Journal of Neuro-Ophthalmology最新文献

Background: Longitudinal changes in the inner retina in patients with optic neuritis (ON) may be helpful in monitoring patients and determining maintenance treatment. The aim of this study was to investigate longitudinal changes in the inner retina after subsiding of acute demyelinating ON and to identify the factors associated with such changes.

Methods: In this multicenter retrospective observational study, we reviewed the medical records of 77 patients with ON, including 23 with neuromyelitis optica spectrum disorder with aquaporin 4 (AQP4)-immunoglobulin G (IgG) (AQP4 group), 23 with myelin oligodendrocyte glycoprotein (MOG)-antibody-associated disease (MOG group), 18 with multiple sclerosis (MS group), and 13 with idiopathic ON (iON group). We measured the thickness of the peripapillary retinal nerve fiber layer (pRNFL) and the macular ganglion cell-inner plexiform layer (mGCIPL) using optical coherence tomography (OCT) at baseline and at follow-up examinations (mean follow-up duration, 29.6 ± 8.6 months; mean number of OCT, 4.2 ± 1.2) in the absence of ON recurrence.

Results: The estimated rate of pRNFL thinning in the AQP4, MOG, MS, and iON groups was 0.66 (95% confidence interval, 0.35-0.97), 0.35 (0.04-0.66), 0.53 (0.16-0.90), and 0.25 (-0.18 to 0.68) μm/year, respectively, indicating that, in the iON group in contrast to the other groups, there was no significant decrease of pRNFL thickness. Among the AQP4, MOG, and MS groups, there was no significant difference in the rate of pRNFL thinning (P = 0.560). The rate of mGCIPL thinning in the AQP4 and MOG groups was 0.25 (0.04-0.46) μm/year and 0.38 (0.23-0.53) μm/year, respectively. Meanwhile, the rate of mGCIPL change in the MS and iON groups was 0.04 (-0.12 to 0.19) and 0.00 (-0.17 to 0.16) μm/year, respectively, which indicates that there was no significant mGCIPL thinning in the latter 2 groups. Between the AQP4 and MOG groups, meanwhile, the rate of mGCIPL change did not significantly differ (P = 0.295). Age older than 40 years was associated with significant progression of mGCIPL thinning (P = 0.005).

Conclusions: We noted inner retina thinning progression independent of relapse activity in AQP4-ON, MOG-ON, and MS-ON. Because subclinical neuroaxonal damage continues to be incurred after an acute attack of ON subsides despite suppression of new attacks, long-term follow-up and neuroprotection should be considered to be integral to the treatment of patients with ON.

Background: Despite the impact of new-onset diplopia on the quality of life, there are few studies concerning new-onset diplopia in seniors. This study aimed to describe the epidemiology, etiology, prognosis, and outcome of different treatments in the older adults compared with younger adult patients presenting with new-onset binocular diplopia.

Methods: A retrospective chart review of patients ≥18 YO with new-onset binocular diplopia presenting between 2010 and 2021. Data collected included age at presentation, gender, duration of time since diplopia onset, imaging results, known trigger, etiology, treatment, and follow-up.

Results: Two hundred ten patients were included. Of them, 75 patients were ≤65 YO (35.7%, the "younger adult group") and 135 > 65 YO (64.3%, the "older adults group"). The common etiology in both groups was neurogenic (54.7% ≤ 65 vs 62.2% >65, P = 0.29). Cranial nerve palsies were more commonly microvascular in the older adults (96.0% vs 74.1%, P = 0.005), whereas tumor-related cranial nerve palsies were more frequent in younger adults (14.81% vs 2.04%, P = 0.03). A restrictive etiology was observed in 20% of younger adult compared with 11.1% of older adults group ( P = 0.08). Sagging eye syndrome (SES) was the second most common etiology in the older adults group at 11.9%, compared with 1.3% in the younger adult group ( P = 0.01). Decompensated phoria/tropia appeared in 16% of younger adult group compared with 11.9% of older adults ( P = 0.4), with an obvious trigger (mostly cataract surgery) in the latter (80% older adults vs 20% younger adults, P = 0.019). Positive imaging findings were found in 46.7% of patients ≤65 compared with 25.3% of >65 ( P = 0.01) and complete spontaneous resolution of diplopia was noted in 32.1% of the older adults compared with 11.8% of younger adults ( P = 0.003).

Conclusions: Neurogenic diplopia was the most common etiology for both groups, but is more prominent in the older adults. Noticeable findings in the older adults were SES diagnosis, identification of triggers for impaired fusion/diplopia, and a paucity of positive findings in imaging results. It is important to know these differences not only for managing seniors better, but also to minimize symptoms of binocular diplopia after lens-related procedures.

Background: Acquired pendular nystagmus is most often seen in patients with demyelinating disease. Although it is often bilateral, rare cases may be monocular. There is paucity of data on the spectrum of clinical presentation, underlying mechanism, and response to treatment in patients with monocular pendular nystagmus.

Methods: Retrospective case series of patients with monocular pendular nystagmus seen in 2 tertiary neuro-ophthalmology clinics between January 2019 and June 2022. All patients underwent a complete neuro-ophthalmological assessment and MRI.

Results: We describe 5 patients (3 women) aged 31-49 with monocular pendular nystagmus. All had a diagnosis of multiple sclerosis. Three patients had horizontal and 2 had vertical pendular nystagmus. The Snellen visual acuity in the eye with pendular nystagmus varied from 20/20 to 20/200. Two patients were asymptomatic and 3 suffered visually debilitating oscillopsia. Treatment response was available for 2 patients, both of which responded well to treatment with memantine. The pendular nystagmus was observed in the eye with worse visual acuity in 4 of 5 cases (80%). Three patients had bilateral pontine lesions, and 2 had unilateral pontine lesion ipsilateral to the side of nystagmus.

Conclusions: Monocular pendular nystagmus in adults is seen most often in patients with multiple sclerosis. Asymmetry in brainstem lesions and afferent visual input may be the culprit. Treatment with memantine may result in significant improvement in symptomatic patients.