We present a comprehensive review of the rare syndrome visual form agnosia (VFA). We begin by documenting its history, including the origins of the term, and the first case study labelled as VFA. The defining characteristics of the syndrome, as others have previously defined it, are then described. The impairments, preserved aspects of visual perception, and areas of brain damage in 21 patients who meet these defining characteristics are described in detail, including which tests were used to verify the presence or absence of key symptoms. From this, we note important similarities along with notable areas of divergence between patients. Damage to the occipital lobe (20/21), an inability to recognise line drawings (19/21), preserved colour vision (14/21), and visual field defects (16/21) were areas of consistency across most cases. We found it useful to distinguish between shape and form as distinct constructs when examining perceptual abilities in VFA patients. Our observations suggest that these patients often exhibit difficulties in processing simplified versions of form. Deficits in processing orientation and size were uncommon. Motion perception and visual imagery were not widely tested for despite being typically cited as defining features of the syndrome - although in the sample described, motion perception was never found to be a deficit. Moreover, problems with vision (e.g., poor visual acuity and the presence of hemianopias/scotomas in the visual fields) are more common than we would have thought and may also contribute to perceptual impairments in patients with VFA. We conclude that VFA is a perceptual disorder where the visual system has a reduced ability to synthesise lines together for the purposes of making sense of what images represent holistically.

Visual agnosia is a neuropsychological impairment of visual object recognition despite near-normal acuity and visual fields. A century of research has provided only a rudimentary account of the functional damage underlying this deficit. We find that the object-recognition ability of agnosic patients viewing an object directly is like that of normally-sighted observers viewing it indirectly, with peripheral vision. Thus, agnosic vision is like peripheral vision. We obtained 14 visual-object-recognition tests that are commonly used for diagnosis of visual agnosia. Our \"standard\" normal observer took these tests at various eccentricities in his periphery. Analyzing the published data of 32 apperceptive agnosia patients and a group of 14 posterior cortical atrophy (PCA) patients on these tests, we find that each patient\'s pattern of object recognition deficits is well characterized by one number, the equivalent eccentricity at which our standard observer\'s peripheral vision is like the central vision of the agnosic patient. In other words, each agnosic patient\'s equivalent eccentricity is conserved across tests. Across patients, equivalent eccentricity ranges from 4 to 40 deg, which rates severity of the visual deficit. In normal peripheral vision, the required size to perceive a simple image (e.g., an isolated letter) is limited by acuity, and that for a complex image (e.g., a face or a word) is limited by crowding. In crowding, adjacent simple objects appear unrecognizably jumbled unless their spacing exceeds the crowding distance, which grows linearly with eccentricity. Besides conservation of equivalent eccentricity across object-recognition tests, we also find conservation, from eccentricity to agnosia, of the relative susceptibility of recognition of ten visual tests. These findings show that agnosic vision is like eccentric vision. Whence crowding? Peripheral vision, strabismic amblyopia, and possibly apperceptive agnosia are all limited by crowding, making it urgent to know what drives crowding. Acuity does not (Song et al., 2014), but neural density might: neurons per deg2 in the crowding-relevant cortical area.