eMedicine Specialties > Radiology > Brain/Spine

Brain, Abscess

Lennard A Nadalo, MD, Clinical Professor, Department of Radiology, University of Texas Southwestern Medical School; Consulting Staff, Envision Imaging of Allen and Radiological Consultants Association
Leigh K Hunter, MD, FACP, Clinical Professor, Infectious Diseases Division, University of Texas Southwestern Medical School; Director, Internal Medicine Residency Program, Methodist Medical Center of Dallas

Updated: Jan 24, 2007

Introduction

Background

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 the infection, 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 all require correlation of medical history, neuroimaging, and results of microbiologic analysis.

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

Pathophysiology

Most commonly, infectious agents gain access to the CNS by spread from a contiguous focus of infection, such as otitis media, mastoiditis, infection of the paranasal sinuses, or dental infection. Infection spreads hematogenously from an extracranial site, via trauma, directly to the CNS through retrograde thrombophlebitis, which may be preceded by empyema, meningitis, or both. Congenital or acquired dural dehiscence and dermal sinuses are less common causes.

Specific organisms involved in cerebritis and abscess vary. In one third of patients, more than one organism is found. Most abscesses are produced by pyogenic bacteria. Overall, the organisms most frequently isolated from cerebral abscesses include streptococci (both aerobic and anaerobic) and staphylococci, although gram-negative organisms are an increasing cause of cerebral abscess. In neonates, the most frequently implicated organisms include Citrobacter, Proteus, Pseudomonas, and Serratia species, as well as Staphylococcus aureus. These abscesses are often large and have poorly formed capsules.

Occasionally, organisms other than pyogenic bacteria cause cerebral abscesses. Examples include Mycobacterium tuberculosis, nontuberculous mycobacteria, fungi, parasites, and Actinomyces and Nocardia species. Focal intracranial infections due to Salmonella organisms are rare and are associated with positive results in blood cultures in some patients.

Four stages have been described in abscess evolution: early cerebritis, late cerebritis, early capsule formation, and late capsule formation.

1. Early cerebritis is the initial phase of abscess formation. The initial infection is focal but not localized. An unencapsulated mass of congested brain tissue is seen, with regional edema. Scattered necrotic foci and microscopic petechial hemorrhages are present, although no gross tissue destruction is seen. Early cerebritis lasts as long as 3-5 days.
2. After 3-5 days, the reaction to the infectious agent progresses to late cerebritis. The infection becomes more focal with zones of necrosis. Blood vessels surrounding the infection proliferate. The central area of the infection becomes necrotic, surrounded by a ring of inflammatory cells, macrophages, granulation tissue, and fibroblasts. The late cerebritis stage lasts 5-14 days.
3. With the beginning of the early capsule stage, collagen and reticulin form a well-delineated capsule. The central core consists of necrotic and inflammatory debris. The abscess capsule increasingly thickens with the addition of more collagen. With the formation of a well-defined capsule, the mass effect and surrounding edema begin to subside. Gliosis around the abscess periphery further defines the region.
4. The wall of a well-defined late abscess consists of an inner inflammatory layer, a middle collagenous layer, and an outer gliotic layer. The late capsule stage may last for months.

Symptoms of brain abscess include an altered mental state, headache, fever, seizure, vomiting, unilateral weakness or hemiparesis, and cranial nerve signs. Imaging prior to a lumbar spinal puncture is critical because lumbar spinal puncture may lead to brain herniation in patients with mass effect. Following successful treatment, many patients are left with significant long-term morbidity. Cavernous sinus thrombosis or brain herniation may be fatal.

Frequency

United States

In developed countries, bacterial abscesses are rare in healthy adults. In children, cerebral abscesses are rare, even in patients with congenital heart disease and immune defects. The frequency of intracranial involvement as a complication of sinusitis is approximately 1.5%.

International

In developing countries, cerebral abscesses are more common than in the developed world. Cerebral abscesses due to Mycobacterium and Salmonella infection are more common in poorer nations in which tuberculosis and GI tract infections are common.

Mortality/Morbidity

Early and improved diagnostic imaging techniques have allowed the discovery of brain abscess at a much earlier stage. Antibiotic treatments have improved the prognosis of patients with cerebral abscess. Mortality rates have decreased from 40-50% to less than 5%.

Regarding altered immunity, the identification and treatment of cerebral abscess often is complicated in patients who are immunosuppressed. Brain abscess due to toxoplasmosis is most common in patients with AIDS. Nocardial infection is seen most commonly in patients with immunosuppression, including patients who have undergone organ transplantation. Fungal brain infections, including mucormycosis, are almost always associated with diabetes, renal failure, or another cause of immunosuppression.

Race

No particular association exists between cerebral abscesses and race.

Sex

No particular predilection is noted in either sex.

Age

Bacterial meningitis is the most common cause of cerebral abscess in neonates and infants. Fungal and nocardial infections tend to occur in patients with diabetes or other causes of immunosuppression that are more common in elderly patients. In neonates, cerebral abscess is caused more commonly by Citrobacter, Proteus, Pseudomonas, and Serratia species, as well as S aureus.

Anatomy

Cerebral abscess formation generally occurs at the corticomedullary (gray-white matter) junction within the frontal and parietal lobes. Fewer than 15% of intracranial abscesses occur in the posterior fossa. Most cerebral abscesses are single. Multiple abscesses are found most commonly in patients who are immunocompromised.

