Because the consequences of delayed treatment of HSE can be devastating, CSF should be obtained for definitive diagnosis by polymerase chain reaction (PCR), and presumptive antiviral therapy should be instituted as the laboratory and imaging workup proceeds (Fig. 2.28).
◆Herpes Encephalitis
Herpes simplex encephalitis (HSE) is the most common cause of sporadic viral en-cephalitis. Its clinical manifestations range from mild headache, sti neck, and fever to profound encephalopathy and coma. The virus migrates to the CNS from a fa-cial infection via either the trigeminal or the olfactory nerve, and cerebritis de-velops in the inferior frontal and medial temporal lobes. Patients often experience malaise, fever, headache, and nausea that progresses to encephalopathy with leth-argy, confusion, and delirium. Psychiatric symptoms and seizures are also common. Because HSE can mimic any toxic or infec-tive encephalopathy and early CT findings are often absent or extremely subtle, the diagnosis may be delayed.
CT aids in the evaluation of encephalitis by excluding brain abscess, neoplasm, and
Fig. 2.28a–fa–d Herpes encephalitis. (a,b) Nonenhanced CT shows subtle low-attenuation parenchymal change in the anterior cingulate gyrus and insula. (c,d) FLAIR MRI better denes high-signal edema within the olfac-tory cortex, cingulate gyrus, medial temporal lobe, and insula. Enlargement of the medial temporal lobe indicates focal swelling.
e,f Herpes encephalitis presenting with intraparenchymal hemorrhage on NCCT. Two ~ 1-cm hemor-rhages in the left inferior frontal and posterior temporal lobes with minimal surrounding vasogenic edema. Brain parenchyma is otherwise normal. (f) T2-weighted MRI shows a swollen medial left temporal lobe with increased T2 signal that extends to the left inferior frontal lobe (gyrus rectus), where a 1-cm low-intensity nodule corresponds to one of the focal hemorrhages visible on CT.
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on CT as a low-attenuation lesion with pe-ripheral enhancement and surrounding vasogenic edema. As acute inflammation resolves, the cyst retracts and appears as an enhancing parenchymal nodule with di-minishing adjacent edema. Over time, the lesion calcifies.
The racemose form of neurocysticer-cosis consists of thin-walled “grapelike” cysts in the subarachnoid, intraventricu-lar, and cisternal CSF spaces. Because the CT attenuation of unruptured cysts corre-sponds to CSF, an intraventricular cyst may be nearly undetectable and a subarachnoid cyst may be indistinguishable from a small arachnoid cyst. MRI imaging with FLAIR sequences readily dierentiates the higher- signal cyst contents from normal CSF. Cysts that obstruct normal CSF flow can cause acute hydrocephalus (Fig. 2.29).
◆Neurocysticercosis
Cysticercosis—systemic infestation by the larval form of the pork tapeworm Taenia so-lium—is endemic to Central America, South America, Asia, and Africa. The incidence in the United States has been steadily rising as a result of immigration and internation-al travel. Infestation can involve almost any tissue, and neurocysticercosis is the leading cause of adult-onset epilepsy worldwide. Obstructive hydrocephalus, meningoen-cephalitis, stroke, headache, and altered mental status are other manifestations.
Clinical and imaging findings depend on the stage of the disease. The encysted larva enjoys immunologic invisibility as long as it is alive, and most patients are as-ymptomatic at this stage. As the larva dies, it elicits an immune reaction that leads to focal cerebritis and seizure. The encysted larva with surrounding cerebritis appears
Fig. 2.29a–fa–d Neurocysticercosis. (a) NCCT. 1-cm right anterior temporal cyst with surrounding vasogenic edema. (b) T2-weighted MRI. High-signal cyst with surrounding vasogenic edema. (c) FLAIR. The cyst is of inter-mediate intensity, indicating complicated uid, and contains a 3-mm hyperintense nodule (larva). Sur-rounding vasogenic edema. (d) T1-weighted MRI + gadolinium. Near-CSF-signal-intensity cyst with thin enhancing rim and surrounding edema.
e,f Neurocysticercosis. (e) NCCT. Right parietal intraparenchymal and left parietal subarachnoid cysts. (f) FLAIR shows an additional intermediate-signal cyst within the left lateral ventricle, not visible on non-enhanced CT.
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cephalus, sulcal eacement, and (rarely) hyperdense subarachnoid or intraventric-ular pus. Meningeal enhancement can be seen if contrast is administered.
FLAIR sequences are particularly sensi-tive to abnormal CSF and can be useful in the early detection of elevated CSF protein seen in meningitis. Oxygen therapy and subarachnoid hemorrhage can have a simi-lar appearance.
The primary role of CT in suspected men-ingitis is not to establish the diagnosis but toexclude subarachnoid or intraparenchymalhemorrhage and ensure the safety of diag-nostic lumbar puncture, which would becontraindicated by significant supratento-rial edema or intracerebral mass (Fig. 2.30).
◆Bacterial Meningitis
Acute bacterial meningitis is most com-monly due to Streptococcus pneumoniae, Neisseria meningitidis,or group B strep-tococcus. Patients present with headache, sti neck, and variable encephalopathy as a result of meningeal inflammation and adjacent cerebral edema. Potential compli-cations include cerebral ischemia, sepsis, and hydrocephalus due to impaired CSF resorption. Viral meningitis, tuberculosis, cryptococcus, and coccidioidomycosis are nonbacterial infections that can mimic bacterial meningitis. Noninfectious con-siderations include neurosarcoidosis, men-ingeal carcinomatosis, and CNS lymphoma.
CT findings are often normal and, when present, subtle. They include mild hydro-
Fig. 2.30a–da,b Bacterial meningitis in an adult. Noncontrast CT. Mild ventricular enlargement; hyperdense debris lls the occipital horns of the lateral ventricles.
c,d Bacterial meningitis in an infant. (c) NCCT. Severe hydrocephalus with transependymal CSF resorption and intraventricular debris. (d) T1-weighted MRI with gadolinium. Diuse leptomeningeal enhancement. Hydrocephalus.
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