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Research-informed explainer · Last reviewed April 12, 2026

Normal Pressure Hydrocephalus: The Treatable Dementia That Mimics Alzheimer's, How the Tap Test Works, and Who Improves With a Shunt

Normal pressure hydrocephalus causes a distinctive triad of gait problems, cognitive decline, and urinary incontinence—and unlike Alzheimer's, it can be treated with surgery.

Research-informed explainer — last updated April 12, 2026

Normal pressure hydrocephalus (NPH) is one of the few causes of dementia-like symptoms that is actually reversible with surgery — yet it is frequently misdiagnosed as Alzheimer's disease, Parkinson's disease, or simply "getting old," and many patients wait years before receiving the correct diagnosis and a chance at improvement. Knowing the classic triad of symptoms, how the diagnostic evaluation works, and what predicts a good response to shunting can help patients and families advocate for proper evaluation.

This article draws on research from five neurologists. James Golomb, MD, Clinical Assistant Professor at NYU Langone Medical College in both Neurology and Psychiatry, published foundational research on Alzheimer's disease comorbidity in NPH patients and shunt response (281 citations), as well as studies on patterns of motor impairment in aging and early cognitive decline (302 citations). Jesse Weinberger, MD, Professor of Neurology and Director of the Neurovascular Laboratory at Mount Sinai Hospital, contributed research on cerebral hemodynamics in NPH diagnosis (62 citations), examining how CSF drainage affects cerebral blood flow and its value in predicting shunt outcomes. Vikas Kotagal, MD, at Michigan Medicine, published a national database analysis of 30-day hospital readmission and surgical complication rates for shunting in NPH (22 citations) and a study of serious adverse events following NPH surgery (8 citations). Melissa Armstrong, MD, Professor at the University of Florida and Director of the UF Health Mangurian Clinical-Research Headquarters for Lewy Body Dementia, contributed the AAN criteria for corticobasal degeneration diagnosis (1,856 citations), a key differential diagnosis that must be distinguished from NPH. Irene Litvan, MD, Tasch Endowed Professor and Director of the Parkinson and Other Movement Disorders Center at UC San Diego, published the SIC Task Force appraisal of parkinsonian diagnostic criteria (1,018 citations) that guides the differential diagnosis of NPH from Parkinson's and related conditions.

What is normal pressure hydrocephalus

NPH is a condition in which excess cerebrospinal fluid (CSF) accumulates in the brain's ventricles, causing them to enlarge. Despite the expanded ventricular size, the pressure of the CSF measured on lumbar puncture is typically within the normal range — which is why the condition is called "normal pressure" hydrocephalus, even though the physiology is abnormal.

The excess fluid exerts pressure on surrounding brain structures, particularly the motor and frontal cortex fibers that travel near the ventricles. This is why the characteristic symptoms of NPH are:

  1. Gait disturbance: Typically described as "magnetic gait" — shuffling, wide-based, and slow, as if the feet are stuck to the floor. Unlike Parkinson's disease, the gait in NPH is not primarily characterized by tremor.
  2. Cognitive impairment: Typically characterized by frontal lobe dysfunction — slowed thinking, poor executive function, reduced attention — rather than the memory-dominant profile of early Alzheimer's disease.
  3. Urinary incontinence: Often urgency-type incontinence, appearing relatively early in the disease.

This triad — gait, cognition, continence — is remembered by the mnemonic "wet, wobbly, and wacky." Not all three features need to be present, and gait disturbance is often the first and most prominent symptom.

Why NPH is mistaken for Alzheimer's and Parkinson's

The cognitive slowing and memory complaints of NPH can strongly resemble early Alzheimer's disease, leading to misdiagnosis — particularly when the gait disturbance is mild or attributed to arthritis or deconditioning. Golomb's research on Alzheimer's comorbidity in NPH found that a substantial proportion of patients clinically diagnosed with NPH have concurrent Alzheimer's pathology at autopsy, and these patients with dual pathology have a significantly blunted response to shunting. This finding has important clinical implications: a patient who improves somewhat with shunting but not completely may have both NPH and Alzheimer's disease.

The gait disturbance in NPH also resembles the parkinsonian gait seen in Parkinson's disease or vascular parkinsonism, particularly in older patients with coexistent cerebrovascular disease. Litvan's SIC Task Force appraisal provides the clinical framework for distinguishing these conditions: in NPH, eye movements are normal (distinguishing it from progressive supranuclear palsy), there is no pill-rolling tremor (distinguishing it from typical Parkinson's disease), and the gait often has a characteristic wide base with poor clearance rather than the narrow-based festinating gait of Parkinson's. Armstrong's criteria for corticobasal degeneration provide another key differential: CBD involves asymmetric limb apraxia and cortical sensory deficits not seen in NPH.

How the diagnosis is made

Diagnosis begins with brain MRI, which in NPH typically shows enlarged ventricles disproportionate to the degree of cortical atrophy — a finding quantified using the Evans index (the ratio of maximum frontal horn width to maximum inner skull diameter; a ratio above 0.3 is consistent with NPH). Periventricular white matter changes and tight sulci over the high convexity are additional supportive features.

