Lorenzo Huang, Fariba Fallahzadeh, Gauti Jóhannesson
<p>An 82-year-old Scandinavian woman with hypertension and diabetes mellitus type 2 experienced 1–2 seconds of blurred vision alternating between right and left eye, never together. There were no associated symptoms such as fatigue, headache or jaw claudication, no sign of temporary visual field loss or ‘dark curtain’. The visual acuity was 0.6/0.6 Snellen explained by moderate cataract with pseudo exfoliation, normal bilateral intraocular pressure and fundoscopy that revealed optic disks with normal size and features bilaterally. There was bilateral calcification-like deposit on the central cornea, initially thought to explain her brief visual disturbances. She was discharged with tear substitutes and instructed to return in case of worsening of symptoms.</p><p>The patient contacted the clinic a week later, reporting altitudinal lower visual field loss in her left eye that worsened to almost total visual loss (Figure 1a). Upon examination, the patient confirmed again absence of the above-mentioned symptoms (no temporal/generalized headache, jaw claudication, scalp pain while combing hair or polymyalgia rheumatica symptoms), no signs of confusion, tiredness, neurological abnormalities, pain in the eye, weight loss or fever. She was a non-smoker and did not have sleep apnoea. Her left eye had 0.4 Snellen visual acuity, optic disc swelling (Figure 1b), no signs of retinal ischemia and a positive left relative afferent pupillary defect (RAPD). C-reactive protein (CRP) and sedimentation rate (SR) were normal, orbital magnetic resonance imaging (MRI) showed no optic abnormalities that could explain the visual field loss. Despite the lack of giant cell arteritis (GCA) symptoms, a rheumatologist was consulted and according to his assessment, an ultrasound (US) evaluation was not deemed necessary. The patient was diagnosed with left sided non-arteritic anterior ischemic optic neuropathy (NA-AION) with a referral to the general practitioner for further cardiovascular risk evaluation.</p><p>The patient was followed up with periodical visual field and visual acuity assessment without reporting new vision deterioration. An additional neck-brain angiography showed no significant findings such as endangering stenosis and the patient was treated with 40 mg oral prednisolone for 2 weeks. Over 2 months of follow up, the left visual field improved from visual field index (VFI) 8–24% and the left optic disc swelling regressed to optic atrophy.</p><p>The patient contacted the eye clinic 3 weeks before the planned final-check due to sudden upper altitudinal hemianopia in her right eye and worsening of her remaining left visual field (Figure 2a). Like before, the patient was totally asymptomatic, no symptoms as listed above besides the sudden right visual field loss. The examinations revealed worsening of visual acuity (0.4/0.3), a fresh right optic disc swelling (Figure 2b) and optic disc atrophy on the left (Figure 2c). Due to bilateral worsening with neither GCA sy
{"title":"Occult GCA: A rare variant of Giant Cell Arteritis","authors":"Lorenzo Huang, Fariba Fallahzadeh, Gauti Jóhannesson","doi":"10.1111/aos.16731","DOIUrl":"10.1111/aos.16731","url":null,"abstract":"<p>An 82-year-old Scandinavian woman with hypertension and diabetes mellitus type 2 experienced 1–2 seconds of blurred vision alternating between right and left eye, never together. There were no associated symptoms such as fatigue, headache or jaw claudication, no sign of temporary visual field loss or ‘dark curtain’. The visual acuity was 0.6/0.6 Snellen explained by moderate cataract with pseudo exfoliation, normal bilateral intraocular pressure and fundoscopy that revealed optic disks with normal size and features bilaterally. There was bilateral calcification-like deposit on the central cornea, initially thought to explain her brief visual disturbances. She was discharged with tear substitutes and instructed to return in case of worsening of symptoms.