PDF icon Download PDF
Open Access
CC BY-NC-ND 4.0 · Asian J Neurosurg 2025; 20(03): 656-659
DOI: 10.1055/s-0045-1809325
Case Report

Vertical Gaze Palsy in Medial Thalamic Infarction Associated with Vein of Galen Malformation: A Case Report

Leve Joseph Sebastian
1   Department of Neuroimaging and Interventional Neuroradiology, All India Institute of Medical Sciences, New Delhi, India
,
Biswamohan Mishra
2   Department of Neurology, All India Institute of Medical Sciences, New Delhi, India
,
Deepti Vibha
2   Department of Neurology, All India Institute of Medical Sciences, New Delhi, India
,
Manoj Kumar Nayak 
3   Department of Radiodiagnosis, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India
› Author Affiliations
› Further Information
Also available ateRef
 
 PDF Download Permissions and Reprints

Abstract

The thalamus, a gray matter structure, is a crucial relay for various afferent and efferent pathways in the brain. It receives its primary blood supply from the thalamoperforating and thalamogeniculate branches of the posterior cerebral arteries. Damage to the thalamus can lead to classical sensorimotor and amnestic syndromes, as well as neuro-ophthalmological manifestations, including vertical gaze palsy (VGP), pseudo-abducens palsy, skew deviation, cerebral ptosis, and Horner's syndrome. While most cases of VGP are self-limiting, some can persist, significantly affecting daily life. This report describes a case involving a 33-year-old man with a vein of Galen malformation who underwent embolization and subsequently developed VGP in the postoperative period. This complication was attributed to a medial thalamic infarct. Notably, the patient experienced spontaneous resolution of the gaze palsy within 3 months.


 

Keywords

thalamic infarct - vertical gaze palsy - vein of Galen malformation - horizontal gaze - syndromes

Introduction

The dorsal section of the diencephalon contains the gray matter structure known as the thalamus, which acts as a relay center for ascending and descending pathways between the cortex and the spinal cord and includes centers for consciousness and sensory perception.[1] Its primary blood supply predominantly originates from the posterior circulation, specifically through the thalamogeniculate and thalamopeduncular branches of the posterior cerebral arteries (PCAs).[2] Any disruption to this arterial supply can result in a thalamic infarct, and the neurological manifestations will depend on the affected and related nuclei.[3] In a study by Agarwal et al, among 36 patients with vein of Galen malformation (VOGM), the posterior choroidal artery was a feeding artery in all cases, while the anterior choroidal artery was involved in 39% (n = 13), the anterior cerebral artery in 12% (n = 4), and thalamoperforators in 12% (n = 4). Additionally, dural feeders were observed in 12% (n = 4), including three adults.[4] Thalamic infarcts account for ∼4% of all cerebral infarctions and 11% of all vertebrobasilar infarctions.[3] In a study by Moon et al, among 40 patients with thalamic infarctions, vertical gaze palsy (VGP) was observed in 47.5% (n = 19), along with skew deviation with an invariable hypotropia of the contralesional eye (n = 18), third nerve palsy (n = 11), pseudoabducens palsy (n = 9), visual field defects (n = 7), and other anomalies such as isolated ptosis and miosis (n = 7).[3] Thalamic infarctions can cause neuro-ophthalmological dysfunctions, most commonly VGP, either in isolation or due to a combination of involvement of the thalamomesencephalic junction and adjacent rostral midbrain, in addition to sensorimotor and amnestic syndromes.[5] These visual deficits can significantly impact daily life, highlighting the importance of understanding how to prevent such infarctions. Herein, we report the case of a young male with a VOGM who underwent embolization and subsequently developed VGP in the postoperative period, attributed to a medial thalamic infarction, which resolved spontaneously within 3 months.


