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.

Mydriasis and anisocoria in a pediatric hyperhidrosis patient with interesting findings in the family cat.

Here, we report a case of unilateral ocular mydriasis in a pediatric patient with longstanding hyperhidrosis, as well as similar findings in her cat. The patient had been undergoing treatment of her hyperhidrosis with topical glycopyrrolate. This case highlights the potential side effect profile of topical antimuscarinics and the importance of counseling patients on proper precautions.

Brimonidine eye drops reveal diminished sympathetic pupillary tone in comatose patients with brain injury.

BACKGROUND: There is an urgent need for easy-to-perform bedside measures to detect residual consciousness in clinically unresponsive patients with acute brain injury. Interestingly, the sympathetic control of pupil size is thought to be lost in states of unconsciousness. We therefore hypothesized that administration of brimonidine (an alpha-2-adrenergic agonist) eye drops into one eye should produce a pharmacologic Horner's syndrome if the clinically unresponsive patient is conscious, but not if the patient is unconscious. Here, in a first step to explore this hypothesis, we investigated the potential of brimonidine eye drops to distinguish preserved sympathetic pupillary function in awake volunteers from impairment of sympathetic tone in patients in a coma. METHODS: We enrolled comatose patients admitted for acute brain injury to one of the intensive care units (ICU) of a tertiary referral center, in whom EEG and/or neuroimaging for all practical purposes had ruled out residual consciousness. Exclusion criteria were deep sedation, medications with known drug interactions with brimonidine, and a history of eye disease. Age- and sex-matched healthy and awake volunteers served as controls. We measured pupils of both eyes, under scotopic conditions, at baseline and five times 5-120 min after administering brimonidine into the right eye, using automated pupillometry. Primary outcomes were miosis and anisocoria at the individual and group levels. RESULTS: We included 15 comatose ICU patients (seven women, mean age 59 ± 13.8 years) and 15 controls (seven women, mean age 55 ± 16.3 years). At 30 min, miosis and anisocoria were seen in all 15 controls (mean difference between the brimonidine-treated pupil and the control pupil: - 1.31 mm, 95% CI [- 1.51; - 1.11], p < 0.001), but in none (p < 0.001) of the 15 ICU patients (mean difference: 0.09 mm, 95% CI [- 0.12;0.30], p > 0.99). This effect was unchanged after 120 min and remained robust in sensitivity analyses correcting for baseline pupil size, age, and room illuminance. CONCLUSION: In this proof-of-principle study, brimonidine eye drops produced anisocoria in awake volunteers but not in comatose patients with brain injury. This suggests that automated pupillometry after administration of brimonidine can distinguish between the extremes of the spectrum of consciousness (i.e., fully conscious vs. deeply comatose). A larger study testing the "intermediate zone" of disorders of consciousness in the ICU seems warranted.

Sudden anisocoria in a healing pediatric multitrauma patient.

ABSTRACT: This article describes a teenager who developed anisocoria with no obvious neurologic deficits or decline after a motor vehicle accident. The condition resolved over several hours before reappearing in the opposite eye 2 days later. Again no clinical neurologic deficits were noted and the condition resolved after several hours. The patient's asymptomatic anisocoria was finally determined to be secondary to aerosolized ipratropium treatments and an ill-fitting mask.

Anisocoria and Poor Pupil Reactivity by Quantitative Pupillometry in Patients With Intracranial Pathology.

