Transient Horner's syndrome and ipsilateral facial hypopigmentation in an acromelanistic cat.

Horner's syndrome (HS) occurs when the sympathetic nerve pathway is disrupted. This case report describes a cat with acromelanism that developed unilateral facial hypopigmentation concurrently with HS after an oesophagostomy tube was placed. Both the hypopigmentation and HS resolved completely following removal of the oesophagostomy tube.

Le syndrome de Horner (HS) survient lorsque la voie nerveuse sympathique est perturbée. Ce rapport de cas décrit un chat atteint d'acromélanisme qui a développé une hypopigmentation faciale unilatérale en même temps qu'une HS après la mise en place d'une sonde d'oesophagostomie. L'hypopigmentation et l'HS ont disparu complètement après le retrait de la sonde d'œsophagostomie.

El síndrome de Horner (HS) ocurre cuando se interrumpe la transmisión nerviosa a través del nervio simpático. Este caso clínico describe un gato con acromelanismo que desarrolló hipopigmentación facial unilateral al mismo tiempo que HS después de la colocación de una sonda de esofagostomía. Tanto la hipopigmentación como la HS se resolvieron por completo tras la retirada del tubo de esofagostomía.

A síndrome de Horner (SH) ocorre quando a via do nervo simpático é danificada. Este relato de caso descreve um gato com acromelanismo que desenvolveu hipopigmentação facial unilateral concomitantemente com SH após a colocação de um tubo de esofagostomia. Tanto a hipopigmentação quanto a HS se resolveram completamente após a remoção do tubo de esofagostomia.

The evaluation of patient demographics, etiologies and apraclonidine test results in adult Horner's syndrome.

PURPOSE: We aimed to demonstrate the patient demographics, etiologies and apraclonidine test results in adult Horner's syndrome. METHODS: This retrospective study was performed by the analysis of medical data of patients who were given 0.5% apraclonidine test. Patients' past medical history, demographic data, etiologies, accompanying neurological findings and pharmacological test results were assessed. RESULTS: Forty patients (21 females and 19 males) with a mean age of 50.3 ± 11.6 years were evaluated. Apraclonidine 0.5% test was positive in 37 patients (92.5%). An etiology could be identified in 20 patients (central [9 patients, 45%], preganglionic [9 patients, 45%] and postganglionic [2 patients, 10%]). Neurological findings accompanying Horner's syndrome were present in 8 patients. CONCLUSION: Despite detailed investigations, in a significant number of patients with Horner's syndrome an underlying cause may not be detected. Among the identifiable lesions, central and preganglionic involvements are still the first leading causes of Horner's syndrome. In addition, apraclonidine test may not be positive in all patients and a negative response does not exclude Horner's syndrome.

Reversal of Iris Heterochromia in Adult-Onset Acquired Horner Syndrome.

ABSTRACT: Iris heterochromia is typically seen in association with congenital Horner syndrome. A man in his 40s with congenital iris heterochromia, blue in the right and brown in the left, presented with left-sided Horner syndrome. This was associated with recent change in color of his brown left iris to blue similar to the right iris. This case demonstrates a unique case of adult-onset Horner syndrome with reversal of iris heterochromia.

Localizing Thalamomesencephalic Afferent and Efferent Pupillary Defects.

ABSTRACT: A 42-year-old Algerian man presented for binocular oblique diplopia, hypersomnolence with drop attacks, bilateral hearing loss, and thoracic pain. He had a right thalamomesencephalic hemorrhage due to an underlying cavernous malformation treated with subtotal surgical resection. On neuro-ophthalmic examination, the patient had a left relative afferent pupillary defect and a right oculosympathetic efferent pupillary defect (i.e., Horner syndrome) in addition to other thalamomesencephalic eye and neurologic signs (right fourth nerve palsy, hearing loss, hemiparesis, and thalamic pain). Clinicians should recognize the localizing value of this unique constellation of mesencephalic afferent and efferent pupillary defects.

