etal bleeding hemorrhoids and a healing anal fissure measuring 5 ‘wn in length. The right and left colon also were biopsied With resultant normal findings. The patient was preseribed ‘nifedipine 0.1% ointment to be applied topically 1 the snug 3uines day for Sweets Wihin nels hoes zeturmed fo normal, and by 6 weeks, he had discontinued al antiyperensive agents, The subject underwent repeat ene. copy under anesthesia several months later, which demon: strated complete resolution ofthe anal fissure DISCUSSION AD isaserious and sometimes life-threatening syndrome that Cccuits most cominonly in patients with SCL ator above the Jevel of TS. AD is more prevalent and more severe among ~ Patents with complete SCI injuries; however, as preseneed here, AD can significantly affect pauents with incomplete injures, AD isa syndrome caused by a noxious stimulus below the Xevel ofthe spinal cord lesion. The stimulus results in gener, alized sympathetic discharge, leading to vasoconstriction, «specially of the splanchnic vascular bed. This leads to hy” Petterson, the hallmark feature of AD, which can range from tnild to life-threatening increases of systolic pressures. The —eaofGLMocks the inhibitory response from the brainstem athe fevelofte lesion. However, stimulation ofthe baroreceptors in the aona and carotid vessels produces a vagal response resulting In the characteristic bradycardia and vasodioees above the level ofthe injury observed in AD. [e clinical presentation of AD often includes a pounding headache, nausea, malaise, nasal obstruction, and anxiety mon precipitating factors include bladder distension, constipation or fecal impaction, urinary tract infection, kid. ney stones, pressure ulcers, tight clothing, and ingrown ‘ocnails. Less commonly reported preciptantsinchude hy. Perthyrotdism, Charcot arthropathy, and intramuscular inc Jeaton 168], Adgtional gastoimestinal causes include ap. Pandlicis, “cholecystiis, hemorhoids, gastroesophageal reflux disease, and anal fissure (9 Gastrointestinal complications are common in persons with SCL The injury disrupts the interactions between she “Mlopomic and somatic inncrvation ofthe bowel leading te Re development of ‘neurogenic bowel.” characerized by disordered defecation incleding constipation. The incidence oes prevalent in the SC pepution, fete eon ea nc tn EUS jus dl wo the mucoconcous juan ie results in spasm ofthe internal anal sphincter, which inhibies healing by pulling the edges ofthe wound apart Healing can AUTONOMIC DYSREFLEXIA CAUSED BY ANAL Fh bs farther tahibited by continued trauma eaused by the Passage of hard stool. Ana fissures can be notoriously dif {ult to treat, and chronie anal fissures often require sugery for efinkive treatment. Although medical therapy. for chronic anal fssure has been shown to have a cure tate that io only marginally beter than placebo, aggressive medical treat, ment of acute anal fissure can be successful (10 This ase presentation describes a SCI patient with persis: tent AD that resolved after treatment of an anal fissure, As described, the development of an anal fissure was not com. Pletely unexpected in this patient, given his chronic coneti. Pation and previous history of anal fissure, However, the ‘egative anoscopy seemed to eliminate an anal fissure as 4 possible cause ofthe AD. In retrospect, it was theorized that increased rectal tone, common in SCI patients, may have Hidden the fissure within the folds of the rectum. The anes, thesia given with the colonoscopy may have allowed the Tectum to relax sufficiently to allow for visualization of the anal fissure CONCLUSION AD 15 a common condition among persons with SCI at or above the level of T6. This ease presentation describes the valuation of persistent AD andthe eventual successful reso lotion after the diagnosis anh tceutmsent cf an anal fceee Although common causes such as urinary tract infection and constipation account for the majority of episodes of AD, Persistent and recurrent episodes of AD necesita diligent 8nd thorough evaluation to uncover less common etiologies REFERENCES 1. Linden 8 Joiner Freehaer AA etal. Incidence nd nical eturesof ‘tnomic daria in patients with spiel cor ny, Pog 1980;18:285 202, 2 Enchson, RP. Autonomic hyperelewe: Pathophysilogy and mada ‘management rch Phys Med Rehabil 1960;61401.448 ‘3% Bors, E. Challenge of quakipegia some personal observations in = eres of 233 ase, Dull Ls Angeles Neuol Soe 195621.105, 09 Gutman 1, Whiteridge D. Elers ober distnsem on nererraie ‘mechanism afer spinal cord inte, Bain 1947.70-501 408 Lee BY, Kammaker MC, Hen BL, Stull RA. Autonome deeded ‘evs. J Spinal Cord Med 1994:1875-87 © Chang JH. 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