Infection CNS Imaging

8/3/2019 Infection CNS Imaging

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CNS tuberculosis

Overview

Tuberculosis (TB) of the central nervous system (CNS) is a granulomatous infection

caused by Mycobacterium tuberculosis. The disease predominantly involves the brain

and meninges, but occasionally, it affects the spinal cord. Clinical diagnosis can bedifficult; therefore, imaging has an important role in establishing the diagnosis (see the

images below).

Contrast-enhanced computed tomography (CT) scan in a patient

with tuberculous meningitis demonstrating marked enhancement in the basal cistern and

meninges, with dilatation of the ventricles. T1-weighted gadolinium-

enhanced magnetic resonance image in a child with a tuberculous abscess in the left

parietal region. Note the enhancing thick-walled abscess.

Preferred examination

Magnetic resonance imaging (MRI) with gadolinium enhancement is the preferredmethod of initial investigation. MRI is the most sensitive test for detecting the extent of

leptomeningeal disease and is superior to computed tomography (CT) scanning in

detecting parenchymal abnormalities, such as tuberculomas, abscesses, and infarctions.MRI also readily depicts hydrocephalus.[1, 2, 3]
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Cerebrospinal fluid (CSF) analysis is usually used to detect a decreased glucose level,

elevated protein levels, and a slight pleocytosis. Results of CSF polymerase chain

reaction (PCR) assays may be diagnostic.

Limitations of techniques

Conventional MRI may cause early meningitis and early infarcts to be missed, and noMRI findings are pathognomonic for TBM. Diffusion-weighted imaging, if available,

depicts infarctions in the hyperacute stage.

For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections

CenterandBrain and Nervous System Center. See also eMedicine's patient educationarticles Tuberculosis and Brain Infection.

Radiography

Skull radiographic findings are usually normal. Rarely, in healed tuberculosis meningitis,faint parenchymal calcification is evident.

Degree of confidence

Calcifications on skull radiographs in patients with healed TBM or healed tuberculomasare nonspecific findings.

False positives/negatives

Skull calcification may indicate choroid plexus, pineal, and/or habenular calcification.

Computed Tomography

In tuberculosis meningitis (TBM), contrast-enhanced CT scanning of the brain depicts

prominent leptomeningeal and basal cistern enhancement. With ependymitis, linearperiventricular enhancement is present. Ventricular dilatation (eg, dilatation of the third

and fourth ventricles) due to hydrocephalus is usually seen. Often, low-attenuating focal

infarcts are seen in the deep gray-matter nuclei, deep white matter, and pons; these

infarcts result from associated vasculitis. The primary differential diagnoses are fungalmeningitis, bacterial meningitis, carcinomatous meningitis, and neurosarcoidosis. Basal

cistern and meningeal enhancement are seen in the first 2 images below. Vasculitis-associated infarcts are seen in the third image.
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Contrast-enhanced computed tomography (CT) scan in a patient

with tuberculous meningitis demonstrating marked enhancement in the basal cistern and

meninges, with dilatation of the ventricles. Contrast-enhancedcomputed tomography (CT) scan of a child with tuberculous meningitis demonstrating

acute hydrocephalus and meningeal enhancement. Extensive

infarcts of the right basal ganglia and internal capsule after the appearance of vasculitis inthe thalamoperforating arteries in a child treated for tuberculous meningitis.

Parenchymal cerebritis may cause hypoattenuation with little or no enhancement.Parenchymal tuberculomas demonstrate various patterns. Noncaseating granulomas arehomogeneously enhancing lesions. Caseating granulomas are rim enhancing; if these

have a central calcific focus, they may form a targetlike lesion. Granulomas may also

form a miliary pattern with multiple tiny nodules scattered throughout the brain. All

lesions are surrounded by hypoattenuating edema. The differential diagnoses includefungal infections, bacterial infections, neurocysticercosis, and cerebral metastases.
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Cryptococcal meningitis also occurs in patients with acquired immunodeficiency

syndrome (AIDS); however, the history is longer (ie, months) than that of TBM, and

perivascular cysts are often seen in the region of the basal ganglia. Perivascular cysts donot occur with TB. Toxoplasmosis usually causes a focal abscess in patients with AIDS.


CT scan findings are typical of granulomatous meningitis with parenchymal involvement.

Fungal infections and neurosarcoidosis may appear similar to CNS TB. At times,

bacterial infections and metastatic disease also may mimic CNS TB. CSF analysis oftenhelps in establishing the diagnosis.

Magnetic Resonance Imaging

MRI is more sensitive than CT scanning in determining the extent of meningeal and

parenchymal involvement.[4, 5]

In tuberculosis meningitis (TBM), gadolinium-enhanced T1-weighted imagesdemonstrate prominent leptomeningeal and basal cistern enhancement. With ependymitis,

linear periventricular enhancement is present. Ventricular dilatation due to hydrocephalus

is usually seen. Deep gray-matter nuclei, deep white matter, and pontine infarctionsresulting from vasculitis are hyperintense on T2-weighted images. Diffusion-weighted

MRI is especially sensitive in depicting early ischemic lesions when findings on the T2-

weighted MRIs are normal. The primary differential diagnoses are fungal meningitis,bacterial meningitis, carcinomatous meningitis, and neurosarcoidosis. (See the images

below.)

T2-weighted magnetic resonance image of a biopsy-proven, right

parietal tuberculoma. Note the lowsignal-intensity rim of the lesion and the surrounding
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hyperintense vasogenic edema. T1-weighted gadolinium-

enhanced magnetic resonance image in a patient with multiple enhancing tuberculomas in

both cerebellar hemispheres. T1-weighted gadolinium-enhanced

magnetic resonance image in a child with a tuberculous abscess in the left parietal region.

Note the enhancing thick-walled abscess. T1-weightedgadolinium-enhanced magnetic resonance image of the thoracic spinal cord in a patient

with acquired immunodeficiency syndrome (AIDS) and leptomeningeal tuberculosis.

Note the numerous granulomas on the dorsal surface of the cord and the dural
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enhancement. T2-weighted magnetic resonance image of the

thoracic spinal cord of a patient with 2 hyperintense intramedullary tuberculomas.

T2-weighted magnetic resonance

image of a patient with a tuberculoma in the right parietal lobe.

Parenchymal cerebritis may show hyperintensity with little or no enhancement on T2-

weighted images.

Parenchymal tuberculomas demonstrate various patterns. They are typically hypointense

on T2-weighted images, but they may be hyperintense as well. Tuberculomas, likebacterial cerebral abscesses, have hypointense walls or rims on T2-weighted MRIs. The

cause is unknown, but free oxygen radicals released by the inflammatory process are

believed to decrease T2 values. Noncaseating granulomas are homogeneously enhancing


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lesions. Caseating granulomas are rim enhancing. Granulomas may also form a miliary

pattern with multiple tiny, enhancing nodules scattered throughout the brain. Lesions are

typically surrounded by hyperintense edema on T2-weighted images. The differentialdiagnoses include fungal infections, bacterial infections, neurocysticercosis, and cerebral

metastases.

MR spectroscopy with a single-voxel proton technique can be used to characterize

tuberculomas and differentiate them from neoplasms (see the image below).Tuberculomas show elevated fatty-acid spectra that are best seen by using the stimulated-

echo acquisition mode technique and a short echo time. The necrosis of the waxy walls of

mycobacteria within the granuloma is believed to cause the elevation of fatty-acid peaks.The lactate peak is caused by anaerobic glycolysis and is found in inflammatory,

ischemic, and neoplastic lesions of the brain; this finding is nonspecific.

Proton spectroscopy trace of a patient with an

intracerebral tuberculoma demonstrating an elevated lactate peak (LA) with diminishedN-acetyl aspartate (NAA) and choline (CH) peaks typical of an inflammatory mass in the

brain.

MRI is especially useful in detecting leptomeningeal involvement of the spinal cord;

cauda equina; and intramedullary tuberculomas, which, although rare, can be detected in

patients with AIDS.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate

dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK],

gadoteridol [ProHance]) have been linked to the development of nephrogenic systemicfibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see

the eMedicine topicNephrogenic Systemic Fibrosis. The disease has occurred in patients

with moderate to end-stage renal disease after being given a gadolinium-based contrastagent to enhance MRI or magnetic resonance angiography scans.

NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or

dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin;yellow spots on the whites of the eyes; joint stiffness with trouble moving orstraightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle

weakness. For more information, see Medscape.

