Abstract
Amblyopia is a neurodevelopmental disorder characterized by visual acuity and contrast sensitivity loss, refractory to pharmacological and optical treatments in adulthood. We studied the response of the visual cortex to transcranial Direct Current Stimulation (tDCS) applied over the primary visual area (V1) contralateral to the “lazy eye”. Visual acuity (logMAR) was assessed before (T0), immediately after (T1) and 60′ following the application of cathodal tDCS (2.0 mA, 20′). At each time point, Visual Evoked Potentials (VEPs) triggered by grating stimuli of different contrasts (K90%, K20%) were recorded in both hemispheres and compared to those obtained in healthy volunteers. Cathodal tDCS improved visual acuity (Holm–Sidak, p
Highlights
Amblyopia is a neurodevelopmental disorder clinically characterized by visual acuity and contrast sensitivity loss, refractory to pharmacological and mechanical treatments in adulthood (Holmes and Clarke, 2006): given the lack of any organic cause, it has been defined as a disorder ‘‘in which the patient sees nothing and the doctor sees nothing’’ (Holmes and Clarke, 2006)
A remarkable improvement occurred at T1 when cathodal polarization was delivered within the hemisphere contralateral to the amblyopic eye, with changes lasting up to 1 h after transcranial Direct Current Stimulation (tDCS) completion (F(2,22) = 8.14, p = 0.0023, two-way analyses of variance (ANOVA), with ‘‘time’’ and ‘‘treatment’’ as factors)
At high contrasts (K90%), we found a persistent enhancement of Visual Evoked Potential (VEP) amplitude in amblyopic subjects but not controls at T2 (Holm-Sidak test, p < 0.0001): transcallosal disinhibition persisted in amblyopic patients, while it vanished in controls
Summary
Amblyopia is a neurodevelopmental disorder clinically characterized by visual acuity and contrast sensitivity loss, refractory to pharmacological and mechanical treatments in adulthood (Holmes and Clarke, 2006): given the lack of any organic cause, it has been defined as a disorder ‘‘in which the patient sees nothing and the doctor sees nothing’’ (Holmes and Clarke, 2006). Amblyopia results in an abnormal binocular experience due to a mismatch between the images perceived with each eye. The retina is generally spared, microscopic anatomical and structural abnormalities in lateral geniculate bodies and visual cortex can occur (von Noorden and Crawford, 1992; Davis et al, 2003); fMRI studies are consistent with the hypothesis of a selective involvement of the parvocellular stream at a precortical or early cortical site, leading to detection and processing deficit for high-contrast stimuli (Li et al, 2007; Hess et al, 2010). Permanent monocular visual impairment is a risk for blindness, if the dominant eye is injured or becomes affected later in life (Williams et al, 2003). For this reason, the early treatment is critical. Eye-patching has been used for centuries, whereas the use of atropine has only recently emerged (Repka et al, 2005)
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