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Purpose: To determine whether the "gatekeeper physician system" for evaluating neuro-ophthalmologic problems is cost effective., Methods: The authors retrospectively reviewed the records of 588 patients referred for neuro-ophthalmologic evaluation between July and December 1989 to determine the frequency and cost of unnecessary diagnostic testing ordered by "gatekeeper physicians." Pre-referral diagnostic testing costs were compared with the cost of neurophthalmologic consultation for four common problems: (1) optic neuropathy; (2) diplopia; (3) ptosis; and (4) proptosis., Results: Between 16% and 26% of patients in the first three diagnostic categories were subjected to overtesting, resulting in $57,900 of excessive costs, a 724% overcharge. Although the evaluation of proptosis was performed correctly, the quality of 10 of the 18 neuro-imaging procedures was substandard., Conclusions: The gatekeeper system managed by primary care physicians for these four neuro-ophthalmologic problems not only did not conserve healthcare dollars but also had a negative impact on cost control. For neuro-ophthalmologic disorders, prompt subspecialty evaluation and examination appear to be a cost-effective strategy.

Color Doppler imaging (CDI) is a technique that provides color-encoded blood flow information on a gray-scale two-dimensional background. Although first reported in the investigation of orbital disease in 1979, it is only in the past 1 to 2 years that CDI has become established as a tool in the assessment of vascular disease of the eye and orbit. Discussed are clinical syndromes in which CDI has been shown to demonstrate abnormalities and also assist in diagnosis and determination of etiology.

Graves' thyroid disease and the orbitopathy which often accompanies it have puzzled physicians and scientists for more than 150 years. Although certain histopathological features have been documented, it is not known what mechanisms are responsible for the systemic and/or ocular disorders. The ocular condition characteristic of Graves' disease may exist in the absence of clinical or biochemical evidence of thyroid dysfunction, and when the systemic and ocular condition exist together, they may follow completely different clinical courses. Because the relationship between the thyroid disorder and the orbitopathy is not established, the authors refer not to "thyroid ophthalmopathy," but to "Graves' ophthalmopathy." In this review, histopathological features of Graves' ophthalmopathy are reviewed. The differential diagnosis of the ophthalmopathy and approaches to its evaluation are discussed, notably the T-4 radioimmunoassay, T-3 resin uptake and TSH tests, as well as CT scanning and ultrasonography. The characteristics of Classes 0-6 ophthalmopathy are outlined and the management of cases in each class is considered. The possible immunological basis for Graves' ophthalmopathy is also reviewed.

We investigated the lymphocyte characteristics of 77 Graves' disease patients with and without infiltrative ophthalmopathy. Thirteen patients with infiltrative ophthalmopathy without prior antithyroid therapy and 20 euthyroid patients with progressive ophthalmopathy demonstrated decreased percentages of active and total erythrocyte rosette-forming lymphocytes compared to thyrotoxic patients without eye disease and to a control population (p less than 0.001). There was no significant difference in rosette-forming cells between untreated thyrotoxic and treated euthyroid patients with ophthalmopathy. No lymphocytotoxic antibodies or rosette inhibitory factor was present in the sera of patients with infiltrative ophthalmopathy. Untreated and treated patients with lid retraction and mild proptosis without extraocular muscle disease had decreased active rosette-forming cells (p less than 0.001) but normal total rosette-forming cells. Five patients with infiltrative ophthalmopathy who failed to improve with systemic corticosteroids demonstrated elevated active but normal total rosette-forming cells. Differences in rosette formation between ophthalmic and nonophthalmic Graves' disease may represent an associated cell-mediated abnormality that may explain why control of the thyrotoxic state need not correlate with the ophthalmic manifestations of the disorder.

