Epidural empyema

An epidural abscess and/or empyema most commonly extends from the paranasal sinuses, especially the frontal sinus. Extension may be via direct bony erosion or retrograde flow via valveless bridging veins. Other etiologies include recent surgery, trauma, and mastoiditis. This purulent collection localizes outside the dura, which protects the underlying brain parenchyma. Therefore, patients with an epidural empyema tend to have a more benign, insidious course than those with a subdural empyema. Patients often complain only of a fever and headache.

On imaging, epidural abscesses are lentiform in shape, tacked down at the sutures, but they can cross the midline, unlike subdural collections ( Fig. 1 ). The MR signal characteristics include T1 hypointensity, which is brighter than pure CSF given its proteinaceous content and inflammatory debris, and T2 hyperintensity, approaching CSF intensity. On post-GAD images, there is profound enhancement of the inflamed dura, often more than seen in subdural empyemas. Another important imaging feature of epidural empyemas is the relatively normal appearance of the underlying brain parenchyma in contrast to subdural empyemas. Empyemas classically have reduced diffusion. However, the DWI signal characteristics can be more complex in epidural as opposed to subdural empyemas. Because epidural empyemas tend to have a more prolonged course, portions of the lesion may become less viscous, allowing for mixed intensity on DWI. Please refer to “ Acute Neuro-Interventional Therapies ,” elsewhere in this issue, for additional imaging information.

Frontal sinusitis and epidural abscess. 11-year-old boy with severe headache. ( A ) Axial contrast-enhanced CT shows a right frontal peripherally enhancing lentiform collection ( arrow ), compatible with epidural abscess. ( B ) An inferior axial CT slice shows contiguous bilateral frontal sinus opacification ( arrow ).

Subdural empyema

The source of most subdural empyemas is also sinusitis or mastoiditis, with frontal sinusitis accounting for most cases. Other etiologies include prior trauma with a superinfected subdural hematoma, postcraniotomy, or a complication of meningitis. Patients may present with fever, headache, seizures, and focal neurologic deficits. The subdural empyema is a medical emergency and usually requires neurosurgical intervention.

Neuroimaging plays a key role in early diagnosis and characterization. CT is often used acutely because of its speed and widespread availability. It is most useful in defining the extent and degree of mass effect and herniation; however, small subdural empyemas can be missed on CT, especially when located along the inner table of the skull. MRI is helpful in diagnosing and differentiating a subdural empyema from other subdural collections, including a subdural effusion, chronic subdural hematoma, and a subdural hygroma that may mimic an empyema on CT ( Fig. 2 ). Subdural empyemas have similar T1 and T2 signal characteristics to epidural empyemas, and classically show reduced diffusion, identified as high signal on DWI and low signal on the apparent diffusion coefficient (ADC) map.

Meningitis with subdural empyema. 56-year-old female with meningitis and new left leg shaking. ( A ) Axial contrast-enhanced CT shows a right parafalcine subdural collection ( arrow ). ( B ) DWI shows reduced diffusion compatible with subdural empyema ( arrow ).

Leptomeningitis

Meningitis refers to acute or chronic inflammation of the pia-arachnoid layers and the adjacent CSF. It may be viral, bacterial, or fungal. The diagnosis usually is based on clinical history, physical examination, and CSF analysis, with imaging playing a limited role. The clinical presentation is often characteristic, with fever, headache, neck stiffness, vomiting, and photophobia being most common.

Imaging is most useful to evaluate the complications of meningitis, including vascular thrombosis, infarctions, brain abscess, ventriculitis, hydrocephalus, and extra-axial empyemas. Post-GAD and FLAIR sequences are most sensitive for detecting abnormal meningeal enhancement and SAS disease, respectively. DWI is particularly helpful in the identification of complications, such as infarction or subdural empyema. Acute bacterial or viral meningitis typically shows enhancement over the cerebrum and interhemispheric fissure, whereas chronic tuberculous or fungal meningitis classically shows enhancement in the basal cisterns ( Fig. 3 ).

