Adie's tonic pupil after COVID-19: a case report and literature review.

Objective: Various neurological complications have been reported after COVID-19. The study aimed to document an unusual case of Adie's tonic pupil following COVID-19. Methods: The study was a case report. Results: A 28-year-old female had suffered a flu-like disease about 2 months before and the SARSCoV-2 polymerase chain reaction test at that time was positive. Two weeks after infection she noticed an asymmetry between the pupils. The only pathological finding on examination was anisocoria with a larger left pupil in ambient light. Light reflexes were observed in the right eye, while in the left eye, they were absent. Also, there was no near response in the left pupil. A 0.1% pilocarpine test results validated Adie's pupil diagnosis. After one year of follow-up, the anisocoria decreased but did not completely recover. Discussion: COVID-19 may cause damage to neural structures due to autoimmune ways by activating immune pathways or because of vascular complications that may affect the vasa nervorum. Adie's tonic pupil is often idiopathic, but it may develop following viral infection. Conclusions: Ocular complications that involve pupil abnormalities may manifest following COVID-19. In the cases of Adie's tonic pupil, infectious diseases, including COVID-19, should be questioned. Abbreviations: RT PCR = reverse transcription polymerase chain reaction.

Anisocoria After Direct Light Stimulus is Associated with Poor Outcomes Following Acute Brain Injury.

BACKGROUND: Assessing pupil size and reactivity is the standard of care in neurocritically ill patients. Anisocoria observed in critically ill patients often prompts further investigation and treatment. This study explores anisocoria at rest and after light stimulus determined using quantitative pupillometry as a predictor of discharge modified Rankin Scale (mRS) scores. METHODS: This analysis includes data from an international registry and includes patients with paired (left and right eye) quantitative pupillometry readings linked to discharge mRS scores. Anisocoria was defined as the absolute difference in pupil size using three common cut points (> 0.5 mm, > 1 mm, and > 2 mm). Nonparametric models were constructed to explore patient outcome using three predictors: the presence of anisocoria at rest (in ambient light); the presence of anisocoria after light stimulus; and persistent anisocoria (present both at rest and after light). The primary outcome was discharge mRS score associated with the presence of anisocoria at rest versus after light stimulus using the three commonly defined cut points. RESULTS: This analysis included 152,905 paired observations from 6,654 patients with a mean age of 57.0 (standard deviation 17.9) years, and a median hospital stay of 5 (interquartile range 3-12) days. The mean admission Glasgow Coma Scale score was 12.7 (standard deviation 3.5), and the median discharge mRS score was 2 (interquartile range 0-4). The ranges for absolute differences in pupil diameters were 0-5.76 mm at rest and 0-6.84 mm after light. Using an anisocoria cut point of > 0.5 mm, patients with anisocoria after light had worse median mRS scores (2 [interquartile range 0-4]) than patients with anisocoria at rest (1 [interquartile range 0-3]; P < .0001). Patients with persistent anisocoria had worse median mRS scores (3 [interquartile range 1-4]) than those without persistent anisocoria (1 [interquartile range 0-3]; P < .0001). Similar findings were observed using a cut point for anisocoria of > 1 mm and > 2 mm. CONCLUSIONS: Anisocoria after light is a new biomarker that portends worse outcome than anisocoria at rest. After further validation, anisocoria after light should be considered for inclusion as a reported and trended assessment value.

A Case of Epstein-Barr Virus Encephalitis and Orbital-Face Inflammation.

Epstein-Barr virus (EBV) can cause follicular conjunctivitis, keratitis, oculoglandular syndrome, meningitis, and encephalitis. We report a 54-year-old Hispanic male who presented with right pupil-involved complete ophthalmoplegia, orbital and masticatory muscle inflammation, trigeminal enhancement, and new corneal infiltrate highly suggestive of EBV. Labwork was negative except for positive EBV polymerase chain reaction (PCR) in serum. Magnetic resonance imaging (MRI) of his brain and orbits with contrast showed enhancement of the right ganglion of the trigeminal nerve, oculomotor nerve, all extraocular muscles in the right orbit, and right masticatory and temporalis muscles and a right subacute lacunar infarct. The patient was diagnosed with encephalitis and orbital-face inflammation secondary to EBV infection. The patient improved with systemic steroids.

