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Optic aphasia is a rare neurological disorder that affects the visual-semantic ability of patients with normal vision and is caused by a lesion in the left occipital lobe. The signs and symptoms of optic aphasia are similar to those of associative visual agnosia, where patients have difficulty recognizing objects both in shape and function, resulting in challenges performing daily tasks. The transformation to optic aphasia or associative visual agnosia is closely related to the degree of damage to the corpus callosum, with some studies hypothetically suggesting that complete damage to the corpus callosum leads to optic aphasia, whereas incomplete damage causes associative visual agnosia. We present a case of a 60-year-old man with a history of intracerebral hemorrhage in the left occipitotemporoparietal lobe. The patient complained of intermittent episodes of painless, blurry vision. Upon examination, we observed that the patient was unable to read the Snellen chart, although he could draw the letter. Furthermore, we discovered that the patient had difficulty naming objects and instruments, even though he was able to express their shape and function through gestures and mimicry. The signs and symptoms of the patient, along with the result of the multi-slice non-contrast CT scan, suggest that he had optic aphasia rather than associative visual agnosia. A comprehensive neuropsychological and aphasia examination needs to be performed to further assess the condition of our patient and establish the diagnosis. [ABSTRACT FROM AUTHOR]

Vision specialists will benefit from increased awareness of posterior cortical atrophy (PCA) syndrome. Failure to adequately identify the chief complaint as a visual symptom may lead to incorrect diagnosis or diagnostic delay. A previously healthy, 59-year-old woman presented with a 5-year history of 'losing her stuff'. Upon psychiatric and neuro-ophthalmological evaluation, this symptom was better recognised as a feature of visual agnosia and simultanagnosia. She also presented with multiple previously unrecognised symptoms indicative of higher visual processing dysfunction, such as alexia without agraphia, ocular motor apraxia, optic ataxia, prosopagnosia, akinetopsia and topographagnosia, so further assessment to investigate for PCA was carried out. After a work-up including cognitive assessment, brain structural/functional imaging, and laboratory tests she was diagnosed with visual-variant Alzheimer's disease. Patients with PCA merit a detailed review of their symptoms, as well as the use of office tests such as cognitive evaluation tools, different types of perimetry, colour vision tests, and non-delayed psychiatric consultation for correct management and assessment. This report will emphasise five key aspects to be considered when evaluating patients with PCA [ABSTRACT FROM AUTHOR]

Aphantasia and prosopagnosia are both rare conditions with impairments in visual cognition. While prosopagnosia refers to a face recognition deficit, aphantasics exhibit a lack of mental imagery. Current object recognition theories propose an interplay of perception and mental representations, making an association between recognition performance and visual imagery plausible. While the literature assumes a link between aphantasia and prosopagnosia, other impairments in aphantasia have been shown to be rather global. Therefore, we assumed that aphantasics do not solely exhibit impairments in face recognition but rather in general visual recognition performance, probably moderated by stimulus complexity. To test this hypothesis, 65 aphantasics were compared to 55 controls in a face recognition task, the Cambridge Face Memory Test, and a corresponding object recognition task, the Cambridge Car Memory Test. In both tasks, aphantasics performed worse than controls, indicating mild recognition deficits without face-specificity. Additional correlations between imagery vividness and performance in both tasks were found, suggesting that visual imagery influences visual recognition not only in imagery extremes. Stimulus complexity produced the expected moderation effect but only for the whole imagery-spectrum and only with face stimuli. Overall, the results imply that aphantasia is linked to a general but mild deficit in visual recognition. [ABSTRACT FROM AUTHOR]

