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Background Polyneuritis cranialis (PNC), a rare variant of Guillain-Barré syndrome (GBS), is usually characterized by ocular and pharyngeal weakness without obvious numbness or weakness of the limbs or ataxia. Horner’s syndrome is extremely rare in patients with PNC. Here, we describe a case of GBS presenting with acute PNC and unilateral Horner syndrome. Case presentation A 53-year-old male presented with headache, abducent paresis, peripheral-type facial palsy, bulbar type dysarthria, decreased gag reflex and tongue palsy. Neurological examination showed Cranial Nerve V, VI, VII, IX, X and XII were affected, and Horner’s syndrome was observed. Cerebrospinal fluid analysis showed albuminocytologic dissociation. Sensorimotor conduction velocity and needle electromyography of limbs were normal. Magnetic resonance imaging of brain was normal. Finally, the patient was diagnosed as PNC combined with Horner’s syndrome. The patient received plasma exchange and intravenous immunoglobulin, which relieved the symptoms rapidly. Conclusion GBS presenting only as Horner syndrome and PNC is a challenge for etiological diagnosis. Clinicians need to know enough to distinguish GBS and its variants from other potential similar diseases.

Abstract A 5-year-old male golden retriever was presented after a subacute onset of left-sided Horner syndrome (HS). The dog had anisocoria with left-sided miosis, ptosis of the upper eyelid, and third eyelid protrusion in the left eye. Because of the absence of additional neurological abnormalities, clinical signs were suggestive of left isolated HS, and the lesion was localized at the level of either the preganglionic or postganglionic neuron of the sympathetic chain. Magnetic resonance imaging (MRI) of the head and total body computed tomography (CT) identified marked narrowing and irregularity of the left internal carotid artery (ICA) in addition to loss of normal vessel flow-void and T1-weighted hyperintensity in the lumen of the left ICA. Except for these abnormalities, MRI and CT results were normal. These findings were suggestive of left internal carotid artery dissection (ICAD), suggesting that ICAD should be considered as a possible differential diagnosis of HS in dogs.

ObjectiveHorner’s syndrome (HS) is characterised by a triad of ocular miosis, ptosis and anhidrosis. HS may be a subtle sign of occult pathology in otherwise asymptomatic children, neuroblastoma (NBL) being the the most common associated malignant tumour. Despite such knowledge, the incidence of underlying malignancy in children with HS remains unclear and robust evidence to guide best clinical practice is sparse. We performed a systematic review of the literature with the aim of identifying the incidence of NBL in children with HS of unknown aetiology, and establishing if screening for NBL should be routinely performed in this patient population.MethodsSystematic review of the literature (PubMed and Ovid/Medline database, 1961–2018).ResultsThe initial search identified 334 manuscripts, of which 8 studies were included in the final analysis. All reports were single-centre retrospective studies without control groups and included a total of 152 patients (age range 0–20 years). All studies investigated patients with HS but without previously established diagnosis. In the studies included, 17 out of a total of 152 patients were diagnosed with a space-occupying lesion. 12 out of the 152 patients were subsequently detected with NBL.ConclusionHS in children may be the first sign of occult malignancy. We report the first systematic review that comprehensively investigates the incidence of malignancy in this unique patient cohort. We show that HS of unknown aetiology in children warrants further investigation(s) to exclude an underlying space-occupying lesion. This should include cross-sectional imaging of the brain, neck and thorax, plus urinary catecholamines for prompt diagnosis and treatment.

M-COPA (1), which contains diene and 3-picolylamine moieties in its side chain and seven stereogenic centers in a multisubstituted octalin skeleton, strongly inhibits the growth of several cancer cell lines. Expecting the improvement of conformational flexibility of basic and coordinating 3-pyridylmethylamino group on M-COPA and its physical properties, we efficiently synthesized its amine analogs by replacing its amide group with an amino group through the Weinreb amide-type Horner–Wadsworth–Emmons reaction. The cytotoxic properties of 1 and its analogs were evaluated against NCI-H226, a lung cancer cell line, HeLa, a cervical cancer cell line, and GIST-T1, a gastrointestinal stromal tumor cell line. The evaluation results indicated that the structural alteration from amide moiety to amine moiety lowered the pharmacological activity but remained strong cytotoxicity.

Horner syndrome is a rare complication following thyroid surgery, typically presenting with ptosis, miosis, and ocular congestion. We report the case of a 30-year-old female diagnosed with papillary thyroid carcinoma who underwent left thyroid lobectomy, isthmectomy, and comprehensive left cervical lymph node dissection. On the first postoperative day, the patient developed left-sided ptosis, a constricted pupil, blurred vision, and conjunctival congestion, leading to a clinical diagnosis of Horner syndrome. Initial treatment with oral neurotrophic agents provided limited improvement, with persistent ocular symptoms. Four months postoperatively, the introduction of topical naphazoline eye drops resulted in marked improvement. Ptosis diminished, the palpebral fissure returned to normal, pupil sizes equalized, and conjunctival congestion resolved, with effects lasting approximately 2 h after each application. This case report summarizes the mechanisms of injury leading to Horner syndrome after thyroid surgery, highlighting the importance of understanding the anatomical relationship between the thyroid gland and the cervical sympathetic nerve trunk during thyroidectomy to minimize the risk of Horner syndrome. This case highlights the potential role of topical α1-adrenergic agonists in managing postoperative Horner syndrome and underscores the need for intraoperative nerve protection strategies.

Disruption of cranial sympathetic tone leads to the symptom complex of miosis, ptosis, and hemifacial anhidrosis. It is widely believed that this phenomenon was discovered in 1869 by the Swiss ophthalmologist Johann Friedrich Horner, and as a result, the term Horner syndrome has become synonymous with the clinical presentation. However, the syndrome that would become Horner syndrome had actually been described several times before his report. François Pourfour du Petit documented the ocular effects of sympathetic trunk lesions in animal studies in 1727. Claude Bernard identified the full clinical triad in animal studies in 1852, and as a result, the condition is sometimes called Bernard syndrome. There were also 2 previous reports of ptosis and miosis resulting from sympathetic nerve damage in humans1 by Edward Selleck Hare in 1838 associated with brachial plexus tumor, and the other by Silas Weir Mitchell in 1864 associated with a gunshot wound to the neck. Although Horner was the first to objectively characterize the co-occurrence of vasomotor and ocular changes in a human patient, he did not identify the etiology of the condition, discuss its relationship to the sympathetic nervous system, or reference any of the previous studies in animals or humans. It is possible that a lack of familiarity with previous investigations delayed the full appreciation of the mechanism underlying this disorder.

PurposeWe aimed to demonstrate the patient demographics, etiologies and apraclonidine test results in adult Horner's syndrome.MethodsThis 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.ResultsForty 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.ConclusionDespite 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.

Our research letter investigates the potential, as well as the current limitations, of widely available text-to-image tools in generating images for medical education. We focused on illustrations of important physical signs in the face (for which confidentiality issues in conventional patient photograph use may be a particular concern) that medics should know about, and we used facial images of hypothyroidism and Horner syndrome as examples.