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

Botulinum A toxin is used intramuscularly in the treatment of spastic neuromuscular disorders, strabismus, and laryngeal dystonia. The toxin has recently been reported as being useful for the cosmetic removal of glabellar furrows. The clinical effect of the toxin lasts four months or longer. Systemic side effects are rare and usually transient. We report the case of a psoriasiform eruption temporally related to the injection of botulinum A toxin into the medial rectus muscle to treat an ocular motility disorder. To our knowledge, this is the first case of a psoriasiform dermatitis caused by this agent.
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PMID:Psoriasiform eruption from intramuscular botulinum A toxin. 148 91

Botulin type A was injected into the eyelids of adult monkeys, and structural alterations in the orbicularis oculi muscle were evaluated after survival times of 7 to 84 days. The most profound change seen at both the light- and electron-microscopic levels was nonselective atrophy of virtually all muscle fibers. Moreover, the botulin-induced blockade of neuromuscular transmission was nonspecific in producing alterations in the three orbicularis fiber types. Muscle structural changes appeared to be reversible, with no apparent long-term consequences. While sprouting of preterminal axons was noted in botulin-treated muscle, formation of collateral sprouts did not appear to be widespread. These changes contrast with the fiber type-specific, long-term alterations induced in extraocular muscle by botulin treatment. However, this differential response may be attributed to the very clear differences in fiber type composition and motor control mechanisms between eyelid and extraocular muscle groups. The efficacy of botulin treatments for strabismus and focal dystonia may then be directly related to both the anatomic fiber type composition and the functional properties of motor control systems of the injected muscle.
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PMID:Botulinum-induced changes in monkey eyelid muscle. Comparison with changes seen in extraocular muscle. 200 2

The National Institutes of Health Consensus Development Conference on Clinical Use of Botulinum Toxin brought together neurologists, ophthalmologists, otolaryngologists, speech pathologists, and other health care professionals as well as the public to address: the mechanisms of action of botulinum toxin, the indications and contraindications for botulinum toxin treatment, the general principles of technique of injection and handling for its safe and effective use, and the short-term and long-term side effects and complications of therapy. Following 2 days of presentations by experts and discussion by the audience, a consensus panel weighed the evidence and prepared their consensus statement. Among their findings, the panel recommended that (1) botulinum toxin therapy is safe and effective for treating strabismus, blepharospasm, hemifacial spasm, adductor spasmodic dysphonia, jaw-closing oromandibular dystonia, and cervical dystonia; (2) botulinum toxin is not curative in chronic neurological disorders; (3) the safety of botulinum toxin therapy during pregnancy, breast feeding, and chronic use during childhood is unknown; (4) the long-term effects of chronic treatment with botulinum toxin remain unknown; and (5) botulinum toxin should be administered by committed interdisciplinary teams of physicians and related health care professionals with appropriate instrumentation. The full text of the consensus panel's statement follows.
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PMID:Botulinum toxin. 209 81

Over recent years botulinum toxin type A has emerged as a safe and effective treatment for a number of previously refractory conditions associated with excessive muscle activity. The list of indications is expanding, but at present it is generally considered to be the treatment of choice for focal dystonias such as blepharospasm, torticollis, laryngeal dystonia, and oromandibular dystonia, as well as hemifacial spasm, strabismus, and some forms of limb spasticity. Carefully targeted intramuscular injections of a small amount of the toxin block the release of acetylcholine at the neuromuscular junction, producing a chemical denervation, with the aim of reducing excessive muscle activity without producing significant functional weakness. In some situations electrophysiological assessment and localisation of the muscles for injection is necessary. Treatment is symptomatic, with effects lasting 3 to 4 months and most patients requiring up to 4 injections per year to maintain the beneficial effect. Appropriate use of the toxin requires both an understanding of the physiological action of the potential muscles involved in each situation, together with a knowledge of the likely dose necessary to reduce muscle activity to the required level. Botulinum toxin represents a major advance in the management of these conditions, many of which responded poorly to previously available forms of therapy.
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PMID:Botulinum toxin in clinical practice. 753 96

A solution containing S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide (NO.-releasing compound, was microinjected in doses of 0.25-2 mumol into a lateral ventricle of conscious rats. SNAP produced dose-dependent convulsions similar to those associated with limbic stimulation, such as tonic extension of the hindlimbs and tail, and dystonia of the forepaws. At 2 mumol, SNAP evoked hyperventilation (arterial hypocapnia), arterial hyperglycemia and caused necrotic lesions of periventricular gray (e.g. lateral septal nucleus) and white matter structures. In the caudate nucleus and lateral septal nucleus ipsilateral to injection, SNAP elicited a bipolar metabolic pattern of low glucose metabolism proximal to the ventricle with higher values occurring more distally. In control studies, we proved that the residue of SNAP decomposition, N-acetylpenicillamine disulfide injected intraventricularly (2 mumol), was without physiological, behavioral, or histological effects. Ventricular pretreatment with methylene blue (2 nmol), a putative inhibitor of guanylate cyclase and superoxide generator, suppressed several of the behavioral manifestations of 1 mumol SNAP, such as the forepaw dystonia, squinting, and facial clonus, but was ineffective on the physiological and histological variables affected by the 2 mumol SNAP dose. Another NO. donor, sodium nitroprusside (2 mumol), produced fewer behavioral and cytotoxic effects over a 55-min observation period, but caused more intense and widely distributed metabolic stimulation, especially in commissural and projection white matter tracts. The results are the basis for a conscious rat model using intraventricular injection of nitrocompounds to examine the physiological, behavioral, metabolic and cytotoxic properties of NO. in the brain.
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PMID:Neurotoxicity in conscious rats following intraventricular SNAP, a nitric oxide donor. 796 12