Coccidiomycosis and basilar meningitis. 23-year-old migrant worker with headache and left upper extremity weakness. ( A ) Noncontrast CT shows hyperdensity in the basilar cisterns ( arrows ). ( B ) Contrast-enhanced CT shows abnormal enhancement of the basilar meninges ( arrows ). ( C ) Noncontrast CT at the level of the basal ganglia shows an infarct in the posterior limb of the right internal capsule ( arrow ), thus explaining the patient’s clinical presentation. Perforating artery infarctions are a potential complication of basilar meningitis secondary to the associated inflammatory arteriopathy.

Tuberculous meningitis, the most common presentation of neurotuberculosis, occurs predominately in young children and adolescents. It usually presents as a long-standing insidious process with exuberant inflammation of the basilar meninges and an obliterative vasculopathy of the basal penetrating vessels. Most infarcts are thus seen in the basal ganglia and internal capsule (see Fig. 3 C). The common imaging triad consists of basal meningeal enhancement, hydrocephalus, and cerebral infarction. Leptomeningeal enhancement is not specific for infectious meningitis, and can also be seen with carcinomatous meningitis, sarcoidosis, or chemical meningitis.

Pyogenic abscess

Pyogenic abscesses can arise from hematogenous dissemination, direct inoculation (trauma or surgery), contiguous extension (paranasal sinus, middle ear, mastoids), or complicating meningitis. The evolution of a pyogenic abscess progresses through 4 stages over approximately 2 weeks: (1) early cerebritis, (2) late cerebritis, (3) early abscess/capsule, and (4) late abscess/capsule. The MRI features of cerebritis and abscess depend on the stage of this infectious process.

In the early cerebritis stage, ill-defined T1 hypointensity and T2 hyperintensity are noted, with mottled heterogeneous enhancement. As the infection matures, the necrotic debris accumulates centrally and the body attempts to isolate the infection with a collagenous capsule. Centrally, the abscess cavity is T1 hypointense (but slightly higher than CSF) and T2 hyperintense ( Fig. 4 ). The abscess capsule is iso- or slightly hyperintense on T1-weighted images and markedly hypointense on T2-weighted imaging; this is thought to be secondary to paramagnetic hemoglobin degradation products or free radicals in macrophages. On post-GAD images, a thin, smooth ring is characteristic, in contrast to necrotic tumors, which typically have a thick nodular ring enhancement ( Fig. 5 ). Another important feature of a brain abscess is its tendency to “grow toward the white matter,” resulting in an oval configuration with a thicker enhancing capsule toward the more well-vascularized cortex. The thinner capsule abutting the white matter helps explain the propensity for intraventricular rupture and subsequent ventriculitis. Imaging features of ventriculitis/ependymitis include enhancement of the ventricular wall and reduced diffusion ( Fig. 6 ). Ventriculitis is rarely isolated and usually occurs in the setting of abscess rupture, meningitis, or shunting and increases mortality to 80%.

Pyogenic abscess. 65-year-old woman with fever and vision loss. ( A ) Sagittal T1-weighted image shows the typical central T1 hypointensity ( arrow ). A T1 hyperintense rim can be seen in some cases. ( B ) Axial post-GAD T1-weighted image shows thin, smooth, ring enhancement that is typical for infection ( arrow ). Also, small daughter cysts are shown anteriorly and posteriorly. ( C ) Axial T2-weighted image shows the typical T2 hypointense rim, central T2 hyperintensity, and marked surrounding vasogenic edema, characteristic of the pyogenic brain abscess ( arrow ). ( D ) Axial DWI shows “light bulb” bright diffusion and hypointensity on the ADC map, consistent with true reduced diffusion.

Brainstem pyogenic abscess mimicking glioblastoma multiforme (GBM). 53-year-old man presented for preoperative evaluation for presumed GBM, without signs and symptoms of infection. ( A ) Axial post-GAD T1-weighted image shows thin, smooth enhancement of the pontine lesion ( arrow ), findings that are more suggestive of infection than neoplasm. ( B ) Axial T2-weighted image reveals ill-defined T2 hyperintensity ( arrow ) rather than the more typical discrete T2 hyperintensity; this finding suggests an earlier stage of infection. ( C ) Axial DWI and ADC map show reduced diffusion. Although GBMs may be hypercellular and show reduced diffusion, the combination of reduced diffusion and thin ring enhancement are key to the diagnosis of an abscess.

