Abnormal Pediatric Background

Abnormal Pediatric Background

John Giang, MD

Purpose

Identify diffuse and focal cerebral dysfunction from the background, with or without seizures.

Why it matters

• Background is the most sensitive but least specific part of the EEG; it reflects current cortical function, not cause.
• In children it is only interpretable against age and state.
• Slowing often carries more localizing and prognostic weight than a single discharge.

Key points

• Confirm abnormal for age and state. Awake PDR: 4–5 Hz at 6 mo, 6 Hz at 1 yr, 7 Hz at 2 yr, 8 Hz at 3 yr, 9 Hz at 8 yr, 10 Hz by 10 yr. Prove wakefulness first, then judge continuity, reactivity, variability, symmetry, synchrony, AP gradient and PDR.
• Generalized slowing: nonspecific but important. Diffuse dysfunction of any cause (metabolic, toxic, infectious, hypoxic, medication, hydrocephalus, neurodegenerative).

Grade it:

• Continuity matters: Discontinuity outside the neonatal period is always highly abnormal; burst-suppression = ≥50% suppressed. Frontal intermittent rhythmic delta activity/generalized rhythmic delta activity (FIRDA/GRDA) and triphasic waves point to encephalopathy; diffuse excess beta usually means benzodiazepines or barbiturates.
• Focal slowing: regional dysfunction. Describe morphology (polymorphic vs rhythmic) and persistence (continuous vs intermittent). Continuous polymorphic delta = structural lesion (tumor, infarct, hemorrhage, malformation); intermittent = smaller lesion, cortical dysfunction or epileptic focus; rhythmic (e.g., TIRDA) = epileptogenic. Asymmetric PDR, lost AP gradient or regional attenuation count as focal abnormality. Severity is judged by lack of reactivity and variability more than by frequency.
• Asymmetry: compare homologous regions in every state.
  • Thresholds: consistent amplitude difference >50% on a referential montage or PDR frequency difference >1 Hz is abnormal; <50% or 0.5–1 Hz is mild. Abnormality usually lies on the side that is slower, lower in voltage or less organized.
  • Awake: unilateral slower or absent PDR, lost AP gradient on one side, regional attenuation (subdural collection, infarct, cortical injury) or unilateral excess beta/breach over a skull defect.
  • Sleep spindles (highest yield): asynchrony is normal to about 12–18 mo and consistent asymmetry is abnormal after 2 yr; before that the total number of spindles per side should still be roughly equal. Persistent unilateral attenuation or absence of spindles points to ipsilateral hemispheric or thalamocortical dysfunction, with 98% specificity for a structural MRI abnormality in one pediatric series. Bilateral absence of spindles in a child with epileptic encephalopathy predicts worse cognitive outcome.
  • Other sleep asymmetries: persistently lateralized vertex waves or K-complexes, and asymmetric photic driving or hyperventilation build-up, carry the same meaning as an asymmetric PDR.
• Background matters without seizures. Delayed PDR is an objective marker of developmental delay; hemispheric polymorphic delta in an infant warrants imaging even without spikes; encephalopathy grade tracks clinical severity and can be followed serially. Report as "mild/moderate/severe generalized slowing" or "continuous/intermittent polymorphic (rhythmic) slowing over [region]" plus its meaning.

Common pitfalls

• Grading slowing before proving the child is awake.
• Calling frontal delta "slowing" when it is blunted spike-and-wave.
• Reading breach activity over a skull defect as spikes or as worse slowing.
• Equating slower frequency with worse pathology instead of unreactivity.
• Missing regional attenuation (subdural collection, infarct) while looking only for slow waves.
• Calling spindle asynchrony abnormal in an infant under 18-24 mo, or missing a truly one-sided spindle deficit in an older child because spindles alternate sides moment to moment; count both sides over the whole N2 record.
• Blaming excess beta on pathology before checking medications.