Review
Visual agnosia
Agnosias visuales
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Álvarez, J. Masjuan" "autores" => array:2 [ 0 => array:4 [ "nombre" => "R." "apellidos" => "Álvarez" "email" => array:1 [ 0 => "r.alvarez.velasco@gmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "J." "apellidos" => "Masjuan" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Servicio de Neurología, Hospital Universitario Ramón y Cajal, Madrid, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Instituto Ramón y Cajal de Investigación Sanitaria, Madrid, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Agnosias visuales" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0020" "etiqueta" => "Figure 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr4.jpeg" "Alto" => 1293 "Ancho" => 1700 "Tamanyo" => 288306 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Farnsworth–Munsell test. (a) The patient has to rearrange the colored tiles using the first and last of each row as reference. (b) The result of a healthy individual. (c) The result of a patient with achromatopsia, the black lines indicate the percentage of error in the placement of each tile. This test can be performed for free at the website <a class="elsevierStyleInterRef" id="intr0005" href="http://www.color-blindness.com/">http://www.color-blindness.com</a>.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Background</span><p id="par0005" class="elsevierStylePara elsevierViewall">Vision is the most developed sensory modality in humans and the one on which we are most dependent. The process starts with the coding of an image by photoreceptor cells in the retina, information which is then projected to the brain by means of the optical nerve, with an initial stop in the geniculate nucleus of the thalamus and from there to the primary visual cortex located around the calcarine fissure of the occipital lobe. Any lesion up to that point will cause a visual field disorder in image acuity or color, i.e., primary visual disorders. From there, the image formed in the primary visual cortex must be recognized and interpreted. To this end, a mental representation of the image is created that can be compared with images previously stored in memory, thereby acquiring sense to the individual. This process occurs in the associative visual cortex, located in the occipital, temporal and parietal lobes. Lesions in the associative visual cortex cause visual agnosia. This disorder is defined as an impairment in the ability to recognize objects visually, in the absence of a loss of visual acuity or cognitive dysfunction that could explain this impairment.</p><p id="par0010" class="elsevierStylePara elsevierViewall">The information received in the primary visual cortex will follow 2 main processing pathways: the ventral stream or the “What?” and the dorsal stream or the “Where?” (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). The ventral stream's function is perception, i.e., building a conscious representation of the world that surrounds us, allowing us to identify and recognize objects, assigning them meaning. The dorsal stream's function is to locate objects in space, determine their movement and trajectory and relate them spatially with the objects that surround them, allowing us to accurately guide our movements toward them.<a class="elsevierStyleCrossRefs" href="#bib0150"><span class="elsevierStyleSup">1,2</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">An example that shows how these 2 pathways work is the mailbox experiment. In this experiment, a patient with a bilateral ventral temporal–occipital lesion is asked if the opening of a mailbox is in the upper or lower part. The patient will not know how to answer the question; however, if they are given a letter, they will insert it into the opening correctly. The patient does not perceive the opening but can locate it and accurately guide their movements toward it.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Depending on which pathway is damaged (ventral or dorsal), there will be 2 types of visual agnosia: the ones consisting of an erroneous perception of objects and the ones consisting of incorrectly locating these objects, which prevents accurate interaction with them.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Agnosia of the ventral visual pathway</span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">General visual agnosia</span><p id="par0025" class="elsevierStylePara elsevierViewall">Patients with this type of agnosia have difficulties recognizing objects in the absence of semantic recognition disorders. For example, when these patients are shown a hammer, they are unable to name it but, conversely, can name it if they touch it or are asked what object drive nails. This ability differentiates them from patients with aphasia.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">4</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">There are 2 types of sequential processes required when recognizing an object:<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1.</span><p id="par0040" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Perception.