 

Case Description

A 33-year-old man with no previous comorbidities presented with intermittent headaches in the occipital region that had persisted for the past 2 years. The headaches were throbbing, occurring more frequently in the morning and upon bending forward, and were occasionally associated with nausea. There was no photophobia, phonophobia, or any other associated symptoms. On examination, the patient was of average build, with complete extraocular movements in all directions of gaze and no papilledema or neck stiffness. The rest of the neurological examination revealed no abnormalities. Magnetic resonance imaging and digital subtraction angiography of the brain revealed multiple choroidal feeders from branches of the posterior choroidal arteries of the PCA with hypoplastic straight sinus, absent internal cerebral veins, and persistent falcine sinus to suggest as VOGM ([Fig. 1A–C]). This VOGM was planned for a staged procedure. After placing a Neuron MAX 088 long sheath (80 cm) (Penumbra Inc, Alameda, California, United States) in the left subclavian artery, a Neuron 058 was parked (Penumbra Inc, Alameda, California, United States) in the distal V2 of left vertebral artery. Then, 165 cm marathon microcatheter segment with distal inner diameter 0.013″ (Covidien Neurovascular, Irvine, California, United States) and synchro 10 guidewire (Stryker Neurovascular, Fremont, California, United States) were used to navigate the feeder vessels. Two large feeders from the posterior choroidal artery were chosen for embolization as the large feeders are relatively easy to navigate and will significantly reduce the flow into the fistula. Subsequently, the feeders were embolized with 90% glue with lipoidal mixture ([Fig. 1D]). Postprocedure, the patient complained of double vision when looking up and down, though he could look sideways without restriction. Examination revealed VGP with normal horizontal eye movements. No other neurological abnormalities were found on examination. A repeat MRI of the brain showed an acute lacunar infarct in the left median thalamus without midbrain involvement ([Fig. 1E–G]). Steroid (dexamethasone 4 mg twice daily for 3 days, the tapered over the next 6 days) treatment was initiated for symptomatic management, and the VGP resolved within 3 months. Follow-up computed tomography scan showed focal gliosis in the left medial thalamus ([Fig. 1H]). Although the intensity of his headache was reduced postprocedure, it persisted, and the patient is now planning for a second embolization due to the persistent headache.

Zoom
Fig. 1 Noncontrast computed tomography (NCCT), digital subtraction angiography (DSA), and follow-up CT scan of the patient with a vein of Galen malformation (VOGM). Axial NCCTof the head (A) showed a VOGM. DSA (preprocedure [B] and postprocedure [C]) showed a reduction in feeders supplying the VOGM. NCCT of the head postprocedure (D), magnetic resonance imaging diffusion-weighted imaging (E), apparent diffusion coefficient (F), and fluid-attenuated inversion recovery (G) showed an acute infarct in the left medial thalamus. After 3 months, follow-up CT (H) showed gliosis in the left medial thalamus.

 

Discussion

Thalamus is supplied from the posterior circulation arteries by thalamogeniculate and thalamopeduncular branches of the PCAs.[2] Any disruption to this arterial supply can result in a thalamic infarct. Thalamic infarctions can lead to various neuro-ophthalmologic abnormalities, with VGP being the commonest. VGP may be caused by lesions affecting the rostral interstitial nucleus of the medial longitudinal fasciculus and the posterior commissure.[6] VGP can result from a lesion in the frontofugal dorsothalamic bundle, which normally travels through the internal medullary lamina of the thalamus and the mediodorsal nucleus to reach the superior colliculus.[7] In contrast to the horizontal gaze, there is a poor understanding of the supranuclear pathway for vertical gaze, which could be because of the involvement of pathways from supplementary eye fields in frontal lobes that traverse through the medial thalamus.[8]

Several prior reports have documented VGPs in patients with unilateral or bilateral paramedian thalamic infarction; however, these cases often attributed the gaze palsy to coexisting midbrain lesions. In contrast, our review of the literature also identified case reports suggesting that VGP can arise from unilateral thalamic infarction alone, potentially due to the decussation of frontobulbar fibers within the medial thalamus. This is supported by a case series describing thalamic infarctions presenting with VGPs.[9] [10] While comprehensive data on the incidence of unilateral thalamic infarctions specifically leading to VGPs remain limited, our case contributes to this growing body of evidence and highlights the need for further investigation into this association.