Four common diseases causing sudden blindness or death in the eye emergency department.

Neuro-ophthalmological emergency disorders typically present with symptoms of visual loss, diplopia, ocular motility impairment or anisocoria. The ocular manifestations of these disorders are sometimes indicative of a more serious global neurology disease rather than an isolated ocular disease. The aim of this review is to highlight four important neuro-ophthalmological emergency disorders that must not be missed by an ophthalmologist. These include acute painful Horner's syndrome, painful cranial nerve III palsy, giant cell arteritis and transient ischaemic attack with amaurosis fugax. The delayed diagnosis of these clinical entities puts the patient at risk of blindness or death. Therefore, prompt diagnosis and management of these conditions are essential. This can be acquired from understanding the main signs and symptoms of the disease presentation together with a high index of suspicion while working at a busy eye emergency department.

Bilateral harlequin syndrome, unilateral Horner syndrome, and Riga-Fede disease as presenting features of hereditary sensory and autonomic neuropathy type IV.

Hereditary sensory and autonomic neuropathy (HSAN) type IV, also known as congenital insensitivity to pain with anhidrosis (OMIM 256800), is part of a family of neurodegenerative disorders that manifest with variable sensory and autonomic neuropathies. In this report, we present a unique dermatological finding in a patient with HSAN type IV: bilateral harlequin syndrome that occurred in association with unilateral Horner syndrome, traumatic alopecia and Riga-Fede disease.

Case report and literature review: Horner syndrome subsequent to endoscopic thyroid surgery.

BACKGROUND: Horner syndrome (HS), mainly characterized by symptoms including ptosis, miosis, and anhidrosis on the affected face, is a condition that is well documented but rarely reported as a postoperative complication of thyroidectomy, particularly in endoscopic thyroid surgery (ETS). We hereby report a case of HS due to ETS with a brief literature review on this topic. CASE PRESENTATION: A 31-year-old female was admitted to our hospital with an unexpected physical examination finding of two thyroid nodules that were hypoechoic, had an irregular shape, and exhibited calcification. Subsequently, the results of a fine-needle aspiration (FNA) biopsy from the thyroid nodules and BRAFV600E mutation further confirmed the malignancy of these nodules. Thus, total thyroidectomy combined with central lymph node dissection (CLND) by ETS via the bilateral axillo-breast approach was performed on this patient. Histology confirmed the diagnosis of papillary thyroid microcarcinoma (PTMC) concurrent with Hashimoto's thyroiditis (HT). However, this patient developed HS with ptosis in her left eye on postoperative day 3. All symptoms gradually resolved before the 3-month follow-up. CONCLUSION: HS subsequent to ETS is a rare complication. Thus, standardized and appropriate operative procedures, as well as subtle manipulation, are essential in preventing and reducing the occurrence of HS. In addition, the early diagnosis and management of this rare complication are also important for a favorable outcome.

High thoracic ossification of ligamentum flavum causing partial Horner syndrome.

We report a case of high thoracic ossification of the ligamentum flavum (OLF) causing a partial Horner's syndrome. A 57-year-old man developed a walking disorder, as well as right-sided miosis and anhidrosis. Magnetic resonance imaging demonstrated a spinal cord compressing T2-T3 OLF. The patient improved after surgery.

[Internal carotid artery dissection in the neurologist's practice - a case study]. / Rozwarstwienie tetnicy szyjnej wewnetrznej w praktyce neurologa ­ opis przypadku.

Dissection of the interior carotid artery is rare in the general population. It can however be a potentially life-threatening condition. In the group of patients below 45 years of age, it constitutes a fairly common cause of cerebral stroke. A CASE REPORT: The study describes the case of a patient with the right interior carotid artery dissection, sustained most probably in the course of work. The patient was admitted to hospital for a severe headache of a few days' duration accompanied by Horner's syndrome on the right side. Promptly undertaken diagnostic procedures allowed for immediate diagnosis and application of the right treatment. The check-up examinations performed showed a healed artery and withdrawal of the neurological syndrome. CONCLUSIONS: The case emphasizes the role of prompt diagnosis and treatment in preventing the development of more serious complications. The article refers also to the standards of treating the dissection of the interior carotid artery which still arouse controversies.

