Bilateral recurrent laryngeal neurectomyas a model for the study of idiopathic

canine laryngeal paralysisCathy L. Greenfield, Joel C. Alsup, Laura L. Hungerford, Brendan C. McKiernan

Abstract - The purposes of this study were to develop an experimental model of canine laryngealparalysis that mimicked the naturally occurring disease and to document the upper airway changesproduced, both clinically and with pulmonary function testing. Ten dogs had bilateral recurrent laryn-geal neurectomy performed and were recovered from anesthesia. Tidal breathing flow-volume loopanalysis and upper airway resistance measurements were taken before and after the development ofclinical laryngeal paralysis while dogs breathed room air and after the individual administration of2 respiratory stimulants. Clinical signs of laryngeal paralysis developed 38 days (median) follow-ing denervation. Although some variations were present, tidal breathing flow-volume loop analy-ses on room air, following denervation, were similar to those reported in naturally occurringcases. Upper airway resistance increased following denervation and was significantly increased withboth respiratory stimulants. We concluded that bilateral recurrent laryngeal neurectomy resulted inclinical signs and respiratory changes similar to those of idiopathic canine laryngeal paralysis.

Resume - Nevrectomie bilaterale du larynge recurrent comme modele pour 1'etude de laparalysie laryngee idiopathique du chien. L'objetif de cette etude consistait a developper un modeleexperimental de paralysie laryngee chez le chien qui ressemblerait 'a la veritable maladie et anoter les changements qui surviendraient dans les voies respiratoires superieures, a la fois d'une faconclinique et par mesure des fonctions pulmonaires. Dix chiens ont subi une nevrectomie bilaterale dularynge recurrent puis se sont remis de leurs anesthesies. Le volume courant mesure par la courtedebit-volume et la mesure de la resistance des voies respiratoires superieures ont ete determines avantet apres l'apparition des signes cliniques de la paralysie laryngee alors que les chiens respiraient l'airambiant et apres l'administration de 2 stimulants respiratoires administres separement.

Les signes cliniques de paralysie laryngee se sont developpes 38 jours (mediane) apres la dener-vation. Bien que quelques variations aient ete observees, le volume courant mesure a l'air ambiantpar la courbe debit-volume apres denervation etait semblable a celui rapporte dans les cas de maladieveritable. La resistance des voies respiratoires superieures a augmente a la suite de la denervation etetait significativement augmentee avec chacun des 2 stimulants respiratoires. Nous avons conclu quela nevrectomie bilaterale du larynge recurrent entrainait des signes cliniques et des modifications res-piratoires semblables a celles rencontrees dans la paralysie laryngee idiopathique du chien.

(Traduit par docteur Andre Blouin)Can Vet J 1997; 38: 163-167

Introductionaryngeal paralysis (LP) is a common upper airwayobstructive disorder of the dog. The cricoarytenoideus

dorsalis muscle is the only intrinsic abductor muscle ofthe larynx. When the dorsal cricoarytenoid muscle failsto contract during inspiration, the arytenoid cartilages andvocal folds remain in a paramedian position, blocking theopening of the rima glottidis and physically obstructingthe passage of air (1-3). In the dog, clinical signs of LPare usually seen when the larynx is bilaterally affected;unilateral LP rarely results in clinical signs in the rest-ing animal (1-3).

Department of Veterinary Clinical Medicine, The Universityof Illinois, College of Veterinary Medicine, 1008 WestHazelwood Drive, Urbana, Illinois 61802 USA.This project was supported by a Biomedical Research SupportGrant (College of Veterinary Medicine, University of Illinois)and Hill's Companion Animal Research Funds (College ofVeterinary Medicine, University of Illinois).