Pharmacologic Anisocoria With Azelastine: The Importance of a Good Anamnesis.

Unilateral pharmacologic mydriasis is one of the differential diagnoses of anisocoria. This is a clinical case of a 37-year-old male patient admitted to the ophthalmology emergency department with unilateral mydriasis, an infrequent side effect of the antihistaminic drug azelastine. A comprehensive medical history including ocular medication was essential to avoid the need for additional tests and to exclude life-threatening conditions responsible for a similar presentation.

Anisocoria in patients with hyperhidrosis: A case series for the primary care physician.

The differential diagnosis for anisocoria is broad and ranges from benign to life-threatening causes. Often, patients with new onset anisocoria present to their primary care physician, an urgent care center, or an emergency room. As such, it is important for non-ophthalmologist physicians to be familiar with its common causes. We present two cases of pharmacologic anisocoria from Qbrexza (glycopyronnium), a wipe used in the treatment of hyperhidrosis. Identifying this medication as a cause of anisocoria in patients with hyperhidrosis can reduce costs and unnecessary testing. Furthermore, physician education about safer usage can be provided.

Isolated Benign Unilateral Episodic Mydriasis in Relation to Anxiety: A Case Report.

Benign episodic mydriasis is a form of anisocoria that is characterised by isolated, episodic, and sporadic mydriasis, in the absence of accompanying neurological or systemic signs or symptoms. The diagnosis is established after other causes of anisocoria have been excluded. The purpose of this case report is to describe a case of benign episodic mydriasis of her right pupil in a 23-year-old female patient. The episodes lasted for 5-10 minutes and occurred spontaneously, without any concomitant symptoms or precipitating factors. The frequency of the episodes was variable, but she reported that it worsened in periods when she felt more mentally stressed or anxious. Contact with any kind of medications, homoeopathic drugs, industrial agents, or any other kind of chemical compounds was excluded, and the remaining neurological and systemic examination was unremarkable. Blood tests were taken and imaging was performed, which ruled out a structural lesion. A diagnosis of isolated benign episodic mydriasis was established. Unlike the typical presentation of the condition, the episodes did not occur in association with any form of migraine or headache. Given the benign nature of the condition, no treatment was instituted. After excluding potentially severe causes, and reassuring the patient, the frequency of the episodes decreased.

A Case of Pharmacologic Anisocoria in Systemic Glycopyrrolate Use from Presumed Local Ocular Inoculation.

Anisocoria is a common finding in ophthalmic clinical practice. History taking and examination is critical in appropriately diagnosing and managing anisocoria, as the differential can be extensive ranging from benign to life-threatening entities. This case discusses the presentation of a 22-year-old female with a history of myopia and hyperhidrosis who presented with pharmacologic anisocoria which was presumed to be from inadvertent topical exposure to conventional glycopyrrolate tablets. To our knowledge, pharmacologic mydriasis from exposure to residue from conventional glycopyrrolate tablets has not been reported in the English literature. This case highlights the importance of medication and contact lens handling with anticholinergic agents.

Internal Carotid Artery Dissection Presenting with Transient or Subclinical Horner Syndrome.

