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Steven A Newman

Publications and source records attributed to Steven A Newman.

8 recordsLinked to original sources
PubMed2006

Development and validation of a computerized expert system for evaluation of automated visual fields from the Ischemic Optic Neuropathy Decompression Trial.

BACKGROUND: The objective of this report is to describe the methods used to develop and validate a computerized system to analyze Humphrey visual fields obtained from patients with non-arteritic anterior ischemic optic neuropathy (NAION) and enrolled in the Ischemic Optic Neuropathy Decompression Trial (IONDT). The IONDT was a multicenter study that included randomized and non-randomized patients with newly diagnosed NAION in the study eye. At baseline, randomized eyes had visual acuity of 20/64 or worse and non-randomized eyes had visual acuity of better than 20/64 or were associated with patients refusing randomization. Visual fields were measured before treatment using the Humphrey Field Analyzer with the 24-2 program, foveal threshold, and size III stimulus. METHODS: We used visual fields from 189 non-IONDT eyes with NAION to develop the computerized classification system. Six neuro-ophthalmologists ("expert panel") described definitions for visual field patterns defects using 19 visual fields representing a range of pattern defect types. The expert panel then used 120 visual fields, classified using these definitions, to refine the rules, generating revised definitions for 13 visual field pattern defects and 3 levels of severity. These definitions were incorporated into a rule-based computerized classification system run on Excel(R) software. The computerized classification system was used to categorize visual field defects for an additional 95 NAION visual fields, and the expert panel was asked to independently classify the new fields and subsequently whether they agreed with the computer classification. To account for test variability over time, we derived an adjustment factor from the pooled short term fluctuation. We examined change in defects with and without adjustment in visual fields of study participants who demonstrated a visual acuity decrease within 30 days of NAION onset (progressive NAION). RESULTS: Despite an agreed upon set of rules, there was not good agreement among the expert panel when their independent visual classifications were compared. A majority did concur with the computer classification for 91 of 95 visual fields. Remaining classification discrepancies could not be resolved without modifying existing definitions. Without using the adjustment factor, visual fields of 63.6% (14/22) patients with progressive NAION and no central defect, and all (7/7) patients with a paracentral defect, worsened within 30 days of NAION onset. After applying the adjustment factor, the visual fields of the same patients with no initial central defect and 5/7 of the patients with a paracentral defect were seen to worsen. CONCLUSION: The IONDT developed a rule-based computerized system that consistently defines pattern and severity of visual fields of NAION patients for use in a research setting.

Automation↗
PubMed2006

Esthesioneuroblastoma: continued follow-up of a single institution's experience.

OBJECTIVES: To analyze outcomes and to provide follow-up for our increasing patient cohort with esthesioneuroblastoma. DESIGN: Retrospective cohort analysis. SETTING: Patients were examined from September 1, 1976, to May 30, 2004, in a tertiary care academic hospital. PATIENTS: Fifty consecutive patients diagnosed as having esthesioneuroblastoma were treated with a standardized protocol during a 28-year period. Patients with tumors staged Kadish A or B received preoperative radiotherapy followed by craniofacial resection, while patients with Kadish stage C disease were treated with preoperative sequential chemotherapy and radiotherapy followed by a craniofacial resection. The mean follow-up is 93 months (range, 1-330 months). RESULTS: The disease-free survival was 86.5% and 82.6% at 5 and 15 years, respectively. There were 17 patients (34%) who developed recurrent disease, most of which was locoregional (12 patients [71%]). There was a long interval to relapse (mean, 6 years), with the longest time to regional recurrence being 10 years. Distant relapses occurred sooner, with poorer outcomes. Of these 17 patients, 7 (41%) underwent successful salvage surgery, while 3 remain alive with disease. CONCLUSIONS: Excellent outcomes for esthesioneuroblastoma are achievable. Long-term follow-up is necessary because of the extended interval for recurrent disease; unlike most sinonasal malignancies, surgical salvage is possible.

Adolescent↗
PubMed2006

Progression of visual field defects in leber hereditary optic neuropathy: experience of the LHON treatment trial.