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MRI improves diagnostic confidence, but images in patients with fungal infections can

appear identical to those in patients with neurosarcoidosis. At times, metastatic disease

and bacterial infections also can mimic CNS TB.

Ultrasonography

In infants, brain ultrasonography can be used to detect hydrocephalus.


Usually, CT scanning or MRI is required for definitive diagnosis.

Nuclear Imaging

Single photon emission CT scanning with hexamethylpropyleneamine oxime (HMPAO)

can be used to assess the degree and extent of cerebral ischemia resulting from TBMcerebral vasculitis.


Findings are specific only for diminished cerebral perfusion.

Angiography

Although not currently in routine use in patients with CNS TB, cerebral angiography

demonstrates findings of vasculitis. These findings include vascular irregularity, vascularnarrowing, and vascular occlusion. Vessels commonly affected include the terminal

portions of the internal carotid arteries, as well as the proximal parts of the middle and

anterior cerebral arteries.


Features of vasculitis and/or vascular occlusion are detected in other inflammatory andischemic cerebral conditions.


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Brain Abscess

Overview

The introduction of infectious agents results in various responses from the central

nervous system (CNS). In the earliest stage of purulent bacterial brain infection, the

generalized initial reaction is cerebritis. Within the background of cellular response to theinfection, cerebritis evolves into a localized abscess in a predictable series of stages.

Neuroimaging of these stages reflects the underlying pathophysiology of abscess

formation. Variations in the brain's reaction at different locations and similarities in the

brain's reaction to certain agents and in the appearances of aggressive neoplasms allrequire correlation of medical history, neuroimaging, and results of microbiologic

analysis.

Early and improved diagnostic imaging techniques have allowed the discovery of brainabscess at a much earlier stage. (See the images below.)

Brain abscess. Axial CT scan in a patient who presented with a

headache, fever, and a history of a recent pneumonia demonstrates a poorly defined area

of posterior parietal brain edema (arrows). Early cerebritis may not outline a focal mass

clearly. Brain abscess. Axial nonenhanced cranial CT scan in a

patient who presented with fever, headache, and a previous paranasal sinus infection

demonstrates a poorly defined pattern of mass effect and low attenuation in the left


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temporal lobe. The pattern is consistent with possible early cerebritis; however, glioma

and infarct may have similar presentations. Brain abscess.Three-dimensional surface model of a cranial CT scan in a patient with a postcraniotomy

abscess. The large deformity in the skull indicates the route of abscess spread.

Brain abscess. Axial T2-weighted MRI in a patient with a

right frontal abscess. Note the mass effect and surrounding edema. The wall of theabscess is relatively thin (black arrows).


The preferred initial examination of the patient in whom brain abscess is suspected is

MRI with and without gadolinium enhancement. Similar diagnostic results can be

expected from cranial CT scans without and with the intravenous administration ofiodinated contrast medium. Both imaging techniques help detect the mass effect of the

abscess; however, findings in MRI with a diffusion protocol are more specific in

differentiating cerebral tumor, stroke, and abscess. In particular, examination of the

metabolite peaks with MR spectroscopy can help to specifically differentiate tumor,radiation necrosis, and abscess by identifying their different spectral profiles.[1, 2]

Perfusion MRI has also been used to differentiate these lesions by evaluating vascularity

with blood flow analysis with dynamic intravenous gadolinium contrast injection studies.

Occasionally, distinguishing brain abscess from neoplasm or postoperative changes frominfection is difficult. In these patients, a nuclear agent can be used to tag white blood cells

or antibodies to help differentiation.


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dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK],

gadoteridol [ProHance]) have been linked to the development of nephrogenic systemicfibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see

the eMedicine topicNephrogenic Systemic Fibrosis. The disease has occurred in patients

with moderate to end-stage renal disease after being given a gadolinium-based contrastagent to enhance MRI or MRA scans.

NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or

dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin;

yellow spots on the whites of the eyes; joint stiffness with trouble moving orstraightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle

weakness. For more information, see Medscape.

Limitations of techniques

Plain radiographs of the paranasal sinuses can only suggest a possible etiology forcerebral abscess. Early findings of CT examinations are not specific for cerebral abscess.The edema pattern and moderate mass effect cannot be differentiated from tumor or

stroke in some patients. MRI findings in patients with cerebritis may resemble findings in

stroke, while findings in the infarcts that result from vasculitis and cerebritis may

resemble those of embolic strokes. Nuclear medicine single photon emission computedtomographic (SPECT) findings are not specific for brain abscess unless a white cell tag is

used.

Follow-up scans for certain infectious agents, such as M tuberculosis, may be necessarybecause infection by these organisms may not follow a predictable response to treatment.

Tuberculosis-related brain abscesses that retain positive results to culture and smearsfollowing 4 weeks of treatment may not represent treatment failure. In addition, treatment

of fungal infections may require many weeks of treatment with interval follow-upimaging studies. Follow-up imaging during the treatment for toxoplasmosis is important

in avoiding brain biopsy.

Intervention

Intervention in patients with cerebral abscess is most commonly limited to biopsy and

aspiration of infectious material that may represent the origin of a CNS infection.

Aspiration and biopsy of small lesions is performed best using a CT-guided computer-assisted technique or with the aid of an external frame, which (with the aid of CT data)

directs the placement of the aspiration needle. More recently, fully computer-aided

virtual imaging programs have provided greater flexibility in the application of both CT

and MRI sets during craniotomy procedures and in the aspiration of selected lesions.Intraoperative ultrasonography may aid in the detection and treatment of relatively large

superficial abscess collections.
http://emedicine.medscape.com/article/1097889-overviewhttp://www.medscape.com/viewarticle/550122http://emedicine.medscape.com/article/1097889-overviewhttp://www.medscape.com/viewarticle/550122


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Recent studies

In a study by Chiang et al, diffusion, perfusion-weighted, and spectroscopic MRIs were

able to differentiate cerebral abscesses from necrotic tumors. The authors found that the

mean apparent diffusion coefficient value at the central cavities of the cerebral abscesses

were significantly lower; the mean relative cerebral blood volume values of the necrotictumor walls were significantly higher; and amino acids were present only in the cerebral

abscesses.[3]

Sepahdari et al found that in 9 cases of orbital cellulitis, including 6 cases of pyogenicabscess, diffusion-weighted imaging confirmed abscess in a majority of cases without

contrast-enhanced imaging. According to the authors, this may be of particular

importance in patients in whom the use of contrast is contraindicated. Diffusion-weightedimaging improved diagnostic confidence in virtually all the patients with orbital abscess

when it was used along with contrast-enhanced imaging.[4]

For excellent patient education resources, visit eMedicine's Brain and Nervous SystemCenter. Also, see eMedicine's patient education article Brain Infection.

Radiography

Radiographic findings usually are limited to paranasal or mastoid sinus opacification;

however, gas bubbles or air-fluid levels within the cranium may indicate a gas-producing

organism or a communication with the paranasal sinuses or the nose.

Direct evidence of osteomyelitis of the skull is generally a mixed pattern of lucency witha destruction of the outer or inner tables of the skull.

Occasionally, foreign bodies (eg, in gunshot wounds) or osteomyelitis of the maxillary

bone may indicate a probable source for an intracranial abscess. Bone destruction of the

roof, floor, or lateral wall of the sinuses may indicate an aggressive osteomyelitis withextension into the intracranial space.


Clouding of the sinuses is not a direct indication of an intracranial abscess, merely a

possible etiology. Air-fluid levels within the cranial vault strongly suggest abscess

formation.


Patients with established intracranial abscesses may develop fluid retention within the

mastoid and paranasal sinuses secondary to endotracheal intubation and chronicdisability. Most patients with osteomyelitis of the mandible or maxilla do not develop

intracranial abscesses.
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Computed Tomography

On nonenhanced CT, Toxoplasma encephalitis appears as areas of isointense or

hypodense mass effect. The basal ganglia and the corticomedullary junction are mostcommonly affected. Contrast-enhanced CT demonstrates a ring or nodular enhancement

pattern with lesions of 1-3 cm in diameter. The enhancement is greatest within theintermediate zone where inflammation is the greatest. (See the images below.)