Introduction: The most frequently encountered symptoms in internal carotid artery dissection (ICAD) are head or neck pain and cerebral ischemia. Ocular symptoms or signs have been reported as the presenting feature in up to 50% of patients, with (painful) Horner syndrome being the most frequently associated. Horner syndrome is part of the classic triad that depicts the characteristic presentation of ICAD and that consists of pain in the ipsilateral neck, head and orbital regions, (partial) Horner syndrome, and cerebral or retinal ischemia. All patients presenting with painful Horner syndrome should therefore require prompt investigations to rule out carotid artery dissection. In patients with confirmed diagnosis, treatment should be started early to prevent permanent ocular or cerebral complications. Case Presentation: Case 1: A 61-year-old woman presented with right temporal headache, an episode of transient visual loss and drooping of the right upper eyelid. Examination revealed anisocoria, which was more important in darkness. Reversal of anisocoria was observed after instilling drops of apraclonidine 0.5%. Neuroimaging demonstrated intrapetrous ICAD. Headaches, eyelid ptosis, and anisocoria all had resolved the next day. Apraclonidine pharmacologic testing a few weeks later was no longer dilating the previously smaller pupil. Case 2: A 48-year-old man presented with drooping of the right upper eyelid and right occipital headache and facial pain that all started one day after an intense yoga workout. Anisocoria was noticed upon examination, with topical cocaine 10% pharmacologic testing confirming a right Horner syndrome. Neuroimaging revealed ICAD. The patient reported resolution of his eyelid ptosis a few days later. Eyelid ptosis and anisocoria had indeed resolved at a follow-up examination a few weeks later. However, cocaine drop testing still produced anisocoria, compatible with subclinical Horner syndrome. Conclusion: Transient or subclinical Horner syndrome can be the presenting feature in ICAD; in such cases, the characteristic eyelid ptosis and anisocoria may be short-lived and resolve in only a few days. If suspected by clinical history, pharmacologic testing may be helpful in identifying subclinical cases.

Holmes-Adie syndrome and vitamin B12 - associated peripheral neuropathy: An association or coincidence?

A 30-year-old male patient presented to the eye department with complaints of blurring of vision of right eye at distance and near for a duration of 1.5 months. Ocular examination revealed Anisocoria with enlarged pupil in the right eye. On instillation of 0.1% pilocarpine, there was a pronounced miosis in the dilated pupil seen at 30 min associated with an improvement in distance and near vision. On slit lamp examination, vermiform movements were seen in the affected pupil on shining the slit from temporal aspect. Fundus examination was within normal limits. Systemic examination revealed absent deep tendon reflexes. Based on the clinical features, a diagnosis of Holmes-Adie syndrome was reached and the patient was started on 0.1% pilocarpine eye drops. This case highlights the importance of thorough systemic examination and investigations in all cases of anisocoria.

[Ocular complications in intense pulsed light therapy (case study)]. / Glaznye oslozhneniya intensivnoi fototerapii (klinicheskoe nablyudenie).

A 24-year-old female patient with photophobia, discoria, redness and dryness in her right eye after intense pulsed light (IPL) therapy applied for posttraumatic subcutaneous hemorrhage received a comprehensive ophthalmic examination including optical coherence tomography (OCT) and OCT angiography of the anterior eye segment. Her best corrected visual acuity was 20/20 in both eyes. Medically induced mydriasis revealed discoria with paresis of pupil dilatator in the left eye (pupil size 4.2 mm and 6.6 mm in the right and left eye, respectively). Anterior segment OCT showed anterior chamber cytosis and increased iris vascularity. The patient was prescribed topical 1.0% tropicamide 2 times per day and 1.0% dexamethasone 4 times per day for two weeks. Examination performed after 3 months showed no restoration of pupil dilatator function in the left eye. The case demonstrates potential ocular complications of IPL therapy, which may include iris burn with iritis and persistent pupil dilatator dysfunction.

Static anisocoria in cats and dogs with naturally occurring tick paralysis (Ixodes holocyclus).

OBJECTIVE: To characterise the novel occurrence and neuro-ophthalmological features of static anisocoria in cats and dogs with tick paralysis (TP) (Ixodes holocyclus) due to a single tick located remote from the head and neck. DESIGN: Observational case series with retrospective analysis. METHODS: Medical records were reviewed from 69 cats and 169 dogs treated for TP from a suburban veterinary hospital in Newcastle, New South Whales, between September 2005 and October 2021. RESULTS: Anisocoria was observed in 2/18 (11.1%) cats and 3/30 (10.0%) dogs with a single tick located remote from the head and neck. These proportions were not different when compared within species to 4 of 28 (14.3%) cats and 16 of 98 (16.3%) dogs with aniscocoria with a single tick located on the head and neck region (P = 1 and 0.56 respectively). Anisocoria arose from pupillary efferent dysfunction and included unilateral oculoparasympathetic dysfunction (internal ophthalmoplegia) in one dog, unilateral oculosympathetic dysfunction (Horner's syndrome) in one cat and one dog, and a combination of bilateral, but asymmetric, oculosympathetic and oculoparasympathetic dysfunction in one cat and one dog. CONCLUSION: It is proposed that anisocoria in cases of TP with a tick located remote from the head and neck is due to an intrinsic latent asymmetry in the safety factor for pupillary efferent function that is unmasked by a systemically distributed holocyclotoxin inhibiting neural transmission within this system, and this is the prevailing pathomechanism, rather than a direct local effect, underscoring anisocoria with a tick located on the head or neck.

