Diagnosis Of Horner's Syndrome Research Articles

Horner syndrome: Clinical image

A 34-year-old man was referred by his primary care physician for left blepharoptosis, ipsilateral miosis, and left facial anhidrosis (Figure 1). His medical history included a recent thoracotomy of the upper left hemithorax for extirpation of a neurogenic mediastinal tumor. A diagnosis of Horner syndrome was made.

PANCOAST TUMOR PRESENTING WITH HORNER SYNDROME: A CASE REPORT

Case Report: A 50-year-old man was referred to Dr. Moewardi General Hospital with history of right chest pain that radiate to the right back and hand for 2 months. His complaint did not improve with medication and physical therapy. On physical examination we observed multiple nodules on the right axilla, scapula, and colli region. Neurological examination revealed right sided partial ptosis, anisocoria, ipsilateral weakness, and ipsilateral allodynia, and anhidrosis T1 dermatome. CT-scan showed a right lung mass in the superior lobe of the apical segment. The diagnosis of Horner syndrome is then established caused by multiple lymphadenopathies. His symptoms then relieved after lymphadenectomy. Conclusion: Horner syndrome, characterized by ipsilateral pupillary anisocoria, ptosis and anhidrosis, is one of the complications of Pancoast tumor invasion to the sympathetic nervous system in the C8, T1, and T2 nerve territory.

Automatic Detection of Horner Syndrome by Using Facial Images.

Horner syndrome is a clinical constellation that presents with miosis, ptosis, and facial anhidrosis. It is important as a warning sign of the damaged oculosympathetic chain, potentially with serious causes. However, the diagnosis of Horner syndrome is operator dependent and subjective. This study aims to present an objective method that can recognize Horner sign from facial photos and verify its accuracy. A total of 173 images were collected, annotated, and divided into training and testing groups. Two types of classifiers were trained (two-stage classifier and one-stage classifier). The two-stage method utilized the MediaPipe face mesh to estimate the coordinates of landmarks and generate facial geometric features accordingly. Then, ten machine learning classifiers were trained based on this. The one-stage classifier was trained based on one of the latest algorithms, YOLO v5. The performance of the classifier was evaluated by the diagnosis accuracy, sensitivity, and specificity. For the two-stage model, the MediaPipe successfully detected 92.2% of images in the testing group, and the Decision Tree Classifier presented the highest accuracy (0.790). The sensitivity and specificity of this classifier were 0.432 and 0.970, respectively. As for the one-stage classifier, the accuracy, sensitivity, and specificity were 0.65, 0.51, and 0.84, respectively. The results of this study proved the possibility of automatic detection of Horner syndrome from images. This tool could work as a second advisor for neurologists by reducing subjectivity and increasing accuracy in diagnosing Horner syndrome.

Safety of apraclonidine eye drops in diagnosis of Horner syndrome in an outpatient pediatric ophthalmology clinic

To describe the efficacy and systemic side effects of apraclonidine drops 0.5% in children clinically suspected of having Horner syndrome. The medical records of patients with clinically suspected Horner syndrome who underwent testing with apraclonidine 0.5% eyedrops were reviewed retrospectively. The following data were retrieved from the record: allergic reactions, somnolence, shallow respiration, pallor, or excessive fussiness noted by the examiner or parents. A total of 46 patients presenting with anisocoria and tested with apraclonidine 0.5% were included. Of these, 15 had a positive result, with reversal of anisocoria. The mean age of patients was 3.2 years (median, 0.91; mode, 0.25 years). Twenty-four patients were ≤1 year of age; 19 were ≤6 months. No systemic side effects were noted during the examination or reported by parents in any patients. The use of topical apraclonidine eyedrops has been described as an effective test for Horner syndrome. However, concerns have been raised regarding the potential systemic side effects in children, especially those under the age of 6 months. In our cohort, no systemic side effects were reported, including in those under 6 months of age.

