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.

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.

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.

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.

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.

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.

Horner Syndrome as the Only Focal Neurologic Manifestation of Hypothalamic Hemorrhage.

A 70-year-old woman suffered an anterior dorsal hypothalamic hemorrhage that caused an ipsilateral Horner syndrome (HS) as the only focal neurologic manifestation. This is only the second reported case of hypothalamic hemorrhage producing HS. Because HS was the sole focal neurologic manifestation, its confirmation with topical apraclonidine drops was a valuable clue toward prompt localization of the patient's confusional state.

MRI detection of cerebral lesions in post-traumatic anisocoria: specificity and prognostic significance.

AIM: To identify whether increased numbers of brainstem lesions are found in the presence of a post-traumatic pupillary function disturbance and classify them anatomically. MATERIALS AND METHODS: In this study, a diagnostic magnetic resonance imaging (MRI) examination was performed within 8 days after traumatic brain injury (TBI) in patients who had been unconscious for more than 24 hours post-TBI. The Glasgow Outcome Scale was evaluated 6 months after TBI. The data obtained from 140 consecutively enrolled patients between 2005 and 2011 were analysed. The clinical study parameter comprised the development of post-traumatic anisocoria at least once over the course between onset of trauma and diagnostic MRI, as a yes/no decision. Significance was presumed at p≤0.05. RESULTS: A total of 57 patients (41%) were found to have a lesion at MRI without involvement of the brainstem; in 83 (59%) the brainstem was (multiple) affected. Of the latter, 66 (46%) of patients had lesions in the midbrain, 38 (27%) in the pons, and seven (5%) in the medulla oblongata. By the time of MRI, anisocoria had been diagnosed in 45 (32%) patients. Mortality was highest, at 58%, in patients with anisocoria and a midbrain lesion, whilst it was 23% in those with anisocoria and no lesion in the midbrain. Mortality was 33% in relation to a midbrain lesion without anisocoria. CONCLUSION: Overall, the study demonstrated that there is a significant correlation between midbrain lesions and post-traumatic anisocoria in unconscious trauma patients. A brainstem lesion in this case can be assumed to be a pathomorphological correlate of anisocoria. The rate of damage to the midbrain was approximately 50% in cases of transient anisocoria. It can be assumed in this situation that there are functional disorders of the peripheral oculomotor nerve or identifiable/unidentifiable lesions of the brainstem.

The First Case of Kernohan-Woltman Notch Phenomenon Caused by Epidural Hematoma in a Pediatric Patient.

Kernohan-Woltman notch phenomenon (KWNP) is an ipsilateral motor weakness due to compression of the contralateral cerebral peduncle. Most of the KWNP cases reported have been due to subdural hematomas, intracranial space-occupying lesions, and spontaneous bleeding of vascular malformations. In this study, we present the first pediatric case of KWNP caused by a traumatic epidural hematoma. Although subdural hematomas are the most frequent reason for KWNP, epidural hematomas may cause paradoxical ipsilateral signs not only in adults but also in pediatric patients.

Anisocoria After Repair of Blowout Fracture.

Anisocoria may indicate a life-threatening neurosurgical emergency, unlike bilateral mydriasis. In patients with periorbital fracture, anisocoria can be caused by direct or indirect injury to the oculomotor nerve, excessive retraction of the orbital contents, or constriction of the muscles responsible for eyeball movement. Herein, the author reports a patient, 15-year-old boy, who developed anisocoria after an operation for a blowout fracture. The anisocoria was improved, self-limiting, and transient. The author has also reviewed the literature regarding anisocoria.

Iatrogenic Horner Syndrome: Etiology, Diagnosis and Outcomes.

BACKGROUND: The identification and prompt diagnosis of Horner syndrome (HS) is essential for preventing permanent damage. HS may arise when a lesion presents anywhere along the three-neuron oculosympathetic pathway that begins at the posterior-lateral nuclei of the hypothalamus all the way through to the orbit. We present four cases and review the literature to familiarize the reader with the identification, diagnosis and treatment of Horner syndrome. The four patients, three adults and one child, were followed for at least 6 months following the initial diagnosis (range 6-18 months). There was partial resolution in three of the four cases, while the fourth resolved completely. There are numerous causes of HS, some of them iatrogenic. While iatrogenic cases of HR are rare in both adults and children, HS is seen more often following surgical procedures. Prompt recognition of the syndrome and correction of the offending agent may prevent permanent damage to the neuronal pathway. It is therefore recommended that practitioners be aware of the risks for development of iatrogenic HS and the signs for early detection.

An approach to anisocoria.

PURPOSE OF REVIEW: Anisocoria is a finding seen on a daily basis in nearly every eye clinic. Although often benign, it can also represent the sole sign of a life-threatening disease making an up-to-date understanding of pathophysiology and diagnosis essential for anyone practicing medicine. RECENT FINDINGS: Many aspects of the traditional approach to anisocoria still hold true today, but advancements in imaging technology and changing trends in pharmacologic diagnosis and localization have led many to rethink that approach. In addition, the differential diagnosis for anisocoria continuously expands with identification and improved understanding of causal disease processes. SUMMARY: The present article discusses an approach to the classic anisocoria diagnostic algorithm modified by current knowledge from the most recent literature.

