Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dysthyroid orbitopathy (DO) is an autoimmune disorder usually associated with Graves' disease. The extra-ocular muscles are the target of the autoimmune attack. As a result, they become enlarged, producing restrictive ophthalmoplegia and proptosis. Other cardinal signs of DO include upper eyelid retraction and lag, conjunctival injection and chemosis, and periorbital edema. Visual loss may occur if the enlarged extra-ocular muscles compress the optic nerve in the orbital apex. These cardinal signs may mimic neurological conditions, including Parinaud's syndrome, sixth nerve palsy, carotid-cavernous fistula, and spheno-orbital meningioma. Treatment is directed at the cardinal signs and is largely palliative. Under certain clinical conditions, judicious use of corticosteroids, radiation therapy, or surgery designed to decompress the orbit, correct strabismus, or restore normal lid position may help to restore visual function.
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PMID:Dysthyroid orbitopathy. 1087 76

It has been hypothesized that the distinct anatomic localization of the Graves' triad may be partially explained by pressure and trauma. While there are reports of local trauma clearly contributing to the pathogenesis of pretibial myxedema, direct evidence for a similar mechanism in Graves' ophthalmopathy (GO) has been lacking. We describe a 65-year-old male patient with stable mild Graves' ophthalmopathy of 24 years' duration in whom a retrobulbar block was administered prior to cataract removal. Three weeks after the procedure, he complained of rapidly progressive bilateral diplopia. In 6 months, there was moderate exophthalmos, exposure keratitis, almost complete ophthalmoplegia, and decreasing visual acuity requiring surgical decompression. Postdecompression, inflammatory signs and vision improved but there was complete ophthalmoplegia. The eye signs remained unchanged for the next 4 months but there was exacerbation of the disease within a week of receiving radioiodine despite concomitant steroid administration. Orbital irradiation was finally administered with rapid improvement in extraocular eye muscle function. We hypothesize that local inflammatory and immune responses stimulated by trauma and/or pressure in the retrobulbar compartment, triggered the development of severe ophthalmopathy in this patient. Thyroid-stimulating immunoglobulin (TSI) levels remained markedly elevated despite the clinical improvement suggesting that the beneficial effects of radiotherapy in this case were not mediated by suppressing TSI production.
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PMID:Severe Graves' ophthalmopathy after retrobulbar anesthesia for cataract extraction in a patient with mild stable thyroid eye disease. 1455 26

A 53-year-old woman with long-standing chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) developed progressive proptosis, lid retraction, and ophthalmoplegia. MRI showed enlarged, enhancing cranial nerves that initially gave rise to diagnostic confusion with Graves disease or orbitocavernous mass lesions. This report further documents that CIDP may cause hypertrophy of ocular motor and trigeminal nerves with imaging features that suggest alternative causes.
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PMID:Ophthalmoplegia, proptosis, and lid retraction caused by cranial nerve hypertrophy in chronic inflammatory demyelinating polyradiculoneuropathy. 1754 92

Many neurological diseases like myopathy, periodic paralysis, ophthalmoplegia, and myasthenia gravis are known associations of thyrotoxicosis. However the association of neuropathy with thyrotoxicosis is not frequently recognized. First described by Charcot in 1889, thyrotoxic neuropathy or 'Basedow's Paraplegia' is a rarely reported entity. We describe here a case of a young woman with subacute distal neuropathy as the presenting manifestation of thyrotoxicosis. The neuropathy improved on antithyroid treatment. A careful literature search leads us to believe that peripheral neuropathy in thyrotoxicosis is under recognised. Thyroid function tests can be helpful in the diagnosis of this treatable neuropathy and should be included in the routine work up.
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PMID:Thyrotoxic neuropathy- an under diagnosed condition. 1768 80

We report a child presenting with intermittent ophthalmoplegia and fluctuating ptosis and facial weakness whose evaluation revealed no evidence of myasthenia gravis but did reveal hyperthyroidism secondary to Graves disease. Successful treatment of the child's endocrinopathy resulted in complete resolution of his presenting symptoms. Children presenting with ophthalmoplegia and ptosis without proptosis should be evaluated for hyperthyroidism if no evidence of a myopathy or disorder of neuromuscular junction transmission is found.
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PMID:Childhood Graves disease masquerading as myasthenia gravis. 2295 13

Diplopia is a frequent neuro-ophthalmologic symptom with diverse etiologies. This article describes elementary diagnostic tests and frequent causes of diplopia. Monocular diplopia persists when the other eye is closed and usually disappears when the patient looks through a pinhole. It is usually caused by errors in the optical media of the eye and has to be differentiated from spectacle-induced side effect and non-organic disorders. A sign of non-organic etiology is absence of change in image position when the head is tilted. Binocular diplopia disappears regardless of which eye is closed. Binocular diplopia occurs when the images of both eyes cannot be fused. The most frequent direct cause of diplopia is acquired strabismus. Knowledge of several specific types of strabismus enables efficient patient management. Congenital and decompensating strabismus like accommodative esotropia, pathophoria, strabismus surso- and deorsoadductorius, retraction syndrome, Brown's syndrome and esotropia in high myopia only need ophthalmologic treatment. Orbital injury, orbital tumor, ocular myositis, Graves orbitopathy and vascular disease usually require multidisciplinary management. Neurogenic paresis, superior oblique myokymia, ocular neuromyotonia, myasthenia, chronic progressive external ophthalmoplegia (CPEO), internuclear ophthalmoplegia (INO) and skew deviation require specific neurologic examination. Treatment of diplopia includes treatment of the fundamental disorder, monocular occlusion, prisms and strabismus surgery.
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PMID:How to deal with diplopia. 2298 79


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