Brain abscess. Axial CT scan with intravenous (IV) contrast

enhancement in a patient who presented with headache and fever. Initial CT scan

demonstrated mass effect and edema within the left temporal lobe. Since the edema and

mass pattern were poorly defined, a biopsy of the left temporal lobe was performed toexclude a tumor. Following resection of the temporal lobe abscess, extracranial, subdural,

and intracerebral abscesses developed (arrows). Brainabscess. Coronal multiplanar reformatted CT scan in a patient who developed temporal

brain abscesses (yellow arrows) and a left-sided extracranial abscess (white arrow)

following surgery of the left temporal skull. Brain abscess.

Axial contrast-enhanced CT scan in a patient who was treated surgically for a depressed


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skull fracture. The left parietal cranial injury has become complicated by an abscess of

the subgaleal space (SGA), of the epidural space (EDA), and within the left cerebral

hemisphere (CA). Edema related to the abscess is indicated by the yellow arrow. The

cerebral abscess wall enhances (white arrow). Brain

abscess. Axial CT scan with intravenous (IV) contrast enhancement in a patient withfever and diplopia demonstrates an enhancing mass arising from within the ethmoid air

cells, with expansion into the medial right orbit (black arrow). The optic nerve is in

contact with the mass (blue arrow).

CT manifestations of an intracranial abscess depend on the stage of the abscessformation. The earliest phase may be related to meningitis, with no findings on

unenhanced CT studies. Enhancement of the meningeal surfaces is a nonspecific and

inconsistent finding in patients with meningitis.[5]

During early cerebritis, nonenhanced CT scans may demonstrate normal findings or mayshow only poorly marginated subcortical hypodense areas. Contrast-enhanced CT studies

demonstrate an ill-defined contrast-enhancing area within the edematous region.

During the early stage of a formed abscess, the lesion coalesces, with an irregularenhancing rim that surrounds a central low-attenuating area.

Scans obtained with a time delay following contrast enhancement in cerebritis may show

contrast "filling in" the central low-attenuating region. A formed abscess will not "fill in"

the central portion of the abscess.

Peripheral edema results in considerable mass effect with sulcal obliteration.

The early capsule stage is characterized by a distinct collagenous capsule, while a

relatively thin, well-delineated capsule marks the final stage of a fully formed abscess.

Ring-enhancing lesions are commonly seen in various disease conditions. Besides

abscess, metastatic brain tumors, some primary brain tumors (particularly grade 4astrocytomas), granulomas, resolving hematomas, and infarctions are associated with a

ringlike enhancement pattern. The cystic pattern is a particularly prominent feature of

cysticercosis, due to the infestation of the larva ofTaenia solium. In most pyogenic

abscesses, the ring is smooth and thin walled (< 5 mm). The medial margin is oftenthinner along the medial margin, which may reflect the variation of cerebral perfusion of

gray and white matter. The wall of a cystic neoplasm is generally thick and irregular,

frondlike, or lobulated. (See the images below.)


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Brain abscess. Axial CT scan obtained with intravenous(IV) contrast enhancement in a patient with fever and headaches. Because a definite

diagnosis of abscess is difficult to determine in some patients in whom ring enhancement

is not associated with an apparent source of infection, stereotactic biopsy and culture of a

walled abscess may be necessary. Brain abscess. Surface

3-dimensional model of a craniofacial CT scan in a patient with headache, orbitalswelling, and diplopia of 48 hours' duration. Note the remarkable degree of right orbital

swelling, which has resulted in the right lid being closed.


The moderate vasogenic edema that is seen in the early stages of cerebritis and abscess

formation must be interpreted in the context of the clinical presentation. The presence offever, known infection, and immunosuppression supports the probable diagnosis of early

abscess formation; however, cerebrovascular accidents (CVAs) and tumors must be

included in the differential diagnosis. Later, the well-formed abscess wall must beinspected within the context of other known malignancies, which may be a source for

cerebral metastatic disease, glioma, lymphoma, and multiple sclerosis.


False-negative CT scans may occur if intravenous contrast enhancement is not adequate

or if imaging of the brain is performed too soon after contrast administration, which can

happen easily when a rapid CT (eg, multisection) scanner is used.

False-positive results primarily are the result of mistaking alternative causes of ringlikelesions of the brain for an abscess. Ring-enhancing lesions must be placed into the

differential diagnosis, which includes some primary brain tumors (eg, anaplastic


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astrocytoma), metastatic brain tumors, abscess, granuloma, resolving hematoma, brain

infarct, thrombosed vascular malformation, demyelinating disease (eg, multiple

sclerosis), thrombosed aneurysm, and other primary brain tumors, particularly primaryCNS lymphoma in patients with AIDS.


MRI of the brain without and with intravenous gadolinium contrast enhancement is the

most sensitive test forToxoplasma encephalitis. Lesions with contrast may behyperintense compared with normal brain tissue and may be difficult to identify

compared to the edema pattern otherwise seen in the surrounding brain. The ring

enhancement, which is best seen on T1-weighted gadolinium-enhanced studies,represents the enhancement within the most active area of the infection. Following

treatment with pyrimethamine and sulfadiazine or clindamycin, the lesions become

reduced in size with resolution of the ring of enhancement. (See the images below.)

Brain abscess. Coronal T1-weighted postgadolinium-enhanced

MRI of the brain in a patient with fever following head trauma. Osteomyelitis of the skull

developed in this patient following cranial trauma. Bilateral subdural abscesses (yellow

arrow) developed by direct extension of the infection beyond the skull. The leading edgeof the cerebritis is marked by the pattern of enhancement within the deeper margins of

the left parietal lobe (white arrow). Brain abscess. Axial T2-weighted MRI in a patient with a right frontal abscess. Note the mass effect and

surrounding edema. The wall of the abscess is relatively thin (black arrows).


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Brain abscess. Gadolinium-enhanced coronal T1-weighted MRI

in a patient who presented with headache, fever, and diplopia. The right frontal lobe ofthe brain is shifted across the midline (double arrow) by an intracranial abscess (single

black arrow) that has extended upward from the medial right orbit and medial ethmoid air

cells (curved dotted arrow). Aspergillus organisms were recovered from the sinuses and

brain tissue. Brain abscess. Coronal T1-weighted

gadolinium-enhanced MRI in a patient with sudden onset of diplopia, fever, and right

orbital swelling. Note the enhancement within the right ethmoid sinuses from which theinfection arose. The medial superior right maxillary sinus has been destroyed (yellow

arrow). Brain abscess. Coronal T1-weighted spin-echogadolinium-enhanced MRI demonstrates a central zone of enhancement within the

abscess, with a zone of decreased brightness (edema, white arrow). Nocardia organisms


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were cultured from within the abscess cavity. Brain abscess.

Axial fluid-attenuated inversion recovery (FLAIR) MRI of a left occipital-parietal brainabscess. The edema pattern (white arrows) surrounds the central abscess (A). A

secondary (daughter) abscess is noted anterior to the primary abscess cavity.

MRI findings of brain abscess vary with time.[6, 7, 8, 9, 10, 11, 12]

Early cerebritis stage

The early cerebritis stage presents as an ill-defined subcortical hyperintense zone that can

be noted on T2-weighted imaging.

Lesions appearing hyperintense on diffusion-weighted imaging with apparent-diffusion-coefficient (ADC) values of < 0.9 are most commonly brain abscess, whereas

hypointense lesions on diffusion-weighted imaging with ADC values > 2 are more likely

nonabscess cystic lesions.

Contrast-enhanced T1-weighted studies demonstrate poorly delineated enhancing areaswithin the isointense to mildly hypointense edematous region.

Late cerebritis stage

During the late cerebritis stage, the central necrotic area is hyperintense to brain tissue onproton-density and T2-weighted sequences.

The thick, somewhat irregularly marginated rim appears isointense to mildly

hyperintense on spin-echo T1-weighted images and isointense to relatively hypointenseon proton-density and T2-weighted scans.

Peripheral edema is common. The rim enhances intensely following contrast

administration. Satellite lesions may be demonstrated.

Early and late capsule stages


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During the early and late capsule stages, the collagenous abscess capsule is visible prior

to contrast as a comparatively thin-walled, isointense to slightly hyperintense ring that

becomes hypointense on T2-weighted MRIs.

Diffusion-weighted imaging aids in depiction of specific features of a brain abscess. If a

cerebral abscess ruptures into the ventricular system, diffusion-weighted imagesdemonstrate specific patterns.

Purulent material within the ventricle appears similar to that of the central abscess cavity,with a strongly hyperintense signal on diffusion-weighted images.

