I had stopped at a florist’s on my way to his apartment and bought myself a slightly extravagant red rose for my lapel buttonhole. I took it off and gave it to her. He took it as a botanist or a morphologist to whom they give a specimen, not as a person to whom they give a flower.

– “About six inches in length. A rolled-up red shape with a green linear addition.”

– “Yes. And what do you think you are?”

– “It’s not easy to say. It lacks the simple symmetry of geometric shapes, although it may have a superior symmetry of its own… it could be an inflorescence or a flower.”

P. was acting exactly like a machine. It was not only that he showed the same indifference as a computer to the visual world but he built the world as a computer builds it, through distinctive features and schematic relationships.

I start today’s entry with this excerpt from a
Oliver Sacks (“The man who mistook his wife for a hat”) in which he tells a case of visual agnosia , which leads the protagonist of the story to a disintegrated vision of the world and to different situations that, although comical, result in a serious problem of visual recognition.

Visual Agnosia: definition and explanation

Since sight is our main sense, we are always shocked and impressed by reading alterations of something as basic as
perception. The brain, through its main window to the world -the eyes-, shows us a simple and ordered image of the world around us.

This creation that our nervous system performs is shared, to a greater or lesser extent, by almost everyone. The basis of all that we call reality is in the light that hits our retinas and travels along the optic nerve in the form of a nerve impulse, to make synapses in the geniculated nucleus of the thalamus – a structure that we could consider a kind of brain toll in which a large number of synapses are made – until it reaches our primary visual cortex in the occipital lobe. But it would be a mistake to believe that this circuit, these three synapses, are the ones that confer meaning to the world we live in. What makes us not live in a chaotic or fragmented world, as in the case of P., is the function of gnosis.

Gnosis , from Latin knowledge, refers to the ability to recognize objects, people, faces, spaces, etc. Furthermore, it is also the faculty that offers us a global and united perception of reality and not schematic or “by parts”. Therefore, the visual agnosia is the loss of this capacity . To better understand this process we will talk about the two main brain pathways involved in this function. We will also talk about the types of agnosia most frequently described in bilbliography

Visual Perception: The Way of the What and Where

As we said, the information from the retina reaches our primary visual cortex after synapses in the thalamus. But the primary visual cortex is not informative in itself in terms of recognition. It only processes the physical characteristics of what the retina perceives. That is: light, contrast, visual field, visual acuity, etc.

Thus, the primary visual cortex, Brodman area 17, has only raw information. It doesn’t tell us that we see a beautiful sunset or a dry leaf. So,
what will it take to recognize an object?

Recognizing objects, faces, places…

First, we must be able to see the object in question, performing those three synapses in order to capture the physical information of the light that hits first the object and then our retina. Secondly,
d e will have to integrate all this information to perceive it as a whole . Finally, we will have to rescue from our memory the memory of that object already present in our memories and its name.

As we can see, this involves more than one source of information. In the brain, the cortex that is in charge of relating different types of information is called the associative cortex. To perform the steps we have described we will need an associative cortex. So the brain will need more synapses, and this is where the what and where pathways come into play.


The what-way, or ventral-way, goes to the temporal lobe and
is in charge of object recognition and identification . It is the way that, if for example we see in the middle of the desert a big green thing with thorns, it helps us to identify it as a cactus and not as the Hulk.

It is not surprising that this path is located in the temporal lobe if we think that this is the main one in charge of memory functions. Therefore the pathway of the
which are nervous projections that link the information of our retina with that of our memory. It is the synthesis of optical and limbic information.


The way of the
where , or dorsal pathway, projects into the parietal lobe. E s the pathway responsible for locating objects in space ; perceiving their movement and trajectory, and relating their location to each other. Therefore, it is the path that allows us to direct our movements effectively in a given space.

These are the neurons that allow us to follow with our eyes the direction a tennis ball takes when it is hit from one court to another. It is also the way that allows us to throw a letter into a mailbox without making mistakes.

Different neurological disorders -infarcts, head injuries, infections, tumors, etc.- may affect these pathways with the expected deficits depending on the affected region. As usual, these brain regions will be affected not only if their cortex is damaged, but also if the fibers that connect these areas to the primary visual cortex are affected.

