place within a population of binocular cells, neurons that receive input from both eyes and are sensitive to image disparity. These cells are prevalent throughout the superficial and deep layers of area V1, as well as several areas

4outside the striate cortex such as areas V2, MT (middle temporal visual area or area V5), and MST (medial superior temporal visual area), and play a major role in the appreciation of stereopsis and in generating disparity vergence (motor fusion).

In the presence of strabismus, inputs from the same point in space will stimulate nonadjacent ocular dominance columns, cells that would ordinarily not communicate with each other horizontally, or synapse with the same binocular cell further downstream in visual processing. Unrepaired, large angle infantile-onset strabismus has been shown to have devastating e ects on the population of binocular cells. The supply of binocular cells throughout area V1 is decimated [3]. Yet objective evidence of binocular cortical processing has been found in human subjects with small angle strabismus and MFS [4, 5]. The question then arises, how is it that these patients can achieve fusion and stereopsis?

One theory is that the cortical adaptation that occurs in response to a small angle ocular deviation is limited to suppression of the foveal ocular dominance columns in area V1. This would preserve the parafoveal columns and allow for normal, though limited binocular communication with gross stereopsis [3]. This theory also implies that the anomalous motor fusion present in MFS is also driven by the disparity-sensitive neurons that are located at this earliest stage of binocular processing [6]. In this paradigm, retinal correspondence would be considered normal, as no cortical rewiring would be needed to maintain fusion in the presence of a small deviation.

Other researchers have found evidence of an adaptation that results in binocular vision in MFS; one that occurs further downstream from area V1, in areas V2,V3, and beyond. This adaptation does involve a rewiring that could be considered the anatomic basis of anomalous retinal correspondence (ARC) [7, 8]. For example, it has been demonstrated in esotropic cats that if the angle of strabismus is small (<10°), the binocular neurons in the lateral suprasylvian cortex (area LS) may be spared, though their receptive fields are shifted so that normally noncorresponding retinal elements may communicate [9, 10].Area LS of the cat is functionally analogous to area MT in the primate.

Regardless of where the adaptation takes place, it appears that the visual cortex may be most successful in achieving fusion in the presence of a tropia when it can combine information from cell populations that are no more than two cortical neurons distant [11]. At approximately 7 mm in length, the typical cortical neuron is

theoretically capable of joining visual receptive fields up to 2.5° (4.4D) distant [6]. In Parks’ original description, manifest deviations no larger than 8D were consistent with MFS. A two-neuron chain could allow the fovea to e ectively communicate with a peripheral retinal element that is up to 8.7D away, providing support to Parks’ clinical observations.

4.2.1Binocular Correspondence: Anomalous, Normal, or Both?

Interestingly, one of the questions raised by Parks and debated for decades is whether the binocular vision that is the prominent feature of MFS should be called ARC, normal correspondence (NRC) with an expansion of Panum’s fusional space in the peripheral field (Parks’ conclusion), or even a combination of the two. Some authors have found NRC in the central visual field, with ARC in the periphery [8, 12]; others have found ARC centrally, and NRC peripherally [13]. Certainly, the angle of strabismus is small enough and the peripheral receptive fields large enough that it is conceivable peripheral fusion might be achieved without requiring a rewiring of the visual cortex (see Sect. 4.2). On the other hand, it seems unlikely that stereoacuity as fine as 70seconds of arc, which has been found in MFS, could be consistent with a foveal suppression scotoma of up to 5° with NRC. Perhaps stereoacuity at this level is the result of an expansion of Panum’s area surrounding the fixation point. However, such an adaptation, should it be found, would surely be termed anomalous.

What do we mean when we say a patient has ARC? The state of retinal correspondence has historically been defined as characteristic responses to specific clinical sensory tests; responses which can be manipulated by many di erent external factors [14]. Test results are also influenced by both the patient’s ability to communicate and the examiner’s interpretation of the response. It is not uncommon for the same subject to demonstrate characteristic ARC responses on some tests and NRC responses on others. It has been assumed that ARC is the result of a shift in the perceptual mapping of the deviated eye under binocular conditions, and these tests are designed to determine the subjective visual direction of at least one retinal element. However, in human subjects with ARC, no cortical shift in topography was found with pattern VEP, though this does not rule out a shift occurring in cortical areas further downstream [7].

It is important to remember that the concepts of the horopter, Panum’s fusional space, and binocular correspondence are simply geometric and psychophysical constructs used to describe binocular vision. Until we know how this binocular vision is achieved in the visual cortex,