case report

Anton’s Syndrome and Cortical Blindness

Gadwalkar Srikant R*, Deepa DV**, P Rama Murthy†, Ravi Dhar**

Abstract
Introduction: Anton’s syndrome is a condition where the patient is unaware of being blind and denies the problem even when
it is pointed out to him. On the contrary, in cortical blindness patient is aware of his blindness and does not deny it. In both,
bilateral lesions of the occipital lobes are seen. Case presentation: We present two cases of cortical blindness, Case 1 being
consistent with diagnosis of Anton’s syndrome where patient denied of her blindness. Both cases revealed bilateral occipital
lobe infarcts. Conclusions: Cerebrovascular disease is the most common cause of cortical blindness. These occur as a result of
successive infarctions as seen in Case 1 or from a single embolic or thrombotic occlusion as seen in Case 2. First case is Anton’s
syndrome with patient denying blindness, whereas second case is cortical blindness. It is due to involvement of other cortical
centers in Anton’s syndrome that patient denies blindness.
Keywords: Anton’s syndrome, cortical blindness, bilateral occipital lobe infarcts

Case Presentation patient had severe visual impairment with no per-

ception of light. She walked into objects but denied of
Case 1 being blind. On asking her to describe the object in front
A 52-year-old married, right-handed woman presented of her, her reply was incorrect. Patient was oriented to
with history of headache and sudden, painless loss of time, place and person; speech, intelligence was normal
vision since five days. Patient was apparently normal but irritable in her behavior. There was no abnormality
five days back when she developed acute onset of any other cranial nerves. Pupillary reflexes were
headache. After around five hours she started colliding intact with normal fundus. Patient had normal power in
into objects suggesting she was blind. Patient denied all four limbs and no sensory loss. Cerebellar functions
being blind and had no ocular symptoms like floaters, were normal. Skull and spine examination was normal.
watering of eyes or ocular pain. She had no history Rest of the examination was normal.
of fever, seizures, trauma or any drug intake. There The laboratory investigations revealed normal hemogram
was no history suggestive of any other cranial nerve and biochemistry. Electrocardiogram, echocardiography,
involvement, motor deficits or sensory loss. There was carotid and vertebral Doppler were normal. Computed
no history of any bladder or bowel involvement. There tomography (CT) revealed ill-defined hypodensity in
was no history of previous medical illnesses or any the right occipital region with surrounding edema and
visual abnormalities. Following this, she was taken to hypodensity in left temporoparietooccipital regions
a general physician where she was found to have high (Fig. 1). Magnetic resonance imaging (MRI) revealed
blood pressure and was prescribed antihypertensive altered signals in the left temporoparietooccipital and
medication and referred to the present hospital. right occipital lobes suggestive of a large subacute
On arrival to the hospital, patient had a Glasgow Coma infarct in the left temporoparietooccipital lobe with
Scale score of 15 out of 15, but was agitated. Her blood a gliotic lesion (chronic infarct) in the right occipital
pressure recording was 130/80 mmHg. On examination, lobe (Figs. 2-4). Patient was subjected to anticerebral
edema measures which reduced her agitated behavior.
Antiplatelet agents and statins were started. There
*Professor and Head was no significant improvement in her vision. Patient
**Postgraduate Student
†Associate Professor was discharged after seven days with focus on
Dept. of General Medicine, Vijayanagar Institute of Medical Sciences secondary prevention and rehabilitation.
Bellary, Karnataka
Address for correspondence
Dr Gadwalkar Srikant R Case 2
Professor and Head, Dept. of Medicine, Vijayanagar Institute of Medical Sciences
Bellary - 534 101, Karnataka
A 60-year-old married, right-handed man presented
E-mail: srikantbly@gmail.com with history of sudden, painless loss of vision since one

106 Indian Journal of Clinical Practice, Vol. 23, No. 2, July 2012
 case report

Figure 4. Radiological findings: Coronal sections of MRI

showing altered signals in the left temporoparietooccipital
lobe and right occipital lobes suggestive of a large subacute
infarct in the left temporoparietooccipital lobe involving
P2 segment of PCA and a gliotic lesion (chronic infarct) in
the right occipital lobe.