Laryngeal paralysis is frequently diagnosed after anepisode of acute dyspnea and respiratory distress, oftenprecipitated by a sudden period of stress, exertion, orexercise. However, this disease may also have aninsidious onset with a slowly progressive clinical course.There may be a period of months to years between thefirst recognizable signs of laryngeal paralysis (hoarsebark and/or stridor during heavy exercise) and the sud-den onset of dyspnea (1-3). It is not currently known ifthe slow development of clinical signs is due to pro-gressive neurologic changes to the recurrent laryngealnerves, progressive changes in the larynx after thedevelopment of laryngeal denervation, or both factors.

Laryngeal paralysis has been created experimentallyby many methods for studying the disease and correctivesurgical procedures (4-18). Methods of creating LPhave included crushing the recurrent laryngeal nerve(4-6), transecting the recurrent laryngeal nerve (7-11),resecting the recurrent laryngeal nerve (12-17), vagusnerve resection (18), and permanently ligating the

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recurrent laryngeal nerve (4). Previous investigatorshave documented LP by noting the lack of abduction ofthe arytenoid cartilages and vocal folds during inspira-tion while the animal was still partially anesthetized. Inthese studies, the investigators did not allow animals withbilaterally induced LP to recover from anesthesia.Documentation of clinical disease of similar severityto that seen in naturally occurring cases of canine LP, hasnot been performed prior to treatment in any prior bilat-eral LP model. Consequently, conclusions drawn fromLP studies using previously reported methods for creatingLP may not be directly applicable to naturally occurringcases of canine LP.The objectives of this study were 1) to develop an

experimental model of bilateral LP that would mimic thenaturally occurring condition in the dog; 2) to documentthe development of clinical signs of LP following bilat-eral recurrent laryngeal neurectomy (BRLN); and 3) toobjectively assess upper airway function (on room air andafter respiratory stimulation), by the use of tidal breath-ing flow-volume loop (TBFVL) analysis and upper air-way resistance (Ruaw) measurement, in dogs before andafter the development of BRLN-induced clinical LP. Thismodel was developed in anticipation of studying varioussurgical procedures used to treat canine LP.

Materials and methodsThe number of animals and all procedures used in thisstudy were approved by the Laboratory Animal CareCommittee of the University of Illinois prior to con-ducting the study. Guidelines for approval were based onthe Animal Welfare Act and the National Institutes ofHealth "Guide for the Care and Use of LaboratoryAnimals."

Presurgical evaluationTen, adult male, healthy mixed-breed dogs weighing22.6 ± 3.9 kg (mean ± SD) were used in this study.Presurgical evaluation consisted of physical examination,laboratory evaluation (including packed cell volume, totalsolids measurement, and blood urea nitrogen (AzostickReagent Strips for Whole Blood, Urea Nitrogen, MilesDiagnostics Division, Elkhart, Indiana, USA), heart-worm testing (Difil-Test, EVSCO Pharmaceuticals,Immunogenetics, Buena, New Jersey, USA), fecalexamination, and thoracic radiography. In addition,TBFVL analysis and Ruaw measurement were obtained,as previously described (19-21). All preoperative testswere performed with the dogs awake and unsedated.Dogs with intestinal parasites were treated with appro-priate anthelmintic agents. Dogs that had any otherabnormalities were excluded from the study.

Tidal breathing flow-volume loops (19,20) and Ruawmeasurements (21) were obtained under 3 separate con-ditions. Initially, these tests were run with dogs breath-ing room air, followed by the separate administration of2 respiratory stimulants. A 10% CO2 mixture, contain-ing IO% C02, 21% 02' and 69% N2, was the 1st respi-ratory stimulant administered. For CO2 administration,dogs breathed through a tight fitting face mask (Narkovetlarge clear mask, Bell Medical, St. Louis, Missouri,USA), which was attached to a Hans Rudolph series 1500

nonrebreathing valve (Hans Rudolph, Kansas City,Missouri, USA) and a 5 L reservoir bag. Each dog wasallowed to breathe the CO2 mixture for approximately2 min before either the TBFVL or Ruaw measurementswere obtained. The 2nd respiratory stimulant, doxapramhydrochloride (Dopram-V, Fort Dodge Laboratories,Fort Dodge, Iowa, USA), was administered, IV, to eachdog, at a dose of 2.2 mg/kg body weight (BW) while thedog breathed room air.