Ventriculitis. 65-year-old man with fever after shunt placement. ( A ) Axial post-GAD T1-weighted image shows a ring-enhancing abscess adjacent to the atrium of the right lateral ventricle ( vertical arrow ). Note also subtle subependymal enhancement and higher signal intensity in the ventricle indicating ventriculitis ( horizontal arrow ). ( B ) Axial DWI at the same level demonstrates reduced diffusion in both the abscess ( vertical arrow ) and the debris within the ventricle ( horizontal arrow ).

DWI is extremely useful in identifying a brain abscess. As mentioned previously, the pyogenic brain abscess typically has “light bulb bright” diffusion signal intensity with corresponding low ADC values. Although some tumors can have low ADC values because of hypercellularity, the necrotic or cystic portions are usually less cellular and therefore do not show the same reduced diffusion.

Tuberculoma

A global increase in the incidence of tuberculosis (TB) can be attributed to increased immigration, AIDS, and multidrug-resistant strains. CNS infection with Mycobacterium tuberculosis can present as either of the following:

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  Diffuse form (eg, basal exudative leptomeningitis, as discussed previously)

  
  
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  Localized form (eg, tuberculoma, abscess, or cerebritis).

The most common parenchymal form of CNS TB is tuberculous granuloma (tuberculoma). In some countries, TB represents up to 10% to 30% of all focal intracranial masses.

Parenchymal TB is more common in HIV-infected patients, can be solitary or multiple, and can occur with or without meningitis. There is hematogenous spread in cases of known pulmonary TB.

Tuberculomas occur at the corticomedullary junction and are more common infratentorially in children and supratentorially in adults. The clinical presentation is often related to the space-occupying mass effect (ie, seizures, focal neurologic signs, headache, papilledema) rather than to the infection.

The MRI features depend on whether the granuloma is noncaseating, solid-caseating, or cystic-caseating. Noncaseating granulomas are T2 hypointense and solidly enhancing. Caseating granulomas have smooth ring enhancement. Solid caseating granulomas have characteristic T2 hypointensity ( Fig. 7 ), whereas cystic-caseating granulomas have central T2 hyperintensity similar to pyogenic abscess. The dark T2 signal is thought to be caused by free radicals, and the solid caseation signal is attributed to cellular density. Finally, the tuberculous abscess is a rare complication developing from parenchymal granulomas that are teeming with tubercle bacilli. Similar to cystic-caseating granulomas, these lesions show central T2 hyperintensity and even reduced diffusion, which can therefore mimic pyogenic abscess. Some investigators suggest that MRS may help differentiate tubercular abscess from pyogenic abscess. Specifically, identification of the amino acids acetate and succinate are found in pyogenic abscesses, but lipid peaks are found in tubercular abscesses.

Caseating tuberculoma. 3-year-old boy with fever, lethargy, and abnormal chest x-ray. ( A ) Axial noncontrast CT shows a round, slightly hyperdense mass with surrounding vasogenic edema located in the left cerebellar hemisphere ( arrow ). Note that the slight hyperdensity would be atypical for pyogenic abscess. ( B ) Axial noncontrast T1-weighted image reveals a thin hyperintense rim around the mass ( arrow ). ( C ) Axial post-GAD T1-weighted image shows smooth ring-enhancement ( arrow ), which favors infection over neoplasm. ( D ) Axial T2-weighted image shows uniform T2 hypointensity ( arrow ), which suggests an atypical infection rather than pyogenic infection. ( E ) Axial CT image obtained 1 year after treatment demonstrates dense calcification that is sometimes termed a “brain stone” ( arrow ).