</span> The process by which the form, size and volume of an object is identified, integrating it into a three-dimensional image. In patients with apperceptive agnosia, the degree of impairment varies significantly. Patients with a greater degree of impairment have an absolute inability to recognize the simplest forms, which impedes them from, for example, differentiating a straight line from a curve or determining the size of objects. In their daily life, these patients have practically the same degree of disability as a patient with total blindness, with the difference that the former are able of avoid obstacles but cannot recognize any of the objects that surround them. Paraphrasing Saramago, there are “blind people who cannot see and blind people who seeing see not,” the latter definition being the most appropriate for these patients. Patients with the less severe forms of this condition have difficulty integrating or grouping the various parts of an object in an item differentiated from the objects that surround them. These patients are unable to differentiate overlapping objects, something they achieve by separating them. Another type of perceptual visual agnosia is that in which the patients have difficulty in identifying objects presented from an atypical perspective (e.g., a painting with a figure lying in perspective). In general, this disorder is rarely limiting from the functional point of view. These disorders are caused by lesions of any type in the bilateral occipital–temporal cortex. These disorders have been reported most often after bilateral cerebral infarctions in the posterior cerebral artery territory, carbon monoxide poisoning and in the posterior variant of Alzheimer's disease,<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">4</span></a> characterized mainly by visuospatial disorders, object agnosia, difficulty with facial recognition, simultanagnosia and alexia.</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2.</span><p id="par0045" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Association</span>. The process by which the generated mental image is compared with previously acquired images stored in memory, enabling us to recognize objects. Patients with associative visual agnosia can draw and copy objects, unlike patients with apperceptive agnosia in its complete form (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). These patients are able to compare an object with another and say whether it is the same object or not. These patients can also describe the object. For example, when they are shown an orange, they are able to say that it is a small, round, rough, orange object but cannot recognize it further.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">5</span></a> This type of disorder has been reported after localized bilateral and, more rarely, unilateral lesions in the parahippocampal, fusiform and lingual gyrus of the dominant hemisphere. The causes are very similar to those of general apperceptive visual agnosia.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">6</span></a></p><elsevierMultimedia ident="fig0010"></elsevierMultimedia></li></ul></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Prosopagnosia</span><p id="par0050" class="elsevierStylePara elsevierViewall">This disorder is the inability to recognize previously known faces. These patients can have difficulties recognizing relatives and celebrities and even themselves when looking in a mirror.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">5</span></a> Patients learn to recognize individuals by specific characteristics, such as having a beard or a large nose, or by nonfacial clues, such as gait. Additionally, almost all such patients are able of recognize individuals by their voice. This is probably the reason why many of these patients compensate, at least partially, for the deficiency and do not spontaneously report their symptoms.<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">7</span></a> The amount of information these patients can extract from a face (e.g., recognition of emotions, gender, age or whether the face is attractive or not) varies.</p><p id="par0055" class="elsevierStylePara elsevierViewall">Isolated prosopagnosia is rare and is frequently accompanied by other manifestations (e.g., general visual agnosia, visual field deficits, hemineglect), which relegate it to a second plane and can go unnoticed if not specifically examined.<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">8</span></a> In the diagnosis of prosopagnosia, we should ensure that the patient does not have general visual agnosia by having them name objects from various categories. We should then confirm that the patient still recognizes individuals through nonvisual clues (e.g., by asking them the name of celebrities using biographical facts or after listening to recordings of their voices) to check that this form of recognition is undamaged. This step, which should be subsequently performed, also helps confirm that the defect in recognizing photographs, is not due to a cultural issue. There are systematic tests to assess patients with prosopagnosia, such as the Warrington Recognition Memory Test<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">9</span></a> and the Cambridge Face Memory Test.<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">10</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Prosopagnosia has been associated with bilateral lesions of the lower occipital–temporal and anterior temporal regions. Unilateral lesions occur less frequently in these regions, in the right hemisphere.