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Background: Horner syndrome often occurs with cervical myelopathies and might provide insight into the underlying disease and prognosis., Objectives: To describe the clinical and imaging features of dogs with cervical myelopathy and concurrent Horner syndrome and to determine association of Horner syndrome with diseases or magnetic resonance images (MRI)., Animals: Ninety-three client-owned dogs with cervical myelopathy and concurrent Horner syndrome and 99 randomly selected client-owned dogs with cervical myelopathy without Horner syndrome (control cases)., Methods: Retrospective study. Medical records were reviewed to identify Horner and control cases and clinical findings recorded. MRI were reviewed, and lesions characterized and recorded. Descriptive and comparative statistics were performed., Results: Non-compressive disease occurred more frequently in the Horner group compared with controls (58%; 95% CI: 48-68 vs 9%; 95% CI: 5-16; P < .0001). The most common diseases were fibrocartilaginous embolism in the Horner group (44/93; 47%) and intervertebral disc extrusion (76/99; 77%) amongst controls. On MRI, parenchymal hyperintensity was seen more commonly in the Horner group (95%; 95% CI: 88-98) compared with controls (51%; 95% CI: 41-60; P < .0001). In the Horner group, dogs that did not survive to discharge (N = 13) had more extensive MRI lesions relative to the adjacent vertebral length (200%; IQR 110%-575%) compared with survivors (N = 80; 110%; IQR 40%-250%; P = .02). Lateralization of Horner signs and MRI changes matched in 54% of cases. The overall survival rate was high in both Horner (80/93; 86%) and control (95/99; 96%) groups., Conclusions and Clinical Importance: Horner syndrome in cervical myelopathy is commonly associated with noncompressive intraparenchymal disease., (© 2023 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.)

Purpose: To evaluate the diagnostic yield of advanced imaging in dogs with Horner's syndrome (HS) both with and without additional clinical signs., Methods: Retrospective review of clinical records from a UK referral hospital (2000-2018). Cases were excluded if HS was trauma- or surgery-related and if no advanced imaging with MRI or CT was performed. Imaging findings were assessed as well as any additional investigations performed., Results: One hundred twenty cases met the inclusion criteria; 88 with additional clinical signs and 32 with isolated HS. MRI or CT of head and neck was performed in 115 cases and/or thoracic CT in eight cases. Causative lesions were identified in 98% (86/88) of cases with additional clinical signs and 3% (1/32) of cases with isolated HS. This was statistically significant (p < .001). Pharmacological localization using phenylephrine (0.1%-10%) was accurate in predicting the site of a causative lesion in 79% (19/24) of tested cases. Overall, 28% (33/120) of cases were idiopathic, of which 49% (16/33) were golden retrievers. When compared to the overall hospital population, and UK Kennel Club records, this confirmed a significant predisposition in this breed (p < .001). No associations between idiopathic HS and concurrent systemic disease were identified., Conclusion: This is the first study to evaluate the diagnostic yield of advanced imaging in dogs with HS. Isolated HS is significantly more likely to be idiopathic than cases presenting with additional clinical signs; this could guide decision-making regarding further investigations performed in a clinical setting. Idiopathic HS is over-represented in the golden retriever., (© 2021 American College of Veterinary Ophthalmologists.)

Objective: To describe the clinical findings, imaging features, underlying conditions, treatment, and progression of dogs presented between 2010 and 2019 with neurogenic keratoconjunctivitis sicca (NKCS)., Methods: Dogs diagnosed with NKCS were searched in the clinical database. Inclusion criteria were STT-1 readings <15 mm/min, clinical signs of KCS with concurrent ipsilateral xeromycteria., Results: Thirty-four cases were identified. Mean age at presentation was 8.2 years, median 8.9 years (0.3-14.7). Twenty dogs were male, and 14 dogs were female. Concurrent neurological deficits included facial neuropathy (n = 13, 38%), peripheral vestibular syndrome (n = 10, 29%), and Horner's syndrome (n = 5, 15%). Advanced imaging was acquired in 53% of cases (n = 18). Etiologies included idiopathic (n = 18, 53%), endocrinopathy (n = 6, 18%), otitis interna (n = 4, 12%), head trauma (n = 3, 9%), iatrogenic (post-TECA-LBO, n = 1, 3%), brainstem mass (n = 1, 3%), and an area of inflammation in the pterygopalatine fossa (n = 1, 3%). Treatment for NKCS was initiated in most cases (n = 30, 88%) including: oral pilocarpine 2% and lacrimostimulant (n = 19), oral pilocarpine 2% only (n = 3), or lacrimostimulant only (n = 8). A mean time follow-up of 3.7 months, median 3 months (1-14) was available in 23 cases (68%). Eleven cases with follow-up were responsive (48%) with resolution of the clinical signs in a median time 4 months (1-10), and all of them were treated with oral pilocarpine (±lacrimostimulant)., Conclusions: Most cases presented as idiopathic NKCS; in others, an underlying cause of facial neuropathy was identified. All responsive cases were treated with oral pilocarpine 2%., (© 2021 American College of Veterinary Ophthalmologists.)