Magnetic resonance spectroscopy

Magnetic resonance (MR) spectroscopy may be helpful in the differential diagnosis of

toxoplasmosis versus CNS lymphoma. CNS lymphoma generally shows a mild pattern of

elevated lipid and lactate peaks, with a prominent choline peak with some other normal

metabolites. In toxoplasmosis, there are elevated lipid and lactate peaks, while othernormal brain metabolites are nearly absent.

Diffusion-weighted MRI

Diffusion-weighted MRI may be useful in differentiating abscess from necrotic tumor.

Diffusion-weighted echo planar images demonstrate an abscess as a high signal intensity

with a corresponding reduction in the apparent diffusion coefficient. The brightness on

diffusion-weighted imaging (DWI) is related to the cellularity and viscosity of thecontents within the abscess cavity. Tumors with central necrosis have marked

hypointensity on diffusion-weighted images and much higher apparent diffusion

coefficient values. The pattern described above for an abscess has also been noted foracute cerebral infarction.


In patients with ring-enhancing cerebral mass lesions, restricted diffusion is characteristic

but is not pathognomonic for abscess. Low apparent diffusion coefficient values also may

be found in brain metastases. Diffusion imaging techniques should be corrected for T2brightness contribution. Corrected diffusion maps more accurately reflect the relative

diffusion within a large or complex lesion. Diffusion imaging is more sensitive than

conventional MRI alone in detection of changes due to infections and ischemic lesions.

Single-voxel proton MR spectroscopy is useful in differentiating ringlike enhancedlesions that cannot be diagnosed correctly using enhanced MRI alone. MR spectroscopy

can help to specifically differentiate tumor, radiation necrosis, or abscess by identifying

their different spectral profiles. Perfusion MRI has also been used to differentiate theselesions by evaluating their degree of vascularity through dynamic blood flow analysis

studies.


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Diffusion MRI does not help in differentiating brain abscess formation from focal brain

infarcts related to venous thrombosis, although superior imaging of the anatomic

distribution of lesions proves useful. Restricted diffusion within ring enhancement is not

pathognomonic for brain abscess.

Ultrasonography

On ultrasonograms, cerebral abscess is depicted as a complex cystic pattern with an

echogenic wall and an ultrasonographically hypoechoic or mildly hyperechoic centralzone of necrosis. Cerebral ultrasonography is rarely used in the evaluation of cerebral

abscess in the adult, except for intraoperative guidance for aspiration procedures, because

the intact skull is a barrier to the procedure.

In the neonate, abscess can be diagnosed by using ultrasonographic images obtained

through the anterior fontanelle. Brain ultrasonograms can reveal the size and number ofabscesses but provide only a limited suggestion of a possible origin for the infection.

Ultrasonography-guided aspiration of brain abscesses through a single burr hole has beenperformed with excellent overall results.

Ultrasonography cannot help to differentiate a cystic neoplasm from an abscess. When

seen in the neonate, periventricular and arachnoid cysts commonly are not abscesses.

Porencephalic cysts may suggest thin-walled abscesses if communication with the

ventricle is not depicted clearly. Arachnoid cysts have thin walls with a marked,hypoechoic pattern.

Nuclear Imaging

Brain SPECT imaging by using thallous chloride Tl 201 (thallium-201;201 Tl)can help

detect and differentiate infectious processes from lymphoma and other primary brainneoplasms. Brain abscess may be evaluated using gallium Ga 67 (gallium-67;67 Ga)

citrate and technetium-99mm hexamethylpropyleneamine oxime (HMPAO)labeled

leukocytes. In patients with an active abscess, nuclear agents collect in the wall of theabscess. Similar findings occur within high-grade brain tumors (glioma). Differential

considerations of rounded (ring) lesions of the brain include some primary brain tumors

(eg, anaplastic astrocytoma), metastatic brain tumors, abscess, granuloma, resolvinghematoma, brain infarct, thrombosed vascular malformation, demyelinating disease,

thrombosed aneurysm, and primary CNS lymphoma in patients with AIDS.


201 Tl brain SPECT imaging appears to be unreliable for differentiating primary

lymphoma from nonmalignant brain lesions in patients with AIDS. Follow-up scans


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showing improvement may help further differentiate the lesions, but brain biopsy is

necessary to establish a definitive diagnosis in questionable cases.


False-positive201

Tl SPECT imaging in brain abscess may indicate focally increasedintracranial201 Tl uptake; however, such activity may be an abscess if positive tumoractivity is reported. Single lesions demonstrated on MRI scans with focal accumulation

of201 Tl strongly suggest lymphoma. Multiple lesions demonstrated on MRIs with201 Tl

SPECT uptake ratios 2.9 also suggest lymphoma; however, uptake ratios < 2.1 do notaid in discrimination.

Differentiation of toxoplasmosis abscess from primary brain lymphoma requires a

difficult combination of clinical history, laboratory findings, and radiographic

considerations. A trial period of treatment against the toxoplasmosis organism withfollow-up imaging is necessary in some patients before excluding the possibility of CNS

lymphoma.

Angiography

Cerebral angiography is rarely performed to define an abscess; however, mycotic cerebralaneurysms may occur related to an infectious vasculitis. These may rupture, resulting in a

cerebral hematoma. If the hematoma is evacuated without adequate antibiotic treatment,

the bed of the hematoma near the site of the mycotic aneurysm may become infected,later forming an abscess.


Cerebral angiography is the best means with which to detect vasculitis or mycoticaneurysms. The mass effect caused by an abscess can be localized using angiographic

criteria.


The beaded appearance of the blood vessels affected by active vasculitis may be mistaken

for movement on the part of the patient.


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Herpes Encephalitis

Overview

Herpes encephalitisis the most common cause of sporadicviral encephalitis, with a

predilection for the temporal lobes and a range of clinical presentations, from aseptic

meningitis and fever to a severe rapidly progressive form involving alteredconsciousness. In adults, herpes simplex virus type 1 (HSV-1) accounts for 95% of all

fatal cases of sporadic encephalitis and usually results from reactivation of the latent

virus. The clinical findings and neuroimaging appearance are both consistent with spread

of the virus from a previously infected ganglion.

More recently, sporadic cases of human herpesvirus 6 (HHV6) have been described in

immunocompromised patients or those with lymphoproliferative disorders. In childrenand neonates, herpes simplex virus type 2(HSV-2) accounts for 80-90% of neonatal andalmost all congenital infections. An isolated case report of an immunocompromised adult

patient developing HSV-2 infection has been described. Magnetic resonance imaging

(MRI) can play an important role in determining the diagnosis and extent of disease. [1, 2, 3,

4, 5, 6, 7, 8, 9, 10, 11, 12] See the image below.

Magnetic resonance image depicting herpes encephalitis.

On pathology, herpes viruses cause a fulminant hemorrhagic and necrotizing

meningoencephalitis, with typical gross findings of severe edema and massive tissue

necrosis, with petechial hemorrhages and hemorrhagic necrosis. Often, the petechial

hemorrhage is not observed on computed tomography (CT) scanning or MRI. Onmicroscopy, a focal necrotizing vasculitis is observed with perivascular and meningeal

lymphocytic infiltration and eosinophilic intranuclear inclusions in glial cells andneurons. Taira et al found that a lower Glasgow Coma Scale score and a greater number

of lesions detected on CT scanning were predictors of prolonged acyclovir therapy.[13]

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MRI is the preferred modality for evaluating the brain.[14, 15, 16] However, early in the

clinical course of the disease, MRI results may be negative. A negative MRI does not rule

out HSV encephalitis. Therapy should be empirically continued until laboratory testsdefinitely exclude the diagnosis. A case report of West Nile Virus causing focal temporal

lobe findings was described in the literature.[17]

Early imaging with CT scanning or radionuclide studies may also reveal normal findings.

CT scanning may not reveal abnormalities until 3-5 days after symptom onset, by whichtime the patient may be stuporous and comatose. As noted above, in the acute setting,

even contrast-enhanced MRIs may be negative.

Computed Tomography

In adults, CT scans classically reveal hypodensity in the temporal lobes either unilaterallyor bilaterally, with or without frontal lobe involvement. Hemorrhage is usually not

observed. A gyral or patchy parenchymal pattern of enhancement is observed. Contrast

enhancement generally occurs later in the disease process.[15, 18]

The herpes virus preferentially involves the temporal lobe and orbital surfaces of the

frontal lobes. This involvement may extend to the insular cortex, posterior occipital

cortex, and cerebral convexity; however, the basal ganglia are spared. Bilateral

involvement is frequent. Involvement of the cingulate gyrus occurs later in the disease.The classic involvement of the medial temporal and frontal lobes is consistent with

intracranial spread along the small meningeal branches of the fifth cranial nerve.