<a class="elsevierStyleCrossRefs" href="#bib0200"><span class="elsevierStyleSup">11,12</span></a> The recognition of objects can be partially affected; however, the clear disproportion between facial and object recognition in patients with prosopagnosia and the results of studies with functional magnetic resonance imaging suggest that the processing of the 2 types of images is performed in different cortical areas. In contrast, a number of studies support the theory that prosopagnosia could be the most pronounced and incapacitating manifestation of a problem with discriminating between highly similar examples from a single category. As an illustration, one of these studies found that the majority of patients with prosopagnosia and good object recognition in the employed tests had, however, greater difficulties than the controls in performing more complex tests of car brand and model recognition.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">13</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">The lesions that cause prosopagnosia are usually secondary to bilateral or unilateral right infarctions in the posterior cerebral artery territory and to neurodegenerative diseases. In particular, these lesions can appear during frontotemporal dementia, although they have also been reported in other types of dementia. The lesions can also occur after infections, trauma, tumors, hypoxic encephalopathy and in congenital disorders.<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">14</span></a> This last cause is surprisingly frequent, given that it affects 2% of the general population.<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">15</span></a> The causes of congenital prosopagnosia are unknown. Functional magnetic resonance imaging has detected structural disorders in the right fusiform gyrus and disorders in this region's connectivity with anterior and frontal temporal regions.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">16</span></a> There have also been reports<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">7</span></a> of families with a total of 38 cases of prosopagnosia, with a transmission suggestive of an autosomal dominant pattern.<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">17</span></a></p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Achromatopsia</span><p id="par0070" class="elsevierStylePara elsevierViewall">This disorder is the inability to differentiate colors. These patients see the world in shades of gray, which might seem a minor disability. However, many patients with achromatopsia are truly affected by the condition in their daily life and perceive the lack of color as extremely unpleasant. Oliver Sacks transcribed the following disquieting history of one of his patients with achromatopsia after a car accident:<span class="elsevierStyleDisplayedQuote" id="dsq0005"><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall"><span class="elsevierStyleItalic">Mr. I. could barely stand the appearance that people now had (“like gray animated statues”) or his own reflection in the mirror. He avoided social life, and sexual relations seemed impossible to him. He saw people's skin, his wife's skin, his own skin as an abominable gray. “Skin color” seemed like “rat color”… He found meals unpleasant due to its deathly, grayish appearance and had to close his eyes to eat.</span><a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">18</span></a></p></span></p><p id="par0075" class="elsevierStylePara elsevierViewall">The Ishihara plates can be used to diagnose these patients. However, they are not very sensitive for partial deficits; the Farnsworth–Munsell test is more appropriate for these patients<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">19</span></a> (<a class="elsevierStyleCrossRefs" href="#fig0015">Figs. 3 and 4</a>).</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0080" class="elsevierStylePara elsevierViewall">Achromatopsia occurs secondary to lesions in the bilateral ventral occipital–temporal region.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">11</span></a> Unilateral lesions are not usually symptomatic; however, a careful examination of these patients can reveal defects in color discrimination in the hemifield contralateral to the lesion.<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">20</span></a> These lesions are generally secondary to cerebral infarctions in the posterior territory and to trauma, encephalitis and neurodegenerative diseases. On rare occasions, we find patients with isolated achromatopsia. Its association with alexia, visual field defects and prosopagnosia, among others, is more common.<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">14</span></a></p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Pure alexia (without agraphia)</span><p id="par0085" class="elsevierStylePara elsevierViewall">Reading is an extremely complex and developed ability in humans, whose mechanism is similar to facial recognition. The latter usually has right predominance, while reading is usually affected by left hemispherical lesions of the lower occipital temporal region (fusiform gyrus). Due to this lateralization of reading, some lesions of the corpus callosum can cause hemialexia of the left visual hemifield. This is due to the fact that the visual information received in the primary visual cortex of the right hemisphere cannot access the contralateral hemisphere, where its processing is performed, resulting in difficulty in understanding the start of written words.<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">21</span></a> In pure alexia, the other verbal skills (nomination, comprehension, repetition and writing) are respected. It is surprising that these patients can correctly write a phrase, but they are incapable of reading something they have written after a few minutes. Some patients are able to “read” by going over the written word with a pen (kinesthetic reading).