Chorioretinal folds: a proposed diagnostic algorithm.

PURPOSE: To create a diagnostic algorithm for the management of chorioretinal folds. METHODS: We reviewed the existing literature about chorioretinal folds focusing our attention on three specific conditions and created a diagnostic algorithm in order to otpimize the choice and the number of investigations. RESULTS: Chorioretinal folds are visible striations of the fundus usually arranged in parallel lines and disposed horizontally. They may be either unilateral or bilateral, symptomatic or asymptomatic and are often associated with different possible ocular and extra ocular pathologies, including systemic diseases like autoimmune disorders and intracranial hypertension. They are named idiopathic when no apparent cause for their development is detectable. However, with improved diagnostic testing, the patients with idiopathic choroidal folds are likely to represent only a smaller portion of the total. CONCLUSIONS: Since choroidal folds be the sole sign of an underlying disease possibly requiring a multidisciplinary approach, an appropriate work-up varying according to the specific clinical features of each case is needed to define the etiology and the treatment. A diagnosting algorithm may be useful in order to optimize the diagnostic approach and management.

Agreement in detecting glaucomatous visual field progression by using guided progression analysis ?and Humphrey overview printout.

PURPOSE: To examine the level of agreement among 3 clinicians in assessing glaucoma visual field progression by using 2 different methods. METHODS: Each visual field was assessed by Humphrey Field Analyzer (HFA), program SITA standard 30-2 or 24-2. In each printout the first 3 fields were excluded to minimize learning effect: the fourth and fifth full-threshold or SITA Standard examinations were used as baseline. Three clinicians assessed the progression status of each series using both HFA overview printouts and the guided progression analysis (GPA). The level of agreement among the clinicians was evaluated using a weighted kappa statistic (k). RESULTS: A total of 510 tests, comprising 83 eyes with an average of 6.1 tests each, was assessed by the 3 specialists. The mean follow-up time was 5.8 ± 1.75 years (mean ± standard deviation). When the intraobserver intermethod agreement was evaluated, k ranged from 0.5 to 0.7. When the interobserver agreement was analyzed, if HFA overview printouts were used, k ranged from 0.4 to 0.7. But when GPA was used, k ranged from 0.2 to 0.6. The level of agreement on progression status between the clinicians was always higher when they used HFA overview printouts (median k = 0.54) than when they used GPA (median k = 0.37). CONCLUSIONS: Agreement among expert clinicians about visual field progression status was moderate when GPA printouts were used. Clinicians' agreement about patients' visual field progression status was better when HFA overview printouts were used than with GPA printouts.

Limits on introspection: distorted subjective time during the dual-task bottleneck.

Which cognitive processes are accessible to conscious report? To study the limits of conscious reportability, we designed a novel method of quantified introspection, in which subjects were asked, after each trial of a standard cognitive task, to estimate the time spent completing the task. We then applied classical mental-chronometry techniques, such as the additive-factors method, to analyze these introspective estimates of response time. We demonstrate that introspective response time can be a sensitive measure, tightly correlated with objective response time in a single-task context. In a psychological-refractory-period task, however, the objective processing delay resulting from interference by a second concurrent task is totally absent from introspective estimates. These results suggest that introspective estimates of time spent on a task tightly correlate with the period of availability of central processing resources.

Partial visual recovery from radiation-induced optic neuropathy after hyperbaric oxygen therapy in a patient with Cushing disease.

Here we describe the case of a 41-year-old woman with a history of Cushing disease who had previously undergone unsuccessful neurosurgery, followed by stereotactic radiosurgery. More than 4 years after this treatment, she presented severe visual impairment, which started in the left eye and was documented by neuro-ophthalmic evaluation. Radiological assessment by contrast-enhanced magnetic resonance (MR) imaging initially suggested the diagnosis of glioma of the optic nerve and the patient started corticosteroid treatment (first with prednisone, 80 mg/day, followed by dexamethasone, 8 mg/day). Despite the therapy, vision in the left eye rapidly worsened until light was no longer perceptible; similar symptoms and signs also developed in the right eye, evolving to complete temporal hemianopsia. The clinical evidence was confirmed by the rapid progression of the MR picture, which showed homogeneous enhancement of the chiasm and optic nerves. On the basis of these findings, the original diagnosis of glioma was excluded, and radiation-induced optic neuropathy was diagnosed. As corticosteroids had proved inefficacious, hyperbaric oxygen (HBO) therapy was promptly instituted and vision steadily started to improve. This improvement was documented and confirmed by the progressive recovery of the visual field in the right eye and the changes in the sequential follow-up MR scanning. Optic neuropathy is an infrequent but dramatic complication of radiation therapy. Symptoms develop, on average, 12 months after treatment, and the onset may be acute and characterized by the progressive loss of vision in one or both eyes. HBO has already been used to treat this complication, but its efficacy is still controversial. Here, in addition to describing this particular case, which presented a significantly delayed radiation injury of the optic pathways, we provide a brief literature review and discuss some important points.

Pathogenesis of degenerative retinopathies induced by thioridazine and other antipsychotics: a dopamine hypothesis.

Thioridazine and other antipsychotics (neuroleptics, dopaminergic antagonists) can cause degenerative retinopathies with histological, electrophysiological and symptomatological features similar to those of primary retinitis pigmentosa. It was formerly suggested that these retinopathies are due to drug absorption by melanin of the eye which damages the choriocapillaris first and subsequently the photoreceptors and the retinal pigment epithelium. An alternative explanation of the still unclear mechanisms involved in the pathogenesis of thioridazine and other phenothiazines retinopathies has underlined the role of the drug effects on the activity of some retinal enzymatic systems which can lead to retinal dystrophy. More recent data on the complex role of dopamine (DA) and of its receptor subtypes in the retina has provided evidence that the D2 family of DA receptors, in particular the D4 receptor, is involved in the control of the synthesis of melatonin, a factor that has been shown to regulate several aspects of retinal physiology and to increase photoreceptor susceptibility to be damaged by light. Based on this knowledge, as well as on clinical data and on pharmacological considerations concerning the differences recently shown to exist among the various antipsychotics as regards their affinity for the DA receptor subtypes, we hypothesize that neuroleptic induced blockade of retinal D2/D4 receptors is among the initial events of these drug-induced degenerative retinopathies. Clinicians should be aware of the retinotoxic effects not only of thioridazine and some others phenothiazines, but also of those possibly caused by other typical and atypical antipsychotics. By evaluating the retinal status and function before and during the treatment of psychiatric patients, it should be possible to choose more accurately the safest drugs, particularly when treating predisposed subjects.