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The pathophysiology of interstitial cystitis/bladder pain syndrome (IC/BPS) may be bladder-centric, with afferent nerve hyperexcitability and/or due to neural central sensitization. In bladder-centric disease, the trigone's unmyelinated nociceptive C-fibers are thought to be upregulated, suggesting this as a potential target for diagnostic modalities and for treatment with local anesthetics and chemodenervation. We propose that the transvaginal trigone treatment (T3) route of administration of such treatments should be considered in women with IC/BPS, as this approach is easier and less invasive than cystoscopy. For T3, or other bladder-centric treatments to be successful, patient selection should attempt to exclude patients with predominantly neural central sensitization.

Purpose of Review Bilateral vocal fold immobility is a challenging life-threatening problem involving multiple treatment options and nuanced clinical decision making. We aim to provide relevant background on the etiology, diagnosis, and management of bilateral vocal fold movement impairment (BVFMI). Recent Findings Over the last 20 years, the management of bilateral vocal fold immobility has advanced significantly with the addition of multiple endoscopic approaches as well as procedures with the goal of returning dynamic function to the larynx, among them: selective reinnervation. Chemodenervation has also demonstrated promising results as a temporizing procedure in appropriately selected patients with BVFMI. Summary Tracheostomy remains the mainstay of emergent treatment for airway obstruction secondary to bilateral vocal fold immobility. However, recent advances in endoscopic approaches allow for avoidance of tracheostomy in many patients. Developments in dynamic procedures with the aim of restoring laryngeal function allow for adequate airway management while maintaining voice quality and limiting aspiration risk.

Botulinum toxin A (BoTA) has proven a safe and effective treatment across a wide variety of medical and cosmetic applications. Recently, studies have explored the use of BoTA to optimize scar formation by reducing the dynamic tension under which traumatic and surgical wounds heal via chemodenervation of underlying muscles. This article reviews advances focusing on the use of BoTA in wound management and scar revision. Several prospective randomized controlled trials provide evidence that BoTA has a positive effect on wound healing and scar formation. This effect extends beyond its chemodenervative properties to include reducing pro-fibrotic factors and minimizing fibroblast growth and differentiation to better prevent pathological scarring. Botulinum toxin is a safe and efficacious adjunct to other interventions intended to optimize scar appearance in traumatic or surgical wounds. Questions remain regarding the optimal technique, timing, and dosing for BoTA administration for ideal wound healing.

Facial paralysis can lead to lagophthalmos, loss of corneal protection, and devastating ocular consequences like corneal ulcers or even blindness. The purpose of this review is to discuss the importance of comprehensive and early eye care. Treatment of paralytic lagophthalmos should be individualized to each patient’s situation; depending on the severity of the problem and the prognosis for recovery, treatment modalities are broad and include lubrication, selective chemodenervation, filler injection, fat augmentation, and surgical procedures like canthopexy and tarsorrhaphy. This paper serves to highlight the importance of treating paralytic lagophthalmos and provides an overview of the optimal management algorithm of the compromised periocular complex to help improve function and quality of life. Prospective studies and long-term comparisons of surgical techniques for repair of paralytic lagophthalmos will help improve our understanding of this complex problem and perhaps introduce novel treatment strategies.

Facial synkinesis is a sequela of facial nerve injury that results in involuntary facial movement occurring simultaneously with volitional facial movement. Inability to control facial movement has functional and psychological consequences and can be socially isolating. This review discusses the involved facial nerves and musculature, evaluation of the synkinetic face, and different treatment options. We reviewed the literature for advancements and outcomes in assessment, rehabilitation, and non-surgical and surgical treatments for facial synkinesis while highlighting anatomical correlates and movement patterns of commonly affected facial musculature. Understanding facial muscular anatomy, including the intended vectors of movement, guides appropriate therapeutic intervention and improves outcomes. Chemodenervation and rehabilitation continue to be the main treatment strategy for facial synkinesis. In select cases, other techniques, such as selective neurolysis, selective myectomy, nerve grafting, or free muscle transfer, are also available.

