PRES Syndrome MCQ — NEET PG Practice Question | NEETPGAI
PRES Syndrome
medium
stethoscope Medicine
A 32-year-old woman at 35 weeks gestation with severe preeclampsia presents with sudden-onset headache, confusion, cortical blindness, and a generalized tonic-clonic seizure. Blood pressure is 210/120 mmHg. MRI brain shows bilateral symmetric T2/FLAIR hyperintensities in the parietooccipital white matter without restricted diffusion. EEG findings are shown in the diagram. The pattern marked **B** (bilateral posterior delta slowing with occasional focal sharp waves, reversible after blood pressure control) is most consistent with which underlying pathophysiological mechanism in PRES?
A. Restricted diffusion from acute ischemic stroke in the posterior cerebral artery territory
B. Cytotoxic edema from direct neuronal toxicity caused by cyclosporine or tacrolimus exposure
C. Vasogenic edema from breakdown of the blood-brain barrier due to failure of cerebral autoregulation in the posterior circulation, which has sparser sympathetic innervation
D. Venous sinus thrombosis with impaired cerebral venous drainage in the posterior fossa
Explanation
Why option 1 is right
The EEG pattern marked B—bilateral posterior delta slowing with occasional focal sharp waves, reversible after blood pressure control—is the hallmark electrophysiological signature of PRES in eclampsia. This pattern directly reflects the underlying pathophysiology: acute severe hypertension (210/120 mmHg) overwhelms cerebral autoregulation, particularly in the posterior circulation, which has sparser sympathetic innervation than the anterior circulation. This leads to endothelial dysfunction, breakdown of the blood-brain barrier, and vasogenic edema (confirmed by the MRI showing T2/FLAIR hyperintensities WITHOUT restricted diffusion). The reversibility of the EEG abnormality after blood pressure control is pathognomonic for vasogenic edema and functional disturbance rather than irreversible tissue damage. The delta slowing reflects cortical and subcortical dysfunction from the edema, while the focal sharp waves over the occipital regions correspond to the parietooccipital predilection of PRES. (Harrison's 21e PRES; Hinchey NEJM 1996)
Why each distractor is wrong
Option 2 (Cytotoxic edema from calcineurin inhibitors): While cyclosporine and tacrolimus are recognized triggers of PRES, this patient's presentation is driven by eclampsia (severe preeclampsia with seizures and hypertension at 35 weeks gestation), not immunosuppressive therapy. Cytotoxic edema would show restricted diffusion on MRI, which is absent here. The reversibility of the EEG after BP control points to vasogenic, not cytotoxic, pathology.
Option 3 (Restricted diffusion from acute ischemic stroke): The MRI explicitly shows NO restricted diffusion, ruling out acute ischemia. PRES is characterized by vasogenic edema, not infarction. Acute stroke would produce persistent EEG abnormalities and neurological deficits, not reversibility with BP control.
Option 4 (Venous sinus thrombosis): Venous sinus thrombosis is a differential diagnosis for PRES but is ruled out here by the bilateral symmetric parietooccipital pattern without restricted diffusion and the rapid reversibility with BP control. Venous thrombosis would typically show more focal findings and would not resolve simply with antihypertensive therapy.
High-YieldNEET PG
PRES = vasogenic edema from autoregulation failure in the posterior circulation; EEG shows reversible posterior delta slowing; MRI shows T2/FLAIR hyperintensities WITHOUT restricted diffusion; full recovery expected with urgent BP control and treatment of the trigger (magnesium sulfate + delivery in eclampsia).
Harrison's 21e PRES; Hinchey NEJM 1996 PRES
Practice similar questions
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.
