Triphasic waves (TWs) are a distinctive but nonspecific electroencephalographic (EEG) pattern originally described in a stuporous patient in 1950 by Foley as “blunted spike and wave.” In 1955, Bickford and Butt coined the term “triphasic wave.” Since their findings were limited to patients with hepatic failure, triphasic wave encephalopathy (TWE) became synonymous with hepatic encephalopathy. Since then, TWE has been associated with a wide range of toxic, metabolic, and structural abnormalities.
TWs are high-amplitude (>70 µV), positive sharp transients that are preceded and followed by negative waves of relatively lower amplitude. They are diffuse and bilaterally synchronous with bifrontal predominance. They often repeat periodically at a rate of 1-2 Hz.
See the image below.
An 89-year-old man with end-stage liver disease. Note the frontally predominant, sharply contoured waveforms with a triphasic morphology, characterized by 3 phases: negative (wave 1), positive (wave 2), and negative (wave 3). Also note the periodicity with 1-second intervals.
Regardless of the underlying etiology, TWs are associated with an impaired consciousness that may range from mild confusion to deep coma. The background may be slower in hepatic failure than in other conditions. Patients with metabolic abnormalities as a cause for TWE are more likely to be in coma than those with another etiology of TWE.
Early theories suggested that moving cortical positivity due to cortical irritation produced TWE. The cause now is believed to be a dysfunction of the thalamocortical relay neurons due to structural or metabolic disruption. Abnormalities in glutamate metabolism may be one of the mechanisms of TWE. Metabolic or structural abnormalities at the thalamocortical level, particularly dysfunction in the thalamocortical relay neurons, are hypothesized to be responsible for the EEG and clinical findings associated with TWE.
A population-based evaluation of TWE has not been completed, but of 5000 patients at the University of Pennsylvania who underwent an EEG, TWs were identified as the dominant abnormality in 42. Of 15,326 EEGs of inpatients at a large psychiatric institute, 83 demonstrated TWs. TWs occur in approximately 25% of patients with hepatic encephalopathy and in more than 10% of patients with septic encephalopathy. The criteria used to define TWs can vary, and this affects its reported frequency.
The morbidity and mortality associated with TWE depends on the underlying etiology. Patients with TWE from anoxic injuries or lithium toxicity have a particularly poor prognosis. Residual neurologic deficits among survivors are common.
TWE has been reported in those aged 1 month to 85 years; however, most patients are older than 60 years. TWE is rarely seen in patients younger than 30 years.
No differences in gender prevalence have been reported. The dominance of females among studied populations probably results from their longer life span.