Anisocoria without extraocular muscle impairment due to moderate traumatic brain injury with midbrain contusion: a case report.

BACKGROUND: New-onset anisocoria is an important clinical clue to life-threatening intracranial injury. Anisocoria alone without impairment of extraocular muscles is a rare presentation of moderate traumatic brain injury (TBI). CASE PRESENTATION: A 79-year-old woman was transported to hospital soon after falling off a bicycle. Glasgow Coma Scale score on arrival was 11 (E3V3M5). On examination at admission, she was found to be drowsy. Bruising was seen around the right eye and pupil diameters differed (right, 4.5 mm; left, 3.0 mm; both reactive to light). Computed tomography of the head revealed hemorrhagic contusion in the left temporal lobe and left pretectal area of the midbrain, right clavicular fracture, and pulmonary contusion with fractures of the 3rd and 4th ribs. Magnetic resonance imaging confirmed hemorrhagic contusion of the midbrain. The patient achieved full recovery of motor and mental functions with conservative treatment and was discharged on hospital day 17. CONCLUSION: We encountered a case of anisocoria without major extraocular muscle impairment due to moderate TBI with midbrain contusion.

Approach to anisocoria in the emergency department.

Anisocoria describes asymmetric pupillary diameter, which can result from traumatic, pharmacologic, inflammatory, or ischemic effects on the eye. In many cases, anisocoria represents a normal physiologic variant. Morbidity associated with anisocoria is directly related to the inciting cause and can vary from benign to life-threatening. A thorough understanding by emergency physicians of normal ocular neuroanatomy, and of common causes of pathologic anisocoria, including medication-induced anisocoria, can facilitate appropriate resource utilization and timely subspecialty consultation, and can help prevent irreversible ocular injury and patient morbidity. We describe a patient who presented to the emergency department with acute onset of blurry vision with anisocoria.

Isolated Internal Ophthalmoplegia from Posterior Cerebral Artery Neurovascular Conflict.

We report a rare case of recurrent isolated internal ophthalmoplegia attributed to oculomotor nerve (CN III) compression by the posterior cerebral artery (PCA). A 30-year-old female patient presented with recurrent right-sided headaches, right periorbital pain, and slight anisocoria. Slit-lamp examination revealed normal anterior and posterior segments except for vermiform movements of the right pupil with a temporal hyporeactive flat area. Tonic pupils were ruled out with pilocarpine 0.1% testing. Suspecting an internal ophthalmoplegia, magnetic resonance imaging was ordered which demonstrated the right CN III indented by the PCA, fulfilling the criteria of a neurovascular conflict. The evaluation of unilateral mydriasis from internal ophthalmoplegia should prompt neuroimaging with exclusion of aneurysmal or compressive lesions. CN III palsy can rarely be caused by vascular anatomical variants because of the proximity of the posterior intracranial circulation and CN III. Newer, more precise imaging techniques will better help characterize neurovascular conflicts presenting as cranial nerve palsies.

Carotid-Cavernous Fistula Presenting as Isolated Painful Anisocoria.

A painful isolated third nerve palsy is an uncommon presenting sign of a carotid-cavernous fistula (CCF). It mostly occurs in dural CCFs with posterior drainage into the petrosal sinuses. We present a case of a 50-year-old woman who developed acute right periorbital facial pain in the territory of the first branch of the right trigeminal nerve and was noted to have a right dilated unreactive pupil with very subtle right ptosis. She was subsequently diagnosed with a posteriorly draining dural CCF.

A Case of Surgery Cancellation Following the Discovery of Anisocoria After Induction of General Anesthesia.

