EEG similarities between TWs and epileptiform sharp and slow wave
complexes were already noted by Foley (1950), who thought that TWs could
not always be clearly distinguished from ictal patterns associated with
petit mal epilepsy (hence the term "blunted spike and wave" he used in
describing TWs).
As a matter of fact, differentiating NCSE from triphasic wave encephalopathy (metabolic or structural) may be difficult since TWs straddle the borders between epilepsy and encephalopathy (Kaplan 1999). Especially when TWs have a frequency higher than I Hz (Figure 4), the distinction between encephalopathy and NCSE may be particularly difficult (Kaplan 1999).
Several investigators proposed EEG criteria in order to clearly differentiate "triphasic-like waves" in NCSE from nonepileptiform "true TWs" in encephalopathies. Litt et al. (1998) reported that monorhythmic TWs could be distinguished from epileptic patterns. An antero-posterior lag was considered to be specific for hepatic encephalopathy (Reiher 1970, Karnze and Bickford 1984), but it was later demonstrated that this time lag is neither a consistent feature of TWs nor of specific value regarding the type of metabolic encephalopathy (Fisch and Klass 1988). The appearance of TWs after noxious stimulation, which was considered a criterium to differentiate nonepileptiform "true TWs" from the epileptic pattern, has been recently challenged by the finding of stimulus-induced rhythmic, periodic or ictal discharges (SIRPIDs) (Hirsch et al. 2004). In a study conducted by Husain et al. (1999) epileptic "triphasic-like waves" in NCSE differed from nonepileptiform "true TWs" with an atypical morphology and variable periods of amplitude suppression between successive waveforms. Boulanger et al. (2006) conducted a retrospective study comparing EEG patterns in patients with diagnosis of NCSE and in patients with metabolic encephalopathy. Authors concluded that when compared with nonepileptiform "true TWs", epileptiform discharges associated with NCSE had a higher frequency, a shorter duration of phase one, extra spike components, and less generalized background slowing. Amplitude predominance of positive phase (wave 2) was similar. A phase lag was absent in all cases of NCSE but present in 40.8% of patients with nonepileptiform "true TWs." Noxious or auditory stimulation frequently increased the nonepileptiform "true TWs" (51%) without effect on epileptic "triphasic-like waves."
Unfortunately none of these criteria, which would be of great utility, have been validated in an observer-blinded study (Bauer and Trinka 2010), so that definitive conclusions are still lacking.
CLINICAL AND DIAGNOSTIC ASPECTS
TWs may be encountered in many conditions, especially in metabolic/toxic disorders, but also in structural encephalopathies, and "triphasic-like waves" may occur during status epilepticus. The most common metabolic/toxic disturbances associated with this pattern are hepatic failure, renal failure, and anoxia. Other metabolic disorders which must be taken into account are hyponatremia, hypernatremia, hypercalcamia, and hypoglycaemia. Sporadic TWs may also occur in stroke, cerebral tumors, and elderly subjects with clinically advanced dementia. Physical and neurological examinations usually show a decline of consciousness ranging from mild confusion to stupor and coma with decreased responsiveness. Postanoxic TWs are frequently associated with myoclonus, whereas TWs during hepatic or renal failure may be accompanied by asterixis, a neurological sign consisting of recurrent sudden loss of muscle tone in the outstretched and dorsiflexed hands.
The following laboratory studies may be useful to determine the presence of a metabolic encephalopathy: electrolytes, liver function tests, blood urea urea nitrogen, creatinine, and lithium levels. When laboratory tests are not suggestive of a metabolic/toxic disorder and when neurological examination shows focal neurological deficits, neuroimaging studies (CT or MRI) should be performed to rule out a structural encephalopathy.
The most useful way to distinguish between "triphasic-like waves" occurring during status epilepticus and nonepileptiform "true TWs" occurring during nonepileptic encephalopathies is to evaluate whether electroclinical improvement following benzodiazepine administration occurs.
