What is the significance of a finding of triphasic waves (TWs) on EEG to evaluate dementia and encephalopathy?

Updated: Oct 09, 2019
  • Author: Eli S Neiman, DO, FACN; Chief Editor: Selim R Benbadis, MD  more...
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Triphasic waves (TWs; see the image below) were initially described by Foley et al in hepatic encephalopathy. They later were described in other metabolic states and brain tumors. [95] Most electroencephalographers now agree that TWs are a relatively nonspecific pattern observed in a number of metabolic conditions, degenerative dementias, and anoxia. In a bipolar montage, TWs usually comprise a high-voltage, positive wave followed by a smaller negative deflection; they usually are bilaterally synchronous and maximal frontally. A fronto-occipital (anteroposterior) phase lag varies from 25 to 140 ms; this is expressed less in referential montages.

Triphasic waves, maximum amplitude bilateral front Triphasic waves, maximum amplitude bilateral frontal.

TWs have not been reported in children. Generally, the TW pattern carries a poor prognosis with a high mortality if it occurs in association with rapid neurologic and clinical deterioration.

However, TWs in a psychiatric population described by Blatt and Brenner carried a different prognosis. In a large retrospective study consisting of 15,326 electroencephalograms (EEGs) performed from 1983 to 1992 in a psychiatric institute, 83 EEGs (62 patients—13 men and 49 women aged 59-90 years, with a mean age of 74 years) had TWs.

All 62 patients were awake, though they often were confused. Most (n=56) had dementia, usually severe; 15 also had delirium. Six patients had no dementia. Infrequent etiologies included neuroleptic malignant syndrome (n=1) and hepatic encephalopathy (n=1); in 4, the cause was uncertain, although all were receiving lithium. [96]

EEG features analyzed included frequency of background rhythms, distribution of the TWs, periodicity, and epileptiform abnormalities. [96] Background rhythms were slow in all but 7 patients. TWs were maximal posteriorly in 47 patients and anteriorly in 6 and were diffuse in 9. Neuroimaging studies demonstrated prominent posterior abnormalities in only 1 individual. Periodicity was prominent in 4 patients; in 2, the TWs were maximal anteriorly. Interictal epileptiform activity was present in 6 patients, a history of seizures in 8, and myoclonus in 4. TWs are uncommon in psychiatric populations; they occur primarily in elderly and severely demented patients.

Aguglia et al discussed nonmetabolic causes of TWs and described 2 patients with TWs on their EEGs in the absence of metabolic disturbances. [97] One patient had coma associated with cerebellar hematoma, the other had mild dementia associated with idiopathic calcifications of the basal ganglia and healthy auditory brainstem responses and subcortical and cortical SEPs. Neurologic examination revealed no asterixis in either patient.

The literature on nonmetabolic causes of TWs also was reviewed, and the clinical and anatomic reports of 10 patients were analyzed. [97] Seven patients had focal brainstem-diencephalic lesions: craniopharyngioma (2), thalamic gliomas (3), or pontine stroke (2). Three patients suffered from diffuse subcortical or multifocal encephalopathies: Binswanger encephalopathy (1), cerebral carcinomatosis (1), or multifocal cerebral lymphoma (1).

From the clinical point of view, patients with nonmetabolic diseases causing TWs presented with either disturbance of higher cerebral functions with no asterixis or sudden onset of coma. Aguglia et al concluded that TWs may result from focal brainstem/diencephalic lesions or from diffuse subcortical or multifocal encephalopathies in the absence of concomitant metabolic abnormalities. [97] Nonmetabolic causes of TW should be suspected in patients presenting with neurologic disturbances not associated with asterixis.

TWs also were evaluated by Sundaram et al, and their clinical correlates and morphology were assessed. [98] Of 63 consecutive patients with TWs, 26 (41%) had various types of metabolic encephalopathies, and 37 patients (59%) had nonmetabolic encephalopathies, usually senile dementia. TWs were not found to be specific for any single type of metabolic encephalopathy. Etiology was linked more closely to level of consciousness at recording than to any morphologic or distributional feature of the TWs themselves. Thus, all 31 alert patients had nonmetabolic encephalopathies, and all 13 comatose patients had metabolic encephalopathies.

The second, positive component (wave II) most often had the highest voltage, while equally maximal waves I and II occurred next most commonly. [98] In these patients, TWs most often were expressed maximally anteriorly. Among patients with metabolic encephalopathies, a posterior-anterior delay or lag of the wave II peak occurred more commonly than did the better known anterior-posterior lag. Lags occurred with both metabolic and nonmetabolic conditions but were more common with the former. No difference in quantity or mode of appearance existed between the metabolic and nonmetabolic groups when matched for consciousness level.

Prognosis for patients with either metabolic or nonmetabolic encephalopathies was unfavorable. [98] Only 4 of 24 patients with metabolic encephalopathy and 1 of 35 patients with nonmetabolic encephalopathy were well at follow-up more than 2 years later. Forty percent of EEGs with sharp and slow-wave complexes (slow spike waves) had sporadically appearing TWs. The relative amplitudes of the 3 components differed from those of TWs in other conditions; equally maximal waves II and III were the most usual form.

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