Infection and Inflammation

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Chapter 34

Infection and Inflammation

Bacterial, viral, fungal, and parasitic organisms are all causative factors in neurologic infection. Brain infection manifests as encephalitis, cerebritis, and meningitis. Encephalitis refers to diffuse infection of the brain parenchyma, whereas cerebritis is a more focal parenchymal infection. Meningitis refers to infection of the pia, arachnoid, and dural membranes, as well as the cerebrospinal fluid (CSF). Ventriculitis is often present in cases of meningitis. Infectious complications most often include abscess, empyema, or both. Infection in the setting of tumor often presents a diagnostic conundrum.

Imaging of central nervous system (CNS) infection is most often initially performed by means of computed tomography (CT) to assess for the possibility of hydrocephalus or increased intracranial pressure prior to the preparation of a lumbar puncture. Nonspecific parenchymal hypoattenuation indicative of edema on CT is sometimes appreciated in cases of more focal infection. CT is superior in the evaluation of bone erosion and destruction. Magnetic resonance imaging (MRI) is warranted in the assessment of infectious complications such as abscess, empyema, vasculitis, and ischemia in the setting of a worsening clinical condition or lack of clinical improvement despite appropriate therapy. Infection is most often manifested on MRI by abnormal hyperintense signal on T2-weighted (T2W), proton density, and fluid-attenuated inversion–recovery (FLAIR) sequences, with corresponding hypointense signal on T1-weighted (T1W) sequences. Postcontrast T1W images are essential in the evaluation for infectious collections and meningeal enhancement. Magnetic resonance venography (MRV) sequences may detect associated venous sinus thromboses. Diffusion-weighted imaging (DWI) may assist in localizing abscess collections, infection associated with ischemia, or both and may at times help distinguish lymphoma from abscess, especially in immunocompromised patients. DWI may also demonstrate lesions earlier than conventional sequences in viral infections such as herpes and West Nile virus (e-Fig. 34-1). Magnetic resonance spectroscopy has shown promise in distinguishing pyogenic abscesses from those caused by atypical organisms, with the former often demonstrating the presence of amino acids and lack of choline.

Bacterial Infections

Nearly two thirds of cases of bacterial meningitis in the United States occur in children. Routes of transmission include hematogenous, direct traumatic, congenital routes, as well as direct extension from adjacent sinus or mastoid disease (Figs. 34-2 through 34-4 and e-Fig. 34-5). Imaging plays a key role in determining the course of treatment for bacterial infection. It is essential to distinguish between focal cerebritis (Fig. 34-6), which tends to respond to antibiotics, and abscess, which often requires surgical intervention. Hypoattenuation on CT, indicative of edema, and corresponding hyperintense T2W and hypointense T1W signal on MRI, with patchy nonspecific postcontrast enhancement, are typical imaging characteristics of cerebritis. Mild to moderate mass effect is often present. Sequential imaging is essential in the assessment of the response to antibiotics as well as for progression to an abscess. Progression from cerebritis to abscess generally takes 1 to 2 weeks but may progress more quickly in neonates. Citrobacter, Serratia, and Proteus are the most common causes of neonatal brain abscess. Citrobacter and Serratia infection may cause medullary vein thrombosis and associated hemorrhage (Fig. 34-7). In general, abscesses tend to be situated at gray-white matter junctions, where the diameter of the end arterioles decreases (Fig. 34-8). Opportunistic organisms are common in immunocompromised neonates.

Differential diagnostic considerations of a peripherally contrast-enhancing fluid-filled structure in the brain includes infectious abscess and tumor. On DWI, abscesses will appear hyperintense (and dark on apparent diffusion coefficient, indicating restricting material within the capsule. On both MRI and CT, abscesses tend to have smooth regular inner margins and are often thinner walled along their medial edge than along their lateral margins. Intraventricular rupture of an abscess portends a poor outcome. Spectroscopy of abscesses is notable for the presence of amino acids and lactate (Fig. 34-9) and the absence of normal metabolite peaks. In neonates, ultrasonography may depict a hypoechoic abscess with peripheral hyperechogenicity, which may contain dependent echogenic debris.

Bacterial meningitis is the most common form of pediatric CNS infection. Although not diagnosed by imaging, imaging is warranted if a diagnosis is unclear, persisting seizures are present, and symptoms persist despite treatment. It is more common in preterm infants and full-term infants within the first month of life. The subarachnoid space tends to resist infection in older children, making meningitis in this age group a rarity. Most cases of neonatal meningitis in the United States are caused by group B Streptococcus (Fig. 34-10) and Escherichia coli. Other less common organisms (e.g., Serratia, enterococci, and Listeria) tend to inflict more extensive destruction. In infants older than 1 month, the most common causative organisms are Haemophilus influenza type B, Streptococcus pneumonia (Fig. 34-11), Neisseria meningitides, and Escherichia coli. Complications of meningitis include cerebritis, abscess, empyema, hydrocephalus, venous thrombosis, infarction (venous and arterial), ventriculitis (e-Fig. 34-12), mycotic aneurysms (Fig. 34-13), and sensorineural hearing loss (Fig. 34-14).