Horner syndrome-A rare complication after thyroidectomy for benign thyroid swelling.

Horner syndrome occurring after thyroidectomy is a rare entity and most of the reported cases have happened after surgeries on malignant thyroid swellings. In the present report, we describe a 27-year-old female who developed ptosis, miosis, enophthalmos, and anhidrosis on the second post-operative day after thyroidectomy for benign goiter. Post-operative ultrasound, computed tomography of neck, nerve conduction study, and electromyography of brachial plexus were unremarkable. Patient was kept on conservative management. She was given short course of Prednisolone orally for 2 weeks and was discharged on 150 mcg thyroxine. She had significant improvement in ptosis, miosis, and enophthalmos after six months. Horner syndrome is a rare but an important complication after thyroidectomy which may lead to cosmetic disfigurement. Surgeons should be well aware of this possibility and its presentation for timely recognition and management postoperatively. Early intervention should be done for any reversible cause, i.e., hematoma and oral steroids should be initiated as early as possible.

Horner Syndrome Caused by Internal Jugular Vein Catheterization.

THE RISK FACTORS, clinical manifestation, and preventive measures of Horner syndrome (HS) caused by internal jugular vein (IJV) catheterization were explored. Electronic databases were searched to identify all case reports of HS caused by IJV catheterization. Two authors independently extracted literature characteristics, IJV catheterization method, clinical manifestations, and prognosis data. Twenty case reports (22 patients in total) were included, 18 of which were written in English and the other 2 in Chinese. Patients were between 19 months to 65 years old, and clinical manifestations included ptosis (n = 22), miosis (n = 21), anhidrosis (n = 8), enophthalmos (n = 3), and hoarseness (n = 1). Onset of HS manifestation ranged from a few hours to 19 days after the procedure. Eight patients with ptosis, 6 patients with miosis, and 1 patient with hoarseness recovered during follow-up. Of the 22 patients, 8 underwent more than 1 attempt of IJV catheterization. Six patients experienced accidental carotid artery puncture or hematoma formation during or after IJV catheterization. Ultrasound guidance was applied in 4 patients and anatomic landmark technique was used in the other 18 patients. The left IJV was catheterized in 3 patients, and the right IJV was catheterized in 19 patients. Repeated attempts of puncture, anatomic landmark technique, accidental carotid artery puncture, or hematoma formation may increase the possibility of HS. Ptosis and miosis are the most common manifestations of HS caused by IJV catheterization.

Postoperative Horner Syndrome After Lung Transplantation.

BACKGROUND: Horner syndrome arises from a disruption along the oculosympathetic efferent chain and can be caused by a variety of pathological and iatrogenic etiologies. We present 3 cases of postoperative Horner syndrome after bilateral lung transplantation. METHODS: The electronic health records of 3 patients with iatrogenic Horner syndrome after lung transplantation were examined, including notes from each patient's medical history, operative and postoperative records, and ophthalmology consultation results. A literature review was performed. RESULTS: All 3 of our patients displayed anisocoria and ptosis, symptoms consistent with Horner syndrome, and the patients from Cases 1 and 2 showed reversal of anisocoria after an application of topical apraclonidine. CONCLUSIONS: Ophthalmologists should be aware of the risk of Horner syndrome after lung transplantation.

Causes of Horner Syndrome: A Study of 318 Patients.

