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Significance of triphasic waves in acute encephalopathy

I read with interest Sutter and Kaplan’s study on the clinical and radiological association of triphasic waves (TWs) in patients with acute encephalopathy [1]. The presence of TWs in the electroencephalogram (EEG) in the setting of a diffusely slow background (theta and delta frequency slowing) is thought to be suggestive of a metabolic-toxic cause of cerebral dysfunction. I have seen these waveforms wax and wane when reviewing continuous EEG recordings of critically ill patients in medical, surgical and neurological intensive care units. At times the record shows bursts of typical triphasic morphology waveforms lasting at times for a few minutes only to be interspersed with long segments where only diffuse background slowing is present. The same patient’s EEG record may be free of TWs on day 1 only to demonstrate florid TWs a day later. Triphasic waves probably occur due to dynamic interplay between various intrinsic factors (age, grade of encephalopathy as assessed by the Glasgow coma scale, metabolic factors such as electrolyte imbalance, degree of derangement of hepatic and renal functions as measured by level of hepatic enzymes, blood urea nitrogen and creatinine and underlying pre-existing cerebral atrophy and white matter disease). Thus TWs are more likely to be seen in the EEG records of some ‘more’ vulnerable encephalopathic patients compared with others.