Neurocysticercosis

Neurocysticercosis, caused by the pork tapeworm Taenia solium, is the most common parasitic infection of the CNS in immunocompetent individuals. Endemic in Latin America and parts of Asia, India, Africa, and Eastern Europe, it is the most common cause of seizures in young patients in developing countries with poor hygiene. Neurocysticercosis may involve the brain parenchyma, the subarachnoid space, and the ventricles.

CT and MRI findings in parenchymal neurocysticercosis depend on the stage of development of the parasite. Four stages have been categorized : (1) viable/vesicular, (2) colloidal, (3) nodular-granular, and (4) calcified.

In the first, vesicular, stage, small cysts follow CSF density on CT and CSF intensity on MRI, and show little to no enhancement or edema. Most of these lesions have a “cyst with a dot” appearance representing an eccentric scolex ( Fig. 8 ).

Vesicular stage of neurocysticercosis. 40-year-old man with seizures. Sagittal T1-weighted image demonstrates multiple lesions that have a “cyst with a dot” appearance ( arrows ). This is a classic finding in vesicular neurocysticercosis where the “dot” represents the scolex. Note the absence of mass effect and edema.

Colloidal lesions develop ring enhancement and surrounding edema as the parasite degenerates and triggers the host immune response. MRI characteristics in the second colloidal phase include central T1 hypointensity, central T2 hyperintensity, ring-enhancement, and increased diffusion ( Fig. 9 ).

Colloidal stage and nodular calcified stage of neurocysticercosis. 39-year-old man with new seizure. ( A ) Axial post-GAD T1-weighted image shows a ring-enhancing lesion ( arrow ) with a thin, smooth ring favoring infection. An eccentric, internal “dot” should always raise the possibility of neurocysticercosis. ( B ) Axial T2-weighted image also shows this eccentric “dot” ( arrow ). The central T2 hyperintensity and T2 hypointense rim can mimic pyogenic infection, but DWI should help distinguish. ( C ) Axial ADC map demonstrates increased rather than reduced diffusion ( arrow ), suggesting atypical infection rather than pyogenic infection. ( D ) Axial gradient-echo image demonstrates a focus of susceptibility ( arrow ). ( E ) Axial CT shows that the abnormal focus of susceptibility corresponds to calcification ( arrow ). Note the lack of edema and mass effect. Such calcifications are an important clue to the diagnosis of neurocysticercosis which represents the late calcified stage that easily seen on CT.

During the nodular-granular phase, the cyst wall thickens, the cyst involutes, and the surrounding edema decreases.

Finally, the lesion mineralizes in the calcified stage and appears as small parenchymal calcifications on CT and small areas of susceptibility on MR gradient sequences (see Fig. 9 D, E).

The colloidal stage mimics other ring-enhancing lesions. In these cases, DWI may be helpful to differentiate a cysticercosis cyst from a pyogenic abscess because cysticercal cysts are dark. Also, ADC values are higher in neurocysticercosis than in TB granulomas.

Subarachnoid lesions may be small in the cortical sulci, but are often large and “grapelike” when located in the basilar cisterns or Sylvian fissures. In the past, the term “racemose” referred to this form in which the scolex was not thought to develop; however, it is now known that the scolex may be present, yet undergoes degeneration, such that the term “racemose” has fallen into disuse. Ruptured subarachnoid lesions may produce a basilar meningitis and lead to vasculitis and lacunar infarction. Ventricular cysticerci are usually isodense to CSF on CT and isointense to CSF on T2-weighted MR imaging, thus making them difficult to detect. Intraventricular cysticercosis occurs in approximately 20% of cases and is most often located in the aqueduct of Sylvius or fourth ventricle. Frequently, the accompanying hydrocephalus is detected before the obstructing cyst is identified. Therefore, FLAIR is a critical sequence to localize intraventricular cysts, because the cysts will appear hyperintense to CSF and become more conspicuous ( Fig. 10 ). Cysts can migrate within the ventricular system (the “ventricular migration sign”) and cause intermittent obstructive hydrocephalus. Treatment includes antiparasitic medications such as oral albendazole, steroids for edema, and antiseizure medications in selected cases.

