Using AI Text-to-Image Generation to Create Novel Illustrations for Medical Education: Current Limitations as Illustrated by Hypothyroidism and Horner 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.

Study in Patients With Unilateral Horner Syndrome Supports the Role of Müller's Muscle in the Eyelid-Dark Reflex.

Purpose: A previous study demonstrated upper eyelid retraction synchronized with pupil dilation following a transition from photopic to scotopic conditions. The current study aimed to evaluate the role of Müller's muscle as the efferent arm of this suggested reflex arc. Methods: A video scan of both eyes of patients with unilateral Horner syndrome was performed using optical coherence tomography infra-red mode to document the transition between photopic and scotopic conditions. The affected side with sympathetic denervation was the study group, whereas the contralateral unaffected side of the same patients served as the control group. The pupil diameter, upper eyelid margin-to-reflex distance 1, lower eyelid margin-to-reflex distance 2, and vertical palpebral fissure height were measured. The control group was compared to the healthy subjects of a previous study to verify any compensatory changes to the side contralateral to denervation. Results: Ten patients with unilateral Horner Syndrome were included in the study. Transitioning from photopic to scotopic conditions, the mean change in margin-to-reflex distance 1 in the study and control groups was 315 ± 276 µm (P < 0.05) and 723 ± 432 µm (P = 0.005), respectively. Margin-to-reflex distance 1 and palpebral fissure height were significantly higher in the control group both in photopic (P = 0.005 and P = 0.017, respectively) and scotopic conditions (P = 0.005 and P = 0.007, respectively). The change in margin-to-reflex distance 1 and palpebral fissure height following the transition from light to dark was significantly greater in the control group (P = 0.022). Conclusions: Reflexive eyelid retraction following a transition from photopic to scotopic conditions was significantly diminished in eyelids with sympathetic denervation compared with the unaffected contralateral side of the same patients. This study provides further evidence that the sympathetically innervated Müller's muscle serves as the efferent arm of this reflex.

Selfie-Induced Diagnostic Challenge in Horner Syndrome.

This case report describes an 18-year-old woman with neurofibromatosis type 1 and prior right brachial plexus neurofibroma resection who reported intermittent, unilateral facial flushing after exertion.

Segmental Zoster Paresis Accompanied by Horner's Syndrome.

We herein report a 90-year-old immunocompromised woman who developed right upper limb weakness and right ptosis with a miotic pupil 1 week after oral therapy for zoster on the right T2 dermatome. The right pupil was dilated with instillation of 1% apraclonidine, indicating Horner's syndrome. The patient was treated with intravenous acyclovir and methylprednisolone. Focal weakness related to zoster, generally known as segmental zoster paresis, improved over five months, but Horner's syndrome remained. We suggest that aggressive intravenous treatment should be considered for rare cases of zoster that occur with a combination of these two neurological conditions.

Lessons of the month: Giant cell arteritis with Horner's syndrome and vertebral dissection.

We present a case of an 82-year-old woman presenting with left-sided Horner's syndrome and stroke. She also had a 6-week history of intermittent dizziness, reduced appetite, lethargy, muscle stiffness and weight loss. Examination revealed left temporal artery and left posterior auricular artery tenderness. Her ESR showed 62 mm/hr and imaging showed left vertebral artery dissection. Temporal artery biopsy was positive.The case highlights a rare presentation of giant cell arteritis with Horner's syndrome and left vertebral artery dissection. High clinical suspicion is required to prevent delay in diagnosis and treatment.

Assessment of the changes in cardiac sympathetic nervous activity using the pupil size changes measured in seated patients whose stellate ganglion is blocked by interscalene brachial plexus block.

BACKGROUND: As a side effect of interscalene brachial plexus block (ISBPB), stellate ganglion block (SGB) causes reductions in pupil size (Horner's syndrome) and cardiac sympathetic nervous activity (CSNA). Reduced CSNA is associated with hemodynamic instability when patients are seated. Therefore, instantaneous measurements of CSNA are important in seated patients presenting with Horner's syndrome. However, there are no effective tools to measure real-time CSNA intraoperatively. To evaluate the usefulness of pupillometry in measuring CSNA, we investigated the relationship between pupil size and CSNA. METHODS: Forty-two patients undergoing right arthroscopic shoulder surgery under ISBPB were analyzed. Pupil diameters were measured at 30 Hz for 2 s using a portable pupillometer. Bilateral pupil diameters and CSNA (natural-log-transformed low-frequency power [0.04-0.15 Hz] of heart rate variability [lnLF]) were measured before ISBPB (pre-ISBPB) and 15 min after transition to the sitting position following ISBPB (post-sitting). Changes in the pupil diameter ([right pupil diameter for post-sitting - left pupil diameter for post-sitting] - [right pupil diameter for pre-ISBPB - left pupil diameter for pre-ISBPB]) and CSNA (lnLF for post-sitting - lnLF for pre-ISBPB) were calculated. RESULTS: Forty-one patients (97.6%) developed Horner's syndrome. Right pupil diameter and lnLF significantly decreased upon transition to sitting after ISBPB. In the linear regression model (R2 =0.242, P=0.001), a one-unit decrease (1 mm) in the extent of changes in the pupil diameter reduced the extent of changes in lnLF by 0.659 ln(ms2/Hz) (95% CI [0.090, 1.228]). CONCLUSIONS: Pupillometry is a useful tool to measure changes in CSNA after the transition to sitting following ISBPB.