<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">14</span></a> The degree of impairment in alexia varies, ranging from patients who are unable to read isolated letters, numbers or symbols to patients whose deficit allows them to read but at a slower pace than normal.</p><p id="par0090" class="elsevierStylePara elsevierViewall">It is worth differentiating between the several types of alexia. Patients with surface alexia can go from a written word to its verbal expression because they still have the mechanism for transforming lexemes to phonemes; however, they are incapable of reading words that are not pronounced the same way they are written (which is not an extremely incapacitating problem in Spanish). Patients with phonological alexia are, in contrast, unable to go from lexeme to phoneme and understand words by going directly from the sequence of written letters to the spelling dictionary stored in their memory (they cannot transform written letters into sounds). The difficulty for these patients lies in reading aloud those words whose meaning they do not know, which is revealed by showing them nonexistent words. For example, when a healthy individual sees the word “QUETU”, they recognize the phonemes |k|, |e|, |t|, |u| and can pronounce the word aloud. However, a patient with phonological alexia would be incapable of performing this step. Lastly, profound alexia consists of performing semantic errors while reading (e.g., if they see the word “dog”, they read it as “animal”).<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">22</span></a></p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Topographagnosia</span><p id="par0095" class="elsevierStylePara elsevierViewall">Spatial orientation depends on a considerable number of different cognitive functions. These functions include the recognition of objects in our local setting, the creation of a mental map and the ability to place ourselves correctly according to this map. Topographagnosia refers to a disorder in the visual recognition of geographical places. This condition is examined by showing images of famous sites or places known to the patient. The patients are unable to recognize them visually although they have no difficulty describing them, giving directions on how to reach them and placing them on maps. The patients’ main problem is that they are unable to recognize landscape clues (e.g., buildings) that can help them determine where they are. These patients can learn to orient themselves following verbal information by memorizing the directions (e.g., take the third on the right then take the first on the left), which becomes useless if the patient attempts to start the trip from a different point than the learned one.</p><p id="par0100" class="elsevierStylePara elsevierViewall">The lesions that explain this symptom are found in the medial temporal–occipital region, in the fusiform, lingual and parahippocampal gyrus and are bilateral and less frequently right unilateral. The most common lesion mechanism is ischemia.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">23</span></a></p></span></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Agnosia of the dorsal visual pathway</span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Akinetopsia</span><p id="par0105" class="elsevierStylePara elsevierViewall">This disorder is the inability to perceive movement. This is an extremely rare condition of which very few cases have been published.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">24</span></a> These patients have the sensation that objects jump into place rather than having a continuous and fluid movement, appearing and disappearing in different positions, which makes it difficult to judge whether the object is getting closer or moving away. For them, running water takes on the appearance of a block of ice. Akinetopsia occurs after bilateral occipital–parietal lesions (cases of unilateral lesions have been reported), generally due to ischemia or trauma.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">5</span></a></p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Simultanagnosia</span><p id="par0110" class="elsevierStylePara elsevierViewall">This disorder is the inability to see more than one object at a time. Although these patients can determine the form, color, size and location of each object separately, they cannot place them in relation with others to create a joint coherent image. They therefore see the world as a chaos of objects without no connection between them. Some of these patients do not stray far from being functionally blind. The patients can have difficulty differentiating between the various parts that make up an object (they see a forest but they cannot see the trees) or differentiating the overall collection formed by several objects (they can see the trees but not the forest). These 2 phenomena can coexist in the same patient depending on the image they are analyzing. A method that can be used when examining these patients, and which illustrates this dichotomy, is the presentation of letters grouped to form another different letter or an image similar to the pictorial representations of Arcimboldo, in which the artist painted portraits by joining various objects (<a class="elsevierStyleCrossRef" href="#fig0025">Fig. 5</a>).