Cingulate gyrus involvement may arise from efferent hippocampal connections. Arhomboencephalitis resulting from pontine involvement may occur and likely arises from

retrograde viral transmission along the cisternal portion of the trigeminal nerve to the

brainstem.

In neonates, involvement is in the periventricular white matter, sparing the medialtemporal and inferior frontal lobes. In addition, meningeal enhancement may be observed

following contrast.[19, 20]

Taira et al analyzed specific variables as predictors of a need for a prolonged course of

acyclovir therapy in 23 patients with HSV encephalitis and reported a lower GlasgowComa Scale score and a greater number of lesions detected on CT scans were predictors

of prolonged therapy.[13] The investigators concluded that standard initial ACV treatment

may not be sufficient for patients with such predictors and that initial treatment

modifications may be necessary in such patients.[13]

Late in the disease process, when temporal and frontal lobe involvement is seen, CT

findings may be characteristic. Reports exist of patients with normal CT results and

cerebrospinal fluid (CSF) studies in the presence of abnormal MRI and EEG findings,indicating that MRI is more sensitive. Early in the disease process, limited sensitivity of

approximately 50% was noted. When typical findings of HSV encephalitis are observed

on CT scan, they often are associated with severe brain damage and a poor prognosis.[15]


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Because of bone artifact, the temporal lobes can be difficult to assess on CT scanning.

Early in the disease process, CT scanning may be normal. Other causes of encephalitis,

tumor, or lymphoma may appear similar.


The diagnosis of herpes encephalitis can be strongly suggested by the typical appearance

of medial temporal abnormalities that do not respect hippocampal borders.

In adults, T2-weighted MRI reveals hyperintensity corresponding to edematous changesin the temporal lobes (see the first 2 images below), inferior frontal lobes, and insula,

with a predilection for the medial temporal lobes. Foci of hemorrhage occasionally can be

observed on MRI (see the third image below).

Axial proton densityweighted image in a 62-year-old womanwith confusion and herpes encephalitis shows T2 hyperintensity involving the right

temporal lobe. Axial gadolinium-enhanced T1-weighted

image reveals enhancement of the right anterior temporal lobe and parahippocampal

gyrus. At the right anterior temporal tip is a hypointense, crescentic region surrounded by


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enhancement consistent with a small epidural abscess. Axial

nonenhanced T1-weighted image shows cortical hyperintensity (arrows) consistent withpetechial hemorrhage. In general, this is a common pathologic finding but less commonly

depicted in herpes encephalitis.

MRI is preferred for imaging and follow-up studies of herpes encephalitis. Typically,

temporal lobe T2 hyperintensity spares the basal ganglia. Although this appearance waspreviously believed to be pathognomonic for herpes involvement, similar findings can be

observed in progressive multifocal leukoencephalopathyand primaryCNS lymphoma.

Patchy parenchymal or gyral enhancement can be observed (see the image below).[21, 22, 23,24, 25, 26]

Axial gadolinium-enhanced T1-weighted imagereveals enhancement of the right anterior temporal lobe and parahippocampal gyrus. At

the right anterior temporal tip is a hypointense, crescentic region surrounded by

enhancement consistent with a small epidural abscess.

Reports of restricted diffusion in herpes encephalitis exist (see the first image below),with corresponding T2 hyperintensity reflecting edema (see the second image below).

Reports suggest diffusion-weighted imaging may be more sensitive in the detection of

HSV involvement than conventional MRI sequences and may mimic an infarct withinvolvement of the cortical regions of the temporal lobe.
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Coronal T2-weighted image reveals hyperintensity in the

left temporal lobe (arrows) in a distribution similar to the restricted diffusion abnormality

seen in the previous image. This finding is typical for herpes encephalitis. In patients withHHV6 infection, one series noted that in addition to mesial temporal lobe abnormality,

abnormal T2 hyperintensity has been seen in the insular and inferior frontal region, which

may suggest the diagnosis. There are felt to be 2 typical imaging appearances: one seen in

older adults involves T2 hyperintensity confined to the medial temporal lobe; in youngadults, a more varied pattern has been described that includes foci of restricted diffusion

with an otherwise normal magnetic resonance, diffuse cortical necrosis, or small focal

regions of abnormal T2 hyperintensity. Coronal T2-weighted image reveals hyperintensity in the left temporal lobe (arrows) in a distribution

similar to the restricted diffusion abnormality seen in the previous image. This finding is

typical for herpes encephalitis. In patients with HHV6 infection, one series noted that in

addition to mesial temporal lobe abnormality, abnormal T2 hyperintensity has been seenin the insular and inferior frontal region, which may suggest the diagnosis. There are felt

to be 2 typical imaging appearances: one seen in older adults involves T2 hyperintensity

confined to the medial temporal lobe; in young adults, a more varied pattern has beendescribed that includes foci of restricted diffusion with an otherwise normal magnetic

resonance, diffuse cortical necrosis, or small focal regions of abnormal T2 hyperintensity.

In neonates, T2-weighted MRI shows hyperintensity of the periventricular white matter,

with the medial temporal and inferior frontal lobes spared. Meningeal enhancement alsomay be observed.[27]

MR spectroscopy using proton spectroscopic MRI has demonstrated a reduction of theN

-acetylaspartate (NAA)-to-choline ratio. A decreased NAA peak has been reported 7-14


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weeks after onset, and in some cases, an elevated choline peak is seen. Occasionally, the

lactate peak may be elevated. The NAA decrease is believed to reflect neuronal injury.

NAA recovery has been noted to parallel clinical improvement.[28, 29]


dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK],gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic

fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, seethe eMedicine topicNephrogenic Fibrosing Dermopathy.

NSF/NFD has occurred in patients with moderate to end-stage renal disease after being

given a gadolinium-based contrast agent to enhance MRI or MRA scans. NSF/NFD is a

debilitating and sometimes fatal disease. Characteristics include red or dark patches onthe skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on

the whites of the eyes; joint stiffness with trouble moving or straightening the arms,

hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more

information, see FDA Information on Gadolinium-Based Contrast Agents orMedscape.

Ultrasonography

The role for ultrasonography in herpes encephalitis is limited. For in utero or neonatal

evaluation, ultrasonography may have a limited role in identifying the periventriculardestructive process.

Nuclear Imaging

The use of technetium-99m (

99m

Tc) hexamethylpropyleneamine oxime (HMPAO) single-photon emission CT (SPECT) scanning in evaluating herpes encephalitis is limited.Results demonstrate that the encephalitis matches the distribution of hyperintensity on

T2-weighted MRIs, with increased HMPAO uptake in the acute stage. Late sequelae are

characterized by decreased HMPAO uptake and postnecrotic widening of the temporalhorns. When abnormal uptake involves the temporal lobes, with characteristic

involvement of the limbic system, the diagnosis of herpes encephalitis is likely.
http://emedicine.medscape.com/article/1097889-overviewhttp://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm142882.htmhttp://www.medscape.com/viewarticle/550122http://www.medscape.com/viewarticle/550122http://emedicine.medscape.com/article/1097889-overviewhttp://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm142882.htmhttp://www.medscape.com/viewarticle/550122


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Meningitis

Overview

Neuroimaging can identify conditions that may predispose to bacterial meningitis; thus, it

is indicated in patients who have evidence of head trauma, sinus or mastoid infection,

skull fracture, and congenital anomalies. In addition, neuroimaging studies are typicallyused to identify and monitor complications of meningitis, such as hydrocephalus,

subdural effusion, empyema, and infarction and to exclude parenchymal abscess and

ventriculitis. Identifying cerebral complications early is important, as some

complications, such as symptomatic hydrocephalus, subdural empyema, and cerebralabscess, require prompt neurosurgical intervention.[1] See the images below.

Frontal sinusitis, empyema, and abscess formation in

a patient with bacterial meningitis. This contrast-enhanced, axial T1-weighted magnetic

resonance image shows a right frontal parenchymal low intensity (edema),

leptomeningitis (arrowheads), and a lentiform-shaped subdural empyema (arrows).

Watershed and lacunar infarcts in a patient with bacterial

meningitis. This axial computed tomography scan shows a left frontoparietal watershed


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infarct, a right basal ganglia lacunar infarct, and a bilateral subdural effusion.