Objectives: To describe and compare the cumulative incidence and clinical progression of ocular neuropathies in diabetic dogs vs nondiabetic dogs following cataract surgery., Methods: Medical records of 196 diabetic and 442 nondiabetic dogs who underwent cataract surgery between 2004 and 2015 were reviewed. The percentage of patients affected by neuropathy and potential risk factors were compared between groups., Results: Patients with diabetes mellitus (DM) were 20.4 times more likely to develop an ocular neuropathy than patients without DM (12.24% vs 0.68%). Twenty-four diabetic patients were affected by mononeuropathies or polyneuropathies including Horner's syndrome (n = 20), facial neuropathy (n = 5), and neurogenic keratoconjunctivitis sicca (NKCS) (n = 5). The odds of a diabetic patient developing Horner's syndrome and NKCS were 86.3 and 20.7 times higher than a nondiabetic patient, respectively. The average duration of DM prior to diagnosis of neuropathy was 659 days (range 110-2390 days; median 559 days). Complete resolution was achieved in 10 of 22 neuropathies (45%) within an average of 248 days (range 21-638 days; median 187 days) after diagnosis., Conclusions: The odds of developing an ocular neuropathy, specifically Horner's syndrome and NKCS, are statistically higher in diabetic patients compared to nondiabetic patients. Neuropathies were observed as a long-term complication in this group of diabetic patients, and complete resolution of the neuropathy was observed in less than half of the affected population., (© 2018 American College of Veterinary Ophthalmologists.)

Case Report: A 4-year-old neutered male Rhodesian Ridgeback dog with right-sided Horner's syndrome, bilateral laryngeal paralysis, neck pain and bilateral hindlimb ataxia was euthanased following deterioration of its neurological status. Necropsy examination revealed an off-white retropharyngeal neoplastic mass (100 × 30 × 30 mm) attached to the base of the skull on the right side and macroscopic nodular metastases in the spleen and three vertebral bodies (C6, C7 and T6), including a nodule attached to the dura at C7. Histological evidence of neuroblastic tumour was detected in these macroscopic lesions, a regional lymph node, bone marrow of a femur and all 15 vertebral bodies (C1-T8) examined, including the three with macroscopic metastases, and in the lumens of small blood vessels in the lungs and liver. Ganglion cell differentiation was detected only in the primary retropharyngeal mass, one splenic nodule and the C7 dural nodule. Neoplastic cells were immunoreactive to neurofilament protein (ganglion cells only), vimentin and synaptophysin, and were negative for S100 protein, GFAP, CD3 and Pax5., Conclusion: The diagnosis was disseminated peripheral neuroblastoma, differentiating subtype (International Neuroblastoma Pathology Classification), with likely primary involvement of the right cranial cervical ganglion. This appears to be the first report of neuroblastoma in a dog with widespread occult haematogenous metastasis to bone marrow., (© 2017 Australian Veterinary Association.)

