Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Paper 003 Disc Veterinary Ophthalmology (1998) 1, 1, 17±20 Idiopathic Horner's syndrome in collie dogs HeÂctor Daniel Herrera,*{ Adriana Patricia Suraniti* and Nuria Fernanda Kojusner{ *Veterinary Medicine Teaching Hospital. School of Veterinary Sciences, University of Buenos Aires, Argentina, {Private practice, Buenos Aires, Argentina Address communications to: H. D. Herrera {ChorroarõÂn 280 1427 Buenos Aires Argentina Fax: +54 1 521 8316 e-mail: [email protected] Abstract Seven cases of idiopathic Horner's Syndrome in the Collie are described. Five males and two females presented with unilateral miosis, ptosis of the upper eyelid, enophthalmos and protrusion of the third eyelid. Thorough examination, pharmacological testing with phenylephrine, complete blood counts and radiography of the tympanic bullae and thorax were performed. The etiology was not identified in any of the cases. Clinical signs improved with pharmacologic testing within 20±40 min. In five dogs, total resolution of clinical signs was observed at 4 and 16 weeks after their initial appearance. Pharmacological testing suggested that the deficit could be at the preganglionic neuron. Ahed Bhed Ched Dhed Ref marKey Words: Horner's syndrome, dog, collie ker Fig marker following road accidents, otitis media/interna, avulsion of T a b l e INTRODUCTION the roots of the brachial plexus, thoracic masses, central marker Horner's syndrome (HS) is a group of clinical signs that result nervous system infection or neoplasia, ischaemic myelo- Ref end from loss or interruption of sympathetic innervation to the pathy, intervertebral disc disease,1,3,4,5,6,8±10 and thyroid Ref start globe and adnexa. These signs include miosis, ptosis of the neoplasia.11 However, in approximately half of affected dogs upper eyelid, enophthalmos and protrusion of the third eyelid. the cause cannot be determined3,9,10 and these cases are The sympathetic innervation of the eye and adnexa may recognized as idiopathic HS. There are no reports of any be divided into three neuroanatomic parts: central, preganbreed predisposition to the disease3,9 but a high incidence of glionic and postganglionic. The central component consists idiopathic HS has been described in the Golden Retriever.2 of fibers descending from the higher centers of the The purpose of this paper is to describe the findings of seven autonomic nervous system in the brain stem.1 They pass cases of idiopathic HS in Collies in a total of eight dogs with from the hypothalamus, tectum and tegmentum down the HS presented to the authors between October 1994 and tegmentospinal tract to synapse with preganglionic cell December 1996. bodies in the intermediate grey column of the cranial thoracic segments of the spinal cord.2 Pain, fear or emotional responses may cause pupillary dilatation by MATERIALS AND METHODS activating this pathway.3,4 The preganglionic cell bodies Eight dogs (seven Collies and a Great Dane) with idiopathic are located in the intermediate grey column of the first three HS were studied between October 1994 and December or four segments of the thoraxic spinal cord. The axons leave 1996. The medical records of the seven Collies were the spinal cord with the ventral roots of the spinal nerves to reviewed in the present study. Five males and two females join the thoracic sympathetic trunk, and then pass through aging from 5 to 11 years (mean 7 years) were included the cervicothoraxic ganglion without synapsing, very close to (Table 1). All of them presented with acute unilateral miosis, the cranial lung lobe.1,4±6 These preganglionic axons travel up the neck in the vagosympathetic trunk ending in the ptosis of the upper eyelid, enophthalmos and protrusion of cranial cervical ganglion, located caudomedial to the the third eyelid. Clinical examination included a complete tympanic bulla, where they synapse with the postganglionic ophthalmic examination (seven cases), thorough ear examcell bodies.5,6 The postganglionic sympathetic axons travel ination (seven cases), complete neurologic examination forward, pass through the middle ear adjacent to the facial (seven cases), pharmacological testing with topical 10% nerve and join the ophthalmic branch of the trigeminal phenylephrine (seven cases), complete blood counts and nerve. The ophthalmic nerve enters the periorbita through blood chemistry parameters (four cases), and radiographs of the orbital fissure and distributes to the smooth muscles of the thorax (three cases) and the tympanic bullae (two cases). the periorbita, eyelids and the dilator muscle of the iris.3,4 In order to localize the site of the lesion, pharmacological Several causes of HS have been proposed including testing was performed through