Neuroinfections in children

Meningitis and its intracranial complications

In uncomplicated bacterial meningitis, CT and MRI are usually normal or show mild meningeal contrast enhancement; therefore, they are not used as primary tests. Scanning is indicated only in cases of unclear diagnosis, persistent seizures, focal neurological deficits, or signs of increased intracranial pressure.

Infection can enter the cranial cavity via five pathways: contiguous spread (sinusitis, otitis), hematogenous spread, via the choroid plexus (choroid plexus), rupture of a cortical abscess, or as a result of open trauma.

The main intracranial complications include:

• Vascular disorders: Venous and arterial infarctions occur in one-third of infants with meningitis. Arterial thrombosis results from inflammation of the vessel wall (e.g., in the basal cisterns), while venous thrombosis is frequently associated with subdural empyema.
• Hydrocephalus: Fibro-purulent masses in the cisterns or ventricular foramina disrupt CSF flow and resorption, causing communicating or obstructive hydrocephalus.
• Ventriculitis: Inflammation of the ependyma with accumulation of purulent debris in the ventricles (often settling in the occipital horns). It can lead to loculation (isolation) of individual parts of the ventricular system.

Subdural collections: effusion or empyema?

Differentiating between these two conditions is critical for choosing the appropriate management strategy.

1. Sterile subdural effusions are a frequent reactive complication of meningitis (especially caused by pneumococcus or Haemophilus influenzae). On CT density and MRI signal, they are identical to CSF. Effusions do not require surgical intervention and resolve with antibiotic therapy.
2. Subdural empyemas are purulent collections with a high protein content. On CT, they are hyperdense compared to CSF; on MRI, they show a high T2 signal and pachymeningeal and leptomeningeal contrast enhancement. Empyemas can provoke brain infarction and require urgent surgical drainage.

Suppurative inflammation of the parenchyma: from cerebritis to abscess

The formation of a purulent focus in brain tissue goes through several stages, and the imaging findings directly depend on the stage of the process.

Cerebritis represents the early stage of purulent inflammation. On CT and MRI, it appears as a diffuse, poorly defined area of edema with mass effect and blurred contrast enhancement. At this stage, the condition may resolve with antibiotics.

As the condition progresses, an abscess forms. Its characteristic radiological signs are:

• A well-defined mass lesion with ring-like contrast enhancement along the capsule.
• The central zone (pus) is hyperintense on T2-weighted images and, crucially, restricts diffusion (unlike necrosis in tumors, where diffusion is elevated).
• Pronounced surrounding perifocal edema.

Specific infections and viral encephalitides

Each type of pathogen may have its own "predilection" sites, which aids in differential diagnosis:

• Viral encephalitides: Classically affect the gray matter asymmetrically. Herpetic encephalitis is localized in the anterior temporal and inferior frontal lobes. Enteroviruses cause extensive hemispheric lesions, while Japanese encephalitis affects the thalami and brainstem.
• Tuberculosis: Characterized by dense, contrast-enhancing basal exudates. Frequently complicated by hydrocephalus and infarctions of the deep nuclei due to involvement of perforating arteries. Tuberculomas may be detected in the parenchyma.
• Neurocysticercosis: Infestation by the pork tapeworm (Taenia solium). Cysts are typically located at the gray-white matter junction. MRI may reveal the scolex within the cyst, perifocal edema (a response to larval death), and punctate calcifications ("burned-out" lesions).
• Congenital infections: HIV encephalopathy is typically characterized by basal ganglia calcification and global atrophy. TORCH infections may manifest as severe malformations (Dandy-Walker malformation) and ocular subatrophy (phthisis bulbi).

CNS inflammation: ADEM vs. Multiple Sclerosis

Acute disseminated encephalomyelitis (ADEM) is an immune-mediated post-infectious disorder that must be differentiated from multiple sclerosis.

Brain MRI in ADEM reveals multiple asymmetric areas of demyelination with subcortical white matter edema. Unlike multiple sclerosis, ADEM frequently involves the cerebral cortex, and the process is monophasic (follow-up scans show no new lesions, and old ones resolve). Classic multiple sclerosis lesions in the corpus callosum ("Dawson's fingers") are not typical for ADEM.

Class and exam questions

What else to study on this topic

• Imaging features in immunocompromised children (fungal infections)
• Ventriculitis: pathways of spread and consequences for the ventricular system
• Deep dural venous sinus thrombosis: staging by MRI signal intensity
• Acute cerebellitis: clinical presentation, etiology, and indications for CSF drainage
• Autoantibody-associated demyelinating diseases (MOG and aquaporin-4)

Other Topics in "Pediatric Diagnostic Radiology"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.