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)

Cranial arteritis (CA) presenting as sudden blindness is well documented, and early recognition of this entity in an elderly patient with visual loss or diplopia is of critical importance. This entity presents a difficult diagnostic problem when temporal artery biopsy is negative, as in our case, or when the erythrocyte sedimentation rate is normal. The present report details an unusual patient with "occult temporal arteritis" who sustained abrupt monocular visual loss and subsequent ipsilateral ophthalmoplegia involving all functions of the oculomotor nerve. Despite negative biopsies of each temporal artery, other probable etiologies of the symptom complex were excluded, and the diagnosis of cranial arteritis is warranted. The patient is unique in that the oculomotor palsy is complete and permanent. This report emphasizes cranial arteritis masquerading as an intracranial aneurysm.
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PMID:Biopsy-negative cranial arteritis with complete oculomotor nerve palsy. 43 39

Sixty-five cases of berry aneurysm on the supraclinoid portion of internal carotid artery were reviewed on the viewpoint of oculomotor palsy. 27 of 65 patients (42%) showed oculomotor palsy. Most cases of complete oculomotor paralysis developed immediately after having subarachnoid hemorrhage, whereas the case of gradually developing oculomotor palsy tended to manifest diplopia first, and followed with blephaloptosis. The recovery rate from oculomotor palsy seemed to be correlated with the duration from the onset of symptom to surgery. The recovery from the complete oculomotor paralysis lasting for a long time seemed to be unsatisfactory unless the surgical direct procedure to the aneurysm was successful in early stage.
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PMID:[Oculomotor palsy due to aneurysm of internal carotid artery (author's transl)]. 49 66

Multiple sclerosis is a disease of the central nervous system whose clinical manifestations include animportant group of ocular pathologies, e.g., unilateral retrobulbar neuritis, uveitis, decreased visual function, nystagmus, internuclear ophthalmoplegia, diplopia, optic papillitis and Marcus Gunn pupil. Additionally, it is not generally appreciated that bitemporal hemianopia, usually associated with tumors of the optic chiasm, may also result from multiple sclerosis. Since most of a patient's life is spent in the remission phase of the disease, it is important for the practitioner to recognize the ocular findings present during this period. Additionally, studies have shown that such patients lead longer and more productive lives than most practitioners realize, and often have prolonged periods of remission. While the onset of the disease may present with ocular symptoms, such as loss of vision or diplopia, the patients tend to recover and retain relatively good function for many years.
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PMID:The ocular manifestations of multiple sclerosis. 59 46

Fifteen patients spontaneously developed paralysis of one superior oblique muscle, which remained unexplained after an initial evaluation. Follow-up evaluation showed that all of the patients' conditions were improved. Twelve of the patients had enjoyed spontaneous, functional recoveries within four months. Three had residual diplopia that was relieved by prisms. No patient subsequently developed evidence of any local or systemic disease that could explain the ophthalmoplegia. One patient suffered a recurrence 3 1/2 years after his first episode that lasted three months and spontaneously cleared.
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PMID:Cryptogenic unilateral paralysis of the superior oblique muscle. 62 75

A study is presented of three patients suffering from internuclear ophthalmoplegia without diplopia. The components of the nystagmus and the dysmetry of the oculomotor changes, as well as the difference in the respective speeds during abduction and adduction toward the side opposite to the lesion were recorded. A dysmetric component was found in the saccadic low amplitude movements (reading movements).
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PMID:[So-called internuclear ophthalmoplegias. Electro-oculographic study]. 73 73

Two hundred and twenty-seven cases of carcinoma metastatic to the eye and orbit have been reviewed previously. The orbit alone was involved in 28 cases: theses lesions constitute the basis of this clinicopathologic study. The most common signs and symptoms produced by orbital metastasis included exophthalmos (75%1, pain (29%), decreased vision (29%), periorbital swelling (25%), a visible mass (21%), ophthalmoplegia, and diplopia (18%). The ophthalmologists' preoperative (or premortem) clinical diagnoses were: orbital mass, 36%; metastatic carcinoma, 29%; leukemia, 7%; melanosarcoma, 4%; mixed tumor of lacrimal gland, 4%; and meningioma, 4%. The sites of the primary tumors in the 28 patients with orbital metastasis were as follows: breast, eight; lung, four; genitourinary tract, four; pancreas, one; and ileum, one. In 10 patients the site of the primary carcinoma was not determined. In 17 of the 28 patients, symptoms of orbital metastasis preceded detection of a primary tumor elsewhere in the body. In 10 of the remaining 11 patients, detection of the primary tumor had preceded the onset of orbital symptoms. In one patient, symptoms of the primary tumor and of orbital metastasis appeared at about the same time. The median survival of patients with carcinoma metastatic to the orbit was 15.6 months from the time of orbital surgery. This was much better than the median survival of the 227 patients in the overall study (7.4 months) and far better than the median survival of the patients with metastasis to the anterior segment of the eye (only 5.4 months).
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PMID:Carcinoma metastatic to the eye and orbit III. A clinicopathologic study of 28 cases metastatic to the orbit. 95 71