The large-volume lumbar puncture (tap test) is the key diagnostic procedure. A physician removes 30–50 mL of CSF via lumbar puncture, and the patient is tested for gait and cognition immediately before and at intervals afterward (typically 30 minutes, 1 hour, and sometimes 24 hours). Improvement in gait — particularly in walking speed and stride length — following CSF removal is the strongest predictor of a favorable response to surgical shunting. Patients who do not improve after the tap test may still respond to shunting, but the likelihood is lower.

Weinberger's research examined cerebral blood flow dynamics after CSF drainage in NPH, finding that cerebral blood flow did not increase after lumbar puncture and did not reliably predict post-shunt outcomes — an important finding that influenced the field's reliance on gait-based functional testing rather than CBF measurements for surgical decision-making.

Who responds to shunting and what the risks are

Ventriculoperitoneal (VP) shunting — placing a catheter in the ventricles to drain excess CSF into the abdominal cavity — improves symptoms in approximately 60–80% of properly selected NPH patients, with gait responding better and more reliably than cognition or continence. Younger patients, shorter symptom duration, prominent gait involvement, and a positive tap test all predict better outcomes.

Kotagal's large national database analysis of 30-day outcomes following NPH shunting found that the procedure carries a 30-day readmission rate and serious complication rate that patients should understand when weighing the decision. Complications include subdural hematoma (from over-drainage), shunt infection, shunt malfunction, and the risks of general anesthesia in an older patient population. Kotagal's study of serious adverse events following NPH surgery documented that adverse events, while manageable at experienced centers, are not trivial — underscoring the importance of realistic expectations and the value of evaluation at high-volume neurosurgery programs.

Questions to ask your doctor

  • My MRI shows enlarged ventricles — has someone specifically considered normal pressure hydrocephalus, and what is my Evans index?
  • Would a large-volume lumbar puncture tap test help determine whether I am a shunt candidate?
  • How much of my cognitive impairment might be reversible with a shunt versus reflecting coexistent Alzheimer's disease?
  • What specific improvements in gait would you expect to see after shunting if it works, and over what timeframe?
  • What is this center's volume and complication rate for NPH shunting?
  • If I have a positive tap test, how soon should shunting occur?

The bottom line

Normal pressure hydrocephalus is a genuinely reversible cause of cognitive and physical decline that is underdiagnosed because its symptoms overlap with Alzheimer's disease and Parkinson's disease. The classic triad of gait difficulty, cognitive slowing, and urinary incontinence in an older adult with enlarged ventricles on MRI should prompt a tap test referral. Patients who respond to CSF drainage are strong surgical candidates, and many who undergo timely shunting experience meaningful improvements in walking and daily function — an outcome that no Alzheimer's drug can offer.

Research informing this article

Peer-reviewed research from the following specialists listed on Convene informs this explainer. They did not write or review the article; their published work is cited throughout.

  • James Golomb

    Clinical Assistant Professor, Department of Neurology & Department of Psychiatry, NYU Langone Medical College

    NYU Langone Hospitals

  • Jesse Weinberger

    Professor of Neurology, Director of the Neurovascular Laboratory

    Mount Sinai Hospital

  • Vikas Kotagal

    Michigan Medicine Pulmonary Clinic, Taubman Center

  • Melissa Armstrong

    Professor and Associate Chair of Faculty Development, Department of Neurology; Director, UF Health Mangurian Clinical-Research Headquarters for Lewy Body Dementia

    UF Health Shands Hospital

  • Irene Litvan

    Tasch Endowed Professor of Neurology and Director, Parkinson and Other Movement Disorders Center, University of California, San Diego

    UC San Diego Health Hillcrest Medical Center

Sources

  1. 1.
    Alzheimer's disease comorbidity in normal pressure hydrocephalus: prevalence and shunt responseJournal of Neurology Neurosurgery & Psychiatry, 2000. DOI
  2. 2.
    Patterns of Motor Impairment in Normal Aging, Mild Cognitive Decline, and Early Alzheimer' DiseaseThe Journals of Gerontology Series B, 1997. DOI
  3. 3.
    Cerebral hernodynamics in the diagnosis of normal pressure hydrocephalusNeurology, 1984. DOI
  4. 4.
    Thirty-Day Hospital Readmission and Surgical Complication Rates for Shunting in Normal Pressure Hydrocephalus: A Large National Database AnalysisNeurosurgery, 2019. DOI
  5. 5.
    Serious adverse events following Normal Pressure Hydrocephalus surgeryClinical Neurology and Neurosurgery, 2018. DOI
  6. 6.
    Criteria for the diagnosis of corticobasal degenerationNeurology, 2013. DOI
  7. 7.
    SIC Task Force appraisal of clinical diagnostic criteria for parkinsonian disordersMovement Disorders, 2003. DOI

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