hemispheric lesions. Ann Neurol 40:465–468. Avisar R, Leshem Y, Savir H. (1991). Unilateral congenital ptosis due to plexiform neurofibroma, causing refraction error and secondary amblyopia. Metab Pediatr Syst Ophthalmol 14:62–63. Barton JJ, Kardon RH, Slagel D, Thompson HS. (1995). Bilateral central ptosis in acquired immunodeficiency syndrome (review). Can J Neurol Sci 22:52–55. Berlit P, Rakicky J. (1992). The Miller Fisher syndrome: review of the literature. J Clin Neuro-ophthalmol 12:57–63. Blumen SC, Nisipeanu P, Sadeh M, Asherov A, Tome F, Korczyn AD. (1993). Clinical features of oculopharyngeal muscular dystrophy among Bukhara Jews. Neuromusc Dis 3:575–577. Boghen D. (1997). Apraxia of lid opening: a review. Neurology 48:1491–1503. Brazis PW. (1997). Enhanced ptosis in Lambert-Eaton myasthenic syndrome. J Neuro-ophthalmol 17:202–203.
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Thieme New York 333 Seventh Avenue
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To our wives, Hilary and Liz and to
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x Preface We would again like to th
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2 Clinical Pathways in Neuro-Ophtha
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10 Clinical Pathways in Neuro-Ophth
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Table 1-12. Clinical Features of Ra
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13 r Sixth Nerve Palsies What is th
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