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1.
Insight ; 41(1): 13-17, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-30230735

RESUMO

Glaucoma is one of the single largest causes of irreversible blindness. Glaucomatous vision loss is preventable with the appropriate diagnostic testing and treatment. Ophthalmic nurses play and important role in ensuring the success of glaucoma diagnosis and treatment.


Assuntos
Glaucoma de Ângulo Aberto/diagnóstico , Glaucoma de Ângulo Aberto/terapia , Profissionais de Enfermagem/estatística & dados numéricos , Enfermeiros Especialistas , Papel do Profissional de Enfermagem , Oftalmologia , Técnicas de Diagnóstico Oftalmológico/enfermagem , Humanos , Pressão Intraocular , Recursos Humanos
2.
J Neuroophthalmol ; 32(4): 313-20, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-22684127

RESUMO

BACKGROUND: In cases of progressive optic neuropathy, diagnostic uncertainty often persists despite extensive work-up. Optic nerve biopsy (ONB) can be considered, especially when visual decline of the affected or fellow eye ensues despite empiric therapy. We aimed to evaluate both diagnostic and therapeutic utilities of ONB based on the long-term experience at a tertiary care institution. METHODS: This was a retrospective chart review of biopsies over 20 years at a single institution involving intrinsic or adherent optic nerve masses. Main outcome measures included the impact of tissue sampling on reaching a diagnosis and on guiding treatment. Secondary measures included vision in the eye of the ONB and the fellow eye. RESULTS: Fifteen patients with a mean age of 51.7 ± 17.4 years underwent biopsies. At the time of biopsy, visual acuity was no light perception in 8 (53%) eyes, light perception to counting fingers in 5 (33%), and 20/400 or better in 2 (13%). The fellow eye of 7 patients (47%) experienced some degree of sequential vision loss before biopsy. Seven specimens included en bloc biopsy of the nerve, 7 contained the dural sheath (usually with a portion of the optic nerve), and 1 only of the compressive mass. Six patients (40%) had tumors. Six of 8 inflammatory lesions biopsied required further clinical data to arrive at specific diagnoses. In one case, a clinical diagnosis could not be made. No patients experienced further vision loss in the fellow eye at last follow-up (median, 8 months). CONCLUSIONS: In diverse circumstances of progressive optic neuropathy, ONB can be beneficial in establishing the diagnosis. ONB can help direct specific local or systemic treatment, particularly when infectious or inflammatory etiologies are identified. ONB, if considered early in the disease course, can potentially halt or prevent vision loss when the fellow eye is threatened.


Assuntos
Doenças do Nervo Óptico/diagnóstico , Nervo Óptico/patologia , Adulto , Idoso , Biópsia , Citocinas/metabolismo , Progressão da Doença , Feminino , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Doenças do Nervo Óptico/fisiopatologia , Estudos Retrospectivos , Acuidade Visual
3.
Ophthalmology ; 116(9): 1808-1813.e1, 2009 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-19643491

RESUMO

OBJECTIVE: To identify and describe patients with idiopathic intracranial hypertension (IIH) with concurrent functional visual loss (FVL). DESIGN: Observational, retrospective case series. PARTICIPANTS: Seventeen patients with IIH and FVL. METHODS: Clinical features were collected retrospectively. Data from 281 cases of IIH were analyzed for concurrence of FVL. MAIN OUTCOME MEASURES: Occurrence of FVL diagnosed at presentation or on subsequent follow-up. RESULTS: Seventeen patients had FVL and IIH. Of the 17 patients with FVL and IIH, 11 (65%) had FVL on presentation, with the remaining 6 patients developing FVL after initial presentation. Two patients in this cohort had documented recurrence of their IIH. There were several common patterns of FVL. All 17 patients had functional visual fields, with 82% having tubular fields and 71% exhibiting nonphysiologic constriction on perimetry testing. Seventy-six percent of patients had nerve/field mismatch showing no atrophic disc changes. Eighty-eight percent of patients had significant psychiatric, psychosocial, or other medical comorbidities. The majority of patients were managed surgically at some point in their clinical history, with 53% having nerve decompression, shunt, or both. Three patients had optic nerve sheath fenestrations after the diagnosis of FVL. CONCLUSIONS: Results suggest a high prevalence of FVL in IIH with a potential association with psychiatric illness and psychosocial stressors requiring careful consideration before surgical intervention. FINANCIAL DISCLOSURE(S): The author(s) have no proprietary or commercial interest in any materials discussed in this article.


Assuntos
Pseudotumor Cerebral/fisiopatologia , Transtornos da Visão/fisiopatologia , Adulto , Feminino , Seguimentos , Humanos , Pessoa de Meia-Idade , Disco Óptico/patologia , Papiledema/diagnóstico , Pseudotumor Cerebral/diagnóstico , Pseudotumor Cerebral/cirurgia , Estudos Retrospectivos , Fatores de Risco , Transtornos da Visão/diagnóstico , Acuidade Visual/fisiologia , Testes de Campo Visual , Campos Visuais/fisiologia
4.
Proc Natl Acad Sci U S A ; 100(26): 15859-64, 2003 Dec 23.
Artigo em Inglês | MEDLINE | ID: mdl-14657382

RESUMO

Degeneration of vessels precedes and precipitates the devastating ischemia of many diseases, including retinopathy of prematurity and diabetic retinopathy. Ischemia then leads to proliferative retinopathy and blindness. Understanding the mechanisms of blood vessel degeneration is critical to prevention of these diseases. Vessel loss is associated with oxygen-induced suppression of vascular endothelial growth factor (VEGF) and with pericyte (vascular smooth muscle cell) dropout. The molecular mechanism of pericyte protection of the vasculature is unknown. We show that transforming growth factor beta1 (TGF-beta1)-expressing pericytes are specifically found on vessels resistant to oxygen-induced loss. TGF-beta1 potently induces VEGF receptor 1 (VEGFR-1) expression in endothelial cells and thereby prevents oxygen-induced vessel loss in vivo. Vessel survival is further stimulated with a VEGFR-1-specific ligand, placental growth factor 1. TGF-beta1 induction of VEGFR-1 in endothelial cells explains pericyte protection of vessels and the selective vulnerability of neonatal vessels to oxygen. These results implicate induction and activation of VEGFR-1 as critical targets to prevent vessel loss.


Assuntos
Endotélio Vascular/fisiologia , Vasos Retinianos/fisiologia , Fator de Crescimento Transformador beta/fisiologia , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/genética , Animais , Bovinos , Primers do DNA , Regulação da Expressão Gênica/efeitos dos fármacos , Reação em Cadeia da Polimerase , RNA/genética , RNA/isolamento & purificação , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fator de Crescimento Transformador beta/genética , Fator de Crescimento Transformador beta/farmacologia , Fator de Crescimento Transformador beta1 , Fator A de Crescimento do Endotélio Vascular/genética , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/genética
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