Chemodenervation

Abstract: This article will discuss many of the key concepts regarding chemodenervation and neurolysis in the management of spasticity. Topics that will be discussed include techniques for localization, strengths and limitations of various agents (botulinum toxin, phenol, and alcohol), the value of combination therapies, and the role of nerve blocks (diagnostic and therapeutic). With advancing technology have come newer methods to improve accuracy of localization for the performance of chemodenervation and neurolysis such as electromyographic guidance, electrical stimulation, and ultrasound guidance. During the last 2 decades, the addition of botulinum toxin chemodenervation as an adjunct to traditional neurolysis, medication, and therapy modalities has expanded the field of treatment of intramuscular hyperactivity in upper motor neuron syndrome. The technique of diagnostic blocks as predictors of response and the therapeutic value of nerve blocks will be discussed.

Abstract: SUMMARY Cerebral hemodynamic responses to arterial hypoxia were studied in 13 normal and 9 chemodenervated anesthetized, paralyzed dogs. Arterial O2 content was lowered from control (18.0 vol%) to 14.0, 8.0, and 4.0 vol%, respectively, by either decreasing arterial Po2 (hypoxic hypoxia) or increasing carboxyhemoglobin saturation (CO hypoxia) at normal Po2. Both hypoxic hypoxia and CO hypoxia at each value of the lowered arterial O2 content resulted in progressive significant increases in cerebral blood flow (134, 169, 276, and 146, 206, 244% of control, respectively). Before chemoreceptor denervation, arterial blood pressure increased with hypoxic hypoxia but decreased with CO hypoxia. After chemodenervation, hypoxic hypoxia and CO hypoxia at each value of lowered arterial O2 content resulted in similar significant increases in cerebral blood flow. These increases were not significantly different from those observed prior to chemodenervation. After chemodenervation, hypoxic hypoxia and CO hypoxia both resulted in similar decreases in arterial blood pressure and cerebral vascular resistance, whereas, before chemodenervation, cerebral vascular resistance decreased more with CO hypoxia than with hypoxic hypoxia. These data show that cerebral vasodilation induced by both forms of hypoxia in chemodenervated dogs resembles that in animals with CO hypoxia and intact chemoreceptors in which Pao2 is high and the carotid chemoreceptors may not be activated. We also have shown that the transient responses to both types of hypoxia are not altered by carotid chemodenervation, and conclude that the carotid chemoreceptors do not play a role in the mechanism by which cerebral blood flow increases during decreased blood O2 content. IN THE PAST several years, there has been renewed interest in the possible role of the autonomic nervous system in the regulation of cerebral blood flow. Despite much evidence supporting an autonomic nerve supply to parts of the cerebral vasculature, the functional significance of these nerves remains uncertain. Neural regulatory mechanisms for the cerebral circulation have been assumed to be negligible or nonexistent' because of the failure of autonomic stimulation and denervation to affect cerebral blood flow significantly. The effect of the sympathetic nervous system on cerebral blood flow remains especially controversial. Many investigators have failed to show any significant effects of sympathetic stimulation on cerebral blood flow, 2 " 4 whereas others using similar tech

Abstract: Purpose of reviewTo review current concept in spasmodic dysphonia management.Recent findingsThe standard of care for spasmodic dysphonia in 2004 remains botulinum toxin chemodenervation for symptomatic management. This is supported by a large body of literature attesting to its efficacy in many diff

Abstract: 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.