assessment of ocular congenital anomalies,7 severe head, neck and chest trauma response to the topical administration of 10% phenylephrine # American College of Veterinary Ophthalmologists Paper 003 Disc 18 HERRERA, SURANITI AND KOJUSNER Table 1 Distribution by sex, age and affected eye, response to pharmacologic testing and recovery times in the seven studied Collies Case Sex Age (years) Affected eye Pupillary response with phenylephrine Recovery time (weeks) 1 2 3 4 5 6 7 9 6 5 8 11 5 5 OD OS OD OS OS OS OD mydriasis incomplete incomplete incomplete mydriasis mydriasis incomplete 12 16 ± ± 8 4 6 F M M F M M M M, male; F, female; OD, right eye; OS, left eye. (Poenefrina: Poen Lab., Buenos Aires). Two drops were placed in each eye using the control eye for comparison. Ocular examination was repeated every 10 min for 50 min; the time when the affected eye resumed to normality and mydriasis occurred in both the control and affected eye was noted. Two cases had a history of otitis externa; radiographs of the tympanic bullae were performed in these two patients, in addition to the otoscopic examination. Follow-up could be carried out by telephone contact with the owners in five of the cases. RESULTS Four dogs were affected on the left side and three dogs were affected on the right side. The cause could not be determined in any of the cases. There was no history of trauma, infectious or non infectious disease of the central nervous system, or ear disease except in two cases with previous mild otitis externa. Ophthalmic and otoscopic examination, and hematological and serum biochemical analysis were normal as well as radiographic examination, except in one case which showed spondylosis deformans from C6 to T2 with no peripheral neurologic signs. All the dogs responded to the pharmacological testing (Figs 1 and 2). All the clinical signs showed a complete improvement within 20±40 min after application of the topical phenylephrine, except the pupil, which had an incomplete response in four of the affected eyes (Table 1). Mydriasis occurred in all the control eyes at the same time as the affected eyes. In the five dogs that could be followed up, total resolution of clinical signs was observed between 4 and 16 weeks (mean 9.2 weeks) after its appearance. DISCUSSION The sympathetic supply of the eye is responsible for maintaining normal tone of the smooth muscles of the periorbita, eyelids and dilator muscle of the iris. It keeps the globe positioned normally, the third eyelid retracted, the pupil partially dilated, and modulates palpebral fissure width.1,4 Horner's syndrome (HS) is the name given to the group of clinical signs which results from interruption or loss of sympathetic innervation. These signs include miosis (actually the affected pupil dilating incompletely in low light conditions2), ptosis of the upper eyelid, enophthalmos, and protrusion of the third eyelid. HS is not an uncommon finding in dogs. Previous reviews of cases of HS have shown a relatively high incidence of the condition. One author diagnosed 74 cases in 10 years.9 In another report, 33 dogs with HS were diagnosed over a period of six years,3 while only two cases were diagnosed in 4 years by another author.8 In our series, eight cases of idiopathic HS were diagnosed in the last two years and seven of these cases were in Collies. Collies are not a common breed in the Argentinian dog population. In fact, only 12 Collies with ophthalmic disease were presented to one of the authors (H.D.H.) in the review period and seven of them had HS. Thorough examination and pharmacological testing with phenylephrine were performed in these seven Collies; complete blood counts and radiographs of the tympanic bullae and thorax were performed in some of them but the cause could not be determined in any case. Boydell has reported a high incidence of idiopathic HS in Golden Retrievers;2 however, there are no reports of any breed predisposition in other studies.3,4,8±10 There is no general agreement about the utility of pharmacologic testing for HS. Use of 0.001% epinephrine and 2 or 4% cocaine,12,13 hydroxyamphetamine,14 hydroxyamphetamine and 10% phenylephrine,4±6 epinephrine,3,9 and phenylephrine2 have been utilized in both humans and dogs in order to localize the site of the lesion. The combined use of an indirect and a direct-acting sympathomimetic agent appears to be the most useful method. Instillation of an indirect-acting sympathomimetic such as 1% hydroxyamphetamine results in normal mydriasis of the miotic pupil if the lesion is preganglionic. This drug acts by releasing endogenous norepinephrine from adrenergic nerve endings. When the lesion is postganglionic, the stores of norepinephrine contained in the nerve terminals are depleted and the pupil remains