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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Complete oculomotor nerve palsy with pupillary involvement is a neuro-ophthalmologic emergency because it is commonly caused by a compressive aneurysm at the junction of the posterior communicating artery and the internal carotid artery. If left untreated, this condition can be potentially fatal within days. The present report describes a 45-year-old African American woman with human immunodeficiency virus who presented with complaint of new-onset nonspecific headache, acute onset of complete oculomotor nerve palsy, and a dilated pupil of the right eye. Results of standard work-up for aneurysm and other etiologic factors were negative. Ten days after presentation, papulovesicular eruptions occurred over the V1 and V2 dermatomes, revealing herpes zoster ophthalmicus. The present case may be the first to identify a patient with complete ophthalmoplegia with pupil involvement as a pre-eruptive manifestation of herpes zoster. The literature on epidemiology, pathogenesis, clinical presentation, diagnosis, and current treatment options for this rare form of shingles are reviewed.
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PMID:Complete ophthalmoplegia with pupillary involvement as an initial clinical presentation of herpes zoster ophthalmicus. 1894 45

Based on a review of 20 well-documented cases reported in the English literature between 1968 and 2008, herpes zoster ophthalmicus (HZO) may rarely be associated with complete unilateral ophthalmoplegia, defined here as impaired ocular ductions in all 4 directions within 3 months of onset of manifestations of HZO. Ophthalmoplegia occurred equally in immune-competent and immune-incompetent individuals. HZO preceded ophthalmoplegia in 75% by a mean interval of 9.5 days and a range of 2 to 60 days, occurred simultaneously with ophthalmoplegia in 20%, and followed by 2 days the onset of ophthalmoplegia in only 5%. Concurrent conjunctival inflammation, keratitis, or anterior uveitis was present in 90%. Lumbar puncture showed features of aseptic meningitis in 88%, slightly more than the 40%-50% found in patients with HZO without ophthalmoplegia. On orbit/brain imaging, abnormal enlargement of the extraocular muscles was present in 33%, and orbital soft tissue swelling was present in 17%. Enhancement of ocular motor cranial nerves was not reported. Complete or near-complete resolution of ophthalmoplegia occurred in 65% within a range of 2 weeks to 1.5 years (mean 4.4 months). A single autopsy report described granulomatous angiitis of the meninges and large vessels in the anterior cerebral circulation, as well as periaxial infarction in the optic nerve, pons, and medulla but without viral inclusion bodies or antigen. Unsettled issues are whether the pathogenesis is direct viral invasion or an immune reaction to the virus, whether the impaired ocular ductions are based on myopathic or neuropathic injury, whether there are predisposing factors to the combination of HZO and complete ophthalmoplegia, and whether treatment is effective.
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PMID:Complete unilateral ophthalmoplegia in herpes zoster ophthalmicus. 1995 8

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with localized herpes zoster is rarely reported and may be under-appreciated. We describe two diabetic men with herpes zoster ophthalmicus (HZO) who developed hyponatremia (114 and 116 mmol/L) during acute illness. Both were euvolemic and had elevated urine osmolality (435 and 368 mmol/kg.H(2)O) and sodium (Na(+)) concentration (61 and 63 mmol/L) along with normal cardiac, renal, liver, and endocrine function consistent with the diagnosis of SIADH. Thorough investigation for other causes of SIADH, including detailed physical examination, laboratory studies, and computed tomography of the brain, chest, and abdomen, were negative. Despite antiviral therapy (acyclovir) for herpes zoster, ophthalmoplegia, keratitis, and post-herpetic neuralgia (PHN) developed. Even with fluid restriction and high salt diet, SIADH lasted for 3 to 4 months and resolved concomitantly with resolution of PHN, suggesting an association between SIADH and HZO. These two cases raise the potential for herpes zoster infection, especially HZO, to involve the regulatory pathway of ADH secretion, contributing to SIADH. The presence of PHN, which reflects greater neural damage may, at least in part, explain the prolonged ADH secretion and hyponatremia.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone associated with localized herpes zoster ophthalmicus. 2087 95

We report a rare instance of favorable outcome in orbital apex syndrome secondary to herpes zoster ophthalmicus (HZO) in a human immunodeficiency virus (HIV)-positive patient. The patient complained of pain and decrease in vision in one eye (20/640) for 2 weeks accompanied with swelling, inability to open eye, and rashes around the periocular area and forehead. The presence of complete ophthalmoplegia, ptosis, relative afferent pupillary defect, and anterior uveitis with decreased corneal sensation prompted a diagnosis of HZO with orbital apex syndrome. The enzyme-linked immunosorbent assay test and a low CD4 count confirmed HIV. Highly active antiretroviral therapy (HAART), systemic acyclovir, and systemic steroids were started. Visual acuity and uveitis improved within 10 days. By the end of the fourth week, ocular motility also recovered and the final visual acuity was 20/25. We highlight the role of HAART, used in conjunction with systemic steroid and acyclovir therapy, in improving the outcome.
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PMID:A rare case of orbital apex syndrome with herpes zoster ophthalmicus in a human immunodeficiency virus-positive patient. 2095 40

