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      Anton's syndrome due to cerebrovascular disease: a case report

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      1 , , 1 , 1
      Journal of Medical Case Reports
      BioMed Central

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          Abstract

          Introduction

          Anton's syndrome describes the condition in which patients deny their blindness despite objective evidence of visual loss, and moreover confabulate to support their stance. It is a rare extension of cortical blindness in which, in addition to the injury to the occipital cortex, other cortical centres are also affected, with patients typically behaving as if they were sighted.

          Case presentation

          We present a case report of an 83-year-old white woman with cortical blindness as a result of bilateral occipital lobe infarcts. Despite her obvious blindness, illustrated by her walking into objects, the patient expressed denial of visual loss and demonstrated confabulation in her accounts of her surroundings, consistent with a diagnosis of Anton's syndrome.

          Conclusions

          A suspicion of cortical blindness and Anton's syndrome should be considered in patients with atypical visual loss and evidence of occipital lobe injury. Cerebrovascular disease is the most common cause of Anton's syndrome, as in our patient. However, any condition that may result in cortical blindness can potentially lead to Anton's syndrome. Recovery of visual function will depend on the underlying aetiology, with cases due to occipital lobe infarction after cerebrovascular events being less likely to result in complete recovery. Management in these circumstances should accordingly focus on secondary prevention and rehabilitation.

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          Most cited references10

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          Bypassing V1: a direct geniculate input to area MT.

          Thalamic nuclei are thought to funnel sensory information to the brain's primary cortical areas, which in turn transmit signals afresh to higher cortical areas. Here we describe a direct projection in the macaque monkey from the lateral geniculate nucleus (LGN) to the motion-selective middle temporal area (MTor V5), a cortical area not previously considered 'primary'. The constituent neurons are mostly koniocellular, send virtually no collateral axons to primary visual cortex (V1) and equal about 10% of the V1 population innervating MT. This pathway could explain the persistence of motion sensitivity in subjects following injury to V1, suggesting more generally that residual perception after damage in a primary area may arise from sparse thalamic input to 'secondary' cortical areas.
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            Selective disturbance of movement vision after bilateral brain damage.

            A patient who suffered bilateral posterior brain damage exhibited disturbance of movement vision in a rather pure form. The patient had no impression of movement in depth, and could only discriminate between a stationary and a moving target in the periphery of her otherwise intact visual fields. She had some movement vision in the central part of her visual fields, provided that target velocity did not exceed 10 deg/s. Neither did she possess visual movement after effects nor apparent (phi) visual movement. In addition, visually guided eye and finger movements were impaired. In contrast to the disturbance of movement perception in the visual modality, movement perception elicited by acoustic and tactile stimuli was not impaired. On the basis of the localization of the cerebral damage (as judged by CT scanning and neuropsychological testing) it is concluded that the observed disorder in movement vision is due to bilateral cerebral lesions affecting the lateral temporo-occipital cortex and the underlying white matter. The selectivity of the visual disturbance supports the idea that movement vision is a separate visual function depending on neuronal mechanisms beyond the primary visual cortex.
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              Complex visual hallucinations in the visually impaired: the Charles Bonnet Syndrome.

              Visually impaired patients may experience complex visual hallucinations, a condition known as the Charles Bonnet Syndrome. Patients usually possess insight into the unreality of their visual experiences, which are commonly pleasant but may sometimes cause distress. The hallucinations consist of well-defined, organized, and clear images over which the subject has little control. It is believed that they represent release phenomena due to de-afferentation of the visual association areas of the cerebral cortex, leading to a form of phantom vision. Cognitive defects, social isolation, and sensory deprivation have also been implicated in the etiology of this condition. This condition, which is most common in the elderly, frequently goes unrecognized in clinical practice, due to both lack of awareness among doctors and patients' reluctance to admit to hallucinatory experiences, for fear of being labeled mentally unstable. Furthermore, patients who comprehend the unreality of their hallucinations may be distressed by the real fear of imminent insanity. Sensitive and sympathetic history taking is essential to ascertain the existence of hallucinations. Reassurance and explanation that the visions are benign and do not signify mental illness have a powerful therapeutic effect. Hallucinatory activity may terminate spontaneously, on improving visual function or on addressing social isolation. There is no universally effective drug treatment but anticonvulsants may play a limited role in aborting the hallucinations. Physician awareness and empathy are the cornerstones of management.
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                Author and article information

                Journal
                J Med Case Reports
                Journal of Medical Case Reports
                BioMed Central
                1752-1947
                2009
                9 September 2009
                : 3
                : 9028
                Affiliations
                [1 ]Stroke Unit, Erne Hospital, Cornagrade Road, Enniskillen BT74 6AY, UK
                Article
                1752-1947-0003-0000009028
                10.4076/1752-1947-3-9028
                2827161
                20226004
                d44b1b58-b7fe-4ec3-9e50-ec0a0a8e686e
                Copyright ©2009 Maddula et al.; licensee Cases Network Ltd. licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 10 October 2008
                : 7 March 2009
                Categories
                Case report

                Medicine
                Medicine

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