Optic Nerve MRI T2-Hyperintensity: A Nonspecific Marker of Optic Nerve Damage.

BACKGROUND: MRI abnormalities are common in optic neuropathies, especially on dedicated orbital imaging. In acute optic neuritis, optic nerve T2-hyperintensity associated with optic nerve contrast enhancement is the typical imaging finding. In chronic optic neuropathies, optic nerve T2-hyperintensity and atrophy are regularly seen. Isolated optic nerve T2-hyperintensity is often erroneously presumed to reflect optic neuritis, frequently prompting unnecessary investigations and neuro-ophthalmology consultations. Our goal was to determine the significance of optic nerve/chiasm T2-hyperintensity and/or atrophy on MRI. METHODS: Retrospective study of consecutive patients who underwent brain/orbital MRI with/without contrast at our institution between July 1, 2019, and June 6, 2022. Patients with optic nerve/chiasm T2-hyperintensity and/or atrophy were included. Medical records were reviewed to determine the etiology of the T2-hyperintensity and/or atrophy. RESULTS: Four hundred seventy-seven patients (698 eyes) were included [mean age 52 years (SD ±18 years); 57% women]. Of the 364 of 698 eyes with optic nerve/chiasm T2-hyperintensity without atrophy, the causes were compressive (104), inflammatory (103), multifactorial (49), glaucoma (21), normal (19), and other (68); of the 219 of 698 eyes with optic nerve/chiasm T2-hyperintensity and atrophy, the causes were compressive (57), multifactorial (40), inflammatory (38), glaucoma (33), normal (7), and other (44); of the 115 of 698 eyes with optic nerve/chiasm atrophy without T2-hyperintensity, the causes were glaucoma (34), multifactorial (21), inflammatory (13), compressive (11), normal (10), and other (26). Thirty-six eyes with optic nerve/chiasm T2-hyperintensity or atrophy did not have evidence of optic neuropathy or retinopathy on ophthalmologic examination, and 17 eyes had clinical evidence of severe retinopathy without primary optic neuropathy. CONCLUSIONS: Optic nerve T2-hyperintensity or atrophy can be found with any cause of optic neuropathy and with severe chronic retinopathy. These MRI findings should not automatically prompt optic neuritis diagnosis, workup, and treatment, and caution is advised regarding their use in the diagnostic criteria for multiple sclerosis. Cases of incidentally found MRI optic nerve T2-hyperintensity and/or atrophy without a known underlying optic neuropathy or severe retinopathy are rare. Such patients should receive an ophthalmologic examination before further investigations.

Nonneurologic causes of binocular diplopia for the neurologist.

PURPOSE OF REVIEW: To review several etiologies of nonneurologic diplopia that the neurologist should be familiar with. The pathophysiology, clinical presentation, neuroimaging findings, and treatment options are briefly summarized for each condition. RECENT FINDINGS: Certain etiologies for diplopia can be associated with life-threatening neurologic conditions and should be investigated thoroughly for proper localization and immediate management of the underlying disease. However, nonneurological causes of binocular diplopia are very common and disabling, but are often nonemergent and may not require in-depth investigation or neuroimaging. Some of the etiologies of nonneurologic diplopia mimic cranial nerve palsies, making them confusing to evaluate when the physician is not familiar with these etiologies. Unfamiliarity with these diagnoses can lead to unnecessary neuroimaging, inefficient utilization of medical resources, and undue alarm to the patient. Recent advances in clinical diagnostic tools and neuroimaging have clarified our understanding of the diverse underlying mechanisms of nonneurologic binocular diplopia. SUMMARY: Diplopia can be a difficult symptom for the neurologist to evaluate. A systematic approach to the evaluation of diplopia can help establish the urgency and necessity of an extensive workup.This review will help to familiarize the neurologist with nonneurological causes of binocular diplopia, minimize expensive and unnecessary evaluations, and reassure patients and physicians alike.

Carotid-Cavernous Fistula Presenting as Isolated Painful Anisocoria.

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

Seizures as the Initial Manifestation of Idiopathic Intracranial Hypertension Spectrum Disorder.

Idiopathic intracranial hypertension (IIH) is a syndrome of isolated elevated intracranial pressure of unknown aetiology. The IIH spectrum has evolved over the past decade making the diagnosis and management more challenging. The neurological examination in IIH is typically normal except for papilloedema and possible cranial nerve 6 palsy. Recent publications have highlighted skull base thinning and remodelling in patients with chronic IIH. Resulting skull base defects can cause meningo-encephalocoeles, which are potential epileptogenic foci. We describe the clinical and radiological characteristics of five IIH patients with seizures and meningo-encephalocoeles as the presenting manifestations of IIH spectrum disorder.

[ASPECTS AFFECTING PEDIATRIC OPHTHALMOLOGY AND STRABISMUS PUBLICATION TIMES].