A tale of ptosis, pharmacological tests, and Pancoast tumour

Horner syndrome (HS) classically presents with ipsilateral blepharoptosis, pupillary miosis, and facial anhidrosis and caused by a lesion along the oculosympathetic pathway from the hypothalamus to eye. The diagnosis of HS in a patient presenting with partial ptosis may be easily missed in the Asian patient. This is mainly due to the dark irides, making detection of anisocoria on direct visualization difficult. Index of suspicion must be high, especially in the absence of any extraocular motility or lid abnormalities. We present a case where a healthy asymptomatic patient presented with partial ptosis and diagnosis of HS was eventually confirmed through pharmacological tests. Non-targeted imaging with a simple chest X-ray revealed an apical lung lesion which eventually turned out to be malignant. Although it is a typical textbook description, this case highlights the importance of careful history and examination in an otherwise healthy patient presenting with mild ptosis.

Nationwide population-based incidence and etiologies of pediatric and adult Horner syndrome.

To determine age- and sex-specific incidence and possible etiologies of pediatric and adult Horner syndrome in South Korea. A nationwide, population-based, cohort study using data from the Korean National Health Claims database from 2007 to 2018. All patients with Horner syndrome from the entire Korean population (n = 51,629,512) were included. To find possible causes of Horner syndrome, we searched concurrent codes for systemic diseases, trauma, or surgical procedures. A total of 139 pediatric patients (59.7% male) and 1331 adults (51.0% male) were newly diagnosed as having Horner syndrome. The cumulative incidence was 2.12 (95% CI 2.08-2.17) per 100,000 pediatric population and 2.95 (2.94-2.96) per 100,000 adults. The peak incidence occurred at 0-4years of age in the pediatric population, and at 50-54years in the adult population. A total of 835 (56.8%) patients had underlying conditions or related surgical procedures associated with Horner syndrome. The underlying causes were recognized in 695 (83.2%) patients before the diagnosis of Horner syndrome, in 75 (9.0%) patients at the same time as the Horner syndrome diagnosis, and in 65 (7.8%) patients after the diagnosis of Horner syndrome. There were four cases of Horner syndrome that preceded neuroblastoma diagnosis. The most common tumor related with Horner syndrome was that of the thyroid in the adult population. This study determined the estimated incidence and possible causes of pediatric and adult Horner syndrome. As Horner syndrome with unknown etiologies may harbor serious malignancy, extensive evaluations are required, especially in children.

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.

Clinical Presentations of Pediatric Horner Syndrome

Purpose: To understand the multiple signs of Horner syndrome and to recommend protocols for pediatricians to obtain an accurate diagnosis of Horner syndrome. Methods: The medical records of 17 pediatric patients with Horner syndrome, neonates to eighteen years of age, were collected and analyzed. Data recorded included age, presenting symptoms, other medical history, allergies, medications, pupil size, presence of anhidrosis, and presence of ptosis. From the available pupil sizes, average degree of anisocoria was calculated. Results: All 17 patients had other clinical findings of Horner syndrome in addition to anisocoria. On initial evaluation, 100% had ptosis and 25% had anhidrosis. Of the available pupil size data, the average level of anisocoria was 2.06 mm, with a standard deviation of 1.17 mm. Conclusion: Physicians are reminded to measure pupil size to determine the degree of anisocoria when present, as it may help distinguish benign conditions from underlying pathology. Educating pediatricians on measurement of anisocoria and additional signs of Horner syndrome will help with proper referral patterns.