Posterior Cortical Atrophy (PCA) is a neurodegenerative disorder characterized by impairment of higher-order visual processing in the setting of progressive atrophy of the parietal and occipital lobes. The underlying pathology is variable but most commonly Alzheimer's disease. The majority of individuals develop symptoms before 65 years of age; however, delayed diagnosis is common due to misattribution of symptoms to ocular rather than cortical pathology. The purpose of this review is to provide readers with an in-depth analysis of Posterior Cortical Atrophy syndrome, including clinical, imaging, pathological, and genetic features, management, and treatments. Most patients present initially with a relatively pure visuoperceptual-visuospatial syndrome, though other cognitive domains become affected over time. Structural neuroimaging demonstrates parieto-occipital or temporo-occipital predominant atrophy. Cerebrospinal fluid Alzheimer's disease biomarkers, or amyloid/tau PET imaging can help evaluate for underlying Alzheimer's disease, which is the most common underlying neuropathology. The cornerstone of management is focused on nonpharmacologic measures. Early etiologic diagnosis is important with the arrival of disease-modifying therapies, especially for Alzheimer's disease. [ABSTRACT FROM AUTHOR]

BACKGROUND: Disorders of higher visual processing often impact patients with acquired brain injury. Even with treatment, these vision conditions can cause chronic challenges for patients. Understanding these conditions and their management can help improve functional independence and quality of life. OBJECTIVES: To discuss the various disorders of higher visual processing that result from acquired brain injury. Discussion to include classification, evaluation, and treatment techniques available to clinicians. METHODS: Peer reviewed journal articles were searched, primarily through PubMed. Articles spanning several decades were included in the review for historical context of these conditions, however an emphasis was placed on more recent publications for purposes of a discussion regarding clinical management of these conditions. RESULTS: Peer-reviewed articles and clinical trials from across several disciplines were included to frame a discussion of this varied group of conditions. CONCLUSION: Visual processing disorders have debilitating impacts on both the rehabilitation process as well as functional independence. Varied approaches are utilized in the treatment of these conditions with limited success. Understanding the benefits and limitations of both restorative and compensatory treatments will better help clinicians manage patients with these conditions. [ABSTRACT FROM AUTHOR]

A 73-year-old woman with posterior cortical atrophy (PCA) presented with progressive apperceptive visual agnosia, alexia, agraphia, ventral simultanagnosia, prosopagnosia, and allocentric (stimulus-centered) left-sided hemispatial neglect. All of these symptoms were attributed to damage to the bilateral occipito-temporal cortices, consistent with ventral variant PCA. While the Pittsburgh compound B uptake was extensively distributed throughout the occipito-parietal (dorsal) and occipito-temporal (ventral) areas, the THK5351 (ligand binding to tau aggregates/astrocyte gliosis) accumulation was limited to the ventral area. These findings suggest that local accumulation of tau proteins and/or astrocyte gliosis over the occipito-temporal cortices can result in ventral variant PCA.

Purpose of Review: Historical and contemporary treatments of visual agnosia and neglect regard these disorders as largely unrelated. It is thought that damage to different neural processes leads directly to one or the other condition, yet apperceptive variants of agnosia and object-centered variants of neglect share remarkably similar deficits in the quality of conscious experience. Here we argue for a closer association between "apperceptive" variants of visual agnosia and "object-centered" variants of visual neglect. We introduce a theoretical framework for understanding these conditions based on "scale attention", which refers to selecting boundary and surface information at different levels of the structural hierarchy in the visual array. Recent Findings: We review work on visual agnosia, the cortical structures and cortico-cortical pathways that underlie visual perception, visuospatial neglect and object-centered neglect, and attention to scale. We highlight direct and indirect pathways involved in these disorders and in attention to scale. The direct pathway involves the posterior vertical segments of the superior longitudinal fasciculus that are positioned to link the established dorsal and ventral attentional centers in the parietal cortex with structures in the inferior occipitotemporal cortex associated with visual apperceptive agnosia. The connections in the right hemisphere appear to be more important for visual conscious experience, whereas those in the left hemisphere appear to be more strongly associated with the planning and execution of visually guided grasps directed at multi-part objects such as tools. In the latter case, semantic and functional information must drive the selection of the appropriate hand posture and grasp points on the object. This view is supported by studies of grasping in patients with agnosia and in patients with neglect that show that the selection of grasp points when picking up a tool involves both scale attention and semantic contributions from inferotemporal cortex. The indirect pathways, which include the inferior fronto-occipital and horizontal components of the superior longitudinal fasciculi, involve the frontal lobe, working memory and the "multiple demands" network, which can shape the content of visual awareness through the maintenance of goal- and task-based abstractions and their influence on scale attention. Summary: Recent studies of human cortico-cortical pathways necessitate revisions to long-standing theoretical views on visual perception, visually guided action and their integrations. We highlight findings from a broad sample of seemingly disparate areas of research to support the proposal that attention to scale is necessary for typical conscious visual experience and for goal-directed actions that depend on functional and semantic information. Furthermore, we suggest that vertical pathways between the parietal and occipitotemporal cortex, along with indirect pathways that involve the premotor and prefrontal cortex, facilitate the operations of scale attention. [ABSTRACT FROM AUTHOR]

