EXERCISE 12-4. INTRACRANIAL INFECTIONS
12-9. In Case 12-9, what is the most likely diagnosis (Figure 12-25 A, B)?
A. Frontal contusion
B. Aneurysm with intraventricular hemorrhage
C. Parietal lobe abscess
D. Intracranial lymphoma
12-10. In Case 12-10, the location of the abnormality is pathognomonic for which type of infection (Figure 12-26 A, B)?
D. Herpes Staphylococcus
12-11. In Case 12-11, the major differential diagnosis for this lesion is toxoplasmosis versus (Figure 12-27)
B. Intracranial lymphoma
D. Metastatic disease
E. Cytomegalovirus (CMV)
12-9. In this case, the contrast-enhanced MR scan shows a ring-enhancing lesion (arrows) in the left parietal lobe with decreased surrounding T1 signal (Figure 12-25 A). A diffusion signal abnormality is present on the corresponding diffusion-weighted image (Figure 12-25 B), within the central aspect of the lesion, and is found to be compatible with an area of restricted water motion. The patient’s history is compatible with an intracranial infection, and the demonstrated MR imaging findings favor an abscess (C is the cor-rect answer to Question 12-9.)
12-10. In this case, the T2-weighted MR image (Figure 12-26shows increased signal in the medial and anterior aspects of the right temporal lobe (single arrow) with small focus of T2 hypointensity (double arrows) con-sistent with the presence of blood products. Postcon-trast axial T1 (Figure 12-26 B) shows abnormal patchyparenchymal and leptomeningeal enhancement along the medial right temporal lobe. These changes are commonly seen in patients with herpes encephalitis (D is the correct answer to Question 12-10).
12-11. In this case, multiple enhancing lesions are present within the basal ganglia, especially on the right (ar-rows), on the gadolinium-enhanced T1-weighted MR image (Figure 12-27). The most common lesions with this appearance in an immunocompromised patient, such as a patient with HIV, are toxoplasmosis and intracranial lymphoma (B is the correct answer to Question 12-11). The patient markedly improved after anti-toxoplasmosis therapy, and the lesions shown on the MR image disappeared.
A host of infectious diseases can involve the brain and its cov-erings. Because the CNS has a limited number of ways of re-sponding to an infectious agent, many intracranial infections appear identical on neuroimaging studies. It is, therefore, very important to closely correlate the imaging findings with the clinical presentation and other diagnostic tests, such as lumbar puncture or stereotactic brain aspiration.
For our purposes, it is useful to classify CNS infections ac-cording to the intracranial compartment involved, especially because this has treatment implications. Intracranial infections can be either parenchymal or extraparenchymal. Parenchymal manifestations include cerebritis/abscess and encephalitis. Ex-traparenchymal disease includes epidural abscess, subdural empyema, and leptomeningitis. Bacterial, viral, fungal, and par-asitic agents can all affect the CNS. Although a few infectious agents preferentially involve a particular anatomic compart-ment of the CNS, most are not site specific.
Case 12-9 demonstrates the classic ring-enhancing lesion of an abscess, in this case, due to Nocardia. No specific fea-tures of this abscess distinguish it from a typical pyogenic ab-scess. The diffusion signal abnormality has been postulated to arise from restricted water motion in the presence of vis-cous, purulent material within the abscess cavity and can mimic an area of acute ischemia. Cerebral infection by No-cardia usually arises from a pulmonary focus in an immuno-compromised host. Similarly, most pyogenic abscesses are the result of hematogenous dissemination from a non-CNS source. Pyogenic brain abscesses can also result from direct extension of an infectious process from an adjacent area (eg, sinusitis or mastoiditis) or from trauma (eg, penetrating wound or surgery).
Abscesses usually occur at gray matter/white matter junc-tions, although they can occur anywhere in the brain. Pa-tients frequently present with seizures or symptoms related to intracranial mass effect. If abscesses develop near the brain surface, they may rupture into the subarachnoid space, pro-ducing meningitis; they may also produce a ventriculitis ifthey rupture into the ventricular system. Most abscesses are treated surgically.
Herpes encephalitis (Case 12-10) is caused by the herpes simplex virus (HSV). Older children and adults are usually infected by HSV-1, either primarily or as a result of reactiva-tion of a latent virus. The ensuing necrotizing encephalitis in this condition typically involves the temporal and inferior frontal lobes, insular cortex, and cingulate gyrus. Focal ab-normalities of attenuation (on CT) or signal (on MR) in these characteristic locations, often with enhancement after contrast administration, are practically pathognomonic of HSV-1 encephalitis. Early diagnosis of this condition is ex-tremely important, because antiviral therapy can signifi-cantly affect patient outcome.
Neonatal herpes simplex infection differs from infection in the older child and adult. The offending organism is usu-ally HSV-2, which may be acquired in utero or during birth from mothers with genital herpes. HSV-2 infection can pro-duce severe destructive changes within the developing brain. Unlike HSV-1 infection in older children and adults, neona-tal herpes encephalitis can involve any area of the brain, hav-ing no predilection for the temporal lobe.
Patients with AIDS (Case 12-11) commonly develop in-tracranial infections during the course of their disease. Human immunodeficiency virus (HIV) itself can directly in-fect the CNS, producing encephalopathy in up to 60% of AIDS patients. The most common neuroimaging finding in HIV encephalopathy is cerebral atrophy, often with patchy white matter hypodensity (on CT) or T2 hyperintensity (on MR imaging) from demyelination and gliosis (Figure 12-28). Other common CNS infections in the immunocompromised AIDS patient include toxoplasmosis, cryptococcosis, and progressive multifocal leukoencephalopathy (from a poly-omavirus infection).
Toxoplasmosis usually presents as multiple lesions of varying size and demonstrates ring enhancement with sur-rounding edema on CT or MR imaging. Lesions commonly occur in the basal ganglia or at the gray matter/white matter junction within the cerebral hemispheres. Individual masses may have a solid appearance or demonstrate central necrosis or hemorrhage. The enhancement pattern is vari-able; both rim-enhancing and more solidly enhancing le-sions can be seen. Their appearance is almost identical to that of primary intracranial lymphoma, another common intracranial condition in AIDS. Metabolic studies, such as PET or SPECT scans (no increase in 18F-FDG activity with toxoplasmosis, increased with lymphoma), MR spec-troscopy (no choline elevation in toxoplasmosis, elevated in lymphoma), and perfusion-weighted sequences (lower cerebral blood volume in toxoplasmosis) may assist in dis-tinguishing these pathologies.
Meningitis is the most frequent manifestation of crypto-coccosis in AIDS, although parenchymal lesions, termed cryptococcomas, are occasionally encountered. In progressivemultifocal leukoencephalopathy, extensive areas of white matter demyelination are shown on MR imaging. A number of other intracranial infections can occur in AIDS patients.
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