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Objective: To report the development of transient Horner's syndrome in horses following local anesthesia of the cervical plexus., Animals: A total of 37 horses., Study Design: Observational retrospective short case series., Methods: Medical records of cases undergoing ultrasound-guided cervical plexus anesthesia for standing prosthetic laryngoplasty at a single referral institution were evaluated (2019-2020)., Results: Five of 37 horses (14%) developed transient signs of Horner's syndrome postoperatively. Obvious clinical signs began 2 to 5 h following local anesthesia and persisted for two to 4 h. Profuse unilateral sweating of the head and upper neck was the most apparent clinical sign., Conclusion: Transient clinical signs of Horner's syndrome were seen following unilateral local anesthesia of the cervical plexus. Long-term adverse sequelae were not observed., (© 2023 The Authors. Veterinary Surgery published by Wiley Periodicals LLC on behalf of American College of Veterinary Surgeons.)

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.)

Case Description: A 9-year-old spayed female Maine Coon cat was presented at the University of Veterinary Medicine Vienna for further investigation of chronic nonpruritic bilateral ear disease and unilateral Horner syndrome., Clinical Findings: Physical examination and otoscopy findings included right sided Horner syndrome, a right head tilt of approximately 20° and a small pink nodule in the right and several smaller nodules in the left proximal horizontal external ear canal. Computed tomography and magnetic resonance imaging revealed soft tissue opacity material in both middle ear cavities, the caudal portion of the nasal cavity, the left nasopharyngeal meatus and the right frontal sinus. Via videootoscopy, 2 multilobular and several flat nodules were detected in the proximal right horizontal external ear canal and in the left tympanic bulla, respectively. Histopathological examination confirmed the diagnosis of cholesterol granulomas., Treatment and Outcome: All otic cholesterol granulomas (CGs) were removed via video-otoscopy (VO), and topical treatment was initiated in addition to oral prednisolone. After the histopathological confirmation, negative microbial cultures from the middle ear cavities, and the remission of the symptoms by the first recheck, topical, and systemic treatment were discontinued. A follow-up 6 months later, did not reveal any recurrence of the CGs., Clinical Relevance: To our knowledge, this is the first case of bilateral CGs diagnosed with a combination of CT, MRI, VO, and histopathology and removed minimal invasively via VO, without a need for ventral bulla osteotomy, which led to complete remission of all signs and no relapse until the follow up 6 months later.

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.)

A juvenile yellow-tailed black cockatoo ( Calyptorhynchus funereus ) was presented with paresis of the right wing, ptosis, and miosis of the right eye; feather erection of the right side of the head and neck; and a penetrating injury over the right pectoral muscle. Temporary reversal of ptosis, miosis, and feather erection after administration of phenylephrine drops confirmed a diagnosis of Horner syndrome. Computed tomographic imaging revealed a fractured rib, traumatic lung lesions, and subcutaneous emphysema. The right-sided Horner syndrome and wing paresis were attributed to a sympathetic nerve trauma of the eye and feathers and to the brachial plexus, respectively. This report describes the diagnosis and resolution of ptosis and miosis within 8 weeks and recovery of feather symmetry and wing function within 11 weeks of the cockatoo's initial presentation with a conservative-management treatment plan.

Horner syndrome, which results from oculosympathetic denervation, has rarely been reported in birds. A retrospective study was conducted in a raptor rehabilitation program to gain further insight into Horner syndrome in birds. Data from 5128 live raptors admitted over 20 years were reviewed. Horner syndrome was identified in 22 individuals from 13 different species. Raptors from the orders Strigiformes, Accipitriformes, and Falconiformes were affected, with the last order being underrepresented. Ptosis of the upper eyelid was the most commonly reported clinical sign in the birds diagnosed with Horner syndrome, having been noted in 21 cases. Signs of traumatic injury, such as fractures, wounds, and hematomas, were documented in 18 cases. Among the 22 cases, 12 birds were euthanatized, 3 died in treatment, and 7 were successfully released back into the wild.

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.)

Horner syndrome was identified in 25 of 30 777 avian admissions to Currumbin Wildlife Hospital during 2010-2016. Unilateral ptosis and erection of facial feathers were distinct findings on physical examination and consistent across 9 species. Affected birds were biased toward adults (64%) suffering traumatic injuries (88%). Concurrent injuries requiring treatment were present in 38% of cases, and 76% had additional neurologic deficits. Prognosis for release was poor, with an overall success rate of 32%. Resolution of clinical signs increased to 44% with higher doses of meloxicam and required an average hospitalization of 22 days (range, 3-78 days). Further investigation of the underlying causes of Horner syndrome in birds to provide treatment and prognostic guidelines is warranted.