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Integration information theories posit that the integration of information is necessary and/or sufficient for consciousness. In this paper, we focus on three of the most prominent information integration theories: Information Integration Theory (IIT), Global Workspace Theory (GWT), and Attended Intermediate-Level Theory (AIR). We begin by explicating each theory and key concepts they utilize (e.g., information, integration, etc.). We then argue that the current evidence indicates that the integration of information (as specified by each of the theories) is neither necessary nor sufficient for consciousness. Unlike GWT and AIR, IIT maintains that conscious experience is both necessary and sufficient for consciousness. We present empirical evidence indicating that simple features are experienced in the absence of feature integration and argue that it challenges IIT's necessity claim. In addition, we challenge IIT's sufficiency claim by presenting evidence from hemineglect cases and amodal completion indicating that contents may be integrated and yet fail to give rise to subjective experience. Moreover, we present empirical evidence from subjects with frontal lesions who are unable to carry out simple instructions (despite appearing to understand their meaning) and argue that they are irreconcilable with GWT. Lastly, we argue that empirical evidence indicating that patients with visual agnosia fail to identify objects they report being conscious of present a challenge to AIR's necessity claim. [ABSTRACT FROM AUTHOR]

Optic aphasia is a rare neurological disorder that affects the visual-semantic ability of patients with normal vision and is caused by a lesion in the left occipital lobe. The signs and symptoms of optic aphasia are similar to those of associative visual agnosia, where patients have difficulty recognizing objects both in shape and function, resulting in challenges performing daily tasks. The transformation to optic aphasia or associative visual agnosia is closely related to the degree of damage to the corpus callosum, with some studies hypothetically suggesting that complete damage to the corpus callosum leads to optic aphasia, whereas incomplete damage causes associative visual agnosia. We present a case of a 60-year-old man with a history of intracerebral hemorrhage in the left occipitotemporoparietal lobe. The patient complained of intermittent episodes of painless, blurry vision. Upon examination, we observed that the patient was unable to read the Snellen chart, although he could draw the letter. Furthermore, we discovered that the patient had difficulty naming objects and instruments, even though he was able to express their shape and function through gestures and mimicry. The signs and symptoms of the patient, along with the result of the multi-slice non-contrast CT scan, suggest that he had optic aphasia rather than associative visual agnosia. A comprehensive neuropsychological and aphasia examination needs to be performed to further assess the condition of our patient and establish the diagnosis., Competing Interests: Conflict of Interest: None declared

Facial agnosia (prosopagnosia) is one of the causes of limitations in the life of patients with focal vascular, inflammatory, traumatic, and tumor lesions of the brain; however, the clinical significance of these lesions in neurological practice is often underestimated.The review briefly presents the current understanding of the neurophysiological basis of facial gnosis and its neuroanatomic correlates. It discusses the clinical variants of prosopagnosia, the features of neuropsychological diagnosis, and adopted approaches to patient rehabilitation. It also highlights the importance of developing standardized methods for facial agnosia to improve the detection of prosopagnosia in focal brain lesions.