Local injections of botulinum toxin is a well-accepted treatment for focal dystonias, hemifacial spasms and strabismus. Its use by skilled neurologists has been reported to be safe and effective. We report our experience with botulinum toxin injections in 108 patients with various central nervous system disorders. Botox was effective in upper face dystonia (86% improvement), spastic dysphonia (92% improvement), platysma muscle spasms and spasmodic torticollis (range of movement 61%, pain and tension 90%). It was also very effective in a few patients with apraxia of eyelid opening, parkinsonian jaw tremor, teeth clenching, palatal myoclonus and adductor leg spasticity. No serious side effects were recorded. Botulinum toxin is a useful symptomatic treatment for many neurological disorders, and one of the leading mode of treatments in the new subspecialty in neurology called "Interventional neurology."
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PMID:Interventional neurology: botulinum toxin as a potent symptomatic treatment in neurology. 798 70

The use of botulinum-A toxin will be described in two conditions--the extrapyramidal syndrome of dystonia and the pyramidal deficit, spasticity. There is no cure for dystonia and its cause is unknown. Drug therapy is unpredictable and dose-limiting side effects frequently occur with little or no alleviation of symptoms. Spasticity of adductor muscles in the lower limbs causes profound disability and major nursing problems in patients with chronic disorders of the pyramidal tract. As in the case with dystonia, drug therapy is unsatisfactory. At the UBC Movement Disorders Clinic treatment with botulinum-A has been applied to over 400 patients since 1985. The results of the first studies using this treatment in spasmodic torticollis (the most common form of focal dystonia) and spasticity (in late stage multiple sclerosis) will be discussed. As well the effects of long term treatment will be addressed. Botulinum-A toxin is approved treatment for strabismus, blepharospasm and hemifacial spasm. Approval for its use in other focal dystonias is anticipated. The very nature of the agent used for treatment requires that patients be well prepared and reassured before they undergo their first treatment. There is a wide gulf between the patients' preconceived notions about the treatment and reality.
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PMID:Local treatment of dystonia and spasticity with injections of botulinum-A toxin. 827 87

Botulinum toxin, the most potent of the neurotoxins, produces paralysis by blocking presynaptic release of the neurotransmitter (acetylcholine) at the neuromuscular junction, with reversible chemical denervation of the muscle fibre, thereby inducing partial paralysis and atrophy. Because chemical denervation is reversible, botulinum toxin has temporary effects, the muscle being progressively reinnervated by nerve sproutings. Type A botulinum toxin (Bix-A) is available under two dosage forms: Botox and Dysport. Although the initial clinical indication was strabismus, subsequent studies have demonstrated the efficacy of Btx-A, mainly in dystonia, hemifacial spasm and spasticity. However, botulinum toxin has been successfully used in various other clinical indications. In regard to spasticity associated with cerebral palsy, Btx-A is a promising treatment requiring a multidisciplinary approach. Btx-A injections lead to effective reduction of muscle hyperactivity with minor side-effects. They are painless, even though electromyographic guidance may be required for the injection of deep muscles. However, the production of antibodies to Btx-A may compromise the effect of long-term treatment.
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PMID:[Mechanism of action, clinical indication and results of treatment of botulinum toxin]. 897 11

Botulinum toxin is a presynaptic neuromuscular blocking agent that, when injected intramuscularly in minute quantities, can produce selective muscle weakness. This property is employed therapeutically to provide symptomatic relief in conditions related to excessive muscle activities in strabismus, blepharospasm, hemifacial spasm, cervical dystonia, spasmodic dysphonia (adductor type), and jaw closing dystonia. It is investigational for a long list of medical conditions. It is a marketed drug in a number of countries in the world, but its use has only been approved by different regulatory agencies for use in a limited number of conditions. The long-term effects, appropriate dose for children, and in pregnancy, and maximum dose without causing toxicity remain unclear.
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PMID:Botulinum toxin as a therapeutic agent. 898 68

Botulinum toxin was introduced as a safe and effective treatment for strabismus and other disorders of the extraocular muscles in the early 1980s. Approved by the U.S. Food and Drug Administration for use in the treatment of strabismus, blepharospasm and seventh cranial nerve disorders, botulinum toxin has also been shown to be effective in the treatment of a wide range of disorders associated with involuntary muscle contraction and spasm, including focal dystonia, hemifacial spasm and spasmodic torticollis. Neurologic syndromes associated with excessive muscle contraction or involuntary movement, disturbances of sphincter function and musculoskeletal pain are other conditions that can be successfully treated with botulinum toxin.
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PMID:Therapeutic uses of botulinum toxin. 905 23


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