A Case of Balint Syndrome Due to Left Basal Ganglia Hemorrhagic Stroke: Exploring the Pathogenesis Through Parietal Lobe Circuits
aDepartment of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk, Virginia
*Corresponding author: David R. Spiegel, MD, Department of Psychiatry and Behavior Sciences, Eastern Virginia Medical School, 825 Fairfax Ave, Norfolk, VA 23507 (firstname.lastname@example.org).
Prim Care Companion CNS Disord 2021;23(2):20l02742
To cite: Spiegel DR, D’Souza HS, Yee KL, et al. A case of Balint syndrome due to left basal ganglia hemorrhagic stroke: exploring the pathogenesis through parietal lobe circuits. Prim Care Companion CNS Disord. 2021;23(2):20l02742.
To share: https://doi.org/10.4088/PCC.20l02742
© Copyright 2021 Physicians Postgraduate Press, Inc.
Balint syndrome (BS) is a rare neurologic disorder associated with bilateral parieto-occipital damage that disrupts connections between the posterior visual association areas and the motor regions of the prefrontal cortex.1 It typically consists of inaccurate reach responses to objects under visual guidance (optic ataxia [OAt]), disturbed organization of eye movements (ocular apraxia [OcA]), and an inability to perceive more than one object at a time (dorsal simultanagnosia [DS]). These symptoms are thought to develop, in part, from an impairment in visual attention, although OAt may also involve a visual proprioceptive deficit.2,3 Additionally, basal ganglia (BG) participates in circuits involving visual attention vis-a-vis the fronto-parietal attention network,4 oculomotor control,5 and prehension movements.6 Thus, lesions in BG potentially could present with DS, OcA, or OAt. We present a case of BS that followed left BG hemorrhagic stroke.
The patient was a 76-year-old woman who came to the hospital after her husband noted she was “uncoordinated.” Her vital signs were stable except for blood pressure of 223 mm Hg/152 mm Hg. Computed tomography (CT) of the brain revealed a left BG hemorrhagic infarct. The patient scored 16 on the National Institutes of Health Stroke Scale.7 Pertinent positives included right-sided gaze palsy and hemiparesis.
Her past medical history was significant for hypertension, although she was not taking medications prior to admission. She had a remote history of nicotine and alcohol usage. Blood alcohol level and urine drug screen were negative. Her husband denied previous history of motor or cognitive deficits. Due to “restlessness,” magnetic resonance imaging (MRI) was unobtainable until hospital day 30, but it corroborated CT findings and revealed additional hematoma encompassing left dorsal BG.
After the patient was reported removing her nasogastric tube, we were consulted on hospital day 35. Mental status examination was remarkable for dysarthria, although our patient was able to follow instructions without difficulty. When asked to track an object with her eyes, the patient had smooth saccadic movements to the left, but kept turning her head while trying to track objects to the right visual field. Her Mini-Mental State Examination8 score was 21, but she had a negative assessment per the Confusion Assessment Method.9 Given improvement in right hemiparesis, we evaluated our patient for BS.
When presented with the “cookie theft” picture,10 our patient was able to identify individual items but could not describe the scene as a whole. She was shown a Navon figure (characters composed of smaller characters),11 wherein she fixated on smaller letters and failed to report the larger letter E when prompted. Our patient was unable demonstrate voluntary right visual field saccades (left-sided saccades were unaffected). Nonetheless, 2 weeks later, difficulty producing voluntary saccades to verbal commands resolved. Finally, per the protocol of Borchers and colleagues,12 misreaching behavior (she neither grasped the target in the first nor had other following movement) was observed using her contralesional arm for movements directed toward the contralesional/right visual half-field.
On the basis of this evaluation, we believed our patient’s phenotype included DS, OcA, and OAt. For a review of BS in our patient, please see Figure 1.13–19
In conclusion, similar to other neuropsychiatric disease, our patient’s case of BS due to BG lesion can plausibly be viewed as a “circuit disorder.”20 BG is structurally represented within and between fronto-parietal attention (posterior parietal cortex [PPC]/dorsal frontal cortex including frontal eye fields), oculomotor (frontal/parietal oculomotor cortex), and dorsomedial reach pathway (primary motor cortex/supplementary motor area and PPC/superior parietal lobule) circuits.16,18,21–23 While BS has overwhelmingly been associated with parieto-occipital pathology, different lesion combinations have been described in the literature.24,25 Thus, per our case, a BG lesion within or between these 3 parietal lobe circuits could present with the phenotype of BS, ie, DS, OcA, and OAt, respectively, yet without the classical bilateral parieto-occipital lesions that typically produce BS.
Published online: April 1, 2021.
Potential conflicts of interest: Dr Spiegel is in the Speaker’s Bureau for Allergen, Alkermers, Otsuka, and IntraCellular Pharmaceuticals, but has no conflict of interest in preparation of this manuscript. Drs D’Souza, Yee, Kot, Yuna, Samaras, and Cook have no disclaimer/conflict of interest to report.
Patient consent: The patient (and husband) did give verbal consent to publish the manuscript, and we have de-identified her to protect anonymity.
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