Communicating hydrocephalus is a condition where cerebrospinal fluid (CSF) builds up in the brain’s ventricles because it can’t be properly absorbed after leaving them. Unlike other forms of hydrocephalus, the passageways between the ventricles remain open, so fluid flows freely within the brain’s internal chambers. The problem lies downstream, in the spaces surrounding the brain where CSF is normally reabsorbed into the bloodstream.
How CSF Normally Flows and Where It Goes Wrong
Your brain constantly produces cerebrospinal fluid, a clear liquid that cushions the brain, delivers nutrients, and carries away waste. This fluid circulates through four connected chambers called ventricles, then exits into the subarachnoid space, a thin layer surrounding the brain and spinal cord. From there, tiny structures called arachnoid granulations act like one-way valves, draining CSF back into the bloodstream.
In communicating hydrocephalus, those drainage structures become damaged or blocked. CSF keeps being produced at a normal rate but can’t be absorbed fast enough, so pressure builds and the ventricles expand. The term “communicating” simply means the ventricles still connect to each other normally. The blockage happens after the fluid has already exited the ventricular system.
What Causes It
The two most common triggers are subarachnoid hemorrhage (bleeding into the space around the brain) and meningitis (infection of the brain’s protective membranes). Both cause inflammation and scarring that can clog the drainage pathways. Other causes include head trauma, brain surgery, and congenital defects present from birth. In one documented case, even severe air pressure buildup inside the skull after a fracture damaged enough of the subarachnoid space to trigger the condition.
When no identifiable cause can be found, the condition is classified as idiopathic. This is especially common in older adults, where it takes the form of normal pressure hydrocephalus, the most common type of hydrocephalus in adults.
Normal Pressure Hydrocephalus: A Special Case
Normal pressure hydrocephalus (NPH) is a subtype of communicating hydrocephalus that develops gradually in older adults. The ventricles enlarge, but CSF pressure measured during a spinal tap often falls within a normal range, which makes it tricky to diagnose. It’s one of the few treatable causes of dementia, which makes catching it early especially important.
NPH produces a characteristic set of three symptoms, sometimes called the Hakim-Adams triad: difficulty walking, cognitive decline, and urinary problems. The full triad appears in 50% to 75% of patients. Walking difficulty is the most common symptom, showing up in 80% to 95% of cases, and it’s typically the first to appear. Over time, the gait becomes slow, shuffling, and wide-based, with feet that seem glued to the floor. Urinary symptoms, present in 50% to 75% of patients, usually begin as sudden urgency and frequency before progressing to full incontinence.
The cognitive changes in NPH look different from Alzheimer’s disease. Instead of the memory loss and language problems typical of Alzheimer’s, NPH tends to cause mental slowness, poor attention, difficulty with planning and organizing, and a general sense of apathy or inertia. These are signs of disruption to the brain’s frontal regions and deeper structures rather than the cortical damage seen in Alzheimer’s.
Symptoms in Acute Cases
When communicating hydrocephalus develops rapidly, such as after a hemorrhage or infection, symptoms are more dramatic. Severe headaches, nausea, vomiting, vision changes, and difficulty staying awake can develop over hours to days as pressure inside the skull climbs. In infants, whose skull bones haven’t yet fused, the head may visibly enlarge. Acute cases require urgent treatment to prevent permanent brain damage.
How It’s Diagnosed
Brain imaging with MRI or CT is the starting point. Doctors look for enlarged ventricles that are out of proportion to the rest of the brain. The standard measurement is the Evans’ Index: the widest point of the front portion of the ventricles divided by the widest internal diameter of the skull at the same level. A ratio greater than 0.3 indicates ventriculomegaly, or abnormally large ventricles.
One key challenge is distinguishing communicating hydrocephalus from enlarged ventricles caused by brain shrinkage, which can happen in Alzheimer’s disease and other neurodegenerative conditions. When the brain atrophies, the ventricles passively expand to fill the space, a condition sometimes called hydrocephalus ex vacuo. On imaging, the two look quite different. In true hydrocephalus, the expanding ventricles compress the top of the brain, narrowing the grooves along the upper surface of the skull and widening the gaps near the base. In brain atrophy, the grooves are uniformly widened everywhere because the brain is shrinking evenly. The angle at which the ventricles meet at the top of the brain is also telling: it’s noticeably sharper in hydrocephalus (averaging around 87 degrees) compared to atrophy (around 111 degrees).
For suspected NPH, a lumbar tap test helps predict whether treatment will work. A doctor removes 30 to 50 mL of spinal fluid through a needle in the lower back, and the patient’s walking is tested before and after. An improvement in walking speed of 10% or more is considered a positive result, suggesting the patient will respond well to surgical treatment.
Treatment With Shunts
The primary treatment for communicating hydrocephalus is a shunt, a thin tube system that drains excess CSF from the brain’s ventricles to another part of the body where it can be absorbed. The most common type is a ventriculoperitoneal (VP) shunt, which routes fluid to the abdominal cavity. The system has three parts: a catheter placed in a ventricle, a valve that controls flow, and a second catheter running under the skin to the abdomen.
Modern shunts use programmable valves, a significant improvement over older fixed-pressure designs. These valves can be adjusted from outside the body using a magnetic device placed against the scalp, letting doctors fine-tune how much fluid drains without additional surgery. This is particularly useful because the ideal drainage rate can change over time or differ between sitting and lying positions. Many shunt systems also include an antisiphon device that prevents too much fluid from draining when you stand up, which could otherwise cause headaches and other problems from overdrainage.
For NPH specifically, walking difficulty is typically the first symptom to improve after shunt placement. Cognitive symptoms may also improve, though the degree of recovery depends on how long the condition went untreated.
Shunt Complications and Long-Term Outlook
Shunts are effective but not without problems. About 22% of patients need at least one shunt revision over time, most commonly because the catheter becomes blocked, disconnected, or shifts out of position. The risk is highest in the first year, with roughly 21 complications per 100 patients during that period. By the second year, the rate drops to about 6 per 100, and by the fifth year, it falls to about 2.5 per 100.
Infection is the most serious short-term risk, occurring in about 6% of cases. Symptoms of a shunt infection include fever, redness or swelling along the tubing path, and a return of hydrocephalus symptoms. Overdrainage can cause headaches that worsen when standing and improve when lying down, though programmable valves have made this easier to manage without reoperation.
Living with a shunt means staying alert to signs of malfunction. A sudden return of headaches, balance problems, confusion, or nausea can signal that the shunt has stopped working properly. Most people with well-functioning shunts, however, return to their normal daily activities and require only periodic follow-up imaging to monitor ventricle size.