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Ping-pong Gaze in a Patient with Bilateral Hemispheric Ischemic Stroke: Case Report and Video
Case Report
Ping-pong Gaze in a Patient with Bilateral Hemispheric Ischemic Stroke: Case Report and Video Kostas Sotiriou, MD, Artemios K. Artemiadis, MD, MSc and Ioannis Papanastasiou, MD, PhD
Ping-pong gaze (PPG) is a rare eye movement abnormality consisting of conjugate smooth rhythmical horizontal eye deviations between the 2 extreme positions. PPG is encountered in cases of severe bilateral hemispheric or posterior fossa brain damage with intact brain stem and more rarely during drug toxicity. In this brief video case report, we present a 91-year-old woman with PPG after sustaining bilateral hemispheric ischemic stroke. We also present the neuroanatomic substrates of PPG along with its main saccadic variant, and we coin the hypothesis that PPG actually represents the paralysis of eye saccades. Key Words: Ping-pong—gaze— periodic alternating—saccades—eye movements. Ó 2015 by National Stroke Association
A 91-year-old woman was admitted to our hospital after sustaining bilateral hemispheric ischemic stroke (Fig 1). Her risk factors for stroke were hypertension and diabetes mellitus type II. During her hospitalization, she stayed in deep coma (Glasgow Coma Scale, 4/15; E1M2V1), and she showed both smooth alternating conjugate ocular deviations (typical ping-pong gaze, PPG) and a saccadic end position cogwheeling on right gaze (Video 1). Intravenous mannitol (60 g in 3 doses) and nadroparin (5700 anti-Xa IU once in day) were given as rescue therapy. The patient died 6 days after admission. In PPG, as first Senelick described, the eyes move horizontally, conjugately, and rhythmically (with a cycle
From the Department of Neurology, 417 Army Share Fund Hospital, Athens, Greece. Received July 27, 2014; accepted October 9, 2014. The authors have no financial disclosures. Address correspondence to Artemiadis K. Artemios, MD, MSc, Department of Neurology, 417 Army Share Fund Hospital, Monis Petraki Str, 10-12, Athens, Greece 115-21. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2014.10.003
lasting few seconds) in a pendular manner between the 2 extreme positions, without any associated head movements.1 PPG arises from severe bilateral hemispheric (implying the disconnection of the cerebrum from the brain stem gaze centers) or posterior fossa damage (especially of the midline deep vermis) with intact brain stem and more rarely drug toxicity (eg, monoamine oxidase inhibitors administered with or without neuroleptics).2-4 The overflow from vestibular inputs has been suggested to account for the emergence of PPG, although other pacemakers such as dentate nucleus and inferior olivary nucleus have been proposed as candidates.5 In our opinion, PPG may represent the paralysis of all saccades, leaving brain stem nuclei involved in the smooth pursuit eye movements (most probably the nucleus prepositus hypoglossi in pons or the dorsomedial pontine nucleus), uninhibited to produce this smooth alternate conjugate horizontal eye movement of PPG.6 In favor of this hypothesis is that transition of the classical smooth PPG to the saccadic (cogwheeling) PPG variant may predict a better prognosis concerning mortality, ostensibly reflecting the recovery, or salvage (due to less extensive cortical lesions) of corticobulbar pathways subserving the saccadic eye movements.7
Journal of Stroke and Cerebrovascular Diseases, Vol. 24, No. 3 (March), 2015: pp e67-e68
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Figure 1. (A) Initial computed tomography (CT) brain scan revealing bilateral middle cerebral artery thrombosis (white arrows). (B) CT brain scan (24 hours after) revealing bilateral frontotemporal ischemic infractions.
Supplementary Data Supplementary data related to this article can be found at http://dx.doi.org/10.1016/j.jstrokecerebrovas dis.2014.10.003.
References 1. Senelick RC. ‘‘Ping-pong’’ gaze. Periodic alternating gaze deviation. Neurology 1976;26:532-535. 2. Ahn SH, Choi KD, Kim JS, et al. Ping-pong gaze in hemifield may indicate bilateral asymmetrical hemispheric lesions. Neurology 2007;68:E8.
3. Prueter C, Schiefer J, Norra C, et al. Ping-pong gaze in combined intoxication with tranylcypromine, thioridazine, and clomipramine. Neuropsychiatry Neuropsychol Behav Neurol 2001;14:246-247. 4. Erich JL, Shih RD, O’Connor RE. ‘‘Ping-pong’’ gaze in severe monoamine oxidase inhibitor toxicity. J Emerg Med 1995;13:653-655. 5. Sieben A, Crevits L, Santens P. Saccadic ping pong gaze in coma. Neurologist 2007;13:161-163. 6. Sharpe JA. Neurophysiology and neuroanatomy of smooth pursuit: lesion studies. Brain Cogn 2008;68: 241-254. 7. Johkura K, Komiyama A, Tobita M, et al. Saccadic pingpong gaze. J Neuroophthalmol 1998;18:43-46.
