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HOME > Res Vestib Sci > Volume 23(3); 2024 > Article
Case Report
Horizontal nystagmus with velocity-increasing waveforms in delayed post-hypoxic leukoencephalopathy: a case report
Eugene Jung, Suk-Min Lee, Seo-Young Choi, Kwang-Dong Choiorcid
Research in Vestibular Science 2024;23(3):111-113.
DOI: https://doi.org/10.21790/rvs.2024.016
Published online: September 15, 2024

Department of Neurology, Pusan National University Hospital, Pusan National University School of Medicine, Biomedical Research Institute, Busan, Korea

Corresponding author: Kwang-Dong Choi Department of Neurology, Pusan National University Hospital, Pusan National University School of Medicine, 179 Gudeok-ro, Seo-gu, Busan 49241, Korea. E-mail: kdchoi@pusan.ac.kr
• Received: August 9, 2024   • Revised: August 18, 2024   • Accepted: August 20, 2024

© 2024 The Korean Balance Society

This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Abnormal eye movements in unconscious patients serve as crucial diagnostic instruments, offering insights into the function of the central nervous system. Understanding these movements can aid in diagnosing the cause of unconsciousness, localizing brain lesions, and predicting outcomes. We report a patient who presented with spontaneous horizontal nystagmus unaffected by light in delayed post-hypoxic encephalopathy. Video-oculography showed exponentially increasing slow phases, with an amplitude ranging from 3° to 9° and a frequency of 0.5 Hz. Based on the results of oculography and neuroimaging, persistent horizontal nystagmus in our patient may be ascribed to an unstable neural integrator, possibly caused by disrupted cerebellar feedback mechanisms for horizontal gaze holding.
  • Keywords: Nystagmus; Hypoxic brain damage; Cerebellum
Abnormal eye movements observed in unconscious patients include ocular bobbing or dipping, reversed ocular bobbing or dipping, ping-pong gaze, periodic alternating gaze deviation, and vertical myoclonus [1]. Rarely, horizontal nystagmus has been observed in unconscious patients with unilateral cerebral hemisphere lesions. This may be due to the asymmetry in horizontal smooth pursuit [2] or to epileptic seizures [3,4].
We report a unique case presenting spontaneous horizontal nystagmus with exponentially increasing slow phases in delayed post-hypoxic encephalopathy.
A 79-year-old male with a medical history of coronary heart disease and diabetes mellitus was referred to the neurology department due to the presence of abnormal eye movements. He had received rehabilitation treatment for 3 months after surgeries for a subdural hematoma with diffuse axonal injury and ruptured cervical disc caused by a traffic collision. Recently, the patient exhibited abnormal eye movements 2 weeks following hypoxic-ischemic brain injury due to sudden cardiac arrest. A neurological examination revealed that he was in a vegetative state with the eye and head fixedly turned to the left and had quadriplegia. Pupils were normal size and reactive to light. Corneal and gag reflexes were also intact bilaterally. Video-oculography showed mainly left-beating nystagmus with small downbeat and counterclockwise (from the patient’s perspective) torsional components in light. The removal of light did not lead to significant change (Fig. 1A, Supplementary Video 1). The nystagmus had exponentially increasing slow phases, with an amplitude ranging from 3° to 9° and a frequency of 0.5 Hz. Head deviation and left-beating nystagmus did not change the direction. Vestibulo-ocular reflex tests could not be performed due to the patient’s tonic neck deviation. Brain magnetic resonance imaging (MRI) including diffusion-weighted images revealed delayed post-hypoxic leukoencephalopathy affecting the bilateral subcortical white matter and basal ganglia (Fig. 1B, C). There were no abnormal signal intensities in the brainstem or cerebellum. An electroencephalogram (EEG) did not show any epileptiform discharges.
We conducted this study in compliance with the principles of the Declaration of Helsinki. Written informed consent for publication of the research details and clinical images was obtained from the patient.
Our patient developed persistent horizontal nystagmus 2 weeks after hypoxic-ischemic injury. Brain MRI revealed characteristic findings of delayed post-hypoxic leukoencephalopathy, affecting the bilateral subcortical white matter and basal ganglia. Remarkably, the nystagmus showed impaired suppression in light and had exponentially increasing slow phases.
The neural integrator for horizontal eye movements depends on a distributed network of neurons located in the brainstem and cerebellum [4]. Lesions in the brainstem that affect the nucleus prepositus hypoglossi and medial vestibular nucleus—both responsible for horizontal neural integrator—can impair gaze holding, leading to gaze-evoked nystagmus. The cerebellum serves to enhance the performance of an inherently leaky neural integrator in the brainstem through a positive feedback loop [5,6]. If such feedback is inappropriate, the integrator becomes leaky, resulting in exponentially decaying drifts of the eyes back to the neutral position. Conversely, if the feedback is excessively strong, the integrator becomes unstable, leading to exponentially increasing velocity drifts of the eyes away from the midline. Such increasing slow-phase waveforms have been reported in patients with horizontal, downbeat, and upbeat nystagmus [7], as well as in monkeys with cerebellar lesions [8]. Accordingly, persistent horizontal nystagmus observed in our patient with delayed post-hypoxic leukoencephalopathy may be attributed to an unstable neural integrator, possibly caused by disrupted cerebellar feedback mechanisms for horizontal gaze holding.
Asymmetry of horizontal smooth pursuit or epileptic seizures could be other possible explanations. However, nystagmus resulting from asymmetric smooth pursuit typically has low amplitude and constant velocity drift [9]. Intermittent nystagmus is characteristic of epileptic nystagmus [3], and EEG in our patient did not show epileptiform discharges during the presence of spontaneous nystagmus.
Forced head deviation to the left in our patient may be attributed to asymmetric damage to the corticospinal tracts due to the lesions of the bilateral subcortical white matter and basal ganglia.