Intraventricular neurocysticercosis. 30-year-old man with increasing headache. ( A ) Axial noncontrast CT shows enlargement of the fourth ventricle and a round eccentric nodule within the fourth ventricle ( arrow ). Note that the nodule appears too small to obstruct the fourth ventricle. ( B ) Axial CT at a higher level reveals enlargement of the lateral and third ventricles compatible with hydrocephalus. A clue to the etiology of the fourth ventricular lesion is the focal calcification in the left inferior frontal lobe ( arrow ). ( C ) Axial noncontrast T1-weighted image shows an atypical appearance consisting of intrinsic T1 hyperintensity in a neurocysticercosis cyst, secondary to proteinaceous debris ( arrow ). ( D ) Coronal FLAIR image shows that the cyst actually fills the entire fourth ventricle ( arrow ), explaining the obstructive hydrocephalus. This case illustrates why FLAIR can be helpful for identifying intraventricular cysts, as they can be difficult to see on CT and on T2-weighted images because they often follow CSF density and intensity, respectively. ( E ) Gross pathologic specimen revealing the proteinaceous components of this cyst.

Aspergillosis

Invasive CNS aspergillosis is rare, but is seen with increased frequency in immunosuppressed patients, particularly after bone marrow transplantation (BMT). Because humans are infected by inhaling spores, the lungs and paranasal sinuses are the main sites of infection. Cerebral involvement may also result from hematogenous spread from the lungs or direct invasion from the sinuses. Invasive CNS aspergillosis has high morbidity and mortality, but case reports do note survival with early, aggressive antifungal therapy and surgical resection. As clinical and laboratory features do not always confirm the diagnosis, neuroimaging plays a key role.

Imaging patterns depend on lesion age and immunologic status of the patient. The angioinvasive nature of the fungus helps explain the CT and MR imaging features of these cortical and subcortical septic infarctions. Aspergillosis also has a unique affinity for perforating arteries that supply the basal ganglia, thalami, and corpus callosum. In severely immunocompromised patients, the lesions appear as poorly defined areas of CT hypodensity or T2 hyperintensity on MRI, without significant mass effect, surrounding edema, or enhancement owing to the lack of a host immune response. In more immunocompetent patients, or as the immune function recovers after BMT, subtle peripheral or ring enhancement may be seen with surrounding vasogenic edema ( Fig. 11 ). Another important clue to the diagnosis is the presence of hemorrhage within these septic infarcts (seen as T1 hyperintensity, T2 hypointensity, and abnormal magnetic susceptibility on gradient sequences). In addition, pyogenic abscesses typically have a smooth outer wall, whereas fungal abscesses tend to have a crenated wall with intracavitary projections. Although early septic infarcts may show reduced diffusion, Luthra and colleagues found reduced diffusion only in the wall and projections of the fungal abscess, whereas the core did not show reduced diffusion, distinguishing it from pyogenic and tubercular abscesses.

Invasive aspergillosis. 11-year-old girl with neutropenia after bone marrow transplantation and new fevers. ( A ) Axial T2-weighted image shows a large, predominately T2 hyperintense lesion that involves most of the right inferior frontal lobe, putamen, and caudate head ( large arrow ). Note the small amount of mass effect given the size of the lesion. Also, note the small T2-hypointense areas within this lesion ( short arrow ). ( B ) Axial post-GAD T1-weighted image shows mild peripheral ring enhancement ( arrow ). Again, there is little to no mass effect. ( C ) Coronal gradient-echo image demonstrates susceptibility within this mass ( arrow ), consistent with hemorrhage. Minimal enhancement, minimal mass effect, and hemorrhage are all clues to diagnosis of invasive aspergillosis in this neutropenic patient. ( D ) Axial ADC map demonstrates reduced diffusion along the margins of the lesion ( arrow ), but no centrally reduced diffusion that is typical for pyogenic infection.

