The
n e w e ng l a n d j o u r na l
of
m e dic i n e
Images in Clinical Medicine Lindsey R. Baden, M.D., Editor
Ping-Pong Gaze
Muthiah Vaduganathan, M.D., M.P.H. Jacob H. Johnson, M.D. Massachusetts General Hospital Boston, MA mvaduganathan@partners.org
A
55-year-old man with alcoholic cirrhosis was found to be unresponsive at home. He was hemodynamically stable but obtunded and minimally responsive to noxious stimuli. Examination revealed spontaneous, slow, horizontal, conjugate eye deviation, alternating every 2 to 4 seconds from one extreme to the other (see video). Eye movements were smooth and continuous without interruption. Pupillary reactivity was maintained. The patient also had rigidity of all four limbs, clonus in the lower extremities, and Babinski signs bilaterally. Magnetic resonance imaging of the brain revealed chronic microangiopathic changes, with no electroencephalographic correlate. The plasma ammonia level was elevated at 359 μmol per liter (611 μg per deciliter; normal range, 12 to 48 μmol per liter [20 to 82 μg per deciliter]). “Ping-pong gaze” has been reported in irreversible comatose states associated with diffuse structural brain lesions, such as bilateral hemispheric infarcts and midline cerebellar hemorrhage. In this case, the neuro-ophthalmologic motility pattern was seen as a transient, reversible phenomenon in a patient with advanced hepatic encephalopathy. After 48 hours of lactulose treatment, the patient’s plasma ammonia level was 28 μmol per liter (48 μg per deciliter), with resolution of hepatic encephalopathy and ping-pong gaze. The patient was discharged home with normal mental status 1 week after presentation. DOI: 10.1056/NEJMicm1408161 Copyright © 2015 Massachusetts Medical Society.
e34
n engl j med 372;26 nejm.org June 25, 2015
The New England Journal of Medicine Downloaded from nejm.org on July 2, 2015. For personal use only. No other uses without permission. Copyright © 2015 Massachusetts Medical Society. All rights reserved.
n e w e ng l a n d j o u r na l
of
m e dic i n e
Images in Clinical Medicine Lindsey R. Baden, M.D., Editor
Ping-Pong Gaze
Muthiah Vaduganathan, M.D., M.P.H. Jacob H. Johnson, M.D. Massachusetts General Hospital Boston, MA mvaduganathan@partners.org
A
55-year-old man with alcoholic cirrhosis was found to be unresponsive at home. He was hemodynamically stable but obtunded and minimally responsive to noxious stimuli. Examination revealed spontaneous, slow, horizontal, conjugate eye deviation, alternating every 2 to 4 seconds from one extreme to the other (see video). Eye movements were smooth and continuous without interruption. Pupillary reactivity was maintained. The patient also had rigidity of all four limbs, clonus in the lower extremities, and Babinski signs bilaterally. Magnetic resonance imaging of the brain revealed chronic microangiopathic changes, with no electroencephalographic correlate. The plasma ammonia level was elevated at 359 μmol per liter (611 μg per deciliter; normal range, 12 to 48 μmol per liter [20 to 82 μg per deciliter]). “Ping-pong gaze” has been reported in irreversible comatose states associated with diffuse structural brain lesions, such as bilateral hemispheric infarcts and midline cerebellar hemorrhage. In this case, the neuro-ophthalmologic motility pattern was seen as a transient, reversible phenomenon in a patient with advanced hepatic encephalopathy. After 48 hours of lactulose treatment, the patient’s plasma ammonia level was 28 μmol per liter (48 μg per deciliter), with resolution of hepatic encephalopathy and ping-pong gaze. The patient was discharged home with normal mental status 1 week after presentation. DOI: 10.1056/NEJMicm1408161 Copyright © 2015 Massachusetts Medical Society.
e34
n engl j med 372;26 nejm.org June 25, 2015
The New England Journal of Medicine Downloaded from nejm.org on July 2, 2015. For personal use only. No other uses without permission. Copyright © 2015 Massachusetts Medical Society. All rights reserved.