Tuberculosis Infection

CNS infection with Mycobacterium tuberculosis (tuberculosis [TB]) differs clinically and radiographically from pyogenic infection. Other granulomatous and fungal organisms are rare in the pediatric age group and often present with similar imaging characteristics as those in TB. The pathogenesis of tuberculous meningitis is different from that of other bacterial meningitides. Hematogenous dissemination of tuberculous bacilli is believed to occur about 1 week following the infected inhalation. Hematogenous spread to the CNS may produce miliary TB (rare in children), but more typically produce tuberculomas in the meninges, the brain (at the gray-white junction), spinal cord, or, rarely, the choroid plexus. After a variable period, organisms from one or more of these foci are discharged into the CSF or subarachnoid space causing meningitis. Isolated meningeal tuberculomas tend to localize in the region of the Sylvian fissures, but meningitis is typically most severe in the basal cisterns. This leads to secondary complications, including cranial nerve palsies, secondary infarction consequent to vasculitis, and hydrocephalus secondary to blockage of fourth ventricular outlet foramina. Clinical presentation ranges from personality change and anorexia to coma and death, with nuchal rigidity being the most common presenting clinical sign. Pathologically, tuberculous exudate fills the subarachnoid spaces. Most of the affected patients demonstrate hydrocephalus.

On CT, exudate within the cisterns is manifested by its greater than CSF attenuation. On contrast-enhanced MRI, marked subarachnoid and cisternal enhancement is seen on T1W sequences (e-Fig. 34-15), with T2W images demonstrating obscuration of the cisterns caused by the hyperintense signal within these affected regions. Microinfarctions are not uncommon. Tuberculomas often occur at gray-white junctions and are more common above the tentorium cerebelli. On CT, they demonstrate high attenuation and ring enhancement (Fig. 34-16), whereas on MRI, they demonstrate hyperintense T1W and hypointense T2W signals and enhance uniformly or peripherally when less than and greater than approximately 2 cm, respectively. The rare tuberculous abscess may be differentiated from a tuberculoma by its central hyperintense T2W signal and more pronounced associated vasogenic edema. Although DWI is not particularly helpful in making a diagnosis, lipid detection on spectroscopy has been reported in some cases.

Lyme Disease

Lyme disease is the most common tickborne disease in the United States and Europe. More than 1 in 5 cases has been reported in children or adolescents. This multisystemic disorder involves the neurologic system in approximately one fifth of affected children, manifesting as lymphocytic meningitis, meningoencephalitis, pseudotumor cerebri-like syndrome, or cranial neuropathy. It is unclear whether the mechanism of CNS involvement is a result of direct invasion by the Borrelia burgdorferi organism or an autoimmune phenomenon.

CT scans are usually normal in Lyme disease, although focal areas of hypoattenuation have been reported. Focal T2W hyperintense white matter lesions are seen in about 1 in 4 neurologically affected patients. Contrast-enhanced MRI may show leptomeningeal enhancement, with or without enhancement of the affected nerves, in children with cranial neuropathy (Fig. 34-17).

Cysticercosis

Although cysticercosis is not very common in the United States, it often presents in immigrants from endemic regions. Presenting symptoms of neurocysticercosis include seizures, developmental delay, and hydrocephalus. The most common form, parenchymal cysticercosis, is caused by an inflammatory reaction secondary to the death of the parasite. Focal lesions are cystic and solid, and demonstrate peripheral enhancement and calcification, respectively. They are most often situated in the cortex, the gray-white matter junction, or both areas (Fig. 34-18). Parenchymal lesions follow CSF signal intensity on DWI, which helps differentiate them from pyogenic abscesses. The typical calcification seen in adults is not always seen in children. Surrounding inflammatory reaction demonstrates hyperintense signal abnormality on T2W imaging. Intraventricular cysterci often cause obstructive hydrocephalus, and thin-slice T1W imaging best depicts the causative intraventricular scolex (Fig. 34-19). The leptomeningeal form of cysticercosis mimics the radiographic appearance of TB, with marked subarachnoid postcontrast enhancement. Subarachnoid granulomata mimic their parenchymal counterparts. Hydrocephalus and vasculitis are common associated findings. Large racemose cysts are most often found in the cerebellopontine angle, Sylvian fissures, and in the basilar and suprasellar cisterns. Multiple coexisting forms of cysticercoids are a clue to the diagnosis. On MRI, clusters of cysts are most commonly depicted.

Viral Infections

All viral CNS infections produce inflammation and neuronal necrosis to a greater or lesser extent. Some viruses such as herpes simplex and Coxsackie may also produce white matter necrosis, whereas the primary inflammatory process involves the parenchyma. Usually, a meningeal inflammatory reaction or even ventriculitis occurs. In general, acute viral infection typically causes marked edema, causing hyperechogenicity on ultrasonography, hypoattenuation on CT, and hyperintense signal on T2W and FLAIR sequences. Restricted diffusion is the earliest imaging sign of viral encephalitis, and DWI should be performed when viral infection is suspected. Fortunately, differences in presentation and location help suggest one viral etiology over another. Viral-like syndromes with autoimmune associations such as acute disseminated encephalomyelitis (ADEM) and posttransplantation lymphoproliferative disorders (Fig. 34-20) often demonstrate imaging characteristics similar to those of viral infections.