The triad of ataxia, areflexia and ophthalmoplegia was first described as a variant of the Guillain-Barre syndrome in 1932 by Collier. In 1956, Miller Fisher reported three patients with ataxia, areflexia, and ophthalmoplegia as a separate entity. Since then, 223 cases of Miller Fisher syndrome have been published. The male/female ratio is 2:1 with a mean age of 43.6 years at the onset of the disease. A viral infection preceded the neurological symptoms in 71.8% of cases with an average symptom-free interval of 10 days. First symptoms were diplopia (38.6%) or ataxia (20.6%). An areflexia was present in 81.6% of cases. Cranial nerves other than the oculomotor nerves were involved in 127 cases (56.9%): cranial nerves 7 (45.7%), 9 and 10 (39.9%), and 12 (13%) were involved. In 53 cases a tetraparesis occurred. An elevated protein value was present in 134 patients (64.4%); cerebrospinal fluid findings were normal in 56 patients. Eighteen patients showed a mild pleocytosis. Besides the cerebellar type of ataxia, initial disturbances of consciousness (n = 8), supranuclear oculomotor signs (n = 22), and pathology findings in electroencephalography (n = 38), computed tomography (n = 8), and magnetic resonance imaging (n = 2) were reported as evidence for a central nervous system involvement in the Miller Fisher syndrome. The prognosis of Miller Fisher syndrome was good--recovery occurred after a mean time period of 10.1 weeks. Residual symptoms were present in 74 cases (33.2%), and a recidivism of the Miller Fisher syndrome was reported in seven patients. Eight patients died. Of six patients with autopsy findings, four exhibited central nervous system lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The Miller Fisher syndrome. Review of the literature. 153 3

We treated one patient with bilateral internuclear ophthalmoplegia and another with skew deviation with extraocular muscle botulinum toxin injection. Both patients had pre-injection symptomatic diplopia in primary position, one for 1 month and the other for 12 months. Resolution of diplopia and complete and permanent binocular fusion in primary position was obtained within 3 to 4 days in both cases.
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PMID:Botulinum toxin treatment of supranuclear ocular motility disorders. 162 Mar 51

This report describes a rare complication after the resection of a tumor of the posterior fossa, the "one-and-a-half" syndrome. The one-and-a-half syndrome is a disturbance of horizontal eye movements in which patients have lateral gaze palsy in one direction and internuclear ophthalmoplegia in the other direction. The patient was a 54-year-old woman who developed headaches, diplopia, and blurred vision over 6 months. Computed tomographic scans and magnetic resonance imaging demonstrated an enhancing, mixed density, midline mass of the cerebellum. After a resection of the mass, an anaplastic astrocytoma, the patient complained of more severe diplopia and facial weakness. An examination disclosed a left one-and-a-half syndrome, left peripheral facial paralysis, dysarthria, dysphagia, mild left hemiparesis, dysmetria of the left upper limb, and truncal ataxia. The brain stem showed no abnormalities on postoperative computed tomographic scans. After 4 months of follow-up, the one-and-a-half syndrome had not improved, even though other signs had improved or resolved. This syndrome is caused by damage to structures within the pontine tegmentum: the medial longitudinal fasciculus, the ipsilateral paramedian pontine reticular formation, or the ipsilateral abducens nucleus. Multiple sclerosis and brain stem infarction are the most common causes of the one-and-a-half syndrome. Less frequently, it is caused by primary and metastatic tumors of the brain stem and cerebellum. Rarely, the one-and-a-half syndrome can develop postoperatively after the removal of tumors of the posterior fossa. The mechanism of pontine tegmental injury remains unknown.
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PMID:"One-and-a-half" syndrome after a resection of a midline cerebellar astrocytoma: case report and discussion of the literature. 196 11

A case of Burkitt's type ALL with numb chin syndrome as the initial manifestation is described. A 57-year-old Japanese male was admitted to our hospital in November 14, 1989 because of paresthesia at the chin and lower lip with diplopia and ptosis. Neurological examination revealed oculomotor paralysis of the right side and hypesthesia on the chin, lower lip and buccal mucous membrane. Laboratory findings showed increased leukocyte count. Bone marrow aspirate revealed hypercellular marrow with 92.3% leukemic cells which had vacuoles in the cytoplasm and surface marker of IgM, kappa type. The abnormalities of karyotype included t(8;14). He was treated with chemotherapy and radiation. His conditions were temporarily improved, but relapsed later and died in March 6, 1990. Leukemic infiltrations to the trigeminal nerve were found in autopsy. The relationship between lymphoid malignancies and numb chin syndrome was discussed.
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PMID:[Burkitt's type ALL with numb chin syndrome as an initial manifestation]. 202 41


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