The term Horner syndrome refers to the clinical presentation of oculosympathoparesis, comprising miosis, ptosis, and facial anhydrosis. To date, there are 2 reports of postoperative Horner syndrome in pigs. In this species the cervical sympathetic chain and cranial cervical sympathetic ganglion are consistently within the carotid artery sheath. This case study describes the sudden onset of Horner syndrome in 2 pigs, from a study cohort of 8, after the placement of a vascular graft between the carotid artery and external jugular vein. Anesthesia and surgery was uneventful in all the pigs in the study, but 2 pigs demonstrated clinical signs including ptosis, enophthalmos and prolapse of the nictitating membrane immediately after recovery from anesthesia. Horner syndrome was diagnosed in light of the clinical signs. These clinical signs persisted throughout the 2-mo study period and did not appear to improve or deteriorate in that time. Gross examination of the surgery site at the end of the study did not reveal an obvious lesion in the carotid artery sheath. The risk of Horner syndrome after surgery involving the carotid artery in pigs had not been reported prior to this study. Without specific measures to protect the cervical sympathetic ganglion during surgery, the incidence of postoperative Horner syndrome was 25% in our population of pigs. Although the welfare implications of this syndrome are minimal, concerted effort to avoid intraoperative damage to the cervical ganglion is essential for future work.

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.)

An 8-month-old Holstein heifer with cervical enlargement was suspected of thymic lymphosarcoma given clinical signs of depression, tendency to lie down, cervical mass, jugular vein distension, conjunctival hyperemia, and ruminal tympany. Unilateral Horner's syndrome was also observed. Increased serum total lactate dehydrogenase (LDH), LDH isozyme (LDH-2, and LDH-3) and serum thymidine kinase activity were observed. The findings of fine needle aspiration cytology of the cervical mass revealed large lymphoblasts with mitoses present. These findings strongly suggested the diagnosis of lymphosarcoma. Necropsy revealed a large mass in the cervical thymic region, which compressed the esophagus and trachea. Cranial masses in the frontal sinus and multiple extradural sites throughout the cranial vault were also recorded. Histopathological examination confirmed the diagnosis of thymic lymphosarcoma and demonstrated the brain involvement of neoplastic lymphoid cells in the cerebrum. This is a rare clinical case of thymic lymphosarcoma accompanied by brain metastasis in a Holstein heifer.

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.)

The close relationship between guttural pouches, cranial nerves, and sympathetic structures make neurologic abnormalities due to diseases of the guttural pouches (especially mycosis) possible. Recognition of epistaxis or mucopurulent nasal discharge, together with signs of dysfunction of the cranial nerves in contact with the guttural pouches, are important key points in order to consider a comprehensive evaluation of these structures and further definitive diagnosis. Diseases of the guttural pouches can also cause signs such as dysphagia, abnormal soft palate positioning, laryngeal paralysis, and Horner syndrome due to lesions in one or more of the cranial nerves or sympathetic structures involved with these functions. Therefore, an accurate diagnosis is essential for treatment.

In an experimental model, iatrogenic Horner syndrome developed after a right carotid sheath surgery in an infant pig (Sus scrofa). Horner syndrome is a classic clinical triad consisting of ipsilateral eyelid ptosis, pupil miosis, and facial anhydrosis. This syndrome results from cervical sympathetic chain (CSC) paresis and usually is acquired in humans. To determine whether the development of Horner syndrome in this situation could be attributed to pig anatomy, we compared the anatomy of the CSC in pigs and humans, by using 10 infant (age, 1 to 3 wk) pig cadavers. The CSC and cranial cervical sympathetic ganglion (CCG) were dissected bilaterally under a surgical microscope. These structures were consistently within the carotid sheaths of the pigs. In contrast, the CSC and CCG are outside the carotid sheath in humans. Awareness of the anatomic variation of the CSC and CCG within the carotid sheath in the pig and the possibility of the same variation in humans may help surgeons to identify and preserve important structures while performing cervical surgery in pigs and humans. Furthermore, this knowledge can aid in the diagnosis and prognosis of schwannoma.

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.

This case report describes the clinical and magnetic resonance imaging (MRI) findings of a 3.5-year-old, male neutered, domestic shorthair cat with second order Horner's syndrome as the only clinical abnormality. The neuroanatomical pathway of the sympathetic innervation to the eye, differential diagnoses for Horner's syndrome in cats, and the interpretation of pharmacological testing are reviewed. The unusual MRI findings and the value of fat-suppressed MRI sequences are discussed.

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 9-year old, Rasa Aragonesa ewe was presented with a left-sided, facial, soft fluctuant swelling. The postmortem examination showed grass awns filling the entire length of the parotid gland duct. The presence of parotid duct obstruction with Horner's syndrome, previously unreported in sheep, is discussed.