Multiple sclerosis (MS) is an autoimmune disorder affecting the central nervous system. Because MS is a chronic disease that can affect any part of the central nervous system, most patients experience voiding dysfunction during the course of the disease. Depending on the site of plaques within the central nervous system, various complaints may arise. Familiarity is required with the evaluation of patients with MS and the available treatment armamentarium. Preservation of the upper urinary tracts is of primary importance. Newer technologies, such as sacral neuromodulation and chemodenervation with botulinum toxin A, can achieve control of urologic symptoms without extensive surgery. This review focuses on the diagnosis, evaluation, and treatment of patients with MS.

Botulinum toxin A (BTX-A) has emerged as a novel treatment option for idiopathic overactive bladder (OAB) refractory to antimuscarinic agents. The clinical needs of refractory OAB patients have been recently met by sacral neuromodulation and augmentation enterocystoplasty. Important features of BTX-A should include safety, efficacy, and ease of delivery during long-term repeated usage. This article reviews the role of repeated BTX-A injections in the treatment of idiopathic OAB.

Botulinum toxin treatment was originally developed 25 years ago by Alan B. Scott to produce reversible weakening of extraocular eye muscles in humans (chemodenervation). The following uses are still helpful today in comparison with eye muscle surgery, prism applications etc.: Preoperative evaluation of possible postoperative diplopia in patients in whom this cannot be done by means of prisms or traction test, etc. Acute paretic loss of ocular muscle function when surgical treatment of the ocular muscles is not yet possible but the patient is obviously disturbed by diplopia or a forced head posture. This applies especially to VI cranial nerve paresis. Depending on the surgical approach in VI nerve palsies, Botulinum toxin may be injected in the medial rectus muscle before muscle transposition surgery to loosen contracture. Strabismus in acute Graves' disease. In strabismus in other conditions, Botulinum toxin is mostly inferior surgical treatment of the ocular muscles; this is the case, for example in congenital esotropia or horizontal strabismus in adults. While the reversibility of the Botulinum toxin A effect by fading out after 3-4 months is seen as an advantage, it does also mean that in these cases of constant strabismus it is necessary to keep repeating the injections.

To evaluate the effectiveness of anterior chemodenervation of levator palpebrae superioris with Botulinum toxin type A (Botox®) to induce temporary ptosis for corneal protection, and assess the incidence of superior rectus underaction. Prospective interventional case series. Patients with ocular surface pathology requiring temporary tarsorrhaphy underwent transcutaneous anterior chemodenervation of levator palpebrae superioris with Botox®. The onset and duration of ptosis, corneal healing, and superior rectus underaction was evaluated. Ten eyes of 10 patients underwent transcutaneous anterior chemodenervation of levator muscle. Five patients had Bells palsy with exposure keratopathy, four patients had persistent epithelial defect, and one had neurotrophic ulcer. The median age at presentation was 30 years. Median dose of Botulinum toxin injection was 12.5 U (range 10–15 U). The mean palpebral fissure height of 9 mm (SD±2.1 mm) before injection, reduced to 2.8 mm (SD±1.9 mm) at 1-week post-injection. More than 50% reduction in palpebral fissure height was seen in nine out of 10 eyes (90%, 95% CI 71.4–100%) at 1 week, seven of nine eyes (77.8%, 95% CI 50.6–100%) at 2 weeks, and two of nine eyes (22.2%, 95% CI 0–49.4%) at 4 weeks, and returned to pretreatment level after mean duration of 9.2 weeks (range 5–16 weeks). Superior rectus underaction was not noted in any of the patient (95% CI 0–30%). Corneal pathology improved in all cases. Anterior chemodenervation of levator palpebrae superioris with Botulinum toxin type A (Botox®) induces significant temporary ptosis and aids in corneal healing. Anterior placement of the toxin injection may avoid superior rectus underaction.