Objective: To investigate whether idiopathic Horner's syndrome (HS) in Golden Retrievers is an exclusively preganglionic disorder based on denervation hypersensitivity pharmacological testing with phenylephrine., Animals Studied: Medical records of dogs presented with HS between 2000 and 2012. Dogs presented with additional ocular or systemic signs were excluded., Procedures: Clinical data examined included age, sex, duration of clinical signs, ancillary diagnostic test results, and time to mydriasis on topical ocular application of 1% phenylephrine. Lesions were diagnosed as postganglionic (mydriasis within 20 min) or preganglionic (mydriasis between 20 and 45 min)., Results: Medical records of 21 dogs of nine different breeds were included. An etiopathogenesis for Horner's syndrome was determined in five dogs, none of which were Golden Retrievers. All diagnoses correlated with pharmacological lesion localization. Ten Golden Retrievers were included (eight male and two female) with a mean age of 8.5 years (range: 4-13). Lesion localization was diagnosed as postganglionic in eight (mean: 10 min [range: 6-18]) and preganglionic in two Golden Retrievers (20 and 24 min). All cases were unilateral and had completely resolved within 15 weeks (range: 11-20). Recurrence was not reported in any of the patients., Conclusions: Idiopathic postganglionic HS was diagnosed in eight of 10 Golden Retrievers contradicting previous reports of a purely preganglionic localization. Etiopathogenesis of canine idiopathic HS remains to be determined; nevertheless, a vascular etiology cannot be excluded. Future studies using magnetic resonance angiography may aid in clarifying the pathogenesis., (© 2013 American College of Veterinary Ophthalmologists.)

The medical records for 133 total ear canal ablations combined with lateral bulla osteotomies (TECA-LBOs) performed on 82 dogs (121 ears) and 11 cats (12 ears) between 2004 and 2010 were reviewed to determine if the duration of preoperative clinical signs was associated with the incidence of postoperative facial nerve injury and Horner's syndrome. Other perioperative complications, such as a head tilt, nystagmus, incisional drainage, draining tracts, hearing loss, as well as bacterial culture results, were noted. Postoperative facial nerve paresis occurred in 36 of 133 ears (27.1%), and paralysis occurred in 29 of 133 ears (21.8%), with no significant difference between species. Thus, postoperative facial nerve deficits occurred in 48.9% of ears. The median duration of clinically evident temporary facial nerve deficits was 2 wk for dogs and 4 wk for cats. Dogs had a significantly longer duration of preoperative clinical signs and were less likely than cats to have a mass in the ear canal. Dogs were less likely to have residual (> 1 yr) postoperative facial nerve deficits. The incidence of postoperative Horner's syndrome was significantly higher in cats than dogs. The duration of preoperative clinical signs of ear disease was not associated with postoperative facial nerve deficits.

There are four major neuroanatomical structures associated with the ear that, when damaged, result in different neurologic clinical signs. These structures are the facial nerve, the ocular sympathetic tract, the vestibular receptors, and the cochlea. The clinical signs associated with disorders of each structure are discussed, followed by a summary of the diseases that should be considered in each case. The article begins with a description of the neuroanatomy of each of these structures., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Objective: To describe a technique for insertion of a thoracic epidural catheter., Study Design: Clinical report., Animals: Dogs (n = 3) undergoing thoracic wall resection and thoracotomy., Methods: A paramedian approach with cephalic angulation was used to place a 24-g epidural catheter in 3 dogs. Dogs 1 and 2 had left caudal thoracic wall resection and dog 3 had left thoracotomy. In dog 1, the epidural catheter was inserted at L2-L3 intervertebral space and the tip of the catheter advanced to the level of T13 vertebral body. In dog 2, the epidural catheter was inserted at T12-T13 intervertebral space and the tip of the catheter was advanced to the level of T8 vertebral body. In dog 3, the epidural catheter was inserted at T13-L1 intervertebral space and its tip advanced until reaching the vertebral body of T10. All dogs were administered a combination of bupivacaine and morphine through the epidural catheter to provide intra- and postoperative analgesia., Results: The peridural space was identified and the tip of the catheter was positioned where intended in all dogs. Dog 1 developed transient Horner's syndrome and dog 3 required intraoperative fentanyl during the first part of the procedure., Conclusion: Paramedian approach with cephalad angulation is a suitable technique to place thoracic epidural catheters in dogs., (© Copyright 2012 by The American College of Veterinary Surgeons.)

This report describes a partial ventral verte-brectomy and interbody fusion for a progressive hemivertebra disease using a ventral transthoracic approach in a 3.6-month-old male Labrador puppy. The goal of this article is to clarify the potential advantages of this uncommon surgical technique for this condition and to discuss its technical aspects.

Observations: A left sided Horner's syndrome (ptosis, prolapse of the nictitating membrane and miosis) was observed in a 4-year-old female, neutered Beagle dog after epidural injection of 0.22 mL kg(-1) ropivacaine (0.75%) in 0.01 mL kg(-1) of saline during isoflurane anaesthesia. Clinical signs disappeared gradually and resolved completely 4 hours and 10 minutes after injection., Conclusions: The epidural injection of 0.22 mL kg(-1) ropivacaine (0.75%) in 0.01 mL kg(-1) of saline during isoflurane anaesthesia caused unilateral (left) Horner's syndrome in a 4-year-old female, neutered Beagle dog.

