Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review, the anatomy of the trochlear nerve, the diagnosis of palsies of the trochlear nerve, and the localization of lesions of the trochlear nerve are discussed. Paresis of the superior oblique muscle is often not evident on duction testing; therefore, subjective diplopia testing with use of a Maddox rod is often necessary. The torsional component of the deviation may be evaluated by double Maddox rod testing. Palsies of the trochlear nerve must be distinguished from other causes of vertical diplopia, such as oculomotor palsy, skew deviation, myasthenia gravis, and Graves' ophthalmopathy. Trauma is the most common cause of isolated, unilateral or bilateral, acquired palsies of the trochlear nerve when a cause can be determined. The localization of lesions of the trochlear nerve to the nucleus or fascicles (or both), subarachnoid space, cavernous sinus and superior orbital fissure, or orbit depends on the associated damage to neighboring neurologic structures. Myokymia of the superior oblique muscle is usually idiopathic and benign but may rarely be an isolated manifestation of tectal disease.
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PMID:Palsies of the trochlear nerve: diagnosis and localization--recent concepts. 847 14

A single 5.5-millimeter to 8.0-millimeter lateral rectus resection eliminated diplopia in five of six adult patients with divergence paralysis and in all three patients with a sixth cranial nerve paresis. Preoperative distance esotropia ranged from 11 to 20 prism diopters in primary gaze. Prism therapy failed in seven of nine patients. Lateral incomitance was reduced in three patients with a mild limitation of abduction preoperatively, but was not induced in the six patients with divergence paralysis. Significant overcorrection of the near esodeviation did not occur. A single lateral rectus resection can effectively eliminate diplopia in selected patients with divergence and partial sixth nerve paralysis.
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PMID:Results of a single lateral rectus resection for divergence and partial sixth nerve paralysis. 850 17

Sixteen patients with combined paresis and restriction of extraocular muscle(s) orbital fracture repair were studied before and after in order to determine the clinical features and management of such patients. All 16 patients showed limited ductions of the involved eye in the field of action of the entrapped, paretic muscle and of the antagonist muscle after orbital fracture. Single extraocular muscles (13 patients) and two extraocular muscles (three patients) were demonstrated adjacent to the fracture site on orbital computed tomography (CT). In three patients prior to orbital surgery, a deviation in primary position was present. After fracture repair with release of the entrapped muscle in all patients, evidence of paresis of the muscle was demonstrated by underaction in its field of action and overaction in the field of its antagonist. There was a resultant manifest tropia or phoria in the primary position. In seven patients, the paresis gradually improved with no tropia and little diplopia in the functional fields of gaze. Three patients had minimal deviations and required no further treatment. Six patients with significant deviations required prisms (three patients) or strabismus surgery (three patients). The latter three patients had two muscles involved. Results of this study demonstrate that the ophthalmologist must appropriately diagnose patients with paresis and restriction of an extraocular muscle and counsel them that "new" diplopia may occur after orbital fracture repair and that this diplopia may require additional therapy.
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PMID:Combined paresis and restriction of the extraocular muscles after orbital fracture: a study of 16 patients. 886 78

Eighteen consecutive patients undergoing vestibular nerve surgery underwent pre- and postoperative examination of ocular motility. Five patients developed a skew deviation following surgery, with the lower eye on the operated side and an incomitant pattern of deviation in all cases. Three patients experienced diplopia lasting from 1 day to 6 months. The magnitude of skew deviation was increased by head tilt away from the operated side in only 1 case. The development of skew deviation was not determined by preoperative ocular alignment or binocular function, or any particular type or pattern of vestibular disease. There was an association with large changes in ocular torsion and subjective visual vertical, which correlated with lesser degrees of canal paresis to preoperative caloric testing on the operated side. No patient developed a head tilt postoperatively. There is a gradation of responses to surgical vestibular deafferentation in humans, skew deviation only occurring in patients suffering marked changes in subjective visual vertical and ocular torsion.
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PMID:Skew deviation following vestibular nerve surgery. 900 70

A 25-year-old man had diplopia caused by abducens nerve paresis on both sides after cranial injury. Because of the patient's reports of persistent diplopia after surgical correction, a specially manufactured, tinted iris claw lens was implanted in the left eye, with the crystalline lens in situ. Fourteen years after surgery, specular microscopy was performed to evaluate the corneal endothelium. The difference in mean endothelial cell density in both eyes was 18.6%. The difference between eyes in polygonality and polymegathism was not significant.
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PMID:Opaque iris claw lens in a phakic eye to correct acquired diplopia. 910 Jan 23

A 36-year-old male presented with a very rare epidermoid tumor in the sphenoid sinus manifesting as paresis of the right sixth cranial nerve and diplopia. Computed tomography and magnetic resonance imaging revealed a mass lesion in the sphenoid sinus expanding to the clivus. The cystic tumor, which contained cholesterin crystals, was extensively removed via the transsphenoidal approach. Histological examination showed epidermoid cell layers, consistent with the diagnosis of epidermoid tumor. Epidermoid tumors should be considered in the differential diagnosis of lesions in the sphenoid sinus.
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PMID:Epidermoid tumor in the sphenoid sinus--case report. 913 62

