Balint syndrome is a rare visuospatial coordination disorder secondary to bilateral parieto-occipital lesions. It is defined by three signs.
Impaired perception of distance between objects may also be added as a fourth element.
In 1909, Hungarian neurologist Rezső Balint first reported the condition. The initial description included inability to perceive multiple items in a visual scene simultaneously, inability to voluntarily shift gaze to a fixation target, and inability to reach with the right hand (left hand was possible). In 1919, Holmes and Horrax reported similar cases and suggested that the symptoms were due solely to visuospatial impairment, as there were no motor or sensory deficits. The term “Balint syndrome” was coined in 1954.
It is a rare disease with limited reported cases in the literature. Isolated corpus callosum infarction accounts for less than 1% of all strokes 1), and posterior circulation strokes account for approximately 20–25% of all strokes 2).
This is an extremely rare disease with limited reported cases in the literature. Isolated corpus callosum infarction accounts for less than 1% of strokes 1), and cases due to typical bilateral watershed infarction are also rare. There may be cases that are overlooked as dementia or delirium.
The characteristics of the three main signs of Balint syndrome are shown below.
Simultanagnosia
Definition: Inability to visually recognize multiple objects at once. The classic description is “cannot see the forest for the trees.”
Dorsal type (bilateral parietal lobe lesions): Inability to see multiple objects within the same scene. Bumps into objects while moving.
Ventral type (left inferior occipitotemporal lobe lesions): Can see multiple items but cannot conceptualize the entire scene. Less likely to bump into objects.
Optic Ataxia
Definition: Inability to accurately point or reach for objects under visual guidance despite normal muscle strength.
Features: Movements can be guided by sound or touch. There is an impairment in converting visual input into motor actions.
Ocular motor apraxia
Definition: Inability to voluntarily shift gaze without paralysis of the extraocular muscles. Balint described it as “psychic paralysis of gaze,” and Holmes as “spasm of fixation.”
Features: Involuntary reflexive saccades are preserved. In acquired cases, smooth pursuit movements are also lost, but the vestibulo-ocular reflex is preserved.
The dorsal type is caused by bilateral parietal lobe lesions, where the patient cannot recognize multiple objects within the same scene, leading to bumping into objects while moving. The ventral type is caused by left inferior occipitotemporal lobe lesions, where multiple items can be seen but the overall scene cannot be conceptualized. The ventral type is characterized by fewer problems with bumping into objects.
The diseases that cause Balint syndrome are diverse. The following table shows the main categories of causes.
The causes are broadly classified into three categories.
| Category | Representative diseases/conditions |
|---|---|
| Cerebrovascular disorders | Watershed infarction, corpus callosum infarction, cerebral hemorrhage |
| Neurodegenerative diseases | Alzheimer’s disease, posterior cortical atrophy, corticobasal degeneration |
| Infectious diseases and others | SSPE, CJD, COVID-19-related thrombosis, brain tumor, PRES |
The most common cause is bilateral parieto-occipital lobe infarction, particularly watershed infarction at the MCA-PCA border. Watershed areas are susceptible to hypoperfusion and cardiac arrest. Posterior circulation stroke accounts for approximately 20-25% of all strokes2).
Isolated bilateral infarction of the corpus callosum (body and splenium) can also cause Balint syndrome1). This is an important report because it can occur without direct parietal lesions. Isolated callosal infarction is rare (<1% of strokes), as the corpus callosum receives dual blood supply from the ACA and PCA1).
Risk factors for cerebrovascular disorders include hypertension, diabetes, hyperlipidemia, arteriosclerosis, smoking, and coronary artery disease.
There are no specific diagnostic criteria. Clinical diagnosis is made based on the presence of the triad (simultanagnosia + optic ataxia + oculomotor apraxia).
The following methods are useful for detecting simultanagnosia.
A comparison with the main differential diagnoses is shown.
| Feature | Balint syndrome | Hemispatial neglect | Cortical blindness |
|---|---|---|---|
| Lesion side | Bilateral parieto-occipital lobes | Right parietal junction (unilateral) | Bilateral occipital lobes |
| Visual acuity | May be preserved | Preserved | Decreased |
| Light reflex | Preserved | Preserved | Preserved |
Unilateral spatial neglect shows similar findings such as visual search deficits, visually guided action deficits, and extinction phenomena, but differs in that it is a unilateral lesion. Cortical blindness presents with bilateral visual acuity loss, but the pupillary light reflex is preserved. If the calcarine fissure is preserved bilaterally, cortical blindness is ruled out4). In elderly patients, it is easily misdiagnosed as delirium, dementia, or cortical blindness2).
Cortical blindness results from bilateral occipital lobe damage causing loss of vision in both eyes, but the pupillary light reflex is preserved. In Balint syndrome, if the calcarine fissure is preserved bilaterally, cortical blindness can be ruled out, and vision may be preserved4). The presence of simultanagnosia can be assessed by checking responses to Navon figures or complex scene descriptions.
There is no specific treatment for Balint syndrome. Addressing the underlying cause is the first priority.
For visual-related central nervous system deficits, perform corresponding rehabilitation. There are two approaches.
Improvement has been reported in cases through neurorehabilitation focusing on visuospatial and visuomotor retraining2).
Depends on the underlying disease.
There are two approaches: compensatory and restorative. Compensatory methods enhance intact functions to compensate for lost functions and are considered most beneficial. Restorative methods aim to recover impaired functions using eye movement and convergence exercises, with some successful studies reported. Improvement has also been seen in some cases with neurorehabilitation focused on visuospatial and visuomotor retraining 2).
Balint syndrome is caused by damage to the bilateral dorsolateral pathways.
In addition to the classic bilateral parietal lobes, lesions involving the bifrontal cortex, pulvinar, Brodmann areas 6 and 8, and the mesial right temporo-occipital area have been reported 1).
From the perspective of neural networks, the following has been demonstrated1).
There are two pathways in visual processing.
All three signs of Balint syndrome reflect damage to the dorsal pathway.
Changlai & Liang (2025) reported a case of a 30-year-old man with isolated corpus callosum (body and splenium) infarction presenting with Balint syndrome1). Despite the absence of direct parietal lobe lesions, Balint syndrome developed, suggesting that the corpus callosum is part of the neural network for attention and visual working memory. Citing fMRI studies, it was shown that fiber coherence of the bilateral superior longitudinal fasciculus and inferior fronto-occipital fasciculus is related to the accuracy of visual working memory.
Storti et al. (2021) reported a case of a 65-year-old woman with Balint syndrome due to bilateral parieto-occipital lobe infarction caused by diffuse thrombosis associated with SARS-CoV-2 infection4). Confirmation of simultanagnosia using Navon figures and exclusion of cortical blindness due to preservation of the calcarine sulcus were key to diagnosis. Dramatic symptom improvement was recorded two months after discharge, making this an important case demonstrating the potential for recovery in acute cerebral infarction.
Parida et al. (2025) reported an extremely rare case of a 22-year-old male with SSPE presenting with Balint syndrome (prosopagnosia, simultanagnosia, optic ataxia, and oculomotor apraxia) as the initial symptom 3). CSF IgG measles antibody was elevated at 16,578 U/mL. Treatment (clobazam 20 mg twice daily, levetiracetam 40 mg/kg/day, isoprenosine 100 mg/kg/day in three divided doses, IFN-α 3 MU/week) was ineffective, and the patient died. Recognition of Balint syndrome as an atypical initial presentation of SSPE is important.