Anisocoria after induction of general anesthesia may indicate a severe cerebrovascular disorder. We encountered a case in which anisocoria in the left and right eyes was noticed after induction of general anesthesia, and the surgery was canceled. The patient was a 53-year-old woman with a history of hypertension. She received general anesthesia 10 years ago, but the details were unknown. Anesthesia was induced with propofol, remifentanil, and rocuronium, followed by nasal intubation. No significant change was observed in vital signs during the induction of anesthesia. After intubation, the pupils were checked according to the protocol for observing pupil diameter. The pupil size was found to be unequal, measuring 1 mm in the left eye and 4 mm in the right eye. A cerebrovascular disorder was suspected; thus, the surgery was canceled, and the patient was awakened and extubated. Neurological symptoms such as limb movements were checked after awakening, and no disorientation or motor dysfunction was detected in the patient. However, her pupils remained unequal, measuring 2 mm in the left eye and 4 mm in the right eye. Regarding light reflex, the left eye was miotic, but the right eye remained mydriatic. The pupillary symptom persisted even during discharge the next day. Since our hospital is a solely dental hospital, following discharge, after consulting the ophthalmology department of a nearby medical university hospital, the patient was diagnosed with pupillotonia, as she had been experiencing light dazzling in only her right eye for seven years, had no light reflex but near reflex, and was miotic due to the use of pilocarpine hydrochloride eye drops, which promotes miosis. The patient has had these symptoms in the right eye for seven years, and it is possible that she had anisocoria during the preoperative examination at this time. If anisocoria had been detected and examined carefully during the preoperative examination, there would have been no need to cancel the surgery. In this case, we strongly felt that the pupils must be checked during the preoperative examination.

Anisocoria and mydriasis after scalp nerve block: a case report.

Strategies for the assessment of abnormal neurological findings during general anesthesia are limited. However, pupil abnormalities may represent serious neurological complications. We herein present a case of new-onset anisocoria and mydriasis that developed after scalp nerve block. The patient's signs were possibly related to increased intracranial pressure with resulting brain shift that ultimately affected the oculomotor nerves. A 45-year-old man was scheduled for left cerebellar tumor resection and ventricular drainage surgery; however, anisocoria and left pupillary mydriasis were observed after induction of general anesthesia and performance of scalp nerve block. After reducing the intracranial pressure, the right pupil showed constriction (1 mm) but the left pupil was dilated (5 mm). The pupils were of similar size postoperatively. Although pupillary dilation during general anesthesia has been previously described, this is the first case in which the mydriasis was considered to have been caused by brain shift due to increased intracranial pressure after scalp nerve block. Thus, we propose this phenomenon as a new possible cause of pupillary changes. Actively monitoring this presentation intraoperatively could enable early detection of and intervention for complications, therefore improving the prognosis.

Atypical Presentation of Enlarged Vestibular Aqueducts Caused by SLC26A4 Variants.

Enlarged vestibular aqueduct is the most common inner ear malformation in pediatric patients with sensorineural hearing loss. Here, we report a new presentation of enlarged vestibular aqueduct in a Korean family. The family consists of two parents and five daughters, and the first and second daughters were diagnosed with bilateral enlarged vestibular aqueducts. The third daughter, who showed no signs of hearing deterioration, came to medical attention with incomplete Horner syndrome. Evaluations for localization of Horner syndrome on the patient and Sanger sequencing of SLC26A4 on the family members were performed. Although auditory brainstem response and pure tone audiometry of the third daughter were normal, temporal bone computed tomography demonstrated bilateral enlarged vestibular aqueducts. Sanger sequencing of SLC26A4 revealed compound heterozygous variants c.2168A>G and c.919-2A>G in the first, second, and third daughters. Diagnosis of enlarged vestibular aqueduct is often delayed because the degree of hearing loss can vary, and a considerable phenotypic variability can be shown even in family members with the same SLC26A4 variations. Fluctuations of CSF pressure into the cochlear duct and recurrent microruptures of the endolymphatic membrane could result in damage of sympathetic nerve supplying to the inner ear, which could explain the mechanism of Horner syndrome associated with enlarged vestibular aqueduct.