Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038379 (strabismus)
 9,317 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The botulinum A toxin inhibits the release of acethylcoline from the vesicles of presynaptic neuronal end plates. Its effect is a transient pharmacological neurectomy. The toxin is used more and more widespreadingly. It selectively inhibits certain muscles or groups of muscles. Its use is of outstanding importance in the treatment of blepharospasm, a disease possibly causing transient functional blindness. This blindness develops randomly, with undetermined duration, therefore it may even threaten the life of the patient. There is no alternative treatment. In ophthalmology, the toxin is used in the therapy of strabismus and nystagmus, as well as replacing entropion operations. Most often its use is suggested in the treatment of focal dystonies, dysphonia, tremor palatinus, dysphagia, spasm of the oesophagus sphincter muscle, nasal hypersecretion, hemifacial spasm, headaches, focal hyperhydrosis, proctalgia fugax, diabetic gastroparesis and difficulties in urination. In the past few years, the toxin has been used for esthetic reasons as well. By relaxing the muscles causing wrinkles, non-permanent result may be reached with its use. The botulinum A toxin does not have general side effects. As local side effects, haematomas and unwanted, transient paresis of the neighboring muscles can be mentioned.
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PMID:[Applications of the botulinum A toxin]. 1278 36

Toxoplasmosis was the most common cause of primary retinochoroiditis. The majority of cases of ocular toxoplasmosis were congenital. However, cases of acquired ocular toxoplasmosis have been reported. The clinical manifestations of congenital ocular toxoplasmosis were choroidal coloboma, strabismus, nystagmus, ptosis, microphthalmia, cataract and enophthalmia. The purpose of this study was to determine the clinical presentation and visual outcome of 173 patients with ocular toxoplasmosis at Dr Sardjito Hospital, Dr Yap Eye Hospital, and private practice during the last six years. A total of 173 subjects were studied--98 males and 75 females. The ages at which first diagnosis was established ranged from 3 months to 68 years, frequently in young adults and occurring mostly in students. The most-reported chief complaint was blurred vision in 70.5% and floaters in 6.1% of cases. The most frequent clinical manifestations were chorioretinitis (71.2%), macular scars (22.4%), squint (6.4%), congenital cataract (2.8%), nystagmus (6.4%) and atrophic optic papilla (2.8%). Bilateral involvement was found in 32.4% of all patients. The therapeutic outcome showed improvement, especially visual acuity in acute cases (25.6%). However, visual acuity categorized as blindness was 13.9%. The results of the study imply that suddenly blurred vision in the quiet eye in the young adult, squint, and nystagmus in children could be chorioretinal inflammation and scar caused by Toxoplasma gondii.
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PMID:Clinical manifestations of ocular toxoplasmosis in Yogyakarta, Indonesia: a clinical review of 173 cases. 1297 52

This review summarizes the knowledge and highlights recent advances in clinical research of retinopathy of prematurity (ROP). This disease is still important, because improvements in neonatal intensive care during the last years have increased the survival of the most immature newborns, but did not diminish the ROP frequency. Ophthalmologic screening and, if applicable, laser treatment at the optimal time for advanced ROP prevents blindness in most cases. The history, classification and the modern concepts of ROP pathophysiology are described. The results of various multicenter treatment trials are summarized. The current German screening guidelines are discussed with the guidelines of other nations. The therapeutic treatment strategies and the treatment results are discussed. The ophthalmologic disorders of former preterm infants, as higher rates of amblyopia, strabismus, and refractive error, are mentioned. Possible future therapies, e. g. anti-angiogenic factors are discussed.
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PMID:[Retinopathy of prematurity]. 1584 53

The pattern of innervation of the extraocular muscles is highly conserved across higher vertebrate species and mediates sophisticated visuomotor processes. Defects in oculomotor development often lead to strabismus, a misalignment of the eyes that can cause partial blindness. Although it has been intensively studied from a clinical perspective, relatively little is known about how the system develops embryonically. We have therefore mapped the development of the oculomotor nerve (OMN) in chick embryos by using confocal microscopy. We show that OMN development follows a series of stereotyped steps that are tightly regulated in space and time. The OMN initially grows past three of its targets to innervate its distal target, the ventral oblique muscle, only later forming branches to the more proximal muscles. We have also investigated spatiotemporal aspects of the unusual contralateral migration of a subpopulation of oculomotor neurons by using molecular markers and have found the semaphorin axon guidance molecules and their receptors, the neuropilins, to be expressed in discrete subnuclei during this migration. Finally, we have created an embryological model of Duane retraction syndrome (DRS), a form of strabismus in which the OMN is believed to innervate aberrantly the lateral rectus, the normal target of the abducens nerve. By ablating rhombomeres 5 and 6 and hence the abducens, we have mimicked a proposed oculomotor deficit occurring in DRS. We find that the absence of the abducens nerve is not sufficient to produce this inappropriate innervation, so other factors are required to explain DRS.
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PMID:Development of oculomotor axon projections in the chick embryo. 1506 26

A 4-year-old boy presented with complete blindness in his left eye after accidentally walking into a merchandise display hook while shopping in a department store. An ophthalmologic examination revealed no light perception, an amaurotic pupil, and nasal conjunctival injection in the eye. Intravenous steroids did not improve his vision.
J Pediatr Ophthalmol Strabismus
PMID:Traumatic optic neuropathy caused by a merchandise display hook. 1530 40

