Lateral Gaze Research Articles

Headache After MVA in Physically Active, Healthcare Professional

HPI: 35 y/o F NP with hx of migraines, presented to the ED 1 day s/p MVA, c/o right-sided headache, nausea, photophobia. The patient went off the road at 30 mph, hitting a snowbank. She had a mild headache after the accident, saying her head whiplashed but denied hitting her head, or LOC. She took an ibuprofen but woke up the following morning with the worst headache of her life, prompting ED visit. Pertinent negatives: No retrograde amnesia, phonophobia, blurred vision, eye pain, hearing loss, tinnitus, neck pain, extremity weakness, paresthesia, dizziness. In the ED, patient was told her eye dilated funny, but otherwise normal exam. CT head was negative. GCS 15. Symptoms improved with prochlorperazine, diphenhydramine. She followed up in the office 2 days later, with continued symptoms. Office SCAT2 scored 52. She was diagnosed with post-concussion syndrome, and treated supportively. Over the next several months, patient developed diplopia, vertigo, neck pain, fatigue. EXAM: Vital signs were stable and afebrile, well-developed, AAxOx3, anxious. NCAT. Pupils were equal, round, and L pupil was sluggishly reactive to light. EOMI Visual acuity: OU20/20, OD/OS20/25. AROM/PROM of head and neck were normal. No ptosis, proptosis. CN 2-12 intact. Romberg test negative. Motor strength 5/5 UE & LE. Sensation intact. Subsequent office visits revealed R neck pain to palpation, asymmetry along R levator and R trapezius muscles, with reduced range of motion. DDX: Post-concussive syndrome, BPPV, chronic migraine with aura, CN injury, malignancy/tumor TESTS/RESULTS: CT head (ED) negative. X-ray cervical spine AP/lateral negative. Non-contrast brain MRI negative. She received OMT for neck pain with mild improvement. While working with OT, patient was noted to have horizontal saccades on lateral gaze along L eye, with lateral deviation of L eye. She was referred to neuro-optometry. She was diagnosed with CN3 palsy. DX: Partial oculomotor (CN3) nerve palsy secondary to whiplash from MVA TX & OUTCOMES: Tx: Optometry rehab with vestibular exercises, prism therapy, OMT, TP injections, PT/OT; Sumatriptan, amitriptyline, melatonin. 17 mo s/p MVA, pt continued to have intermittent headaches, light/noise sensitivity, trouble focusing. Symptoms have improved and pt resumed training for local 5K, which she completed. She is not at baseline.

A Case of Traumatic Isolated Unilateral Sixth Cranial Nerve Palsy

Traumatic isolated sixth cranial nerve palsy is a rare condition that has been reported to be as low as 1% to 2, 7% following traumatic brain injury. The sixth nerve innervates the ipsilateral lateral rectus which abducts the eye. Isolated loss of lateral gaze with no other cranial nerve signs and muscular entrapment is thought to be resulted from an injury to the peripheral nerve along its course from the brain stem to the lateral rectus. We presented a case of traumatic isolated unilateral sixth cranial nerve palsy in a female patient with diplopia and restriction left eye movement to lateral following head trauma after accident. Head Computed Tomography (CT) scan showed left frontal bone fracture involving the lateral wall of the orbit and also left retro orbital hemorrhage with no other lesions noted in the brain. Eye examination revealed isolated sixth cranial nerve palsy with normal vision of both eyes. Here we discussed about the possible mechanism, differential diagnosis and also management of the patient.

The hidden Niemann-Pick type C patient: clinical niches for a rare inherited metabolic disease