A one-year-old female English Cocker Spaniel dog with idiopathic Horner's Syndrome is described. The specific clinical signs in this specimen were miosis, ptosis, enophthalmos, and prolapsed nictitans for 2 days following sudden onset. According to history taking, ophthalmic, neurological, and radiological examination, the patient was diagnosed with idiopathic Horner's syndrome. Manual acupuncture treatment was applied to the dog on local points two times in 2 days. The local acupoints were ST-4 (Di Chang) and GB-1 (Tong Zi Liao). The day after the initial acupuncture treatment, clinical signs related to idiopathic Horner's syndrome had almost disappeared. The day after the second treatment, specific clinical signs were completely absent. During this period, the dog did not receive any orthodox treatment. Thus, it is suggested that manual acupuncture might be an effective therapy for idiopathic Horner's syndrome.

A small-cell carcinoma of the lung was identified in a six-year-old female German shepherd dog with a history of chronic lameness of the left forelimb, Horner's syndrome and sensory deficits on the caudal portion of the left forelimb below the elbow. A mass, the exact location of which was difficult to ascertain, was identified during radiographic examination of the thorax. It was easily identified, using magnetic resonance imaging, as an apical tumour of the left lung with dorsal extension and involvement of paraspinal structures, such as spinal nerve roots C8 to T1 and the sympathetic trunk. Postmortem examination confirmed a mass in the left apical lobe of the lung, compatible with a diagnosis of small-cell carcinoma by histopathology and immunohistochemistry. This clinical presentation is similar to Pancoast syndrome described in humans.

Diseases of the ear often cause signs of neurologic dysfunction because of damage of peripheral nervous system structures associated with the middle and inner ear. Vestibular dysfunction, facial paralysis, Horner's syndrome, and hearing deficits are the most common neurologic deficits that accompany middle and inner ear disease. Differentiating these signs from disease of the central nervous system is crucial for an accurate diagnosis and prognosis but can be difficult. Understanding the normal anatomy of the ear and its association with the brain is crucial to interpretation of the neurologic examination. This article reviews neurologic dysfunction commonly associated with diseases of the ear and differentiating these signs from central disease.

A 9-year-old, spayed female, Airedale Terrier was euthanatized and necropsied after a progressive clinical course that included Horner's syndrome of the left eye and unilateral atrophy of the masticatory muscles. Although gross lesions were limited, a polyradiculoneuritis and ganglionitis that was most severe in the trigeminal nerves and ganglia were confirmed histologically. The inflammatory infiltrate consisted predominantly of macrophages and B and T lymphocytes that were phenotypically confirmed by immunostaining. Horner's syndrome was the result of damage to postganglionic sympathetic fibers that were incorporated in segments of the inflamed trigeminal nerve and its ophthalmic branch. Histologically, the character and distribution of the inflammation was similar to previously described syndromes of suspected immune-mediated etiology in humans and animals.

A working collie cross was presented with a three-month history of vague neurological signs and a right-sided Horner's syndrome. Denervation hypersensitivity testing suggested a first order syndrome. There was a significant positive titre to Neospora and clinical signs resolved completely following treatment.

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.

A retrospective study was made of 43 dogs with Horner's syndrome (HS). In the group studied the golden retriever was found to be predisposed for Horner's syndrome. No predisposition in gender or age seemed to exist. Symptomatic treatment with topical 10% phenylephrine alleviates the clinical signs. Generally patients recover in 2 to 6 months.

An 8-year-old female German Shepherd dog showed first order Horner's syndrome associated with progressive right-sided hemiplegia and mega-oesophagus. Intramedullary and leptomeningeal arteriovenous malformation (AVM) was identified in the cervical spinal cord. The morphological characteristics were arteriovenous shunting, intramedullary multiple thromboses and haemorrhage, non-inflammatory necrosis of white and grey matter around the shunt, and intervening neural gliosis with neovascularization. These findings suggested that the malformation induced a focal circulatory disturbance within the cervical spinal cord and that fatal thrombosis was responsible for the sudden onset of the nervous signs and progressive neurological deterioration. This is the first report of intramedullary spinal AVM in a dog., (Copyright 1999 W.B. Saunders Company Ltd.)

