Vol.23 March 2009 BTXA Treatment for Vasomotor Rhinitis Rhinitis is the inflammation of nasal mucosa. Its symptoms include itching, sneezing, congestion and rhinorrhea of nasal system. It constitutes a major worldwide health problem. Vasomotor Rhinitis (VMR) is known as non-allergic and non-infectious rhinitis. It is unrelated to allergy, infection, structural abnormalities and systemic diseases. Patients with VMR always suffer from nasal obstruction and numerous watery nasal discharge. Use of botulinum toxin to treat hypersecretory disorders is increasing in popularity in recent years. In this issue, further information concerning this topic will be introduced to the readers. Introduction Rhinitis is inflammation of nasal mucous membranes, "dry" patients, in which nasal obstruction and airflow characterized by nasal discharge, itching, and resistance exist with minimal rhinorrhea. Triggers of congestion. It vasomotor rhinitis symptoms vary among patients. infectious, occupational can be classified into idiopathic rhinitis. It allergic, rhinitis, nares, and Odors or irritants in air, changes in weather, always coexists with medications, foods and chronic health conditions are respiratory disorders such as asthma and greatly some possible factors. impacts life quality of patients. It may contribute to Cause sinus problem, ear problem, sleep problem and Exact pathogenesis of VMR is not fully known. It is learning problem. thought to be the result of autonomic imbalance with Vasomotor Rhinitis (VMR), almost 50% of chronic a relative dominance of the parasympathetic nervous rhinitis, is non-allergic rhinitis. Possible reasons are system in the nasal mucosa. Emotional disturbance, thought to be allergy, infection, structural lesions, hormones, physical agents, and trauma are some possible factors. systemic disease and drug abuse. Its symptoms include nasal blockage to rhinorrhea; sneezing. The nasal airway is under the control of the autonomic nervous system. Sympathetic nervous system decreases nasal airway resistance; parasympathic system produces nasal discharge. Patients with vasomotor rhinitis are divided into two subgroups: "runners", who have "wet" rhinorrhea; and 1 ICBA Newsletter Vol. 23 Some studies showed that VMR is caused by an Botulinum Toxin Type A Treatment autonomic nervous system dysfunction (relative Botulinum Toxin Type A selectively inactivates parasympathetic of peripheral cholinergic nerve terminals by blocking the Parasympathetic release of acetylcholine. Its most important effect is hyperactivity in the nasal cavity causes clear nasal at the neuromuscular junction where it causes discharge from submucosal glands; on the other hand, temporary and reversible weakness and atrophy of sympathetic hypoactivity can give rise to nasal striated muscle. Botulinum Toxin Type A also blockage. Therapeutic efforts to decrease rhinorrhea provokes in human beings have attempted to either cut the sympathetic and parasympathetic ganglion cells and parasympathetic vidian postganglionic parasympathetic neurons. It exerts neurectomy or chemically block the receptors with action at the molecular level by selectively cleaving the short-acting, topical ipratropium. the sympathic hyperactivity) as hypoactivity. nerve supply a result through medical decongestants, treatment nasal of VMR ipratropium bromide, blocking (synaptosomal-associated on regulated exocytosis, the release of synaptic and vesicles in response to electrical depolarization. Blocking the release of acetylcholine from the potential side effects. Nasal steroids may be cholinergic nerve terminal in the nasal mucosa or appropriate treatment option, but the efficacy of preganglionic these drugs has been inconsistent. Surgical treatment short-term effect and cholinergic nerve endings in sphenopalatine ganglion are the two suggested such as concha resections, vidian nerve section has SNAP-25 by BTX-A damages SNAP-25, the most obvious effect is including antihistamines needs long time usage and has some generally protein dysfunction protein with a molecular weight of 25 kD). When the Current treatment The autonomic mechanisms of BTX-A action in the nasal cavity. some Rohrbach complications. and colleagues demonstrated a degeneration of nasal glands and ducts in addition to Exercise may be a useful treatment addition because diffuse glandular apoptosis in guinea pigs after nasal it produces decreased airway resistance and assists application of 20U BTX-A. They also observed the natural nasal decongestion by I-adrenergic-mediated absence of necrosis or inflammation after application mechanisms. However, the effect of exercise on nasal of BTX-A. decongestion is rather short-lived. The cost-effectiveness is an important issue in the Traditional oral antihistamines have no established management of chronic diseases such as vasomotor beneficial effect in patients with vasomotor rhinitis rhinitis. With the high price of the treatment of VMR and may be associated with sedation. Newer, with nasal steroids or oral antihistamines, intranasal less-sedating antihistamines also have no proven injection of BTX-A is a highly effective, safe, and effectiveness for vasomotor rhinitis, and their simple administration delays proper treatment and incurs long-lasting effect for patients with VMR. Botulinum significant cost and burden to the health care system. Toxin Type A provides good alternative for the symptomatic treatment option with a treatment of resistant VMR cases. 