We report a case of large cystic acoustic neurinoma. A 52-year-old male was admitted to hospital with a history of progressive dysphagia, gait disturbance and diplopia for 2 months. On admission, neurological examinations revealed Bruns' type nystagmus to the left side, hypesthesia in the distribution of the second and third divisions of the left trigeminal nerve, and partial paresis of cranial nerves IX, X, and XII on the left side, and truncal ataxia. A pure-tone threshold audiogram indicated the presence of 32 dB hearing loss in the left ear. Speech discrimination was 80%. Caloric vestibular responses were absent on the left side. Skull radiographs with polytomographs of the internal auditory canal (IAC) were normal. Bony changes in the IAC were not found by high-resolution bone-window computed tomography (CT) scan. A plain CT scan revealed a large low-attenuated cystic mass in the left cerebellopontine angle (CPA), which was associated with displacement of the fourth ventricle. An enhanced CT scan demonstrated a thin rim-enhancement in the cyst wall. Magnetic resonance imaging (MRI) scans disclosed a large rim-enhanced cystic mass extending superiorly into the tentorial incisura and inferiorly into the foramen magnum. At surgery via a left suboccipital approach, a large cystic mass was found at the left CPA arising from the VIIIth nerve, and compressing the Vth, VIth, VIIth and lower cranial nerves. The cyst was filled with a xanthochromic fluid and was firmly attached to the internal auditory meatus (IAM). However no tumor extension into the IAM was confirmed. The tumor was excised completely. The postoperative course was uneventful, except for impairment of the VIIth and VIIIth nerves. At 6 months after the first operation, the facial nerve had improved up to grade III (Hause-Brackmann stage). Histological examinations revealed a typical benign acoustic neurinoma with predominant representation of Antoni B tissues. The cyst wall contained numerous abnormal sinusoid and telangiectasia-like vessels which showed occasional thromboses. The vessel walls displayed endothelial proliferations and were frequently hyalinized. Hemosiderin deposits and hemosiderin-containing phagocytes were also found near these vessels. Myxoid degeneration and necrosis were evident in vast areas. These degenerative changes appeared to be the principal causes of the large cystic formation. 16 cases including our case have been reported. The broad characteristics of the clinical symptoms and radiological findings of these tumors are discussed.
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PMID:[Large cystic neurinoma: a case report]. 921 60

Arachnoid cysts in the middle cranial fossa usually present with skull deformity, intracranial hypertension, epilepsy, focal symptoms and delayed mental development. Some cases, however, have neither symptoms nor signs. We have encountered a patient with an arachnoid cyst of the middle cranial fossa with extraocular muscle paresis and who was treated with cyst wall fenestration with good results. An 11-year-old boy presenting with double vision was diagnosed as having an arachnoid cyst in the middle cranial fossa with extraocular muscle paresis. He had no signs of increased intracranial pressure. This patient underwent a cyst membranectomy. Postoperatively this symptom rapidly subsided. Double vision disappeared two months postoperatively. To our knowledge, if those cases associated with increased intracranial pressure signs are excluded, this is the first case reported so far of a middle cranial fossa arachnoid cyst with extraocular muscle paresis. This report illustrates that extraocular muscle paresis can be caused by an arachnoid cyst in the middle cranial fossa and that knowledge of this could be helpful in its early diagnosis and treatment.
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PMID:[Arachnoid cyst of the middle cranial fossa with extraocular muscle paresis: case report]. 926 65

We report a case of partial fascicular oculomotor paresis in a 22-year-old woman. The patient noticed sudden onset diplopia which had transiently occurred twice in the past two months for several hours. She also had left blepharoptosis. Neurological examination revealed left blepharoptosis and diplopia caused by paresis of the left inferior oblique and superior rectus muscles. No other focal neurological signs were detected. Laboratory data, CSF examinations, ABR, SEP and VEP studies were all normal. Brain MRI revealed a high-signal-intensity lesion of about 7 mm in diameter in the left paramedian area of the midbrain at superior colliculus level on T2-weighted images. Cerebral angiography showed no significant findings. The lesion was limited to the left oculomotor fascicles. Either demyelinating or vascular lesion might be responsible for her oculomotor paresis. The symptomatic differences between this and previously reported cases suggest that the topographical organization of the oculomotor fascicles for the superior rectus, levator palpebrae superioris, inferior oblique, medial rectus, and inferior rectus muscles and the sphincter muscles of the pupils consists of fibers that lie in a lateromedial order.
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PMID:[A case of partial fascicular oculomotor paresis]. 943 Oct 5

A 17-year-old girl with acute pomyelocytic leukemia (APL) went into complete remission following Daunorubicin, Ara-C and ATRA chemotherapy for 1 month. Unfortunately, prolonged administration of ATRA 6 weeks later caused binocular diplopia with left abducent nerve paresis, which gradually disappeared upon withdrawal of ATRA. We propose that it is ATRA induced pseudotumour cerebri and present this case to discuss the relationship between the ATRA and pseudotumour cerebri.
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PMID:ATRA-induced pseudotumour cerebri--one case report. 951 92


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