The four types of hydrocephalus are communicating, non-communicating (obstructive), normal pressure hydrocephalus (NPH), and hydrocephalus ex-vacuo. Each involves enlarged fluid-filled spaces in the brain, but they differ in what causes the buildup, who they typically affect, and how they’re treated. Hydrocephalus occurs in roughly 1 in every 1,000 births in high-income countries, though it can also develop later in life from injury, infection, or aging.
Your brain constantly produces cerebrospinal fluid (CSF), a clear liquid that cushions the brain, delivers nutrients, and carries away waste. This fluid circulates through a series of connected chambers called ventricles, then gets absorbed back into the bloodstream. Hydrocephalus develops when something disrupts that cycle, whether the fluid can’t drain, can’t be absorbed, or the brain tissue itself shrinks and leaves extra space.
Communicating Hydrocephalus
In communicating hydrocephalus, fluid moves freely through the ventricles but isn’t absorbed properly once it exits. The problem lies at the absorption site: tiny structures on the brain’s surface that normally pull CSF back into the bloodstream stop working efficiently. Fluid keeps being produced at the normal rate, but with nowhere to go, pressure builds and the ventricles expand.
The most common triggers are conditions that irritate or scar the brain’s surface membranes. Bleeding around the brain (subarachnoid hemorrhage), bacterial meningitis, and complications from brain surgery can all damage the absorption pathways. In some cases, no clear cause is ever identified. This type can develop at any age, from newborns to older adults, and the speed of onset varies widely depending on how severely absorption is impaired.
In infants, whose skull bones haven’t yet fused, the head may enlarge noticeably as fluid accumulates. The soft spot on top of the head can bulge, and the eyes may appear to gaze downward, a sign sometimes called “sunsetting.” In older children and adults, symptoms tend to involve headaches, nausea, vision problems, and difficulty with balance or coordination, because the rigid skull can’t expand to accommodate the extra fluid.
Non-Communicating (Obstructive) Hydrocephalus
Non-communicating hydrocephalus happens when something physically blocks CSF from flowing between the ventricles. The fluid is being produced and could theoretically be absorbed, but a barrier prevents it from reaching the absorption site. This creates a backup, like water building behind a dam.
The blockage most commonly occurs at a few narrow points in the ventricular system: the passages connecting the first two ventricles to the third, the narrow channel connecting the third ventricle to the fourth (called the aqueduct of Sylvius), or the exits from the fourth ventricle. Because these passages are already small, even a modest obstruction can cause significant fluid buildup. On brain imaging, a blocked aqueduct produces a characteristic pattern where the front portions of the ventricles balloon outward.
Tumors are the most frequent cause. Growths in the back of the brain are especially likely to trigger this type because of their proximity to narrow drainage pathways. Cysts, congenital narrowing of the aqueduct, and scarring from infections or bleeding can also create blockages. Congenital aqueduct stenosis, where a baby is born with an abnormally narrow connecting channel, is one of the leading causes of hydrocephalus in newborns. Non-communicating hydrocephalus often develops more rapidly than the communicating form because a complete blockage stops flow entirely rather than just slowing absorption.
Normal Pressure Hydrocephalus (NPH)
Normal pressure hydrocephalus is a unique form that primarily affects adults over 60. The ventricles enlarge, but CSF pressure measurements come back in the normal range, which is part of why it’s so often misdiagnosed. The exact mechanism is still debated, but it likely involves a gradual failure of fluid absorption that the brain partially compensates for, keeping pressure relatively stable even as ventricles slowly expand and compress surrounding tissue.
NPH produces a distinctive trio of symptoms. Walking problems come first in most cases: a slow, wide-based, shuffling gait that looks like the person’s feet are stuck to the floor. Cognitive decline follows, typically affecting attention, processing speed, and the ability to plan or organize rather than memory loss in the early stages. Urinary urgency and eventually incontinence round out the pattern. Not everyone develops all three symptoms, and because each one individually overlaps with other conditions common in older adults (Parkinson’s disease, Alzheimer’s, prostate problems), NPH frequently goes unrecognized.
What makes NPH especially important to identify is that it’s one of the few causes of dementia-like symptoms that can be reversed with treatment. A surgically placed shunt that redirects excess fluid can significantly improve walking and cognition, particularly when the condition is caught early. In people with NPH, the Evans index, a ratio comparing ventricle width to skull width on a brain scan, typically measures around 0.36, well above the 0.3 threshold that suggests abnormal enlargement.
Hydrocephalus Ex-Vacuo
Hydrocephalus ex-vacuo is not a true hydrocephalus. The ventricles appear enlarged on brain imaging, but the cause isn’t excess fluid or blocked drainage. Instead, the brain tissue itself has shrunk, and the ventricles passively expand to fill the empty space. There’s no increased pressure and no disruption of normal fluid circulation.
This happens after events that destroy brain tissue: strokes, traumatic brain injuries, or degenerative diseases like Alzheimer’s. As damaged or atrophied brain tissue breaks down and shrinks, the ventricles grow larger simply because there’s less brain surrounding them. The National Institute of Neurological Disorders and Stroke describes it as a hydrocephalus “look-alike” condition. It matters because it can show up on a brain scan and mimic the appearance of other types, potentially leading to unnecessary treatment. The key difference is that draining fluid won’t help, because the problem isn’t fluid buildup. Treatment focuses instead on managing the underlying condition that caused the brain tissue loss.
How Hydrocephalus Is Diagnosed
Diagnosis starts with brain imaging, typically a CT scan or MRI. Doctors measure the Evans index to determine whether the ventricles are abnormally large. This ratio compares the widest point of the front ventricle chambers to the widest internal diameter of the skull. A value above 0.3 has traditionally been the cutoff for diagnosing ventriculomegaly, though this threshold has limitations. Healthy adults over 80 can naturally have an Evans index at or slightly above 0.3 due to normal age-related brain shrinkage, so the number has to be interpreted in context.
Distinguishing between types requires looking at the pattern of enlargement and the clinical picture. If only certain ventricles are enlarged while others are normal-sized, that points toward a blockage (non-communicating type). If all ventricles are uniformly enlarged, communicating hydrocephalus or NPH is more likely. For suspected NPH, a large-volume spinal tap that temporarily removes fluid can serve as a diagnostic test: if walking and thinking improve noticeably in the hours or days afterward, it’s a strong sign that a permanent shunt would help.
Treatment and What to Expect
For communicating and non-communicating hydrocephalus, the most common treatment is a shunt, a thin tube placed surgically that diverts excess CSF from the brain to another part of the body (usually the abdominal cavity) where it can be absorbed naturally. Shunts are effective but not problem-free. Infection rates range from about 5% to 13% after placement, and shunt malfunction over time is common enough that many people require at least one revision surgery during their lifetime. Infections account for roughly 21% of all shunt revision procedures.
For non-communicating hydrocephalus specifically, an alternative procedure creates a small opening in the floor of the third ventricle, allowing fluid to bypass the blockage entirely without implanting hardware. This approach avoids the long-term complications of a shunt but isn’t suitable for every patient or every type of obstruction.
NPH treatment follows the same shunt approach, though outcomes depend heavily on timing. People treated earlier in the disease course, particularly those whose primary symptom is gait difficulty rather than advanced cognitive decline, tend to see the most improvement. Hydrocephalus ex-vacuo doesn’t require shunting at all, since the enlarged ventricles aren’t causing the symptoms. Management targets whatever caused the brain tissue loss in the first place.