A 58-year-old man with hypertension presents to the emergency department 36 hours after acute onset of left-sided weakness and aphasia. CT head shows a large right middle cerebral artery territory infarct. Continuous EEG monitoring is initiated due to altered mental status. The EEG reveals the pattern marked **B** in the diagram—stereotyped, repetitive sharp-wave complexes occurring at regular intervals of 1 Hz, confined to the right hemisphere. Which of the following best explains the pathophysiological basis for this EEG finding?

Question

Accepted Answer

B. Electrical instability and metabolic stress in the ischemic penumbra surrounding the infarct core. ## Why "Electrical instability and metabolic stress in the ischemic penumbra surrounding the infarct core" is right

The pattern marked **B** (PLEDs/LPDs) arises specifically from the ischemic penumbra—the hypoperfused but potentially salvageable cortex surrounding the infarct core. Neurons in this region are metabolically stressed and electrically unstable, generating the characteristic periodic discharges at regular intervals (0.5–2 Hz) confined to one hemisphere. This reflects cortical hyperexcitability in tissue that is neither dead nor fully recovered. The ACNS 2021 terminology and pathophysiology explicitly link PLEDs to penumbral injury and the ictal-interictal continuum of seizure-prone cortex.

## Why each distractor is wrong

- **Irreversible necrosis and loss of electrical activity in the infarct core**: The infarct core is electrically silent; PLEDs originate in the penumbra, not the necrotic center. Dead tissue does not generate periodic discharges.
- **Hyperexcitability of the contralateral hemisphere due to loss of interhemispheric inhibition**: PLEDs are strictly unilateral (confined to one hemisphere). Bilateral patterns (BIPLEDs) are a separate, more severe entity. The contralateral hemisphere is not the source of the pattern marked **B**.
- **Acute inflammatory demyelination of white matter tracts in the affected territory**: While inflammation may contribute to post-stroke injury, PLEDs are a marker of acute cortical irritability and ischemic penumbral dysfunction, not demyelination. This mechanism does not explain the regular periodic discharge pattern.

**High-Yield:** PLEDs = penumbral hyperexcitability; they appear 24–72 hours post-stroke, carry 40–60% seizure risk, and resolve over 1–3 weeks as tissue either infarcts or recovers.

[cite: ACNS Standardized Critical Care EEG Terminology 2021]

Answer

A. Hyperexcitability of the contralateral hemisphere due to loss of interhemispheric inhibition

Answer

C. Irreversible necrosis and loss of electrical activity in the infarct core

Answer

D. Acute inflammatory demyelination of white matter tracts in the affected territory

Explanation

Why "Electrical instability and metabolic stress in the ischemic penumbra surrounding the infarct core" is right

Why each distractor is wrong

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