Variable functional recovery and minor cell loss in the ganglion cell layer of the lizard Gallotia galloti after optic nerve axotomy

In the model of experimentally induced ischemia- reperfusion injury, retinal ganglion cells (RGC) expressing the gene AP-1 result apoptosis. The inflammation mediators, such as TNF-α, IL-1β, etc. lead RGC to apoptosis, that may lead the thinning of the retinal ganglion cell layer (RGCL) followed by the optic nerve fiber layer (RNFL) thinning. In his study we observed retinal ganglion cell and optic nerve fiber layer thinning in patients with various uveitis, that the pathological features appear obliterative vasculitis, using the optical coherence tomography (OCT) imaging analyses. Subjects were 182 eyes of 91 uveitis patients without glaucoma. Comparison were patients with normal tension glaucoma (NTG). Image analyses were conducted with 3D OCT-2000. As a result average RGCL thickness values in the patients with uveitis were significantly(p<0.01) thinner than those in healthies. Cycle scan findings of RNFL around the optic disc in the patients with uveitis showed significant thinning especially at nasal side. The retinal ganglion cell layer thinning followed by the retinal nerve fiber thinning in the patients with various uveitis was observed, and the thinning was similar to that in patients with glaucoma. The observation of RGCL and RNFL thickness may be useful for the diagnosis and the follow-up of uveitis.

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Spectral-domain OCT changes in retina and optic nerve in children with hypoxic–ischaemic encephalopathy

Graefe s Archive for Clinical and Experimental Ophthalmology ◽

10.1007/s00417-020-04996-y ◽

2020 ◽

Author(s):

L. Grego ◽

S. Pignatto ◽

E. Busolini ◽

N. Rassu ◽

F. Samassa ◽

...

Keyword(s):

Optic Nerve ◽

Ganglion Cell ◽

Therapeutic Hypothermia ◽

Nerve Fibre ◽

Cerebral Oedema ◽

Ganglion Cell Layer ◽

Cell Layer ◽

Control Group ◽

Fibre Layer ◽

Nerve Fibre Layer

Abstract Purpose To evaluate the effect of neonatal hypoxic–ischaemic injury on the retina and the optic nerve and to correlate ocular damage with systemic parameters, laboratory tests, neurological imaging and therapeutic hypothermia at birth. Methods Forty-one children with hypoxic–ischaemic encephalopathy (HIE) at birth (9.09 ± 3.78 years) and a control group of 38 healthy subjects (9.57 ± 3.47 years) were enrolled in a cohort study. The HIE population was divided into three subgroups, based on the degree of encephalopathy according to Sarnat score and the treatment with therapeutic hypothermia (TH): Sarnat score I not treated with hypothermia, Sarnat score II-III treated with TH and Sarnat score II-III not subjected to TH. Total macular thickness, individual retinal layers and peripapillary nerve fibre layer thickness were measured with spectral-domain optical coherence tomography. Clinical data of perinatal period of HIE children were collected: APGAR score, pH and base excess of funiculus blood at birth, apnoea duration, brain ultrasound, cerebral MRI ischaemic lesions and blood chemistry tests. Results Children with Sarnat score I did not show a reduction of peripapillary nerve fibres and ganglion cell layer compared to the control group (p = 0.387, p = 0.316). Peripapillary nerve fibre layer was 109.06 ± 7.79 μm in children with Sarnat score II-III treated with TH, 108.31 ± 7.83 μm in subjects with Sarnat score II-III not subjected to TH and 114.27 ± 6.81 μm in the control group (p = 0.028, p = 0.007). Ganglion cell layer was thinner in children with Sarnat score II-III treated with TH (50.31 ± 5.13 μm) compared to the control group (54.04 ± 2.81 μm) (p = 0.01). Inner retinal layers damage correlated with C-reactive protein and lactate dehydrogenase increase, while higher levels of total bilirubin were protective against retinal impairment (p < 0.05). Cerebral oedema was related to peripapillary nerve fibre layer damage (p = 0.046). Conclusions Thickness reduction of inner retinal layer and peripapillary nerve fibre impairment was related to encephalopathy severity. Ocular damage was associated with inflammation and cerebral oedema following hypoxic–ischaemic damage.

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