We report our findings for a patient with orbital apex syndrome associated with herpes zoster ophthalmicus. Our patient was initially admitted to a neighborhood hospital because of nausea and loss of appetite of 10 days' duration. The day after hospitalization, she developed skin vesicles along the first division of the trigeminal nerve, with severe lid swelling and conjunctival injection. On suspicion of meningoencephalitis caused by varicella zoster virus, antiviral therapy with vidarabine and betamethasone was started. Seventeen days later, complete ptosis and ophthalmoplegia developed in the right eye. The light reflex in the right eye was absent and anisocoria was present, with the right pupil larger than the left. Fat-suppressed enhanced T1-weighted magnetic resonance images showed high intensity areas in the muscle cone, cavernous sinus, and orbital optic nerve sheath. Our patient was diagnosed with orbital apex syndrome, and because of skin vesicles in the first division of the trigeminal nerve, the orbital apex syndrome was considered to be caused by herpes zoster ophthalmicus. After the patient was transferred to our hospital, prednisolone 60 mg and vidarabine antiviral therapy was started, and fever and headaches disappeared five days later. The ophthalmoplegia and optic neuritis, but not the anisocoria, gradually resolved during tapering of oral therapy. From the clinical findings and course, the cause of the orbital apex syndrome was most likely invasion of the orbital apex and cavernous sinus by the herpes virus through the trigeminal nerve ganglia.
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PMID:Orbital apex syndrome associated with herpes zoster ophthalmicus. 2214 Mar 5

Herpes zoster ophthalmicus (HZO) with oculomotor nerve involvement is rare, even rarer as an acute presentation rather than sequelae of HZO. In this paper we present a case of cutaneous HZO in which our patient's initial presentation was one of complete ophthalmoplegia.
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PMID:An acute case of herpes zoster ophthalmicus with ophthalmoplegia. 2264 45

An 86-year-old female presented with eye pain, complete ophthalmoplegia, a visual acuity of 1/60, vitritis, ptosis, displacement of the eye, and a partially dilated pupil unresponsive to light. A computed tomography of the cerebrum was normal. Herpes zoster ophthalmicus was suspected and treatment with i.v. acyclovir and prednisolone was commenced, which led to a gradual improvement of the clinical condition. Complete ophthalmoplegia due to herpes zoster ophthalmicus is a very rare condition and no evidence-based treatment is available. The prognosis is very good with almost complete remission of the symptoms within 18 months.
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PMID:[Complete ophthalmoplegia following outburst of herpes zoster]. 2273 24

An 80-year-old Caucasian woman had been diagnosed with right herpes zoster ophthalmicus 2 ½ weeks before presentation to our department. Ten days after stopping oral aciclovir, she presented with periorbital pain, visual loss, ptosis and complete ophthalmoplegia. On examination, visual acuity in her right eye was hand movements, with a relative afferent pupillary defect and 2 mm proptosis. MRI demonstrated contrast enhancement within the orbit extending into the apex, suggestive of an inflammatory process. Oral treatment was started with oral aciclovir and corticosteroids for 2 months, when she had resolution of the optic neuropathy and ophthalmoplegia. Vision recovered to 6/9 and repeat neuroimaging revealed regression of the inflammatory process.
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PMID:Ophthalmoplegia secondary to herpes zoster ophthalmicus. 2279 18

Orbital apex syndrome is a rare manifestation of Herpes Zoster Ophthalmicus. Herein we report on a case of orbital apex syndrome secondary to Herpes Zoster Ophthalmicus. A 75 year-old male complained of vision loss, conjunctival hyperemia and proptosis on the left eye, was referred to our clinic. Visual acuity was 5/10 Snellen lines and he had conjunctival hyperemia, chemosis, minimal nuclear cataract and proptosis on the left eye. A diagnosis of orbital pseudotumor was demonstrated firstly. The patient received oral and topical corticosteroids, antiinflammatory and antibiotic agents. On day 2, vesiculopustular lesions were observed, Herpes Zoster Ophthalmicus was diagnosed and corticosteroid treatment stopped, oral acyclovir treatment initiated. Two days later, total ophthalmoplegia, ptosis and significant visual loss were observed on the left. The diagnosis of orbital apex syndrome was considered and the patient commenced on an intravenous acyclovir treatment. After the improvement of acute symptoms, a tapering dose of oral cortisone treatment initiated to accelarate the recovery of ophthalmoplegia. At 5-month follow-up, ptosis and ocular motility showed improvement. VA did not significantly improve because of cataract and choroidal detachment on the left. We conclude that ophthalmoplegia secondary to Herpes Zoster Ophthalmicus responds favourably to intravenous acyclovir and steroids.
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PMID:Orbital apex syndrome in herpes zoster ophthalmicus. 2283 66

A male patient with herpes zoster ophthalmicus (HZO) presented with left exophthalmos, external and internal ophthalmoplegia and decreased visual acuity. A CT scan revealed myositis without significant compression of the optic nerve. Intravenous acyclovir and oral steroids were started with improvement of the symptoms and eventual complete recovery.Orbital apex syndrome is a rare complication of HZO. Multiple pathogenic mechanisms are involved, including a direct cytopathic effect of the virus as in the present case. Early diagnosis and therapy may lead to complete recovery of visual function.
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PMID:Orbital apex syndrome secondary to herpes zoster virus infection. 2461 76


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