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)

A series of 16 patients with unilateral ophthalmoplegia due to mass lesions of the cavernous sinus was analyzed; there were six cavernous meninglomas and nine intracavernous aneurysms. All meningiomas were characterized by painless, insidiously progressive partial nerve palsies, as were half of the aneurysms; the remaining aneurysm patients experienced acute painful episodes. Pharmacologic pupillary tests failed to confirm a coexisting Horner syndrome in the majority of cases with anisocoria. Although plain skull films were unremarkable or misinterpreted as normal, bone tomograms, computerized axial tomograms, radionuclide scans, and cerebral angiograms established the diagnosis in all cases. Because cavernous meningiomas show slow progression and are surgically inaccessible, craniotomy is advised only if the visual pathways or brain stem is compromised. Intractable pain appears to be the only distinct indication for intervention with cavernous aneurysms.
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PMID:Meningiomas and aneurysms of the cavernous sinus. Neuro-ophthalmologic features. 62 85

A rare case of systemic lupus erythematosus (SLE) associated with lateral medullary syndrome and unilateral internuclear ophthalmoplegia was reported. A 15 year old girl was admitted to Kyushu University hospital on 2 September in 1987 because of vertigo, occular symptom, and sensory disturbance. She had noted vertigo since 28 August. On admission she had nystagmus, left Horner syndrome, sensory disturbance of left hemiface and right limbs and trunk and mild hemiparesis of right limbs. She also had a discoid erythema behind the left ear, butterfly rash on her cheek. She developed right internuclear ophthalmoplegia on 6 September. Investigations revealed biological false positive of serological test for syphilis, positive antinuclear antibodies, and prolonged APTT. Peripheral blood cell count and erythrocyte sedimentation rate were normal. There was no proteinuria. Computed tomography and magnetic resonance imaging failed to detect any lesions in the brain. Cerebrospinal fluid cell count was 20/3 and Ig-G index was 17.1%. Her neurological signs were thought to be related to SLE. Lupus anticoagulant might be responsible for the development of impairment of central nervous system (CNS). She was treated with prednisolone, initial dose of 40mg, and the symptoms and signs were improved quickly. Early diagnosis and treatment for SLE with CNS involvement is primarily important.
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PMID:[A case of systemic lupus erythematosus associated with lateral medullary syndrome and unilateral internuclear ophthalmoplegia]. 250 Oct 49

Ophthalmoplegia and blindness caused by squamous cell carcinoma were reported in a cat. Unilateral functional deficits of cranial nerves II, III, IV, and VI and of the sympathetic nerve supply caused blindness, complete ophthalmoplegia, and Horner syndrome. Radiography and computed tomography revealed a proliferating bony lesion associated with the right tympanic bulla, right temporal bone, right side of the mandible, and left frontal bone. A focal area of bony destruction involved the right sphenoid bone. The cat was euthanatized and necropsied. Squamous cell carcinoma was identified invading the bones and rostral part of the right side of the skull. The tumor had extended through the sphenoid bones into the region of the cavernous sinus and had surrounded the cranial nerves passing through this region. It also had invested connective tissue surrounding the optic nerves and had invaded the right globe through the lamina cribrosa. This represents an unusual distribution for ocular cranial squamous cell carcinoma in a cat.
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PMID:Squamous cell carcinoma causing blindness and ophthalmoplegia in a cat. 279 81

A 47-year-old woman presented with headache, acute monocular vision loss, and ipsilateral Horner syndrome. Apart from the optic neuropathy, all cranial nerve function was intact. Magnetic resonance imaging revealed an enlarged pituitary gland with compression of the orbital apex. The surgical specimen was consistent with pituitary apoplexy. The combination of headache, acute visual loss, and ipsilateral Horner syndrome without ophthalmoplegia, which may suggest carotid artery dissection, is evidently an unusual manifestation of pituitary apoplexy.
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PMID:Pituitary apoplexy causing optic neuropathy and horner syndrome without ophthalmoplegia. 1450 93

In multiple sclerosis (MS), nystagmus or internuclear ophthalmoplegia (INO) are the usual ocular motor dysfunctions. However, in patients with focal brainstem lesions, other rare manifestations may be observed, such as an isolated ocular motor nerve palsy or complex ocular motor disturbances. We report five MS patients with unusual ocular motor disturbances (bilateral third nerve palsy [n = 2], opsoclonus, Horner's syndrome and one-and-a-half syndrome). We discuss possible correlations between clinical disturbances and MRI abnormalities. Patients were seen in two MS centres. They had a confirmed diagnosis of MS and underwent a brain MRI and a complete neuro-ophthalmological work-up. In one case (opsoclonus), ocular motor manifestations were the first manifestation of MS. In the other four cases they occurred 3 months (Horner syndrome), 6 years and 12 years (bilateral third nerve palsy) and 2 years (one-and-a-half syndrome) after the disease onset, respectively. Four out of five patients were still in a relapsing-remitting form of MS. In the opsoclonus case, there was no evidence of a brainstem lesion. A gadolinium-enhanced lesion (2 cases) or a new T2-weighted lesion located in the brainstem correlated with the clinical presentation. All patients completely or partially recovered after corticosteroid infusions. Our study shows some rare or previously undescribed complex ocular motor symptoms in MS.
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PMID:Unusual ocular motor findings in multiple sclerosis. 1646 46

The gathering of visual information is a complex process that relies on concerted movements of the eyes, and cranial nerves II-VIII are at least partially involved in the visual system. The cranial nerves do not function in isolation, however, and there are multiple higher-order cortical centers that have input into the cranial nerves to coordinate eye movement. Among the functions of the cortical reflex pathways are (a) controlling vertical and horizontal gaze in response to vestibular input to keep the eyes focused on an object as the head moves through space, and (b) controlling rapid, coordinated eye movement to a new visual target (saccades). There are also reflex pathways connecting the cranial nerves involved in vision that produce consensual blinking of the eyes in response to corneal stimulation of one eye and consensual pupillary constriction in response to light input on one pupil. A variety of intracranial pathologic conditions, including benign and malignant neoplasms, infection, trauma, autoimmune diseases, vascular anomalies, degenerative diseases, and inherited-congenital disorders, can disrupt the cranial nerves and visual reflex pathways. This disruption can manifest in myriad ways-for example, as extraocular muscle paresis, afferent pupillary defect, oculosympathetic paresis (Horner syndrome), internuclear ophthalmoplegia, dorsal midbrain (Parinaud) syndrome, or loss of the corneal reflex. Knowledge of the function and anatomy of the cranial nerves and visual reflex pathways, coupled with selection of the proper magnetic resonance pulse sequence, will allow the radiologist to order appropriate imaging of the involved cranial nerve or visual reflex pathway based on the patient's symptoms and thereby play an essential role in establishing the diagnosis and planning appropriate therapy.
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PMID:Intracranial causes of ophthalmoplegia: the visual reflex pathways. 2402 40