Background/aim: Retinal vein occlusion (RVO) is one of the most frequent ocular vascular diseases and leads to severe vision impairment. Colour Doppler imaging (CDI) is the first method which allows distinct evaluation of arterial and venous velocities in RVO. CDI is valuable for diagnosis of RVO and shows the effects of isovolaemic haemodilution. Patients with RVO were monitored by CDI for 1 year in order to clarify venous and arterial involvement in the pathogenesis of this disease. Methods: Patients with RVO were monitored prospectively for 1 year with clinical examinations, fluorescein angiography, and CDI every 3 months. 102 adults referred for RVO for less than 2 months were enrolled. Unaffected eyes were used as control. The maximum systolic and diastolic flow velocities and the resistance index (RI) were measured in the central retinal artery (CRA) and the maximum and minimum blood flow velocities in the central retinal vein (CRV). Results: During the year of observation, branch retinal vein occlusion (BRVO), ischaemic central retinal vein occlusion (CRVO), and non-ischaemic CRVO had a distinct pattern of venous velocity changes. BRVO had a similar profile to that observed in controls. Venous velocities were continuously lower in central forms, with the lowest values in ischaemic occlusion. In contrast, a brief decrease in arterial diastolic velocity was observed in ischaemic CRVO at presentation, correlated with arteriovenous passage time on fluorescein angiography, but with rapid normalisation. Conclusions: CDI findings were correlated with the type of RVO at all times during follow up. CDI showed persistent impairment of central venous velocity in CRVO whereas there was a fast initial values recovery of the arterial velocity. These results using CDI show strong evidence of a primary venous mechanism in RVO.

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Purpose We report the first case of acute and late‐onset Autosomal Dominant Optic Atrophy with a novel mutation. Autosomal Dominant Optic Atrophy (ADOA) is an inherited primary optic neuropathy that leads to reduced visual acuity. ADOA has often been associated with mutations in OPA1 gene. OPA1 encodes a large dynamin‐related GTPase, involved in mitochondrial structure, mitochondrial DNA maintenance and apoptosis regulation. Methods We conducted direct DNA sequencing of the entire coding sequence and the exon/intron junctions of OPA1 gene. Results A 62‐year‐old woman noticed blurred vision with a central scotoma. Visual loss was sudden, painless and severe in her right eye. Papillary edema was noted. Left visual loss occurred one year after initial presentation. The ophthalmoscopic feature of our patient was diffuse optic disc atrophy. MRI examination confirmed the diagnosis of isolated bilateral optic neuropathy. We did not found any neurological, metabolic, toxic, or ophtalmic causes. One novel heterozygous missense mutation in exon 27 was characterized. This mutation has not been previously reported, was absent in 400 control chromosomes and affected highly conserved amino acids. Conclusion The age of onset, like ADOA penetrance must be accepted to be more variable than initially thought, including late‐onset cases. The presence of an OPA1 mutation reveales that this sporadic late‐onset and acute case of optic neuropathy is related to ADOA. This result shows that the mutation screening of OPA1 gene could be justified in every case of optic nerve atrophy with no clear cause.