The size-weight illusion is a perceptual illusion where smaller objects are judged as heavier than equally weighted larger objects. A previous informal report suggests that visual form agnosic patient DF does not experience the size-weight illusion when vision is the only available cue to object size. We tested this experimentally, comparing the magnitudes of DF's visual, kinesthetic and visual-kinesthetic size-weight illusions to those of 28 similarly-aged controls. A modified t-test found that DF's visual size-weight illusion was significantly smaller than that of controls (zcc = −1.7). A test of simple dissociation based on the Revised Standardized Difference Test found that the discrepancy between the magnitude of DF's visual and kinesthetic size-weight illusions was not significantly different from that of controls (zdcc = −1.054), thereby failing to establish a dissociation between the visual and kinesthetic conditions. These results are consistent with previous suggestions that visual form agnosia, following ventral visual stream damage, is associated with an abnormally reduced size-weight illusion. The results, however, do not confirm that this reduction is specific to the use of visual size cues to predict object weight, rather than reflecting more general changes in the processing of object size cues or in the use of predictive strategies for lifting. [ABSTRACT FROM AUTHOR]

The aim of this article is to discuss the logic and assumptions behind the concept of neural reuse, to explore its biological advantages and to discuss the implications for the cognition of a brain that reuses existing circuits and resources. We first address the requirements that must be fulfilled for neural reuse to be a biologically plausible mechanism. Neural reuse theories generally take a developmental approach and model the brain as a dynamic system composed of highly flexible neural networks. They often argue against domain-specificity and for a distributed, embodied representation of knowledge, which sets them apart from modular theories of mental processes. We provide an example of reuse by proposing how a phylogenetically more modern mental capacity (mental rotation) may appear through the reuse and recombination of existing resources from an older capacity (motor planning). We conclude by putting arguments into context regarding functional modularity, embodied representation, and the current ontology of mental processes.

Acquired focal visuoperceptual deficits are rarely reported, and rehabilitation strategies are not well established. This is a report on visuoperceptual deficit after traumatic brain injury that initially went unnoticed.Missing visual agnosia is not unusual especially when perceptual deficits present with visual field defects, impaired insight, and inattention. This case is made more interesting because of the rarity of visual agnosia with predominant ventral pathway involvement, affecting object and face recognition. This report provides a brief discussion on visual agnosia spectrum deficits and rehabilitation measures. [ABSTRACT FROM AUTHOR]

Posterior cortical atrophy (PCA) is a rare disease that manifestsmainly as disturbance of cortical visual function, agnosia.Blints syndrome (optic ataxia) is one of the clearest clinicalmarkers of the disease. The disease is caused by progressive atrophyof the visual cortex. Many researchers define PCA as anindependent disease, while others suggest that it is a posteriorvariant of Alzheimers disease, corticobasal degeneration, etc. Morphological studies of brain tissues support the neurodegenerativenature of the disease.

Visual agnosia and Balint's syndrome are complex neurological disorders of the higher visual system that can have a remarkable impact on individuals' lives. Rehabilitation of these individuals is important to enable participation in everyday activities despite the impairment. However, the literature about the rehabilitation of these disorders is virtually silent. Therefore, the aim of this systematic review is to give an overview of available literature describing treatment approaches and their effectiveness with regard to these disorders. The search engines Psychinfo, Amed, and Medline were used, resulting in 22 articles meeting the criteria for inclusion. Only articles describing acquired disorders were considered. These articles revealed that there is some information available on the major subtypes of visual agnosia as well as on Balint's syndrome which practising clinicians can consult for guidance. With regard to the type of rehabilitation, compensatory strategies have proven to be beneficial in most of the cases. Restorative training on the other hand has produced mixed results. Concluding, although still scarce, a scientific foundation about the rehabilitation of visual agnosia and Balint's syndrome is evolving. The available approaches give valuable information that can be built upon in the future. [ABSTRACT FROM AUTHOR]

