How is an EEG finding of slow activity interpreted?

Updated: Aug 06, 2019
  • Author: Selim R Benbadis, MD; Chief Editor: Helmi L Lutsep, MD  more...
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Answer

Continuous focal slow activity is the only nonepileptiform focal abnormality that can be interpreted unequivocally as abnormal when it is an isolated finding. Other focal abnormalities are quite frequent but are of such low specificity that they almost never constitute an abnormality in themselves. To be interpreted as abnormal, these usually require the coexistence of a more definite abnormality such as slowing or epileptiform discharges.

As already outlined, focal slowing is nonspecific as to etiology, and in the era of neuroimaging the EEG has no role in diagnosing the nature of a lesion. Focal slowing is the most common abnormality associated with focal lesions of any type, including (but not limited to) neoplastic, vascular, subdural collections, traumatic, and infectious (see images below). It occasionally may be seen even in more subtle structural abnormalities such as mesiotemporal sclerosis or focal malformations of cortical development.

Continuous slow, lateralized right hemisphere. Whi Continuous slow, lateralized right hemisphere. While "spilling over" to the left frontal region, the polymorphic delta activity is clearly predominant over the right hemisphere. This type of slowing almost invariably is associated with a structural hemispheric lesion. This patient had a large right middle cerebral artery infarct.
Continuous slow, lateralized left hemisphere. This Continuous slow, lateralized left hemisphere. This polymorphic delta activity was continuous throughout the record. This patient had a left hemisphere neoplasm.
Continuous slow, regional right temporal. This pol Continuous slow, regional right temporal. This polymorphic delta activity is somewhat more focal than that shown in the first image above, with a maximum in the temporal chain. Little such activity is evident in the central chain, but enough to exclude a T4 electrode artifact. The slowing shows phase reversals at T4, indicating a maximum at that electrode.
Continuous slow, regional left temporal. This poly Continuous slow, regional left temporal. This polymorphic delta activity is somewhat more focal than that in the second image above, with a maximum in the temporal chain. The phase reversals at T3 indicate a maximum at that electrode.

The physiologic basis for focal polymorphic delta activity caused by focal cortical lesions is not fully understood. It is probably due to abnormalities in the underlying white matter rather than the cortex itself. When present, focal slow activity correlates highly with the side of the lesion, but it is not reliable for lobar localization. The likelihood of a structural lesion (ie, specificity) diminishes when the slow activity lacks these characteristics and is intermittent (see image below), in the theta rather than the delta range, and of low amplitude. This type of slowing may be normal (eg, temporal slowing of the elderly; see the article Normal EEG Variants). This is essentially the difference between focal "continuous slow" and "intermittent slow." [1]

Intermittent slow, lateralized left hemisphere. Th Intermittent slow, lateralized left hemisphere. This brief burst of delta activity is seen in the temporal and central areas. This is a much "weaker" finding than continuous slowing, and much less reliably associated with a structural lesion. This is indicative of mild dysfunction in that region.

In a few situations in clinical neurology, the EEG may show clear evidence of focal dysfunction (ie, focal slow) while no structural abnormality is found. The typical cases in point are the focal epilepsies. A readily demonstrable structural lesion usually is not found on neuroimaging, typically MRI (see Localization-Related Epilepsies on EEG).

Focal brain dysfunction without structural abnormalities has been observed in transient ischemic attacks (TIA), migraine, and postictal states. Polymorphic delta activity in these cases may be indistinguishable from that caused by a structural lesion, except that it is short-lived (ie, it disappears over time). The postictal state is the most common cause of nonstructural polymorphic delta activity, but the activity disappears within minutes to hours after the ictal event. Patients with ongoing TIAs or migraine rarely undergo an EEG during the symptomatic period, so clinical data are scarce.


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