Myasthenic pseudo-internuclear ophthalmoplegia due to penicillamine.

George, Justin; Spokes, E.G.

doi:10.1136/jnnp.47.9.1044

Cited by 17 publications

(2 citation statements)

References 7 publications

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“…Any pattern of incomitant strabismus may develop, from single muscle paresis to total external ophthalmoplegia. It can mimic peripheral nerve palsies, such as IV nerve palsy, 41 VI nerve palsy, and partial III nerve palsy, 42 and also central disorders of gaze, including unilateral or bilateral internuclear ophthalmoplegia, [56][57][58] one-and-a-half syndromes 59 and double elevator palsy. Although any muscle may be affected, the medial rectus, inferior rectus, and superior oblique may be more commonly affected.…”

Section: Extra-ocular Musclesmentioning

confidence: 99%

Ocular Aspects of Myasthenia Gravis

Barton¹,

Fouladvand²

2000

Semin Neurol

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Ocular myasthenia gravis is a not uncommon autoimmune disorder causing diplopia, ptosis, and weakness of lid closure. The predilection of myasthenia for the ocular muscles may be related to differences between limb and extraocular muscles in either physiological function or antigenicity. Clinically, ocular myasthenia can mimic any form of pupil-sparing ocular motility disorder. Dynamic abnormalities of myasthenic eye movements may reflect the primary hallmarks of the disease, which are fatigability and variability in strength, or secondary adaptive effects by the central nervous system. Tests to confirm the diagnosis include edrophonium challenge, repetitive nerve stimulation, single-fiber electromyography (EMG) of the frontalis, and assays for antibody directed against the acetylcholine receptor: all are less sensitive for ocular myasthenia than for generalized myasthenia. There is a higher incidence of other autoimmune conditions in myasthenia, notably thymoma and thyroid dysfunction. The differential diagnosis includes other diseases of the neuromuscular junction, such as Lambert-Eaton syndrome and botulism. Treatment consists of symptomatic use of acetylcholinesterase inhibitors and immunosuppression with steroids or azathioprine. Between 50 and 70% of patients with ocular myasthenia will eventually develop generalized disease: there is some retrospective data that steroids or azathioprine may reduce this by about 75%. The role of thymectomy in ocular myasthenia remains unclear.

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Section: Extra-ocular Musclesmentioning

confidence: 99%

Ocular Aspects of Myasthenia Gravis

Barton¹,

Fouladvand²

2000

Semin Neurol

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“…However, internal ophthalmoplegia is also rare in MS [11]. Ptosis can be present [2,7,12] or absent [5] in MG. Ptosis would be important as indicating MG when it is consistent and reliable, because it is rare in MS [11]. Convergence was full in some patients with pseudo-INO [2,4], weak but present in some [2,5] including ours, and impaired in another [7], As convergence is usually preserved with an MLF lesion posterior to the oculomotor nerve nucleus [ 1 ], it can be a clue to the diagnosis when convergence is absent or severely impaired.…”

Section: Discussionmentioning

confidence: 99%

Bilateral Pseudo-internuclear Ophthalmoplegia in Myasthenia gravis

Ito¹,

Mizutani²,

Murofushi³

et al. 1997

ORL

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A 38-year-old male with bilateral pseudo-internuclear ophthalmoplegia (-INO) in myasthenia that could have been misdiagnosed as INO in multiple sclerosis is reported. He experienced fluctuating symptoms including double vision, imbalance, and tinnitus. His eye movements simulated bilateral INO, with a downshoot in abduction. After thymectomy, his eye movements became normal. From our case and a review of the literature, we propose that ptosis, downshoot, and fatigability are likely to be signs of pseudo-INO in myasthenia, whereas an impaired vertical smooth pursuit is unlikely. Dissociated nystagmus and monocular overshoot might be the results of central compensation.

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