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Ocular Motor Cranial Neuropathies
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Zane Foster, Ashwini Kini, Bayan Al-Othman, Andrew G. Lee
Lastly, it is important to remember the causes of acute-onset ophthalmoplegia which include myasthenia gravis, Miller Fisher variant of Guillain-Barre syndrome, botulism, brainstem encephalitis, Wernicke encephalopathy, carcinomatous meningitis, or leptomeningeal disease when the ophthalmoplegia is acute, bilateral, or appears to involve multiple cranial nerves.
Neuromuscular Junction Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Diana Mnatsakanova, Qin Li Jiang
Chronic progressive external ophthalmoplegia: Patients generally do not complain of diplopia in the presence of very restricted extraocular movements, which is typically more severe than seen in MG.Retinal degeneration can coexist, and more generalized muscle weakness can occur later in the disease course.
Thyroid ophtalmopathy manifesting as superior oblique paralysis
Published in Jan-Tjeerd de Faber, 28th European Strabismological Association Meeting, 2020
V. Oğuz, M. Yolar, H. Pazarli, S. Özkan
within the differential diagnosis in all cases showing an ophthalmoplegia [9]. As in the thyroid ophtalmomyopathy the involvement of the inferior rectus is the most frequent, often appearing with a vertical diplopia [4,5].
Infantile and Early Acquired Ophthalmoplegic Syndromes
Published in Journal of Binocular Vision and Ocular Motility, 2018
CCDDs, extraocular muscle dysgenesis, and profound congenital myopathy should be considered when static ophthalmoplegia presents at birth. Episodic ophthalmoplegia could be ophthalmoplegic migraine, while acute and profound ophthalmoplegia in association with respiratory distress could be botulism. Progressive ophthalmoplegia with a variable course or in association with ptosis raises the possibility of myasthenia, while ophthalmoplegia with relentless progression to systemic weakness or in association with generalized weakness could be associated with neurodegenerative disease, muscular dystrophy, or other rare, progressive myopathies. Nonsurgical treatment of ophthalmoplegia in children and adults is reviewed by Arnoldi,22 and surgical management is reviewed by Archer23 elsewhere in this issue. Treatment of each of these conditions is challenging, and by necessity must be context-dependent.
Ophthalmoplegia: When the Eyes Don’t Move: An Introduction
Published in Journal of Binocular Vision and Ocular Motility, 2018
Ophthalmoplegia is often perceived as a complex entity with a confusing combination of clinical presentations and overlapping diagnostic entities. Ophthalmoplegia may also be an indicator of more serious neurological or systemic pathology. Thus, many eye-care providers, when presented with such patients, simply refer them to the nearest subspecialist. However, the care of these patients is not only interesting but also highly rewarding, and a multidisciplinary, team-based approach ensures optimal clinical and functional outcomes. In this symposium, the essentials of assessment and initial treatment are reviewed with updates on clinical and surgical approaches to management.
Recurrent Painful Ophthalmoplegic Neuropathy with Unilateral Oculomotor and Trochlear Nerve Palsy in an 8-year-old Girl
Published in Journal of Binocular Vision and Ocular Motility, 2022
Javad Akhondian, Farah Ashrafzadeh, Farrokh Seilanian Toosi, Mahla Esmaeilzadeh, Mehran Beiraghi Toosi, Shima Imannezhad, Nazanin Saeedi Zand, Narges Hashemi
Ultimately, she was diagnosed with RPON based on clinical and laboratory findings, so we started prednisolone treatment (1 mg/Kg.day) for a week. There was no response to prednisolone; therefore, we also added indomethacin 25 mg/day, and the treatment continued. By the end of the second week of the treatment, the patient’s ptosis relatively improved and we started to taper prednisolone to 0.5 mg/Kg/day. By the end of the third week, the ptosis had completely resolved. By the end of the fourth week of the treatment, the ophthalmoplegia partially improved. On the fifth week of treatment, all symptoms were completely gone.