Talk:Anton syndrome

Which specific areas relate to eyesight and to "the presence of vision"?
It's believed that the cause is damage to two areas:[specify] the portion of the brain responsible for eyesight and the portion responsible for detecting the presence of vision[which?].[citation needed]

From the psych courses I took and the research I've just done to refresh my memory, it seems like these areas are BA17 and BA19, respectively (I've noted this in the edit I made on the article). Can someone confirm this?

Or are the specific locations of these areas not yet known to researchers?? — chirographa   diverbia   cognatō  01:06, 24 July 2008 (UTC)

Well, about half the brain is "responsible for eyesight" (i.e., necessary, in one way or another, for normal vision). On the other hand, although I am quite widely read in the neuroscience of vision, I have never heard of a "portion [of the brain] responsible for detecting the presence of vision." I think this sentence is just a redescription of the symptoms (they can't see but they don't know that they can't see) dressed up with spurious speculative neuroscience. Presumably, Anton's is a form of anosognosia, which in other cases can cause sufferers to deny they have symptoms such as paralysis. I think anosognosia in general is associated with right hemisphere parietal lobe damage.

That said, as cognatus suggests, destruction of BA17 (which is the primary visual cortex, AKA V1) would certainly account for the cortical blindness. Also, it might be relevant that at least some people who have lost part of this brain area experience hallucinations (as well as "blindsight") in the part of their visual field that is blinded, although if their brains are otherwise reasonably intact they generally know that these visions are not real (see: Ashwin, P.T. & Tsaloumas, M.D. (2007). Complex Visual Hallucinations (Charles Bonnet Syndrome) in the Hemianopic Visual Field Following Occipital Infarction. Journal of the Neurological Sciences, 263, 184-186; Weiskrantz, L., Warrington, E. K., Sanders, M. D., & Marshall J. (1974). Visual capacity in the hemianopic field following a restricted occipital ablation. Brain, 97, 709-728). Treharne (talk) 14:51, 24 January 2009 (UTC)

Reverted move of this page
I have reverted the move of this page, which was done without any consultation at this talkpage. If anyone wants to move it, please go through the full correct procedure of flagging, notifying, discussion, and consultation.

A further point: when moving an article page, and putting a redirect at the page from which the content is moved, leave the talkpage of that redirecting page intact. I mean, do NOT redirect it as well. Editors may need to discuss the redirect; for example, perhaps some other new article will come to seem more appropriate to redirect to, or a disambiguation page may need to be discussed.

In fact the syndrome discussed on this page is most accurately called Anton's syndrome; Anton-Babinski syndrome more accurately refers either to some anosognosia in general, or to unilateral asomatognosia (or asomat a gnosia). See for example this specialised source. I may well, therefore, call for a move of this page back to Anton's syndrome (yes, that's where this content started out).

– ⊥ ¡ɐɔıʇǝo N oetica! T– 02:11, 16 February 2009 (UTC)

Tone
The tone of this article seems a little critical of people with Anton-Babinski syndrome.

Specifically:

"Those who have it are cortically blind, but affirm, often quite adamantly and in the face of clear evidence of their blindness, that they are capable of seeing. Failing to accept being blind, people with Anton-Babinski syndrome dismiss evidence of their condition and employ confabulation to fill in the missing sensory input."

This reads as though people have a choice about whether or not they have Anton-Babinski, but from the information in the rest of the article (and I don't know much about this, so that's why I've not edited it myself), it seems like this is out of the patient's control. It doesn't seem like this should be phrased as a failure, or as a refusal to acknowledge the obvious. Waitalie Nat (talk) 19:13, 3 May 2018 (UTC)

This section is trying to get at one of the most fascinating aspects of Anton-Babinski Syndrome: the patients don't think that they are blind! If you asked patients with ABS to read something, they will tell you that *obviously* they can read, but not right now because someone's turned out the lights, smeared the ink, taken their glasses, etc. "Confabulation" does sound a little....aggressive, but I think it is the preferred term for when patients invent plausible but ungrounded reasons for their symptoms. 104.163.141.5 (talk) 22:47, 3 July 2022 (UTC)

Two conditions need two articles
The lead states, without citing any reference: Anton syndrome must not be confused with Anton–Babinski syndrome … then proceeds to characterise the latter in a couple of (rather technical) lines, stating — again without references — that Anton–Babinski syndrome is the right-hemisphere equivalent of Gerstmann syndrome and it is due to non-dominant inferior parietal lobule damage. — whatever that means. This appears to consign ABS to the status of "nothing but …" and virtually dismisses it from further discussion, not giving the reader even one wikilink to follow for more in-depth information. However, the remainder of the article deals solely with Anton syndrome. It is thus quite illogical to have this article labelled "Anton–Babinski syndrome" as at present. Clearly, we should label it "Anton syndrome" instead, and create a new and separate article to deal with ABS in a properly encyclopaedic manner. yoyo (talk) 15:00, 29 September 2019 (UTC)

I noticed that too. Even worse, the article is titled “Anton-Babinski Syndrome,” so the fact that it says ABS is a separate disorder is problematic ImVeryAwesome (talk) 01:45, 12 December 2020 (UTC)

Wiki Education assignment: Science Communication
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Inclusion of management stratergies and more case studies
Firstly, I believe that a section on Treatment and Management Strategies for Anton syndrome should be included. This section will detail various rehabilitation techniques and cognitive therapies that are essential for managing the condition effectively.

Secondly, currently, the article only features two case studies. I think adding relevant cases, including those by Chaudhry et al. (2019), Menon et al. (1985), and Swartz (1984), illustrate the diversity of symptoms and the varied responses to rehabilitation, which are crucial for addressing the complex syndrome in both academic and clinical contexts. Sairah Mamik (talk) 20:03, 30 April 2024 (UTC)