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.

A 10-year-old neutered male Persian cat and a 4-year-old spayed female domestic shorthair (DSH) cat were evaluated for acute-onset severe lateralising tetraparesis and hemiplegia, respectively. Both cats also had left-sided Horner's syndrome. Neurological examination of the cats localised the lesion to cranial to C5 in the Persian and the left cervical intumescence (C6-T2) in the DSH. Physical examinations were otherwise generally unremarkable. Routine laboratory tests and spinal radiography were normal for the Persian cat and were not performed for the DSH cat. A cerebrospinal fluid (CSF) tap was attempted for the Persian cat but aborted because of gross blood contamination, and was not performed for the DSH cat. Magnetic resonance imaging (MRI) of the Persian cat revealed a lesion within the spinal parenchyma at segments C1 to C3 (slightly more left-sided) which was iso- to hypointense on T1-weighted scans and hyperintense on T2-weighted scans, and which enhanced slightly with gadolinium. MRI of the DSH cat revealed a lesion within the spinal parenchyma at segment C7 (predominantly left-sided) which was hypointense on T1-weighted scans and hyperintense on T2-weighted gradient echo scans. Contrast was not administered. The MRI findings in both cases were highly suggestive of acute spinal cord infarction, based upon comparison to human cases. Both cats made full neurological recoveries with supportive treatment only. This paper describes two cases of suspected acute spinal cord infarction in the cat, demonstrates the potential diagnostic value of MRI, and discusses the clinical syndrome of this condition with a brief review of published cases.

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.

Fifty-two total ear canal ablation (TECA) procedures in 44 cats were reviewed. The indication for surgery was neoplasia in 41 per cent of the cats, 86 per cent of which had ceruminous gland adenocarcinoma. Chronic inflammatory or polypoid disease accounted for 50 per cent of surgical procedures. Postoperative complications included Horner's syndrome (42 per cent) and facial paralysis (56 per cent) and these were permanent in 14 per cent and 28 per cent of cases, respectively, with the rest resolving in the ensuing weeks or months. The higher incidence of Horner's syndrome and facial paralysis in the cat, compared to the dog, was attributed to greater fragility of the feline tympanic plexus and facial nerve. The median survival time of cats with ceruminous gland adenocarcinoma was 50-3 months, and did not differ significantly from that for inflammatory or polypoid disease. A potential prognostic indicator for this tumour was the mitotic index (MI): cases with MI < or = 2 survived significantly longer than those with MI > or = 3.

A 5 year old, neutered male, domestic shorthaired cat had acute left hemiparesis and Horner's syndrome. Magnetic resonance imaging (MRI) revealed a loss of the normal signal from the nucleus pulposus of the intervertebral disc at C3/4, narrowing of the ventral subarachnoid space and slight dorsal displacement of the spinal cord and a focal hyperintense lesion affecting the left side of the spinal cord at the same level. The presumptive diagnosis was focal spinal cord oedema associated with intervertebral disc extrusion. A traumatic aetiology was suspected. The cat was treated conservatively and improved gradually over a period of 6 months., (Copyright 2002 ESFM and AAFP.)

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.

Interruption of the postganglionic neuron in the sympathetic pathway to the eye is reported to be a common cause of Horner's syndrome in the cat, although there are few clinical reports identifying the site and nature of the lesion responsible. A case of Horner's syndrome resulting from trauma to the periorbital structures following reduction of temporomandibular joint luxation is presented. In this case, the ophthalmic abnormalities resolved spontaneously over eight days.

An adult domestic female pig (Sus scrofa) exhibited clinical signs of right-sided Horner's syndrome after experimental placement of a woven aortic stent followed by aortic catheterization. The clinical signs included a miotic pupil, ptosis of the upper eyelid, prolapse of the nictitating membrane, and enophthalmos. Necropsy revealed a large mass in the right midcervical region that encased or was in contact with the carotid artery, internal jugular vein, and vagus nerve. Closer evaluation of the mass revealed that it was a small piece of surgical suture material that was embedded within the lumen of the carotid artery. This extrinsic material served as a nidus for an inflammatory reaction involving the vagus nerve.

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 young adult male white Bengal tiger (Panthera tigris tigris) presented with hindlimb ataxia. Cervical and lumbar myelography revealed a compressive lesion of the cord at C(6-7). Corticosteroid therapy and confinement failed to provide lasting remission of signs. A modified, inverted cone ventral slot decompression was used to remove the fibrous material causing cord compression at C(6-7). Temporary Horner's syndrome and laryngeal paresis developed postsurgically because of excessive tissue retraction. The animal recovered normal ambulatory function 6 wk after surgery.

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.)