Browsing by Author "Tavares Ferreira, J"
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- Ocular Ischaemia Due to a Spontaneous Carotid Artery DissectionPublication . Frazão, S; Perry da Câmara, C; Proença, R; Tavares Ferreira, JInternal carotid artery dissection (ICAD) is caused by the disruption of the tunica intima, with the formation of an intramural haematoma that can cause stenosis or occlusion of the artery's lumen, leading to reduced blood flow and secondary thrombus formation. Up to two-thirds of patients with ICAD show ophthalmological symptoms or signs, which are, frequently, the first manifestations of this clinical condition, often preceding for weeks the neurological signs of cerebral infarction. Central retinal artery occlusion (CRAO) is a rare complication of ICAD, secondary either to haemodynamic compromise, with ocular hypoperfusion and reverse flow within the ophthalmic artery, or to thromboembolic events, in rarer cases. We report a case of CRAO secondary to a spontaneous ICAD, in an otherwise healthy middle-aged patient.
- Optic Neuropathy Due to Chronic Lymphocytic Leukemia: the First Manifestation of the DiseasePublication . Maleita, D; Serras Pereira, R; Hipólito-Fernandes, D; Moura-Coelho, N; Cunha, JP; Tavares Ferreira, JPurpose: Chronic lymphocytic leukemia (CLL) is the most common lymphoproliferative disorder in the western world. The involvement of the central nervous system (CNS) or the optic nerve in CLL, however, is rare. We report a case of a previously untreated patient with CLL whose first manifestation of the disease was a progressive visual loss caused by optic neuropathy. Observations: Clinical manifestations, optical coherence tomography (OCT), and automated visual fields pointed to the diagnosis of neuropathy. Leukemic involvement of the CNS was confirmed after cells suggestive of CLL were found by cerebrospinal fluid analysis. Optic nerve infiltration is thought to be the cause of this optic neuropathy, and the clinical course and treatment are described herein. Conclusions: When readily diagnosed, optic nerve infiltration is a rare, yet manageable complication of CLL.
- Retinal Neurodegeneration in Diabetic Patients Without Diabetic RetinopathyPublication . Tavares Ferreira, J; Alves, M; Dias-Santos, A; Costa, L; Santos, B; Cunha, JP; Papoila, AL; Abegão Pinto, LPURPOSE: To compare the thickness of all retinal layers between a nondiabetic group and diabetic patients without diabetic retinopathy (DR). METHODS: Cross-sectional study, in which all subjects underwent an ophthalmic examination including optical coherence tomography. After automatic retinal segmentation, each retinal layer thickness (eight separate layers and overall thickness) was calculated in all nine Early Treatment Diabetic Retinopathy Study (ETDRS) areas. The choroidal thickness (CT) also was measured at five locations. Generalized additive regression models were used to analyze the data. RESULTS: A total of 175 patients were recruited, 50 nondiabetic subjects and 125 diabetic patients without DR, stratified into three groups according to diabetes duration: group I (<5 years, n = 55), group II (5-10 years, n = 39), and group III (>10 years, n = 31). Overall, groups I and III of diabetic patients had a decrease in the photoreceptor layer (PR) thickness, when compared with the nondiabetic subjects in six ETDRS areas (P < 0.0007). Patients with more recent diagnosis (group I) had thinner PR than those with moderate duration (group II). Interestingly, patients with longer known disease (group III) had the thinnest PR values. There were no overall differences in the remaining retinal parameters. CONCLUSIONS: Retinal thickness profile is not linear throughout disease duration. Even in the absence of funduscopic disease, PR layer in diabetic patients seems to differ from nondiabetic subjects, thus suggesting that some form of neurodegeneration may take place before clinical signs of vascular problems arise.
- Retinal Structural Changes in Preterm Children without Retinopathy of PrematurityPublication . Maleita, D; Serras-Pereira, R; Passos, I; Elisa-Luís, M; Alves, M; Papoila, AL; Brito, C; Cunha, JP; Tavares Ferreira, JPurpose: The aim of this study was to compare all retinal layers' thickness in full-term and preterm children without retinopathy of prematurity (ROP). Methods: Cross-sectional study including two groups of patients: group 1 children with history of preterm gestation without ROP (gestational age < 37 weeks) and group 2 healthy children with history of full-term gestation. All subjects underwent an ophthalmic examination including spectral domain-optical coherence tomography. After automatic retinal segmentation, each retinal layer thickness (eight separate layers and overall thickness) was calculated in all nine Early Treatment Diabetic Retinopathy Study areas. Demographic, systemic, gestational, and birth data were collected. Generalized additive regression models were used to analyze the data. Results: Fifty-one children (51 eyes) were recruited, 19 full-term and 32 preterm children, mean age at ophthalmic examination of 10.58 (4.21) and 14.13 (3.16), respectively. In multivariable analysis, the preterm group's retinal thickness was significantly decreased in total retina nasal outer sector, ganglion cell layer (GCL), and inner plexiform layer (IPL), specifically GCL temporal outer (p = 0.010), GCL superior outer (p = 0.009), IPL temporal outer (p = 0.022), and IPL superior outer (p = 0.004), when compared with full-term group. From the variables compared only with birth head circumference that influenced the models, a non-linear association was identified and consequently modeled with splines through a generalized additive model. Conclusion: This study suggests that preterm children without ROP have structural retinal alterations, mostly in GCL and IPL in outer areas of the macula. Therefore, it is crucial to question gestational history since these retinal changes may be found later in life leading to useless investigation.
- The Role of Ophthalmic Imaging in Central Nervous System Degeneration in Systemic Lupus ErythematosusPublication . Dias-Santos, A; Proença, R; Tavares Ferreira, J; Pinheiro, S; Cunha, JP; Proença, R; Moraes-Fontes, MFSystemic lupus erythematosus (SLE) is an autoimmune connective tissue disorder that can involve any organ system. Central nervous system involvement can be a severe life threatening complication, ultimately resulting in severe neurodegenerative changes. Magnetic resonance imaging suggests that neurodegeneration, which may have deleterious effects on brain function, may occur early in SLE and experimental models suggest that neuroprotection may be feasible and beneficial. The retina is an extension of the brain. Recent ophthalmic imaging technologies are capable of identifying early changes in retinal and choroidal morphology and circulation that may reflect CNS degeneration. However, their utility in monitoring CNS involvement in SLE has been poorly studied as these have only been performed in small cohorts, in a cross-sectional design, non-quantitatively and without correlation to disease activity. The authors aim to review the current understanding of neurodegeneration associated with SLE, with particular focus on the visual pathway. We describe the neuropathology of the visual system in SLE and the evidence for retinal and choroidal neurodegenerative and microvascular changes using optical coherence tomography technology. We aim to describe the potential role of optical imaging modalities in NPSLE diagnosis and their likely impact on the study of neuronal function.