Background: Niemann-Pick disease type C (NP-C) is a rare, inherited neurodegenerative disease of impaired intracellular lipid trafficking. Clinical symptoms are highly heterogeneous, including neurological, visceral, or psychiatric manifestations. The incidence of NP-C is under-estimated due to under-recognition or misdiagnosis across a wide range of medical fields. New screening and diagnostic methods provide an opportunity to improve detection of unrecognized cases in clinical sub-populations associated with a higher risk of NP-C. Patients in these at-risk groups (“clinical niches”) have symptoms that are potentially related to NP-C, but go unrecognized due to other, more prevalent clinical features, and lack of awareness regarding underlying metabolic causes.Methods: Twelve potential clinical niches identified by clinical experts were evaluated based on a comprehensive, non-systematic review of literature published to date. Relevant publications were identified by targeted literature searches of EMBASE and PubMed using key search terms specific to each niche. Articles published in English or other European languages up to 2016 were included.Findings: Several niches were found to be relevant based on available data: movement disorders (early-onset ataxia and dystonia), organic psychosis, early-onset cholestasis/(hepato)splenomegaly, cases with relevant antenatal findings or fetal abnormalities, and patients affected by family history, consanguinity, and endogamy. Potentially relevant niches requiring further supportive data included: early-onset cognitive decline, frontotemporal dementia, parkinsonism, and chronic inflammatory CNS disease. There was relatively weak evidence to suggest amyotrophic lateral sclerosis or progressive supranuclear gaze palsy as potential niches.Conclusions: Several clinical niches have been identified that harbor patients at increased risk of NP-C.

頭位性めまいを主訴とした脊髄小脳失調症6型 (SCA6) 例の ENG 検討

A 57-year-old woman presented at our outpatient clinic with the recent and frequent experience of paroxysmal positional vertical vertigo similar to the sensation of a somersault, especially changing position from sitting to lying supine, accompanied with spells of nausea and blackout. On examination, we observed prominent downbeat nystagmus in the primary eye position and lateral gaze. MRI disclosed prominent cerebellar cortical atrophy, especially in the vermal regions. The patient had a family history of spinocerebellar ataxia type 6 (SCA6) and had herself received a definitive diagnosis of the same phenotype disease from genetic studies. The points of the ENG findings were as follows: (1) downbeat nystagmus was prominent in the primary eye position and was combined with gaze nystagmus in the lateral gaze; (2) both horizontal & vertical rebound nystagmus were noted; and (3) impairment of both horizontal & vertical smooth pursuit were seen. In horizontal and upward pursuit, catch-up saccades (lower gain) were intermingled. In contrast, backup-saccades (higher gain) were intermingled in downward pursuit. Furthermore, (4) Horizontal saccades were hypometric, though vertical saccades were hypermetric (overshoot); (5) In both horizontal and vertical OKN, the slow phase of OKN was severely impaired. Finally, (6) vestibular caloric nystagmus was well induced bilaterally. Both sides of visual suppression of caloric nystagmus were severely impaired. Most of present results are well explainable with the pure cerebellar cortical atrophy as the typical pathological finding of SCA6. However, two important findings should be mainly discussed and stressed here. One, the gain of the horizontal smooth pursuit was lower, while the gain of the downward pursuit was higher. It seemed to be inconsistent that a single part of the cerebellum would simultaneously modulate decreasing gain of the horizontal and increasing gain of vertical smooth pursuit systems. Therefore, this finding suggested that several parts, not a single part, of the cerebellum would be simultaneously engaged in the gain modulation of the smooth pursuit system. Second, the severe impairments of both horizontal and vertical OKN implied disturbances of both the pursuit and the velocity storage systems. In Cohen & Raphan's model, the slow phase of OKN is composed of the “direct pathway” and the “indirect pathway.” The “direct pathway” utilizes the ocular pursuit system in the flocculus/paraflocculus, while the “indirect pathway” is mediated through the velocity storage system in the medial vestibular nuclei/prepositus hypoglossi nuclei or the interstitial nuclei of Cajal in the brainstem. Consequently, the present results of OKN strongly suggested that the neural circuits related to the velocity storage integrator in the brainstem would also be perturbed, together with the disturbance of the ocular pursuit system in the cerebellum.