Visual aperceptive agnosia

In this kind of agnosia
components of perception fail, and therefore, there is no recognition . Perception is the faculty that integrates the physical characteristics of an object so that we can grasp them as a three-dimensional whole.

In aperceptive visual agnosia this integration is severely affected and the patient shows deficits in even the simplest form recognition. These patients, when faced with the drawing of a hammer, will not recognize it as a hammer. Nor will they know how to copy it or match it with another drawing of the same hammer. Nevertheless, visual acuity is normal, as is the perception of light, darkness, etc. In fact, patients can even avoid obstacles when walking. However, the consequences for the patient are so dire that they are often functionally almost blind with serious problems in their level of independence.

Some authors, in a very timely manner, have paraphrased Saramago “there are blind men who do not see, and blind men who see do not see”. The case of a patient with aperceptive agnosia would be the second. These patients may recognize the object by means of another sensory modality such as touch -sometimes touching the different parts of the object in question- or with contextual clues or descriptions by the examiner. In addition, these types of actions by the examiner help to make a differential diagnosis and rule out that the anomie-inability to say the name of what is seen-is not due to a language deficit, for example.

It is a rare type of agnosia and has been described most frequently following bilateral infarctions of the regions of the posterior arteries, carbon monoxide poisoning and in the later variant of Alzheimer’s disease. Thus, s
and is produced by pathologies affecting occipitotemporal regions .

Associative visual agnosia

In this type of agnosia, in addition to visual acuity, color perception, light, contrast…
the perception is also preserved . However, despite normal perception, recognition is affected. As in the previous case, before the drawing of a hammer the subject will not know that it is a hammer, but in this case he will be able to match it with another drawing of a hammer. He can even copy the drawing or describe the object.

They may identify the drawing due to one of the details of the object depicted. As a rule, objects are more difficult to identify than real ones , possibly due to a contextual factor. Again, the other sensory modes can help in their recognition.

Associative agnosia
seems to be due to the disconnection between the visual and limbic systems . The substrate may be the bilateral lesion of the white substance (lower longitudinal fascicle) from the occipital associative cortex to the medial temporal lobe, which leads to a disconnection of the visual and memory systems. This is why this agnosia is also called amnesic agnosia. The causes are similar to those of aperceptive agnosia.

Other types of agnosia

There are many more types of agnosia and perception disorders . Here are some of them. I will simply make a small definition to identify the disorder,


It’s the inability to distinguish colors. Patients who suffer from it see the world in shades of gray. A bilateral lesion of the occipitotemporal region appears secondarily. There are very few recorded cases. If the lesion is unilateral it will not cause symptoms. I highly recommend reading “Anthropologist on Mars” which tells the story of a case of acromatopsia. Besides, reading Oliver Sacks is always a pleasure. I show you an excerpt from that case which will be much more explanatory of the disorder than my definition:

“Mr. I. could hardly stand the way people looked now (“like gray, animated statues”), and neither could he bear his own appearance in the mirror: he avoided social life, and sexual relations seemed impossible to him: he saw the flesh of people, the flesh of his wife, his own flesh, of an abominable gray; the “color of flesh” seemed to him “rat color” [. . .] He found the foods unpleasant because of their dull, grayish appearance, and had to close his eyes to eat “.


It is the inability to recognize faces of relatives, previously known famous people or even one’s own face in the mirror .

Prosopagnosia is a specific deficit in face recognition and therefore we must rule out other types of agnosia for diagnosis. In general, other functions such as reading are not affected. They can also estimate whether they are human or primate faces and even recognize the emotional expression of the face in question. It should be noted that the deficits are more evident when recognizing photographs than when looking at the person in question, as there will be other contextual clues such as the movement of the person. It is also very interesting the proposal of Damasio et al (1990) that would consider that prosopagnosia would not be so much a failure in the recognition of faces, but rather the inability to identify individuality within a set of similars.


Is the inability to perceive objects in movement . It is frequently due to posterior occipitoparietal injuries. The first case of acinetopsy was described in 1983 in a 43-year-old woman who had suffered several bilateral cerebrovascular infarctions. The deficits severely affected her level of independence. For example, she needed to touch the edge of the cup to know when to serve coffee.