OBJECTIVES: To describe the prevalence and associated risk factors of new onset anisocoria (new pupil size difference of at least 1 mm) and its subtypes: new onset anisocoria accompanied by abnormal and normal pupil reactivities in patients with acute neurologic injuries. DESIGN: We tested the association of patients who experienced new onset anisocoria subtypes with degree of midline shift using linear regression. We further explored differences between quantitative pupil characteristics associated with first-time new onset anisocoria and nonnew onset anisocoria at preceding observations using mixed effects logistic regression, adjusting for possible confounders. SETTING: All quantitative pupil observations were collected at two neuro-ICUs by nursing staff as standard of care. PATIENTS: We conducted a retrospective two-center study of adult patients with intracranial pathology in the ICU with at least a 24-hour stay and three or more quantitative pupil measurements between 2016 and 2018. MEASUREMENTS AND MAIN RESULTS: We studied 221 patients (mean age 58, 41% women). Sixty-three percent experienced new onset anisocoria. New onset anisocoria accompanied by objective evidence of abnormal pupil reactivity occurring at any point during hospitalization was significantly associated with maximum midline shift (ß = 2.27 per mm; p = 0.01). The occurrence of new onset anisocoria accompanied by objective evidence of normal pupil reactivity was inversely associated with death (odds ratio, 0.34; 95% CI, 0.16-0.71; p = 0.01) in adjusted analyses. Subclinical continuous pupil size difference distinguished first-time new onset anisocoria from nonnew onset anisocoria in up to four preceding pupil observations (or up to 8 hr prior). Minimum pupil reactivity between eyes also distinguished new onset anisocoria accompanied by objective evidence of abnormal pupil reactivity from new onset anisocoria accompanied by objective evidence of normal pupil reactivity prior to first-time new onset anisocoria occurrence. CONCLUSIONS: New onset anisocoria occurs in over 60% of patients with neurologic emergencies. Pupil reactivity may be an important distinguishing characteristic of clinically relevant new onset anisocoria phenotypes. New onset anisocoria accompanied by objective evidence of abnormal pupil reactivity was associated with midline shift, and new onset anisocoria accompanied by objective evidence of normal pupil reactivity had an inverse relationship with death. Distinct quantitative pupil characteristics precede new onset anisocoria occurrence and may allow for earlier prediction of neurologic decline. Further work is needed to determine whether quantitative pupillometry sensitively/specifically predicts clinically relevant anisocoria, enabling possible earlier treatments.

Comparison of out of hospital cardiac arrest due to acute brain injury vs other causes.

BACKGROUND: Acute brain injury (ABI) can cause out of hospital cardiac arrest (OHCA). The aim of this study was to compare clinical features, mortality and potential for organ donation in patients with OHCA due to ABI vs other causes. METHODS: From January 2017 to December 2018, all adult patients presenting to ED for OHCA were considered for the study. Two physicians established the definitive cause of OHCA, according to clinical, laboratory, diagnostic imaging and autoptic findings. Clinical features in patients with OHCA due to ABI or other causes were compared. RESULTS: 280 patients were included in the analysis. ABI was the third most frequent cause of OHCA (21, 7.5%); ABIs were 8 subarachnoid hemorrhage, 8 intracerebral hemorrhage, 2 ischemic stroke, 2 traumatic spinal cord injury and 1 status epilepticus respectively. Neurological prodromes such as seizure, headache and focal neurological signs were significantly more frequent in patients with OHCA due to ABI (OR 5.34, p = 0.03; OR 12.90, p = 0.02; and OR 66.53, p < 0.01 respectively) while among non-neurological prodromes chest pain and dyspnea were significantly more frequent in patients with OHCA due to other causes (OR 14.5, p < 0.01; and OR 10.4, p = 0.02 respectively). Anisocoria was present in 19% of patients with OHCA due to ABI vs 2.7% due to other causes (OR 8.47, p < 0.01). In 90.5% of patients with ABI and in 53.1% of patients with other causes the first cardiac rhythm was non shockable (OR 8.1; p = 0.05). Multivariate logistic regression analysis revealed that older age, active smoking, post-traumatic OHCA, neurological prodromes, anisocoria at pupillary examination were independently associated with OHCA due to ABI. Patients with ABI showed a higher mortality compared with the other causes group (19 pts., 90.5% versus 167 pts., 64.5%; p = 0.015). Potential organ donors were more frequent among ABI than other causes group (10 pts., 47.6% vs 75 pts., 28.9%) however the difference did not reach the statistical significance (p = 0.07). CONCLUSIONS: ABI is the third cause of OHCA. Neurological prodromes, absence of chest pain and dyspnea before cardiac arrest, anisocoria and initial non-shockable rhythm might suggest a neurological etiology of the cardiac arrest. Patients with OHCA due to ABI has an unfavorable outcome, however, they could be candidate to organ donation.

Pharmacologic Mydriasis Secondary to Topical Glycopyrronium Tosylate Cloths: Clinical Characterization From a Multicenter Analysis.

