The Emergency Department Patient You’re Already Seeing
An older adult male arrives after “just another fall.” Family members report that the patient is “slowing down” and seems mildly confused. There have been frequent falls and his gait is worse, especially when trying to turn. You order a head CT, consider trauma or stroke, and move on.
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ACEP Now: June 2026 (Digital)Hidden in that familiar presentation is one of the few truly reversible causes of what is often labeled “dementia:” idiopathic normal pressure hydrocephalus (iNPH). Population data suggest that 3.7 percent of adults over age 65, and nearly 9 percent of those over age 80, meet criteria for probable iNPH, yet only a small fraction is ever diagnosed or treated.
Why This One Is Worth Finding
Most dementias that present to the emergency department (ED)—Alzheimer’s disease, Lewy body dementia, frontotemporal dementia—are proteinopathies that progressively destroy cortex and are not reversible. iNPH is fundamentally different. It is a disorder of cerebrospinal fluid hydrodynamics: impaired absorption and altered intracranial compliance lead to ventriculomegaly despite normal opening pressure.
That mechanical pathophysiology makes iNPH uniquely amenable to shunting. In appropriately selected patients, draining excess ventricular CSF through a shunt leads to meaningful improvement in gait and function for most, with reduced fall risk and delayed nursing home placement compared with conservative management. Your role is not to decide who gets a shunt; it is to recognize the pattern and ensure referral to someone who can.
Think “Gait-First,” Not “Memory-First”
In the ED, cognitive complaints in older adults most often reflect delirium superimposed on baseline impairment, infection, or medication effects. iNPH is missed when the story is prematurely closed as “urinary tract infection and dementia,” or dismissed as inevitable aging.
A simple forcing question helps: Is there a gait-first syndrome here? In iNPH, gait disturbance appears early and dominates; cognitive changes and urinary symptoms follow. When families describe months of progressive gait dysfunction and recurrent falls with only modest early cognitive decline, iNPH deserves a prominent place on your differential.
Your Best Test: Watch Them Walk
The classic triad—gait disturbance, cognitive impairment, and urinary symptoms—is colloquially known as “wobbly, wacky, and wet,” a mnemonic widely used among clinicians. While the phrase reduces the lived experience of these patients to dismissive shorthand, gait is the most discriminating feature in the ED.
The characteristic iNPH gait is:
- Broad-based;
- Short-stepped;
- “Magnetic,” with reduced foot clearance and the appearance of feet stuck to the floor; and
- Marked-start hesitation, with turning accomplished by multiple small steps rather than a pivot.
Notably, the gait impairment is often far more dramatic than limb strength testing on the stretcher would predict.
Contrast this with common alternative gait patterns encountered in the ED (see Table 1 below):
- Antalgic (pain-avoidance) gait: Suggests a pain generator
- Narrow-based shuffling with tremor and rigidity: Parkinson’s disease
- Spastic gait with hyperreflexia: Cervical myelopathy
- True limb ataxia with nystagmus: Cerebellar disease or intoxication
A practical ED maneuver is simply to have the patient walk 10–20 feet, turn, and return, when safe. If time permits, a Timed Up and Go test longer than approximately 20 seconds is clearly abnormal, and a 10-meter walk speed under 0.6 m/s indicates substantial impairment. Even without formal testing, a single focused sentence describing base width, step length, initiation, and turning can be invaluable to consulting neurologists or neurosurgeons.
