Effect of botulinum-A toxin to cremaster muscle: an experimental study

Çakmak, Murat; Çağlayan, Fatma; Erdemoğlu, Ali Kemal; Ulusoy, Sevgi

doi:10.1007/s00240-003-0357-7

Cited by 9 publications

(6 citation statements)

References 13 publications

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“…Oral medication with different types of drugs frequently used to treat hyperactivity of nerve function such as antidepressants, anticonvulsants, and anti‐parkinsonian drugs were not successful in this patient. Efficacy of Btx A in the cremasteric muscles has been proven in an animal model 4. The success of the treatment with Btx A is in line with previous reports of treatment of synkinesias of other parts of the body, especially of the facial nerve 1, 2.…”

Section: Discussionsupporting

confidence: 80%

Treatment of cremaster synkinesias with botulinum toxin A: A video case report

et al. 2006

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Synkinesias secondary to nerve lesions and aberrant re-innervation are well-known phenomena especially after lesions of the facial nerve. Synkinesias can successfully be treated with botulinum toxin A (BTx A). Synkinesias of the cremaster muscle have not been described or treated to date. We present the case of a 62-year-old man who developed synkinesias of both cremaster muscles after extensive laparatomy for esophageal cancer. Treatment of synkinesias with various oral medications had been unsuccessful. Electromyography-guided injections of BTx A in both cremaster muscles (15 MU on the right and 10 on the left) led to significant symptom relief for an average of 8 weeks. We present the case including pre- and posttreatment video clips.

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Section: Discussionsupporting

confidence: 80%

Treatment of cremaster synkinesias with botulinum toxin A: A video case report

et al. 2006

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“…Pretreatment with gallamine minimized the confounding effects of BoNTA-mediated muscle paralysis and isolated BoNTA's blockade of sympathetic neural transmission. 30 Inhibition of norepinephrine release from vascular smooth muscle nerve terminals resulted in relaxation of arterial smooth muscle and increased vessel diameters. The observed maximal response might have been due to a saturation of the nerve terminals or simply sufficient synaptosomal-associated protein 25 cleavage to block soluble N-ethylmaleimide-sensitive factor attachment protein receptor-mediated neurotransmission.…”

Section: Discussionmentioning

confidence: 99%

“…29 Gallamine paralysis eliminated the confounding effect of vascular responses to altered metabolic rate due to toxin-mediated muscle paralysis. 30 Baseline measurements were repeated 10 minutes after the addition of gallamine. Because gallamine did not cause a significant change in vessel diameter over the pre-gallamine treatment diameters, all vessel measurements were normalized to resting diameter in the presence of gallamine.…”

Section: Drug Treatment and Vessel Measurementmentioning

confidence: 99%

The Effect of Botulinum Neurotoxin-A on Blood Flow in Rats: A Potential Mechanism for Treatment of Raynaud Phenomenon

Stone

Koman

Callahan

et al. 2012

The Journal of Hand Surgery

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“…Early research into the mechanisms of action of BoNT‐A commonly involved in vivo injections of BoNT‐A, and then a wait of several days before experiments were undertaken in vitro [7–9]. For example, human extensor digitorum brevis muscles showed a reduction in end‐plate noise after i.m.…”

Section: Discussionmentioning

confidence: 99%

Lack of effectiveness of botulinum neurotoxin A on isolated detrusor strips and whole bladders from mice and guinea‐pigs in vitro

et al. 2009

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OBJECTIVE To differentiate between the effects of parasympathetic and sensorimotor stimulation of isolated mouse and guinea‐pig bladders in vitro by measuring the pressure increases to electrical field stimulation (EFS) and then comparing the effects of botulinum neurotoxin A (BoNT‐A) applied either to the lumen or to the external bathing medium. MATERIALS AND METHODS Isolated mouse and guinea‐pig bladders and detrusor strips were exposed to EFS in vitro before and after the addition of BoNT‐A. The rationale of this method was that BoNT‐A applied to the outside of the bladder would first affect the parasympathetic nerves before diffusing inwards to affect the sensorimotor innervation. BoNT‐A applied intravesically would first reach the sensorimotor nerves and only later the parasympathetic nerves. Initial experiments on strips of detrusor were conducted to establish the correct dosage and application time of BoNT‐A. RESULTS Contrary to our expectations, BoNT‐A application failed to produce any significant effects on either the detrusor strips or whole bladders. CONCLUSIONS Our experimental design failed to show any effect of BoNT‐A on the contractility of detrusor muscle strips or whole bladders from mice and guinea‐pigs. The reason for this is unclear, but may be related to tissue spending inadequate time incubated with BoNT‐A under physiological conditions.

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Effect of botulinum-A toxin to cremaster muscle: an experimental study

Cited by 9 publications

References 13 publications

Treatment of cremaster synkinesias with botulinum toxin A: A video case report

Treatment of cremaster synkinesias with botulinum toxin A: A video case report

The Effect of Botulinum Neurotoxin-A on Blood Flow in Rats: A Potential Mechanism for Treatment of Raynaud Phenomenon

Lack of effectiveness of botulinum neurotoxin A on isolated detrusor strips and whole bladders from mice and guinea‐pigs in vitro

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