Evaluation and neuroimaging of the Horner syndrome

ObjectiveTo define the efficacy, safety, and cost-effectiveness of a single centre’s approach to evaluating Horner syndrome (HS) including a simplified single neuroimaging protocol. DesignCase series study. ParticipantsMedical records of 34 patients diagnosed with HS at Houston Methodist Hospital (HMH) were reviewed after obtaining Institutional Review Board approval. MethodsA retrospective chart review was performed for all patients presenting with the diagnosis of HS at the HMH from January 2010 to November 2013. All patients had diagnostic imaging with contrast-enhanced brain magnetic resonance imaging (MRI) extending to the T2 level in the chest. They had either documented causative diagnosis for HS or were “idiopathic.” Efficacy and cost-effectiveness of the proposed neuroimaging technique were analyzed compared with other recommended protocols. ResultsWe initially reviewed 34 charts with presumed diagnosis of HS; 27 charts were included in the analysis. The average age of patients was 46.6 years. Eleven patients (41%) had a final diagnosis of HS secondary to a proven cause, and 16 patients (59%) were diagnosed as “idiopathic.” Ten patients (63%) in the idiopathic group had follow-up, and none of those with follow-up had an alternative cause. The estimated cost of our recommended MRI protocol was US$667.76 without magnetic resonance angiography (MRA) or US$1501.71 with MRA. ConclusionsA single contrast-enhanced brain MRI extending to the T2 level in the chest is an effective and simple means of ruling out life-threatening and other causative factors of HS. Compared with previous imaging recommendations, this proposed protocol may be simpler for clinicians to use and more cost-effective.

Adult Horner’s syndrome: a combined clinical, pharmacological, and imaging algorithm

The diagnosis of Horner's syndrome (HS) can be difficult, as patients rarely present with the classic triad of ptosis, miosis, and anhydrosis. Frequently, there are no associated symptoms to help determine or localise the underlying pathology. The onset of anisocoria may also be uncertain, with many cases referred after incidental discovery on routine optometric assessment. Although the textbooks discuss the use of cocaine, apraclonidine, and hydroxyamphetamine to diagnose and localise HS, in addition to reported false positive and negative results, these pharmacological agents are rarely available during acute assessment or in general ophthalmic departments. Typically, a week is required between using cocaine or apraclonidine for diagnosis and localisation of HS with hydroxyamphetamine, leaving the clinician with the decision of which investigations to request and with what urgency. Modern imaging modalities have advanced significantly and become more readily available since many of the established management algorithms were written. We thus propose a practical and safe combined clinical and radiological diagnostic protocol for HS that can be applied in most clinical settings.

Irreversible Horner’s syndrome diagnosed by aproclonidine test due to benign thyroid nodule

We are reporting an irreversible Horner Syndrome (HS) in a patient with benign thyroid gland nodule in which thyroidectomy was performed for treatment. A 37-year-old female was admitted to our clinic with a swelling in the left lobe of the thyroid gland and ptosis at the left eyelid. The clinical diagnosis of HS was confirmed pharmacologically by aproclonidine. Histopathologic examination of thyroidectomy specimen was reported as benign nodule. To the best of our knowledge, this is a very rare report in terms of thyroid benign nodule associated with irreversible HS due to cervical sympathetic chain compression.

El uso de apraclonidina en el diagnóstico del Síndrome de Horner

We present four cases: two males with Horner Syndrome, who were diagnosed by means of apraclonidine 0.5% and cocaine 4% tests respectively. Two children with anisocoria, one of whom had Horner Syndrome confirmed with apraclonidine 1% and the other, in whom an apraclonidine test ruled out this syndrome but in whom pilocarpine 0.125% confirmed Adie's pupil. Apraclonidine drops (1% and 0.5%) may aid in the diagnosis of Horner Syndrome and are easier to obtain than cocaine.

Anisokorie und Übelkeit

We present the case of a 40-year-old female patient with sudden onset of anisocoria and unilateral ptosis of the left eye. With the exception of several previous episodes of nausea and vomiting, mild headache and tiredness, combined with the early death of the patient's mother following aortic rupture, patient history and clinical condition showed no pathological findings. Following indicative findings on duplex sonography, a dissection of the left internal carotid artery from its origin to its distal section was detected on CT angiography of the brain vessels and the diagnosis of Horner syndrome due to internal carotid artery dissection was made. Since this condition is associated with serious embolic complications, prompt treatment following diagnosis is of utmost importance. Our patient was treated conservatively using PTT (partial thromboplastin time)-effective heparinisation. Regular checks including kidney ultrasound, blood pressure measurement, imaging and continuous therapy with acetylsalicylic acid are recommended.