2 ICBA Newsletter Vol. 23 The Effect of Botulinum Toxin Type A on Vasomotor Rhinitis and Frey’s Syndrome and Morphological Study Wang Jinling, Chen Fuquan, Zhang Xu, Liu Shunli1, Wang Yinchun2 (1Department of Otolaryngology, Xijing Hospital, Fourth Military Medical University, Xi’ an 710032; 2Lanzhou Institute of Biological Prodcuts) Abstract Objective: To investigate the effect and mechanisms of botulinum toxin type A (BTXA) on vasomotor rhinitis and Frey’s syndrome. Method: A retrospective study of 82 patients with vasomotor rhinitis who received BTXA injection at 4 points in bilateral nasal cavities with 2.5U each point had been done. The state of rhinorrhea, nasal obstruction, sneeze and nasal mucosa edema of each patient were recorded and scored before and after the application of BTXA respectively. 1 patient of gustatory sweating who had done operation for hemifacial spasm underwent Minor’s starch iodine test before and after treatment with intracutaneous injections of botulinum toxin A. 48 guinea pigs were randomly divided respectively into 3 groups: BTXA group and control group. Merocel sponge soaked with 10U (0.2ml) BTXA was put into left nasal cavity for one hour in BTXA group. Saline replaced BTXA in control group. The inferior turbinate mucosa of guinea pigs was harvested under general anesthesia at 1, 2 and 4 weeks after BTXA treatment. The first group was observed with HE staining and electron microscope. The tissues of the second group were fixed in 4% paraformaldehyde and paraffin embedded. The concentration of acteylcholinesterase was determined with immunohistochemistry staining. Apoptosis was detected with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) staining and the types of gland cells were determined with AB-PAS staining in the third group. Result: Rhinorrhea improved significantly in all 82 patients while sneeze, nasal obstruction and mucosa edema reduced partly. The reducing of rhinorrhea lasted averagely 10 weeks. Patients had an episode of nasal dryness or increased rhinorrhea at the day of injection. No other complications were found. 1 patient of Frey’s syndrome did not experience any gustatory sweating at follow-up. The only side effect was a transitory affection of the lower orbicularis oris muscle. 1 and 2 weeks after local BTXA application in nasal mucosa of guinea pigs, the degenerations of glandular epithelium and canal epithelium were observed. Most of the glandular cells showed normal at 4 weeks after BTXA treatment. 1 and 2 weeks after local BTXA application, the expression of acteylcholinesterase in nasal glandular and canal cells decreased significantly (P<0.01). It became normal at 4 weeks after BTXA treatment. 1 and 2 weeks after local BTXA application, apoptosis of glandular and canal cells in nasal mucosa of guinea pigs increased significantly (P<0.01). The apoptosis index became normal at 4 weeks after BTXA treatment. Apoptosis mainly occurred in serous gland. 3 ICBA Newsletter Vol. 23 Conclusion: BTXA can induce the degeneration of glandular cells in nasal mucosa of guinea pig, and induce apoptosis in nasal serous glands, decrease the concentration of acetylcholinesterase in nasal glands. BTXA can obviously relieve rhinorrhea of patients with vasomotor rhinitis, and disappearance of gustatory sweating with Frey’s syndrome that was effective, simple and minimally invasive method of treatment. References 1. Tae YY, Yoon GJ, Young HK, Tae YJ. A comparison of the effects of botulinum toxin A and steroid injection on nasal allergy. Otolaryngology-Head and Neck Surgery 2008; 139:367-71. 2. Cengiz O, Yusuf V, Okan D, Kemal G. The effect of intranasal injection of botulinum toxin A on the symptoms of vasomotor rhinitis. American Journal of Otolaryngology-Head and Neck Medicine and Surgery 2006; 27:314-8. For further information, please feel free to contact us by the following means: International C-BTXA Association (ICBA) Room 1312, New East Ocean Centre, 9 Science Museum Road, Tsim Sha Tsui East, Kowloon, HK +852 2771 6622 +852 2782 5249 hughs@hughsource.com 4 ICBA Newsletter Vol. 23