Brainstem somatosensory and auditory evoked responses in central pontine myelinolysis

Excerpt

A 49-year-old woman with a history of chronic ethanol abuse was admitted to a first hospital for generalized tonic–clonic seizures related to ethanol withdrawal. Initial treatment included diazepam, valproic acid and thiamine supplementation. The patient regained rapidly consciousness, but remained disorientated and confused. Treatment with diazepam was pursued. The electroencephalogram was symmetric with predominant beta waves and no epileptiform discharges. There was a mild hyponatremia on admission (122 mmol/l). The following values were recorded: 127 mmol/l (day 2), 130 (day 3), 137 (day 4), 148 (day 5). She was admitted to the intensive care unit on day 7, following progressive deterioration of consciousness with flaccid quadriplegia and preservation of the horizontal and vertical eye movements. The Glasgow Coma Score was only 5/15 (E3,V1, M1). Diazepam overdose or valproate-induced hyperammonemic encephalopathy were ruled out by laboratory investigations. Brain computed tomography was unremarkable. Electromyography did not show peripheral nerve involvement and median nerve conduction velocity was 56 m/s. The patient was transferred to our intensive care unit on day 27. Brainstem auditory and somatosensory evoked potentials (BAEP and SSEP, respectively) were performed. Somatosensory conduction intervals above the bulbo-medullary junction were increased symmetrically, as shown by the significant delay in the N20 waves and the increase in the P14–N20 intervals (Fig. 1c). Auditory conductions within the pons were also increased (Fig. 1b). Brain magnetic resonance imaging (MRI) was performed the next day. T2-weighted and fluid attenuated inversion recovery sequences were consistent with extensive central pontine myelinolysis (CPM) (Fig. 1a). The patient made a progressive recovery over a 2-month period. Follow-up SSEPs at 1 month did not show improvement.

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