BACKGROUND: To better understand and analyze various aspects of scientific publication, bibliometric data analysis is useful. OBJECTIVES: An analysis of the factors associated with shorter publication times in pediatric ophthalmology and strabismus (POS) between the years 2002 and 2007, compared to 2014 and 2018. METHODS: In this retrospective bibliometric analysis, we analyzed 2,487 articles related to POS from the official websites of 8 preselected ophthalmology journals. Time from submission to acceptance, from acceptance to publication, and from submission to publication were calculated for each article. RESULTS: Median peer review durations were 156 days from submission to acceptance; 79 days from acceptance to publication, and 244 days from submission to publication. Journals such as the American Journal of Ophthalmology, JAMA Ophthalmology, and Strabismus reported the shortest time from submission to publication. Annually, all time intervals decreased, but in the first decade, the decline was significantly greater. The time between submission and acceptance of female senior authors increased during the first decade; however, this disappeared during the second decade. CONCLUSIONS: There was an improvement in most journals and the gender gap in senior authorship decreased with time. DISCUSSION: Since digital technology has rapidly developed over the past two decades, authors have been able to communicate with editorial and production teams more quickly and efficiently. Journal names and the gender of the last author are the main factors affecting publication times.

Applying the 2022 optic neuritis criteria to noninflammatory optic neuropathies with optic nerve T2-hyperintensity: an observational study.

INTRODUCTION: Recent diagnostic criteria for optic neuritis include T2-hyperintensity of the optic nerve (ON), even without associated contrast enhancement. However, isolated ON-T2-hyperintensity is a nonspecific finding found in any optic neuropathy or severe retinopathy. We applied the 2022 optic neuritis diagnostic criteria to a cohort of patients with noninflammatory optic neuropathy and ON-T2-hyperintensity in at least one eye, to assess the rate of optic neuritis misdiagnosis using these criteria. METHODS: Retrospective study of consecutive patients who underwent brain/orbit MRI with/without contrast between 07/01/2019 and 06/30/2022. Patients with ON-T2-hyperintensity in at least one eye were included. The 2022 optic neuritis diagnostic criteria were applied to patients with noninflammatory optic neuropathies who had an ophthalmologic examination available for review. RESULTS: Of 150 patients included, 85/150 had compressive optic neuropathy; 32/150 had glaucoma; 12/150 had papilledema; 8/150 had hereditary (3), radiation-induced (3), nutritional (1), traumatic (1) optic neuropathies (none fulfilled the criteria); 13/150 had ischemic optic neuropathy and 4 fulfilled the criteria as definite optic neuritis due to contrast enhancement of the ON head. Seven additional patients would have satisfied the diagnostic criteria if red flags for alternative diagnoses had been overlooked. DISCUSSION: The application of the 2022 optic neuritis diagnostic criteria in patients with noninflammatory optic neuropathy and ON-T2-hyperintensity in at least one ON resulted in misdiagnosis of optic neuritis in only 4 patients because of ON head enhancement, all with nonarteritic anterior ischemic optic neuropathy. Neuro-ophthalmologic evaluation and exclusion of the ON head as a location in the MRI criteria would have prevented optic neuritis misdiagnosis in our study.

Glaucoma as a cause of optic nerve abnormalities on magnetic resonance imaging.

BACKGROUND/OBJECTIVES: To report a series of patients with glaucoma and optic nerve abnormalities on magnetic resonance imaging (MRI) in at least one-eye, and to determine whether these findings correlate with the severity of glaucoma. PATIENTS AND METHODS: Retrospective study of all patients who underwent a brain/orbits MRI without and with contrast at our institution between 07/1/2019-6/30/2022. Patients with optic nerve T2-hyperintensity and/or MRI optic nerve atrophy in at least one-eye and a diagnosis of isolated glaucoma in at least one-eye were included. Demographic information, glaucoma clinical characteristics, glaucoma severity parameters, and MRI indication were collected. RESULTS: Fifty-six patients (112 eyes) (age 65 years-old [range 26-88]; 70% male) had isolated bilateral glaucoma with at least one-eye MRI optic nerve abnormality. The indication for MRI was atypical/asymmetric glaucoma in 91% of patients. Of the 112 eyes, 23 had optic nerve T2-hyperintensity alone; 33 had both optic nerve T2-hyperintensity and MRI optic nerve atrophy; 34 had MRI optic nerve atrophy alone; and 22 did not have abnormal optic nerve MRI-findings. None had optic nerve enhancement. A statistically significant association between optic nerve T2-hyperintensity or MRI optic nerve atrophy and glaucoma severity parameters was found. CONCLUSIONS: Glaucoma is a clinical diagnosis and MRI brain is usually not required, except in atypical or asymmetric cases. Optic nerve T2-hyperintensity and MRI optic nerve atrophy are nonspecific MRI-findings that can be found in severe glaucomatous optic nerves and should not systematically prompt investigations for another cause of optic neuropathy.