Surgical techniqueAfter completion of the presurgical evaluation, eachdog was lightly anesthetized with thiamylal sodium(Bio-tal, Boehringer Ingelheim Animal Health, St. Joseph,Missouri, USA), in multiple fractional doses of 1-2 mg/kgBW, IV, as needed, for laryngoscopic examination oflaryngeal anatomy and function. Fractional doses weregiven to ensure a light plane of anesthesia and avoiddepressing laryngeal function. Only dogs with grosslynormal laryngeal anatomy and intrinsic laryngeal func-tion were included in the study. Following laryngoscopy,additional thiamylal sodium was administered (8-16 mg/kgBW, IV, to effect) and an endotracheal tube was placed.Anesthesia was maintained with halothane and oxygen.The ventral cervical region from the middle of themandible to the manubrium of the sternum in eachdog was prepared for aseptic surgery, using standardprocedures.The recurrent laryngeal nerves were exposed through

a midventral cervical incision. A 2 cm section of eachrecurrent laryngeal nerve was resected from the mid-cervical region. The resected ends of each nerve werefolded back on the remainder of the nerve and tied inplace with 4-0 polyglyconate (Maxon, Davis & GeckMonofil, Manati, Puerto Rico) suture material. Removedsections of the nerves were placed in formaldehyde forhistological examination. The sternothyroideus andsternohyoideus muscles were reapposed using a simplecontinuous pattern with 3-0 polyglyconate. The sub-cuticular tissue was closed with a continuous horizontalpattern using 3-0 polyglyconate, and the skin was reap-posed with a simple interrupted pattern of 3-0 mono-filament nylon (Ethilon, Ethicon, Somerville, New Jersey,USA) suture material. Denervation (lack of arytenoidabduction during inspiration) was confirmed postopera-tively while each dog was still lightly anesthetized andrecovering from the general anesthesia. Followingrecovery from anesthesia, each dog was housed in a1.8 m by 3.6 m run for the remainder of the study.

Postsurgical examinationDogs were examined daily for the presence of respira-tory abnormalities including, but not limited to, stridor,dyspnea, and cyanosis. Dogs were evaluated both atrest in their runs and during mild (walking 30-60 m) tomoderate (jogging 30-60 m) exercise. Once clinicalabnormalities consistent with LP had developed,TBFVL analysis and Ruaw measurements were repeatedwhile the dog was awake, as previously described.Following completion of these tests, each dog waslightly anesthetized with thiamylal sodium for laryn-geal examination to confirm the diagnosis of LP andthe lack of any anatomical abnormalities (such as