The concept of functional modularity in human visual processing was proposed 25 years ago with the distinction between a ventral pathway for object recognition and a dorsal pathway for action processing. Lesions along these pathways yield selective deficits. A 15-year-old patient (MW) presented with a seizure due to a lesion in the left occipitotemporal cortex. Surgical resection of the lesion was performed with sparing of the classic language areas and visual fields. Postoperatively MW had great difficulty reading and had a specific agnosia for more complex visual stimuli in the right hemifield. No deficit was seen for lower level visual discrimination tasks. Gradual improvement of hemi-agnosia was paralleled by slower reaction times reflecting a speed-accuracy trade-off. Absolute reading speed improved markedly over time, doubling at 6 weeks. MW fully recovered after 18 months. Postoperative functional Magnetic Resonance Imaging (fMRI) illustrated an overlap of the lesion with object and word processing areas. Diffusion Tensor Imaging showed damage to the white matter tracts [inferior fronto-occipital fasciculus and inferior longitudinal fasciculus (ILF)] interconnecting ventral temporal areas. A transient higher order deficit can result from a disruption of the neural network supporting visual word and object processing. Most visual system research has focused on cortical areas, while the underlying subcortical network received much less attention. We believe that white matter tracts, in particular the ILF, play a critical role in object perception by connecting visual areas along the ventral visual stream. Lesions of the ILF should be taken into consideration in agnosia. [ABSTRACT FROM AUTHOR]

The inferior longitudinal fasciculus (ILF) is a long-range, associative white matter pathway that connects the occipital and temporal-occipital areas of the brain to the anterior temporal areas. In view of the ILF’s anatomic connections, it has been suggested that this pathway has a major role in a relatively large array of brain functions. Until recently, however, the literature data on these potential functions were scarce. Here, we review the key findings of recent anatomic, neuromodulation, and neuropsychological studies. We also summarize reports on how this tract is disrupted in a wide range of brain disorders, including psychopathologic, neurodevelopmental, and neurologic diseases. Our review reveals that the ILF is a multilayered, bidirectional tract involved in processing and modulating visual cues and thus in visually guided decisions and behaviors. Accordingly, sudden disruption of the ILF by neurologic insult is mainly associated with neuropsychological impairments of visual cognition (e.g., visual agnosia, prosopagnosia, and alexia). Furthermore, disruption of the ILF may constitute the pathophysiologic basis for visual hallucinations and socio-emotional impairments in schizophrenia, as well as emotional difficulties in autism spectrum disorder. Degeneration of the ILF in neurodegenerative diseases affecting the temporal lobe may explain (at least in part) the gradual onset of semantic and lexical access difficulties. Although some of the functions mediated by the ILF appear to be relatively lateralized, observations from neurosurgery suggest that disruption of the tract’s anterior portion can be dynamically compensated for by the contralateral portion. This might explain why bilateral disruption of the ILF in either acute or progressive disease is highly detrimental in neuropsychological terms.

A number of studies have investigated the cognitive deficits underlying dyslexia and dyscalculia. Yet, it remains unclear as to whether dyslexia and dyscalculia are associated with the common visual perception deficits. The current investigation analyzed cognitive performance in children with dyslexia, dyscalculia, comorbidity, and typically developing subjects. The results showed that children with dyslexia, dyscalculia and comorbidity exhibited common deficits in numerosity processing and visual perception. Furthermore, visual perception deficits accounted for deficits in numerosity processing in all three groups. The results suggest that visual perception deficits are a common cognitive deficit underlying both developmental dyslexia and dyscalculia. [ABSTRACT FROM AUTHOR]

