Anton’s Syndrome is the delusion of denial that vision has been lost, in contravention of the facts. It is one manifestation of bilateral cortical blindness due to disruption of visual pathways in the brain beyond the lateral geniculate body. The eyes respond to the usual opthalmological testing – there is little or no specific damage.
A recent article in the Case Notes section of the magazine ‘Progress in Neurology and Psychiatry’ describes the condition and the case of an older male patient who came into the emergency room with a supposed hypertensive emergency, including reduced vision and confusion.
For some years, I have been challenging the description ‘confusion’ when describing people with dementia because it has always seemed to me that it is actually a judgement that many of the rest of us make about someone else’s feelings. The confusion may well be between what the person thinks, and what we, ourselves, think. Within their own heads, they may not be confused at all! Only they can say.
In the case of sudden loss of vision, even if it is not admitted, though, there could well be a sense of internal confusion …
Because of the need for speed in the emergency room, the taking of medical history often must be rushed, and it can be very difficult to take into account all the factors which are needed – especially if the patient is suffering from delusions which are not well understood, even though the Austrian neuropsychiatrist, Gabriel Anton described the condition in 1899.
Anton described bilateral damage in the occipital lobe causing blindness which was not reported by the patients. They were, in fact, liable to confabulation about this – denying it, and showing surprising apathy towards it.
Although there is generally no pain, the condition is secondary to, usually, stroke, head trauma, occipital lobe epilepsy, severe hypoglaecemia, and hypertensive encephalopathy, and will probably appear on MRI. According to Aldrich et al (1987 Annals of Neurology), the condition is commonly caused by cerebrovascular disease.
The latest ideas of why patients with Anton’s Syndrome deny blindness are around the disconnection of the speech-language areas from the visual area, which leads to confabulation. It is also believed that, perhaps, the lesions affecting the occipital lobes on both sides can also damage the visual association cortex, and that this could account for the patient’s lack of awareness of their blindness.
In this case study, the patient was given intravenous glyceryl trinitrate infusion, to reduce arterial blood pressure, and supplemental oxygen was administered. He was given aspirin pre-MRI scan. Testing showed-up a new diagnosis of Type 2 diabetes. There was a subjective improvement of visual acuity after treatment.
He was followed-up a month later and no significant improvement in visual acuity was present, although he had developed a certain level of awareness of his condition, i.e. the delusion had lessened, and he accepted the fact that he needed assistance with daily living.
Apart from the underlining of the absolute necessity to obtain a useful medical history (always necessary but rarely entirely satisfactory), the conclusion of the Case History, was of most interest, to a researcher in delusions. The last paragraph says:
‘The cognitive and behavioural problems that accompany blindness pose challenges in the trial of therapy and make rehabilitation difficult. Rehabilitation goals depend on the degree of vision loss, extent of occipital damage, age, and degree of cognitive impairment.’
‘Cortical blindness: diagnostic issues in sudden bilateral visual loss’
Iqbal, R, Das, S, Progress in Neurology & Psychiatry, 1 Vol.27, Issue 3, 2023
I would add that what is desperately needed is skill, knowledge, and experience in the rehabilitating therapist(s). Although how to obtain this is a serious issue.
