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This chapter reviews the effects of early deprivation of sight in one or both eyes. The discussions cover the effects of dark rearing; monocular deprivation; the critical period; amblyopia; and amblyopia and stereopsis.

Visual deprivation in early life disrupts the development of the visual system, especially binocular vision. The chapter starts with a review of the effects of rearing animals in darkness and the effects of blindness in humans. Monocular deprivation in early life produces permanent defects in the deprived eye—a condition known as amblyopia. The amblyopic eye has reduced acuity and stereoscopic vision is lost. Monocular deprivation disrupts vision only when applied during a critical period in early life, and different types of monocular deprivation such as loss of one eye, squint, and monocular occlusion, produce different types of amblyopia. A review of retinal, subcortical, and cortical effects of monocular deprivation is followed by a review of what is known about mechanisms of neural plasticity responsible for amblyopia.

Lamberto Maffei has been a scientific explorer of new trails in uncharted territories. In his early work, Lamberto explored the functions of the mammalian visual system. He moved on to an investigation of the development and plasticity of the brain. In addition, he analyzed the role of environmental enrichment in visual development and in visual cortical plasticity in adults. He demonstrated that living in an enriched environment can potentiate visual cortical plasticity in adult rats to the point of allowing complete recovery from amblyopia, acting on the balance between cortical excitation and inhibition.

Masking has been used for several decades as an experimental technique to investigate the temporal properties of visual information-processing in specific populations of human observers. Among these are individuals suffering from amblyopia, psychiatric patients suffering from major depression and from schizophrenia, neurological patients, and individuals with specific attentional, learning, and reading disabilities. While differences of masking performance between control observers and observers from these specific populations are generally expected, these differences can also be theoretically relevant when they are clearly predictable from properties or processes underlying visual information processing.

Amblyopia has been attributed to a shift in sensitivity of the visual system toward low spatial-frequency filter mechanisms. This chapter analyzes the capacity to recognize moving signals and how colour can help in this task. It shows that changes in perceived form or colour can cause changes in perceived motion.

This chapter, as its title suggests, is concerned primarily with practical issues surrounding amblyopia therapy. Imprecise or inappropriate measurement techniques have limited understandings of occlusion therapy. To examine these issues the chapter draws upon observations made in the literature and on some techniques recently developed in the laboratory. Finally, experimental data that indicate how proposals work in practice are presented. The discussions are necessarily restricted in scope and do not address the many neuroscientific contributions that have increased the understandings of this curious condition. Throughout this chapter the attention is focused on the amblyopic child as opposed to the infant and the chapter defines the former as being of an age at which a visual task involving ‘linear’ optotypes can be performed, either by the elicitation of a verbal response or by the child indicating the target seen at distance on a hand-held key card. Also, it makes no specific reference to the taxonomy of amblyopia although it acknowledge this to be an obvious factor likely to influence treatment outcome. At the beginning of this chapter, attention is drawn to the lack of empirical (as opposed to clinical, anecdotal) support for the use of occlusion therapy. It is suggested that this arose because of inadequate or inappropriate measurement of compliance and visual outcome.

An understanding of the ways in which vision develops following treatment of an infantile cataract is of considerable interest to a broad spectrum of basic scientists and clinicians. Devising improved methods for treatment, or ideally methods for prevention, of the amblyopia that typically develops following the surgical removal of the cataract poses a significant challenge for clinicians. Psychophysicists are interested in the precise nature of the perceptual deficits that sometimes develop in these children. Neuroscientists are particularly interested in questions regarding the neuropathology in the visual pathways in the brain that correlate with reduced visual function. Developmental psychologists are intrigued by the implications this topic has for broad issues having to do with the relative importance of ‘nature versus nurture’ in guiding development. This chapter attempts to summarize some of the main findings from the literatures from all of these disciplines in order to synthesize an understanding of visual development in children being treated for infantile cataracts.

Visual−deprivation experiments on cats and monkeys have showed that complete unilateral eye occlusion of these animals until twelve weeks of age can produce a permanent amblyopia and a decrease in cell density along the geniculocortical pathway. Reversal of the amblyopia was possible if the occlusion was removed before eight weeks of age in monkeys. Although this critical age is established for animals, the exact critical period has not been determined for humans, partly because of the problem with assessment of infant vision. This chapter focuses on the relationship between visual development and age at surgery for patients with total congenital cataract. In patients with total congenital cataract, retinal image formation is severely degraded from birth until the lens is removed by surgery and the optics is restored by a contact lens.

This chapter deals with the visual processing of adults with amblyopia. Plasticity is deemed to exist in the process and can be used to improve the vision of such patients. Through perceptual learning, particularly repetitive practice of target detection, lateral interactions between cortical neurons can be normalized, and improved visual functions can be achieved.

This chapter presents new perspectives in amblyopia treatment. It provides evidence for plasticity in the adult nervous system. It illustrates that substantial neural plasticity exists in the visual system of adults and older children with naturally occurring amblyopia. This chapter suggests that treatment for amblyopia is generally undertaken only in children; however, there is now considerable data that treatment of amblyopia may also be effective in adults. It proposes that it might be time to reconsider the notions about neural plasticity in amblyopia.

A number of non-independent factors, such as neurotransmitter and receptor excesses and reductions, a reduced ability to generate oscillations and synchrony, and changes in gene expression due to primary genetic or environmental causes, may compromise dynamic coordination. This chapter focuses on brain disorders that have been linked to dynamic coordination failures, including autism, epilepsy, amblyopia, schizophrenia, Williams syndrome, Parkinson’s disease, and Alzheimer’s disease.

The purpose of any medical test is to confirm or rule out a diagnosis based on the clinical facts. In performing perimetry, the printout of the defect is not the end of the test. For even the most experienced reader, the test results at best tell the location of the defect. The next step is to consider the causes of such a defect in that part of the vision system. The experienced perimetrist will look at the results and suggest a differential list of causes. The primary diagnostic list is frequently aided by adding to the perimetry the medical history and other physical signs. The results of both then lead to the next step: ordering tests to confirm the cause of the field defect. It may require the ordering of a magnetic resonance (MR) image, but that may not be the proper test if the original differential diagnosis is faulty. Sedimentation rate and C-reactive protein may be more appropriate tests if the clinical facts suggest cranial arteritis. If carotid disease is suspected, a computed tomography (CT) angiogram may be more appropriate. In the following discussion of these defects, there has been a melding of a discussion explaining anatomically why these defects occur in certain areas. Because the course and relations of the primary visual sensory pathway have been frequently and well described (including in other chapters of this monograph), this chapter concentrates on the multiple anatomic substrates that may explain each particular pattern of visual field abnormality. Visual field abnormalities are represented by three categories: monocular, binocular, and junctional. Monocular field defects include those that can be caused by lesions of one eye or optic nerve. Binocular field defects include those that may result from single or multiple lesions at one or more points along the visual pathway. Junctional field defects include three types of visual field defects resulting from a lesion at the junction of the optic nerve and optic chiasm or of the optic tract and optic chiasm.