Abstract

A 66 year-old Indian gentleman with a background of type II diabetes, Crohn's disease and previously treated tuberculosis presented with double vision and unsteadiness.

He was found to have a right-sided internuclear opthalmoplegia (INO) along with weakness and fasciculations in the lower limbs associated with brisk reflexes and an ataxic gait.

An MRI scan of the brain and spinal cord revealed multiple supratentorial and infratentorial lesions. There was a hyperintensity in the right medial longitudinal fasciculus, which was felt to explain the INO. Cord and nerve root changes were also present. A CT angiogram of the brain was unrevealing.

A lumbar puncture showed a mildly cellular CSF. CSF protein was 1.24 g/L and CSF glucose was 3.0 mmol/L compared to the paired plasma sample of 10.4 mmol/L. CSF ACE was raised at 1.59 µmol/L. Lactate dehydrogenase was raised at 773IU/L. CSF microbiology, immunology, cytology and flow cytometry were unrevealing. The clinical diagnosis at the time was neurosarcoidosis. The patient was managed with prednisolone and azathioprine.

His condition worsened and his Glasgow Coma Scale score dropped requiring admission to the Intensive Care Unit. Whilst on ICU, the patient's eyes began deviating conjugately from one lateral side to the other without any rest period, the cycle lasting around 3 seconds. This was an example of “ping-pong gaze”.

Ping pong' gaze (PPG) is a term used to define slow conjugate eye deviation from one lateral side to the other with a fixed frequency. The term was coined by Selenick in 1976 after observing the phenomenon in a patient with a cerebellar haemorrhage.¹ PPG has been chiefly observed in unconscious patients with bilateral cerebral impairment. It has, however been described in further cases of cerebellar haemorrhage,² tricyclic toxicity³ and monoamine oxidase inhibitor toxicity.⁴

Different pathophysiological mechanisms have been described, most involving the lack of cortical inhibition on the horizontal gaze centres in the brain stem. This lack of input may permit vestibular or other nuclei to act as pacemakers.⁵ The majority of cases have been described in patients with persistent vegetative state however it has been demonstrated in awake patients.²

Unfortunately the patient's condition did not improve and he died. Post-mortem findings from the central nervous system confirmed a diagnosis of intravascular large B-cell lymphoma.

In this case the cause of PPG was severe bihemispheric brain injury secondary to intravascular large B-cell lymphoma, a disease which can present with a wide variety of symptoms and often evades diagnosis.