Table 1: How iNPH Differs from Common Mimics
| Feature | iNPH | Alzheimer’s disease | Vascular Dementia | Parkinson’s disease |
|---|---|---|---|---|
| Pathophysiology | CSF hydrodynamic dysfunction with impaired absorption and ventriculomegaly. | Amyloid and tau–mediated cortical neurodegeneration. | Cerebrovascular disease with white matter ischemia and lacunar infarcts. | Alpha-synuclein pathology with dopaminergic neuron loss. |
| Reversibility | ~80% improve or stabilize (gait>dementia) with ventricular shunt. | Not reversible; symptomatic therapy only. | Not reversible; focus on vascular risk modification. | Not reversible; dopaminergic therapy for motor symptoms. |
| Earliest predominant symptom | Gait disturbance (broad based, magnetic, short stepped). | Episodic memory loss and word finding difficulty. | Variable; often executive dysfunction, slowed processing, often stepwise decline. | Resting tremor, bradykinesia, rigidity. |
| Gait pattern | Broad-based, magnetic, reduced foot clearance, multistep turning. | Often near normal until late stages. | Variable; may be cautious, hemiparetic, or apraxic. | Narrow-based, shuffling, festinating with reduced arm swing. |
| Cognitive profile | Subcortical: psychomotor slowing, executive dysfunction, apathy, memory relatively preserved early. | Cortical: early amnestic deficit with later language and visuospatial loss. | Subcortical/mixed: executive dysfunction and slowed processing speed; patchy deficits. | Subcortical: bradyphrenia, executive dysfunction, hallucinations with PD dementia. |
| Urinary symptoms | Early urgency and frequency progressing to incontinence; follows gait abnormality. | Usually late and functional incontinence in advanced disease. | Variable; often related to comorbidities. | Autonomic dysfunction may cause urgency; usually later. |
| CT/MRI findings | Disproportionate ventriculomegaly; Evans index ≥0.30; tight high-convexity sulci (DESH); limited cortical atrophy. | Diffuse cortical and hippocampal atrophy; proportional ventricular enlargement. | White matter hyperintensities, lacunar infarcts; cortical atrophy; proportional ventricular enlargement. | Often normal or mild generalized atrophy; no disproportionate ventriculomegaly. |
| Time course | Insidious over months; gait first, then urinary, then cognitive. | Gradual decline over years; memory first. | Stepwise or gradual; linked to vascular events. | Gradual; motor symptoms precede dementia by years. |
Use the Triad, but Focus on Its Sequence
Most frail older adults present with some combination of gait difficulty, bladder symptoms, and cognitive complaints. What distinguishes iNPH is the quality and temporal sequence of these features.
Cognitive impairment in iNPH is typically subcortical, i.e., psychomotor slowing, poor attention, apathy, and executive dysfunction, rather than the early amnestic syndrome of Alzheimer’s disease. Urinary symptoms usually begin with urgency and frequency, progressing later to incontinence. They tend to follow gait impairment but precede severe cognitive decline, unlike other dementias in which incontinence signals advanced disease.
The course is insidious over months, helping distinguish iNPH from delirium (hours to days) and from the stepwise decline of pure vascular dementia, which may also coexist with iNPH.
Don’t Let Ventriculomegaly Be Hand-Waved Away
You are already ordering non-contrast head CTs on these patients. When iNPH is on your radar, that CT becomes your second critical data point. The essential concept is simple: ventricles that are too large for the degree of cortical atrophy present.
Radiologists often quantify this using the Evans index—the ratio of maximal frontal horn width to inner skull diameter—with values greater than or equal to 0.30 supporting ventricular enlargement. A complementary pattern, disproportionately enlarged subarachnoid space hydrocephalus (DESH), characterized by tight high-convexity sulci and enlarged Sylvian fissures, increases specificity for iNPH. In contrast, Alzheimer’s disease and vascular dementias show diffuse cortical atrophy with proportionate ventricular enlargement.
You do not need to calculate the Evans index in the ED. You can, however, ask the radiologist about it and document clearly: “Ventriculomegaly disproportionate to sulcal atrophy; CT pattern compatible with possible iNPH.”
What “Screen-Positive” Looks Like in the ED
You are not diagnosing iNPH or selecting patients for shunting. You are screening, documenting, and referring (see figure 1). A reasonable screen-positive ED profile includes:
- Objective gait disturbance with recent falls or mobility decline; and
- CT evidence of ventriculomegaly not fully explained by diffuse cortical atrophy.
Subcortical cognitive slowing or new urinary urgency/incontinence is common but not required.
When these elements align, name the possibility. Your consult or discharge documentation should include:
- A concise gait description, including turning;
- The sequence and approximate timing of gait, urinary, and cognitive symptoms;
- Specific CT language raising concern for iNPH; and
- A direct recommendation for neurology or neurosurgery follow-up for evaluation, including consideration of a high-volume lumbar tap with formal pre- and post-tap gait assessment.
For patients and families, it is helpful to frame iNPH not as an inevitable consequence of aging but as a potentially reversible condition, akin to a slow, correctable plumbing problem in the brain’s drainage system. Recognizing iNPH is a matter of justice in geriatric emergency care: it counters diagnostic ageism and preserves access to a life-altering intervention for many of our patients.
Dr. Iserson is professor emeritus in the department of emergency medicine at the University of Arizona, Tucson, AZ.






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