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Strabismus

MA M27 M27.002 Bontoxilysin Therapeutic use for local paralysis of neuromuscular function, as in strabismus... [Pg.879]

Hakim RB, Stewart W, Tielsch J. 1989. A case-control study of parental occupational lead exposure and strabismus. Am J Epidemiol 130 834. [Pg.530]

Botulinum toxin from Clostridium botulinum is the most potent poison known. The lethal dose in an adult is approx. 3x10 mg. The toxin blocks exo-cytosis of ACh in motor (and also parasympathetic) nerve endings. Death is caused by paralysis of respiratory muscles. Injected intramuscularly at minuscule dosage, botulinum toxin type A is used to treat blepharospasm, strabismus, achalasia of the lower esophageal sphincter, and spastic aphonia. [Pg.182]

Strabismus and blepharospasm associated with dystonia (Botox only) For the... [Pg.1339]

Strabismus (Botox only) The volume of botulinum toxin type A injected for treatment of strabismus should be between 0.05 to 0.15 mL per muscle. [Pg.1341]

For vertical muscles, and for horizontal strabismus of less than 20 prism diopters 1.25 to 2.5 units in any 1 muscle. [Pg.1341]

Safe and effective use Safe and effective use of botulinum toxin type A depends upon proper storage of the product, selection of the correct dose, and proper reconstitution and administration techniques. Physicians administering botulinum toxin type A must understand the relevant neuromuscular or orbital anatomy of the area involved and any alterations to the anatomy caused by prior surgical procedures. An understanding of standard electromyographic techniques is also required for treatment of strabismus and may be useful for the treatment of CD. [Pg.1343]

Retrobulbar hemorrhages During the administration of botulinum toxin type A for the treatment of strabismus, retrobulbar hemorrhages sufficient to compromise retinal circulation have occurred from needle penetrations into the orbit. It is recommended that appropriate instruments to decompress the orbit be accessible. Ocular (globe) penetrations by needles have also occurred. An ophthalmoscope to diagnose this condition should be available. Inducing paralysis in 1 or more extraocular P.788... [Pg.1344]

Primary axillary hyperhidrosis Adverse events (in at least 3% of patients) included injection site pain and hemorrhage, nonaxillary sweating, infection, pharyngitis, flu syndrome, headache, fever, neck or back pain, pruritus, and anxiety. Blepharospasm The most frequently reported treatment-related adverse reactions were ptosis (20.8%), superficial punctate keratitis (6.3%), and eye dryness (6.3%). Strabismus Extraocular muscles adjacent to the injection site can be affected, causing ptosis, vertical deviation, spatial disorientation, double vision, or past-pointing, especially with higher doses of botulinum toxin type A. [Pg.1345]

Overdose results in blurred vision, seizures, myosis, mydriasis, severe muscle weakness, strabismus, respiratory depression, and vomiting. [Pg.117]

Accommodative esotropia (strabismus caused by hypermetropic accommodative error) in young children is sometimes diagnosed and treated with cholinomimetic agonists. Dosage is similar to or higher than that used for glaucoma. [Pg.144]

A 0.1% ophthalmic preparation is recommended for prevention of postoperative ophthalmic inflammation and can be used after intraocular lens implantation and strabismus surgery. A topical gel containing 3% diclofenac is effective for solar keratoses. Diclofenac in rectal suppository form can be considered for preemptive analgesia and postoperative nausea. In Europe, diclofenac is also available as an oral mouthwash and for intramuscular administration. [Pg.803]

Although IEF of serum transferrin is relatively easy to perform, it is assumed that many CDG patients are still missed. Due to the complex clinical presentation of CDG, all patients suffering from unclear multi-organ diseases, especially in combination with mental and psychomotor retardation, strabismus, cerebellar atrophy and blood-clotting problems, should be investigated for CDG. [Pg.383]

BT has also been tested for the relief of crossed eyes (strabismus) in children where it relieved that condition for two years in more than 50% of those treated. [Pg.74]

Strabismus -treatment of [FLUORINE COMPOUNDS, INORGANIC - PHOSPHORUS] (Vol 11)... [Pg.933]

Kaye LD, Kalenak JW, Price RL, Cunningham R. Ocular implications of long-term prednisone therapy in children. J Pediatr Ophthalmol Strabismus 1993 30(3) 142-4. Cumming RG, Mitchell P, Leeder SR. Use of inhaled corticosteroids and the risk of cataracts. N Engl J Med 1997 337(1) 8-14. [Pg.56]