Herpes Simplex Virus Type I

Herpes simplex virus type 1 (HSV-1), as opposed to the prenatally or perinatally acquired HSV type 2 (HSV-2), is a spontaneous infection most often caused by reactivation of an orofacial herpes infection. HSV-1 CNS infection occurs in all ages but has a pediatric predominance. Early symptoms of fever and malaise may progress to seizures and hemiparesis. Restricted diffusion on MRI is the earliest radiologic manifestation, with unilateral or bilateral medial temporal lobe hyperintense signal on T2W and FLAIR sequences and more heterogeneous restricted diffusion appearing several days later (Fig. 34-21). CT findings of low attenuation within the temporal lobe and insular cortex do not manifest until several days following the onset of symptoms. Leptomeningeal and cortical contrast enhancement, as well as foci of calcification hemorrhage, or both, may also be present.

Human Immunodeficiency Syndrome

In the United States, greater than 90% of children with human immunodeficiency virus (HIV) are infected as a result of maternal transmission to the fetus. CNS imaging manifestations of congenital HIV include atrophy as well as basal ganglia and subcortical calcifications (Fig. 34-22). Superinfection and neoplasm, not uncommon in adults with HIV, are seldom seen in children. Progressive multifocal leukoencephalitis (PML) caused by the John Cunningham polyomavirus, is radiologically identical to its presentation in adults. PML demonstrates white matter hypoattenuation on CT, as well as hyperintense signal on T2W and FLAIR sequences. These lesions characteristically lack mass effect and do not enhance following contrast administration. HIV infection may also lead to vasculitis (Fig. 34-23).

Acute Disseminated Encephalomyelitis

ADEM is a monophasic perivascular inflammatory and demyelinating disorder that often affects both the brain and the spinal cord, following a vaccination or viral infection. Lesions are generally hyperintense on T2W sequences and have corresponding hypointensity or isointensity on T1W sequences. MRI characteristics of ADEM (Fig. 34-24) are variable, with enhancement patterns, ranging from solid or ringlike enhancement to no enhancement at all, in lesions that range from small to large and which affect gray matter, white matter, or both. A clinical history of a recent viral illness, vaccination, or both is the key to properly diagnosing these lesions.

Congenital Infections

Transplacental and less often transvaginal transfer of infection to the fetus is often the result of TORCH (toxoplasmosis, other, rubella, cytomegalovirus, herpes) infection (Fig. 34-25). Insults occurring during the first two trimesters most often manifest as severe congenital malformations. Those occurring during the third trimester often result in destructive lesions.

Cytomegalovirus

Cytomegalovirus (CMV) is the most common serious viral infection to affect newborns in the United States, occurring in nearly 1% of all live births. Up to 25% of infected infants develop neurologic or developmental abnormalities, including microcephaly, hearing impairment, chorioretinitis, and seizures, in the first year of life. Neonatal ultrasonography in affected patients often demonstrates nonspecific mineralizing vasculopathy of the basal ganglia (e-Fig. 34-26). MRI and CT demonstrate the sequelae of infection in the third trimester as periventricular calcification, hemorrhage, or both; ventricular and sulcal prominence; and periventricular and subcortical white matter changes (Figs. 34-27 and 34-28). Intrauterine infection with this virus is associated with polymicrogyria, especially in the region of the Sylvian fissures.

Herpes Simplex Virus Type 2

Most cases of neonatal HSV-2 are contracted transvaginally as the baby passes through the birth canal. Neonatal CNS herpetic infection is believed to occur in approximately 1 in 10,000 births. CNS manifestations generally present between 2 to 4 weeks of life and include meningoencephalitis with seizures, lethargy, and fever. Sequelae include mental retardation, severe neurologic deficits, or even death, secondary to virulent destruction of the brain. The disease may produce ischemic infarction of parts or all of the brain, necrosis, atrophy, encephalomalacia, demyelination, and gliosis (Fig. 34-29). Watershed distribution ischemia is also fairly common in areas remote from the primary herpetic lesions. MRI-restricted diffusion, which may be multifocal or limited to the temporal lobes, brainstem, or cerebellum, is the first radiologic sign of herpetic brain destruction. CT in early disease is either normal or demonstrates subtle areas of low attenuation. Later, patchy white matter low attenuation on CT and corresponding hyperintense signal on T2W imaging with rapid progression is demonstrated. Meningeal enhancement reflects the extent of the disease. Also of note is classic persisting hyperattenuation of cortical gray matter on CT, and corresponding T1 and T2 shortening on MRI. Eventually, diffuse cerebral and cerebellar (in about 50% of cases) atrophy and encephalomalacia ensue (Fig. 34-30). It should be noted that HSV-1 encephalitis, which affects older children and adults, is different from neonatal herpes infection.

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