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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association of congenital ophthalmoplegia and facial paresis (Moebius syndrome) with a variety of other developmental somatic defects has been widely recognised. Its co-existence with hypogonadism of hypothalamic/pituitary origin and subclinical peripheral neuropathy has been reported and in this paper we describe the second case of the Moebius syndrome in association with hypogonadotrophic hypogonadism and a progressive peripheral neuropathy of mixed axonal and demyelinating type.
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PMID:Moebius syndrome, peripheral neuropathy and hypogonadotrophic hypogonadism. 20 51

The anterior internuclear ophthalmoplegia, a dissociated ophthalmoplegia of adduction secondary to an ipsilateral supranuclear paresis of the internal rectus, represents a well-know clinical picture. The dissociated ophthalmoplegia of abduction, however, sometimes referred to as posterior internuclear ophthalmoplegia, is debated. Such an oculomotor disturbance emerging from an ophthalmoplegic polyneuropathy (Fisher syndrome) is presented and illustrated by oculographic tracings. A secondary finding was a limited range of accommodation. Oculographically, the dissociated ophthalmoplegia of abduction reflects a true mirror image of the anterior internuclear ophthalmoplegia. Because of anatomical considerations the dissociated ophthalmoplegia of abduction cannot be regarded as internuclear ophthalmoplegia, and the terminology of posterior internuclear ophthalmoplegia is not tenable. Discussing the pathophysiology of the Fisher Syndrome, it is reflected upon an infranuclear lesion causing an ocular motility disorder featuring supranuclear aspects, and avoiding limitations of peripheral nerve damage.
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PMID:[Dissociated ophthalmoplegia of abduction: so-called posterior internuclear ophthalmoplegia in Fisher's syndrome]. 53 May 53

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

Diagnosis of Tolosa-Hunt syndrome was made in a 25-year-old woman on the basis of unilateral third and sixth nerve paresis and possible involvement of the first branch of the ipsilateral trigeminal nerve, accompanied by headaches and ocular pain, which responded promptly to corticosteroid administration. Irregular narrowing of the right carotid siphon and occlusion of the homolateral superior ophthalmic vein were observed. During steroid therapy this stenosis improved in association with almost complete clinical recovery, although the vein was not recanalized. Of ten reported cases with contrast radiographic abnormalities, including our own, only two showed pupillary involvement. We hypothesize that the third nerve paresis with pupillary sparing in this syndrome may be attributable to the same underlying mechanism as that of diabetic ophthalmoplegia.
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PMID:Tolosa-Hunt syndrome. Arteriographic evidence of improvement in carotid narrowing. 63 55

Three cases of histologically verified neurinomas of the oculomotor nerve are reported. The preoperative diagnosis in all three cases was not made; on the contrary all cases were diagnosed as sphenoid ridge meningiomas. The oculomotor neurinoma manifests itself in the beginning with a discrete progressive palsy of the oculomotor nerve leading in later stages to complete ophthalmoplegia. Proceeding the oculomotor nerve paresis or going parallel to it is a functional loss of the homolateral optic nerve sometimes progressing to amaurosis. Unilateral exophthalmos as well as frontal or orbital neuralgic pain with or without sensory disorders in the area of trigeminus-I are characteristic for the clinical picture in later stages, all symptoms characteristic for the syndrome of the apex orbitae, resp. the superior orbital fissure, resp. the anterior cavernous sinus. The differential diagnosis has to consider above all the sphenoid ridge meningioma, the trigeminal neurinoma and the numerous tumors within the cavernous sinus (aneurysmas, meningiomas, chondromas, metastases of carcinomas, pituitary adenomas etc.) or the middle cranial fossa. Plain X-ray, carotid angiogram and computer tomogram are essential diagnostic means for localization and extension of the tumor but not for histological diagnosis. Oculomotor neurinomas are very seldom. The three observed cases did not have any relation to a possible generalized neurofibromatosis.
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PMID:[Neurinoma of the oculomotor nerve (author's transl)]. 65 Dec 44