Nonetheless, Moon et al reported that the range and extent of VGP were not significantly affected by whether the infarction was unilateral or bilateral.[3] Similar findings of VGP with intact horizontal gaze were observed in a 62-year-old male with bilateral paramedian thalamic infarction.[11] The spontaneous resolution of VGPs, as observed in our patient, aligns with findings from prior literature. For instance, previous reports have documented transient vertical diplopia and nystagmus in cases of thalamic infarction, attributing these deficits to temporary disruptions in the vestibulo-ocular pathways traversing the thalamus, coupled with the brain's inherent plasticity (Moon et al).[3] In our case, the patient's VGP resolved spontaneously within 3 months postembolization, despite follow-up imaging revealing focal gliosis in the left medial thalamus. This suggests that the initial impairment likely stemmed from a transient disturbance—possibly edema or ischemic stunning rather than permanent structural damage to critical gaze control pathways. Brain plasticity, including compensatory mechanisms involving unaffected neural circuits (e.g., contralateral thalamic or cortical inputs), may have facilitated this recovery.[5] The gliosis observed on follow-up CT likely represents a residual scar from the infarct, which did not preclude functional restoration of vertical gaze. This is consistent with reports indicating that neuro-ophthalmological deficits in thalamic infarctions can resolve even when imaging shows persistent changes, possibly due to the reorganization of supranuclear pathways or resolution of reversible factors such as local inflammation.[10] [12] While the exact mechanism remains speculative without longitudinal functional imaging, our case underscores the potential for recovery despite gliotic changes and highlights the need for further studies to elucidate the interplay between structural damage, gliosis, and functional plasticity in such scenarios.

Skew deviation, believed to involve the thalamus and can result from disorders affecting the vestibulo-ocular pathway, was not observed in our case.[12]

Thalamic esotropia (tonic inward ocular deviation), known as pseudo-abducens palsy, can occur in thalamic infarction. Gaze-evoked nystagmus can be seen in thalamic infarctions due to a defective gaze-holding mechanism.[3] [13]

Cerebral ptosis can also result from thalamic lesions.[14] Previous studies have demonstrated that any disorder which affects the connections between the frontal eye fields and internal medullary lamina of the thalamus will cause cerebral ptosis.[15] However, these were not present in our case. Most of these abnormalities resolve spontaneously within months, but some cases show persistent findings, necessitating follow-up.


 

Conclusion

While VGP associated with thalamic infarction has been documented in the literature, our case uniquely highlights this neuro-ophthalmological deficit as a rare postoperative complication following embolization for a VOGM—an association not previously emphasized in published reports. While various neuro-ophthalmological issues due to thalamic infarctions resolve within months, some persist, underscoring the need for clinicians to understand these conditions. This distinction adds a novel dimension to the existing knowledge, as it underscores a potential risk specific to neurointerventional procedures for VOGM. By reporting this case, our aim is to raise awareness among neurointerventionists about this possible complication, emphasizing the importance of early recognition and management to potentially prevent or mitigate such outcomes in future cases.


 

 

Conflict of Interest

None declared.

Authors' Contributions

L.J.S. contributed to the concept design, literature search, and manuscript preparation. B.M edited and reviewed the manuscript. M.N. contributed to the concept design and manuscript editing. D.V. contributed to the patient care and management and edited and reviewed the manuscript.



Address for correspondence

Manoj Kumar Nayak, DM
Department of Radiodiagnosis, All India Institute of Medical Sciences
Bhubaneswar 751019, Odisha
India   

Publication History

Article published online:
21 May 2025

© 2025. Asian Congress of Neurological Surgeons. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

Thieme Medical and Scientific Publishers Pvt. Ltd.
A-12, 2nd Floor, Sector 2, Noida-201301 UP, India


  Permissions and Reprints
Zoom
Fig. 1 Noncontrast computed tomography (NCCT), digital subtraction angiography (DSA), and follow-up CT scan of the patient with a vein of Galen malformation (VOGM). Axial NCCTof the head (A) showed a VOGM. DSA (preprocedure [B] and postprocedure [C]) showed a reduction in feeders supplying the VOGM. NCCT of the head postprocedure (D), magnetic resonance imaging diffusion-weighted imaging (E), apparent diffusion coefficient (F), and fluid-attenuated inversion recovery (G) showed an acute infarct in the left medial thalamus. After 3 months, follow-up CT (H) showed gliosis in the left medial thalamus.