164 Can Vet J Volume 38, March 1997

Table 1. Mean baseline and postdenervation tidal breathing flow-volume loop values in10 dogs with experimentally induced bilateral laryngeal paralysis breathing room air, carbondioxide, or following administration of doxapramhydrochlorideVariable BLra PDra BLC02 PDC02 BLdp PDddpTE/TI 1.2 ± 0.2 0.99 ± 0.2a 1.0 ± 0.2 0.91 ± 0.2a 1.0 ± 0.1 0.82 ± 0.3aPEF (mL/s) 502 ± 113 529 ± 154 894 ± 199 719 ± 262a 897 ± 214 800 ± 154aPIF (mL/s) 545 ± 117 486 ± 120 847 ± 157 656 ± 240 861 ± 194 679 ± 136PEF/PIF 0.93 ± 0.1 1.1 ± 0.3a 1.1 ± 0.2 1.1 ± 0.3 1.1 ± 0.2 1.2 ± 0.2aIF50 (mL/s) 490 ± 114 426 ± 126 795 ± 158 SS5 ± 271a 779 ± 204 548 ± 144aEF25(mL/s) 340±74 433± 129a 717± 183 627±242 740±207 703± 165EF50(mL/s) 394± 104 455 ± 139 778 ± 194 637 ± 259 786± 195 702 ± 150PEF/EF50 1.3 ± 0.1 1.2 ± O. la 1.2 ± 0.1 1.2 ± 0.1 1.2 ± 0.2 1.2 ± 0.1PEF/EF25 1.5 ± 0.3 1.2 ± 0.2a 1.3 ± 0.3 1.2 ± 0.1 1.2 ± 0.2 1.1 ± 0.1EF5,EF25 1.2±0.3 1.1 ±0.1 1.1±0.0 1.0±0.1 1.1 ±0.2 1.0±0.2aPIF/IF25 1.3 ± 0.1 1.2 ± O.la 1.2 ± 0.1 1.1 + 0.1 1.2 ± 0.1 1.1 ± 0.1IF5dIF25 1.2 ± 0.1 1.0 ± O.la 1.2 ± 0.1 0.98 ± 0.2a 1.2 ± 0.1 0.92 ± 0.laaSignificant difference from baseline value of same parameter following same treatmentData are expressed as the mean ± standard deviationBL = baseline values; PD = postdenervation values; ra = room air; CO2 = 10% carbon dioxide mixture; dp = doxapram hydrochlorideTE= expiratory time, T, = inspiratory time, PEF = peak expiratory flow, PIF = peak inspiratory flow, IF50 = midtidal inspiratory flow,EF50 = midtidal expiratory flow, EF25 = expiratory flow at end expiration plus 25% of tidal volume, IF25 = inspiratory flow at endexpiration plus 25% of tidal volume

granulomas or laryngeal collapse that could cause airwayobstruction).

Data collection and statistical analysisThe number of days it took for clinical signs of laryngealparalysis to develop was recorded for each dog. Themedian, mean, standard deviation, and range of days todevelopment of clinical LP were calculated for the10 dogs.Twelve parameters routinely obtained during TBFVL

analysis were chosen for evaluation. We selected thoseparameters, based on our clinical experience and onchanges previously documented in clinical cases ofcanine LP (20), so that we could evaluate variablesused to assess loop shape and alterations in respira-tion. Tidal breathing flow-volume loops were exam-ined graphically, and 6 representative loops were selectedfrom each treatment for each dog, as previously described(19). A minimum of 6 representative values were alsoused in calculating the Ruaw measurements, as previouslydescribed (21). The mean value for each respiratoryvariable (TBFVL and Ruaw) was calculated presurgicallyand postdenervation (following BRLN and develop-ment of clinical signs of LP). Postdenervation TBFVLand Ruaw values were compared with the presurgicalTBFVL and Ruaw values in dogs breathing room air,breathing CO2, and after the administration of doxapramhydrochloride. Changes in respiratory measures betweenthese 2 times were analyzed for the data collected whiledogs breathed room air, while dogs breathed CO2, andafter the administration of doxapram hydrochlorideusing the Wilcoxon signed rank test (data were notnormally distributed) with a P value of < 0.05 being con-sidered significant (22).

ResultsPreoperative physical examination, laboratory evalua-tion, and thoracic radiographs were within normal lim-its for all dogs in the study. All dogs were negativefor heartworm microfilaria. Eight of the 10 dogs hadintestinal parasites (hookworms, roundworms, whip-

worms, or a combination of these) and all were treatedwith an appropriate anthelmintic agent prior to thebeginning of the study.On gross laryngeal examination, all dogs had normal

