Full sample analysis of cerebral venous sinus thrombosis in ophthalmology inpatients.

PURPOSE: We hope that by analyzing the clinical features of cerebral venous sinus thrombosis (CVST), we can help ophthalmologists reduce misdiagnosis or delayed diagnosis. DESIGN: We evaluated 47 patients with CVST in terms of clinical manifestations. METHODS: All cases were analyzed in terms of risk factors, clinical symptoms, ophthalmic examination, imaging examination and lumbar puncture. RESULTS: The body mass indices (BMIs) of 41 patients (87.2%; 95% CI, 77.7-96.8%) were≥24, which is overweight by Chinese standards. There were 22 patients (46.8%; 95% CI, 32.5-61.1%) with BMIs≥28, who were considered obese. Thirteen were hypertensive (27.7%; 95% CI, 14.9-40.5%). The initial symptoms included blurred vision (23, 48.9%; 95% CI, 34.6-63.2%), amaurosis fugax (13, 27.7%; 95% CI, 14.9-40.5%), headache (11 patients, 23.4%; 95% CI, 11.3-35.5%), dizziness (3, 6.4%; 95% CI, -0.6-13.4%), and bilateral diplopia (3, 6.4%; 95% CI, -0.6-13.4%). There were 9 patients (9, 19.2%; 95% CI, 7.9-30.4%) with blindness, 23 patients (48.9%; 95% CI, 34.6-63.2%) with pupillary abnormalities, and 40 patients (85.1%; 95% CI, 74.9-95.2%) with papilledema. Forty-three of the 45 patients who successfully underwent a routine lumbar puncture showed high intracranial pressure (91.7%; 95.6% CI, 89.6-101.6%). Finally, two cases are reported in greater detail for illustrative purposes. CONCLUSION: The main reasons interfering with the diagnosis of CVST might be its nonspecific ocular symptoms and the physicians' clinical thought process being limited to the scope of common ophthalmological diseases.

Optic nerve sheath fenestration: Current status in France and comparison of 6 different surgical approaches.

PURPOSE: Optic nerve sheath fenestration (ONSF) is a surgical procedure commonly performed in the Anglo-Saxon countries for the treatment of medically refractory idiopathic intracranial hypertension (IIH). We chose to compare 6 different trans-orbital surgical approaches to ONSF. We also desired to determine the number of optic nerve decompression procedures performed in France in 2019 and 2020. METHODS: Four fresh frozen orbits were dissected at the University of Nice anatomy laboratory. We performed the following surgical approaches: (i) eyelid crease, (ii) lid-split, (iii) medial transconjunctival with medial rectus disinsertion, (iv) medial transconjunctival without rectus disinsertion, (v) lateral transconjunctival and (vi) lateral orbitotomy. For each surgical approach, we measured the distance between the incision and the optic nerve dura mater. We also extracted data from the French National PMSI (Programme de Médicalisation des Systèmes d' Information) database from January 2019 through December 2020 to determine the annual number of optic nerve decompression procedures. RESULTS: The lid crease and medial transconjunctival approaches provided the shortest distance to the optic nerve (average 21mm and 24mm, respectively) and the lowest levels of difficulty compared to the other surgical routes. A total of 23 and 45 optic nerve decompressions were performed in France in 2019 and 2020, respectively. Among them, only 2 and 7 procedures, respectively, were performed through a trans-orbital approach. CONCLUSION: Upper lid crease incision and medial transconjunctival approaches are the most direct and easiest surgical routes when performing an ONSF. We found that ONSF was rarely performed in France. We strongly recommend close cooperation between ophthalmologists, neurologists, neurosurgeons and interventional radiologists.

[Idiopathic intracranial hypertension: From physiopathological mechanisms to therapeutic decision]. / Hypertension intracrânienne idiopathique : des mécanismes physiopathologiques à la décision thérapeutique.

Clinical features include visual disturbances, headaches, and pulsatile tinnitus that can be associated with reduced quality of life, and a risk of irreversible visual impairment in some cases. Obese women of childbearing age represent the main at-risk population, and the incidence of the disease is increasing because of rising prevalence of obesity worldwide. In addition, an imbalance in sex hormones is reported as a contributing risk factor. The pathophysiology of idiopathic intracranial hypertension involves a disturbance of the evacuation pathway of intracranial fluids caused by the increase in intracranial venous pressure. Brain imaging is useful for diagnosis with several signs including bilateral stenosis of the transverse sinuses that plays a major role in the pathogenesis of the disease by creating a positive feedback loop that increases intracranial venous hypertension and contributes to clinical manifestations. Treatment aims to relieve symptoms and prevent permanent visual impairment. Drug therapies including acetazolamide and topiramate have moderate effectiveness. Among invasive treatments, transverse sinus stenting seems to be the most interesting option to consider in drug-resistant patients. Weight loss remains essential to achieve a sustainable improvement by reducing central venous pressure. Future randomized trials are expected to reach a consensus on this treatment.