Toxoplasmosis

Toxoplasmosis is caused by the parasite Toxoplasma gondii and is the most common mass lesion in patients with AIDS. Fortunately, the number of cases has declined significantly within the past decade because of the advent of highly active antiretroviral therapy (HAART). T gondii is an obligate intracellular protozoan that exists in 3 forms: oocysts, tachyzoites, and bradyzoites. Tachyzoites are the rapidly multiplying form and they convert to bradyzoites or tissue cysts when they localize to the CNS. Toxoplasmosis is a ubiquitous organism with titers as high as 70% in the normal adult population. The primary form of transmission is ingestion of undercooked meat, but also blood transfusions, contaminated needles, and contact with cat feces can result in the infection. HIV-infected patients become most susceptible to toxoplasmosis when their CD4 counts are less than 100 cells/μL. The most common presenting symptom is headache, but fever, altered mental status, and focal deficits are also seen.

On noncontrast CT, lesions are usually multiple, hypodense, and located in the basal ganglia, thalami, and corticomedullary junction. The lesions frequently calcify after treatment. On MRI, the T2 signal characteristics can be variable, ranging from T2 hyperintense to T2 iso- or even hypointense. On T1-weighted images, the lesions are hypointense, but intrinsic T1 shortening has been described in a few cases, thought to represent hemorrhage. Smooth, ring enhancement is typically seen on post-GAD images, but smaller lesions may have more nodular enhancement. An imaging finding highly suggestive of toxoplasmosis is the “asymmetric target sign,” which consists of a small eccentric nodule of enhancement along the enhancing wall, thought to represent infolding of the cyst wall ( Fig. 12 ). This sign is specific, but not sensitive (seen in ∼30% cases). Recently, a similar target sign has been described on FLAIR and T2-weighted imaging that consists of 3 layers: T2 hypointense core alternating with an intermediate zone of T2 hyperintensity and a T2 hypointense rim. Although DWI signal can be variable in toxoplasmosis, most investigators have found that most lesions have increased diffusion on DWI.

Toxoplasmosis. 41-year-old HIV-positive man with new right-sided weakness. ( A ) Axial T2 image shows 3 dominant lesions with surrounding vasogenic edema: left caudate head, right parahippocampal gyrus, and right frontal lobe ( arrows ). Note that the 2 larger lesions are T2 hypointense centrally ; this would be atypical for pyogenic abscess. ( B ) Axial T1-weighted post-GAD image shows ring enhancement ( arrows ). Note the “eccentric target sign,” which is shown best in the right parahippocampal lesion. Although this sign is not sensitive, it is fairly specific for toxoplasmosis. ( C ) An additional axial T1-weighted post-GAD image shows another lesion in the right inferior frontal lobe, which also demonstrates the “eccentric target sign” ( arrow ). ( D ) Axial DWI shows no evidence of reduced diffusion within the left basal ganglia lesion ( arrow ).

In the HIV-infected patient, the major differential consideration for multiple ring-enhancing lesions is primary CNS lymphoma. Imaging features that favor lymphoma include subependymal spread, reduced diffusion owing to hypercellularity, and corpus callosum involvement. Most patients are treated empirically for toxoplasmosis with pyrimethamine and sulfadiazine for a duration of 6 weeks. Radiographic improvement should occur in most (>90%) patients by 14 days. If a follow-up MRI does not show improvement after empiric therapy, thallium-201 brain single-photon emission computed tomography (SPECT) or fluorodeoxyglucose positron emission tomography (FDG PET) may be useful. Both studies classically show increased uptake only in lymphoma, but have variable sensitivities. Other useful MR techniques include DWI, MRS, and MR perfusion. Lymphoma tends to have reduced diffusion because of its hypercellularity, whereas toxoplasmosis tends to show facilitated diffusion. MRS in lymphoma shows marked elevation of choline owing to hypercellularity and membrane turnover. In contrast, MRS in toxoplasmosis confirms the infectious origin with elevated lactate and lipid peaks. On MR perfusion, because lymphoma is a hypervascular neoplastic process, there is elevated relative cerebral blood volume (rCBV), whereas toxoplasmosis shows decreased rCBV. In persistently equivocal cases, a biopsy is usually the next course of action.