CLINICAL AND TECHNICAL TIPS FOR A CORRECT INTERPRETATION OF TRIPHASIC WAVES
Improvement in EEG pattern after intravenous administration of benzodiazepine may occur in both NCSE and metabolic encephalopathies (Fountain and Waldman 2001, Brenner 2002), being therefore of limited utility in the differential diagnosis.
As a matter of fact, instead of considering only EEG modification after benzodiazepine or antiepileptic drug administration, an electroclinical response should be taken into account. After intravenous antiepileptic drug or benzodiazepine administration a clearly marked clinical improvement may occur in NCSE; such a clinical improvement does not occur in metabolic encephalopathies. The clinical response to benzodiazepines should be considered when interpreting TWs.
The evaluation of the patient's consciousness impairment is another clinical aspect which should be considered when interpreting TWs. In metabolic encephalopathies, the impairment of consciousness is mild or moderate when TWs are seen, almost never reaching the level of coma. On the other hand, patients with anoxic encephalopathy following cardiopulmonary arrest are often in deep coma, at the time when "triphasic-like waves" are recorded. The epileptic nature of TWs may be suspected if they are associated with spikes (which, however, may be absent in 31% of the cases [Boulanger et al. 2006]). There are still no valid criteria for a differential diagnosis between epileptic and nonepileptic TWs in coma following cardiopulmonary arrest (Bauer and Trinka 2010).
As a consequence, it is essential to interpret the EEG recording always considering clinical features and laboratory data. When only EEG is taken into account, electroencephalographers should not be dogmatic in distinguishing metabolic periodic discharges from seizure-related periodic discharges, because such a distinction is often not possible (Chong and Hirsch 2005).
CONCLUSION
In conclusion, nonepileptic "true TWs" with sharply contoured morphology may resemble epileptic patterns encountered in NCSE and may lead to misinterpretation and overinterpretation of this pattern as epileptic "triphasic-like waves" if only EEG is considered. Both the electroclinical response to benzodiazepines and evaluation of consciousness impairment should be considered when interpreting TWs. Evaluating only the EEG without considering also clinical and laboratory findings is not only useless and meaningless, but it may even lead to serious consequences.
As a matter of fact, differentiating NCSE from triphasic wave encephalopathy (metabolic or structural) may be difficult since TWs straddle the borders between epilepsy and encephalopathy (Kaplan 1999). Especially when TWs have a frequency higher than I Hz (Figure 4), the distinction between encephalopathy and NCSE may be particularly difficult (Kaplan 1999).
Several investigators proposed EEG criteria in order to clearly differentiate "triphasic-like waves" in NCSE from nonepileptiform "true TWs" in encephalopathies. Litt et al. (1998) reported that monorhythmic TWs could be distinguished from epileptic patterns. An antero-posterior lag was considered to be specific for hepatic encephalopathy (Reiher 1970, Karnze and Bickford 1984), but it was later demonstrated that this time lag is neither a consistent feature of TWs nor of specific value regarding the type of metabolic encephalopathy (Fisch and Klass 1988). The appearance of TWs after noxious stimulation, which was considered a criterium to differentiate nonepileptiform "true TWs" from the epileptic pattern, has been recently challenged by the finding of stimulus-induced rhythmic, periodic or ictal discharges (SIRPIDs) (Hirsch et al. 2004). In a study conducted by Husain et al. (1999) epileptic "triphasic-like waves" in NCSE differed from nonepileptiform "true TWs" with an atypical morphology and variable periods of amplitude suppression between successive waveforms. Boulanger et al. (2006) conducted a retrospective study comparing EEG patterns in patients with diagnosis of NCSE and in patients with metabolic encephalopathy. Authors concluded that when compared with nonepileptiform "true TWs", epileptiform discharges associated with NCSE had a higher frequency, a shorter duration of phase one, extra spike components, and less generalized background slowing. Amplitude predominance of positive phase (wave 2) was similar. A phase lag was absent in all cases of NCSE but present in 40.8% of patients with nonepileptiform "true TWs." Noxious or auditory stimulation frequently increased the nonepileptiform "true TWs" (51%) without effect on epileptic "triphasic-like waves."