Visual crowding is a phenomenon that impairs object recognition when the features of an object are positioned too closely together. Crowding limits recognition in normal peripheral vision and it has been suggested to be the core deficit in visual agnosia, leading to a domain-general deficit in object recognition. Using a recently developed tool, we test whether crowding is the underlying deficit in four patients with category specific agnosias: Two with pure alexia and two with acquired prosopagnosia. We expected all patients to show abnormal crowding. We find that the two patients with acquired prosopagnosia show abnormal crowding effects in foveal vision, while the pure alexic patients do not, and that this constitutes a significant dissociation. Thus, abnormal crowding cannot explain all cases of visual agnosia. Much recent work has focused on similarities between pure alexia and acquired prosopagnosia. Here we show a difference in a basic visual mechanism—visual crowding. [ABSTRACT FROM AUTHOR]

The inferior longitudinal fasciculus (ILF) is a long-range, associative white matter pathway that connects the occipital and temporal-occipital areas of the brain to the anterior temporal areas. In view of the ILF's anatomic connections, it has been suggested that this pathway has a major role in a relatively large array of brain functions. Until recently, however, the literature data on these potential functions were scarce. Here, we review the key findings of recent anatomic, neuromodulation, and neuropsychological studies. We also summarize reports on how this tract is disrupted in a wide range of brain disorders, including psychopathologic, neurodevelopmental, and neurologic diseases. Our review reveals that the ILF is a multilayered, bidirectional tract involved in processing and modulating visual cues and thus in visually guided decisions and behaviors. Accordingly, sudden disruption of the ILF by neurologic insult is mainly associated with neuropsychological impairments of visual cognition (e.g., visual agnosia, prosopagnosia, and alexia). Furthermore, disruption of the ILF may constitute the pathophysiologic basis for visual hallucinations and socio-emotional impairments in schizophrenia, as well as emotional difficulties in autism spectrum disorder. Degeneration of the ILF in neurodegenerative diseases affecting the temporal lobe may explain (at least in part) the gradual onset of semantic and lexical access difficulties. Although some of the functions mediated by the ILF appear to be relatively lateralized, observations from neurosurgery suggest that disruption of the tract's anterior portion can be dynamically compensated for by the contralateral portion. This might explain why bilateral disruption of the ILF in either acute or progressive disease is highly detrimental in neuropsychological terms. [ABSTRACT FROM AUTHOR]

The sudden inability to recognize individual faces following brain damage was first reported in a scientific journal 150 years ago and termed ‘prosopagnosia’ 70 years ago. While the term originally identified a face‐selective neurological condition, it is now obscured by a sequence of imprecisions. First, prosopagnosia is routinely used to define symptoms of individual face recognition (IFR) difficulties in the context of visual object agnosia or other neurological conditions, or even in the normal population. Second, this over‐expansive definition has lent support to a long‐standing within‐category recognition account of prosopagnosia, that is, that the impairment of IFR reflects a general impairment in recognizing within‐category objects. However, stringent experimental studies of classical cases of prosopagnosia following brain damage show that their core impairment is not in recognizing physically similar exemplars within non‐face object categories. Instead, the impairment presents specifically for recognizing exemplars of the category of faces. Moreover, compared to typical observers, the impairment appears even more severe for recognizing individual faces against physically dissimilar than similar distractors. Here, I argue that we need to limit accordingly our definition of prosopagnosia to a clinical (i.e., neurological) condition in which there is no basic‐level object recognition impairment. Other criteria for prosopagnosia are proposed, with the hope that this conservative definition enables the study of human IFR processes in isolation, and supports progress in understanding the nature of these processes. [ABSTRACT FROM AUTHOR]