Ventriculitis in a patient with bacterial meningitis. This

contrast-enhanced computed tomography scan shows ependymal enhancement.

The diagnosis of acute bacterial meningitis is not made on the basis of imaging studies.Rather, it is established by the affected patients history, physical examination findings,

and laboratory results.

[2, 3]

Lumbar puncture is the single most important diagnostic study.

Imaging studies performed in patients with acute meningitis may provide normal

findings. The results of an imaging study do not exclude or prove the presence of acutemeningitis.

For excellent patient education resources, visit eMedicine's Brain and Nervous System

Center. Also, see eMedicine's patient education articlesMeningitis in Adults, Meningitis

in Children, and Brain Infection.

Preferred Radiologic Examination

Computed tomography (CT) scanning is often performed first to excludecontraindications for lumbar puncture. Unfortunately, while increased intracranial

pressure is considered a contraindication to lumbar puncture, normal CT scan findings

may not be sufficient evidence of normal intracranial pressure in patients with bacterial

meningitis. Nonenhanced CT scans and magnetic resonance images (MRIs) of patientswith uncomplicated acute bacterial meningitis may be unremarkable.

Currently, MRI is the most sensitive imaging modality, because the presence and extent

of inflammatory changes in the meninges, as well as complications, can be detected. MRI

is superior to CT scanning in the evaluation of patients with suspected meningitis, as well

as in demonstrating leptomeningeal enhancement and distention of the subarachnoidspace with widening of the interhemispheric fissure, which is reported to be an early

finding in severe meningitis. See the image below.
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Acute bacterial meningitis. This contrast-enhanced, axial

T1-weighted magnetic resonance image shows leptomeningeal enhancement (arrows).

Effusion, hydrocephalus, cerebritis, and abscess can be evaluated well with CT scanningand ultrasonography (US) in infants; however, MRI is the most effective modality for

localizing the level of the pathology. Chest radiographs may be obtained to look for signs

of pneumonia or fluid in the lungs, especially in children.

In uncomplicated cases of purulent meningitis, early CT scans and MRIs usuallydemonstrate normal findings or small ventricles and effacement of sulci. The value of CT

scanning in the early diagnosis of subdural empyema is limited because of the presence

of bone artifact.


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Acute bacterialmeningitis. This axial nonenhanced computed tomography scan shows mild

ventriculomegaly and sulcal effacement. Acute bacterial

meningitis. This axial T2-weighted magnetic resonance image shows only mild


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ventriculomegaly. Acute bacterial meningitis. Thiscontrast-enhanced, axial T1-weighted magnetic resonance image shows leptomeningeal

enhancement (arrows).

Enhancement of the meninges is seen on contrast-enhanced CT scans and MRIs in cases

of bacterial meningitis. However, meningeal enhancement is nonspecific and may also becaused by the following 5 different etiologic subgroups:

Infectious

Carcinomatous meningitis

Reactive (eg, surgery, shunt, trauma)

Chemical (eg, ruptured dermoid and cysticercoid cysts, intrathecal chemotherapy)

Inflammatory (eg, sarcoidosis, collagen vascular disease

RadiographyPlain radiographs do not have diagnostic importance in bacterial meningitis. Chestradiography may be obtained to look for signs of pneumonia or fluid in the lungs. As

many as 50% of patients with pneumococcal meningitis also have evidence of pneumonia

on initial chest images.

Computed Tomography

The most important role of CT scanning in imaging patients with meningitis is to identify

contraindications to lumbar puncture and complications that require prompt neurosurgical

intervention, such as symptomatic hydrocephalus, subdural empyema, and cerebralabscess. Contrast-enhanced CT scans may also help in detecting complications such as

venous thrombosis, infarction, and ventriculitis. Ventriculitis is a complication of

bacterial meningitis that is seen commonly in neonates. Ependymal enhancement can beseen on contrast-enhanced CT scans.

The value of CT scanning in the early diagnosis of subdural empyema and effusion has

been controversial, as this modality may not detect meningitis, especially nonenhanced
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CT scans in the early stage of the disease. Normal results on CT imaging do not exclude

the presence of acute meningitis.

CT scans may reveal the cause of meningeal infection. Obstructive hydrocephalus canoccur with chronic inflammatory changes in the subarachnoid space or in cases of

ventricular obstruction. Otorhinologic structures and congenital and posttraumaticcalvarial defects can be evaluated (see image below).

Cerebritis and developing abscess formation in a patient

with bacterial meningitis. This contrast-enhanced, axial computed tomography scan wasobtained 1 month after surgery and shows a small, ring-enhanced, hypoattenuating mass

(recurrence of abscess) in the left basal ganglia and a left lentiform-shaped subdural fluid

collection with enhanced meninges (arrowhead).

Coronal thin-section CT scanning is useful for evaluating patients with recurrent bacterialmeningitis; CT cisternography may depict CSF leaks, which may be the source of

infection in cases of recurrent meningitis.

Sequelae from meningitis may be depicted on CT scans as periventricular and meningealcalcifications, localized areas of encephalomalacia, porencephaly, and ventricular

dilatation secondary to brain atrophy.

Nonenhanced CT scan findings may be normal (>50% of patients), or the studies may

demonstrate mildventricular dilatation and effacement of sulci, cerebral edema, and focallow-attenuating lesions. See image below.


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Acute bacterialmeningitis. This axial nonenhanced computed tomography scan shows mild

ventriculomegaly and sulcal effacement.

Obliteration of the basal cisterns may result from increased attenuation, perhaps owing to

the presence of exudate in the subarachnoid space or leptomeningeal hyperemia.Increased attenuation in the CSF spaces due to meningitis may simulate acute

subarachnoid hemorrhage on CT scans.

CT scans for patients with suggested meningitis must be performed with iodinated

contrast material. Diffuse enhancement of the subarachnoid space is characteristic. Seethe image below.


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Cerebritis and developing abscess formation in a patient

with bacterial meningitis. This contrast-enhanced axial computed tomography scan shows

leptomeningitis and parenchymal enhancement (cerebritis) with a low-attenuating area(edema) in the left basal ganglia.

Curvilinear meningeal enhancement over convexities, interhemispheric and sylvian

fissures, and obliteration of basal cisterns are usually seen on contrast-enhanced CTscans. Dural enhancement also may occur. However, meningeal enhancement isnonspecific and may be caused not only by bacterial meningitis but also by neoplasm,

hemorrhage, sarcoidosis, and other noninfectious inflammatory disorders.

Subdural Effusion

Subdural effusion is a common complication of meningitis, especially in young children.

CT scans have shown that as many as 25-40% of children develop this complication

during or after treatment for meningitis. Some subdural effusions resolve spontaneously,whereas others may require aspiration or drainage. Important diagnostic features on CT

scans are high-attenuating effusions from the CSF and prominent enhancement of themargin of an empyema. The marked degree of enhancement of an empyema that is seenon CT scan rarely occurs in cases of a subdural hematoma, although a thin rim of

enhancement is not uncommon in imaging of a chronic subdural hematoma. See images

below.
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Subdural empyemaand arterial infarct in a patient with bacterial meningitis. This contrast-enhanced axial

computed tomography scan shows left-sided parenchymal hypoattenuation in the middle

cerebral artery territory, with marked herniation and a prominent subdural empyema.

Subdural empyema and diffuse cerebral edema in a patientwith bacterial meningitis. This axial computed tomography scan shows bilateral subdural

effusion (empyema) and parenchymal low-attenuating areas.


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Subdural empyema with strand in a patient with bacterial

meningitis. This contrast-enhanced, axial computed tomography scan shows a bilateral

subdural effusion with cortical surface enhancement (empyema). Note that theattenuation of the effusion is higher than that of the cerebrospinal fluid.

Sinus Thrombosis

Sinus thrombosis can be demonstrated on CT scans. In the acute phase (when the clot is

dense), a hyperattenuating thrombus can be seen in the sagittal sinus on a nonenhanced

scan. The so-called empty delta sign, which is a triangle of decreased attenuation in theposterior portion of the affected sinus, can be seen on contrast-enhanced CT scans and is

visible only after the clot becomes less dense than the contrast-enhanced blood that flows

around it.

Infarcts

Infarcts can be reliably diagnosed with CT scanning. Infarcts tend to be sharply

marginated and confined to a specific arterial vascular territory. Commonly, multiplelacunar infarcts are seen in the distribution of perforating vessels in the brainstem, basal

ganglia, and white matter. See the images below.