BACKGROUND: Topical glycopyrronium tosylate (GT) is an anticholinergic medication for treatment of axillary hyperhidrosis. Pharmacologic mydriasis and anisocoria from topical GT has been reported and may be underrecognized. This study aims to clinically characterize patients presenting with pharmacologic mydriasis from exposure to this medication. METHODS: This study is a retrospective observational case series. A multicenter chart review of 16 patients diagnosed with pharmacologic mydriasis secondary to topical GT was performed. RESULTS: Eight patients (50.0%) were age 18 years and younger, and 14 patients (87.5%) were female. Unilateral mydriasis (anisocoria) occurred in 14 patients (87.5%). Fourteen patients (87.5%) did not initially volunteer topical GT as a "medication," and the history of topical GT exposure needed to be elicited with further questioning. Hand hygiene details were known for 12 patients, and all reported that they did not wash their hands after GT application. Six patients (37.5%) were soft contact lens users. One patient had possible exposure through a family member's use of the medication. Ocular symptoms were common (blurry vision [11 patients, 68.8%] and eye dryness [7 patients, 43.8%]), but systemic anticholinergic symptoms were uncommon (such as constipation [1 patient, 6.3%] and urinary symptoms [3 patients, 18.8%]). CONCLUSIONS: Mydriasis associated with topical GT seems to be a consequence of local exposure rather than systemic toxicity. Because patients may not volunteer topical GT as a medication, eliciting a history of exposure often requires further specific questioning. Soft contact lens wear and poor postapplication hand hygiene seem to be associated with mydriasis in GT use.

Characteristics of Postoperative Anisocoria After Medial Orbital Wall Fracture Repair.

ABSTRACT: The purpose of this study was to present the clinical characteristics and etiology of patients with anisocoria after medial wall fracture repair. This study was a retrospective, noncomparative case series of postoperative anisocoria after medial orbital wall fracture repair. Data regarding patient demographics, laterality, signs and symptoms at presentation, interval between injury and surgery, fracture size using orbital computed tomography, pupil size of mydriasis, time of discovery of postoperative mydriasis, time of resolution of anisocoria, surgical outcomes, and complications were collected. Twelve patients were included in this study. The mean interval between injury and surgery was 19.17 ±â€Š4.95 (range, 12-30) days. The mean fracture size of the anteroposterior meridian was 25.22 ±â€Š2.15 (range, 21.8-28.4) mm and that of the horizontal meridian was 16.02 ±â€Š2.02 (range, 12.5-21.2) mm. Postoperatively, unilateral pupil dilation was observed at a mean of 5.33 ±â€Š1.61 (range, 3-8) hours after surgery, and mean pupil size was 5.13 ±â€Š0.61 (range, 4-6) mm in the dilated eye and 3.29 ±â€Š0.26 (range, 3-3.5) mm in the normal eye. The dilated pupils all recovered within a mean of 3.42 ±â€Š1.08 (range, 2-5) days. Postoperative anisocoria after medial orbital wall blowout fracture surgery may occur in delayed repair of the posterior location of large fractures. Transient mydriasis caused by parasympathetic nerve injury returned to normal pupil size.

A well-appearing infant with a sudden anisocoria.

Case presentationA 10-month-old boy was admitted to the emergency department due to a sudden onset of left unilateral mydriasis (figure 1). His medical history was unremarkable. A minor head trauma 2 days before was reported, without alarming signs or symptoms. His mother was putting him to sleep, after coming back from work, when she noticed a different pupil size and promptly went to the ED with her husband. The parents denied any use of medications, including nebulised therapy or direct contact with plants. The child was well appearing and his vital signs were within the standard age limits. His extraocular motility was normal as well as the rest of his neurological and physical examination. Parents' behaviour was somehow remarkable. Even though the child was not suffering, the mother seemed very worried while the father was nervous and aggressive, repeatedly asking for a discharge.

Reversible Mydriasis of Sudden Onset: Think Before You Act.

BACKGROUND: The presence of abrupt anisocoria in clinical examination usually leads to the performance of urgent neuroimaging studies to exclude intracranial hemorrhage, although unilateral mydriasis might be the result of other benign etiologies. CASE REPORT: In this work, we report an illustrative case of a patient presenting with sudden-onset anisocoria while receiving ipratropium bromide nebulization in the emergency department to treat acute asthma. No other abnormalities were found on neurological examination and the computed tomography scan was normal. As a muscarinic antagonist, ipratropium bromide can produce mydriasis if accidentally instilled on one eye, thus leading to the suspicion of pharmacologic mydriasis. The pupils became isocoric after the discontinuation of the drug. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: A careful neurological examination and the history of treatment with mydriatic drugs might avoid unnecessary tests and radiation exposure.