BACKGROUND Masseteric hypertrophy is a unilateral or bilateral enlargement of the masseteric muscle of various aetiologies. The therapeutic options range from solely conservative measures, especially in functionally induced abnormalities, up to surgical ablation of the muscle. The presented study evaluates the application of botulinum toxin serotype A for the treatment of masseteric hypertrophy. PATIENTS AND METHODS Between June 2000 and August 2004 seven patients with a unilateral and one patient with a bilateral manifestation of the condition were treated by an injection of botulinum toxin. RESULTS A significant improvement of facial asymmetry caused by chemodenervation and following reduction of the hypertrophic muscle mass could be achieved in all cases. Complications during the injection, side effects, signs of intoxication, and therapy failure were not observed. CONCLUSION The results of this treatment series show in agreement with the reports in the literature that the application of botulinum toxin can be currently considered as the therapy of choice in masseteric hypertrophy.

Botulinum toxin preparations can provide patients with a therapeutic modality that may improve both their medical condition and quality of life. The mechanism of action of the various botulinum toxin preparations and serotypes is similar: they all block neurotransmitter release. The majority of clinical conditions treated are based upon the targeted temporary chemodenervation of the selected organ. The antinociceptive effects of botulinum toxin type A (BTX-A), based on preclinical studies and clinical experiences in treating movement disorders and other painful conditions, will also be reviewed to illustrate how this compound may act as it alleviates the discomfort associated with various conditions. Chronic therapies with preparations with the lowest amount of neurotoxin protein provide the best chance for long-term therapy by minimizing the potential of the patient to form neutralizing antibodies. Differences in formulations or serotypes impart unique efficacy and safety profiles and thus does not support a simple dose ratio conversion between products.

Intramuscular injections of botulinum neurotoxin type A cause reversible chemodenervation and subsequent paralysis by blocking the presynaptic release of acetylcholine. Botulinum toxin type A has emerged as the most effective form of symptomatic treatment for abnormabilities in muscle movement (blepharospasm, hemifacial spasm, torticollis) and has been approved for use in these conditions. First results in the treatment of patients suffering from oromandibular dystonia, myogenic craniomandibular dysfunction and recurrent dislocation of the temporomandibular joint are presented. In most cases, therapeutic effects occurred within 1-6 days post-injection. Muscular hyperfunction was reliably reduced and involuntary activity patterns gradually ceased. No severe side effects of the local injections were noted.

Ruptured extraocular muscle loses its function and shows severe restriction of eye movement even after muscle-to-muscle anastomosis or muscle transposition surgery. We present the case of a patient who developed a large exotropia after near-total rupture of the medial rectus muscle following a blowout fracture.Case report.A 12-year-old girl presented at our clinic with 45 prism diopters' exotropia after a blunt trauma. A forced duction test was unrestricted, and orbital computed tomography showed a medial orbital wall fracture and an impinged medial rectus muscle. Upon surgical exploration, an almost totally ruptured medial rectus muscle was found. The median margin of the ruptured muscle was 6.0 mm from its insertion, and the distal end that we could examine was 15.0 mm from the limbus. Recession-resection surgery combined with intraoperative botulinum toxin A chemodenervation to the ipsilateral lateral rectus muscle achieved a good primary alignment and binocular single visual field, even at a 9-month follow-up.Recession-resection surgery augmented by intraoperative botulinum toxin A chemodenervation to the ipsilateral rectus muscle appears to be highly effective in the treatment of a large exotropia produced by subtotal rectus muscle rupture following orbital wall fracture, with a lower risk of anterior segment ischemia.