laryngeal anatomy and function prior to BRLN. BaselineTBFVL values were within the reported reference rangefor awake, untrained dogs, breathing room air (Table 1)(19). The mean ± SD baseline Ruaw values for the 10 dogswere 8.4 ± 2.1 cm H2O/L/s on room air, 8.1 ± 1.0 cmH2O/L/s on CO2, and 7.9 ± 1.2 cm H20/L/s after admin-istration of doxapram hydrochloride. Baseline roomair Ruaw measurements were also within the normalreference range for dogs (21).No dog had any respiratory problems in the immedi-

ate postoperative recovery period. When clinical signsof LP did develop, the onset of signs was slow andprogressive. Clinical signs of LP (including stridor,dyspnea, and some exercise intolerance) developed38 d (median) following BRLN, with a mean and stan-dard deviation of 56 ± 50 d, and a range of 7 to 140 d.Mild respiratory stridor was noted in most dogs whenthey were excited (jumping, barking, and running) intheir runs. Clinical signs of dyspnea, difficulty breath-ing, or exercise intolerance were only noted with mild(walking 30-60 m) to moderate (jogging 30-60 m)exercise. Laryngeal paralysis was confirmed in all dogsby laryngoscopic examination. No other anatomicalabnormalities of the larynx, such as, laryngeal granu-lomas or collapse, which could have accounted for theclinical signs, were noted in any dog. Histologicalexamination of all of the sections of the recurrent laryn-geal nerves removed during BRLN revealed normalnerve tissue.

Following the development of clinical signs of LP, thedogs in this study developed TBFVL loop shapes con-sistent with those previously reported in canine LP(20). Significant changes were present in 7 of the 12selected TBFVL variables while the dogs were breath-ing room air (Table 1). Significant increases were seenpostdenervation in peak expiratory flow/peak inspiratoryflow (PEF/PIF) and expiratory flow at end expiration plus25% of tidal volume (EF25), while significant decreases

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occurred in expiratory time/inspiratory time (TE/TI),peak expiratory flow/midtidal expiratory flow (PEF/EF50), peak expiratory flow/expiratory flow at endexpiration plus 25% of tidal volume (PEF/EF25), peakinspiratory flow/inspiratory flow at end expiration plus25% of tidal volume (PIF/IF25), and midtidal inspiratoryflow/inspiratory flow at end expiration plus 25% oftidal volume (IF50/IF25). The changes in the TBFVL vari-ables following the administration of CO2 or doxapramhydrochloride were more pronounced than those seen onroom air (Table 1). The direction of change (increase ordecrease) between the presurgical and postdenervationevaluations in most of the TBFVL variables was the sameafter respiratory stimulation as it was on room air(Table 1). Significant changes seen at the postdenerva-tion evaluation and following the administration of therespiratory stimulants included decreases in TE/T1,peak expiratory flow (PEF), midtidal inspiratory flow(IF50) and IF50/IF25 with CO2 or doxapram hydrochlo-ride stimulation, and an increase in PEF/PIF and adecrease in midtidal expiratory flow/expiratory flowat end expiration plus 25% of tidal volume (EF50/EF25)after the administration of doxapram hydrochloride,but not with CO2.

At the postdenervation evaluation, the mean ± SD Ruawvalues were 10.7 ± 5.4 cm H2O/L/s on room air, 15.3 ±7.7 cm H20/L/s after breathing CO2, and 17.3 ± 9.5 cmH2O/L/s after administration of doxapram hydrochloride.These values were all increased when compared with thebaseline Ruaw values, but were significantly different onlyafter administration of the 2 respiratory stimulants.

