Meningitis

Acute bacterial meningitis is inflammation of the meninges caused by bacterial microorganisms that seed the leptomeninges through hematogenous spread (most common mechanism), local spread from an adjacent nidus of infection, retrograde perineural spread, or direct introduction from a recent procedure, surgery, or trauma. Cerebrospinal fluid (CSF) studies from a lumbar puncture (LP) are often diagnostic, but neuroimaging is useful to exclude other pathologies, identify complications, and confirm the diagnosis in an equivocal setting.

CT is usually pursued in the evaluation of an acutely comatose patient, but scans are often normal in the setting of acute bacterial meningitis. Specific signs of meningitis include high density in the subarachnoid space (similar to hemorrhage) and effacement of the basilar cisterns.3 On contrast-enhanced CT scans, leptomeningeal enhancement may be seen.3 In addition to enhancement of the basal cisterns, occasionally enhancement of the subarachnoid space between the horizontal folia of the vermis may lead one to the diagnosis. CT can also be diagnostic of the complications of meningitis, such as hydrocephalus, subdural effusions (often seen in infants) and empyema, infarction (venous or arterial), and abscess formation.3 Before LP, CT should be performed to identify the cause of increased intracranial pressure, such as diffuse cerebral edema, hydrocephalus, and cerebral herniation.

MR imaging is far superior to CT in visualizing the abnormalities of bacterial meningitis. The inflammatory exudate of meningitis is often isointense on T1-weighted images and hyperintense on T2-weighted images compared with adjacent parenchyma. Unenhanced fluid-attenuated inversion recovery (FLAIR) images may be abnormal, reflecting altered protein content of the CSF and/or inflammation of the leptomeninges; however, they are unfortunately often normal. Contrast-enhanced FLAIR images are extremely sensitive, and likely more so than conventional T1-weighted post-contrast images, in detecting early leptomeningeal inflammation. Contrast-enhanced T1-weighted images are, however, more specific in detecting associated parenchymal abnormalities and should be retained in MR protocols focused on CNS infection.4 Diffuse pachymeningeal enhancement should be interpreted with caution in the post-LP setting because this finding has been reported in 1% of all patients after uncomplicated LP procedures.5

Diffusion-weighted imaging (DWI) is extremely sensitive in the early detection of arterial infarction from meningitis-induced vasospasm, or subdural empyema ( Fig. 4.1 ), and venous infarction secondary to venous or dural sinus thrombosis. The area of infarction develops increased signal on FLAIR and T2-weighted images 12 to 24 hours later. In the acute stage, subcortical T2-hyperintensity is the key finding in meningitis-induced cortical venous infarction. MR angiography and MR venography may be considered when arterial or venous infarction is suggested on standard MR pulse sequences. Spread of subdural empyema into the interhemispheric fissure presages a potentially ominous course of the disease.

Viral or “aseptic” meningitis is typically caused by enteroviruses, and neurologic deficits are uncommon. Because imaging studies are usually normal, they are not part of routine work-up. Occasionally, subtle meningeal enhancement can be detected on post-contrast turboFLAIR MR images ( Fig. 4.2 ).

Tuberculous (TB) meningitis is increasing in incidence in the United States because of immigration from areas of endemicity, acquired immunodeficiency syndrome (AIDS), and multidrug resistance. This infection is typically a secondary infection from a primary pulmonary source and is the most common form of CNS TB. High rates of morbidity and mortality from TB meningitis and its predilection for infants and children make early diagnosis and treatment imperative. CT has a limited role in detecting TB meningitis.

The classic MR finding of TB meningitis ( Fig. 4.3 ) is marked nodular thickening and enhancement of the meninges at the base of the brain (in distinction to bacterial meningitis, which involves the convexities to a greater extent). This MR finding is often difficult to distinguish from the MR appearance of neurosarcoidosis, carcinomatous meningitis, and fungal meningitis. Associated tuberculomas are often seen and are characterized by single or multiple intraparenchymal masses with variable enhancement. Nodular meningeal thickening in addition to tuberculomas is highly suggestive of CNS TB. Vasculitis and subsequent infarction can result from infiltration of the exudate into the perivascular spaces. DWI is invaluable in the early detection of this complication.3

Fungal meningitis, like TB meningitis, must be considered in immunocompromised patients. Numerous organisms are included under this umbrella term, and imaging findings are often nonspecific. In cryptococcal meningitis, dilated perivascular spaces in the deep gray nuclei maybe seen on MR. With time, these may evolve into gelatinous pseudocysts. Absence of enhancement is typical in an AIDS patient. As the patient′s immune status improves after initiation of antiretroviral therapy, enhancement may appear in the areas of signal abnormality. In the angioinvasive form of zygomycosis (mucormycosis), a stroke protocol MR with MR angiography may be useful in evaluating complications such as arteritis, arterial occlusion with or without infarction, and mycotic aneurysms.6 CT has no established diagnostic role in the specific diagnosis of fungal meningitis.

Encephalitis

Encephalitis is most commonly caused by viruses. The location of parenchymal abnormality depends on the specific pathogen.

Herpes encephalitis results from reactivation of the herpes simplex virus in immunocompetent patients, has a predilection for the limbic system, and carries a high mortality rate (50–70%). CT is often normal, especially early in the disease course. In the late acute or subacute stage, CT may show low attenuation in the temporal lobes and insula. Hemorrhage on CT is often a late finding and is associated with a poor prognosis.

The best imaging clue on MR is increased signal on T2 and FLAIR images in the limbic system cortical and subcortical areas (particularly medial temporal and inferior frontal), with relative sparing of the white matter and basal ganglia ( Fig. 4.4 ). Limbic encephalitis can have a similar MR appearance, although a history of primary malignancy (often lung) and subacute onset of symptoms distinguish it from herpes encephalitis. Additionally, the constellation of DWI restriction, cingulate gyrus involvement, and contralateral temporal lobe involvement is highly suggestive of herpes encephalitis.7 Although bilateral signal abnormalities are present in 60% of cases in the acute stage, findings are often more prominent on one side.6 In the setting of hemorrhage, susceptibility-weighted sequences (such as T2* images) show “blooming” of decreased signal in the areas of edematous brain.7 Atrophy is a typical finding in the chronic or treated stage of herpes encephalitis.

Human immunodeficiency virus (HIV) encephalitis and progressive multifocal leukoencephalopathy (PML) are discussed in the section of this chapter on immuno-compromised patients.

Prion Diseases

Creutzfeldt-Jacob disease (CJD) is a rare, transmissible spongiform encephalopathy that is invariably fatal. On MR, symmetric FLAIR hyperintensity in the caudate and putamen with relative sparing of the pre- and postcentral gyri is typical in this condition. Thalamic involvement is less common in CJD than in variant CJD (vCJD), also known as bovine spongiform encephalopathy (BSE).

BSE, also known as mad cow disease, is a chronic neurodegenerative disease that affects the CNS of cattle. There is strong evidence that vCJD is linked to the consumption of meat produced from BSE-infected cattle. In contrast to the classic form of CJD, vCJD affects younger patients (mean age, 28 years) and is characterized by prominent psychiatric and sensory symptoms.8 Two classic findings are often present on the MR images of patients with vCJD ( Fig. 4.5 ). The “pulvinar sign” arises from a relative T2 hyperintensity in the pulvinar of the thalamus compared with the anterior putamen, whereas the “hockey stick sign” is the result of symmetric pulvinar and dorsomedial thalamic nuclear hyperintensity.