SAH-induced Vasospasm MCQ — NEET PG Practice Question | NEETPGAI
SAH-induced Vasospasm
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stethoscope Medicine
A 54-year-old woman is admitted on day 1 with a Hunt-Hess grade 3 subarachnoid hemorrhage from a ruptured anterior communicating artery aneurysm (coiled immediately). Continuous EEG monitoring is initiated per neurocritical care protocol. On day 7, she develops progressive left hemiparesis and decreased alertness. CT angiography shows severe narrowing of the right MCA and A1 segment. The EEG pattern marked **B** in the diagram—progressive focal delta slowing with a falling alpha-delta ratio over the right frontotemporal region—is observed over 8 hours preceding her clinical deterioration. Which of the following best explains the pathophysiology underlying this EEG finding and the patient's clinical presentation?
A. Rebleeding with acute mass effect causing midline shift and bilateral EEG changes
B. Delayed cerebral ischemia due to cerebral vasospasm, which typically peaks 7–10 days post-SAH and is preceded by qEEG changes hours to days before clinical manifestation
C. Acute hydrocephalus causing diffuse increased intracranial pressure with generalized EEG suppression
D. Nonconvulsive seizure activity requiring immediate antiepileptic therapy rather than vasospasm management
Explanation
Why "Delayed cerebral ischemia due to cerebral vasospasm..." is right
The clinical anchor is that progressive focal delta slowing with a falling alpha-delta ratio (pattern B) over the affected hemisphere is a hallmark qEEG finding of delayed cerebral ischemia (DCI) from vasospasm. This occurs typically between days 4–14 post-SAH (peak 7–10), and quantitative EEG changes—particularly a drop in alpha-delta ratio ≥10% from baseline or worsening focal slowing—precede clinical and angiographic vasospasm by hours to days. The patient's day 7 presentation, focal neurological deficit (left hemiparesis), and imaging confirmation of severe MCA/A1 narrowing all align with vasospasm-induced DCI. The qEEG finding is the earliest warning sign, enabling early intervention with nimodipine, induced hypertension, and endovascular rescue if needed (Neurocritical Care SAH Guidelines 2023; Claassen 2004).
Why each distractor is wrong
Acute hydrocephalus causing diffuse increased intracranial pressure: Hydrocephalus typically produces generalized EEG suppression or diffuse slowing, not focal delta activity with a falling alpha-delta ratio over one hemisphere. The imaging shows vasospasm, not obstructive hydrocephalus.
Nonconvulsive seizure activity requiring immediate antiepileptic therapy: While nonconvulsive seizures occur in ~20% of severe SAH patients, they present with generalized periodic discharges (pattern C) or triphasic waves (pattern D), not the focal delta slowing and falling ADR of pattern B. The clinical context (focal hemiparesis, angiographic vasospasm) points to ischemia, not seizure.
Rebleeding with acute mass effect: Rebleeding would cause acute, diffuse EEG changes with bilateral abnormalities and rapid deterioration. The focal, progressive nature of the EEG change over 8 hours and the angiographic finding of vasospasm (not hemorrhage) exclude this.
High-YieldNEET PG
A falling alpha-delta ratio on qEEG is an early, sensitive marker of vasospasm-induced DCI and precedes clinical symptoms by hours to days—enabling timely intervention before irreversible ischemia.
Neurocritical Care SAH Guidelines 2023; Claassen 2004 Continuous EEG SAH
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