Apraclonidine hydrochloride: pharmacology and clinical use

Apraclonidine hydrochloride is a potent and relatively selective α2-adrenergic receptor agonist. The α2-adrenoceptor is widely expressed in the eye, located in regions of the anterior segment including the cornea, trabecular meshwork, iris, ciliary body epithelium and ciliary muscle and in the posterior segment in structures such as the retina, retinal pigment epithelium and choroid. Apraclonidine is useful in the diagnosis of Horner Syndrome. It is also used to prevent intraocular pressure spikes after anterior segment laser surgery or following cataract surgery. It can also be used as a temporary adjunctive drug for patients with open-angle glaucoma on maximal therapy before laser trabeculoplasty or surgery, and as a treatment for ptosis secondary to injections of botulinum toxin on the upper third of the face.

Medical Decision Making

Topical cocaine is used to confirm the clinical diagnosis of ocular sympathetic denervation, or Horner Syndrome (HS). Cocaine blocks re-uptake of norepinephrine (NE) by sympathetic nerve terminals in the iris dilator muscle, transiently increasing its concentration in the synaptic junction. Norepinephrine activates alpha1 receptors in the iris dilator to cause pupil dilation. In HS, cocaine fails to dilate the affected pupil as much as the unaffected pupil, but its indirect action makes it a weak dilator, and the test can give equivocal results. Cocaine is also a controlled substance and therefore difficult to obtain. A practical and reliable alternative to cocaine is apraclonidine, an ocular hypotensive agent that has a weak direct action on alpha1 receptors and therefore minimal to no clinical effect on the pupils of normal eyes. Patients with HS have denervation supersensitivity of the alpha1 receptors in the iris stroma of the affected eye, making the pupil dilator responsive to apraclonidine. In patients with HS, reversal of anisocoria occurs after bilateral instillation of apraclonidine 1% or 0.5%. Two cases that demonstrate this effect are reported. Apraclonidine should be considered a candidate to replace cocaine in the pharmacologic diagnosis of HS if a gold-standard comparison study confirms these results.

Adverse effects of apraclonidine used in the diagnosis of Horner syndrome in infants

Apraclonidine, a selective alpha(2)-agonist, was developed to lower intraocular pressure and minimize the systemic side effects associated with the use of its parent drug, clonidine.(1) An investigation of the site of action of apraclonidine incidentally uncovered a reversal of anisocoria in patients with absent sympathetic innervation of one pupil (Horner syndrome) due to its alpha(1)-effect on a pupil with denervation supersensitivity.(2) It has been used as a diagnostic test for Horner syndrome.(3,4) We report adverse effects of topical apraclonidine when used in the diagnosis of Horner syndrome in infants.

Comparing efficacies of 0.5% apraclonidine with 4% cocaine in the diagnosis of Horner Syndrome in pediatric patients

This interesting study compared the use of cocaine 4% and apraclonidine 0.5% in the diagnosis of Horner syndrome in pediatric patients. Ten subjects ranging in age from 1 to 18 years were tested using a crossover study design in which patients, using either apraclonidine or cocaine, were evaluated 1 week apart. The effect on pupil size was measured using external photography 1 hour following drop instillation.

