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CASE SNIPPET
Year : 2021  |  Volume : 67  |  Issue : 4  |  Page : 245-246

Atypical ocular movement disorder after hypoxic-ischemic brain injury


Department of Neurology, King George's Medical University, Lucknow, Uttar Pradesh, India

Date of Submission25-Sep-2020
Date of Decision24-Dec-2020
Date of Acceptance18-Jan-2021
Date of Web Publication25-Oct-2021

Correspondence Address:
R Verma
Department of Neurology, King George's Medical University, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpgm.JPGM_921_20

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How to cite this article:
Verma R, Sharma P K, Giri P. Atypical ocular movement disorder after hypoxic-ischemic brain injury. J Postgrad Med 2021;67:245-6

How to cite this URL:
Verma R, Sharma P K, Giri P. Atypical ocular movement disorder after hypoxic-ischemic brain injury. J Postgrad Med [serial online] 2021 [cited 2022 Aug 18];67:245-6. Available from: https://www.jpgmonline.com/text.asp?2021/67/4/245/329131




There are various types of ocular movements reported in the literature. Many ocular motility disorders have localization values and prognostic significance.[1] We report an atypical ocular movement disorder after hypoxic-ischemic brain injury which, to our knowledge, has not been described earlier.

A 65-year-old male, a known case of chronic obstructive pulmonary disease, was admitted in the emergency ward with complaints of sudden onset, severe chest pain, and breathlessness. He had an acute exacerbation of his respiratory illness. Computerized tomography (CT) scan of chest revealed bilateral pneumothoraces [Figure 1]. Bilateral intercostal drains were inserted by the pulmonary physician to alleviate the breathlessness.
Figure 1: Computerized tomography (CT) scan of chest revealed bilateral pneumothoraces

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The next day, the patient became unconscious and was referred to our department for further evaluation. Our examination showed that he was unconscious, making asymmetric flexion movements of bilateral upper limbs with more involvement of the left upper limb, eye-opening and, making only incoherent sounds on painful stimuli (Glasgow coma scale -8). He had bilateral normal sized pupils with normal width and reaction. Doll's eye movements were present. The ocular examination revealed [Video 1] abnormal spontaneous, high frequency vertical ocular movement in both eyes, equal in amplitude and velocity without inter-saccadic pause. Bilateral deep tendon jerks were exaggerated, and plantar responses were upgoing. He underwent a CT scan of the brain, which showed multiple infarcts [Figure 2]a. On magnetic resonance imaging, the diffusion-weighted images showed bilateral inferior cerebellar discrete acute infarcts, internal border zone, and cortical border zone infarcts [Figure 2]b.
Figure 2: (a) Computerized tomography of brain revealed multiple watershed infractions; (b) magnetic resonance imaging diffusion-weighted images showed bilateral inferior cerebellar discrete acute infarcts, internal border zone and, cortical border zone infarcts

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After 10 days, the patient regained consciousness and was able to walk with support, and communicate. At time of discharge, he continued to have complaints of blurring of vision with oscillopsia, and his abnormal ocular movements persisted. The eye movement abnormality can be labeled as ocular flutter-like vertical eye movements. Ocular flutter is to and fro oscillating eyeball movement without inters-saccades pause and limited only in the horizontal direction.[2] Our patient had to- and- fro eyeball movements without inter-saccadic latency, limited only in the vertical direction. It classically resembled flutter but manifested in the vertical direction. Ocular flutter was explained by dysfunction of brain stem structures regulating the oculomotor system, including excitatory burst neurons (EBN), inhibitory burst neurons, and omnipause neurons (OPN). The dysfunction of OPN and IBN leads to unchecked EBN and is the current explanation of saccadic oscillation.[3] Ocular flutter is mainly described in the brain stem and cerebellar lesion. Here our patient was a case of hypoxic-ischemic injury because of watershed infraction of the brain with atypical ocular saccades.

To conclude, ocular flutter is a burst of to- and fro- horizontal saccades without intersaccadic interval. Ocular flutter-like movements in the vertical direction has not been reported earlier. The dysfunction in brain stem and cerebellum neural integrators for saccades is responsible for ocular flutter. The clinician should be aware of atypical vertical ocular flutter-like eye movements, caused by hypoxic-ischemic encephalopathy.

Declaration of patient consent

The authors certify that appropriate patient consent was obtained.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 :: References Top

1.
Leigh J, Zee DS. Diagnosis of nystagmus and saccadic intrusion. In: Leigh RJ, Zee DS, editors. The Neurology of Eye Movements. 4th ed. Oxford: Oxford University Press; 2006. p. 475–558.  Back to cited text no. 1
    
2.
Verhaeghe S, Diallo R, Nyffeler T, Rivaud-Péchoux S, Gaymard B. Unidirectional ocular flutter. J Neurol Neurosurg Psychiatry 2007;78:764–6.  Back to cited text no. 2
    
3.
Kaneko CR. Effect of ibotenic acid lesions of the omnipause neurons on saccadic eye movements in rhesus macaques. J Neurophysiol 1996;75:2229–42.  Back to cited text no. 3
    


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Online since 12th February '04
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