Mechanisms of development and forms
Depending on the mechanism of impaired CSF dynamics and the level of obstruction, several variants of hydrocephalus are distinguished.
Extraventricular obstructive (communicating) hydrocephalus occurs secondary to prior hemorrhages, infections (due to the accumulation of proteinaceous cellular debris), dissemination of malignant tumors, as well as venous hypertension or decreased arterial compliance. On CT and MRI scans, the picture ranges from pronounced dilatation of the ventricles and sulci to a complete absence of visual abnormalities.
Interestingly, CSF hyperproduction causes ventricular dilatation extremely rarely. This mostly occurs in choroid plexus papillomas. However, even these neoplasms more frequently cause obstruction due to mass effect or hemorrhages. When unexplained dilatation of CSF spaces is detected, spinal cord imaging is recommended to rule out an occult oncologic process causing dissemination along the leptomeninges.
Age-related features and benign expansion
In children under two years of age, the subarachnoid spaces and brain ventricles are normally wider than in adults. This physiological feature must not be mistaken for atrophy or hydrocephalus.
Often, neurologically healthy infants exhibit benign enlargement of the subarachnoid spaces. This is due to the cranial bones growing faster than the brain develops (head circumference frequently exceeds the 95th percentile). As a rule, proportions normalize by the age of two.
The main criteria for distinguishing this condition from pathological subdural collections are:
- Presence of crossing veins within the expanded space.
- Complete absence of mass effect on the adjacent brain parenchyma.
During the second decade of life, the ventricles and sulci become visually less prominent. This is a normal process that should not be confused with cerebral edema; however, it is important to remember that basal cisterns in a healthy child should never be effaced.
Levels of ventricular system obstruction
CSF flow block in structural obstructive hydrocephalus most commonly occurs at anatomically narrow sites:
- Foramina of Monro. May be obstructed by suprasellar tumors, colloid and arachnoid cysts, as well as subependymal giant cell astrocytomas (a characteristic finding in tuberous sclerosis).
- Cerebral aqueduct (Sylvian aqueduct). Its stenosis can be congenital (developmental anomalies, membranes) or acquired (gliosis following intraventricular hemorrhage). Sagittal MRI reveals localized narrowing and posterior displacement of the superior colliculi plate. The lateral and third ventricles dilate, while the fourth ventricle remains normal.
- Outflow foramina of the fourth ventricle. Typical localization of obstruction in Chiari II malformation (Chiari II). In this anomaly, the foramina are displaced into the spinal canal, where CSF absorption is impaired.
Evaluation of shunts and ventriculostomy
The mainstay of treatment is surgical diversion of fluid (placement of an external ventricular drain, ventriculoperitoneal shunt, or endoscopic third ventriculostomy).
To check the integrity of the shunting system, plain radiography (skull-to-pelvis) or CT scout view is used. In case of tubing fracture, the fragments separate, and calcification may appear at their ends due to localized inflammation and fibrosis.
Patency of a surgical ventriculostomy is evaluated using MRI. On T2-weighted images (T2WI), a functioning stoma appears as areas of signal void due to rapid CSF flow (flow voids) into the suprasellar cistern.
Shunt complications
Shunt placement carries specific risks, with an infection rate of approximately 1–5%.
- Ventriculitis. Severe inflammation of the ventricular ependyma. On CT, the ependyma appears hyperdense, shows contrast enhancement (ependymal enhancement), and debris is visualized within the ventricles. Inflammation may spread to the brain parenchyma (cerebritis).
- Abdominal complications. Pseudocysts can form around the distal shunt tip in the peritoneal cavity, and ascites or bowel perforation may develop.
- Slit ventricle syndrome (Slit ventricle syndrome). A rare condition: a shunted patient develops symptoms of intracranial hypertension, yet the ventricles remain small. The causes lie in overdrainage or the formation of rigid, non-compliant ventricular walls.
Briefly: answers to topical questions
What radiologic signs and symptoms are characteristic of normal pressure hydrocephalus on brain MRI?
Normal pressure hydrocephalus is characterized by a specific clinical presentation and signs of communicating hydrocephalus on MRI.
Symptoms of the disease:
- Pelvic disorders — urinary urge incontinence.
- Gait disturbances — gait instability, wide-based gait, frequent falls, difficulty lifting feet off the floor, and gait apraxis.
- Cognitive impairment — progressive memory loss and inattention.
Radiological signs:
- Pathology type — normal pressure (communicating) hydrocephalus.
- Scanning sequences — T2-weighted image with FLAIR sequence.
Class and exam questions
Is the "copper-beaten skull" sign a reliable indicator of hydrocephalus?
No, according to current data, erosion of the dorsum sellae and the "copper-beaten skull" sign on skull radiographs are considered unreliable classical signs.
How to differentiate a subdural collection from benign enlargement of the subarachnoid spaces?
Benign enlargement shows a complete absence of mass effect on the brain parenchyma, and crossing veins are clearly visualized within the subarachnoid space itself on MRI.
What are flow voids and why look for them postoperatively?
This is the phenomenon of MRI signal loss on T2WI due to rapid CSF flow. Its presence in the created third ventricle floor stoma confirms ventriculostomy patency.
What else to study on this topic
- MRI findings and complications of neonatal ventriculitis
- Neuroimaging specifics in Chiari II malformation
- Slit ventricle syndrome: pathophysiology and CT diagnosis
- Causes of intracranial venous hypertension
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