Pediatric Horner Syndrome: Etiologies and Roles of Imaging and Urine Studies to Detect Neuroblastoma and Other Responsible Mass Lesions

To evaluate the frequency of etiologies of Horner syndrome in children and suggest an imaging and laboratory diagnostic protocol to evaluate for neuroblastoma and other lesions in a child presenting with Horner syndrome and no known cause. Retrospective chart and data review. A retrospective review of all children seen at a large pediatric neuro-ophthalmology referral center with a diagnosis of Horner syndrome between 1993 and 2005 with particular attention to underlying etiologies and the results of imaging and urine catecholamine studies. Fifty-six children met criteria for Horner syndrome and further review. Twenty-eight children (50%) had no previously identified cause for Horner syndrome. Of these children, 24 (85.7%) had urine catecholamine metabolite studies, and all had negative results. Twenty (71.4%) had complete modern imaging of the brain, neck, and chest. Of the 18 children who had complete imaging and urine studies, responsible mass lesions were found in six (33%). Four had neuroblastoma, one had Ewing sarcoma, and the other had juvenile xanthogranuloma. Of all patients (diagnosis known and unknown), neoplasm was the etiology in 13 of 56 (23%) of patients. We confirm that Horner syndrome in a child of any age without a surgical history requires a complete examination to exclude a mass lesion. In such patients, we recommend brain, neck, and chest magnetic resonance imaging (MRI) with and without contrast as well as urinary catecholamine metabolite testing. However, imaging is more sensitive than urine testing in this setting.

Efficacy of Apraclonidine 0.5% in the Diagnosis of Horner Syndrome in Pediatric Patients Under Low or High Illumination

To evaluate the efficacy and safety of apraclonidine 0.5% in the diagnosis of Horner syndrome in pediatric patients. Prospective, interventional case series. Ten pediatric patients with a diagnosis of Horner syndrome and 10 age-matched controls with physiologic anisocoria underwent pharmacological testing with apraclonidine. The difference between the pupil diameters of both eyes under low (room light off) and high (room light on) ambient illumination before and one hour after apraclonidine was instilled was recorded. Any adverse effects during the examination or reported by the patient's parents were recorded. The mean differences in pupil diameters before and after apraclonidine testing in the Horner syndrome group were -2.05 mm and 0.97 mm, respectively, under low illumination (P = .0049) and -1.48 mm and 1.1 mm, respectively, under high illumination (P = .0051). Three patients with Horner syndrome showed positive values (reversal of anisocoria) only under high ambient illumination, but not under low illumination. There was no statistical difference in the mean differences in pupil diameter before and after apraclonidine testing in the control group. Conjunctival hyperemia was noted in two patients with Horner syndrome and in three patients in the control group. No systemic adverse effects were noted during the examination or were reported by patients' parents. The application of apraclonidine in pediatric patients is safe and effective in the diagnosis of Horner syndrome. The reversal of anisocoria was more obvious under high (room light on) ambient illumination.

Comparing Efficacies of 0.5% Apraclonidine with 4% Cocaine in the Diagnosis of Horner Syndrome in Pediatric Patients

The aim of this study was to compare the efficacy of 0.5% apraclonidine with that of 4% cocaine and to evaluate its safety in the diagnosis of Horner syndrome in pediatric patients. This was a randomized, crossover study, wherein 10 patients with a probable diagnosis of Horner syndrome were assigned to undergo pharmacological testing with 4% cocaine and 0.5% apaconidine. The difference in the pupil diameters of each eye was recorded under dim light before and 1 h after 0.5% apraclonidine or 4% cocaine was instilled. Any adverse effects were noted during examination or reported by the patients' parents were recorded. The mean differences in pupil diameter before and after 4% cocaine testing were -2.08 and -2.97 mm, respectively (P = 0.0047). All patients had an anisocoria greater than 1 mm after 4% cocaine testing. The mean difference in pupil diameter before and after 0.5% apraclonidine was instilled were -2.04 and +1.08 mm, respectively (P = 0.005). All patients showed a reversal of anisocoria after 0.5% apraclonidine testing. Conjunctival hyperemia was noted in 2 patients, but systemic adverse effects were not noted during examination nor reported by the patients' parents. The application of 0.5% apraclonidine in pediatric patients is safe and effective in the diagnosis of Horner syndrome.