Papilledema secondary to vestibular schwannoma: An atypical case without intracranial hypertension.

In most cases, vestibular schwannomas with papilledema are associated with intracranial hypertension secondary to hydrocephalus (obstructive or communicating). We describe the atypical case of a 39-years-old man who presented with bilateral papilledema revealing a vestibular schwannoma, but without hydrocephalus and with normal intracranial pressure. Ophtalmologic signs were completely resolved after tumor removal. The pathophysiological mechanism generally described to explain bilateral papilledema in such cases is tumor-induced hyperproteinorachia. However, in the absence of hydrocephalus or intracranial hypertension, this case raises the question of the mechanisms involved in the visual impairment related to vestibular schwannoma.

[Clinical and paraclinical examination of non-traumatic optic neuropathy in the adult population]. / Examen clinique et paraclinique d'une neuropathie optique non traumatique de l'adulte.

Optic neuropathies (ON) occur in a variety of clinical presentations depending on their pattern of occurrence, their topography and the amount of functional visual impairment. Management of an ON requires a sequence of steps: confirm its existence (positive diagnosis): the diagnosis of ON is usually clinical and must be considered in the case of decreased visual acuity, change in color vision, visual field defect, relative afferent pupillary defect (RAPD), and absence of macular pathology; rule out differential diagnoses: determine the cause; etiologic diagnosis is sometimes complex and takes shape from clinical and paraclinical building blocks. The etiology may be vascular, inflammatory or demyelinating, infectious, toxic, vitamin-deficient, compressive (neoplastic or non-neoplastic), hereditary, congenital, traumatic or even pressure-related (glaucoma or advanced intracranial hypertension). Cerebral and orbital imaging with fine cuts of the optic nerves is often a mandatory examination, which is sometimes useful to repeat; identify therapeutic emergencies.

[Ischemic optic neuropathies]. / Neuropathies optiques ischémiques.

Ischemic optic neuropathies include any vascular disease of the optic nerve. Anterior ischemic optic neuropathies are classically distinguished from posterior ischemic optic neuropathies by the presence of optic disc edema in the former, and the absence thereof in the latter. Non-arteritic acute anterior ischemic optic neuropathy is the most common ischemic optic nerve disease. Its exact cause remains unknown. A disc at risk (small and crowded optic nerve) is a typical backdrop for the development of non-arteritic ischemic optic neuropathy. There is no curative or preventive treatment. Posterior ischemic optic neuropathy is exceedingly rare, compared to anterior ischemic optic neuropathy. It is more frequent in patients with cardiovascular risk factors or in the perioperative period. There is no treatment. In any case of ischemic optic neuropathy, an arteritic cause must be ruled out urgently through clinical and paraclinical examinations. The most frequent cause is giant-cell arteritis. In this case, emergency treatment with intravenous methylprednisolone is required in order to limit vision loss in the affected eye and to prevent vision loss in the other eye.

[Amiodarone-induced optic neuropathy: A rare side effect]. / Un effet indésirable rare de l'amiodarone : la neuropathie optique.

INTRODUCTION: The diagnosis of bilateral papilledema implies emergency medical care to look for intracranial hypertension and arteritic ischemic neuropathy. However, other causes must also be mentioned, including drugs. Too often underrated because of their usual benignity, drug side ophthalmological effects can be severe and are typically bilateral. CASE REPORT: An 80-year-old woman was hospitalized for bilateral papilledema, predominantly in the left eye, with lowered visual acuity. After ruling out intracranial hypertension, arteritic ischemic optic neuropathy, non-arteritic, and inflammatory bilateral papilledema, the diagnosis was toxic optic neuropathy. CONCLUSION: Bilateral edematous optic neuropathy is a known side effect of amiodarone, uncommon but to be known because of the large number of patients benefiting from this treatment.

[Clinical features and etiologies of acute neuroretinitis in southern Tunisia]. / Profil clinique et étiologique des neurorétinites aiguës dans le sud tunisien.