Effect of decompressive hemicraniectomy in patients with acute middle cerebral artery infarction

Background/aim: We aimed to determine in which cases this procedure may be more effective based on the data of patients who underwent decompressive hemicraniectomy (DHC). Material and methods: Overall, 47 patients who underwent DHC due to acute middle cerebral artery (MCA) infarction between January 2014 and january 2019 were retrospectively investigated. These patients were divided into two groups: those who died after DHC (Group A) and those who survived DHC (Group B). The groups were compared in terms of various parameters. We investigated whether the patient's modified Rankin scale (mRS) status changed depending on age (> 60 and < 60 years). Results: The median age of all patients was 65 (37­80) years; groups A and B had median ages of 66.5 (37­80) and 61 (44­79) years (p = 0.111), respectively; 55.3% patients were male. The elapsed times until hospitalization after the onset of symptoms were 4.5 and 3 h in groups A and B, respectively (p = 0.014). The median GCS score at the time of admission was 7 (5­12) and 10 (8­14) in groups A and B, respectively (p = 0.0001). At the time of admission, 63.3% patients in group A had anisocoria, whereas no patient in group B had anisocoria (p = 0.0001). In postoperative period, 40% patients in group A and all patients in group B received AC/AA treatment. The survival of patients aged < 60 and > 60 years who underwent DHC for MCA infraction was 61.5% and 26.5%, respectively (p = 0,041). The median mRS of patients < 60 and > 60 years were 4 (1­6) and 6 (1­6), respectively (p = 0.018). Conclusion: Age, DHC timing, and elapsed time until hospitalization or access to treatment directly affect the functional outcome and survival in MCA-infarcted patients who underwent DHC. In patients in whom the medical treatment fails, early DHC administration will increase survival without waiting for neurological worsening once herniation is detected radiologically.

[Iatrogenic anisocoria after using a scopolamine patch for PONV prophylaxis]. / Iatrogene Anisokorie nach Scopolaminpflaster zur PONV-Prophylaxe.

This is a case report of a 29-year-old female patient who developed unilateral mydriasis following the use of a scopolamine patch for the prevention of postoperative nausea and vomiting (PONV).Given a medical history showing multiple risk factors for PONV, a preauricular scopolamine patch was applied prior to the induction of anesthesia. General anesthesia was induced with 150 mg propofol and 25 µg sufentanil and maintained with total intravenous anesthesia, using propofol (5 mg/kg per h) and remifentanil (2-3 µg/kg per h).Following an uneventful surgery of 90min duration, the patient was extubated and transferred to the recovery room, where the patch was removed. During the orthopedic ward round the following day, the clinical examination revealed anisocoria of the left eye in the form of unilateral mydriasis. In order to determine the cause of this clinical presentation, further neurological and ophthalmological examinations and investigations were carried out. In addition, magnetic resonance imaging was conducted to rule out a central nervous cause. The results of the investigations were negative and no pathology was identified. In addition, the symptoms resolved within 24 h of onset without any therapeutic intervention. Therefore, a suspected diagnosis of a pharmacologically induced anisocoria from the scopolamine patch was made, whereby the substance accidentally reached the affected left eye.Previous studies showed that scopolamine patches may reduce early emetic symptoms. Case reports describing the occurrence of anisocoria following the application of scopolamine patches have been previously published. In all of these cases the patches were used to prevent PONV and each case was comprehensively investigated using various diagnostic and clinical tools. It should be noted, however, that a dysfunctional accommodation is listed as a common side effect of the drug, affecting more than 1 in 10 patients.Even though the efficacy of scopolamine patches for the prevention of PONV is proven, clinicians should be aware of the common ophthalmological side effect. Particularly with respect to various surgical disciplines, where anisocoria may indicate an underlying surgery-related complication, the application of scopolamine patches should be well- considered.

Pharmacologic anisocoria due to nebulized ipratropium bromide: A diagnostic challenge.

Anisocoria may be physiological or seen in fatal conditions, such as intracranial hemorrhage. Newly developing anisocoria may cause confusion and diagnostic difficulty in the emergency department (ED). A 35-year-old female was admitted to the ED with an asthma attack and dyspnea. On examination, the patient was observed to have bilateral rhonchi and was treated with nebulized albuterol (salbutamol) and ipratropium bromide. After the treatment, the dyspnea improved, and mydriasis developed in the left eye (left pupil diameter 9 mm, right 4 mm). An examination revealed that the left pupil was dilated and unreactive to light, but there was no neurological finding. Afterwards, the patient reported that, during the treatment, some aerosol had leaked from the left side of the mask and may have come into contact with her left eye. Given this information, a pilocarpine test was performed, and the patient was diagnosed with pharmacologic anisocoria. The pupil returned to normal within 24 h. Ipratropium bromide is a drug frequently used in patients presenting to the ED with dyspnea. During treatment, nebulized ipratropium may leak from the edge of the facial mask into the ipsilateral eye and may cause mydriasis. A pilocarpine test can be used to differentiate pharmacological anisocoria from other causes, such as third nerve palsy and Adie's pupil. Through the awareness of emergency physicians and the use of the pilocarpine test, a diagnosis can be made without engaging in time-consuming and costly analyses. In addition, this complication can be prevented using masks that better fit the face, as well as protective goggles or eye patches, during treatment.