BACKGROUND: Some reports have indicated that when a cause for Horner syndrome can be determined, it is most often chest and neck tumors and stroke. Others have suggested that Horner syndrome is more frequently caused by surgical procedures in the neck and chest. These differences may be explained by disparate accrual methods. Therefore, we decided to compare the cause of Horner syndrome in cases where the diagnosis was confirmed by apraclonidine testing conducted by ophthalmologists to cases in which the diagnosis was made entirely on clinical grounds mostly by nonophthalmologists. METHODS: We applied a new search engine to the inpatient and outpatient electronic medical records text at the University of Michigan Medical Center from 1996 to 2018 for Horner syndrome with and without pharmacologic confirmation through ocular instillation of apraclonidine 0.5%. Among apraclonidine-confirmed cases, 159 met inclusion criteria. Among apraclonidine-unconfirmed cases, more than 2,000 cases were identified, so that we included only the first 159 cases that met inclusion criteria. In these 318 cases, we documented patient demographics, ophthalmologic features, imaging, underlying cause, and whether the cause was discovered before or after the diagnosis of Horner syndrome. RESULTS: In the cohort of 159 apraclonidine-confirmed cases of Horner syndrome, a cause was identified in 97 (61%). Procedures in the neck, chest, skull base, and paraspinal region accounted for most of the identified causes, with cervical carotid dissection the next most common cause. In a cohort of 159 cases of Horner syndrome not tested with apraclonidine because the clinical diagnosis appeared firm, procedures again accounted for the largest percentage, but tumor was the next most common cause. In both groups, when a cause for Horner syndrome could be identified, that cause was nearly always known before Horner syndrome was identified. However, in an important minority of cases, mostly involving carotid dissection or tumor, the identification of Horner syndrome was critical to the discovery of those conditions. CONCLUSIONS: The prevalence of causes of Horner syndrome depends on the accrual method. Among pharmacologically-confirmed cases, the cause was often undetermined or due to a preceding neck or chest procedure. Among pharmacologically-unconfirmed cases, a substantial proportion had also been caused by neck and chest procedures, but tumors in that region were also common. When a cause of Horner syndrome was found in both cohorts, it was usually known before Horner syndrome was discovered, making Horner syndrome an afterthought. However, in an important minority of cases where the cause was not yet known, the identification of Horner syndrome was valuable in leading to important diagnoses such as carotid dissection and tumor.

A Rare Catheter Complication in a Patient With Neuroblastoma: Horner's Syndrome.

Neuroblastoma is the most common type of extracranial solid tumor during childhood. Clinical presentation includes ipsilateral ptosis, myosis, anhydrosis and enophthalmos. The case of a 2.5-year-old boy who had a complaint of constriction of the left pupil for 3 days is presented. In the physical examination, the pupil of the OD was moderately dilated; there was myosis on the OS and ptosis on the left eyelid. Horner syndrome was considered due to these findings. History of the patient revealed that a central venous catheter insertion procedure was tried from the left side.

Investigation of Pupillary Changes After Carotid Endarterectomy and Carotid Stent Placement Using Automated Pupillometry.

INTRODUCTION: Horner's syndrome has been reported after carotid artery endarterectomy (CEA) and carotid artery stenting (CS). This study evaluates pupillary changes after these procedures using automated pupillometry. METHODS: Retrospective analysis from a prospective database of pupillometry readings. Cases (14 patients with CEA/CS) were matched to controls (14 patients without CEA/CS). t test models were constructed to examine pupillary light reflex measures for CEA, CS, and controls. RESULTS: The 28 subjects had a mean age of 70 years, 50% were male, and 96% were Caucasian. There was no significant difference in the mean pupil size, constriction velocity (CV), dilation velocity (DV) between the procedural side compared to the contralateral side. However, the mean DV in the left eye after a left sided procedure among CS patients (.67) was lower than mean DV in left eye among controls (.88; P < .0001) and patients undergoing CEA (1.03; P < .0001). DISCUSSION: CS may result in disruption of the carotid artery plexus and decreased sympathetic response thereby reducing DV in the ipsilateral pupil. In addition, decreased CV can also been seen. CONCLUSION: The findings confirm and extend those of previous authors suggesting that pupillary changes may be seen after CS and automated handheld pupillometry may aid in the detection of Horner Syndrome.