PURPOSE: To describe the visual fields of patients with Leber hereditary optic neuropathy (LHON), a maternally inherited disorder characterized by bilateral, often sequential vision loss, before and during progressive visual deterioration. DESIGN: Prospective longitudinal follow-up of serial visual fields in patients enrolled onto an open-label, nonrandomized pilot study of topical brimonidine purite as prophylactic treatment after first eye involvement in LHON. METHODS: Nine molecularly confirmed primary mutation patients with LHON with monocular vision loss for less than six months and normal visual function in the other eye were followed prospectively for up to two years. Visual fields were performed on automated perimetry at baseline and on many follow-up visits. RESULTS: Despite normal visual acuity at baseline in all patients, seven patients had some minimal changes in the central visual field of the second eye. All patients had subsequent deterioration of visual acuity, mean deviation, and foveal sensitivity in their second eye. The earliest pattern of abnormality was typically a cecocentral defect enlarging to become a central defect, often with a superior or inferior predilection. The visual field defects in the two eyes of any given patient were remarkably similar. CONCLUSIONS: LHON may be a bilateral condition at onset more frequently than appreciated. Automated static perimetry of the "normal" eye may reveal subclinical findings that typically worsen rapidly over weeks to months to similar central scotomatous damage. Quantitative automated static perimetry is helpful in elucidating the natural history of LHON and in understanding the underlying pathology and pathophysiology of this disease.

Administration, Topical↗
PubMed2006

Capillary hemangioma of the cauda equina presenting with radiculopathy and papilledema.

A 42-year-old, non-obese man with a three-month history of headache, pulsatile tinnitus, transient visual obscurations, and scintillations later developed low back pain with right lower extremity radiation. Brain MRI and magnetic resonance venography were normal, but spine MRI revealed a mass in the cauda equina. Neuro-ophthalmologic examination disclosed bilateral optic disc edema with normal visual function. During spine surgery, cerebrospinal fluid, released under high pressure despite prior hyperventilation, contained a glucose level of 51 mg/dl and a protein level of 1840 mg/dl. Histologic and immunohistochemical features of the lesion were compatible with a capillary hemangioma. Although spinal cord tumors have been associated with papilledema, this is the first report of a capillary hemangioma of the cauda equina in this context. If papilledema is present, spinal cord imaging should be performed when lumbar puncture discloses unexplained protein elevation and in cases that lack clinical features typical of idiopathic intracranial hypertension.

Adult↗
PubMed2005

Prophylaxis for second eye involvement in leber hereditary optic neuropathy: an open-labeled, nonrandomized multicenter trial of topical brimonidine purite.

PURPOSE: To test a topical agent with purported antiapoptotic properties as prophylactic treatment after first eye involvement in Leber hereditary optic neuropathy (LHON), a maternally-inherited disorder characterized by bilateral, often sequential, visual loss. DESIGN: Open labeled, nonrandomized prospective pilot study. METHODS: Nine primary mutation molecularly confirmed LHON patients with one eye vision loss for less than 6 months and normal visual function in the fellow eye were treated with brimonidine purite 0.15% (Alphagan P) 4 times daily in the unaffected eye for up to 2 years. Visual acuity was the primary efficacy outcome. Secondary measures included changes on automated perimetry and quantification of the relative afferent pupillary defect. RESULTS: There were 8 men and 1 woman enrolled, aged 13 to 54 years (mean 32 years), eight with the 11778 mitochondrial DNA (mtDNA) mutation, and one with the 3460 mutation. Despite normal visual acuity at baseline in all patients, 7 patients had some minimal changes in the central visual field of the study eye. All patients had deterioration of vision in their second eye. In 1 of the 2 patients who had treatment initiated within 16 days after first eye involvement, good visual acuity was maintained in the study eye at 15 month followup, despite a mildly abnormal study eye baseline visual field. CONCLUSIONS: LHON may be a bilateral condition at onset more frequently than appreciated, with asymmetric severity at presentation. Topical brimonidine purite in this dosage was unsuccessful in preventing second eye involvement in recently monocularly-symptomatic LHON.

Administration, Topical↗
PubMed2004

Neuro-ophthalmology of von Hippel-Lindau.

von Hippel-Lindau (VHL) disease is a multisystem inherited cancer syndrome with characteristic tumors and a known genetic basis. Patients with VHL develop, among other tumors, retinal capillary hemangiomas, central nervous system hemangioblastomas, renal clear cell carcinomas, and pheochromocytomas. Nearly all patients can be shown to have a mutation in the VHL gene, which is located on chromosome 3p25. Genetic abnormalities result in abnormal levels of pVHL, which in turn lead to the different tumors. Four distinct phenotypes of VHL disease have been identified based on the relative frequency of and propensity for the development of different VHL tumors. Aggressive screening of patients with VHL disease can prevent morbidity and mortality from these tumors. Although these tumors typically have been treated with observation or surgery, trials of newer medical therapies that target some of the cellular dysregulation caused by mutation in pVHL are ongoing. Even though these trials have not been wholly successful, they present an exciting direction for future research. This article presents a summary of new developments in VHL disease with a focus on ophthalmic and neuro-ophthalmic practice.

Adolescent↗
PubMed2002

Commentary.

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Journal Article↗