</p><elsevierMultimedia ident="fig0025"></elsevierMultimedia><p id="par0115" class="elsevierStylePara elsevierViewall">Simultanagnosia can be considered a visual attention defect. Patients have difficulty in directing their attention to different objects at once and focus on highly limited points in the visual field. A patient once described her/his disease by likening her/his visual attention to a spotlight. By increasing the area of the spotlight in order to have a better view of the whole, the intensity of the light decreases, losing detail on each object. In contrast, if the patient wanted to pay attention to a specific object with more detail, she/he had to concentrate this spotlight, losing her/his attention on nearby objects. This analogy only helps explain a part of the symptoms that appear in patients with simultanagnosia. The ability to fix one's attention on one or several objects depends not only on the visual field the objects reside in but also on the characteristics of the objects. For example, these patients are able to see a complete star of David if the 2 triangles that make up the star are the same color; however, they see only one triangle if the colors of each one are different. There is increasing interest in this type of experiment, due to the understanding it provides on the functioning of the visual attention and consciousness.<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">25</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">Simultanagnosia has been associated with bilateral lesions of the medial occipital–parietal junction, the cuneus and the intraparietal sulcus, generally secondary to ischemia or neurodegenerative diseases.<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">26</span></a></p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Optical ataxia</span><p id="par0125" class="elsevierStylePara elsevierViewall">This is a disorder in the ability to reach objects and direct movements under visual guidance. Unlike patients with cerebellar ataxia, these patients can reach objects when guided by another sensory modality. For example, they should be able to reach parts of their own body guided by somatosensory stimuli. Holmes described this characteristic in a patient who was wounded by a gunshot in the First World War:<span class="elsevierStyleDisplayedQuote" id="dsq0010"><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall"><span class="elsevierStyleItalic">He had extreme difficulty locating objects in space using his vision […]. When asked to hold a pencil in front of his eyes, he fumbled his hand making errors in judging its position. However, if his hand reached my arm, the hand moved quickly toward my hand, reaching the object it was holding.</span><a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">27</span></a></p></span></p><p id="par0130" class="elsevierStylePara elsevierViewall">These patients are able to accurately move food toward their mouth and, unlike patients with cerebellar ataxia, do not have intention tremors or dysdiadochokinesia. Unlike ocular motor apraxia, which will be discussed later in this document, the patient's ability to direct their gaze toward a certain object is intact.</p><p id="par0135" class="elsevierStylePara elsevierViewall">Optical ataxia is caused by lesions of the occipital-parietal junction. Bilateral lesions cause generalized optical ataxia. However, when the lesions are unilateral, the deficiency might occur only in the limb or visual hemifield contralateral to the lesion. Optical ataxia generally develops in the context of Balint's syndrome (optical ataxia, ocular motor apraxia and simultanagnosia) due to the proximity of the areas responsible for each of these symptoms. The most common causes of Balint's syndrome are ischemia in the border territory between the anterior and posterior circulation, the posterior variant of Alzheimer's disease and trauma.<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">28</span></a></p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Ocular motor apraxia</span><p id="par0140" class="elsevierStylePara elsevierViewall">This is the inability to direct one's gaze toward visual objectives. When the impairment is mild, it causes a delay in the start of saccadic eye movements aimed at directing the gaze toward a visual stimulus. When the defect is more severe, the patient is unable to change their gaze from one object to another. In addition to a defect in the start of eye movements, these movements tend to be inaccurate and miss the objective. The saccades are therefore not direct but instead visual scanning occurs until the patient reaches the target. In severe cases, even after managing (with some effort) to fixate on an object, this attention is transient, and the patient cannot maintain it for the desired amount of time.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">5</span></a></p><p id="par0145" class="elsevierStylePara elsevierViewall">Ocular motor apraxia is associated with bilateral lesions of the fronto-parietal eye field located in the intraparietal sulcus. This disorder usually occurs as part of Balint's syndrome.<a class="elsevierStyleCrossRefs" href="#bib0215"><span class="elsevierStyleSup">14,29</span></a></p></span></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Conclusion</span><p id="par0150" class="elsevierStylePara elsevierViewall">The study of patients with lesions in visual associative regions has provided significant developments in the understanding of visual agnosia and the functioning of visual processing. However, this understanding is far from complete. There is still a long journey ahead, during which time patients with these types of lesions and the new techniques, such as functional magnetic resonance imaging, will have much to teach us.