Ophthalmic artery occlusion with total ophtalmoplegia and anisocoria revealing cavernous sinus thrombosis.

AIM: To describe a case of ophthalmic artery occlusion associated with anisocoria and revealing a cavernous sinus thrombosis due to sinusitis. OBSERVATION:   A 48-year-old man with a history of diabetes presented acutely with loss of vision and proptosis in the left eye. Ophthalmologic examination concluded in a left ophthalmic artery occlusion with anisocoria and total ophthalmoplgia. Cardiac assessment was normal. Magnetic resonance imaging (MRI) revealed left ophthalmic artery and internal carotid occlusions, left cavernous and transverse sinus thrombosis and sphenoid sinusitis. The patient underwent extensive haematological and medical assessment to search for embolic sources and disease causing thrombophilia. The patient recovered from the thrombosis episode, but sustained permanent blindness. CONCLUSION: Ophthalmic manifestations may be the only signs revealing cavernous sinus thrombosis which must be usually suspected. Visual prognostic was very poor.

Orbital apex syndrome: an unusual complication of herpes zoster ophthalmicus.

BACKGROUND: Herpes zoster ophthalmicus is defined as herpes zoster involvement of the ophthalmic division of the trigeminal nerve. Ocular involvement occurs in 20-70% of patients with herpes zoster ophthalmicus and may include blepharitis, keratoconjunctivitis, iritis, scleritis, and acute retinal necrosis. Orbital apex syndrome is a rare but severe ocular complication of herpes zoster ophthalmicus. We present here the first reported case of herpes zoster ophthalmicus complicated by orbital apex syndrome in a patient from Taiwan. CASE PRESENTATION: A 78-year-old man initially presented with patchy erythema and herpetiform vesicles on his left forehead and upper eyelid. He subsequently developed left-sided ocular complications including reduced visual acuity, anisocoria, ptosis, and complete ophthalmoplegia. Orbital magnetic resonance imaging (MRI) was performed on day 6 of admission to search for signs of the common causes of orbital apex syndrome such as hemorrhage, neoplasm, and cavernous sinus thrombosis. The MRI showed only orbital myositis and enhancement of the retro-orbital optic nerve sheath. The patient was diagnosed with herpes zoster ophthalmicus complicated by orbital apex syndrome. Although the ocular complications partially resolved after systemic antiviral therapy for 15 days and steroid therapy tapered over 12 weeks, there was residual limitation of abduction and paralysis of the left upper eyelid at follow-up at 180 days after the onset of symptoms. The orbital MRI findings at 180 days showed no significant changes compared with the MRI findings on day 6 of admission. CONCLUSIONS: Primary care physicians should be aware of this rare but potentially sight-threatening complication of herpes zoster ophthalmicus. The appropriate therapy for orbital apex syndrome due to herpes zoster ophthalmicus and the potential outcomes of this condition require further investigation.

Unilateral mydriasis after maxillary osteotomy: a case series and review of the literature.

PURPOSE: To present 4 cases of unilateral mydriasis associated with orthognathic surgery and to review the differential diagnosis and management related to this condition. MATERIALS AND METHODS: Four cases of unilateral mydriasis associated with orthognathic surgery were identified from the authors' institutional experience. All maxillary osteotomies performed by the authors' department from 2001 to 2013 were identified based on Current Procedural Terminology codes; 4 cases of unilateral mydriasis were found. Cases are presented and the literature is reviewed. RESULTS: Two male and 2 female patients with an age range of 16 to 34 years developed unilateral mydriasis after maxillary osteotomy; the estimated prevalence is 0.004%. Although the precise cause can be difficult to determine, in this series 1 case was attributable to swelling affecting contents of the superior orbital fissure, 1 was related to edema or medications, and 2 were pharmacologically induced. CONCLUSION: Although rare, a review of the differential diagnosis for and management of unilateral mydriasis associated with orthognathic surgery is pertinent to those who perform corrective jaw surgery.

Eye on children: acute work-up for pediatric Horner's syndrome. case presentation and review of the literature.

BACKGROUND: Ptosis and anisocoria in a child may be subtle indications of occult pathology, and making the observation acutely in the emergency department (ED) is important in guiding patient management and treatment. Emergency physicians must evaluate patients to exclude serious or life-threatening emergencies and ensure correct disposition of patients. Horner syndrome in children may be considered congenital or acquired and may be from benign or malignant causes. When an isolated, acquired Horner syndrome is suspected in a pediatric patient, physical examination of the neck and abdomen for masses, as well as spot urine catecholamines, vanillylmandelic acid and homovanillic acid, and varying degrees of imaging are recommended as part of the initial evaluation. These evaluations may be performed in the ED or may require hospitalization, depending on the suspected anatomical localization and diagnostic considerations. CASE REPORT: A 21-month-old, normally developed girl presented to the University Hospital ED with a 2-h history of right-sided eyelid drooping in the setting of a febrile illness. An eventual diagnosis of Horner syndrome from cervical lymph node compression was made on the basis of history, examination, and imaging findings. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: ED evaluations of pediatric patients differ from adults. Evaluation and work-up of Horner syndrome in children can be challenging and can require varying degrees of assessment and evaluation, depending on the diagnostic considerations. This article will address the common pathologies responsible for isolated pediatric Horner syndrome and the recommended ED evaluation.