Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intramuscular injections of botulinum toxin (Botox) are followed by a dose-dependent focal paresis which can be used to treat several focal movement disorders. Botox injections are recommended as effective for the treatment of blepharospasm, hemifacial spasm, and cervical dystonia (torticollis). Focal dystonias elsewhere (for example, writer's cramp) can often be treated with similar success. Others, such as oromandibular dystonia, are more difficult to treat. In the case of more generalized dystonias, some focal muscle spasms can be treated with success by local intramuscular injections. New indications are still being investigated, for example in focal tremors and spasticity. Side effects are in general slight and disappear at the end of toxin effect. In general, it is necessary to repeat the injections after a couple of months, due to a cessation of effect after regrowth of nerve terminals. New injections have similar effects even over years of treatment.
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PMID:[Treatment of movement disorders using botulinum toxin]. 141 87

Selective facial neurectomy in combination with bilateral musculocutaneous resection, plication brow lift, upper lid blepharoplasty, and limited rhytidectomy was performed on 18 patients with essential blepharospasm, eight with hemifacial spasm, and two with CNS vascular compression malformations. Microscopy showed the nerve tissues to be normal. Initial results were excellent. At 3 months there was a slight, persistent spastic twitching of the affected muscles in five nerves (a 14% failure rate in correcting blepharospasm). After 13 months there were four additional failures resulting from nerve regrowth in three and from one patient not completing therapy. The overall blepharospasm failure rate was 26%. On repeat neurectomy those with nerve regrowth presented with a diffuse, fine meshwork of nerve fibers reinnervating the mimetic facial musculature. In six of seven patients operated on again, spasticity was eliminated. The initial surgical failure rate has been corrected by resecting the frontal branch and the superior division of the buccal branch of the facial nerve. Only repeat neurectomy can correct long-term failures resulting from facial nerve regrowth.
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PMID:Selective facial neurectomy for spastic disorders of the facial nerve. 392 7

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

Structure, biological activity, mode and mechanism of action of botulinum toxin as well as its therapeutic use is described. Botulinum toxin type A, one of the most potent biologic toxins, has been found to be of therapeutic value in the treatment of several neurologic and ophthalmologic diseases. Its ability to produce chemical denervation of muscles makes it option for treatment of disorders in which traditional therapeutic procedures are of limited value (e.g. blepharospasm and other focal dystonias, strabismus, spasticity).
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PMID:[Botulinum toxin: structure, mode of action and therapeutic use]. 763 99

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 toxins, exotoxins of Clostridium botulinum, are the most toxic naturally occurring substances known to man. For more than a century they are known to be the cause of botulism, a nowadays rare intoxication with spoiled food that leads to generalized flaccid weakness of striated muscle including pharyngeal and respiratory musculature. The toxins act primarily at peripheral cholinergic motor nerve endings by blocking the release of the neurotransmitter acetylcholine. As a consequence, action potentials in the motor nerve can no longer be transmitted to the muscle. This lack in transmission, clinically appearing as weakness, may disable or actually critically endanger affected patients. However, in certain neurological diseases characterized by an abnormal increase in muscle tone or activity, for example dystonia or spasticity, a reduction in signal transmission may actually be beneficial. Around 1980 local injections of minute amounts (in the order of 0.5 ng) of Botulinum toxin type A were first successfully used in a neurological disorder named blepharospasm which is characterized by an involuntary squinting of the eyes. Since then Botulinum toxin has developed rapidly from a frightful poison to a safe therapeutic agent with a remarkable beneficial impact on the quality of life of many thousands of patients worldwide. This review tries to outline in brief the characteristics of Botulinum toxins, their mechanism of action and the various indications for clinical use as a therapeutic agent.
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PMID:Botulinum toxin: from poison to remedy. 933 23

Since Botulinum toxin A became a mainstay therapy for blepharospasm, its use in treating other dystonic conditions, spasticity disorders, as well as hyperfunctional lines of the face has increased exponentially in recent years. The following article summarizes our experience in establishing a safe and reliable method of administration of botulinum toxin A for treating hyperfunctional lines of the face.
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PMID:Treatment of hyperfunctional lines of the face with botulinum toxin A. 983 39

Toxins are increasingly being used as valuable tools for analysis of cellular physiology, and some are used medicinally for treatment of human diseases. In particular, botulinum toxin, the most poisonous biological substance known, is used for treatment of a myriad of human neuromuscular disorders characterized by involuntary muscle contractions. Since approval of type-A botulinum toxin by the US Food and Drug Administration in December 1989 for three disorders (strabismus, blepharospasm, and hemifacial spasm), the number of indications being treated has increased greatly to include numerous focal dystonias, spasticity, tremors, cosmetic applications, migraine and tension headaches, and other maladies. Many of these diseases were previously refractory to pharmacological and surgical treatments. The remarkable therapeutic utility of botulinum toxin lies in its ability to specifically and potently inhibit involuntary muscle activity for an extended duration. The clostridia produce more protein toxins than any other bacterial genus and are a rich reservoir of toxins for research and medicinal uses. Research is underway to use clostridial toxins or toxin domains for drug delivery, prevention of food poisoning, and the treatment of cancer and other diseases. The remarkable success of botulinum toxin as a therapeutic agent has created a new field of investigation in microbiology.
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PMID:Clostridial toxins as therapeutic agents: benefits of nature's most toxic proteins. 1054 1

Botulinum toxin (BTX), a potent biologic neurotoxin, commonly is associated with lethal outbreaks of food poisoning; however, it also plays a role as a therapeutic agent. Since the 1970s physicians have investigated BTX therapy in patients with neurologic disorders. The number of applications greatly expanded over the years to include certain focal dystonias (blepharospasm, torticollis, laryngeal dystonias, writer's cramp), strabismus, and a wide variety of other indications (gastrointestinal disorders, cosmetic wrinkle correction, spasticity, hyperhidrosis). BTX's safety and efficacy are reviewed.
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PMID:Pharmacotherapy with botulinum toxin: harnessing nature's most potent neurotoxin. 1099 1

Botulinum toxin is more and more frequently used as a therapeutic agent. The toxin blocks selectively and reversibly the neuromuscular junction, causing a muscle relaxation. Indications are mainly muscular hypercontraction, such as dystonia, blepharospasm, focal spasticity, strabismus or tics. The range of action extend to focal hyperhydrosis, palmar, axillary or plantar. It seems now that some painful syndrome such as migraine or tension headache may benefit from toxin injections. Esthetic indications constitute an extension to the pure medical indications.
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PMID:[Current indications for the treatment with botulin toxin]. 1172 14


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