</p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Conflict of interest</span><p id="par0155" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:10 [ 0 => array:3 [ "identificador" => "xres611128" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec625116" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres611127" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec625117" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Background" ] 5 => array:3 [ "identificador" => "sec0010" "titulo" => "Agnosia of the ventral visual pathway" "secciones" => array:5 [ 0 => array:2 [ "identificador" => "sec0015" "titulo" => "General visual agnosia" ] 1 => array:2 [ "identificador" => "sec0020" "titulo" => "Prosopagnosia" ] 2 => array:2 [ "identificador" => "sec0025" "titulo" => "Achromatopsia" ] 3 => array:2 [ "identificador" => "sec0030" "titulo" => "Pure alexia (without agraphia)" ] 4 => array:2 [ "identificador" => "sec0035" "titulo" => "Topographagnosia" ] ] ] 6 => array:3 [ "identificador" => "sec0040" "titulo" => "Agnosia of the dorsal visual pathway" "secciones" => array:4 [ 0 => array:2 [ "identificador" => "sec0045" "titulo" => "Akinetopsia" ] 1 => array:2 [ "identificador" => "sec0050" "titulo" => "Simultanagnosia" ] 2 => array:2 [ "identificador" => "sec0055" "titulo" => "Optical ataxia" ] 3 => array:2 [ "identificador" => "sec0060" "titulo" => "Ocular motor apraxia" ] ] ] 7 => array:2 [ "identificador" => "sec0065" "titulo" => "Conclusion" ] 8 => array:2 [ "identificador" => "sec0070" "titulo" => "Conflict of interest" ] 9 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec625116" "palabras" => array:5 [ 0 => "Agnosia" 1 => "Visual" 2 => "Prosopagnosia" 3 => "Achromatopsia" 4 => "Simultanagnosia" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec625117" "palabras" => array:5 [ 0 => "Agnosia" 1 => "Visual" 2 => "Prosopagnosia" 3 => "Acromatopsia" 4 => "Simultagnosia" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Visual agnosia is defined as an impairment of object recognition, in the absence of visual acuity or cognitive dysfunction that would explain this impairment. This condition is caused by lesions in the visual association cortex, sparing primary visual cortex. There are 2 main pathways that process visual information: the ventral stream, tasked with object recognition, and the dorsal stream, in charge of locating objects in space. Visual agnosia can therefore be divided into 2 major groups depending on which of the two streams is damaged. The aim of this article is to conduct a narrative review of the various visual agnosia syndromes, including recent developments in a number of these syndromes.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Las agnosias visuales se definen como una alteración en la capacidad de reconocer objetos con la vista, en ausencia de pérdida de agudeza visual o disfunción cognitiva que explique esta alteración. Están producidas por lesiones de la corteza visual asociativa, respetando la corteza visual primaria. Existen 2 vías principales de procesamiento de la información visual: la vía ventral, encargada del reconocimiento de objetos, y la vía dorsal, encargada de su localización en el espacio. Las agnosias visuales pueden, por tanto, dividirse en 2 grandes grupos dependiendo de cuál de las 2 vías esté lesionada. El objetivo de este artículo es realizar una revisión narrativa sobre los diferentes síndromes agnósicos visuales, incluyendo los últimos avances realizados en algunos de ellos.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Álvarez R, Masjuan J. Agnosias visuales. Rev Clin Esp. 2016;216:85–91.</p>" ] ] "multimedia" => array:5 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1012 "Ancho" => 1650 "Tamanyo" => 214752 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Schematic representation of the 2 visual association pathways.</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 675 "Ancho" => 1776 "Tamanyo" => 105509 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Drawings by a patient with apperceptive (left) and associative (right) visual agnosia. Please note the level of detail achieved in the first drawing even though the patient is unable to recognize the object they are copying.</p>" ] ] 2 => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 947 "Ancho" => 950 "Tamanyo" => 203968 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Ishihara plate in which a healthy individual differentiates the number.</p>" ] ] 3 => array:7 [ "identificador" => "fig0020" "etiqueta" => "Figure 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr4.jpeg" "Alto" => 1293 "Ancho" => 1700 "Tamanyo" => 288306 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Farnsworth–Munsell test. (a) The patient has to rearrange the colored tiles using the first and last of each row as reference. (b) The result of a healthy individual. (c) The result of a patient with achromatopsia, the black lines indicate the percentage of error in the placement of each tile. This test can be performed for free at the website <a class="elsevierStyleInterRef" id="intr0005" href="http://www.color-blindness.com/">http://www.color-blindness.com</a>.</p>" ] ] 4 => array:7 [ "identificador" => "fig0025" "etiqueta" => "Figure 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr5.jpeg" "Alto" => 848 "Ancho" => 1664 "Tamanyo" => 216720 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Example of simple tests for assessing patients with simultanagnosia. 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