What is focal polymorphic delta slowing on EEG?

Updated: Oct 09, 2019
  • Author: Alexis D Boro, MD; Chief Editor: Selim R Benbadis, MD  more...
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Answer

These activities consist of arrhythmic slow waves that vary in frequency, amplitude, and morphology. Polymorphic slowing on the basis of a structural lesion requires involvement of white matter. Lesions involving the cortex alone do not cause polymorphic slowing; these lesions are typically associated with focal attenuation of normal rhythms. Continuous polymorphic delta slowing (CPD) is highly, but not inevitably, correlated with structural lesions. In studies that rely on CT, a structural lesion was present in about two thirds of adult patients with CPD. [4, 5] Seizures occur in more than 50% of cases of CPD in which no structural lesion is present. In these series, transient ischemic attack was the next most common cause of CPD.

CPD that resolves with prolonged recording or on subsequent routine EEGs often is a postictal effect, analogous to a Todd paresis. This phenomenon can be highly lateralizing. Other causes of CPD include migraine and trauma. Like postictal CPD, the slowing in these settings would be expected to resolve on subsequent EEGs. When focal slowing is intermittent, involves substantial theta, or disappears with eye opening or in sleep, a structural lesion is less likely.

When CPD is due to a structural lesion, the EEG is usually not helpful in determining its etiology. Ischemic stroke, hemorrhage, and tumors can all cause overlapping and occasionally indistinguishable EEG findings. Rapidly changing intraparenchymal lesions, such as acute strokes and high-grade gliomas, are more likely to produce profound EEG changes. Slowly changing extra-axial lesions such as meningiomas tend to produce relatively subtle changes in the EEG.

The EEG can usually lateralize the lesion, although at times the slowing produced by parasagittal lesions can project to the contralateral hemisphere and frontal lesions often produce bilateral abnormalities. In the latter case, the polymorphic slowing is typically of larger amplitude and has a wider field on the side of the lesion. There is often significant discordance between the localization of the polymorphic slowing and the corresponding lesion. In particular, frontal and parietal lesions often produce delta activity that is of highest amplitude and phase-reverses over the temporal regions.

A small amount of focal polymorphic slowing involving the temporal regions is frequently seen in elderly subjects. Norms are difficult to establish. This finding has been argued to correlate with cerebrovascular disease. When the slowing is encountered rarely in the record, incorporates significant theta rather than delta, and is restricted to drowsiness, it is often not of clinical significance. See the image below.

Continuous polymorphic delta. This EEG is from a 2 Continuous polymorphic delta. This EEG is from a 23-year-old woman who suffered a right middle cerebral artery stroke. She had a history of rheumatic fever and mitral valve replacement. There is continuous polymorphic delta slowing over the left temporal lobe. Faster activities are attenuated in the same region. Note the irregularly irregular heart rate, consistent with atrial fibrillation.

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