A 76-year-old man presents with a 12-month history of progressive gait disturbance described as "walking through molasses" with shortened, shuffling steps and a magnetic quality. He reports increasing forgetfulness and has developed urinary incontinence with urgency over the past 6 months. On examination, he demonstrates gait apraxia. T2-weighted MRI shows the pattern marked **B** in the diagram: marked ventriculomegaly with Evans index of 0.38, disproportionately enlarged subarachnoid spaces with dilated Sylvian fissures and tight high-convexity sulci, callosal angle <90°, and aqueductal flow void. Lumbar puncture opening pressure is 16 cm H₂O (normal). Which of the following best explains the pathophysiology of the condition shown at **B**?
A. Communicating hydrocephalus with impaired CSF absorption at the arachnoid villi despite normal mean intracranial pressure
B. Ex vacuo ventriculomegaly from cortical atrophy with proportionate ventricular enlargement and normal CSF dynamics
C. Obstructive hydrocephalus from aqueductal stenosis causing elevated intracranial pressure
D. Non-communicating hydrocephalus from fourth ventricular outlet obstruction with elevated opening pressure
Explanation
Why "Communicating hydrocephalus with impaired CSF absorption at the arachnoid villi despite normal mean intracranial pressure" is right
The pattern marked B represents idiopathic Normal Pressure Hydrocephalus (NPH), characterized by the Hakim triad (gait apraxia, dementia, incontinence), DESH sign (disproportionately enlarged subarachnoid spaces with tight high-convexity sulci), Evans index >0.3, and normal lumbar puncture opening pressure. The pathophysiology is communicating hydrocephalus—CSF flows freely between ventricles and subarachnoid space—but with impaired CSF absorption at the arachnoid villi. This causes intermittently elevated intracranial pressure despite normal mean pressure, leading to the characteristic clinical presentation. The normal opening pressure is the diagnostic paradox of NPH (Hakim/Adams; Mori 2012).
Why each distractor is wrong
Obstructive hydrocephalus from aqueductal stenosis causing elevated intracranial pressure: This describes pattern D (obstructive hydrocephalus), not B. Obstructive hydrocephalus presents with persistently elevated opening pressure and does not show the DESH sign; the subarachnoid spaces are typically compressed, not disproportionately enlarged.
Ex vacuo ventriculomegaly from cortical atrophy with proportionate ventricular enlargement and normal CSF dynamics: This describes pattern C (Alzheimer atrophy). In ex vacuo ventriculomegaly, cortical atrophy is proportionate to ventriculomegaly, and the subarachnoid spaces are enlarged diffusely. Pattern B shows cortical atrophy OUT OF PROPORTION to ventriculomegaly, with the distinctive DESH pattern (tight sulci despite dilated ventricles).
Non-communicating hydrocephalus from fourth ventricular outlet obstruction with elevated opening pressure: This is obstructive hydrocephalus with elevated pressure, inconsistent with the normal opening pressure and communicating pattern of NPH. The aqueductal flow void in B indicates patent CSF flow, not obstruction.
High-YieldNEET PG
NPH = communicating hydrocephalus + impaired arachnoid villus absorption + normal mean pressure (paradox) + DESH sign (tight convexity sulci + dilated ventricles) + Hakim triad. Gait responds best to shunt; cognition responds least.
Hakim/Adams; Mori 2012
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