Objective Verification of Physiologic Changes during Accommodation under Binocular, Monocular, and Pinhole Conditions.

BACKGROUND: To objectively investigate accommodative response to various refractive stimuli in subjects with normal accommodation. METHODS: This prospective, non-randomized clinical trial included 64 eyes of 32 subjects with a mean spherical equivalent -1.4 diopters (D). We evaluated changes in accommodative power, pupil diameter, astigmatic value, and axis when visual stimuli were applied to binocular, monocular (dominant eye, non-dominant eye, ipsilateral, and contralateral), and pinhole conditions. Visual stimuli were given at 0.25 D (4 m), 2 D (50 cm), 3 D (33 cm), and 4 D (25 cm) and accommodative response was evaluated using open view binocular autorefractor/keratometer. RESULTS: The accommodative response to binocular stimulus was 90.9% of the actual refractive stimulus, while that of the monocular stimulus was 84.6%. The binocular stimulus induced a smaller pupil diameter than did the monocular stimulus. There was no difference in accommodative response between the dominant eye and non-dominant eye or between ipsilateral and contralateral stimuli. As the refractive stimuli became stronger, the absolute astigmatic value increased and the direction of the astigmatism axis became more horizontal. Pinhole glasses required 10%-15% less accommodative power compared with the monocular condition. CONCLUSION: Binocular stimuli enable more precise and effective accommodation than do monocular stimuli. Accommodative response is composed of 90% true accommodation and 10% pseudo-accommodation, and the refractive stimulus in one eye affects the contralateral eye to the same extent. This should be taken into account when developing guidelines for wearing smart glasses while driving, as visual stimulation is applied to only one eye, but far distance attention is constantly needed. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT03557346.

Isolated Anisocoria as a Presenting Stroke Code Symptom is Unlikely to Result in Alteplase Administration.

BACKGROUND: Acute stroke codes may be activated for anisocoria, but how often these codes lead to a final stroke diagnosis or alteplase treatment is unknown. The purpose of this study was to assess the frequency of anisocoria in stroke codes that ultimately resulted in alteplase administration. METHODS: We retrospectively assessed consecutive alteplase-treated patients from a prospectively-collected stroke registry between February 2015 and July 2018. Based on the stroke code exam, patients were categorized as having isolated anisocoria [A+(only)], anisocoria with other findings [A+(other)], or no anisocoria [A-]. Baseline demographics, stroke severity, alteplase time metrics, and outcomes were also collected. RESULTS: Ninety-six patients received alteplase during the study period. Of the 94 who met inclusion criteria, there were 0 cases of A+(only). There were 9 cases of A+(other) (9.6%). A+(other) exhibited higher baseline National Institutes of Health (NIH) Stroke Scale scores compared to A- (17 versus 7; P = .0003), and no additional differences in demographics or alteplase time metrics. Final stroke diagnosis and other outcome measures were no different between A+(other) and A-. Of the A+ patients without pre-existing anisocoria, 5 of 6 (83%) had posterior circulation events or diffuse subarachnoid hemorrhage. CONCLUSIONS: In this exploratory analysis, zero patients with isolated anisocoria received alteplase treatment. Anisocoria as a part of the neurologic presentation occurred in 10% of alteplase patients, and was strongly associated with a posterior circulation event. Therefore, we conclude that anisocoria has a higher likelihood of leading to alteplase treatment when identified in the presence of other neurologic deficits.

DEFENSIVE Stroke Scale: Novel Diagnostic Tool for Predicting Posterior Circulation Infarction in the Emergency Department.