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Subdural empyemaand arterial infarct in a patient with bacterial meningitis. This contrast-enhanced axial

computed tomography scan shows left-sided parenchymal hypoattenuation in the middle

cerebral artery territory, with marked herniation and a prominent subdural empyema.


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Watershed andlacunar infarcts in a patient with bacterial meningitis. This axial computed tomography

scan shows a left frontoparietal watershed infarct, a right basal ganglia lacunar infarct,

and a bilateral subdural effusion. Subdural empyema and

diffuse cerebral edema in a patient with bacterial meningitis. This contrast-enhanced

computed tomography scan shows diffuse cerebral edema and lacunar infarcts in thethalamus.

Cerebritis

In cerebritis, CT scans can show ill-defined areas of low attenuation, which are evidence

of edema in the affected brain. On nonenhanced CT scans, abscesses, which are most

commonly located near the gray matterwhite matter junction, can appear as areas of low


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attenuation with a thin wall of slightly increased attenuation. After the administration of

contrast material, the abscess wall and surrounding inflammatory tissue enhancement are

ring shaped. See the images below.

Cerebritis and

developing abscess formation in a patient with bacterial meningitis. This contrast-enhanced, axial computed tomography scan was obtained 1 month after surgery and

shows a small, ring-enhanced, hypoattenuating mass (recurrence of abscess) in the left

basal ganglia and a left lentiform-shaped subdural fluid collection with enhancedmeninges (arrowhead).


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Cerebritis anddeveloping abscess formation in a patient with bacterial meningitis. This contrast-

enhanced axial computed tomography scan shows a ring-enhancing, lobulated,

hypoattenuating mass (abscess) in the left basal ganglia.

Abscess in a patient with bacterial meningitis. This contrast-enhanced computed

tomography scan shows a ring-enhancing, hypoattenuating mass (abscess) withperipheral edema and mass effect.


Routine contrast-enhanced brain MRI is the most sensitive modality for the diagnosis ofbacterial meningitis because it helps to detect the presence and extent of inflammatory

changes in the meninges as well as complications. The increased sensitivity and


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specificity of MRI results from direct multiplanar imaging, increased contrast resolution,

and the absence of artifact caused by bone.

Nonenhanced MRI studies performed in patients with uncomplicated acute bacterialmeningitis may demonstrate unremarkable findings; however, such results do not exclude

acute meningitis.

Some authors suggest performing MRI with a high dose of contrast material (0.3

mmol/kg), which is the most important factor.[4] They also recommend imagingimmediately after the injection and then performing magnetization transfer imaging,

which can help to depict abnormal meningeal enhancement and which facilitates the

diagnosis of early brain meningitis. Meningeal enhancement is nonspecific, however, and

may be caused not only by bacterial meningitis but also by neoplasm, hemorrhage,sarcoidosis, and other noninfectious inflammatory disorders.

Noncontrast MRIs of patients with uncomplicated acute bacterial meningitis may

demonstrate obliterated cisterns and the distention of the subarachnoid space withwidening of the interhemispheric fissure, which is reported to be an early finding in

severe meningitis or may be unremarkable. T2-weighted images are sensitive to abnormal

tissue water distribution and, thus, may show cortical hyperintensities that are reversible

and believed to represent edema. Diffuse enhancement of the subarachnoid space ischaracteristic. See the images below.

Frontal sinusitis, empyema, and abscess formation in a patient

with bacterial meningitis. This T2-weighted axial magnetic resonance image showsfrontal sinusitis, a bone defect (arrow) with adjacent cortical edema (arrowhead), and

right occipitoparietal subdural fluid collection (empyema).


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Acute bacterial meningitis. This axial T2-weightedmagnetic resonance image shows only mild ventriculomegaly.

Pachymeningitis and cerebritis in a patient with bacterial

meningitis. This T2-weighted axial magnetic resonance image shows parenchymal focal

edema (cerebritis).

Contrast-enhanced MRI has been shown to be more sensitive than CT scanning in the

detection of meningeal inflammation. Gadolinium-enhanced MRI studies can

demonstrate abnormal leptomeningeal enhancement that more closely approximates theextent of inflammatory cell infiltration. See the images below.


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Frontal sinusitis, empyema, and abscess formation ina patient with bacterial meningitis. This contrast-enhanced, axial T1-weighted magnetic

resonance image shows a right frontal parenchymal low intensity (edema),

leptomeningitis (arrowheads), and a lentiform-shaped subdural empyema (arrows).

Acute bacterial meningitis. This contrast-

enhanced, axial T1-weighted magnetic resonance image shows leptomeningealenhancement (arrows).

Dural enhancement may occur, and extension of enhancing subarachnoid exudate deep

into the sulci can be seen in severe cases. See the images below.


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Pachymeningitis in a patient with bacterial meningitis. This

contrast-enhanced, axial T1-weighted magnetic resonance image shows diffuse dural

enhancement.

Pachymeningitis and cerebritis in a patient with bacterial meningitis. This contrast-

enhanced, T1-weighted axial magnetic resonance image shows left-sided dural

enhancement (pachymeningitis) and focal pial enhancement.

Revealing the cause of meningeal infection is best accomplished with MRI. MRI can help

to detect inflammatory changes in the paranasal sinuses and mastoid air cells, which are

usually depicted as areas of increased signal intensity on T2-weighted images. See theimages below.


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Frontal sinusitis, empyema,and abscess formation in a patient with bacterial meningitis. This T2-weighted axial

magnetic resonance image shows frontal sinusitis, a bone defect (arrow) with adjacent

cortical edema (arrowhead), and right occipitoparietal subdural fluid collection

(empyema). Frontal sinusitis, empyema, and abscessformation in a patient with bacterial meningitis. This T2-weighted axial magnetic

resonance image shows a developing abscess formation with mass effect and bilateral

subdural fluid collections (empyema).

Enhancement may be prominent. See the image below.


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with bacterial meningitis. This contrast-enhanced, axial T1-weighted magnetic resonance

image shows a right frontal parenchymal low intensity (edema), leptomeningitis(arrowheads), and a lentiform-shaped subdural empyema (arrows).

MRI also can help to exclude congenital and posttraumatic calvarial defects.

Coronal and sagittal thin-section, heavily T2-weighted MRIs may show CSF leaks, which

may be the source of infection in cases of recurrent meningitis.

Plain and contrast-enhanced MRIs help to depict the complications of meningitis betterthan other images. Such complications include empyema/effusion, cerebritis/abscess,

venous thrombosis, venous and arterial infarcts, ventriculitis, hydrocephalus, and edema

(with or without cerebral herniation). See the images below.

Frontal sinusitis, empyema, and abscess formation in apatient with bacterial meningitis. This T2-weighted axial magnetic resonance image

shows a developing abscess formation with mass effect and bilateral subdural fluid


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collections (empyema). Pachymeningitis and cerebritis in a

patient with bacterial meningitis. This contrast-enhanced, T1-weighted axial magnetic

resonance image shows left-sided dural enhancement (pachymeningitis) and focal pial

enhancement. Pachymeningitis and cerebritis in a patientwith bacterial meningitis. This T2-weighted axial magnetic resonance image shows

parenchymal focal edema (cerebritis).

Subdural Empyema/Effusion

Sterile fluid collections may develop within the subdural space in patients with

meningitis. Effusions may be slightly hyperintense relative to CSF on MRIs and are mostcommonly located in cerebral convexities and interhemispheric fissures. See the images

below.


with bacterial meningitis. This contrast-enhanced, axial T1-weighted magnetic resonance
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image shows a right frontal parenchymal low intensity (edema), leptomeningitis

(arrowheads), and a lentiform-shaped subdural empyema (arrows).

Frontal sinusitis, empyema, and abscess formation in a patientwith bacterial meningitis. This T2-weighted axial magnetic resonance image shows

frontal sinusitis, a bone defect (arrow) with adjacent cortical edema (arrowhead), and

right occipitoparietal subdural fluid collection (empyema).

Frontal sinusitis, empyema, and abscess formation in a patient with bacterial meningitis.

This T2-weighted axial magnetic resonance image shows a developing abscess formationwith mass effect and bilateral subdural fluid collections (empyema).

Occasionally, a portion of the medial subjacent cerebral surface of an effusion

demonstrates mild enhancement, presumably from an inflammatory surroundingmembrane. These effusions are not empyemas and typically resolve spontaneously.

In the early stages of subdural empyema, T2-weighted images can demonstrate a thin

hyperintense convexity and interhemispheric collection usually not visible on CT scans.