Acute disseminated encephalomyelitis

Acute disseminated encephalomyelitis (ADEM) is a monophasic inflammatory demyelinating disorder associated with a recent infection or vaccination. Infection or vaccination is thought to trigger an autoimmune attack, possibly via “molecular mimicry.” Patients usually present with nonspecific symptoms, including headache, vomiting, fever, and lethargy. Children are affected more often than adults. On MR imaging, multifocal T2 hyperintense lesions are typically seen in the subcortical white matter, thalami, and basal ganglia, but lesions may be tumefactive and mimic other ring-enhancing infections and tumors ( Fig. 13 ). Therefore, it is crucial for the radiologist to consider tumefactive demyelination with all ring-enhancing lesions because of the drastically different management. Specifically, ADEM is treated medically with intravenous high-dose steroids and surgery should be avoided. Nonresponsive patients can also be treated with plasma exchange or immunoglobulins.

Acute disseminated encephalomyelitis (ADEM). 43-year-old man with acute altered mental status. ( A ) Axial T1-weighted post-GAD image shows multiple ring-enhancing lesions along with additional smaller nodules of enhancement. ( B ) Axial FLAIR image shows T2 hyperintensity within these lesions; however, there is little to no surrounding vasogenic edema or mass effect. This is a clue that the lesion is a demyelinating process rather than tumor or infection. ( C ) Axial DWI shows no reduced diffusion, also mitigating against pyogenic infection. ( D ) Axial T1-weighted post-GAD image obtained 1 week following steroid treatment shows marked interval improvement with near resolution of many of the lesions.

The imaging features most suggestive of tumefactive demyelinating lesions include large lesions with little to no mass effect, minimal edema, incomplete ring of enhancement at the “leading edge” of demyelination on the white matter side of the lesion, central dilated veins within the lesion, and decreased perfusion (rCBV).

Herpes encephalitis and other viral encephalitis

Encephalitis refers to a diffuse parenchymal inflammation seen as T2 hyperintensity on MR imaging. The most common viral encephalitides include herpes simplex viruses (HSV-1 and HSV-2), herpes zoster, arboviruses, and enteroviruses.

HSV-1 is responsible for 95% of herpes encephalitides and occurs primarily in adults and older children. This devastating necrotizing encephalitis results from reactivation of latent HSV-1 infection within the trigeminal (or gasserian) ganglion, and is the most common cause of fatal sporadic encephalitis. The infection spreads intracranially along meningeal branches of the trigeminal nerve, thus explaining the predilection for the temporal lobe. Patients typically present with fever, headaches, seizures, and focal neurologic deficits. The high mortality rate of HSV-1 herpes encephalitis, approaching 70% without treatment, and the availability of effective antiviral drugs, make early diagnosis key. Because polymerase chain reaction (PCR) is not 100% sensitive, early recognition of MR imaging findings can be critical.

The spectrum of imaging findings reflects the edema, hemorrhage, and necrosis seen pathologically. CT can be normal or show ill-defined areas of hypodensity in the medial temporal lobes and/or inferior frontal lobes. MRI better characterizes the extent of injury and classically shows bilateral, but asymmetric, involvement of the limbic system. Cortical swelling with T2 hyperintensity and T1 hypointensity are seen in the medial temporal lobe, insular cortex, cingulate gyrus, and inferior frontal lobe ( Figs. 14 and 15 ). The pons may also be involved, likely from retrograde transmission along the cisternal segment of the trigeminal nerve. Petechial hemorrhages can manifest as T1 shortening or abnormal susceptibility on gradient-echo sequences. T1 shortening can also be seen in a gyriform configuration owing to cortical hemorrhage. Enhancement is variable, may be patchy or gyral, and generally develops later in the infection (after the T2 abnormality). Areas of reduced diffusion have been shown to be one of the earliest findings ; however, DWI can be variable. Some investigators report more severe, nonresponsive cases to have reduced diffusion, whereas cases with a good response to treatment and more favorable outcome show resolution of reduced diffusion, or even increased diffusion at the onset.