Acute Horner syndrome secondary to glandular fever due to Epstein Barr virus infection.

We present a clinical situation where a 47-year old female patient consulted with left partial ptosis and miosis that started, two weeks before, with an episode of glandular fever secondary to Epstein-Barr infection. Apraclonidine 0.5% and Phenylephrine 1% drop testing was performed with results consistent with suspected left Horner Syndrome (HS), with a probable postganglionic location. Magnetic Resonance Angiography (MRA) at the moment of the acute presentation did not show any image suggesting carotid arterial dissection but showed irregular narrowing of the left internal carotid artery on its paravertebral extracranial way, consistent to enlarged intra-carotid sheath lymphoid tissue. A week later, a Doppler ultrasound was performed, showing bilateral images compatible with internal carotid arterial dissection. When Postganglionar HS is suspected, the first aetiology to rule out is a carotid arterial dissection because of its potentially fatal outcome and for being a more described entity as postganglionic HS aetiology. However, it is also evidenced that a certain diagnose is not always possible. Furthermore, we describe the enlarged internal carotid artery sheath lymphoid tissue as a possible cause of sympathetic nerve disruption causing a Postganglionar HS, although not common.

Síndrome de Horner agudo secundario a mononucleosis infecciosa por virus de Epstein Barr / Acute Horner syndrome secondary to glandular fever due to Epstein Barr virus infection

Presentamos el caso clínico de una mujer de 47 años que consultó por miosis y ptosis del ojo izquierdo cuyo inicio coincidió, 15 días antes, con un episodio de mononucleosis infecciosa con serología positiva para virus de Epstein-Barr. Se realizaron test con colirios de apraclonidina al 0,5% y fenilefrina al 1%, que apoyaron el diagnóstico de síndrome de Horner(SH) izquierdo posganglionar. En el momento agudo se practicó una angiografía por resonancia magnética que descartó disección carotídea, pero evidenció una imagen de arrosariamiento de la arteria carótida interna izquierda a lo largo de su trayecto extracraneal paravertebral compatible con inflamación del tejido linfático de la capa adventicia de la arteria. Una semana más tarde la ecografía Doppler de troncos supraaórticos con la que se completó el estudio mostraba una imagen compatible con disección de la arteria carótida interna bilateral. Ante un caso de SH posganglionar la primera causa a descartar por su gravedad, y por ser una entidad más ampliamente descrita como etiología del SH de 3.ª neurona, es la disección carotídea. Sin embargo, con este caso ponemos de manifiesto que no siempre se puede llegar a un diagnóstico certero. Asimismo, describimos la inflamación del tejido linfático carotídeo como posible etiología de una lesión de la cadena simpática cervical como causa infrecuente de SH posganglionar (AU)

We present a clinical situation where a 47-year old female patient consulted with left partial ptosis and miosis that started, two weeks before, with an episode of glandular fever secondary to Epstein-Barr infection. Apraclonidine 0.5% and Phenylephrine 1% drop testing was performed with results consistent with suspected left Horner Syndrome (HS), with a probable postganglionic location. Magnetic Resonance Angiography (MRA) at the moment of the acute presentation did not show any image suggesting carotid arterial dissection but showed irregular narrowing of the left internal carotid artery on its paravertebral extracranial way, consistent to enlarged intra-carotid sheath lymphoid tissue. A week later, a Doppler ultrasound was performed, showing bilateral images compatible with internal carotid arterial dissection. When Postganglionar HS is suspected, the first aetiology to rule out is a carotid arterial dissection because of its potentially fatal outcome and for being a more described entity as postganglionic HS aetiology. However, it is also evidenced that a certain diagnose is not always possible. Furthermore, we describe the enlarged internal carotid artery sheath lymphoid tissue as a possible cause of sympathetic nerve disruption causing a Postganglionar HS, although not common (AU)

Horner syndrome after cervical spine corticosteroid injection.

Horner syndrome is a rare condition caused by a lesion of the sympathetic cervical chain. Multiple cervical disorders are associated with such lesions. Here we report the first case of Horner syndrome after cervical facet joint corticosteroid injection.

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.

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.