Cohen syndrome is a rare genetic disorder caused by autosomal recessive inheritance and is characterized by the following features: mental retardation, infantile hypotonia, micrognathia, narrow and high-arched palate, microcephaly, prominent upper central incisors, poor dentition, short stature, and truncal obesity. Some patients have strabismus, myopia, optic atrophy, and total blindness. A small number of cases present with heart defects or mitral valve prolapse. Only approximately 100 cases have been reported in the world literature. The administration of general anesthesia in patients with Cohen syndrome can be a challenge because most of these patients are mentally retarded and uncooperative and have facial malformations that may make intubation difficult. We present our experience with the anesthetic management of a patient with Cohen syndrome.
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PMID:The anesthetic management of a patient with Cohen syndrome. 1533 97

This study presents clinical and laboratory findings and outcome of infants with intracranial hemorrhage (ICH) due to vitamin K deficiency after the newborn period, and evaluates vitamin K prophylaxis. The hospital records of 19 infants with a diagnosis of ICH due to vitamin K deficiency after the newborn period, seen in our clinic in less than 4 years, were retrospectively evaluated. The mean age at onset of the symptoms was 49 +/- 18 days. The most frequent presenting complaints were convulsion (58%), vomiting (47%), and irritability (47%). The most frequent examination findings were coma (74%), fontanel bulging (68%), and absence of pupil reaction (42%). The localizations of the ICHs were as follows: parenchymal (47%), subarachnoid (47%), subdural (42%), and intraventricular (26%). Four patients had used antibiotics and 1 patient had suffered diarrhea before the onset of the symptoms. One patient had a mild hepatic dysfunction that resolved spontaneously in a few weeks and its cause was not found. Mortality was observed in 6 (32%) patients. Ten patients were followed up for a mean period of 26.9 +/- 22.6 months. The follow-up findings were developmental delay (40%), microcephaly (30%), epilepsy (30%), blindness (20%), strabismus (20%), spastic tetraparesis (10%), spastic hemiparesis (10%), growth retardation (10%), and hydrocephaly (10%). Three (30%) patients remained neurologically normal. Vitamin K deficiency leads to death and neurological defects. Vitamin K prophylaxis at birth is therefore a priority. In this series, hepatic dysfunction had been detected in only 1 patient. The authors speculate that additional vitamin K to breast-fed infants with liver problem, antibiotic use, diarrhea, etc., should be considered.
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PMID:Intracranial hemorrhage due to vitamin K deficiency after the newborn period. 1562 14

Oculomotor nerve disease is a common cause of diplopia. When strabismus is present, absence of diplopia has to induce the research of either uncovering of visual fields or monocular suppression, amblyopia or blindness. We describe the case of a 41-year-old woman presenting with right oculomotor paresis and left object-centred visual neglect due to a right fronto-parietal haemorrhage expanding to the right peri-mesencephalic cisterna caused by the rupture of a right middle cerebral artery aneurysm. She never complained of diplopia despite binocular vision and progressive recovery of strabismus, excluding uncovering of visual fields. Since all other causes were excluded in this case, we hypothesise that the absence of diplopia was due to the object-centred visual neglect. Partial internal right oculomotor paresis causes an ocular deviation in abduction; the image being perceived deviated contralaterally to the left. Thus, in our case, the neglect of the left image is equivalent to a right monocular functional blindness. However, bell cancellation test clearly worsened when assessed in left monocular vision confirming that eye patching can worsen attentional visual neglect. In conclusion, our case argues for the possibility of a functional monocular blindness induced by visual neglect. We think that in presence of strabismus, absence of diplopia should induce the search for hemispatial visual neglect when supratentorial lesions are suspected.
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PMID:Could visual neglect induce amblyopia? 1574 7

Bilateral convergent strabismus with exophthalmus (BCSE) is a heritable eye defect prevalent in many cattle breeds and known worldwide. BCSE shows a progressive course often terminating in complete blindness. The onset of the defect can sometimes be slowly progressing (late in life) and, as the first signs of the defect are frequently not noticed prior to first breeding, prevention cannot be achieved only by exclusion of affected animals from the breeding program. This paper provides an overview of the clinical signs, histopathology and genetics of BCSE, its distribution in different cattle breeds and analyses the association between milk production traits and US Brown Swiss. There were different modes of inheritance proposed for BCSE, but although an autosomal dominant major gene is considered most likely in German Brown cattle, an association with milk production traits could not be found. Comparative molecular genetic approaches could help to characterize the responsible genes for this ocular disease in cattle.
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PMID:Bilateral convergent strabismus with exophthalmus (BCSE) in cattle: an overview of clinical signs and genetic traits. 1643 18

Cerebral visual impairment is one of the main causes of childhood visual impairment in developed countries. These disorders are often linked with pre- or perinatal hypoxic brain injuries. The patterns of brain injuries depend on the severity and duration of hypoxia and the child's age. In premature children, periventricular leukomalacia affects the optic radiations and the subcortical visual brain. In full-term newborn babies, chronic hypoxia leads to the damage of the visual cortex and acute hypoxia damages the basal ganglia. They recover from cortical blindness in variable ways. Visual dysfunction is characterized by fixation troubles, subnormal acuity (crowding), difficulty with perceiving visual fields, movements, depth, cognitive defects (agnosia of images, objects or faces, visuospatial disorders), ocular motility disorders (tonic gaze deviation, strabismus, nystagmus). Accompanying these cerebral injuries, there are accommodation defects and optic disk abnormalities that vary according to the gestational age at the time of hypoxia.
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PMID:[Cerebral visual impairment in brain-damaged children - four case studies]. 1646 20


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