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Show Journal of" A'euro- Ophthalmology 20( 4): 288- 290, 2000. © 2000 Lippincott Williams & Wilkins, Inc., Philadelphia Idiopathic Horner Syndrome in the Golden Retriever Pip Boydell, B Vet Med, MRCVS Objectives: Various reports have noted a high incidence of idiopathic Horner syndrome in golden retriever dogs. The author seeks to document this condition in the breed. Materials and Methods: A prospective study was made of cases of Horner syndrome in dogs referred to the author throughout a 10- year period. As part of the general clinical, ophthalmic, and neurologic examination, denervation hypersensitivity testing was performed to localize the responsible lesion. Follow- up results were obtained in all cases by repeat examination or telephone contact. Results: Of 155 dogs in the study, 110 were golden retrievers, 100 of which were diagnosed as having idiopathic second order Horner syndrome. Ninety- five of the golden retrievers were male, some neutered. Signs resolved spontaneously in all cases within 6 months. Conclusions: There is a high incidence of idiopathic second order Horner syndrome in the male golden retriever. Key Words: Horner's syndrome- canine- denervation hypersensitivity, Horner syndrome results from interference with the sympathetic innervation of the eye and adnexa. Clinical signs in dogs ( Fig. 1) include anisocoria; incomplete dilation of the affected pupil in low- light conditions; enophthalmos; and third eyelid protrusion, ptosis, and an increase in temperature of the face and pinna resulting from peripheral vasodilation. The sympathetic pathway to the eye can be divided schematically into three parts: central, preganglionic, and postganglionic ( 1). The site of the responsible lesion can be determined by denervation hypersensitivity testing ( 2; Boydell P, The accuracy of denervation hypersensitivity testing with 10% phenylephrine eyedrops in Horner's syndrome in the dog, Presented at the Proceedings of the 30th Annual Meeting of the American College of Veterinary Ophthalmologists, Chicago, 1999). Ten- percent phenylephrine drops instilled into the conjunctival sac will lead to mydriasis after an amount of time dependent on the position of the lesion in the sympathetic pathway. When the postganglionic neuron is affected, mydriasis Manuscript received February 9, 1999; accepted June 27, 2000. From the Department of Ophthalmology, Animal Medical Centre Referral Services, Manchester, United Kingdom. Address correspondence and reprint requests to Pip Boydell, Department of Ophthalmology, Animal Medical Centre Referral Services, 511 Wilbraham Road, Manchester M21 0UB, UK. will occur within 20 minutes. In cases with a preganglionic lesion, mydriasis is expected 20 to 45 minutes after administration. Previous reviews have shown that the cause remains undiagnosed in approximately half the affected dogs, and trauma accounts for a large proportion of those cases that are diagnosed ( 3- 5). Reported etiologies in the dog include congenital anomalies, central nervous system infection, neoplasia, ischemic myelopathy and intervertebral disc disease, brachial plexus avulsion, carotid artery catheterization and surgery of the carotid body, thoracic and cervical neoplasia, thoracic drain placement, surgery of the shoulder joint, middle ear disease and its management, trigeminal neuritis and orbital disease, and cervical spinal surgery ( 6- 15). Idiopathic Horner syndrome has been described in the golden retriever ( 16), but no reference has been made to the relative incidence. METHODS A prospective study was made of cases of dogs with Horner syndrome referred to the author throughout a 10- year period ( 1987- 1997) at several different centers. Breed, age, and sex were recorded, and all patients underwent a complete general clinical, ophthalmic, and neurologic examination. These examinations included routine hematology and blood biochemistry screens ( albumen, globulin, urea, creatinine, liver enzymes, cholesterol, bile acids, and electrolytes); thyroid function testing; and chest, neck, and head radiographs. Computed tomography was performed in only one instance as part of an orbital work- up. Other investigations, such as endoscopy of the tympanic bullae and electrodiagnostic investigation, were performed when appropriate. Dogs referred for the investigation of other clinical signs, and in which Horner syndrome was also noted, were not included in this study, but those dogs that only presented with Horner signs and an underlying cause for the signs were determined were included in the study. Denervation hypersensitivity testing was performed, instilling one drop of 10% phenylephrine eyedrops ( Martindale Pharmaceuticals, Romford, UK) and timing the appearance of substantial pupillary dilation. One drop was placed in the ventral conjunctival sac OU, and the eyes were assessed at 5- minute intervals. No other pharmacologic tests were performed. 