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Triphasic Waves: Clinical Correlates and Morphology

Published online by Cambridge University Press:  18 September 2015

Mecheri B.M. Sundaram
Affiliation:
Department of Clinical Neurological Sciences, University of Saskatchewan, Saskatoon
Warren T. Blume*
Affiliation:
Department of Clinical Neurological Sciences, University Hospital, University of Western Ontario, London, Ontario
*
EEG Department, University Hospital, 339 Windermere Road, London, Ontario, Canada N6A 5A5
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Abstract:

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Twenty-six (41%) of 63 consecutive patients with triphasic waves had various types of metabolic encephalopathies while 37 patients (59%) had non-metabolic encephalopathies, usually senile dementia. Triphasic waves were not found to be specific for any single type of metabolic encephalopathy.

Etiology was more closely linked to conscious level at recording than any morphological or distributional feature of the triphasic waves themselves. Thus, all 31 alert patients had non-metabolic encephalopathies while 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. Triphasic waves were most often maximally expressed 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 non-metabolic groups when matched for conscious level.

Prognosis for patients with either metabolic or non-metabolic encephalopathies was unfavourable. Only 4 of 24 metabolic and one of 35 non-metabolic patients were well at follow-up over 2 years later.

Forty percent of EEGs with sharp and slow wave complexes (slow spike waves) had sporadically-appearing triphasic waves. The relative amplitudes of the 3 components differed from triphasic waves in other conditions: equally maximal Waves II and III were the most usual form.

Type
Original Articles
Copyright
Copyright © Canadian Neurological Sciences Federation 1987

References

REFERENCES

1.Foley, JM, Watson, CW, Adams, RD. Significance of the electroencephalographic changes in hepatic coma. Trans Amer Neurol Ass 1950; 75: 161164.Google Scholar
2.Bickford, RG, Butt, HR. Hepatic coma: the electroencephalographic pattern. J Clin Invest 1955; 34: 790799.CrossRefGoogle ScholarPubMed
3.Silverman, D. Some observations of the EEG in hepatic coma. Electroenceph Clin Neurophysiol 1962; 14: 5359.CrossRefGoogle ScholarPubMed
4.Reiher, J. The electroencephalogram in the investigation of metabolic comas. Electroenceph Clin Neurophysiol 1970; 28: 104P.Google ScholarPubMed
5.Simsarian, JP, Harner, RN. Diagnosis of metabolic encephalopathy: significance of triphasic waves in the electroencephalogram. Neurology 1972; 22: 456.Google Scholar
6.Karnaze, DS, Bickford, RG. Triphasic waves: a reassessment of their significance. Electroenceph Clin Neurophysiol 1984; 57: 193198.CrossRefGoogle ScholarPubMed
7.Markand, ON. Abnormalities associated with diffuse encephalopathies. State of the Science in EEG. Presented at the American Electroencephalographic Soci ty annual course New Orleans, Louisiana, October 1983.Google Scholar
8.Adams, RD, Foley, JM. The neurological disorder associated with liver disease. Assoc Res Nerv and Ment Dis Proc 1953; 32: 198237.Google ScholarPubMed
9.Fischgold, H, Mathis, P. Obnubilations, comas etstupeurs. Electroenceph Clin Neurophysiol 1959; Suppl 11: 50.Google Scholar