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Normal Pressure Hydrocephalus: The Treatable Dementia

Not every dementia is permanent. Normal pressure hydrocephalus is one of the few causes of cognitive decline that can be reversed with treatment—but only if someone identifies it first. Most cases are missed entirely, diagnosed as Alzheimer’s or written off as aging. We find the ones that aren’t supposed to be permanent.

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The Dementia That Isn’t Supposed to Be Permanent

In 1965, neurosurgeon Raymond Adams and his colleagues published a landmark case series describing patients with enlarged cerebral ventricles, normal cerebrospinal fluid pressure on lumbar puncture, and a distinctive clinical triad: difficulty walking, progressive cognitive decline, and urinary incontinence. The patients improved after surgical shunting of CSF. Adams called the condition normal pressure hydrocephalus—and in doing so, identified one of the very few causes of dementia that medicine can actually reverse.

Six decades later, NPH remains dramatically underdiagnosed. Epidemiological studies suggest that NPH may account for 5 to 6 percent of all dementia cases, yet most patients never receive the diagnosis. A 2005 study led by Norman Relkin at Weill Cornell Medical Center estimated that fewer than 20 percent of NPH cases in the United States are identified and treated. The rest are labeled Alzheimer’s disease, Parkinson’s disease, vascular dementia, or simply “old age.”

The cost of this diagnostic failure is staggering. Every month a patient with treatable NPH spends undiagnosed is a month of progressive neurological damage that may become irreversible. The gait instability that begins as a subtle shuffle can progress to immobility and nursing home placement. The cognitive slowing that starts as word-finding difficulty can deepen into frank dementia. And the urinary urgency that a primary care physician attributes to prostate enlargement or pelvic floor weakness can become permanent incontinence.

This is not a rare condition. It is a common condition that is rarely considered.

Recognizing the Triad

The classic presentation of NPH involves three cardinal features, often remembered by the mnemonic “wet, wacky, and wobbly.” But that shorthand undersells the complexity. Each element of the triad has a distinct neurological basis, and recognizing the pattern requires more than checking three boxes.

The gait disturbance is typically the earliest and most prominent feature. Patients develop a wide-based, shuffling walk with short steps and difficulty initiating movement—a pattern neurologists call “magnetic gait,” as though the feet are stuck to the floor. This differs from the festinating gait of Parkinson’s disease and from the cautious gait of someone with balance anxiety. On examination, the feet barely clear the ground, turns are multi-step, and postural reflexes are impaired. Falls become increasingly common.

The cognitive decline in NPH tends to affect executive function and processing speed more than memory per se—a profile that differs from the amnestic pattern typical of Alzheimer’s disease. Patients have difficulty with planning, sequencing, and multitasking. They become slow to respond, lose track of conversations, and struggle with decision-making. Family members often describe a progressive “dulling” rather than the specific memory lapses that characterize early Alzheimer’s.

Urinary symptoms typically begin as urgency and frequency before progressing to frank incontinence. The mechanism involves disruption of frontal lobe circuits that inhibit the micturition reflex. This symptom is frequently attributed to urological causes without considering a neurological origin.

Not every patient presents with all three features simultaneously. Gait disturbance alone, or gait disturbance combined with cognitive decline, should prompt consideration of NPH in any older adult—particularly when brain imaging shows enlarged ventricles.

How We Diagnose NPH

Accurate NPH diagnosis requires more than a single MRI report that mentions “ventriculomegaly.” Many conditions produce enlarged ventricles—cerebral atrophy from Alzheimer’s disease, prior stroke, chronic alcohol use—and the clinical question is whether the ventricular enlargement is the cause of the patient’s symptoms or a consequence of something else entirely.

Our evaluation begins with advanced neuroimaging. MRI sequences are reviewed for the hallmark findings of NPH: ventriculomegaly that is disproportionate to the degree of sulcal enlargement, narrowing of the callosal angle, periventricular white matter hyperintensities, and a patent cerebral aqueduct. These imaging features distinguish NPH from the ex vacuo ventriculomegaly of neurodegenerative disease. When indicated, PET scanning provides additional data on regional metabolic patterns that help differentiate NPH from Alzheimer’s disease.

The diagnostic cornerstone is the large-volume lumbar puncture—sometimes called a “tap test.” We remove 30 to 50 milliliters of CSF and perform standardized gait analysis and cognitive testing before and after the procedure. Improvement in gait speed, stride length, or cognitive scores following fluid removal is a powerful predictor of response to surgical shunting. Research by Wikkelso et al. (2013, published in Acta Neurologica Scandinavica) demonstrated that the tap test carries a positive predictive value exceeding 90 percent for shunt responsiveness when performed with quantitative outcome measures.

We also run metabolic and inflammatory lab panels to rule out concurrent conditions that can mimic or exacerbate NPH symptoms—thyroid dysfunction, B12 deficiency, chronic inflammatory states—and to establish a baseline for monitoring after treatment. Learn more about our diagnostic approach on our brain imaging page.

Our Diagnostic Approach

Every step of our NPH evaluation is designed to answer one question: will this patient improve with treatment?

Advanced Neuroimaging

MRI with targeted sequences to assess ventricular-to-sulcal ratio, callosal angle, aqueductal flow, and periventricular white matter changes. PET scanning when needed to differentiate NPH from concurrent neurodegenerative disease.