Suspension recession of inferior oblique versus graded recession technique in V-pattern strabismus with primary inferior oblique overaction

Purpose The aim of this study was to evaluate the efficacy of inferior oblique suspension recession ‘modified hang-back’ in cases with V-pattern strabismus and primary inferior oblique overaction (IOOA), compared with standard graded recession technique.Patients and methods Thirty patients (60 eyes) presenting with V-pattern strabismus with primary IOOA were enrolled and randomized for inferior oblique weakening intervention − that is, suspension recession (group A), or standard graded recession (group B).Results In group A, the mean postoperative V-pattern exotropia was 4.8±2.7 PD as compared with a mean of 26.42±6.26 PD preoperatively (P≤0.001). Meanwhile, for the esotropic subgroup, the values were 2.57±1.13 and 15.62±4.17 PD, respectively (P≤0.001). For group B patients, the mean V-pattern exotropia was 2±1.5 PD, compared with a preoperative mean value of 23.12±10.66 PD (P≤0.001), and the mean pattern esotropia was 2.28±1.79 PD, compared with a preoperative mean value of 17.14±3.93 PD (P≤0.001), with a highly significant statistical difference between patients within the same group (P≤0.001), as well as between the two groups as regards the exotropic subgroups (P≤0.02). A significant improvement in IOOA was noted in group B, whereas the postoperative hypertropia in lateral gaze was 0.97±1 PD, compared with 5.06±2 in group A (P≤0.001).Conclusion Although considerable results were achieved with the suspension recession technique, the postoperative impact of the procedure as regards the control of IOOA may be still questionable, with significant superior results of the standard recession technique.

Wernicke’s Encephalopathy in A Young Adult Affected by T Cell Acute Lymphoblastic Leukemia and Ileotiphlytis with Review of the Literature

Wernicke-Korsackoff Syndrome is a potentially fatal neurological complication caused by a deficiency of thiamine. The clinical diagnosis is a challenge and the syndrome is frequently misdiagnosed. In this paper we describe the case of a young man affected by T-ALL and ileotyphlitis who developed Wernicke’s Encephalopathy after a month of total parenteral nutrition. Neurological symptomatology, consisting of confusion, nystagmus on lateral gaze, impairment of consciousness state, prosopagnosia and weakness in the four limbs, appeared progressively. An MRI of brain permitted to confirm the diagnosis and high-dose thiamine reintegrating therapy was started obtaining complete resolution of the syndrome.

Kindle the Spindle: To Bring in Light a Rare Case of Eyelid Spindle Cell Sarcoma

Purpose: To bring in perspective a rare case of spindle-cell sarcoma of lid with intra-orbital metastasis. Methods: A seventy-five year old female presented with complaints of severe pain in right eye and right sided headache for 2 months along-with constant watering. She had a history of cataract surgery with IOL implantation in bag in right eye 4 months back. During the same time, a mass lesion was also removed from underside of right lower lid which was present for about 7-8 years. She was asthenic in built and was found to have pallor. On ophthalmic examination she was found to have Snellen’s visual acuity of 6/60 OD, 6/18 OS. Intra-ocular pressure was 37.5 mm of Hg OD, 18.6 mm of Hg OS. Ocular movements were restricted in lateral and superior gaze in right eye. On palpation stony hard, tender induration could be appreciated along the right infero-nasal lid margin. Fundus examination revealed chorio-retinal folds in inferior quadrant peripherally. No palpable lymph nodes were observed. CT scan brain and orbit was advised along-with routine blood investigations and IOP control medications. Results: CT scan revealed a heterogeneous cystic lesion measuring 17 × 16 × 21 mm in antero-inferior right orbit, abutting the globe and inferior rectus with thickening of uveo-scleral ring. The right globe was compressed and displaced supero-laterally. No bony erosion or infiltration of orbital fat or optic nerve was seen. Earlier histo-pathological report of excised lid tumor revealed low grade spindle cell sarcoma. Conclusion: Spindle cell sarcoma of lid is rare entity. This case report reveals a spindle cell sarcoma of lid with intraorbital metastasis.

Changing Vertical Nystagmus in the Opposite Direction: Is the Transition From Upbeat to Downbeat Nystagmus a Diagnostic Clue for Wernicke’s Encephalopathy?

