Clinical EEG slowing correlates with delirium severity and predicts poor clinical outcomes
Abstract
Objective
To determine which findings on routine clinical EEGs correlate with delirium severity across various presentations and to determine whether EEG findings independently predict important clinical outcomes.
Methods
We prospectively studied a cohort of nonintubated inpatients undergoing EEG for evaluation of altered mental status. Patients were assessed for delirium within 1 hour of EEG with the 3-Minute Diagnostic Interview for Confusion Assessment Method (3D-CAM) and 3D-CAM severity score. EEGs were interpreted clinically by neurophysiologists, and reports were reviewed to identify features such as theta or delta slowing and triphasic waves. Generalized linear models were used to quantify associations among EEG findings, delirium, and clinical outcomes, including length of stay, Glasgow Outcome Scale scores, and mortality.
Results
We evaluated 200 patients (median age 60 years, IQR 48.5–72 years); 121 (60.5%) met delirium criteria. The EEG finding most strongly associated with delirium presence was a composite of generalized theta or delta slowing (odds ratio 10.3, 95% confidence interval 5.3–20.1). The prevalence of slowing correlated not only with overall delirium severity (R2 = 0.907) but also with the severity of each feature assessed by CAM-based delirium algorithms. Slowing was common in delirium even with normal arousal. EEG slowing was associated with longer hospitalizations, worse functional outcomes, and increased mortality, even after adjustment for delirium presence or severity.
Conclusions
Generalized slowing on routine clinical EEG strongly correlates with delirium and may be a valuable biomarker for delirium severity. In addition, generalized EEG slowing should trigger elevated concern for the prognosis of patients with altered mental status.
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Information & Authors
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© 2019 American Academy of Neurology.
Publication History
Received: January 18, 2019
Accepted: April 30, 2019
Published online: August 29, 2019
Published in issue: September 24, 2019
Disclosure
E. Kimchi received funding from NIH–National Institute on Aging (1R03AG050878) and NIH–National Institute of Mental Health (1K08MH11613501). A. Neelagiri, W. Whitt, A. Sagi, S. Ryan, G. Gadbois, and D. Groothuysen report no disclosures relevant to the manuscript. M. Westover received funding from NIH–National Institute of Neurological Disorders and Stroke (1K23NS090900, 1R01NS102190, 1R01NS102574, 1R01NS107291) and the Department of Neurology, Massachusetts General Hospital, Boston. Go to Neurology.org/N for full disclosures.
Study Funding
E.Y.K. received funding from NIH–National Institute on Aging (1R03AG050878) and NIH–National Institute of Mental Health (1K08MH11613501). M.B.W. received funding from NIH–National Institute of Neurological Disorders and Stroke (1K23NS090900, 1R01NS102190, 1R01NS102574, 1R01NS107291) and the Department of Neurology, Massachusetts General Hospital, Boston.
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I read with interest Kimchi et al.1 article on clinical EEG slowing correlating with delirium severity. My own experience has been that, while in most patients with delirium, the EEG shows the absence of a well-defined posterior dominant rhythm, diffuse theta or delta or a mixed frequency background with, at times, superimposed broad sharp waves manifesting triphasic morphology, the degree of slowing by itself does not correlate with delirium severity or clinical outcomes. Rather, it is the presence or absence of reactivity, state changes, and sleep architecture which correlates with the degree of diffuse cerebral dysfunction.
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