Funding/Support

This work was supported by a 2-Year Research Grant of Pusan National University.

Conflicts of Interest

No potential conflict of interest relevant to this article was reported.

Availability of Data and Materials

All data generated or analyzed during this study are included in this published article. For other data, these may be requested through the corresponding author.

Authors’ Contributions

Conceptualization: KDC

Formal analysis: All authors

Methodology: KDC

Writing–Original Draft: EJ, KDC

Writing–Review & Editing: All author

All authors read and approved the final manuscript.

Supplementary materials can be found via https://doi.org/10.21790/rvs.2024.016.

Supplementary Video 1.

The patient shows persistent left-beating nystagmus unaffected by light.
Fig. 1.
(A) Video-oculography shows mainly left-beating nystagmus with small downbeat and counterclockwise torsional components from the patient’s perspective. (B, C) Diffusion-weighted magnetic resonance images reveal delayed post-hypoxic leukoencephalopathy affecting the bilateral subcortical white matter and basal ganglia. Upward deflection indicates rightward, upward, and clockwise torsional (from the patient’s perspective) eye motion. RH-P, horizontal position of the right eye; RV-P, vertical position of the right eye; RT-P, torsional position of the right eye; RH-V, horizontal velocity of the right eye.
rvs-2024-016f1.jpg
  • 1. Rosenberg ML. Spontaneous vertical eye movements in coma. Ann Neurol 1986;20:635–637.ArticlePubMed
  • 2. Sharpe JA, Lo AW, Rabinovitch HE. Control of the saccadic and smooth pursuit systems after cerebral hemidecortication. Brain 1979;102:387–403.ArticlePubMed
  • 3. Moster ML, Schnayder E. Epileptic periodic alternating nystagmus. J Neuroophthalmol 1998;18:292–293.ArticlePubMed
  • 4. Sanchez K, Rowe FJ. Role of neural integrators in oculomotor systems: a systematic narrative literature review. Acta Ophthalmol 2018;96:e111–e118.ArticlePubMedPDF
  • 5. Glasauer S. Cerebellar contribution to saccades and gaze holding: a modeling approach. Ann N Y Acad Sci 2003;1004:206–219.PubMed
  • 6. Zee DS, Leigh RJ, Mathieu-Millaire F. Cerebellar control of ocular gaze stability. Ann Neurol 1980;7:37–40.ArticlePubMed
  • 7. Leigh RJ, Zee DS. The neurology of eye movements. Oxford University Press; 2015.
  • 8. Zee DS. New concepts of cerebellar control of eye movements. Otolaryngol Head Neck Surg 1984;92:59–62.ArticlePubMedPDF
  • 9. Zee DS. Mechanisms of nystagmus. Am J Otol 1985;Suppl:30–34.PubMed

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        Horizontal nystagmus with velocity-increasing waveforms in delayed post-hypoxic leukoencephalopathy: a case report
        Res Vestib Sci. 2024;23(3):111-113.   Published online September 15, 2024
        DOI: https://doi.org/10.21790/rvs.2024.016
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      Horizontal nystagmus with velocity-increasing waveforms in delayed post-hypoxic leukoencephalopathy: a case report
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      Fig. 1. (A) Video-oculography shows mainly left-beating nystagmus with small downbeat and counterclockwise torsional components from the patient’s perspective. (B, C) Diffusion-weighted magnetic resonance images reveal delayed post-hypoxic leukoencephalopathy affecting the bilateral subcortical white matter and basal ganglia. Upward deflection indicates rightward, upward, and clockwise torsional (from the patient’s perspective) eye motion. RH-P, horizontal position of the right eye; RV-P, vertical position of the right eye; RT-P, torsional position of the right eye; RH-V, horizontal velocity of the right eye.

      Fig. 1.

      Horizontal nystagmus with velocity-increasing waveforms in delayed post-hypoxic leukoencephalopathy: a case report
      Res Vestib Sci : Research in Vestibular Science
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