DiscussionIt is difficult to explain the large variation in time it tookfor the development of clinical signs of LP and why acuterespiratory distress did not occur immediately followingBRLN, although clinical signs frequently develop slowlyand progressively in dogs with naturally occurring idio-pathic LP (1-3). Many dogs with idiopathic LP havesome clinical signs, such as, voice changes and minorstridorous breathing, for weeks to months prior to devel-oping respiratory distress (1-3). Severe respiratory dis-tress and cyanosis develop later in the disease and areoften precipitated by situations, such as, hot weather,heavy exercise, or stress, where greater than normalair movement through the upper respiratory system isrequired (1-3). The use of BRLN to experimentallyinduce LP in dogs resulted in a similar clinical course tomany of the naturally occurring cases of LP.The most common cause of naturally occurring LP in

the dog is loss of normal neurologic function of therecurrent laryngeal nerves (23). It is not known whetherthe slow onset of clinical signs in the typical naturallyoccurring case is due to progressive neurologic changesin the recurrent laryngeal nerves, progressive changes inthe larynx following loss of laryngeal innervation, or acombination of both factors. It has been suggested thatthe condition usually arises from a progressive loss ofinnervation to the intrinsic laryngeal muscles, and thatthe clinical signs worsen as denervation becomes morecomplete (23). The fact that no dog in this study devel-oped clinical signs of LP immediately following acute

denervation of the larynx supports the theory that sec-ondary laryngeal changes likely occur before clinicalsigns are recognized, at least in this model of LP. Theincreased resistance to air flow across the narrowedrima glottidis in dogs with LP often results in the devel-opment of laryngeal edema and may also cause weak-ening of laryngeal cartilages. Some dogs with natu-rally occurring LP, as well as other obstructive upperairway disorders, do develop laryngeal collapse as an endstage change (1-3). However, neither laryngeal edemanor collapse were visible at the time of development ofclinical signs of LP in any of the dogs in this study. Therole that atrophy of the intrinsic laryngeal musclesplays in the development of clinical signs of LP is alsounknown. Consequently, although an exact explana-tion for the delayed onset of clinical signs was notfound, the delayed onset is similar to that seen in manycases of naturally occurring LP.

Airway changes and clinical signs of laryngeal hemi-plegia are often not apparent in horses unless the animalis exercising (10,24,25). In humans with early respira-tory disease, such as, laryngeal hemiplegia or LP, clin-ical signs and abnormalities in pulmonary functiontests also may not be detected unless the patient ismaximally inspiring or exercising (26). Similarly, dogswith naturally occurring LP often do not show abnor-malities in pulmonary function tests when they are at restand breathing room air. Since dogs cannot be made tobreathe maximally on command and some dogs with LPcannot tolerate exercise, we elected to evaluate CO2and doxapram hydrochloride as respiratory stimulants inan attempt to drive the respiratory system and, thereby,determine if there were significant changes comparedwith breathing room air. All dogs tolerated both stimu-lants well and breathed with visibly greater effort fol-lowing the administration of the stimulant. Subjectively,the greatest changes in respiratory effort were seenafter doxapram hydrochloride, especially in those dogsthat had more marked clinical signs of LP after BRLN.

Tidal breathing flow-volume loop analysis has beenused previously to help in evaluating canine LP patients(20). Although 3 types of loop shape have been describedin naturally occurring LP patients (20), no attempt wasmade to classify the type of loops seen in this study,because of the small number of animals involved andbecause we used TBFVL analysis to help us objec-tively confirm that the respiratory changes present afterBRLN were similar to those previously reported in nat-urally occurring cases of canine LP, not for the purposeof studying the types of loop shapes produced by BRLN.For most of the TBFVL variables, the changes thatoccurred between the presurgical and postdenervationevaluations in the dogs breathing room air were thesame as those previously reported in many of thenaturally occurring cases of LP that have been evalu-ated with TBFV loops (20). All variables that changedsignificantly changed in the same direction as reportedin dogs with naturally occurring LP (20). Interestingly,some of the inspiratory variables, including PIF andIF50, that would be expected to decrease in a predomi-nantly inspiratory type of obstruction, such as LP, didnot change significantly in either of our study dogsbreathing room air or reported clinical cases of LP

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(20). However, in our study, both PIF and IF50 decreasedin room air evaluations following denervation, whereasin naturally occurring cases of LP, these variables eitherdid not change or increased only slightly (but not sig-nificantly) from values reported in normal dogs (19,20).Additionally, IF50 significantly decreased in our studydogs when respiration was stimulated with either CO2or doxapram hydrochloride.