trauma or any drug intake. There was no history

Figure 1. Radiological findings: Axial CT brain plain suggestive of any other cranial nerve involvement,
showing ill-defined hypodensities in the right occipital and motor deficits or sensory loss. There was no history of
left temporoparietooccipital regions suggesting infarcts. any bladder or bowel involvement. He was a known
hypertensive on antihypertensive medication since past
eight years. He is married, having two children. He was
a smoker and alcoholic since 20 years.
On arrival to the hospital, patient had a Glasgow Coma
Scale score of 15 out of 15. His blood pressure recording
was 160/92 mmHg. On examination, patient had
severe visual impairment with no perception of light.
His higher mental functions were normal. There was
no abnormality of any other cranial nerves. Pupillary
reflexes were intact with normal fundus. Patient had
normal power in all four limbs and no sensory loss.
Skull and spine examination was normal. Cerebellar
functions were normal. Rest of the examination was
normal.
The laboratory investigations revealed normal
hemogram and biochemistry. Electrocardiogram,
echocardiography, carotid and vertebral Doppler were
normal. CT revealed ill-defined hypodensities in the
right occipitotemporal and left occipital regions with
Figure 2 and 3. Radiological findings: Axial sections of
MRI showing altered signal in the left temporo-
surrounding edema.
parietooccipital lobes and right occipital lobe suggestive of Patient was managed for anticerebral edema and anti-
a large subacute infarct in the left temporoparietooccipital platelet agents and statins were started. There was
lobe involving P2 segment of PCA and a gliotic lesion
no significant improvement is his vision. Patient
(chronic infarct) in the right occipital lobe.
was discharged after four days with focus on secondary
prevention and rehabilitation.
day. Patient was apparently normal on the previous day,
when he developed sudden, painless loss of vision and With further follow-up, both patients had a slight
had no ocular symptoms like floaters, watering of eyes improvement in vision though recovery in visual acuity
or ocular pain. He had no history of fever, seizures, remained low.

Indian Journal of Clinical Practice, Vol. 23, No. 2, July 2012 107
case report

Discussion in all cases of suspected stroke as patient may have

visual anasognosia and deny blindness.
The ability to recognize visually presented objects and
words depends on the integrity not only of the visual Less-complete bilateral lesions leave the patient with
pathways and primary visual area of the cerebral varying degrees of visual perception. There may
also be visual hallucinations of either elementary or
cortex (area 17 of Brodmann) but also of those cortical
complex types. The mode of recovery from cortical
areas that lie just anterior to area 17 that is areas 18
blindness has been studied carefully by Gloning and
and 19 of the occipital lobe and area 39 - the angular
colleagues, who describe a regular progression from
gyrus of the dominant hemisphere (visual association
cortical blindness through visual agnosia and partially
areas).1 Bilateral infarction in the distal PCAs produces
impaired perceptual function to recovery. Even with
cortical blindness (blindness with preserved pupillary
recovery, the patient may complain of visual fatigue
light reaction). The patient is often unaware of the
(asthenopia) and difficulties in fixation and fusion.4 In
blindness or may even deny it (Anton’s syndrome).
our cases, there has been no remarkable improvement
Tiny islands of vision may persist, and the patient may in visual acuity.
report that vision fluctuates as images are captured in
the preserved portions. Rarely, only peripheral vision References
is lost and central vision is spared, resulting in ‘gun-
1. Ropper AH, Brown RH. Adams & Victor’s Principles of
barrel’ vision.2
Neurology. 8th edition, The McGraw-Hill Companies:
Although cerebrovascular disease is the most common USA 2005; 34:676.
cause, surgery, particularly cardiac surgery and cerebral 2. Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL,
angiography are also major causes.3 Loscalzo S. Harrison’s Principles of Internal Medicine.
18th edition, Vol. 2. The McGraw-Hill Companies: USA
We have presented two cases of cortical blindness due 2012; 370:p.3287.
to infarcts in the PCA territory. The first case consistent
3. Aldrich MS, Alessi AG, Beck RW, Gilman S. Cortical
with diagnosis of Anton’s syndrome had chronic infarct blindness: aetiology, diagnosis, and prognosis. Ann
on the right side and acute infarct on the left side. She Neurol 1987; 21(2):149-58.
did not complain of any symptoms of visual loss related 4. Ropper AH, Brown RH. Adams & Victor’s Principles of
to the old infarct probably not noticed by the patient. Neurology. 8th edition, The McGraw-Hill Companies:
This highlights the detailed examination of visual fields USA 2005; 22:404-5.

108 Indian Journal of Clinical Practice, Vol. 23, No. 2, July 2012