Neurological Sciences
https://doi.org/10.1007/s10072-018-3490-3

LETTER TO THE EDITOR

Bálint syndrome caused by bilateral medial occipital infarcts
Michel Godel 1,2 & Radek Ptak 1 & Armin Schnider 1 & Nicolas Nicastro 1,3
Received: 18 April 2018 / Accepted: 3 July 2018
# Springer-Verlag Italia S.r.l., part of Springer Nature 2018

A 78-year-old woman known for treated hypertension presented a 3-day history of spatial disorientation, attention deficit, word-finding difficulties, and diffuse visual impairment.
Examination showed mild anomic aphasia, verbal anterograde
amnesia, partial right homonymous hemianopsia (with preservation of the right inferior quadrant for the right eye), and
Bálint syndrome. This consisted of optic ataxia for both hands
in her preserved visual field, ocular apraxia with difficulties to
shift gaze to targets in her intact visual field, visual
simultagnosia with inability to detect more than one out of
two or more points simultaneously presented to her visual
field during a few seconds. However, she was able to describe
single parts of pictures and letters of a word. Additional visual
phenomena were palinopsia and Bvanishing^ objects perception, i.e., the persistence of visual stimuli perception after they
left the visual field and, conversely, the sudden perceptive loss
of an object which yet remained in the visual field. Brain MRI
showed acute ischemic lesions in the left posterior cerebral
artery territory, including medial temporal and occipital lobes,
but no parietal lesion. In addition, it revealed a previously
unknown chronic right medial occipital lobe infarct and diffuse leukoaraiosis (Fig. 1).
While aphasia rapidly resolved, visuospatial deficits only
partially improved. The three features of Bálint syndrome
persisted for 10 weeks, thus severely impairing the patient’s
autonomy. She returned to her home with the help of home
care after intensive rehabilitation.
Bálint syndrome was first described by the Reszö Bálint in
1909 as a combination of three complex visual symptoms [1]:

* Nicolas Nicastro
nn311@medschl.cam.ac.uk
1

Division of Neurorehabilitation, Department of Clinical
Neurosciences, Geneva University Hospitals, Geneva, Switzerland

2

Faculty of Medicine, University of Geneva, Geneva, Switzerland

3

Department of Psychiatry, University of Cambridge, Addenbrooke’s
Hospitals, Hills Road, Cambridge CB2 0SP, UK

1. Spatial disorder of attention, later called dorsal visual
simultagnosia, inducing an inability to simultaneously
perceive multiple stimuli in the preserved visual field. It
has been attributed to an extreme shrinkage of the attentional visual field, also called Bspatial window of
attention^ [2]. Other authors attribute simultagnosia to
an inability of the brain to build a visual spatial frame in
which it can compute multiple visual informations, i.e., to
Bbind^ them [3]. Typical lesions are bilateral parietal or
parieto-occipital. The present case is exceptional by the
absence of parietal damage.
2. Optic ataxia describes the difficulty to reach a target under
visual guidance in the absence of any motor, proprioceptive, or primary visual deficits. It can occur independently
from simultagnosia and ocular apraxia, with unilateral
lesions, and is thought to rely on two potentially impaired
pathways: a visual proprioceptive deficit or a visual attentional deficit [4]. Both imply the dorsal visual pathway
within the posterior parietal cortex.
3. Psychic paralysis of gaze, or acquired ocular apraxia, describes the difficulty to shift gaze from one target to another—i.e., to visually Bgrasp^ objects in the visual field.
It has been described in lesions involving the posterior or
frontal eye field. When occurring in Bálint syndrome, a
decrease of visual attentional flexibility has been proposed as an explanation. This mechanism may be shared
by simultagnosia and ocular apraxia [5].
In addition, many visual phenomena such as palinopsia or
vanishing objects have been reported in cases of Bálint syndrome [5].
Etiologies are very diverse—ischemic, degenerative, inflammatory, tumoral, or traumatic [6]. This syndrome has
been classically described in patients with bilateral dorsolateral parietal lesions, and sometimes with other localizations;
bilateral involvement appears to be necessary.
Our patient suffered from a chronic infarct in the right medial occipital lobe. It was not associated with any clinical deficit
before the current episode and was revealed by the MRI. Still,

Neurol Sci
Fig. 1 a Axial diffusion-weighted
MRI showing acute ischemia of
the left medial temporal and occipital lobes. b Axial T2-weighted
MRI showing a chronic infarct of
the right medial occipital lobe and
diffuse leukoaraiosis

its localization is compatible with disconnection of the superior
longitudinal fasciculus, a component of the visual attention
network potentially implicated in Bálint syndrome. Moreover,
the MRI revealed diffuse leukoaraiosis. Thus, our patient potentially already had asymptomatic disruption of attentional
pathways before the present episode, and we can hypothesize
that, since the first silent stroke, her left hemisphere was assuming the main visual attentional functions through a neural compensation strategy involving a shift in hemispheric lateralization. Then, the second (left medial occipito-temporal) ischemia
would have impaired her compensation network and resulted in
Bálint syndrome. To support our hypothesis, we can cite the
recent works about the impact of cognitive reserves on the
symptomatology and recovery of stroke, and more specifically
on the attentional deficits [7].
An alternative (but not exclusive) hypothesis [5] posits that
with two lesions happening at different timepoints, the first
causing left hemineglect and the second right hemianopsia,
the combination of both results in Bálint syndrome in the
remaining left visual field. In our case, the recent stroke
caused a partial right hemianopsia, and it is difficult to predict
if her right visual field would also have suffered from severe
attentional deficit had it been preserved.
Rehabilitation of Bálint syndrome consists of functional
adaptation programs to develop compensatory strategies and
visuoperceptive trainings to reduce deficits [8]. Effects of

rehabilitation versus the natural course of the condition are
not established.

Compliance with ethical standards
Conflict of interest The authors declare that they have no conflict of
interest.

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