Some conclusions

I think it is not necessary to justify how basic the function of gnosis is for our lives. In a way,
our consciousness depends on what we see and on the reality that makes up our brain . This “reality”, manufactured by our circuits, is possibly far from reality as such. Let’s think for a moment: when we see how someone speaks we usually see and hear what we see in synchrony. That is to say, if a friend speaks to us we should not see that first he moves his mouth and then we hear the sound, as if it were a badly dubbed film. But, instead, the speed of light and the speed of sound are very different.

The brain, in some way, integrates reality so that we understand it in an orderly and logical way . When this evil Cartesian genius fails the world can become chaotic and aberrant. Like the fragmented world of P. or the colorless world of I. But is their world more unreal than ours? I think not, we all somehow live deceived by our brains. Like we’re in The Matrix. A Matrix created by ourselves.

Patients like P. or I. have contracted pathologies that have made them move away from the “reality” that we are used to share with the rest of human beings. Although these specific cases had happy endings characterized by personal improvement, in the usual tone of Oliver Sacks, it should be noted that not all cases are equally beautiful. Neurologists and neuropsychologists only see clinical manifestations of these pathologies and, unfortunately, on many occasions we are forced to adopt a “voyeur” attitude when faced with these cases. That is to say,
many times we cannot do much more than follow the case and see how it evolves .

Pharmacological therapies for neurodegenerative disorders are currently of very limited use. Science must develop new drugs. But neuropsychologists must develop new non-pharmacological therapies beyond classical cognitive stimulation. In this regard, centers such as the Guttmann Institute, specialists in neurorehabilitation, are making a great effort and dedication. My subjective opinion is that perhaps the new therapies with virtual reality will mark the 21st century of neuropsychology. In any case, we should work on this or other options and not be satisfied with just the diagnosis.

Text corrected and edited by
Frederic Muniente Peix

Bibliographic references:

Books that tell the story of Agnosia and that I highly recommend reading:

  • Luriia, A., Lemos Giráldez, S., & Fernández-Valdés Roig-Gironella, J. (2010). Lost and recovered world. Oviedo: Krk Ediciones.
  • Sacks, O. (2010). The man who mistook his wife for a hat. Barcelona: Anagram.
  • Sacks, O. An anthropologist on Mars. Barcelona: Anagram


  • Arnedo A, Bembire J, Tiviño M (2012). Neuropsychology through clinical cases. Madrid: Editorial Médica Panamericana.
  • Junqué C (2014). Manual of Neuropsychology. Barcelona: Synthesis


  • Álvarez, R. & Masjuan, J. (2016). Visual agnosias. Revista Clínica Española, 216(2), 85-91. http://dx.doi.org/10.1016/j.rce.2015.07.009

I highly recommend this article above. It is very well explained and very clear and concise.

  • Barton, J. (1998). Higher cortical visual function. Current Opinion In Ophthalmology, 9(6), 40-45. http://dx.doi.org/10.1097/00055735-199812000-00007
  • Barton, J., Hanif, H., & Ashraf, S. (2009). Relating visual to verbal semantic knowledge: the evaluation of object recognition in prosopagnosia. Brain, 132(12), 3456-3466. http://dx.doi.org/10.1093/brain/awp252
  • Bouvier, S. (2005). Behavioral Deficits and Cortical Damage Loci in Cerebral Achromatopsia. Cerebral Cortex, 16(2), 183-191. http://dx.doi.org/10.1093/cercor/bhi096
  • Naccache, L. (2015). Visual consciousness explained by its impairments. Current Opinion In Neurology, 28(1), 45-50. http://dx.doi.org/10.1097/wco.0000000000000158
  • Riddoch, M. (1990). M.J. Farah, Visual agnosia: Disorders of object recognition and what they tell us about normal vision. Biological Psychology, 31(3), 299-303. http://dx.doi.org/10.1016/0301-0511(90)90068-8
  • Zeki, S. (1991). Cerebral Akinetopsia A Review.Brain, 114(4), 2021-2021. http://dx.doi.org/10.1093/brain/114.4.2021