With the exception of PEF, EF25, and EF50, all TBFVLvariable changes following denervation and the admin-istration of either respiratory stimulant were in the samedirection as those seen in dogs breathing room air. Thesedifferences between the stimulated and unstimulatedcondition may be explained by the fact that tidal volumedecreased following the development of clinical LP andrespiratory stimulation. With a smaller tidal volume, thelungs do not expand as much and the elastic recoil is less,resulting in lower flow values during the expiratoryphase of respiration (27). There was also a significantdecrease in IF50 following respiratory stimulation, but notwhen dogs were breathing room air. This change reflectedthe limitation to inspiratory flow that occurs in an inspi-ratory obstructive disorder, such as LP, and becamemore pronounced when the dogs breathed following res-piratory stimulation. Although PIF was decreased afterrespiratory stimulation, the changes were not signifi-cantly different because of the large standard deviations.

Measurement of upper airway resistance in the dog hasrecently been described (21). Change in resistance canbe a sensitive indicator of airway obstruction (10,21).Upper airway resistance has been reported to be elevatedin horses with laryngeal hemiplegia, when they areexercised (10). In dogs breathing room air, Ruaw wasincreased following BRLN, but the change was notsignificant. Dogs showing clinical signs of LP inducedby BRLN had significant increases in Ruaw following res-piratory stimulation with either CO2 or doxapramhydrochloride. An increase in Ruaw was expected in anobstructive inspiratory disorder, such as LP, and docu-ments the obstruction produced by BRLN. The necessityto stimulate the respiratory system before the increase inresistance is significant is consistent with that reportedin other species (10,24-26).

Bilateral recurrent laryngeal neurectomy in dogs is asurgical procedure that can be used experimentally to pro-duce a clinical syndrome that closely resembles naturallyoccurring canine LP. This model is associated withminimal adverse effects to the experimental animals.However, dogs with BRLN should be closely moni-tored for any signs of respiratory distress during the post-operative period. Bilateral recurrent laryngeal neurec-tomy, as described in this study, differs from othermodels previously described because it creates bilateralLP, as is typical of most naturally occurring cases ofcanine LP, and because the animals are allowed torecover from BRLN and develop the clinical signs thatare seen in naturally occurring cases of LP, rather thanhaving immediate surgical correction. The objectivemeasurements obtained from TBFVL analysis and Ruawmeasurement, although quite variable, helped todemonstrate that BRLN produces airway changes that aresimilar to those that occur in naturally occurring canineLP. The use of the BRLN in future studies should allow

objective assessment of the effectiveness of specificsurgical procedures used in the treatment of cases ofnaturally occurring canine LP. cvi

References1. Greenfield CL. Canine laryngeal paralysis. Comp Contin Educ

Pract Vet 1987; 9: 1011-1020.2. Gaber CE, Amis TC, LeCouteur RA. Laryngeal paralysis in dogs:A review of 23 cases. J Am Vet Med Assoc 1985; 186: 377-380.

3. Wykes PM. Canine laryngeal diseases, Part I. Anatomy and dis-ease syndromes. Comp Contin Educ Pract Vet 1983; 5: 8-13.

4. Siribodhi C, Sundmaker W, Atkins JP, et al. Electromyographicstudies of laryngeal paralysis and regeneration of laryngeal motornerves in dogs. Laryngoscope 1963; 73: 148-164.

5. Boles R, Fritzell B. Injury and repair of the recurrent laryngealnerves in dogs. Laryngoscope 1969; 79: 1405-1418.

6. Duncan ID, Baker GJ. Experimental crush of the equine recurrentlaryngeal nerve: A study of normal and aberrant reinnervation.Am J Vet Res 1987; 48: 431-438.