Background: Changes of vertical nystagmus in the opposite direction are very rarely reported. This study aimed to report an unusual case of Wernicke’s encephalopathy (WE) presenting with a transition from upbeat nystagmus (UN) to downbeat nystagmus (DN) and to investigate the clinical pattern of changing vertical nystagmus in the opposite direction reported in the literature.Methods: We present a WE patient with primary position UN that changed to DN with an upward or horizontal lateral gaze. Additionally, we review previously reported cases and analyze the clinical patterns of changing vertical nystagmus in the opposite direction.Results: Among 10 cases, including our case, the most common type of changing vertical nystagmus in the opposite direction was a transition from UN to DN (n=9, 90%). The most common diagnosis was WE, which is accompanied by changes in vertical nystagmus from UN to DN (n=6, 60%). The most commonly associated neuro-radiological localizations for the changing of vertical nystagmus were the brainstem and the cerebellum.Conclusion: The results of this clinical investigation may provide support for the diagnosis of WE. In addition, if young or middle-aged patients exhibit transitions from UN to DN with brainstem or cerebellar signs, a diagnosis of WE should be considered. Furthermore, clonazepam and thiamine might be helpful for improving nystagmus symptoms.

Gaze Palsy in Children: What is Underneath? - A Review Article

Eye movement abnormalities always clench the eyes of a neurologist to reach an interesting diagnosis most of the time in children. The common etiologies affecting the complex brainstem pathways and frontal eye field controlling conjugate eye movement are childhood stroke (pontine infarct), demyelinating disorders, mass lesions, trauma and metabolic or mitochondrial diseases. Horizontal eye movements are conducted by the medial rectus and the lateral rectus muscles. Medial rectus is innervated by oculomotor nerve (cranial nerve III) and the lateral rectus is innervated by abducens nerve (cranial nerve VI) respectively. The oculomotor and the abducens nuclei are interconnected by medial longitudinal fasciculus (MLF). The disorders of horizontal eye movement that are caused by brainstem lesions are classified into three groups: lateral gaze palsy, internuclear ophthalmoplegia, and one-and-a-half syndrome. In the present study, three interesting cases with gaze palsy have been taken into account. Case 1 is an 8-year-old boy presented with left sided hemiparesis and right sided gaze palsy with loss of adduction in right eye (One–and-half syndrome). MRI showed large areas of increased T2W signal intensity both in subcortical white matter and brain stem (involving abducens nucleus, PPRF and ipsilateral MLF). Case 2 is also of a 10-year-old boy, diagnosed to be a case of Clinically Isolated Syndrome (CIS) with ataxia and ophthalmoplegia. MRI showed areas of sub-cortical demyelination in both fronto-parietal region (right side more involved than left) with brain stem and cerebellum unaffected. Case 3 is about an 18-month-old boy presented with complete ophthalmoplegia (Inability to move both the eyes with absent conjugate movement in all directions) and delayed developmental milestones. Lactate was raised in venous blood and MRI showed necrosis in basal ganglia (thalami) and brain stem, with MR spectroscopy showed double lactate peak consistent with Leigh disease (mitochondrial encephalomyopathy).

Myasthenic symptoms in anti-low-density lipoprotein receptor-related protein 4 antibody-seropositive amyotrophic lateral sclerosis: two case reports

BackgroundMyasthenic symptoms can be present in patients with amyotrophic lateral sclerosis (ALS). These symptoms have been considered to be caused by the degeneration of distal motor neurons and the neuromuscular junction (NMJ). Recent studies suggested that antibody to low-density lipoprotein receptor-related protein 4 (LRP4) was a pathogenic agent of myasthenia gravis (MG), and it was also detected in ALS patients.Case presentationPatient 1: A 58-year-old Japanese man developed progressive weakness and subsequent myasthenic symptoms including oculomotor disturbance. Clinical examination and electrophysiological studies confirmed upper and lower motor neuron involvement and NMJ dysfunction, and anti-LRP4 antibody was detected in his serum. A series of immunotherapies, including steroid pulse therapy, intravenous immunoglobulin, and plasmapheresis, was performed, and the myasthenic symptoms partially improved. The titer of anti-LRP4 antibody subsequently decreased. However, the therapeutic effect was transient, and ALS symptoms progressed. His clinical findings fulfilled the criteria of probable ALS using the Awaji criteria. Patient 2: A 74-year-old Japanese man suffered from progressive weakness of all limbs and dropped head in the evening. He complained of diplopia with a lateral horizontal gaze. Probable ALS was diagnosed because of the upper and lower motor neuron signs, whereas anti-LRP4 antibody was detected. Several immunotherapies were administered, and the myasthenic symptoms partially responded to each therapy. However, the truncal muscle weakness progressed, and he died of respiratory failure.ConclusionWe report two anti-LRP4 antibody-seropositive ALS patients with myasthenia who were not typical of ALS patients, and showed partial responses to immunotherapies. The anti-LRP4 antibody-seropositive status may influence developing ALS and cause additional ALS symptoms.

