Neurocrit Care
https://doi.org/10.1007/s12028-018-0550-8

NEUROIMAGE

Insight into Ping‑Pong Gaze in the
Neurosciences Intensive Care Unit
Devon A. Cohen, Ali Daneshmand and Eelco F. M. Wijdicks*
© 2018 Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society

Keywords: Ping-pong gaze, Periodic alternating gaze, Bilateral hemispheric infarction

Case Description
A 76-year-old, right-handed-woman presented with leftgaze deviation, right homonymous hemianopia, global
aphasia, and right-sided hemiplegia with severe sensory
loss. A computed tomography (CT) head scan head showed
a dense left middle cerebral artery (MCA) stroke sign.
Mechanical thrombectomy achieved recanalization of the
left common carotid artery and MCA. She required intubation and did not recover after recanalization, showing
no eye opening to pain and a combination of flexion and
extension responses without clinical improvement. Repeat
CT showed a maturing MCA territory infarct. The second
day, she developed smooth side-to-side horizontal movements consistent with ping-pong gaze (PPG) or short-cycle
periodic alternating gaze deviation (Supplementary video),
as first described by Fisher in 1967 [1]. Magnetic resonance
imaging (MRI) of the brain was performed to evaluate for
additional infarcts given known bilateral hemispheric localization of PPG. An MRI revealed multiple territorial infarctions with large left MCA, bilateral occipital, and smaller
right basal ganglia/capsulostriatal infarcts (Fig. 1).
PPG has predominantly been described in bilateral
basal ganglia and hemispheric lesions, though has also
occurred in midbrain and vermis lesions and toxic metabolic encephalopathies (carbon monoxide poisoning,
hepatic encephalopathy, and serotonin syndrome) [2].
PPG has been attributed to cerebral disconnection from
horizontal gaze centers in the relatively intact brainstem.
PPG can be smooth or saccadic [3]. Smooth PPG consists
of continuous conjugate eye movements between lateral
*Correspondence: wijde@mayo.edu
Division of Critical Care Neurology, Department of Neurology, Mayo
Clinic, 200 First Street, SW, Rochester, MN 55905, USA

extremes, whereas saccadic PPG features reduced eye
deviation amplitudes with a rapid lateral deviation phase
and slow centripetal phase. A transition from smooth to
saccadic PPG has occurred with clinical improvement
[3], but there is no definitive prognostic dichotomy. A
patient with smooth PPG secondary to carbon monoxide
poisoning recovered [2], whereas a patient with saccadic
PPG secondary to hypoxia remained in a coma [3].
Neurointensivists should recognize this eye movement
abnormality as it points toward bilateral hemispheric
involvement, particularly in the absence of metabolic
derangements.

Fig. 1 Diffusion-weighted (magnetic resonance) imaging showing
large areas of restricted diffusion in middle cerebral artery stroke territory and opposite basal ganglia

Electronic supplementary material
The online version of this article (https​://doi.org/10.1007/s1202​8-018-0550-8)
contains supplementary material, which is available to authorized users.

Informed Consent
Informed consent was obtained from all individual participants included in
the study.

Authors Contribution
DAC wrote the manuscript, AD helped with the concept, EFMW is a consulting
physician and the editor of the manuscript.
Source of Support
No funding.
Compliance with Ethical Standards
Conflict of Interest
The authors declare that they have no conflict of interest.
Human and Animal Rights
All procedures performed in studies involving human participants were in
accordance with the ethical standards of the institutional and/or national
research committee and with the 1964 Helsinki declaration and its later
amendments or comparable ethical standards.

References
1. Fisher CM. Some neuro-ophthalmological observations. J Neurol Neurosurg Psychiatry. 1967;30(5):383–92.
2. Ishikawa H, Ishikawa S, Mukuno K. Short-cycle periodic alternating (pingpong) gaze. Neurology. 1993;43(6):1067–70.
3. Johkura K, et al. Saccadic ping-pong gaze. J Neuroophthalmol.
1998;18(1):43–6.