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Muscle Paralysis (muscle + paralysis)
Selected AbstractsMuscle paralysis with an accidental overdosage of neostigmineACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2008R. Sharma No abstract is available for this article. [source] Effect of muscle activity and botulinum toxin dilution volume on muscle paralysisDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 3 2003Hyeon Sook Kim MD PhD The purpose of this study was to evaluate the effects of botulinum toxin A (BTX-A, Botox) dilution volume and post-injection exercise with electrical stimulation on muscle paralysis. We injected 10 units of BTX-A diluted with 0.1 ml (B1, n=8) or 0.5 ml (B5, n=8) normal saline into both gastrocnemius muscles of 16 New Zealand white rabbits; two controls received no BTX-A. After BTX-A injection, all rabbits received calf muscle stretching exercise and electrical stimulation for 2 hours on the left leg. The compound muscle action potential (CMAP) decrease was most pronounced at 1 week and progressive recovery was observed (i.e. recovery from paralysis, increase of CMAP). There was a significant decrease of CMAP amplitudes in the B5 group compared with the B1 group at week 1 and week 4 (p<0.001). Left limbs with stretching exercise and electrical stimulation showed lower CMAP amplitudes compared with control right limbs of all rabbits. To maximize the muscle paralysis effect of BTX-A, increasing dilution volume and performing post-injection stretching exercise with electrical stimulation may be a promising strategy for increasing the beneficial effect of BTX-A treatment. Future studies are needed to investigate the clinical application of this finding. [source] Effects of Botox® and Neuronox® on muscle force generation in miceJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 12 2007Austin V. Stone Abstract The current study determined the dose,response relationship for inhibition of muscle force of two commercially available botulinum neurotoxin type-A (BoNTA) preparations (Botox® and Neuronox®) in a murine model and characterized the time course of recovery from the toxin-induced muscle paralysis. The effect of freezing reconstituted toxin on toxin potency was also determined. The gastrocnemius muscles in male CD-1 mice were injected with either saline or BoNTA (0.3,3.0 U/kg), and muscle force generation was examined following stimulation of the tibial nerve (single twitch and 15,200 Hz tetany). Botox and Neuronox produced nearly equivalent decrements in muscle force (30%,90%) at 4 days after toxin injection. At 28 days after injection (1 U/kg), muscle force had recovered from the effects of both toxin preparations. Maintaining reconstituted toxin at ,80°C for up to 5 months did not result in significant loss of toxin activity. The results of this study suggest that Botox and Neuronox produce equivalent responses in a murine model, and, in contrast to other models, muscle recovery is rapid with doses of toxin that produce less than maximal decrements in muscle force. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:1658,1664, 2007 [source] Historical notes on botulism, Clostridium botulinum, botulinum toxin, and the idea of the therapeutic use of the toxinMOVEMENT DISORDERS, Issue S8 2004Frank J. Erbguth MD Abstract Food-borne botulism probably has accompanied mankind since its beginning. However, we have only few historical sources and documents on food poisoning before the 19th century. Some ancient dietary laws and taboos may reflect some knowledge about the life-threatening consumption of poisoned food. One example of such a dietary taboo is the 10th century edict of Emperor Leo VI of Byzantium in which manufacturing of blood sausages was forbidden. Some ancient case reports on intoxications with Atropa belladonna probably described patients with food-borne botulism, because the combination of dilated pupils and fatal muscle paralysis cannot be attributed to an atropine intoxication. At the end of the 18th century, some well-documented outbreaks of "sausage poisoning" in Southern Germany, especially in Württemberg, prompted early systematic botulinum toxin research. The German poet and district medical officer Justinus Kerner (1786,1862) published the first accurate and complete descriptions of the symptoms of food-borne botulism between 1817 and 1822. Kerner did not succeed in defining the suspected "biological poison" which he called "sausage poison" or "fatty poison." However, he developed the idea of a possible therapeutic use of the toxin. Eighty years after Kerner's work, in 1895, a botulism outbreak after a funeral dinner with smoked ham in the small Belgian village of Ellezelles led to the discovery of the pathogen Clostridium botulinum by Emile Pierre van Ermengem, Professor of bacteriology at the University of Ghent. The bacterium was so called because of its pathological association with