Paratentorial and subtemporal extension is well demonstrated on coronal MRIs.

Prominent enhancement of the margin of an empyema is an important diagnostic featureon MRI and results from the formation of a membrane of granulomatous tissue on the

leptomeninges and from inflammation in the subjacent cerebral cortex.

Subdural empyema may be differentiated from subacute/chronic subdural hematoma. On

MRI, even a noninfected subdural hematoma enhances markedly on gadolinium-


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enhanced T1- and T2-weighted images because of the presence of extracellular

methemoglobin and other forms of iron.

Cerebritis/Abscesses

Cerebritis is the earliest stage of a purulent brain infection. If bacterial cerebritis is notsuccessfully treated medically, the affected portion of the brain liquefies and asurrounding capsule of granulation tissue and collagen forms, resulting in abscess

formation. The corticomedullary (gray matterwhite matter) junction is the most

commonly affected location, and the frontal and parietal lobes are the most frequent sites.Less than 15% of intracranial abscesses occur in the posterior fossa. Multiple abscesses

are uncommon except in patients who are immunocompromised. MRI findings of

pyogenic brain abscesses are characteristic.

On MRIs, stage I cerebritis appears as an ill-defined edematous area on both T1- and T2-weighted images. See the images below

Pachymeningitis and cerebritis in a patient with bacterialmeningitis. This contrast-enhanced, T1-weighted axial magnetic resonance image shows

left-sided dural enhancement (pachymeningitis) and focal pial enhancement.

Pachymeningitis and cerebritis in a patient with bacterialmeningitis. This T2-weighted axial magnetic resonance image shows parenchymal focal

edema (cerebritis).

In late stage II cerebritis/early abscess, the abscess wall is hyperintense on T1-weightedimages and slightly hypointense on T2-weighted images. In stage III (subacute abscess),


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the abscess wall is hyperintense on both T1- and T2-weighted images. In stage IV

(chronic phase), the abscess wall is isointense on T1-weighted MRIs and markedly

hypointense on T2-weighted MRIs. Although abscesses in stages II-IV all exhibit ring-type enhancement after the infusion of a paramagnetic contrast agent, better edge

definition is seen in the enhancing wall of stage II lesions than in stages III and IV.

Abscesses may imitate brain tumors and can be differentiated with use of proton

magnetic resonance spectroscopy. Brain tumors usually demonstrate elevated choline andpossibly decreased creatine peaks, as well asN-acetyl-aspartate peaks. Abscesses do not

demonstrate these abnormal peaks; instead, they have lactate peaks and the lipid peaks of

amino acids.

Venous Thrombosis

Thrombosis of the deep veins, cortical veins, and venous sinuses is an uncommoncomplication of meningitis; however, thrombosis more often develops in the presence of

superimposed dehydration.

Gradient-echo and spin-echo MRIs can demonstrate cortical vein and/or dural sinus

thrombosis, as well as the characteristic signal-intensity properties of acute and subacutehemorrhagic infarctions.

MRI-aided diagnosis for acute and chronic sinus thrombosis may be complex; however,

sinus thrombosis is readily diagnosed when the thrombus is subacute because they are

hyperintense on T1-weighted images.

Magnetic resonance venography (2-dimensional time-of-flight or phase-contrast) can aid

the diagnosis of venous sinus thrombosis.

Cavernous sinus thrombosis is an uncommon sequela of meningitis. The signal intensity

of this condition varies depending on the state of infection, inflammation, and clotevolution. The sinus may be enlarged with a narrowed or occluded cavernous carotid

artery. T2-signal prolongation may occur in the adjacent clivus or petrous apex.

Venous and Arterial Infarcts

Venous infarcts are diagnosed on the basis of their characteristic location and appearance.

Typically, infarcts from a sagittal sinus thrombosis involve the parietal lobes; those from

the straight sinus/vein of Galen thrombosis involve the thalami; and infarcts from thetransverse sinus or sigmoid sinus thrombosis involve the temporal lobe.

Arterial infarctions in bacterial meningitis are usually the result of arteritis caused by

involvement of the vascular spaces and the arterial walls. When major cerebral arteries

are involved, large cortical infarctions result. Frequently, multiple lacunar infarcts areseen in the distribution of the perforating vessels in the brainstem, basal ganglia, and

white matter.


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Ventriculitis

In ventriculitis associated with meningitis, the infecting organisms enter the ventricles via

the choroid plexuses. On MRIs, as on CT scans, proteinaceous debris in the trigone or

occipital horn of the lateral ventricle and intense enhancement of the ependyma are seen.

Hydrocephalus

Ventriculomegaly can occur in the course of meningitis and is usually mild to moderate

in severity. See the image below.

Acute bacterial meningitis. This axial T2-weighted magneticresonance image shows only mild ventriculomegaly.

Obstructive hydrocephalus can occur with chronic inflammatory changes in the

subarachnoid space or ventricular obstruction.

Gadolinium Warning


dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK],gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic

fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). The disease has occurred in

patients with moderate to end-stage renal disease after being given a gadolinium-basedcontrast agent to enhance MRI or MRA scans. NSF/NFD is a debilitating and sometimes

fatal disease. Characteristics include red or dark patches on the skin; burning, itching,

swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes;

joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain

deep in the hip bones or ribs; and muscle weakness.

Ultrasonography

The role of ultrasonography in patients with bacterial meningitis is limited to theevaluation of complications or deterioration in the patient's clinical situation.

Commercially available equipment is used with a 3- to 7.5-MHz transducer, depending


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on the size of the patient's head. Transducers of 5-7.5 MHz are used for newborns,

whereas transducers of 3-5 MHz are used for older infants. US is a heavily operator-

dependent technique. Experience is needed to demonstrate the meningeal andparenchymal findings of bacterial meningitis.

In newborns and older infants, complications of meningitis that are depicted on cranialCT scans and MRIs can also be demonstrated on cranial sonograms obtained with a

transfontanel approach.

Important US findings in infants with bacterial meningitis have been described. These

findings include echogenic sulci, ventriculomegaly and obstructive hydrocephalus,

ventriculitis, prominent leptomeninges, subdural effusions, empyema, parenchymal

echogenicity, and abscess formation. US can help to identify these complications, but thefindings are usually not specific.

Echogenic sulci that appear as a result of the accumulation of inflammatory debris are the

most common and transient US finding in meningitis; these resolve gradually as theexudate is cleared.

On US, inflammatory debris in the CSF creates low-level intraventricular echoes in acute

ventriculitis. This appearance may imitate that which is seen in the breakdown of

intraventricular hematomas; however, these 2 clinical settings can usually bedistinguished because ventriculitis produces other signs of inflammation.

Ventriculomegaly

Mild to moderate ventriculomegaly, which is usually reversible, can occur in the course

of meningitis. Exudates may produce CSF loculations and pathway obstruction, resultingin a communicating hydrocephalus, whereas obstructive hydrocephalus may occur with

ventricular obstruction or chronic inflammatory changes in the subarachnoid space.Intraventricular septa formation may result in ventricular compartmentalization.

Progressive ventriculomegaly can be excluded with the use of serial sonograms.

Ventriculitis

Ventriculitis, which is seen in 65-90% of patients, is suggested by the US findings of

hydrocephalus, which include a thickened, hyperechoic, irregular ependymal surface and

echogenic debris and fibrous septa formation within the enlarged ventricles. The septa

occur over the 2 weeks following bacterial meningitis; US is best for identifying septa,compared with CT scanning or MRI.

Subdural Effusion

Subdural effusion is a common US finding in infants withHaemophilus influenzae

meningitis. Subdural empyemas are uncommon findings and result when the effusionsbecome infected; US features may help differentiate effusions from empyemas.[5]


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Abnormal Parenchymal Echogenicity

Areas of abnormal parenchymal echogenicity are a significant finding. The lesions

represent cerebritis, infarction, encephalomalacia, or, rarely, abscess formation.

Abscesses appear as homogeneous echogenic masses with a hypoechoic center that is

surrounded by a thin hyperechoic rim.

Doppler Ultrasonography

Doppler US can easily demonstrate the major intracranial vessels via the anteriortransfontanel approach; in older children, these vessels can be demonstrated via the

transtemporal approach. The cerebral blood flow can be evaluated qualitatively. Serial

transcranial Doppler examinations performed to assess for disease-related arterialnarrowing have been described. An association between an unfavorable course of the

di

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Infection CNS Imaging

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