You are in: eMedicine Specialties > Neurology > Electroencephalography and Evoked Potentials EEG Triphasic WavesArticle Last Updated: Feb 27, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 9
  Author: Kalyani Korabathina, MD, Department of Neurology, University of South Florida College of Medicine Kalyani Korabathina is a member of the following medical societies: American Academy of Neurology Coauthor(s): Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital; Gretchen L Birbeck, MD, Departments of Neurology and Epidemiology, Assistant Professor, Michigan State University Editors: Anthony M Murro, MD, Laboratory Director, Professor, Department of Neurology, Medical College of Georgia; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Norberto Alvarez, MD, Assistant Professor, Department of Neurology, Harvard Medical School; Consulting Staff, Department of Neurology, Boston Children's Hospital; Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital; Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants Author and Editor Disclosure Synonyms and related keywords: Triphasic waves, electroencephalography, EEG, EEG pattern, triphasic wave encephalopathy, TWE, nonconvulsive status epilepticus, NCSE INTRODUCTIONSection 2 of 9
  Background 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 (Ebersole, 2003). See Image 1. Pathophysiology 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. Epidemiology 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. Morbidity/mortality 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. Demographics 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. CLINICALSection 3 of 9
History
Physical
Causes The 3 most common causes of TWE are hepatic encephalopathy, renal failure, and anoxic injury. Other causes of TWs include the following:
DIFFERENTIAL DIAGNOSISSection 4 of 9
Often, TWs are interpreted as generalized periodic patterns, slow spike-wave complexes, or rhythmic sharp waves. This is significant because such patterns are usually associated with nonconvulsive status epilepticus (NCSE). However, some studies have also suggested an association with nonepileptic encephalopathies (ie, anoxic, toxic, metabolic). One study reported the incidence of NCSE in patients with anoxic brain injury to be as high as 8% (Towne, 2000). This raises the possibility of overinterpretation of some EEG patterns as NCSE. This notion of variable interpretation of generalized periodic epileptiform discharges was further examined in one study that compared general neurologist and electroencephalographer interpretations of an EEG sample depicting a generalized periodic pattern. Indeed, variability exists in the interpretation of generalized periodic epileptiform discharges in that more than 50% of general neurologists did not consider the possibility of NCSE (Korabathina, 2006). This is important because NCSE is treatable. A limited number of studies have attempted to differentiate between patterns of nonepileptic encephalopathy from those of NCSE by considering the morphology of the waveforms and their response to external stimulation (Boulanger, 2006). In addition, the clinical response to benzodiazepines should also be part of diagnostic evaluation (Fountain, 2001). WORKUPSection 5 of 9
Lab studies
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Other tests
Procedure
TREATMENTSection 6 of 9
Medical care Medical care should address the underlying cause of TWE. If in fact a metabolic, toxic, or drug-induced etiology is unequivocal, then treatment should specifically address this problem. If NCSE is suspected, then an evaluation of the patient clinical response after the administration of intravenous benzodiazepines should be considered. Consultation Consult a neurologist and neurophysiologist for EEG. FOLLOW-UPSection 7 of 9
Follow-up care Clinical assessment should be performed to exclude underlying seizures. EEG need not be repeated if there is notable clinical response. Transfers In severe cases, transfer to ICU may be required for airway management. Prognosis
Patient education For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patient education article Electroencephalography (EEG). MULTIMEDIASection 8 of 9
REFERENCESSection 9 of 9
Article Last Updated: Feb 27, 2007 | |||||||