INTRODUCTION: The diagnosis of neuroretinitis is clinical, with optic nerve involvement and a macular star. The most common etiology is cat scratch disease. MATERIALS AND METHODS: Study of 7 patients (7 eyes) with neuroretinitis. A complete ophthalmic examination, fluorescein angiography and optical coherence tomography were performed for all patients. A focused etiological work-up was conducted. RESULTS: The mean age of the patients was 41.6 years [27-51 years]. Decreased visual acuity was the most common reason for consultation. The neuroretinitis was unilateral in all cases. Subclinical serous retinal detachment was noted in 5 patients. The common etiologies were rickettsiosis (4 cases) and tuberculosis (1 case). Leber's idiopathic stellate neuroretinitis was concluded by the negativity of the etiological investigation. Doxycycline was the treatment of choice for rickettsiosis. CONCLUSION: Rickettsiosis appears to be more common than cat scratch disease as an etiology of neuroretinitis in the present study in southern Tunisia. Moreover, the clinical association of a serous retinal detachment, rarely reported in the literature, seems to be more frequent in our series.

[Diabetic papillopathy after intensification of insulin therapy: A case report]. / Papillopathie diabétique après insulinothérapie intensive : à propos d'un cas.

INTRODUCTION: Diabetic papillopathy is a rare ocular complication of diabetes. Its pathophysiology is not well known. It is a unilateral or bilateral optic disc edema with variable degrees of visual loss. OBSERVATION: A 66-year-old woman, with a twelve years old type 2 diabetes mellitus, suddenly presented a unilateral decreased vision. Her ocular examination was normal eight months earlier. Ocular examination, radiological investigations and laboratory analysis were conclusive of diabetic papillopathy. Medical history revealed a recent rapid improvement of blood glucose control after intensification of insulin therapy. A visual acuity improvement with spontaneous regression of papillary edema was observed. CONCLUSION: There is a risk of diabetic papillopathy associated with the rapid control of blood glucose levels after intensification of insulin therapy, even in diabetic patients without known retinopathy.

[Bilateral papilledema]. / Œdème papillaire bilatéral.

This article will review the current standard of care in the diagnosis and management of bilateral optic disc edema. Two emergent conditions must be considered first: secondary intracranial hypertension (cerebral tumor, cerebral thrombophlebitis…) and arteritic ischemic optic neuropathy (or giant cell arteritis). Having ruled out these two diagnoses, the management follows various steps in order to: (i) rule out pseudo-edema, and (ii) determine the underlying cause of the edema: papilledema, non-arteritic ischemic optic neuropathy or papillitis. Systematic cerebral imaging with contrast is required.

[Optic disc changes by optical coherence tomography in optic disc edema in Lomé]. / Modifications papillaires en tomographie par cohérence optique dans l'œdème papillaire à Lomé.

OBJECTIVE: To study the influence of optic disc edema (ODE) on the dimensions of the disc and the thickness of the retinal nerve fiber layer (RNFL) by optical coherence tomography (OCT) in Lomé. PATIENTS AND METHODS: This was a retrospective study which took place in a general ophthalmology office in the city. Twenty-six eyes were examined for ODE (cases) between January 2013 and May 2015, and 26 healthy eyes (control group) were considered in this study. The control group was recruited taking age into account with a variation not exceeding 5 years compared to the ODE cases. Topcon 3D-OCT 2000 software was used to analyze the disc and to measure the thickness of the peripapillary RNFL. The results were compared with software integrated into the OCT device, to the normal range of databases (normative basis) of RNFL thickness. The variables studied were age, gender, etiology of the edema, disc dimensions (optic disc surface area, vertical cup to disc ratio [CDR]), and the thickness of the peripapillary RNFL. Chi2 tests were used for comparison of proportions with a significance level less than or equal to 0.05. RESULTS: Twenty-six eyes of 16 patients with ODE (mean age 25.88±14.35years) and 26 eyes of 16 control group patients (mean age 25.73±15.90 years) were recruited. The ODE was caused by inflammatory optic neuropathies in 10 cases, malignant hypertension in 8 cases and intracranial hypertension in 8 cases. The surface area of the disc was 3.77±1.82mm2 for the ODE group vs. 2.74±0.57mm2 for the control group (P=0.009). The vertical CDR was 0.11±0.15 for the ODE group vs. 0.50±0.15 for the control group (P=0). The mean RNFL thickness was 117.12±18.30µm for the ODE group vs. 95.77±2.52µm for the control group (P=0.006). This study reveals an increase in RNFL in all quadrants (superior, P=0.027; inferior, P=0.007; nasal, P=0.026; temporal, P=0.032). Of the 26 ODE cases, we noted an increase beyond the normative base; superiorly (in 9 cases), inferiorly (in 12 cases), nasally (in 10 cases) and temporally (in 11 cases). CONCLUSION: The study of papillary changes with OCT in ODE has allowed us to note an increase in the surface area of the disc, a reduction of the vertical CDR, and an increase in the thickness of the average RNF in all quadrants.