A pharmacological study was performed in the involved pupils to demonstrate the site of lesion in a patient with Fisher's syndrome who showed marked ptosis, complete external ophthalmoplegia, pupillary involvement with anisocoria, facial paresis, ataxia, areflexia, and albuminocytological dissociation in the cerebrospinal fluid. The instillation of 2.5% methacholine produced mild constriction of one pupil. This response was not detectable in the recovery stage. The instillation of 1.25% l-epinephrine produced marked bilateral dilation of the pupils, in both the early and recovery stages. Instillation of 5% tyramine produced pupillary dilation as in the normal pupil. The response to 5% cocaine, tested only in the recovery stage, was weak in one pupil. These results imply that the pupillary involvement was due to peripheral involvement of the sympathetic and parasympathetic nervous systems. The lesion in the sympathetic nervous system was preganglionic, but in the parasympathetic nervous system the precise localization could not be determined.
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PMID:Fisher's syndrome: a pharmacological study of the pupils. 90 Sep 8

Six members of a family--the mother, three daughters, and two sons--have a unique syndrome consisting of congenital external ophthalmoplegia, bilateral facial weakness, lingua scrotalis, progressive chorioretinal sclerosis, and an intellectual deficit. Bilateral ptosis and almost complete ophthalmoplegia were found in three of the family members, bilateral facial weakness in two, and Parinaud's syndrome and convergence paresis in one. Electromyographically, a lesion of the lower motor neurons--"nuclear ophthalmoplegia"--was found. Three members of the family had different stages of progressive chorioretinal sclerosis and two had myopia. All the family members had lingua scrotalis, and all of those who had ophthalmoplegia had low IQs. Electroretinographic reactions were subnormal or absent in patients with chorioretinal degeneration. It was concluded that an extensive abiotrophic process, genetically conditioned, was a possibility.
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PMID:Progressive nuclear ophthalmoplegia associated with mental deficiency, lingua scrotalis, and other neurologic and ophthalmologic signs in a family. 116 9

In agreement with other clinical reports we observed in 20 patients that Parinaud's syndrome may be associated with other midbrain symptoms. Most frequently we found convergence insufficiency or pupillary changes. In contrast to textbooks in most cases that was an incomplete, absolute paralysis of pupillary constriction. Some patients had also paresis of the 3rd and 4th cranial nerve or lesions of the medial longitudinal fasciculus (internuclear ophthalmoplegia). All clinical patterns which we noted were understandable in view of the topographical relationship of their presumed lesions. However, none of the symptoms was invariably associated with Parinaud's syndrome.
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PMID:[Clinical patterns of Parinaud's syndrome (author's transl)]. 120 46

The Aarskog syndrome is characterized by short stature with typical facial, digital and genital anomalies. A further case is reported which presented with the uncommon finding of ophthalmoplegia and three previously unreported oral-facial findings: enamel dysplasia, a "col" deformity of the anterior mandible and a paresis of the facial muscles innervated by the VII cranial nerve. The implications of genetic heterogeneity in this nosologic classification are discussed.
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PMID:Aarskog syndrome: new oral-facial findings. 124 61

The nuclear syndrome of the third nerve was first described in 1981. It has the very characteristic disturbance of an ophthalmoplegia with complete ipsilateral third nerve palsy associated with paresis of elevation in contralateral eye. This particularly presentation is due to the innervation of the superior rectus which comes mainly from the contralateral oculomotor nucleus. As associated signs were described contralateral cerebellar and or pyramidal syndromes, uni or bilateral parasympathetic disfunction and sometimes gaze disorders. The etiology es usually a vascular damage (ischemic most frequently) located in mesencephalon. We report on a case of a 60 years old man who developed acute nuclear ophthalmoplegia of the third right nerve accompanied with cerebellar and pyramidal syndrome and focal asterixis in left extremities. MRI showed an ischemic lesion in right paramedial mesencephalic territory with extension to the ipsilateral thalamic region. Pyramidal and cerebellar syndromes and asterixis disappeared in a few weeks, while ophthalmoplegia remained unchanged. Semiologic characteristics and anatomic basis of the nuclear oculomotor syndrome which allow to make the differential diagnosis between this syndrome and intra-axial fascicular disturbances of the third nerve (Weber, Claude and Benedikt syndromes) are discuss.
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PMID:[Nuclear syndrome of the oculomotor nerve caused by a mesencephalic infarction confirmed by MRI]. 141 24


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