L’halothane diminue la reponse ventilatoire a l’hypoxie et l’activite des chemorecepteurs arteriels peripheriques, realisant une «chemodenervation chimique». Afin d’evaluer le role de cette «chemodenervation chimique» dans les modifications de l’equilibre acido-basique et des gaz du sang arteriel provoquees par l’halothane, ces parametres ont ete mesures chez des rats intacts eveilles, puis anesthesies, et chez des rats chemodenerves, eveilles puis anesthesies. Le niveau de l’anesthesie pouvant etre modifie par la chemodenervation anatomique, l’ED50 inspiree d’halothane a ete mesuree chez six rats avant et apres chemodenervation anatomique. D’eventuelles modifications hemodynamiques dues a l’halothane et /ou a la chemodenervation anatomique pouvant interferer avec les resultats, la pression arterielle systemique et la frequence cardiaque ont ete mesurees chez six rats intacts eveilles, puis anesthesies, et chez les six memes rats chemodenerves, eveilles puis anesthesies. Chez neuf rats intacts et chez 19 rats chemodenerves, le pH arteriel, la concentration arterielle de bicarbonates, et les gaz du sang arteriel (PaO2 et PaCO2) ont ete mesures avant et apres administration d’halothane. La chemodenervation anatomique ne modifia ni l’ED50 inspiree (1,1%), ni la pression arterielle moyenne et la frequence cardiaque. Les effets hemodynamiques de l’halothane furent comparables chez les rats intacts et chez les rats chemodenerves. Les modifications des gaz du sang et de l’equilibre acido-basique provoquees par l’halothane chez les rats intacts, et par la chemodenervation anatomique chez les rats eveilles, ne furent pas significativement differentes: diminution significative de PaO2 et de pHa, augmentation significative de PaCO2 Chez les rats chemodenerves, l’halothane provoqua une diminution supplemental de PaO2 et une augmentation supplementaire de PaCO2. Le fait que l’halothane et que la chemodenervation anatomique modifient de la meme maniere les gaz du sang et l’equilibre acido-basique est en faveur de l’action «chemodenervatrice chimique» de l’halothane. Mais les effets additionnels de l’halothane chez l’animal chemodenerve anatomiquement confirment que les effets de l’halothane sur les gaz du sang et l’equilibre acido-basique resultent de multiples points d’impact sur le systeme respiratoire. Halothane decreases the ventilatory response to hypoxia and the activity of peripheral arterial chemoreceptors, resulting in “chemical chemodenervation.” In order to evaluate the role of this halothane-induced “chemical denervation” in acid-base and arterial blood gas changes, these values were measured in intact and chemodenervated rats, awake and under anaesthesia. Since the depth of anaesthesia could be modified by the anatomical chemodenervation, the ED50 of inspired halothane was determined in six rats before and after anatomical chemodenervation. To prevent haemodynamic changes due to halothane and/ or anatomical chemodenervation from interfering with the results, systemic arterial blood pressure and heart rate were measured in six intact rats, awake and then anaesthetized, and in the same rats after chemodenervation, awake and then anaesthetized. In nine intact rats and in 19 chemodenervated rats, arterial pH, arterial bicarbonate concentration, and arterial blood gases (PaO2 and PaCO2 were measured before and after administration of halothane. Anatomical chemodenervation modified neither the inspired ED50 (1.1%), nor the mean arterial blood pressure or heart rate. The haemodynamic effects of halothane were comparable in intact and in chemodenervated rats. Changes in arterial blood gases and acid-base balance due to halothane in intact rats and due to chemodenervation in awake rats were not different, but there was a decrease in PaO2 and pHa, and an increase in PaCO2. In chemodenervated rats, halothane caused a further decrease in PaO2 and a further increase in PaCO2. The fact that halothane and anatomical chemodenervation have similar effects on arterial blood gases and acid-base balance favours a “chemical chemodenervating” action of halothane. However, the additional effects of halothane in the anatomically chemodenervated animal show that the action of halothane on blood gases and acid-base balance is the result of multiple sites of impact on the respiratory system.