the sausages (Latin word for sausage = "botulus") and not,as it was suggested,because of its shape. Modern botulinum toxin treatment was pioneered by Alan B. Scott and Edward J. Schantz. © 2004 Movement Disorder Society [source] Spinal muscular atrophy: Recent advances and future prospectsMUSCLE AND NERVE, Issue 1 2002Sophie Nicole PhD Abstract Spinal muscular atrophies (SMA) are characterized by degeneration of lower motor neurons associated with muscle paralysis and atrophy. Childhood SMA is a frequent recessive autosomal disorder and represents one of the most common genetic causes of death in childhood. Mutations of the SMN1 gene are responsible for SMA. The knowledge of the genetic basis of SMA, a better understanding of SMN function, and the recent generation of SMA mouse models represent major advances in the field of SMA. These are starting points towards understanding the pathophysiology of SMA and developing therapeutic strategies for this devastating neurodegenerative disease, for which no curative treatment is known so far. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 4,13, 2002 [source] Using botulinum toxin for pelvic indications in womenAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 4 2009Archana RAO Background: Botulinum toxin (BoNT) is a potent neurotoxin. Its ability to cause muscle paralysis is increasingly being utilised for the management of a number of conditions of interest to the gynaecologist. Aims: This review aims to give the reader an overview of the use of BoNT for conditions presenting a management challenge for the gynaecologist, such as chronic pelvic pain and idiopathic detrusor overactivity. Methods: The literature was reviewed regarding the use, side-effects and complications of BoNT in the pelvis, focussing on chronic pelvic pain, provoked vestibulodynia, conditions involving the lower gastrointestinal tract and detrusor overactivity. Results: In terms of pain caused by pelvic floor spasm, daily pelvic pain and dyspareunia are the symptoms most likely to be improved by BoNT. Limited data regarding use for provoked vestibulodynia indicate an improvement in pain scores. In the lower gastrointestinal tract, injection into puborectalis has been showed to objectively improve intravaginal pressures, though there are no randomised controlled trials (class I studies) validating its use in this setting. Class I studies demonstrate a role for BoNT in the management of idiopathic detrusor overactivity, though long-term follow-up data are lacking. Potential problems with BoNT injection include toxin reactions, urinary and faecal incontinence, urinary retention and secondary treatment failure due to antibody production. Conclusions: A single class I study supports the use of BoNT for refractory pelvic floor spasm; however, further adequately powered class I studies for this indication and for provoked vestibulodynia are warranted. [source] Restoration of motor function of the deep fibular (peroneal) nerve by direct nerve transfer of branches from the tibial nerve: An anatomical study,CLINICAL ANATOMY, Issue 3 2004Kale D. Bodily Abstract Traction injuries of the common fibular (peroneal) nerve frequently result in significant morbidity due to tibialis anterior muscle paralysis and the associated loss of ankle dorsiflexion. Because current treatment options are often unsuccessful or unsatisfactory, other treatment approaches need to be explored. In this investigation, the anatomical feasibility of an alternative option, consisting of nerve transfer of motor branches from the tibial nerve to the deep fibular nerve, was studied. In ten cadaveric limbs, the branching pattern, length, and diameter of motor branches of the tibial nerve in the proximal leg were characterized; nerve transfer of each of these motor branches was then simulated to the proximal deep fibular nerve. A consistent, reproducible pattern of tibial nerve innervation was seen with minor variability. Branches to the flexor hallucis longus and flexor digitorum longus muscles were determined to be adequate, based on their branch point, branch pattern, and length, for direct nerve transfer in all specimens. Other branches, including those to the tibialis posterior, popliteus, gastrocnemius, and soleus muscles were not consistently adequate for direct nerve transfer for injuries extending to the bifurcation of the common fibular nerve or distal to it. For neuromas of the common fibular nerve that do not extend as far distally, branches to the soleus and lateral head of the gastrocnemius may be adequate for direct transfer if the intramuscular portions of these nerves are dissected. This study confirms the anatomical feasibility of direct nerve transfer using nerves to toe-flexor muscles as a treatment option to restore ankle dorsiflexion in cases of common fibular nerve injury. Clin. Anat. 17:201,205, 2004. © 2004 Wiley-Liss, Inc. [source] | |||||||||||||