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

A patient with Friedreich's disease and chronic progressive external ophthalmoplegia is descirbed. An investigation was performed into the nature of the ocular motor disorders, which appeared clinically to be supranuclear. The EMG of the ocular muscles suggested myopathy. A specimen of ocular muscle was obtained by biopsy and examined with the light microscope and-for the first time-under the electron microscope. Signs of mitochondrial myopathy were found alongside neurogenic features. Postmortem examination of the central nervous system confirmed the diagnosis of Friedreich's disease with lesions of the motor cells in the anterior horn of the spinal cord. No evidence was found for a supranuclear or inernuclear origin of the ocular palsies, but 20-30 per cent of the neutrons in the nuclei III and IV were atrophic. Lesions of the non-medullated motor nerve fibres were also visible under the electron microscope. That the origin of the c. p. e. o. in this heredo-ataxia is neurogenic-nuclear is postulated on the grounds of the neuropathological and electronmicroscopic findings. Resemblances to the microscopic and submicroscopic and submicroscopic appearance of many types of "ocular myopathy" and "ophthalmoplegia-plus" throw doubt upon the myogenic character of these conditions. Possibly chronic, slowly progressive atrophy in the nuclear areas of the ocular motor nerves must in these cases also be held responsible for the c. p. e. o. Perhaps Moebius's Kern-Schwund theory may be revived after 85 years.
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PMID:Chronic progressive external ophthalmoplegia in a heredo-ataxia: neurogenic or myogenic? A clinical, neuropathological and submicroscopic study. 60 73

A syndrome of acute periorbital pain, followed by the onset of ophthalmoplegia, has, in recent years, been recognised as a distinct entity. Six patients conforming to this clinical picture are presented from Zambia, and the characteristics of the syndrome is described. Attention is drawn to the existence of the condition in Arica and to its dramatic improvement with systemic steroid treatment. Particularly in those areas with limited investigatory facilities, the use of steroids can constitute a therapeutic test.
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PMID:Painful ophthalmoplegia. 61 21

Ocular motor involvement is uncommon in post-infective polyneuropathy. Details of the evolution and recovery of the ophthalmoplegia are presented in 11 patients in whom ocular motor involvement was a major or notable feature of the illness. Follow-up examinations after intervals of up to 6 years in 10 of the 11 patients showed no residual ocular motor impairment. Saccadic eye movement studies carried out in 6 cases at the time of follow-up showed no abnormality in 2 cases while in the other 4 cases there was mild reduction of saccadic velocities and/or increased saccade reaction times with saccade inaccuracy. In spite of the variability of the ophthalmoplegia and of the remainder of the clinical syndrome in these cases, we conclude that they all represent variants of the classical form of the Guillain-Barre syndrome.
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PMID:Ocular motor involvement in post-infective polyneuropathy. 61 10

The clinical details and results of some laboratory investigations are described in 4 patients who initially presented with severe external ophthalmoplegia, ataxia and areflexia. In 3 of these patients paresis of the limbs was restricted and minimal as in the syndrome first described by Fisher (1956). The fourth patient initially presented with similar symptoms but his illness progressed to a more typical form of acute idiopathic polyneuropathy, confirming Fisher's (1956) contention that this syndrome is an unusual variant of acute idiopathic polyneuritis.
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PMID:Syndrome of ophthalmoplegia, ataxia and areflexia. 61 11

The eye movements of 25 patients with internuclear ophthalmoplegia were recorded by electrooculography. The velocity of adducting saccades was markedly less than normal. The velocity of abducting saccades was within the normal range, but statistically there was a wider distribution. Recordings were made in 2 patients several months after the onset of internuclear ophthalmoplegia, at which time the adducting eye velocity was greater than the abducting eye velocity. A patient with a unilateral medial fasciculus lesion showed marked overshoot of the abducting eye on contralateral saccades and overshoot of both eyes toward the side of the lesion. Optokinetic and postcaloric nystagmus were recorded, and the slow phase showed increasing velocity exponential waveform for the abducting eye. The recordings also showed decreasing velocity exponential waveform for the abducting eye. Downbeat nystagmus was as common as upbeat nystagmus in our patients. The findings appear to confirm the theoretical analysis of the eye movement disorder in internuclear ophthalmoplegia provided by Pola and Robinson as modified by recent experimental work in primates.
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PMID:An electrooculographic study of internuclear ophthalmoplegia. 61 77

A case resembling the syndrome of "ophthalmoplegia plus" or "oculo-cranio-somatic neuromuscular disease" is reported. A biopsy of deltoid muscle showed that 23% of the fibers were "ragged-red fibers" and were all type 1. Study of their ultrastructure revealed clusters of abnormal skeletal muscle mitochondria in subsarcolemmal and intermyofibrillar spaces. A liver biopsy also revealed a considerable increase in the number and size of the mitochondria. In some instances the mitochondria contained osmiophilic rounded inclusions surrounded by myelin-like structures. Metabolic studies revealed an increase of blood lactate concentration after very light exercise, while the O2 consumption was increased within the expected range. It is concluded that: a) the association of ophthalmoplegia and ultrastructural alterations of the mitochondria in muscle fibers may represent a specific nosographic entity: b) mitochondrial abnormalities are not limited to the skeletal muscles and c) the dysmetabolic basis of such a clinico-pathological entity might lie in an alteration of the mechanism which regulates the mitochondrial oxidative phosphorylation.
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PMID:Morphologic and metabolic studies in a case of oculo-cranio-somatic neuromuscular disease. 61 6

This paper describes 6 patients with the syndrome of ophthalmoplegic polyneuritis fairly identical to that described by Fisher. The most striking symptom of the ophthalmoplegic polyneuritis is the acute ophthalmoplegia, usually total and bilateral, often with sparing of the pupillary reflexes and of the levater palpebrae. The disturbances may simulate a paralysis of gaze or a internuclear palsy. Following features may announce this illness: mild harmless infectious disease, sensory deficits, generalized hyporeflexia or areflexia, albuminocytologic dissociation. There is without a specific treatment a complete recovery within months. Often it is impossible to clarify the etiology.
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PMID:[Ophthalmophlegic polyneuritis. A clinical contribution to Fisher's syndrome]. 62

A woman was noted to have chronic progressive external ophthalmoplegia, pigmentary degeneration of retina and third degree AV block. She was admitted to hospital because of syncopes and was successfully treated with a permanent pacemaker. Since 1958, 12 similar cases have been noted. Three of 7 patients without pacemaker treatment died, and 5 were successfully treated with pacemaker. The disturbances in AV-conduction are not thought to be a mere coincidence to the ocular disorder. Cardiomyopathy has been suggested.
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PMID:Third degree atrioventricular block, chronic progressive external ophthalmoplegia and pigmentary degeneration of retina. Case report and survey of the literature. 62 12

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 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


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