An abnormal ocular motor manifestation of Joubert syndrome

Joubert syndrome is a congenital neurodevelopmental disorder primarily affecting the midbrain and hindbrain. It is characterized by ataxia, hypotonia, and developmental delay as well as apnea or abnormal ocular motor function. We describe and present a video of a child with Joubert syndrome with an alternating skew deviation in primary position rather than on lateral gaze, which is a more characteristic phenotype of this condition.

A Severe Case of Septic Cavernous Sinus Thrombosis Caused by a Rare Pathogen

SESSION TITLE: Student/Resident Case Report Poster - Critical Care IV SESSION TYPE: Student/Resident Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM INTRODUCTION: Cavernous Sinus Thrombosis (CST) is thrombophlebitis in the cavernous sinuses. Before the availability of antibiotics, this dramatic and lethal illness carried a 100% mortality, therefore, the onus is on the clinician to have early recognition of this disease and treatment options, which include antibiotics, anticoagulation, and surgery. Although there have been case reports of CST as a complication of paranasal sinusitis, otitis media, and pharyngitis in pediatric population, literature review reveals few cases of CST in adults causing multi-organ impairment similar to our patient. We report a case of CST causing cranial nerve palsy and internal carotid artery narrowing from ethmoid and sphenoid sinusitis secondary to Group C, Beta Hemolytic Streptococcus. This is a common flora of upper airways and skin and bacteremia is almost always seen in immunocompromised individuals and rarely seen in an immunocompetent patient like ours. CASE PRESENTATION: 36 year old female with no significant past medical history presented to the ED with a three day history of left sided headaches, subjective fevers, diplopia and left periorbital swelling. On exam, she was febrile with left eye proptosis and left lateral gaze palsy. Labs revealed significant leukocytosis with left shift and elevated inflammatory markers. CTA head and neck showed left cavernous sinus thrombosis/thrombophlebitis as well as narrowing of left internal carotid artery with MRI/MRV confirming these findings. Imaging also revealed bilateral complete opacification of sphenoid and ethmoid cells suggestive of severe sphenoiditis and ethmoiditis. She was admitted to ICU and her course was complicated by septic shock and acute hypoxemic respiratory failure requiring pressors and mechanical ventilation as per ARDS protocol. Further septic workup revealed the patient to have beta hemolytic, group C strep bacteremia with nasal culture showing the same speciation. She was started on IV antibiotics and heparin drip in ICU and was later discharged home on oral warfarin and IV ceftriaxone. DISCUSSION: The likely mechanism in our patient is that she initially had ethmoiditis causing orbital inflammation and thrombophlebitis of the ophthalmic vein, which extended posteriorly to cause septic CST. Literature review shows that S. aureus encompasses two-thirds of the cases followed by streptococci, especially pneumococci, but there have been no cases, to our knowledge, of group C beta hemolytic strep causing CST. CONCLUSIONS: Aggressive multidisciplinary approach to management remains key in these patients due to high mortality if there is a delay in early and proper diagnosis. Sinusitis and ethmoiditis are relatively common and a physician should be aware of the potential adverse consequences, especially in the setting of ptosis, proptosis, and external opthalmoplegia. Reference #1: Hiroshi Sakaida, Masayoshi Kabayashi, Ai Ito. Cavernous Sinus Thrombosis: linking a swollen red eye and headache. Lancet 2014: 384: 928 DISCLOSURE: The following authors have nothing to disclose: Hemal Mehta, Anthony Saleh, Ravish Singhal No Product/Research Disclosure Information