Between October, 1978 and August, 1986, 35 patients with thyroid ophthalmopathy were treated with radiotherapy. Twenty-eight patients had treatment with corticosteroids prior to radiotherapy and either progressed on steroids or relapsed during tapering. Seven patients with contraindications to steroids were treated primarily with radiotherapy. After radiotherapy, 25 patients (71%) did not require any further steroids or orbital decompression and ten (29%) failed. Patients who required steroids or decompression for active disease after radiotherapy were considered treatment failures. A total of 14 (40%) patients required eye muscle or lid surgery for correction of stable soft tissue defects after radiotherapy, more commonly in patients treated with radiotherapy after steroids or decompression than those irradiated primarily; the median time between radiotherapy and surgery was 8 months (range 1-48). Various factors were examined for prognostic significance in predicting radiotherapy failure. Review of the interval between onset of eye disease and radiotherapy demonstrated that six of ten (60%) failures versus only five of 25 (20%) successful treatments received radiotherapy within 6 months of onset of eye disease. No relation between outcome and sex, age or hyperthyroid versus euthyroid Graves' disease was apparent. Radiotherapy has been used for patients with thyroid ophthalmopathy who failed steroids, decompression, or had steroid contraindications. Morbidity of radiotherapy was minimal and most patients were spared the morbidity of continued steroid therapy.

Two patients with presumed ocular histoplasmosis syndrome developed optic disc edema. In both cases the edema resolved without residual impairment of visual function. Although peripapillary changes in ocular histoplasmosis are common, optic disc edema is rare. The pathogenesis of the edema is unknown.

The authors examined eight patients with dementia of the Alzheimer's type (DAT), five with prominent visual symptoms early in the illness (VS) and three with no visual symptoms (NVS). Results of neuro-ophthalmologic examinations on VS patients showed relatively consistent abnormalities in figure copying, color vision tested by isochromatic plates, and stereopsis. Cerebral glucose metabolism determined by 18F-fluoro-2-deoxyglucose positron emission tomography (PET) was unchanged in primary visual cortex of VS and NVS patients compared with 12 normal volunteers of similar age and sex. Glucose metabolism in VS patients was decreased by 45 and 34% in left and right visual association cortex (P less than 0.01 and P less than 0.05, respectively) and 34 and 37% in left and right inferior parietal cortex (P less than 0.05) compared with controls; NVS patients had no significant metabolic alteration in these areas. Symptoms, physical examination, and metabolic imaging imply that these patients are a heterogenous but distinct clinical subgroup of DAT often with mild dementia who have visual symptoms due primarily to visual agnosia.

Plant GT, Sergott RC. Understanding and interpreting vision safety issues with vigabatrin therapy. Acta Neurol Scand: 2011: 124 (Suppl. 192): 57-71. © 2011 John Wiley & Sons A/S. Vigabatrin is an irreversible inhibitor of γ-aminobutyric acid (GABA) transaminase. It is effective as adjunctive therapy for adult patients with refractory complex partial seizures (rCPS) who have inadequately responded to several alternative treatments and as monotherapy for children aged 1 month to 2 years with infantile spasms. The well-documented safety profile of vigabatrin includes risk of retinopathy characterized by irreversible, bilateral, concentric peripheral visual field constriction. Thus, monitoring of visual function to understand the occurrence and manage the potential consequences of peripheral visual field defects (pVFDs) is now required for all patients who receive vigabatrin. However, screening for pVFDs for patients with epilepsy was conducted only after the association between vigabatrin and pVFDs was established. We examined the potential association between pVFDs and epilepsy in vigabatrin-naïve patients and attempted to identify confounding factors (e.g., concomitant medications, method of vision assessment) to more accurately delineate the prevalence of pVFDs directly associated with vigabatrin. Results of a prospective cohort study as well as several case series and case reports suggest that bilateral visual field constriction is not restricted to patients exposed to vigabatrin but has also been detected, although much less frequently, in vigabatrin-naïve patients with epilepsy, including those who received treatment with other GABAergic antiepileptic therapy. We also reviewed published data suggesting an association between vigabatrin-associated retinal toxicity and taurine deficiency, as well as the potential role of taurine in the prevention of this retinopathy. [ABSTRACT FROM AUTHOR]

Aim: To determine the anatomical site and extent of electrophysiological dysfunction in patients with ethambutol associated visual loss. Methods: A comparative case series. Four patients with ethambutol associated visual loss underwent multifocal electroretinography (mERG). Two patients had advanced visual loss while two had early signs of toxicity. The N1-P1, N1, P1 amplitudes, N1, and P1 latencies were compared to 10 age and sex matched controls. Results: mERG latencies were detected in the ethambutol treated patients. The N1 amplitude was significantly lower in the ethambutol treated patients than in the control group. Conclusion: Ethambutol is possibly toxic the retina, and not only the optic nerve. The multifocal ERG may be of value to diagnose and monitor patients taking ethambutol. [ABSTRACT FROM AUTHOR]