7. Tucker HM, Ogura JH. Vocal cord remobilization in the canine lar-ynx: An histologic evaluation. Laryngoscope 1971; 81: 1602-1606.

8. Iwamura S. Functioning remobilization of the paralyzed vocal cordin dogs. Arch Otolaryngol 1974; 100: 122-129.

9. Sato F, Ogura JH. Reconstruction of laryngeal function for recur-rent laryngeal nerve paralysis: Historical view, advancement oflatest investigations, and a preliminary experiment. Laryngoscope1978; 88: 689-696.

10. Derksen FJ, Stick JA, Scott EA, et al. Effect of laryngeal hemi-plegia and laryngoplasty on airway flow mechanics in exercisinghorses. Am J Vet Res 1986; 47: 16-20.

11. Shappell KK, Derksen FJ, Stick JA, et al. Effects of ventriculec-tomy, prosthetic laryngoplasty, and exercise on upper airwayfunction in horses with induced left laryngeal hemiplegia. Am J VetRes 1988; 49: 1760-1765.

12. Hengerer AS, Tucker HM. Restoration of abduction in the para-lyzed canine vocal cord. Arch Otolaryngol 1973; 97: 247-250.

13. Lyons RM, Tucker HM. Delayed restoration of abduction in theparalyzed canine larynx. Arch Otolaryngol 1974; 100: 176-179.

14. Venker-van Haagen, Hartman W, Goedegebuure A, et al. Thesource of normal motor unit potentials in supposedly denervatedlaryngeal muscles of dogs. Zentralbl Veterinarmed A 1978; 25:751-761.

15. Greenfield CL, Walshaw R, Kumar K, et al. Neuromuscularpedicle graft for restoration of arytenoid abductor function indogs with experimentally induced laryngeal hemiplegia. Am J VetRes 1988; 49: 1360-1366.

16. Fex S. Functioning remobilization of vocal cords in cats with per-manent recurrent laryngeal nerve paresis. Acta Otolaryngol(Stockh) 1970; 69: 294-301.

17. Ducharme NG, Homey FD, Partlow GD, et al. Attempts to restoreabduction of paralyzed equine arytenoid cartilage I. Nerve-musclepedicle transplants. Can J Vet Res 1989; 53: 202-209.

18. Taggart JP. Laryngeal reinnervation by phrenic nerve implantationin dogs. Laryngoscope 1971; 81: 1330-1336.

19. Amis TC, Kurpershoek C. Tidal breathing flow-volume loopanalysis for clinical assessment of airway obstruction in consciousdogs. Am J Vet Res 1986; 47: 1002-1006.

20. Amis TC, Smith MM, Gaber CE, et al. Upper airway obstructionin canine laryngeal paralysis. Am J Vet Res 1986; 47: 1007-1010.

21. Rozanski EA, Greenfield CL, Alsup JC, et al. Measurement ofupper airway resistance in the awake untrained dog. Am J Vet Res1994; 55: 1055-1059.

22. Zar JH. Biostatistical Analysis, 2nd ed. Englewood Cliffs,New Jersey: Prentice-Hall, 1984: 153-156.

23. Venker-van Haagen AJ. Diseases of the larynx. Vet Clin North AmSmall Anim Pract 1992; 22: 1155-1172.

24. Robinson NE, Sorenson PR. Pathophysiology of airway obstruc-tion in horses: A review. J Am Vet Med Assoc 1978; 172: 299-303.

25. Robinson NE, Sorenson PR, Goble DO. Patterns of airflow in nor-mal horses and horses with respiratory disease. Proc Annu MeetAm Assoc Equine Pract 1975; 21: 11-21.

26. West JB. Respiratory Physiology -The Essentials, 4th ed.Baltimore, Maryland: Williams & Wilkins, 1990: 147-161.

27. West JB. Respiratory Physiology -The Essentials, 4th ed.Baltimore, Maryland: Williams and Wilkins, 1990: 87-113.

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