</p><p>The patient contacted the clinic a week later, reporting altitudinal lower visual field loss in her left eye that worsened to almost total visual loss (Figure 1a). Upon examination, the patient confirmed again absence of the above-mentioned symptoms (no temporal/generalized headache, jaw claudication, scalp pain while combing hair or polymyalgia rheumatica symptoms), no signs of confusion, tiredness, neurological abnormalities, pain in the eye, weight loss or fever. She was a non-smoker and did not have sleep apnoea. Her left eye had 0.4 Snellen visual acuity, optic disc swelling (Figure 1b), no signs of retinal ischemia and a positive left relative afferent pupillary defect (RAPD). C-reactive protein (CRP) and sedimentation rate (SR) were normal, orbital magnetic resonance imaging (MRI) showed no optic abnormalities that could explain the visual field loss. Despite the lack of giant cell arteritis (GCA) symptoms, a rheumatologist was consulted and according to his assessment, an ultrasound (US) evaluation was not deemed necessary. The patient was diagnosed with left sided non-arteritic anterior ischemic optic neuropathy (NA-AION) with a referral to the general practitioner for further cardiovascular risk evaluation.</p><p>The patient was followed up with periodical visual field and visual acuity assessment without reporting new vision deterioration. An additional neck-brain angiography showed no significant findings such as endangering stenosis and the patient was treated with 40 mg oral prednisolone for 2 weeks. Over 2 months of follow up, the left visual field improved from visual field index (VFI) 8–24% and the left optic disc swelling regressed to optic atrophy.</p><p>The patient contacted the eye clinic 3 weeks before the planned final-check due to sudden upper altitudinal hemianopia in her right eye and worsening of her remaining left visual field (Figure 2a). Like before, the patient was totally asymptomatic, no symptoms as listed above besides the sudden right visual field loss. The examinations revealed worsening of visual acuity (0.4/0.3), a fresh right optic disc swelling (Figure 2b) and optic disc atrophy on the left (Figure 2c). Due to bilateral worsening with neither GCA sy","PeriodicalId":6915,"journal":{"name":"Acta Ophthalmologica","volume":"102 8","pages":"968-973"},"PeriodicalIF":3.0,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/aos.16731","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141503823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chandrakumar Balaratnasingam, Christine A. Curcio, William H. Morgan, Elon H. C. van Dijk
Central serous chorioretinopathy (CSC) is a frequently occurring chorioretinal disease, that is commonly associated with subretinal fluid accumulation in a generally young population. Even though choroidal abnormalities have been found to be of importance, the exact pathogenesis of CSC is still being learned. The origin of pigment epithelial detachments, seen in many CSC patients, is also unclear. Based on the follow-up of a CSC patient for more than 5 years, we hypothesize that intraocular pressure and, by extension, the pressure gradient across the Bruch's membrane, may be one factor in the pathogenesis of pigment epithelial detachments in CSC, which might very well have implications for the occurrence of and possible ways to prevent subretinal fluid in CSC.
{"title":"A possible association between intraocular pressure changes and pigment epithelial detachment in central serous chorioretinopathy","authors":"Chandrakumar Balaratnasingam, Christine A. Curcio, William H. Morgan, Elon H. C. van Dijk","doi":"10.1111/aos.16730","DOIUrl":"10.1111/aos.16730","url":null,"abstract":"<p>Central serous chorioretinopathy (CSC) is a frequently occurring chorioretinal disease, that is commonly associated with subretinal fluid accumulation in a generally young population. Even though choroidal abnormalities have been found to be of importance, the exact pathogenesis of CSC is still being learned. The origin of pigment epithelial detachments, seen in many CSC patients, is also unclear. Based on the follow-up of a CSC patient for more than 5 years, we hypothesize that intraocular pressure and, by extension, the pressure gradient across the Bruch's membrane, may be one factor in the pathogenesis of pigment epithelial detachments in CSC, which might very well have implications for the occurrence of and possible ways to prevent subretinal fluid in CSC.</p>","PeriodicalId":6915,"journal":{"name":"Acta Ophthalmologica","volume":"102 7","pages":"843-848"},"PeriodicalIF":3.0,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/aos.16730","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141299686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}