Choroidal Thickness in Eyes with Band Atrophy of the Optic Nerve from Chiasmal Compression.

Background: The choroid is a vascular tissue that helps maintain retinal and prelaminar optic nerve head function. Choroidal thickness has been previously studied in diseases accompanied by retinal neural loss, but the relationship between the two sets of measurements is not clear. In eyes with temporal hemianopia as a result of chiasmal compression lesions (CCL), retinal neural loss tends to be greater in the nasal than the temporal hemiretina, a fact that may be useful in evaluating the effect of inner retinal layer loss on choroidal thickness. Purpose: To evaluate macular and peripapillary choroidal thickness on swept-source optical coherence tomography (SS-OCT) in eyes with temporal hemianopia as a result of chiasmal compression and in healthy controls. Methods: 33 eyes of 26 patients with band atrophy of the optic nerve and temporal visual field defects as a result of previously treated suprasellar tumors (CCL group) and 40 eyes of 21 healthy controls underwent SS-OCT scanning. The thickness of the peripapillary retinal nerve fiber layer (pRNFL), the peripapillary choroid (pChoroid), the macular RNFL (mRNFL), the macular ganglion cell layer (mGCL), and the macular choroid (mChoroid) was expressed globally and by sector (peripapillary quadrants and macular hemifield and quadrants). Ratios between macular nasal and temporal hemifield and quadrantic measurements were calculated using generalized estimated equation models, and the two groups were compared. Results: The pRNFL, mRNFL, and mGCC thicknesses were significantly smaller in the CCL group than in the control group (64.67 ± 10.53 µm, 29.68 ± 5.80 µm, and 80.60 ± 10.17 µm vs. 103.78 ± 12.23 µm, 39.89 ± 3.82 µm, and 105.51 ± 7.76 µm, respectively; p < 0.001). For the choroid, the only difference between the groups was increased macular nasal hemifield and superonasal quadrant thickness in CCL (222.47 ± 61.05 µm and 230.45 ± 58.59 µm in the CCL group, respectively vs. 190.68 ± 52.54 µm and 197.65 ± 54.80 µm in the control group, respectively; p < 0.05). The temporal/nasal ratios were significantly higher for the mRNFL and mGCC parameters and significantly lower for the mChoroid parameters in the CCL group, except for the superotemporal/superonasal quadrant ratio. Conclusions: The choroid does not thin after the inner retinal layer becomes damaged due to CCL and may even be thicker in some areas with corresponding severe retinal neural loss. While further studies are needed to interpret these findings, choroidal thinning is most likely not secondary to optic nerve disease-related inner retinal neural loss.

Unilateral papilledema and peripapillary polypoidal choroidal vasculopathy as the presenting manifestations of intracranial hypertension.

We have reported here the case of a 54-year-old woman with intracranial hypertension that presented with the unique features of unilateral papilledema and peripapillary polypoidal choroidal vasculopathy. Our investigations lead to the diagnosis of idiopathic intracranial hypertension and an incidental small right frontal meningioma. The patient was accordingly treated with oral acetazolamide, followed by three consecutive monthly intravitreal injections of bevacizumab, which resulted in the inactivation of the polypoidal choroidal vasculopathy, marked reduction of lipid exudation, and complete absorption of the subretinal fluid. This case serves as the first documentation of polypoidal choroidal vasculopathy associated with papilledema. It also demonstrates that choroidal vascular abnormalities may occur even when optic disk edema is unilateral, which is an uncommon manifestation of increased intracranial pressure. Prompt recognition of such findings and its appropriate management are essential for adequate treatment and prevention of irreversible visual loss.

Circumpapillary and macular vessel density assessment by optical coherence tomography angiography in eyes with temporal hemianopia from chiasmal compression. Correlation with retinal neural and visual field loss.

AIMS: To compare the circumpapillary and macular vessel density (cpVD/mVD) of eyes with temporal visual field (VF) defect and band atrophy (BA) of the optic nerve and normal controls using OCTA and to verify the association of VD parameters with circumpapillary retinal nerve fibre layer (cpRNFL) thickness, macular ganglion cell complex (mGCC) thickness and VF loss. METHODS: Thirty-three eyes of 26 patients with BA and 42 eyes of 22 age-matched normal controls underwent OCT + OCTA scanning. cpVD and cpRNFL were expressed as average and sector measurements. mVD and mGCC were calculated as averages and in quadrants and hemiretinas. VF loss was estimated using the 24-2 and the 10-2 protocols. Generalized estimated equation models were used for comparisons and area under the receiver operating characteristics (AROC) were calculated. RESULTS: Compared with controls, BA eyes displayed smaller average cpVD and mVD values (p < 0.001 and AROC = 0.91 for both). Sectorial measurements were also reduced, especially the nasotemporal sector average cpVD (p < 0.001 and AROC = 0.96) and the nasal retina mVD measurements (p < 0.001 and AROC = 0.93). cpVD and mVD correlated strongly with corresponding cpRNFL and mGCC thickness measurements in affected regions (r range: 0.67-0.78 and 0.56-0.76, respectively). Similarly, cpVD and mVD parameters correlated significantly with corresponding VF loss (r range: 0.45-0.68). CONCLUSIONS: cpVD and mVD are significantly reduced in BA eyes compared with controls and are strongly correlated with retinal neural and VF loss. cpVD and mVD reduction on OCTA could serve as a surrogate for retinal neural loss in compressive optic neuropathy and might be useful in its management.

Unilateral papilledema and peripapillary polypoidal choroidal vasculopathy as the presenting manifestations of intracranial hypertension / Papiledema unilateral e vasculopatia polipoidal da coroide peripapilar como sinais de apresentação de hipertensão intracraniana

ABSTRACT We have reported here the case of a 54-year-old woman with intracranial hypertension that presented with the unique features of unilateral papilledema and peripapillary polypoidal choroidal vasculopathy. Our investigations lead to the diagnosis of idiopathic intracranial hypertension and an incidental small right frontal meningioma. The patient was accordingly treated with oral acetazolamide, followed by three consecutive monthly intravitreal injections of bevacizumab, which resulted in the inactivation of the polypoidal choroidal vasculopathy, marked reduction of lipid exudation, and complete absorption of the subretinal fluid. This case serves as the first documentation of polypoidal choroidal vasculopathy associated with papilledema. It also demonstrates that choroidal vascular abnormalities may occur even when optic disk edema is unilateral, which is an uncommon manifestation of increased intracranial pressure. Prompt recognition of such findings and its appropriate management are essential for adequate treatment and prevention of irreversible visual loss.

RESUMO Relatamos um caso de uma paciente de 54 anos com hipertensão intracraniana que apresentava achados atípicos de papiledema unilateral e vasculopatia polipoidal da coroide peripapilar. A investigação levou ao diagnóstico de hipertensão intracraniana idiopática e de um pequeno meningioma incidental. A paciente foi tratada com acetazolamida por via oral, seguida de três injeções intravítreas mensais de bevacizumabe, resultando em inatividade da vasculopatia polipoidal da coroide, redução da exsudação e completa absorção do líquido subretiniano. A apresentação deste caso serve para documentar pela primeira vez vasculopatia polipoidal da coroide associada a papiledema. Ele também demonstra que podem ocorrer anormalidades vasculares da coroide mesmo quando o edema do disco óptico é unilateral, uma manifestação incomum do aumento da pressão intracraniana. O reconhecimento imediato desses achados e seu manejo adequado são essenciais para o tratamento adequado e para prevenção da perda visual irreversível.