288 IDIOPATHIC HORNER SYNDROME IN THE GOLDEN RETRIEVER 289 FIG. 1. Golden retriever with idiopathic Horner syndrome. Follow- up investigation was performed by physical examination of the dog or by telephone contact with the owner 4 months after the initial presentation, and later, if appropriate. The data were subjected to statistical analysis by a chi square test. RESULTS One hundred fifty- five dogs presenting only with signs of Horner syndrome were investigated. Ocular examination was unremarkable except for the Horner signs. There was a relevant history of trauma to the head, neck, or axilla in 12 dogs. Blood tests were performed in 108 dogs and results were unremarkable in all instances, except for 2 dogs in which there was evidence of hypothyroidism. Radiographic examination of the chest and neck was performed in 58 dogs. Anterior thoracic neoplasia ( lymphoma and mediastinal adenocarcinoma) was detected in 2 cases, and evidence of otitis media was evident in 14 dogs. Signs of middle ear disease were detected by otoscopy in 22 dogs ( including the 14 dogs in which there were radiographic signs). Orbital ultrasonography and computed tomography demonstrated a soft tissue mass in one dog. Electromyography showed involvement of the brachial plexus in three cases. Of the 155 dogs in the sample, 110 were golden retrievers or golden retriever/ Labrador retriever crosses. In 100 of these golden retrievers, no cause for the Horner signs was apparent. Sixty- one dogs were unneutered males, 34 dogs were neutered males, and 5 dogs were neutered females. Of the 45 dogs of other breeds, no cause for the Horner signs was identified in 10 cases. In all the idiopathic cases, the time recorded for dilation of the Horner pupil after instillation of 10% phenylephrine drops was 35 to 45 minutes. The contralateral control pupil dilated after 60 to 90 minutes. The age range of the retrievers with idiopathic Horner syndrome was 2 to 10 years, with an average age of 5.28 years. In all these cases, the third eyelid protrusion and ptosis resolved within 30 minutes, noticeably before substantial pupillary change. Two dogs were reported to have impaired visual function; this symptom was attributed to excessive protrusion of the third eyelid. No treatment was given, and all idiopathic cases had partial or complete resolution of Horner signs within 16 weeks of the initial examination. All idiopathic cases had resolved completely within 6 months of the initial examination. No recurrence has been reported in any of these patients. Exact numbers of the hospital population of referred golden retrievers and all breeds are not available because the studies involved several different centers. However, numbers are available for the past 3.5 years when the number of dogs referred to the Animal Medical Centre in Manchester was 8,876. Two hundred sixty- nine of these dogs were golden retrievers, and 7 of these had idiopathic second order Horner syndrome. Three idiopathic second order cases were noted in other breeds during this time at this clinic. The incidence in golden retrievers was 2.6%; the incidence in all other breeds was 0.03%, and the incidence in all breeds was 0.11%. Chi square analysis gives a 0.01 to 0.02% chance that this difference in incidence could occur by chance alone. DISCUSSION No accurate numbers of breed populations in the United Kingdom are available, although golden retriever numbers are high in the Kennel Club registration. Similarly, there are no available data concerning the sex of pet dogs in the general population. Thus, there is no possible statistical correlation between the breed incidence of Horner syndrome in dogs seen at a single referral center and the breed incidence of Horner syndrome in dogs in the general population. However, the results of this study suggest that golden retrievers have a relatively high incidence of idiopathic Horner syndrome, and male dogs are much more likely to be affected. Although full details of the relative populations are not available, it is unlikely that there would have been substantial changes during the past 10 years, and some interpretation may be made of the relative incidence in the data acquired from a single center for 42 months. Disease involving the middle ear was seen to be the second most common cause of Horner syndrome in me dog. The accuracy of pharmacologic localization of the site of a lesion in the sympathetic pathway has been questioned, and emphasis has been placed on the importance of accompanying clinical signs ( 3,4). The author has found the technique of denervation hypersensitivity testing using 10% phenylephrine drops to be easy to perform, consistent, and reliable in