Myasthenia Gravis after Botulinum Toxin Type A Injection

Botulinum toxin type A (BoNT type A) is a neurotoxin produced by Clostridium botulinum, which causes paralysis by presynaptically binding to the cholinergic nerve terminals at the neuromuscular junction and decreasing the release of acetylcholine (1). BoNT type A, first used to treat strabismus, is now widely used to treat dystonia, spasticity, and other movement disorders, and also autonomic nervous system disorders including hyperhidrosis and sialorrhea (2). As with the effects of the toxin, the adverse effects are also reversible. The most common and severe adverse effects of the toxin are unwanted and excessive weakness of muscle after injection, paralysis of adjacent muscles caused by diffusion of the toxin and iatrogenic botulism characterized by widespread paralysis including the bulbar muscles. Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction, which is caused by antibodies produced against acetylcholine receptors. Fluctuating weakness is the main characteristic of the disease. A woman aged 80 years who presented with forceful contractions of the jaw and tongue, which caused difficulty in opening the mouth, was diagnosed as having oromandibular dystonia. Ten MU (mouse units) of BoNT type A was administered to each hypoglossal muscle once every 3 months. The patient was admitted to the emergency service with bilateral dropping of the eyelids, diplopia, dysphagia, general weakness, and shortness of breath, ten days after the 9th injection. Neurologic examination showed right dominant bilateral ptosis, mild restriction of lateral gaze of the right eye, isochoric pupils, and weakness of eye tightening. Her speech had a nasal quality. The masseter muscles, tongue, and the flexors of neck were weak. Motor examination of other muscles was normal. Generalized botulism, a rare adverse effect of BoNT type A injection, was considered in the patient. Supportive treatment and pyridostigmine 60 mg 5 times per day were given. Worsening of the symptoms, fluctuating weakness, and inadequate response to pyridostigmine suggested the diagnosis of MG. Repetitive nerve stimulation performed 6 weeks after BoNT type A injection revealed dysfunction of neuromuscular junction and autoantibodies against acetylcholine receptors were found positive in serum. Thorax computerized tomography performed for diagnosis of thymoma was normal. Treatment of 0.5 mg/kg/d prednisolone following 0.4 g/kg/d intravenous immunoglobulin was given because dysphagia and shortness of breath worsened. In time, necessity for pyridostigmine decreased and a significant improvement in neurologic status was achieved. Neurologic examination after 6 months was normal except bilateral mild ptosis. Unfortunately, the patient died of acute myocardial infarction 3 weeks after her last follow-up examination. After BoTN type A injection, symptoms including unilateral ptosis, diplopia, and dysphagia can occur and mimic MG (3). Patients with MG are rarely reported to show movement disorders including blepharospasm and cervical dystonia in the literature (4). The occurrence of symptoms of MG after BoTN type A injection

The Mechanism of Lateral Gaze Bias for Faces

The Mechanism of Lateral Gaze Bias for Faces

Posterior diversion suture to treat symptomatic vertical diplopia isolated to lateral gaze

Vertical strabismus that is present and symptomatic only in lateral gaze presents a challenging treatment problem. We developed a novel technique to treat symptomatic vertical diplopia that is isolated to lateral gaze positions.

Treatment of convergence insufficiency exotropia in adults using a selective muscle fiber surgery treatment algorithm

Treatment of adults with convergence insufficiency (CI) exotropia is challenging as surgery frequently results in distance and lateral gaze esotropia. Recent evidence demonstrates differential compartmental function of extraocular muscle fiber groups. Selective surgery of muscle fiber groups may diminish distance–near disparities (NDD) while maintaining alignment at distance.

Maxillary tuberosity fracture and ophthalmologic complications following removal of maxillary third molar