Infants are exposed to auditory and visual information during sleep as well as wakefulness. Little is known, however, about the differences in cortical processing of sensory input between these different behavioral states. In the present study, cortical hemodynamic responses to auditory and visual stimuli during wakefulness and sleep were measured in infants aged 2–10 months using functional near-infrared spectroscopy (fNIRS). While asynchronously presented auditory and visual stimuli during wakefulness induced focal responses in the corresponding sensory regions of the occipital and temporal cortices, the responses to the same stimuli during sleep were dramatically different. Auditory stimuli during sleep induced global responses over the frontal, temporal, and occipital regions, and the response pattern did not change between 2 and 10 months of age. In contrast, visual stimuli during sleep induced responses in the occipital cortex, and the response pattern exhibited developmental changes from a pattern of activation to one of deactivation around a half year of age. The functional connectivity among the cortical regions was generally higher during sleep than during wakefulness. The hemoglobin phase of oxygenation and deoxygenation (hPod) and the phase locking index of hPod (hPod L ) showed general developmental changes and behavioral state dependent differences but no significant differences were seen between the stimulus types. The results suggest that the behavioral states have a fundamental impact on cortical sensory processing; (1) sensory processing during wakefulness is performed in more localized regions, (2) auditory processing is active during both wakefulness and sleep, (3) visual processing undergoes development of inhibitory mechanisms during sleep, and (4) these phenomena primarily reflect neural development rather than vascular and metabolic development. [ABSTRACT FROM AUTHOR]

Molyneux’s question famously asks about whether a newly sighted subject might immediately recognize, by sight alone, shapes that were already familiar to her from a tactile point of view. This paper addresses three crucial points concerning this puzzle. First, (a) the presence of two different questions: the classic one concerning visual recognition and another one concerning vision-for-action (the second question has been almost completely neglected in the literature and even those who mention this second formulation do not fully investigate it). Second, (b) the explicit distinction, reported in the literature, between ocular and cortical blindness. Third, (c) the importance of making reference to our best neuroscientific account on vision, ‘the two visual systems model’, in order to better address Molyneux’s problem(s). Then, by offering a new, deeper analysis of the relation between (a), (b) and (c), this paper suggests that the subjects of Molyneux’s two different questions show the same visual impairment as brain-damaged subjects with different lesions of the visual cortex. In particular, the subject of the first (classic) question shows the same impairment in visual recognition as a visual agnosic subject, while the subject of the second question shows the same visual impairment in visuomotor processing as an optic ataxic subject. These impairments still hold even if ocular processing is restored. Therefore, I suggest the following. For the first classic question, the required experimental setting cannot be properly reached. By contrast, concerning the second question, based on the interpretation we select, either the answer is negative, or, as with the first question, the experimental setting cannot be properly reached. This proposal constitutes, with the other approaches offered in the literature, a further attempt to tackle the enormous complexity of Molyneux’s puzzle. [ABSTRACT FROM AUTHOR]

Goodale and Milner's two visual system hypothesis is an influential model for the understanding of the primate visual system. Lesions of either the ventral (occipito‐temporal) or the dorsal (occipito‐parietal) stream produce distinct and dissociated syndromes in humans: visual agnosia is typical for ventral damage, whereas optic ataxia (OA) for dorsal damage. We studied the case of a 59‐year‐old left‐handed woman with a circumscribed lesion around the left posterior occipital sulcus, extending to the underlying white matter. Initially, she presented with a central visual field OA, which regressed to an OA to the right visual hemifield during the 3 months observation period. In addition, tachistoscopic experiments showed visual hemiagnosia to the right visual hemifield. In line with the findings of the neuropsychological experiments, the analysis of the structural MR data by means of a trackwise hodologic probabilistic approach revealed damage to the left superior longitudinal fasciculus and to the left inferior longitudinal fasciculus, indicating an impairment of both the dorsal and the ventral stream. The combination of OA and visual hemiagnosia in the same patient has never been previously described. The present case study thus provides further insights for the understanding of visual processing. [ABSTRACT FROM AUTHOR]