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Query: UMLS:C0038379 (strabismus)
 9,317 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A motor theory is proposed to explain monocular eccentric fixation of amblyopic eyes. Clinical observations that suggest the involvement of a motor anomaly related to strabismus are cited. The model proposes that potentiation (after discharge) of the agonist muscle in strabismus results in a nonregistered error of monocular fixation of the amblyopic eye. The position error goes undetected as a result of reduced sensitivity of the amblyopic eye. Evidence is cited for normal muscle potentiation in nonamblyopic eyes. A suggestion is made that amblyopia be considered both a sensory and a motor disorder. The sensory disorder is the reduced acuity at the fovea of the amblyopic eye. The motor disorder is muscle potentiation that causes the amblyopic eye to fixate with an eccentric retinal region that has lower acuity than the fovea. A distinction is made between motor anomalies that have a sensory basis, such as unsteady fixation in anisometropic amblyopia, and motor anomalies that have a motor basis, such as eccentric fixation in strabismic amblyopia.
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PMID:A motor theory for monocular eccentric fixation of amblyopic eyes. 67 59

A 41-year-old man was doing well until July 1989, when he noted numbness over soles, followed 4 months later by difficulty in walking. These symptoms were progressively getting worse, and he was admitted to our department on June 12, 1990. General physical examination was unremarkable. Neurologically cranial nerves were intact except old right, traumatic strabismus. Muscle tone and deep tendon reflexes were normal throughout, but bilateral Babinski and Chaddock reflexes were present. Mild weakness of lower extremities were found on muscle testing (4/5). In sensory system, superficial sensory disturbance below T10 was seen, and markedly diminished vibration and position senses of lower extremities were noted. Cerebellar test was intact, although unsteadiness was found on heel-shin test. Romberg sign was definitely positive. His gait was wide-based and ataxic. Laboratory data showed no abnormalities in CBC, chemistry, urinalysis, serological tests and endocrinological examinations. Spinal MRI (Siemens 1.5 Tesla) showed abnormal deposition of epidural fatty tissues compressing spinal cord with flattening of cord from T4 to T8. Spinal ataxia as compressive myelopathy due to epidural lipomatosis was considered and he underwent laminectomy from T4 to T8 with improvement in walking. Epidural lipomatosis is an unusual cause of spinal cord compression, presenting compressive myelopathy, radiculopathy, cauda equina syndrome, intermittent claudication, or back pain. Most of cases were associated with long-term administration of adrenocortical steroid hormone, or underlying diseases, except only 3 cases including ours. This is the first case of spinal epidural lipomatosis presenting progressive gait disturbance due to spinal ataxia.
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PMID:[A case of epidural lipomatosis presenting spinal ataxia]. 206 Feb 46

A male, born on December 8, 1956, during the period when many Minamata diseases broke out in a district. His parents who ate much fish and shell fish taken in Minamata Bay suffered from the light, incomplete Minamata disease showing sensory disturbance, the constriction of the visual field, muscular weakness, etc. He weighed 3,225 gr. upon the normal birth given 10 months after pregnancy. His abnormalities were noted since his head was not stabilized on the neck even six months after the birth. Because of the delay in the development of the motor function, he became barely able to sit, stand up and begin walking at the ages of 3, 5 and 6 respectively. In 1962 (at the age of 6), his congenital Minamata disease was diagnosed in view of his clinical symptoms and epidemiological conditions. The mercury value in the hair and blood upon the birth is not known because a considerable time had elapsed after the birth when his mercury poisoning was discovered. However, the clinical symptoms included intelligence disturbance, character change, dysarthria, primitive reflexes, strabismus, hypersalivation, ataxia and hyperkinesia, indicating a typical congenital Minamata disease. Until he became 13 years old (1969) or so, his mental and motor function developed, both gradually. In the same year, he was admitted to a special class for the handicapped. EEG examination revealed that there was a slow alpha activity in the basic pattern and that 6 Hz positive spike was found in the sleep EEG. The constriction of the visual field was classified through examination.2+
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PMID:[Congenital Minamata disease accompanied by arachnoid cyst (author's transl)]. 709 64

Horizontal and vertical small-field optokinetic nystagmus (OKN) were examined in persons with strabismic or anisometropic amblyopia. Reduced velocity for the slow phase of OKN driven by temporalward and upward target motion presented monocularly was observed in both the amblyopic and nonamblyopic eyes of some subjects. Several experiments were conducted in search of a sensory disturbance of perceived motion sensitivity which could account for the abnormal OKN. Comparisons between the frequency response for OKN and the contrast sensitivity function for perceived motion revealed that amblyopes with asymmetric OKN had equal sensitivity to nasal and temporal target motion. Contrast thresholds for driving the temporal slow phase of OKN were elevated by over 1 log unit above contrast thresholds for perceived temporal target motion, whereas contrast thresholds for stimulating nasal movement and driving the nasalward slow phase of OKN were equal. Contrast sensitivity to nasal and temporal target motion was symmetrical at the fovea and parafovea of the amblyopic eye. These studies did not reveal a sensory a /mso observed in both eyes of persons with congenital strabismus without amblyopia and in the nondeprived eye in monocular congenital cataract. These observations suggest a relationship between directional asymmetries of OKN and the incomplete development of binocular vision.
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PMID:Disturbances of small-field horizontal and vertical optokinetic nystagmus in amblyopia. 738 Jun 25

Postoperative diplopia and strabismus may result from a variety of ocular surgical procedures. Common underlying mechanisms include sensory disturbance, scarring, direct extraocular muscle injury, myotoxicity from injections of local anesthesia or antibiotics, and malpositioning of extraocular muscles by implant materials. The most common patterns are vertical and horizontal motility disturbance. Treatment options include prisms, botulinum, occlusion, or surgery.
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PMID:Diplopia and strabismus following ocular surgeries. 2045 37

Motility disorders and strabismus after vitreo-retinal surgical intervention have multiple etiologic factors. The main focus here is strabismus following scleral buckling surgery. The preoperative evaluation of these patients must be inclusive for restrictions, redirected muscle forces, adherence syndromes, muscle weakness, and visual sensory disturbance. Restoration of binocular function is generally the goal of surgical intervention, but paramount to surgery is assessing the potential for binocular function. Surgical techniques for overcoming the barriers to fusion are discussed with clinical vignettes to illustrate the principal. Surgery, which is appropriately planned, based on theses principals can by highly successful in restoring visual functioning.
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PMID:Surgical management of strabismus following vitreo-retinal surgery. 2300 75