AbstractThird molar removal is one of the most common procedures performed by dentists and oral surgeons. Removal of maxillary third molar is associated with a lower rate of complication compared to the mandible, and maxillary tuberosity fracture or ophthalmologic complications after removal of maxillary third molar are very rare. We report maxillary tuberosity fracture and ophthalmologic complications following removal of maxillary third molar. A 35‐year‐old female underwent removal of left maxillary third molar at private dental clinic. Following the complete extraction, excessive haemorrhage occurred and maxillary tuberosity fracture was seen and the patient was brought by ambulance to our hospital. The bleeding was controlled by vacuum‐formed splint and nasal packing. Computed tomography revealed that lateral maxillary tuberosity and posterior wall of the maxillary sinus was defect and there was a slight intraorbital haematoma via the inferior orbital fissure as well as with extension in the maxillary sinus and adjacent spaces such as buccal, masticator, pterygomaxillary and infratemporal spaces. Because an ophthalmologist noted only slight diplopia in lateral gaze without abnormal signs in other examinations and nasal and oral bleeding were controlled, the surgical treatment was not required. The patient was immediately hospitalised for close observation. Intravenous antibiotics and steroids were administered. Because swelling of the cheek and buccal mucosa was gradually decreasing without further haemorrhage, the patient was discharged 4 days after the extraction. The diplopia was recovered completely 11 days after the extraction.

Delayed Superior Orbital Fissure Syndrome After Reconstruction of Blowout Fracture

The superior orbital fissure syndrome (SOFS) has been known to be a condition caused by impairment of the nerves that cross the superior orbital fissure. Traumatic SOFS is an uncommon complication which occurs usually within 48 hours after a facial injury. A 25-year-old male sustained facial trauma following an altercation. Clinical findings on presentation included swelling, ecchymosis, hyphema, subretinal hemorrhage, and mild extraocular movement limitation upon lateral gaze on his right eyelids. Facial computed tomography scan confirmed fractures of the medial walls of the right orbit and herniation of orbital soft tissue without the incarceration of medial rectus muscle. Ten days after the trauma, the operation was performed. On postoperative day 16, the patient showed ptosis of the right upper eyelid with a fixed pupil, and there was a hypoesthesia over the distribution of the right supraorbital and supratrochlear nerves. The authors diagnosed as a delayed SOFS and prescribed 4 mg of methylprednisolone q.i.d. for 30 days. After steroid therapy, extraocular movement limitations improved progressively. After 8 months, movement was completely restored. The authors experienced delayed SOFS on posttrauma day 27, and it was treated by steroid therapy. Surgical intervention is required when there is an evident etiology such as underlying hematoma or plate migration. If the reason is not clear like our case, steroid therapy can be considered as one of the options. Particularly, the authors should give special attention to the patient who has congenitally narrow superior orbital fissure, like Fujiwara et al suggested.

A Patient with Newly Diagnosed Diabetes Presenting with Sino-Orbital Mucormycosis

ABSTRACT Objective: To present the case of a patient who developed sino-orbital mucormycosis after an occupational exposure and was found to have newly diagnosed uncontrolled diabetes. Methods: We present the patient's clinical, laboratory, imaging, and histopathology findings and review literature relevant for the evaluation and management of patients with diabetes and suspected mucormycosis. Results: A 53-year-old man with a past medical history of mild-intermittent asthma presented with nasal congestion for 1 month and left-eye pain, swelling, and double vision for 3 days. Patient was employed as a construction worker and reported working on water-damaged houses, pulling out rotten wood and wet plasterboard after Hurricane Sandy. Examination revealed left-eye proptosis, erythema of the superior lid, and diplopia upon upward and right lateral gaze. The left nasal cavity contained mucopurulent discharge. Laboratory analyses were significant for blood glucose of 450 mg/dL with a hemoglobin A1c of 12.2%. A...

Modified Harada-Ito Procedure in Acquired Superior Oblique Palsy with Exotropia

Superior oblique palsy is the most common isolated cranial nerve palsy and is commonly associated with exotropia. Modified Harada-Ito procedure can be used to correct excyclotorsion in symptomatic patients. We report a case of acquired superior oblique palsy with exotropia undergoing modified Harada-Ito procedure. A 33 years old man presented with torsional diplopia. On examination there was 10 degrees of left excyclotorsion on double Maddox rod with 25-diopter of exotropia on primary gaze and 20-diopter on lateral gaze suggestive of lateral incomitancy. He underwent a Fells modification of Harada-Ito procedure with bilateral rectus recession. Three months postoperative, he was orthophoric. Modified Harada-Ito procedure is a successful procedure in overcoming torsional diplopia. It is important to identify lateral incomitancy to prevent overcorrection of the horizontal deviation.