A puppy was presented with unilateral Horner's syndrome thought to have been in existence since the eyes first opened. No other clinical signs were evidence and the condition was attributed to trauma during assisted birth. All abnormalities resolved spontaneously by 11 weeks of age.

Two dogs developed unilateral Horner's syndrome attributable to the placement of a thoracic drainage tube. Signs resolved following removal of the chest drains.

A seven-year-old entire male Irish setter was presented because of a neck mass, prolapse of the third eyelid and apparent drooping of the upper eyelid. Historical findings included increased appetite as well as polyuria and polydipsia for about two weeks. The most remarkable findings on physical examination were right-sided Horner's syndrome, pre-scapular lymphadenopathy and a large, ventral cervical mass. Lateral cervical radiographs showed a large, soft tissue opacity surrounding the trachea and retropharyngeal area which was causing displacement and narrowing of the cervical trachea and oesophagus. Results of thyroid testing suggested hyperthyroidism. At necropsy, a large, invasive tumour was identified in the ventral cervical region and multiple metastases of various sizes were detected in the lungs. Histopathological examination of the tumour revealed follicular thyroid carcinoma and confirmed widespread pulmonary metastasis.

Two dobermanns exhibited Horner's syndrome following the surgical treatment of cervical spondylopathy. Denervation hypersensitivity testing demonstrated a 2nd order lesion in both. Spontaneous resolution occurred within one month.

A prospective study was made of cases of idiopathic Horner's syndrome in dogs referred to the author. Over a six-year period the condition was recorded in 62 golden retrievers. Examination suggested that the lesions affected the preganglionic neuron.

The medical records of 74 dogs and 26 cats with Horner's syndrome (HS) that were admitted to the New York State College of Veterinary Medicine between January 1975 and October 1985 were reviewed. In dogs, but not cats, HS was associated significantly (P less than 0.01) with increasing age. Dogs with hypothyroidism (defined liberally but not rigorously), intracranial neoplasia, or thoracic neoplasia, cats with otitis media/interna (defined liberally), and dogs and cats with brachial plexus root avulsion were at greater risk for developing HS than were animals that were hit by a car. Dogs and cats with otitis externa were at less risk of developing HS than were animals that were hit by a car. The cause of HS could not be determined in 50% of dogs and 42.3% of cats. The results of topical adrenergic drug testing in dogs were inconclusive in localizing lesion site. In dogs and cats, HS appeared to be unassociated with gender, breed, or right vs left side. The important causes of HS in dogs and cats were trauma (hit by car), brachial plexus root avulsion, intracranial and thoracic neoplasia, and otitis media/interna.

Acute hemiplegia and Horner's syndrome developed in a 6-year-old female black Labrador Retriever 24 hours after a day of exercise. Radiographic, cerebrospinal fluid, and electromyographic studies did not detect the site or nature of the suspected cervical lesion. The dog showed no improvement after evaluation for 5 days on corticosteroid and antibiotic therapy. Gross and microscopic examination revealed the presence of an ischemic infarct in the C6 segment of the cervical spinal cord and associated fibrocartilaginous emboli. The nature of the clinical signs and the pathologic findings in this case are similar to previous reports of human and canine cases.

Medical records of 49 dogs and cats with Horner's syndrome were reviewed. Causes included head, neck, and chest trauma, chronic otitis, cranial thoracic mass, and injury attributable to cleaning of the external ear canal. Cause could not be delineated in 54.5% of the dogs. Numerous diagnostic tests and pharmacologic challenge exposure with epinephrine were used to localize the site of injury. Resolution of all clinical signs was observed in 36 animals and required a mean of 7.7 weeks.

A 5-year-old male Doberman Pinscher had nasal stenosis, dropped mandible, bilateral atrophy of masseter and temporalis muscles, and Horner's syndrome caused by aleukemic myelomonocytic leukemia. Neoplastic cellular neurotropism, diffuse turbinate and nodular peribronchial infiltrate, and a hepatic portal infiltrative pattern similar to that of lymphoma were microscopic features of interest.

Four cases of Horner's syndrome, two in dogs and two in cats, are described. Miosis, ptosis, and enophthalmos were present in three of the cases and in addition, protrusion of the nictitating membrane was present in the fourth case. In the two cases described in cats, there was also evidence of peripheral vasodilation in the skin of the face on the same side as the Horner's syndrome.