Botulinum toxin has been used for some time to control localized muscle dystonias, including conditions such as spasmodic torticollis, blepharospasm, laryngeal dystonia, strabismus, and several other types of focal dystonias.6 25,26,87 93 When used therapeutically, small amounts of this toxin are injected directly into the dystonic muscles, which begin to relax within a few days to 1 week. This technique appears to be fairly safe and effective in many patients, but relief may only be temporary. Symptoms often return within 3 months after each injection, necessitating additional treatments.40 Still, this technique represents a method for treating patients with severe, incapacitating conditions marked by focal dystonias and spasms. [Pg.172]

Arnold RW, Gionet E, Hickel J, et al. Duration and effect of single-dose atropine paralysis of accommodation in penalization treatment of functional amblyopia. Binocul Vis Strabismus Q. 2004 19 81-86. [Pg.272]

Ozcan AA, Gunes Y, Haciyakupoglu G. Using diazepam and atropine before strabismus surgery to prevent postoperative nausea and vomiting a randomized, controlled study. J AAPOS. 2003 7 210-212. [Pg.272]

This chapter deals with botulinum toxin type A (BOTOX) in the treatment of strabismus, blepharospasm, and related disorders. Botulinum toxin type A (BOTOX) has been used to treat strabismus, blepharospasm, Meige s syndrome, and spasmodic torticollis. By preventing acetylcholine release at me neuromuscular junction, botulinum toxin A usually causes a temporary paralysis of the locally injected muscles. The variability in duration of paralysis may be related to me rate of developing antibodies to me toxin, upregulation of nicotinic cholinergic postsynaptic receptors, and aberrant regeneration of motor nerve fibers at me neuromuscular junction. Complications related to this toxin include double vision (diplopia) and lid droop (ptosis). [Pg.213]

Botulinum, a neurotoxin with muscle relaxant properties, is used in me treatment of strabismus. [Pg.213]

The toxin also inhibits release of Ach in all parasympathetic and cholinergic postganglionic sympathetic neurons. This has fueled interest in its use as a treatment for overactive smooth muscles (for example, in achalasia) or abnormal activity of glands (for example, hyperhidrosis). Over the past 15 years, botulinum toxin has been shown to be useful in many conditions, especially strabismus and various movement disorders (Table 16.1). [Pg.214]

Paralytic strabismus (III, IV, VI nerve palsy, internuclear opthalmoplegia, skew deviation)... [Pg.215]

Note Many drugs and toxins block neuromuscular transmission by other mechanisms, such as interference with the synthesis or release of acetylcholine, but most of these agents are not employed clinically for this purpose. One exception is botulinus toxin, which has been administered locally into muscles of the orbit in the management of blepharospasm and strabismus. This treatment produces a long-lasting interruption of neuromuscular transmission and reduction of spasmodic ocular movements. Another exception is dantrolene, which blocks release of Ca2+ from the sarcoplasmic reticulum and is used in the treatment of malignant hyperthermia. [Pg.215]

Diabetic neuropathy may be associated with neuropathic ulcer, ptosis, diplopia, strabismus, loss of deep tendon reflexes, ankle drop, wrist drop, paresthesia, hyperalgesia, hyperesthesia, and orthostatic hypotension (because of autonomic dysfunction). [Pg.502]

Injection of BoNT is currently recognized as the best available treatment for dystonias and for certain types of strabismus, and new uses are continuously found (Bhidayasiri and Truong 2005 Montecucco and Molgo 2005). In addition, BoNT/A inhibit ACh release at autonomic nerve terminals which innervate the glands and smooth muscle, and it is currently used to treat diseases such as hypersalivation and hypersudoration (Brisinda et al. 2004 Naumann and Jost 2004). [Pg.156]

Schiavo G, Papini E, Genna G, Montecucco C (1990) An intact interchain disulfide bond is required for the neurotoxicity of tetanus toxin. Infect Immun 58 4136 11 Scott AB, Magoon EH, McNeer KW, Stager DR (1989) Botulinum treatment of strabismus in children. Trans Am Ophthalmol Soc 87 174-180 discussion 180 1 Scott D (1997) Phospholipase A2 structure and catalytic properties. In Kini R (ed) Venom phospholipase A2 enzymes structure, function and mechanism. John Wiley Sons, Chichester, p 97-128. [Pg.167]


See other pages where Strabismus is mentioned: [Pg.933]    [Pg.227]    [Pg.1319]    [Pg.622]    [Pg.401]    [Pg.404]    [Pg.688]    [Pg.669]    [Pg.1340]    [Pg.1341]    [Pg.1341]    [Pg.92]    [Pg.130]    [Pg.130]    [Pg.496]    [Pg.381]    [Pg.92]    [Pg.74]    [Pg.215]    [Pg.62]   
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Strabismus surgery

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