Herpes encephalitis. 26-year-old man with new seizure and fever. ( A ) Axial FLAIR image demonstrates right medial temporal lobe enlargement and hyperintensity ( arrow ). ( B ) Axial T1-weighted post-GAD image shows slight linear enhancement posteriorly ( arrow ). Note that enhancement in HSV is variable and dependent on the time after onset. ( C ) Axial DWI shows reduced diffusion ( arrow ) and confirms involvement of the left medial temporal lobe.

Herpes encephalitis (typical distribution). 44-year-old woman with mental status changes. ( A, B ) Axial T2-weighted images at 2 different levels show bilateral, asymmetric involvement of the right temporal lobe, insula, and cingulate gyrus ( arrows ). ( C ) Axial T1-weighted post-GAD image shows little to no enhancement. ( D ) Axial DWI demonstrates reduced diffusion.

The primary differential considerations for abnormalities of the temporal lobe include MCA infarct, infiltrating gliomas, and limbic encephalitis. The basal ganglia are usually spared, and the medial temporal lobe is usually involved before the lateral temporal lobe, in herpes encephalitis, thus helping to differentiate from an acute MCA infarct ( Fig. 16 ). The clinical history, including the onset and chronicity of symptoms, should help differentiate infarct from infiltrating tumor.

Middle cerebral artery infarction (contrast with HSV). ( A ) Axial CT shows hypodensity involving the left basal ganglia and temporal lobe. Note that involvement of the basal ganglia is atypical for HSV and this distribution suggests a large left MCA infarct involving the M1 segment and lenticulostriate vessels. ( B ) Coronal FLAIR in a different patient shows hyperintensity in the lateral temporal lobe with relative sparing of the medial temporal lobe, suggesting MCA infarction rather than HSV. HSV usually involves the medial temporal lobe first.

Cryptococcus

Cryptococcus neoformans is the most common CNS fungal infection in patients with AIDS and the third most common cause of CNS infection in AIDS, after HIV encephalopathy and toxoplasmosis. It typically manifests as a chronic basilar meningitis or meningoencephalitis with minimal inflammation. C neoformans is a ubiquitous yeastlike fungus found in soil contaminated by bird excreta. Patients are most vulnerable to Cryptococcus when their CD4 counts drop below 100 cells/μL. The diagnosis of CNS cryptococcosis can be made on the basis of a series of microbiologic investigations, including CSF culture and positive identification of the yeast with India ink staining; elevations in cryptococcal antigen latex agglutination titers in CSF and blood; and positive results with blood culture.

The most common imaging finding for cryptococcal meningitis, albeit nonspecific, is communicating or noncommunicating hydrocephalus. Cryptococcus tends to spread along the perivascular (Virchow-Robin) spaces resulting in “gelatinous pseudocysts.” These appear as multiple, nonenhancing, rounded, T2 hyperintense, T1 hypointense lesions in the basal ganglia ( Fig. 17 ). Other imaging findings include meningeal enhancement and ring-enhancing granulomas (“cryptococcomas”) with a predilection for the choroid plexus. Immunocompromised patients are less likely to have hydrocephalus or enhancing parenchymal lesions and are more likely to have gelatinous pseudocysts on imaging. Patients are treated with antifungal agents such as fluconazole or amphotericin B.

Cryptococcal gelatinous pseudocysts. 47-year-old HIV-positive man with headache. ( A ) Axial T2-weighted image shows innumerable tiny T2 hyperintense foci within the caudate head, lentiform nuclei, and thalamus, bilaterally ( arrows ). ( B ) Axial T1-weighted post-GAD image shows no enhancement , thus excluding other entities found in the basal ganglia such as toxoplasmosis and lymphoma. ( C ) Axial DWI shows no reduced diffusion , thus excluding acute and/or subacute ischemic injury. ( D ) Coronal gross specimen at the level of the right frontal horn demonstrates mucinous material filling the putaminal perivascular spaces. ( E ) Histology slide shows positive India ink staining.

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