BACKGROUND: Dizziness is the most common posterior circulation symptom; however, diagnosing a posterior circulation infarction is difficult due to a lack of typical symptoms. We aimed to investigate the frequency of misdiagnosis of a posterior circulation infarction in patients who presented with dizziness and to develop a new stroke scale that increased the diagnostic accuracy for stroke among these subjects. METHODS: We retrospectively analyzed consecutive data from subjects hospitalized with ischemic stroke who presented with dizziness (the developmental phase). Based on these results, we created a novel stroke scale, which was used as a diagnostic procedure in the prospective validation phase. We compared the rate of misdiagnosis of ischemic stroke between phases. RESULTS: During the development phase, 115 subjects were hospitalized for ischemic stroke accompanied by dizziness. Six ischemic stroke subjects were not properly diagnosed (6/115, 5.2%). We created the new DisEquilibrium, Floating sEnsation, Non-Specific dizziness, Imbalance, and VErtigo (DEFENSIVE) stroke scale to prevent underdiagnosis of a posterior circulation infarction. During the validation phase, 949 subjects with dizziness were examined with the DEFENSIVE stroke scale; among these subjects, 100 were hospitalized for ischemic stroke accompanied by dizziness. No subject with ischemic stroke was overlooked. The new DEFENSIVE stroke scale had a sensitivity of 100% and decreased the rate of improper diagnosis of stroke (5.2% versus 0%; P = .022). CONCLUSIONS: Our new stroke recognition instrument for a posterior circulation infarction presenting with dizziness and related symptoms (the DEFENSIVE stroke scale) is easy to administer and has good diagnostic accuracy.

Response anisocoria in the pupillary light and darkness reflex.

The pupil constricts or dilates in response to a luminance increase or decrease, and these transient pupillary responses are controlled by the parasympathetic and sympathetic pathways. Although pupillary responses of the two eyes are highly correlated, they are not always identical (referred to as anisocoria). For example, there are unequal direct and consensual pupillary constriction responses after an increase in luminance to one eye. While contraction anisocoria (i.e. constriction) has been demonstrated in the pupillary light reflex, it is not yet known if there is also dilation anisocoria in the pupillary darkness reflex. Unlike previous studies that focused on the pupillary light reflex, we examined response anisocoria in both pupillary light and darkness reflexes. While requiring participants to maintain central fixation, we presented a light or dark stimulus to either the right or left visual field to induce transient pupillary constriction or dilation. Both the pupillary light and darkness reflexes had significantly larger ipsilateral responses compared to the contralateral responses relative to the stimulated visual field. The observed ipsilateral effects occurred significantly faster in the light than darkness reflex, suggesting that larger ipsilateral pupillary dilation after a luminance decrease cannot be only attributed to the inhibition of the parasympathetic system, but is also mediated by the excitation of the sympathetic system. Together, our results demonstrated a larger ipsilateral pupil response in both the pupillary light and darkness reflex, indicating an asymmetry in ipsilateral and contralateral neural circuitry of the pupillary darkness reflex.

Invited Commentary: Evaluation of Horner Syndrome in the MRI Era.

This Invited Commentary discusses the following article: BACKGROUND:: To identify the etiologies of adult Horner syndrome (HS) in the MRI era using a targeted evaluation approach and to assess the value and yield of targeted imaging. METHODS: A retrospective chart review was performed of 200 adult outpatients with HS, confirmed with cocaine eyedrop testing. Patients were divided into subgroups based on the presence or absence of symptoms and those who did or did not receive additional testing with hydroxyamphetamine drops. Imaging was obtained based on pharmacologic localization and/or clinical evaluation. The etiology of HS and the yield of imaging were determined in all subgroups. RESULTS: Imaging showed causative lesions in 24 of 179 (12.84%) imaged patients with HS, and 13 (69.0%) were determined "idiopathic." Of the patients who underwent testing with hydroxyamphetamine drops (132 patients), 86 had a postganglionic localization with an imaging yield of 8.1%, and 46 had preganglionic cause with an imaging yield of 21.7%. Fifty-three patients (26.5%) never noticed ptosis/anisocoria before examination, and the imaging yield in this subgroup was 2.8%. Eighteen of the 200 patients (9.0%) had serious pathology, including carotid artery dissection, brain, or neck mass, and 6 of these (31.6%) had acute symptoms and/or pain. CONCLUSION: HS is most often idiopathic with serious pathology being relatively infrequent. When determining etiology, the absence of symptoms is not predictive of the pathology. However, acute onset of symptoms and/or pain are possible indicators for serious pathology. Localizing the lesion using hydroxyamphetamine drops whenever obtainable and available is still an efficient way to target imaging evaluation.