Large-Volume Lumbar Puncture

Removal of 30 to 50 mL of cerebrospinal fluid with standardized gait and cognitive testing before and after. Measurable improvement following fluid removal predicts shunt response with high accuracy.

Quantitative Gait Analysis

Timed walking tests, stride length measurement, and turn assessment performed under standardized conditions before and after the lumbar puncture. Objective gait data removes subjectivity from the diagnostic decision.

Cognitive Testing

Standardized neuropsychological screens administered before and after CSF removal to quantify changes in processing speed, attention, and executive function. These scores become part of the dataset presented to the neurosurgical team.

Metabolic & Inflammatory Labs

Comprehensive blood panels to rule out thyroid dysfunction, vitamin B12 deficiency, folate deficiency, and chronic inflammatory conditions that can mimic or worsen NPH symptoms. These labs also establish baseline values for post-treatment monitoring.

Neurosurgical Coordination

When our evaluation supports shunt candidacy, we compile the complete diagnostic package—imaging, tap test results, gait and cognitive data—and coordinate directly with a neurosurgical team. We follow the patient after surgery to monitor outcomes and adjust ongoing care.

Related Treatments

Memory Loss Evaluation

Comprehensive neurological evaluation for cognitive decline, including the diagnostic workup that differentiates treatable causes from progressive neurodegenerative disease.

Imbalance & Gait Disorders

Neurological assessment of walking difficulty, balance impairment, and fall risk. Gait disturbance is often the earliest and most prominent feature of NPH.

Brain Health Lab Panels

Metabolic, inflammatory, and nutritional blood panels that identify concurrent conditions affecting brain function and establish baselines for monitoring treatment response.

Frequently Asked Questions

What is normal pressure hydrocephalus?+
Normal pressure hydrocephalus is a condition in which cerebrospinal fluid accumulates in the brain's ventricles, enlarging them and compressing surrounding tissue, even though the measured CSF pressure on lumbar puncture may fall within the normal range. It produces a characteristic triad of gait difficulty, cognitive decline, and urinary incontinence. Unlike most causes of dementia, NPH can be treated — typically with a surgical shunt that diverts excess fluid away from the brain.
How is NPH different from Alzheimer's disease?+
NPH and Alzheimer's disease share overlapping symptoms — memory impairment, slowed thinking, and difficulty with daily tasks — which is why NPH is frequently misdiagnosed as Alzheimer's. The critical difference is that NPH is potentially reversible with treatment, while Alzheimer's is not. NPH also tends to present with prominent gait disturbance and urinary symptoms early in its course, whereas Alzheimer's typically begins with isolated memory loss. MRI findings also differ: NPH shows ventricular enlargement out of proportion to the degree of cortical atrophy, a pattern distinct from the diffuse atrophy seen in Alzheimer's.
What diagnostic tests does The Neurogenesis Project use for NPH?+
We begin with advanced neuroimaging — MRI with specific sequences to evaluate ventricular size relative to sulcal width, assess for periventricular white matter changes, and rule out obstructive causes. The cornerstone of our diagnostic process is the large-volume lumbar puncture, in which we remove 30 to 50 milliliters of cerebrospinal fluid and perform standardized gait and cognitive testing before and after the procedure. Measurable improvement in walking speed, stride length, or cognitive scores after fluid removal is a strong predictor that the patient will respond to surgical shunt placement.
Does The Neurogenesis Project perform shunt surgery?+
No. We are a diagnostic neurology practice, not a neurosurgical center. Our role is to identify NPH accurately, differentiate it from conditions that mimic it, and determine through objective testing whether a given patient is likely to benefit from shunt surgery. When our evaluation supports a shunt candidacy, we coordinate the referral to a neurosurgeon and provide the diagnostic data they need to proceed with confidence. We also follow patients after shunt placement to monitor cognitive and functional outcomes.
Why is NPH so often missed?+
Several factors contribute. The symptoms of NPH — unsteady gait, memory problems, urinary urgency — overlap with conditions that are far more common in older adults, including Alzheimer's disease, Parkinson's disease, cervical myelopathy, and age-related bladder dysfunction. Many clinicians attribute these symptoms to aging itself. Additionally, the name 'normal pressure' hydrocephalus is misleading — it implies nothing is wrong with CSF dynamics, when in fact the intermittent pressure waves and impaired CSF absorption driving the condition simply do not produce a sustained elevated reading on a single lumbar puncture measurement.
What happens if NPH is not treated?+
Untreated NPH follows a progressive course. Gait instability worsens, increasing the risk of falls and fractures. Cognitive decline deepens, often to the point of frank dementia. Urinary incontinence becomes persistent. Over time, the ventricular enlargement compresses white matter tracts and cortical structures, and some of this damage becomes irreversible. The longer NPH goes undiagnosed, the less likely the patient is to experience full recovery after shunt placement. Early identification is the single most important factor in treatment outcome.

Dementia Is Not Always Permanent

If you or a family member has been diagnosed with dementia or Alzheimer’s disease and also experiences difficulty walking or urinary problems, normal pressure hydrocephalus should be ruled out before that diagnosis is accepted as final. Dr. Orr and the team at The Neurogenesis Project provide the diagnostic evaluation that most neurology practices skip.

Schedule Your EvaluationCall (912) 268-3097