The pioneer ophthalmologist Johann Friedrich Horner (1831-1886) and the clinical anatomy of the homonymous syndrome.

Johann Friedrich Horner is remembered in ophthalmology due to his brief report in the German scientific journal 'Klinische Monatsblatter fur Augenheilkunde', in which emphasized the clinical value of a cluster of external signs of damage to the cervical sympathetic nerve. Although J .F .Horner was not the first to describe such a syndrome, he was credited with the nomination. For the French, Francois Pourfour du Petit was the pioneer in that case. Born in Zurich, travelled Europe to be further educated, becoming later on Professor and Director of the University Clinic of Ophthalmology in his native city. In conclusion, J .F .Horner's adamantine character, hard work, assiduous teaching and skills in eye surgery made him one of the main contributors for the evolution of ophthalmology in the nineteenth century Central Europe.

Horner Syndrome With Ipsilateral Wing Paresis in a Wild, Juvenile Yellow-Tailed Black Cockatoo (Calyptorhynchus funereus).

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.

Harlequin Syndrome in Acute Thalamic Hemorrhage.

Harlequin syndrome is a disorder of the autonomic nervous system. It clinically presents as a distinct line of hemifacial sympathetic denervation. We describe a case of Harlequin syndrome with co-existing central first-order Horner syndrome in the setting of a large thalamic hemorrhage with intraventricular extension.

A review of Horner's syndrome in small animals.

Horner's syndrome arises from dysfunction of the oculosympathetic pathway and is characterized by miosis, enophthalmos, protrusion of the third eyelid, and ptosis. It has been recognized in a wide variety of breeds and ages in small animal patients. The oculosympathetic pathway is a 3-neuron pathway. The central/first order neuron arises from the hypothalamus and extends down the spinal cord. The preganglionic/second order neuron arises from the first 3 thoracic spinal cord segments and travels through the thorax and cervical region until it synapses at the cranial cervical ganglion. The postganglionic/third order neuron travels from this ganglion to the orbit. Topical application of cocaine is the gold standard for differentiating Horner's syndrome from other causes of miosis. Topical 1% phenylephrine allows for identification of a post-ganglion Horner's syndrome. Numerous etiologies have been reported for Horner's syndrome, but idiopathic disease is most common. Ancillary diagnostics include otoscopic examination, thoracic radiographs, or advanced imaging. Treatment and prognosis are determined by the etiology.

Examen du syndrome de Horner chez les petits animaux. Le syndrome de Horner provient d'une dysfonction de la voie oculo-sympathique et est caractérisée par la miose, l'enophtalmie, la protrusion de la troisième paupière et la ptose. Elle a été reconnue chez une grande variété de races et d'âges chez les patients petits animaux. La voie oculo-sympathique est une voie à trois neurones. Le neurone central/de premier ordre provient de l'hypothalamus et s'étend vers le bas sur la colonne vertébrale. Le neurone préganglionnaire/de deuxième ordre provient des trois premiers segments thoraciques de la colonne vertébrale et se déplace dans le thorax et la région cervicale jusqu'à la synapse au ganglion cervical crânien. Le neurone postganglionnaire/de troisième ordre se déplace de ce ganglion jusqu'à l'orbite. L'application topique de cocaïne est le test de référence pour la différenciation du syndrome de Horner des autres causes de miose. La phényléphrine topique 1 % permet l'identification d'un syndrome de Horner postganglionnaire. Plusieurs étiologies ont été signalées pour le syndrome de Horner, mais la maladie idiopathique est la plus commune. Les diagnostics auxiliaires incluent l'examen otoscopique, des radiographies thoraciques ou une imagerie avancée. Le traitement et le pronostic sont déterminés par l'étiologie.(Traduit par Isabelle Vallières).