[Ocular syphilis: 9 cases]. / Syphilis oculaire : à propos de 9 cas.

Syphilis is a disease with ocular involvement may be opening and cover all ocular structures. The objective of the study was to retrospectively identify and describe all cases of ocular syphilis diagnosed in the ophthalmology department of Besançon University Hospital from March 2004 to April 2014. Between March 2004 and April 2014, we diagnosed and monitored 9 male patients (13 eyes) with ocular syphilis (1 interstitial keratitis, chorioretinitis associated with a 1 hyalite, 3 panuvéites, 1 chorioretinitis after placoid, 3 bilateral papillary edema). Patients had a mean age of 52.6 years (32-77 years) at diagnosis and the inaugural symptoms were in 100% of cases decreased visual acuity. The follow-up period ranged from 1 month to 5 years. The curative treatment included intravenous antibiotics penicillin G for 3 weeks. All patients had an improvement in their AV (AV initial range "counting fingers" and 0.6 versus AV final between 0.5 and 1 in decimal scale). Syphilis is a disease currently on the rise. It must be systematically sought before any inflammatory disease of the eye or papilledema.

[Neuro-ophthalmic emergencies]. / Urgences en neuro-ophtalmologie.

Neuro-ophthalmic emergencies can cause life-threatening or sight-threatening complications. Various conditions may have acute neuro-ophthalmic manifestations, including inflammatory or ischemic processes, as well as tumoral, aneurysmal compression or metabolic and systemic diseases. Diplopia related to a partial third nerve palsy with pupillary involvement may reveal an intracranial aneurysm. Abnormalities of conjugate gaze may reveal an inflammatory or ischemic lesion, most often of the brainstem. An intracranial tumor may also manifest itself as a single or multiple oculomotor palsy, or causing various visual field defects, due to optic nerve, chiasm or retrochiasmal involvement. Arteritic anterior ischemic optic neuropathy may be the first manifestation of giant cell arteritis, prompting rapid treatment with steroids to prevent contralateral involvement. A (painful) Horner syndrome may be the presenting sign of carotid dissection, or it may be a sign of a central or thoracic sympathetic lesion. Beyond these classical emergencies, this non-exhaustive review will also present more rare clinical situations, describing novel algorithms for quick recognition and prompt intervention in acute neuro-ophthalmology.

Two cases of bilateral amiodarone-associated optic neuropathy.

INTRODUCTION: The widespread use of amiodarone is limited by its toxicity, notably to the optic nerve. We report two cases of bilateral optic nerve neuropathy due to amiodarone, and provide a detailed description of the disease. OBSERVATIONS: The first case was a 59-year-old man complaining from insidious monocular loss of vision within ten months of initiating amiodarone. Funduscopy and optical coherence tomography showed bilateral optic disc edema. The second case was a 72-year-old man presenting with a decrease in visual acuity in his left eye for a month. Funduscopy showed a left optic nerve edema, and fluorescein angiography showed bilateral papillitis. In both cases, the clinical presentation was not suggestive of ischemic neuropathy, because of the preservation of visual acuity and the insidious onset. In addition, both cardiovascular and inflammatory work-up were normal. An amiodarone-associated neuropathy was suspected, and amiodarone was discontinued with the approval of the cardiologist, with complete regression of the papilledema and a stabilization of visual symptoms. DISCUSSION: Differentiating between amiodarone-associated optic neuropathy and anterior ischemic optic neuropathy may be complicated by the cardiovascular background of such patients. The major criterion is the absence of a severe decrease in visual acuity; other criteria are the normality of cardiovascular and inflammatory work-up, and the improvement or the absence of worsening of symptoms after discontinuation of amiodarone. CONCLUSION: Amiodarone-associated neuropathy remains a diagnosis of exclusion, and requires amiodarone discontinuation, which can only be done with the approval of a cardiologist, and sometimes requires replacement therapy.