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    Subjects/Medicine/Posterior Reversible Encephalopathy Syndrome
    Posterior Reversible Encephalopathy Syndrome
    medium
    stethoscope Medicine

    A 34-year-old woman at 32 weeks gestation presents with severe occipital headache, blurred vision, photophobia, and one generalized convulsion. BP is 198/118 mmHg with 3+ proteinuria. Brain MRI shows bilateral parieto-occipital T2/FLAIR hyperintensities with vasogenic edema. An EEG is performed due to persistent altered mental status and cortical blindness. The pattern marked **A** in the diagram—posterior dominant slow-wave and epileptiform activity—is observed maximal over bilateral parieto-occipital regions with superimposed sharp waves and spike-and-slow-wave complexes. Which of the following best describes the clinical significance of this EEG finding in the context of her presentation?

    A. Indicates generalized cerebral dysfunction with loss of autoregulation affecting all cortical regions equally, requiring immediate intubation
    B. Represents primary brainstem involvement with secondary cortical effects, necessitating urgent neurosurgical intervention
    C. Reflects focal cortical dysfunction and seizure susceptibility in the region of vasogenic edema, localizing the structural lesion to the posterior circulation territory
    D. Demonstrates primary white matter demyelination with secondary gray matter involvement, suggesting a demyelinating rather than hypertensive etiology

    Explanation

    Why option 1 is correct

    The posterior dominant slow-wave and epileptiform activity (marked A) maximal over bilateral parieto-occipital regions directly reflects focal cortical dysfunction in the territory of vasogenic edema seen on MRI. In posterior reversible encephalopathy syndrome (PRES) secondary to eclampsia, failure of posterior circulation autoregulation causes vasogenic edema predominantly in parieto-occipital white matter. The EEG finding of focal rhythmic theta-delta slowing (2–4 Hz) with superimposed sharp waves and spike-and-slow-wave complexes over the occipital and parietal leads (O1, O2, P3, P4) localizes electrographic abnormality to the region of structural lesion and indicates heightened seizure susceptibility in that cortical territory. This pattern is pathognomonic for PRES and guides clinical management: seizure prophylaxis with magnesium sulfate and blood pressure control target reversal of the underlying hypertensive encephalopathy. The finding is reversible—as demonstrated by normalization of EEG and MRI within 72 hours to 2 weeks—confirming the diagnosis (Fugate JE, Rabinstein AA. Lancet Neurol. 2015;14(9):914–925).

    Why each distractor is wrong

    • Option 2: Generalized cerebral dysfunction would produce diffusely slowed background with symmetric changes across all regions (frontal, temporal, central, parietal, occipital). This patient's EEG shows relatively spared frontal regions with focal maximal abnormality posteriorly—the opposite of global dysfunction. Generalized patterns do not localize the lesion.
    • Option 3: Brainstem involvement in PRES is rare and would produce different EEG patterns (vertex sharp waves, sleep spindles disruption, or burst suppression). The posterior parieto-occipital localization on EEG and MRI is cortical/subcortical white matter, not brainstem. Neurosurgical intervention is not indicated in PRES; medical management (antihypertensives, seizure prophylaxis) is definitive.
    • Option 4: The vasogenic edema in PRES is primarily in subcortical white matter with secondary cortical effects, not primary demyelination. Demyelinating diseases (MS, ADEM) produce different MRI patterns (periventricular, juxtacortical lesions) and do not reverse with blood pressure control. The rapid reversibility with antihypertensive therapy excludes demyelination.
    High-YieldNEET PG
    In PRES, focal posterior EEG slowing with epileptiform activity localizes the region of vasogenic edema and seizure risk; it is reversible with control of hypertension and is the hallmark electrographic signature of the syndrome.

    Fugate JE, Rabinstein AA. Posterior reversible encephalopathy syndrome. Lancet Neurol. 2015;14(9):914–925.

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