Branch Retinal Vein Occlusion Causes Topographic Optic Neuropathy and Retrograde Maculopathy

Background To evaluate retinal ganglion cell (RGC) loss and axonal affection in branch retinal vein occlusion (BRVO).Methods 13 eyes of 12 non-glaucomatous BRVO patients were included. Thickness of peripapillary and macular retinal nerve fiber layer (pRNFL, mRNFL), ganglion cell-inner plexiform layer (GCIPL), inner nuclear layer, outer and total retina were measured at baseline and after a mean follow-up of 14 months. We compared the thickness between the affected and their internal reference regions. Additionally, pRNFL thickness was compared between the occluded and the healthy fellow eyes in the 11 unilateral cases.Results Significant degeneration of the pRNFL was observed in the affected sector of the BRVO eyes (P < 0.01 versus reference sector and versus fellow eye). In contrast, mRNFL and GCIPL thickness showed no difference between affected and reference regions and no correlation with pRNFL thickness. Degenerative microcystic macular edema (MME) was present in 25% of the eyes with macular edema following BRVO.Conclusion Axonal degeneration occurs in pRNFL, which suggests that anterograde degeneration is the mechanism of RGC affection in BRVO. Our results emphasized the importance of pRNFL monitoring in BRVO treatment, and considering degenerative MME in persistent edema following BRVO.

Attack-related damage of thalamic nuclei in neuromyelitis optica spectrum disorders

ObjectivesIn neuromyelitis optica spectrum disorders (NMOSD) thalamic damage is controversial, but thalamic nuclei were never studied separately. We aimed at assessing volume loss of thalamic nuclei in NMOSD. We hypothesised that only specific nuclei are damaged, by attacks affecting structures from which they receive afferences: the lateral geniculate nucleus (LGN), due to optic neuritis (ON) and the ventral posterior nucleus (VPN), due to myelitis.MethodsThirty-nine patients with aquaporin 4-IgG seropositive NMOSD (age: 50.1±14.1 years, 36 women, 25 with prior ON, 36 with prior myelitis) and 37 healthy controls (age: 47.8 ± 12.5 years, 32 women) were included in this cross-sectional study. Thalamic nuclei were assessed in magnetic resonance images, using a multi-atlas-based approach of automated segmentation. Retinal optical coherence tomography was also performed.ResultsPatients with ON showed smaller LGN volumes (181.6±44.2 mm3) compared with controls (198.3±49.4 mm3; B=−16.97, p=0.004) and to patients without ON (206.1±50 mm3 ; B=−23.74, p=0.001). LGN volume was associated with number of ON episodes (Rho=−0.536, p<0.001), peripapillary retinal nerve fibre layer thickness (B=0.70, p<0.001) and visual function (B=−0.01, p=0.002). Although VPN was not smaller in patients with myelitis (674.3±67.5 mm3) than controls (679.7±68.33; B=−7.36, p=0.594), we found reduced volumes in five patients with combined myelitis and brainstem attacks (B=−76.18, p=0.017). Volumes of entire thalamus and other nuclei were not smaller in patients than controls.ConclusionThese findings suggest attack-related anterograde degeneration rather than diffuse thalamic damage in NMOSD. They also support a potential role of LGN volume as an imaging marker of structural brain damage in these patients.

Damage of the lateral geniculate nucleus in MS

ObjectiveTo study if the thalamic lateral geniculate nucleus (LGN) is affected in multiple sclerosis (MS) due to anterograde degeneration from optic neuritis (ON) or retrograde degeneration from optic radiation (OR) pathology, and if this is relevant for visual function.MethodsIn this cross-sectional study, LGN volume of 34 patients with relapsing-remitting MS and 33 matched healthy controls (HC) was assessed on MRI using atlas-based automated segmentation (MAGeT). ON history, thickness of the ganglion cell–inner plexiform layer (GC-IPL), OR lesion volume, and fractional anisotropy (FA) of normal-appearing OR (NAOR-FA) were assessed as measures of afferent visual pathway damage. Visual function was tested, including low-contrast letter acuity (LCLA) and Hardy-Rand-Rittler (HRR) plates for color vision.ResultsLGN volume was reduced in patients vs HC (165.5 ± 45.5 vs 191.4 ± 47.7 mm3, B = −25.89, SE = 5.83, p < 0.001). It was associated with GC-IPL thickness (B = 0.95, SE = 0.33, p = 0.006) and correlated with OR lesion volume (Spearman ρ = −0.53, p = 0.001), and these relationships remained after adjustment for normalized brain volume. There was no association between NAOR-FA and LGN volume (B = −133.28, SE = 88.47, p = 0.137). LGN volume was not associated with LCLA (B = 5.5 × 10−5, SE = 0.03, p = 0.998), but it correlated with HRR color vision (ρ = 0.39, p = 0.032).ConclusionsLGN volume loss in MS indicates structural damage with potential functional relevance. Our results suggest both anterograde degeneration from the retina and retrograde degeneration from the OR lesions as underlying causes. LGN volume is a promising marker reflecting damage of the visual pathway in MS, with the advantage of individual measurement per patient on conventional MRI.

Combination unilateral amygdaloid and ventromedial hypothalamic lesions: evidence for a feeding pathway

Previous studies have reported hyperphagia and obesity in female rats with bilateral lesions of the most posterodorsal part of the amygdala. In rats with unilateral posterodorsal amygdaloid lesions, a dense pattern of anterograde degeneration appears in the ipsilateral ventromedial hypothalamus, but not the contralateral nucleus. In the present study, female rats with unilateral ventromedial hypothalamic lesions or sham lesions were given either sham lesions or unilateral lesions of the posterodorsal amygdala (PDA) 20 days later. Unilateral lesions of the ventromedial hypothalamus resulted in hyperphagia and excessive weight gain. Subsequent amygdaloid lesions that were contralateral to the initial hypothalamic lesions resulted in hyperphagia and additional excessive weight gains, but amygdaloid lesions ipsilateral to the initial hypothalamic lesions did not. It is concluded that the effects of the two lesions on body weight are not additive and that the PDA and ventromedial hypothalamus are part of the same ipsilateral pathway regulating feeding behavior and body weight regulation.