Infectious and Inflammatory Conditions

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Meningitis is the most common CNS infection affecting children. The diagnosis of meningitis is based on the analysis of CSF, obtained by lumbar puncture; the absence of inflammatory changes such as leptomeningeal enhancement on CT or MRI must not be used to exclude this diagnosis. Affected children present with fever, irritability, lethargy, headaches and nuchal rigidity; seizures, cranial neuropathies or stroke may develop. Imaging is performed mainly for the evaluation of children who are deteriorating neurologically despite apparently appropriate antibiotic therapy, in order to determine the cause of deterioration.

Complications of meningitis include hydrocephalus, cerebral infarction, subdu-ral effusion or empyema, cerebritis and cerebral abscess. Sterile subdural fluid collections are not uncommon in the setting of meningitis and do not usually require surgical intervention. However, if seeded with bacteria, they can be transformed into infected collections (empyemas), which require drainage. Paranasal sinusitis, mastoiditis, otitis media, calvarial osteomyelitis and orbital cellulitis are other causes of empyema. On CT and MRI, both effusions and empyemas appear as peripherally enhancing extra-axial low-intensity fluid collections. They are most frequently located along the frontal and temporal lobes. Empyemas are typically unilateral, have a thick rim of enhancement, and may also have internal septations and locula-tions. Cerebritis can be seen in underlying brain parenchyma in both effusions and empyemas, and has the appearance of local edema (hypodensity on CT, and low T1 and high T2 signal on MRI) with variable contrast enhancement. Progression of cerebritis eventually leads to abscess formation. Cerebral abscesses appear as fluid collections with a thin, smooth rim of peripheral enhancement on CT and MRI (Fig. 10). Their central contents are hypodense on CT but have variable signal intensity on MRI depending the age of the abscess. Necrotic glial neoplasms, resolving hematomas, and metastases can, in rare instances, mimic an abscess.

Granulomatous meningitides, such as those seen in CNS tuberculosis, fungal infections and sarcoidosis, will often cause thick meningeal enhancement that may fill the basal cisterns. Granulomas, represented by foci of T2

hyperintensity and parenchymal en. . . Figure 10. Brainstem abscess. Well-

hancement, or true abscesses can also defined, peripherally enhancing fluid develop in tuberculosis and fungal in- collection located in the midbrain and fections. pons. (sagittal T1-WI with contrast)

Figure 11. ADEM. Numerous scattered foci of T2-hyperintensity in the subcortical white matter, right thalamus and bilateral cerebellum. No significant mass effect. (transaxial T2-WI)

Viral encephalitis encompasses a heterogeneous group of viruses with a predilection for invading the CNS. Some examples include herpes simplex, herpes zoster, mumps, coxsackie, rabies and polio. These typically cause focal areas of edema (hypodensity on CT, and low T1 and high T2 signal on MRI) accompanied by gyral and/or meningeal enhancement. Herpes simplex encephalitis is the most common cause of meningoencepha-litis in the U.S., and has a preference for involving the anterior and medial temporal lobes and inferior frontal lobes (particularly the cingulum). It can be unilateral or bilateral, and frequently results in hem-orrhagic necrosis. Herpes zoster, coxsackie and polio, and Epstein-Barr viruses have been shown to cause acute cerebellitis. Other causes of bilateral cerebellar edema include demyelinating disease and cyanide and lead poisoning.

Demyelinating disorders, such as acute disseminated encephalomyelitis (ADEM) and multiple sclerosis (MS) can have clinical and imaging presentations that are very similar to those of vasculitis and collagen vascular diseases. ADEM is an autoimmune demyelinating encephalomyelitis that typically begins several days after onset of a viral (e.g., varicella) or bacterial infection, or following a vaccination. Initial symptoms can be very much like those seen in meningitis or viral encephalitis. CT and MRI reveal scattered, variably enhancing areas of demyelinated (T1 hypointense and T2 hyperintense) subcortical white matter and often the deep gray nuclei, in an asymmetric, pattern (Fig. 11). The cerebellum, brainstemal and spinal cord are less frequently involved. Demyelinating MS plaques affect the corpus callo-sum and periventricular white matter more specifically, and also the brainstem and cerebellum more commonly than does ADEM.

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