Ping-pong Gaze in a Patient with Bilateral Hemispheric Ischemic Stroke: Case Report and Video Kostas Sotiriou, MD, Artemios K. Artemiadis, MD, MSc and Ioannis Papanastasiou, MD, PhD
Ping-pong gaze (PPG) is a rare eye movement abnormality consisting of conjugate smooth rhythmical horizontal eye deviations between the 2 extreme positions. PPG is encountered in cases of severe bilateral hemispheric or posterior fossa brain damage with intact brain stem and more rarely during drug toxicity. In this brief video case report, we present a 91-year-old woman with PPG after sustaining bilateral hemispheric ischemic stroke. We also present the neuroanatomic substrates of PPG along with its main saccadic variant, and we coin the hypothesis that PPG actually represents the paralysis of eye saccades. Key Words: Ping-pong—gaze— periodic alternating—saccades—eye movements. Ó 2015 by National Stroke Association
A 91-year-old woman was admitted to our hospital after sustaining bilateral hemispheric ischemic stroke (Fig 1). Her risk factors for stroke were hypertension and diabetes mellitus type II. During her hospitalization, she stayed in deep coma (Glasgow Coma Scale, 4/15; E1M2V1), and she showed both smooth alternating conjugate ocular deviations (typical ping-pong gaze, PPG) and a saccadic end position cogwheeling on right gaze (Video 1). Intravenous mannitol (60 g in 3 doses) and nadroparin (5700 anti-Xa IU once in day) were given as rescue therapy. The patient died 6 days after admission. In PPG, as first Senelick described, the eyes move horizontally, conjugately, and rhythmically (with a cycle
From the Department of Neurology, 417 Army Share Fund Hospital, Athens, Greece. Received July 27, 2014; accepted October 9, 2014. The authors have no financial disclosures. Address correspondence to Artemiadis K. Artemios, MD, MSc, Department of Neurology, 417 Army Share Fund Hospital, Monis Petraki Str, 10-12, Athens, Greece 115-21. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2014.10.003
lasting few seconds) in a pendular manner between the 2 extreme positions, without any associated head movements.1 PPG arises from severe bilateral hemispheric (implying the disconnection of the cerebrum from the brain stem gaze centers) or posterior fossa damage (especially of the midline deep vermis) with intact brain stem and more rarely drug toxicity (eg, monoamine oxidase inhibitors administered with or without neuroleptics).2-4 The overflow from vestibular inputs has been suggested to account for the emergence of PPG, although other pacemakers such as dentate nucleus and inferior olivary nucleus have been proposed as candidates.5 In our opinion, PPG may represent the paralysis of all saccades, leaving brain stem nuclei involved in the smooth pursuit eye movements (most probably the nucleus prepositus hypoglossi in pons or the dorsomedial pontine nucleus), uninhibited to produce this smooth alternate conjugate horizontal eye movement of PPG.6 In favor of this hypothesis is that transition of the classical smooth PPG to the saccadic (cogwheeling) PPG variant may predict a better prognosis concerning mortality, ostensibly reflecting the recovery, or salvage (due to less extensive cortical lesions) of corticobulbar pathways subserving the saccadic eye movements.7
Journal of Stroke and Cerebrovascular Diseases, Vol. 24, No. 3 (March), 2015: pp e67-e68
e67
K. SOTIRIOU ET AL.
e68
Figure 1. (A) Initial computed tomography (CT) brain scan revealing bilateral middle cerebral artery thrombosis (white arrows). (B) CT brain scan (24 hours after) revealing bilateral frontotemporal ischemic infractions.
Supplementary Data Supplementary data related to this article can be found at http://dx.doi.org/10.1016/j.jstrokecerebrovas dis.2014.10.003.
References 1. Senelick RC. ‘‘Ping-pong’’ gaze. Periodic alternating gaze deviation. Neurology 1976;26:532-535. 2. Ahn SH, Choi KD, Kim JS, et al. Ping-pong gaze in hemifield may indicate bilateral asymmetrical hemispheric lesions. Neurology 2007;68:E8.
3. Prueter C, Schiefer J, Norra C, et al. Ping-pong gaze in combined intoxication with tranylcypromine, thioridazine, and clomipramine. Neuropsychiatry Neuropsychol Behav Neurol 2001;14:246-247. 4. Erich JL, Shih RD, O’Connor RE. ‘‘Ping-pong’’ gaze in severe monoamine oxidase inhibitor toxicity. J Emerg Med 1995;13:653-655. 5. Sieben A, Crevits L, Santens P. Saccadic ping pong gaze in coma. Neurologist 2007;13:161-163. 6. Sharpe JA. Neurophysiology and neuroanatomy of smooth pursuit: lesion studies. Brain Cogn 2008;68: 241-254. 7. Johkura K, Komiyama A, Tobita M, et al. Saccadic pingpong gaze. J Neuroophthalmol 1998;18:43-46.