No, You Cannot Rule Out NPH Based on Ex Vacuo Dilatation Alone
The presence of ex vacuo dilatation from cerebral atrophy does NOT exclude NPH—in fact, distinguishing between these two conditions is one of the most challenging diagnostic dilemmas in elderly patients, and approximately 75% of NPH patients severe enough to require treatment have coexisting neurodegenerative disease. 1, 2
Why This Distinction Is Critical But Difficult
The fundamental problem is that both NPH and age-related atrophy cause ventricular enlargement, but through different mechanisms:
- NPH causes ventriculomegaly disproportionate to cortical atrophy, meaning the ventricles are larger than expected for the degree of brain shrinkage 1, 3
- Ex vacuo dilatation occurs when ventricles passively expand to fill space left by brain tissue loss 1
- These conditions frequently coexist in elderly patients, making pure radiographic distinction often impossible 2, 4
Key Imaging Features That Favor NPH Over Pure Atrophy
Your patient's imaging shows several features that warrant careful NPH evaluation rather than dismissal:
Features Supporting Possible NPH:
- Prominent temporal horns of lateral ventricles—this is specifically listed as a supportive feature for probable NPH diagnosis 1, 5
- Disequilibrium as presenting symptom—gait disturbance is the cardinal sign occurring in ~70% of NPH patients and often the first symptom 5
Critical Missing Information You Need:
- Evans index (maximal width of frontal horns/maximal width of inner skull): NPH requires >0.3 1, 5, 6
- Callosal angle: NPH shows <90° 1, 5, 6
- Aqueductal flow void on MRI: presence correlates with good shunt response and cannot be seen on CT 3, 7
- DESH pattern: tight high-convexity sulci with enlarged Sylvian fissures despite ventriculomegaly 3, 8
- Frontal horn morphology: rounded/ballooned frontal horns favor NPH 6
The Diagnostic Algorithm You Should Follow
Step 1: Complete the Imaging Assessment
Request formal measurement of 1, 5:
- Evans index
- Callosal angle
- Presence/absence of aqueductal flow void
- Pattern of sulcal effacement (high convexity vs. Sylvian fissure)
Step 2: Clinical Correlation
Assess for the NPH triad 5, 6:
- Gait disturbance: "magnetic" or "glued to floor" appearance (your patient has disequilibrium—this needs detailed characterization)
- Cognitive impairment: typically develops after gait issues
- Urinary incontinence: often last to appear
Step 3: If Imaging and Clinical Features Align, Proceed to Predictive Testing
This is the critical step that distinguishes NPH from atrophy 5, 6:
- Large-volume lumbar puncture (30-50 mL CSF removal) with pre/post gait and cognitive testing
- Extended lumbar drainage (3-5 days, removing ≥150 mL/day): This has 50-100% sensitivity and 80-100% positive predictive value for shunt response 6
- Phase-contrast MRI measuring aqueductal CSF stroke volume: elevated values have 100% positive predictive value for shunt responsiveness in some studies 5, 7
Critical Pitfalls to Avoid
Pitfall #1: Assuming Atrophy Excludes NPH
The most dangerous assumption—NPH guidelines explicitly state that ventricular enlargement should be "not entirely attributable to cerebral atrophy" 1, 5. The word "entirely" is crucial: some atrophy can coexist with NPH 2, 4.
Pitfall #2: Relying on Radiology Interpretation Alone
Radiologists often report "ex vacuo" when they see any atrophy, but this doesn't exclude disproportionate ventriculomegaly 1. You need quantitative measurements (Evans index, callosal angle) 1, 5.
Pitfall #3: Missing a Treatable Dementia
NPH accounts for up to 10% of dementia cases and is one of the few reversible causes 7. Properly selected patients have 80-90% chance of improvement with shunting, with only ~6% serious complication rate 5, 4.
Pitfall #4: Dismissing Cases with Atypical Features
One case report demonstrated dramatic NPH recovery despite PET findings typical of Alzheimer's disease and EEG suggesting Creutzfeldt-Jakob disease 9. The presence of core NPH features warrants consideration regardless of ancillary findings 9.
Your Next Steps
Do not assume NPH is ruled out. Instead 5, 2:
- Obtain formal measurements of Evans index and callosal angle from the existing MRI
- Review for aqueductal flow void and DESH pattern
- Perform detailed gait assessment looking for "magnetic" gait
- If measurements support possible NPH (Evans >0.3, callosal angle <90°, prominent temporal horns), proceed to CSF tap test or extended lumbar drainage
- Clinical improvement after CSF removal is the gold standard for predicting shunt responsiveness 5, 6
The pronounced temporal lobe atrophy and microangiopathic changes indicate coexisting pathology, but this is expected in 75% of NPH cases requiring treatment 1, 2, 4. The question is whether there is a treatable NPH component contributing to this patient's disequilibrium.