cases in which a cause has been determined, although Kay ( 2) comments that the test can be subjective and inconsistent. When no other localizing signs are available, this test assumes greater importance. Pharmacologic localization of the responsible lesion in Horner syndrome has been documented using other agents, such as hydroxyamphetamine and cocaine in dogs and people ( 17- 19), but these agents J Neuro- Ophthalmol, Vol. 20, No. 4, 2000 290 P. BOYDELL were unavailable in the United Kingdom during this study. However, it is unlikely that the use of these agents would have added any additional information because the results of the tests using phenylephrine were considered definitive. Epinephrine has been used, but this agent is thought to be of minimal use because of reported poor corneal penetration and a wide variation in sensitivity ( 17,20). By definition, the etiology remains undetermined. Many patients were boisterous and were reported to pull on the lead, often with a choke chain, and it can be surmised that this may lead to minor traumatic damage to structures within the neck, including the sympathetic pathway. Arguments against this position are that one might expect to see a greater incidence in puppies and immature dogs during training. Similarly, there are other breeds that have a reputation for pulling against restraint, yet have no apparent predisposition toward the condition. Although there is no evidence of a hereditary nature, the high breed incidence suggests some inherited component or predisposing feature. The author can offer no explanation for the predominance of male dogs affected, although male dogs, perhaps, had a tendency to pull harder against normal restraint of collar and lead or choke chain. Such a theory remains speculative, but no others have been offered. However, anecdotally, veterinary ophthalmologists and neurologists recognize the high incidence of idiopathic Horner syndrome in the breed. The author welcomes any explanations. REFERENCES 1. Scagliotti RH. Neuro- Ophthalmology. In: Gelatt KN, ed. Veterinary Ophthalmology, 2nd ed. Philadelphia: Lea & Febiger, 1991: 706- 743. 2. Kay WJ. Neuro- Ophthalmology. In: Gelatt KN, ed. Textbook of Veterinary Ophthalmology. Philadelphia: Lea & Febiger, 1981: 672- 698. 3. Van den Broek AHM. Homer's syndrome in cats and dogs: a review. J Small Anim Pract 1987; 28: 929- 940. 4. Kern TJ, Aromando MC, Erb HN. Horner's syndrome in dogs and cats: 100 cases ( 1975- 1985). J Am Vet Med Assoc 1989; 195: 369- 373. 5. Morgan RV, Zanotti SW. Horner's syndrome in dogs and cats: 49 cases ( 1980- 1986). J Am Vet Med Assoc 1989; 194: 1096- 1099. 6. Brightman AH, Helper LC, Parker AJ. Congenital Homer's syndrome. Canine Practice 1977; 4: 19- 20. 7. Boydell P. Horner's syndrome in a puppy. J Small Anim Pract 1998; 39: 448^ 49. 8. De Lahunta A, Alexander JW. Ischemic myelopathy secondary to presumed fibrocartilaginous embolism in 9 dogs. J Am Anim Hosp Assoc 1976; 12: 37^ 18. 9. Griffiths IR, Duncan ID, Lawson DD. Avulsion of the brachial plexus- 2: clinical aspects. J Small Anim Pract 1974; 15: 177- 182. 10. Obradovich JE, Withrow SJ, Powers BE, et al. Carotid body tumors in the dog: eleven cases ( 1978- 1988). J Vet Intern Med 1992; 6: 96- 101. 11. Meliln C, Morales M, Espinosa de los Monteros A, et al. Horner's syndrome associated with a functional thyroid carcinoma in a dog. J Small Anim Pract 1996; 37: 591- 593. 12. Boydell P, Pike R, Crossley D, et al. Homer's syndrome following intrathoracic tube placement. J Small Anim Pract 1997; 38: 466- 467. 13. Steidl T, Zimmerman M. Operationsbedingtes Homer- syndrome beim hund. Kleintierpraxis 1989; 34: 363- 364. 14. De Lahunta A. Cranial nerve- lower motor neuron: general somatic efferent system, special visceral efferent system. Lower motor neuron- general visceral efferent system. In: Veterinary Neuroanatomy and Clinical Neurology, 2nd ed. Philadelphia: WB Saunders, 1983; 110- 120. 15. Boydell P. Horner's syndrome following cervical spinal surgery in the dog. J Small Anim Pract 1995; 36: 510- 512. 16. Boydell P. Idiopathic Homer's syndrome in the golden retriever. J Small Anim Pract 1995; 36: 382- 384. 17. Bistner S, Rubin L, Cox TA, et al. Pharmacologic diagnosis of Horner's syndrome in the dog. J Am Anim Hosp Assoc 1970; 157: 1220- 1224. 18. Neer TN. Horner's syndrome: Anatomy, Diagnosis and Causes. Compendium on Continuing Education for the Practicing Veterinarian 1984; 6: 740- 746. 19. Maloney WF, Younge BR, Moyer NJ. Evaluation of the causes and accuracy of pharmacologic localization in Homer's syndrome. Am J Ophthalmol 1980; 90: 394- 402. 20. Grimson BS, Thompson HS. Homer's syndrome: overall view of 120 cases. In: Thompson HS, ed. Topics in Neuroophthalmology. Baltimore: Williams & Wilkins, 1979: 151- 156. J Neuro- Ophthalmol, Vol. 20, No. 4, 2000 |