Unfortunately none of these criteria, which would be of great utility, have been validated in an observer-blinded study (Bauer and Trinka 2010), so that definitive conclusions are still lacking.
CLINICAL AND DIAGNOSTIC ASPECTS
TWs may be encountered in many conditions, especially in metabolic/toxic disorders, but also in structural encephalopathies, and "triphasic-like waves" may occur during status epilepticus. The most common metabolic/toxic disturbances associated with this pattern are hepatic failure, renal failure, and anoxia. Other metabolic disorders which must be taken into account are hyponatremia, hypernatremia, hypercalcamia, and hypoglycaemia. Sporadic TWs may also occur in stroke, cerebral tumors, and elderly subjects with clinically advanced dementia. Physical and neurological examinations usually show a decline of consciousness ranging from mild confusion to stupor and coma with decreased responsiveness. Postanoxic TWs are frequently associated with myoclonus, whereas TWs during hepatic or renal failure may be accompanied by asterixis, a neurological sign consisting of recurrent sudden loss of muscle tone in the outstretched and dorsiflexed hands.
The following laboratory studies may be useful to determine the presence of a metabolic encephalopathy: electrolytes, liver function tests, blood urea urea nitrogen, creatinine, and lithium levels. When laboratory tests are not suggestive of a metabolic/toxic disorder and when neurological examination shows focal neurological deficits, neuroimaging studies (CT or MRI) should be performed to rule out a structural encephalopathy.
The most useful way to distinguish between "triphasic-like waves" occurring during status epilepticus and nonepileptiform "true TWs" occurring during nonepileptic encephalopathies is to evaluate whether electroclinical improvement following benzodiazepine administration occurs.
CLINICAL AND TECHNICAL TIPS FOR A CORRECT INTERPRETATION OF TRIPHASIC WAVES
Improvement in EEG pattern after intravenous administration of benzodiazepine may occur in both NCSE and metabolic encephalopathies (Fountain and Waldman 2001, Brenner 2002), being therefore of limited utility in the differential diagnosis.
As a matter of fact, instead of considering only EEG modification after benzodiazepine or antiepileptic drug administration, an electroclinical response should be taken into account. After intravenous antiepileptic drug or benzodiazepine administration a clearly marked clinical improvement may occur in NCSE; such a clinical improvement does not occur in metabolic encephalopathies. The clinical response to benzodiazepines should be considered when interpreting TWs.
The evaluation of the patient's consciousness impairment is another clinical aspect which should be considered when interpreting TWs. In metabolic encephalopathies, the impairment of consciousness is mild or moderate when TWs are seen, almost never reaching the level of coma. On the other hand, patients with anoxic encephalopathy following cardiopulmonary arrest are often in deep coma, at the time when "triphasic-like waves" are recorded. The epileptic nature of TWs may be suspected if they are associated with spikes (which, however, may be absent in 31% of the cases [Boulanger et al. 2006]). There are still no valid criteria for a differential diagnosis between epileptic and nonepileptic TWs in coma following cardiopulmonary arrest (Bauer and Trinka 2010).
As a consequence, it is essential to interpret the EEG recording always considering clinical features and laboratory data. When only EEG is taken into account, electroencephalographers should not be dogmatic in distinguishing metabolic periodic discharges from seizure-related periodic discharges, because such a distinction is often not possible (Chong and Hirsch 2005).
CONCLUSION
In conclusion, nonepileptic "true TWs" with sharply contoured morphology may resemble epileptic patterns encountered in NCSE and may lead to misinterpretation and overinterpretation of this pattern as epileptic "triphasic-like waves" if only EEG is considered. Both the electroclinical response to benzodiazepines and evaluation of consciousness impairment should be considered when interpreting TWs. Evaluating only the EEG without considering also clinical and laboratory findings is not only useless and meaningless, but it may even lead to serious consequences.
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