miotic.4±6 A direct-acting sympathomimetic such as 10% phenylephrine or 0.001% epinephrine can be used to confirm a postganglionic lesion in cases of incomplete or absent mydriasis after instillation of hydroxyamphetamine. In these cases of sympathetic denervation, adrenergic nerve endings become supersensitive to direct-acting sympathomimetics and mydriasis quickly occurs in postganglionic lesions.4±6,12 Boydell refers to the criteria developed by Kay (1981)15 of noting the time when mydriasis occurs after instillation of 10% phenylephrine.2 If mydriasis occurs within 20 min of the instillation, a postganglionic lesion is suggested. If dilatation occurs between 20 and 45 min, a preganglionic lesion is diagnosed. Finally, if mydriasis takes longer than 45 min, a central lesion may exist. Different authors have reported, however, that 10% phenylephrine does not consistently produce mydriasis in preganglionic lesions.4±6 In our cases all pharmacological testing was performed with 10% phenylephrine. Clinical signs improved within 20 and 40 min # American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 1, 17±20 Paper 003 Disc IDIOPATHIC HORNER'S SYNDROME 19 Figure 1. Case no. 6. Protrusion of the third eyelid; enophthalmos and ptosis of the upper eyelid are present on the left eye. Figure 2. Same dog as in Fig. 1, 30 min after instillation of 10% phenylephrine. The clinical signs including miosis show complete recovery. after application in all cases except for the pupils demonstrating incomplete recovery in four of the affected eyes. Control eyes dilated at the same time as the affected eyes. Regarding recovery times, Morgan mentioned that 25 out of 33 dogs showed complete reversal of clinical signs in a time ranging from 24 h to 30 weeks.3 In our study, five out of seven patients demonstrated total spontaneous resolution between 4 and 16 weeks. According to our results, Collies may have a breed predisposition to idiopathic Horner's syndrome. Pharmacological testing performed in these cases suggested that the lesion could be affecting the preganglionic neuron, but the correct site is not able to be confirmed using only phenylephrine. ACKNOWLEDGEMENTS The authors wish to thank Dr Dennis Brooks of the Department of Small Animal Clinical Sciences, Uni- versity of Florida, Gainesville, for the correction of the manuscript. REFERENCES 1 DeLahunta A. Veterinary Neuroanatomy and Clinical Neurology. 2nd edn. WB Saunders Co.: Philadelphia, 1983; 116±120. 2 Boydell P. Idiopathic Horner's syndrome in the Golden Retriever. Journal of Small Animal Practice 1995; 36(9): 382±384. 3 Morgan RV, Zanotti SW. Horner's syndrome in dogs and cats: 49 cases Journal of the American Veterinary Medical Association 1989; 194(8): 1096±1099. 4 Neer TM. Horner's syndrome: anatomy, diagnosis and causes. Compendium of Continuing Education for Practicing Veterinarians 1984; 6(8): 740±746. 5 Scagliotti RH. Current concepts in veterinary neuro-ophthalmology. Veterinary Clinics of North America (Small Animal Pract) 1980; 10(2): 431±434. 6 Scagliotti RH. Neuro-ophthalmology. In: Veterinary Ophthalmology, 2nd edn. (ed. Gelatt KN). Lea & Febiger: Philadelphia, 1991; 706±743. # American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 1, 17±20 Paper 003 Disc 20 HERRERA, SURANITI AND KOJUSNER 7 Brightman AH, Helper LC, Parker AJ. Congenital Horner's syndrome. Canine Practice 1977; 4: 19±23. 8 Jones BR, Studdert VP. Horner's syndrome in the dog and cat as an aid to diagnosis. Australian Veterinary Journal 1975; 51: 329±332. 9 Kern TJ, Aromando MC, Erb HN. Horner's syndrome in dogs and cats: 100 cases. Journal of the American Veterinary Medical Association 1989; 195(3): 369±373. 10 Van Den Broek AHM. Horner's syndrome in cats and dogs: a review. Journal of Small Animal Practice 1987; 28(10): 929±940. 11 Melian C, Morales M, Espinosa de los Monteros A, Peterson ME. Horner's syndrome associated with a functional thyroid carcinoma in a dog. Journal of Small Animal Practice 1996; 37(12): 591±593. 12 Bistner S, Rubin L, Cox TA, Condon WE. Pharmacologic diagnosis of Horner's syndrome in the dog. Journal of the American Veterinary Medical Association 1970; 157(9): 1220±1224. 13 Maloney WF, Younge BR, Moyer NJ. Evaluation of the causes and accuracy of pharmacologic localization in Horner's syndrome. American Journal of Ophthalmology 1980; 90(3): 394±402. 14 Skarf B, Czarnecki JS. Distinguishing postganglionic from preganglionic lesions. Studies in rabbits with surgically produced Horner's syndrome. Archives of Ophthalmology 1982; 100(8): 1319±1322. 15 Kay WJ. Neuro-ophthalmology. In: Veterinary Ophthalmology, 1st edn. (ed. Gelatt KN) Lea & Febiger: Philadelphia, 1981; 672±698. # American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 1, 17±20