The location of an abscess may depend on the location of the primary infection. Abscesses secondary to otitis media usually are localized to the temporal lobe or cerebellum. Infection spread from the paranasal sinuses most commonly presents in the frontal and subfrontal brain. Fungal abscesses are often contiguous with an infection of the orbit or sinuses. Hematogenous pyogenic abscesses usually result from a cardiac, pulmonary, or vascular source. In these patients, abscess formation is seen most commonly in the supratentorial brain.

Other less commonly associated conditions include congenital or acquired dural dehiscence and dermal sinuses, which may provide a pathway for the spread of the infective agent.

Presentation

Clinical manifestations of cerebral abscess most commonly are a result of the size and location of the space occupied by the overall reaction of the brain to the presence of the organism. While the abscess cavity may be significant, the associated edema pattern is often a greater factor in producing midline and transtentorial shifts. Presentation and clinical progression of a brain abscess depends on the nature of infectious agents that have gained access to the CNS. Responses can be pyogenic or nonpyogenic.

Pyogenic inflammatory reaction to an infectious organism represents the host response. Abscess formed in reaction to infection by Pneumococcus species represents a prototypical pyogenic abscess. Other organisms, such as Nocardia species and certain fungi are opportunistic pathogens that cause serious disseminated disease in patients who are immunocompromised, such as patients who have undergone organ transplantation or patients with HIV infection or endstage renal disease.

Nocardia asteroides accounts for 80% of invasive nocardial infections resulting in systemic and CNS disease. Pulmonary infection is the most common initial infection, with hematogenous spread to other organs, such as the skin, soft tissues, CNS, bone, heart, and kidneys, which occurs later in the clinical course. Tissue infected with Nocardia species often demonstrates acute pyogenic inflammation with gram-positive, beaded, filamentous rods with variable acid-fast staining. The organism is best demonstrated in tissue sections by using silver staining.

Nocardial species stimulate little humoral immunity. Protective immune responses are primarily T-cell mediated. Both immunocompetent and immunocompromised hosts can be affected. Low CD4 cell counts and failure to receive prophylaxis were found in patients with HIV infection with Toxoplasma -related brain abscess. Seropositive patients with CD4 counts below 200 cells per cubic millimeter benefit from effective anti– Toxoplasma encephalitis prophylaxis.

Other organisms that may have similar clinical features include M tuberculosis, Actinomyces species, fungi, nontuberculous mycobacteria, and parasites.

Unusual agents have been recovered from neonates with no immunosuppression. Klebsiella pneumoniae is rarely a causative organism in the healthy neonate. When such infections occur, an antenatal infection in the mother may be the source.

Listeria monocytogenes infection may present as a mass within the brain with a confusing pattern that is difficult to differentiate without biopsy and culturing. Most Listeria -related brain abscesses occur in patients who have a compromised immune response.

Toxoplasma encephalitis is caused by Toxoplasma gondii. In the US, seropositivity has been reported in up to 70% of those tested. The primary transmission of Toxoplasma organisms is via raw meat, while bodily secretions, milk, transfusions, and organ transplantation are other sources of exposure. After the acute infection, the parasite becomes latent in the form of a bradyzoite. As cell-mediated immunity declines, the cytes rupture, releasing invasive tachyzoites.

Clinical Toxoplasma encephalitis represents a recurrent infection. In AIDS, the risk of recurrent infection is associated with CD4 counts of less than 100 cells per cubic millimeter. In AIDS patients, Toxoplasma encephalitis is often progressive and may be fatal, if untreated. The primary symptoms seen in the patient with AIDS include fever, altered mental status, seizure, and focal neurologic deficits.

The lesion of toxoplasmosis presents with a central zone, which contains few organisms and is avascular; an intermediate zone, which contains enlarged blood vessels and free extracellular and intracellular tachyzoites; and a peripheral zone, with few prominent blood vessels and mainly encysted organisms.

On nonenhanced CT, Toxoplasma encephalitis appears as areas of isointense or hypodense mass effect. The basal ganglia and the corticomedullary junction are most commonly affected. Contrast-enhanced CT demonstrates a ring or nodular enhancement pattern with lesions of 1-3 cm in diameter. The enhancement is greatest within the intermediate zone where inflammation is the greatest.

MRI of the brain both without and with intravenous gadolinium contrast enhancement is the most sensitive test for Toxoplasma encephalitis. Lesions with contrast may be hyperintense compared to 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.

Preferred Examination

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 of iodinated 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.

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 from infection is difficult. In these patients, a nuclear agent can be used to tag white blood cells or antibodies to help differentiation.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease 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. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. 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 the FDA Public Health Advisory or Medscape.

Limitations of Techniques

Plain radiographs of the paranasal sinuses can only suggest a possible etiology for cerebral 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 computed tomographic (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 necessary because infection by these organisms may not follow a predictable response to treatment. Tuberculosis-related brain abscesses that retain positive results to culture and smears following 4 weeks of treatment may not represent treatment failure. In addition, treatment of fungal infections may require many weeks of treatment with interval follow-up imaging studies. Follow-up imaging during the treatment for toxoplasmosis is important in avoiding brain biopsy.

Differential Diagnoses

Other Problems to Be Considered

HIV encephalitis

Radiography

Findings

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 with a 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 with extension into the intracranial space.

Degree of Confidence

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.

False Positives/Negatives

Patients with established intracranial abscesses may develop fluid retention within the mastoid and paranasal sinuses secondary to endotracheal intubation and chronic disability. Most patients with osteomyelitis of the mandible or maxilla do not develop intracranial abscesses.

Computed Tomography

Findings

CT manifestations of an intracranial abscess depend on the stage of the abscess formation. 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.

• During early cerebritis, nonenhanced CT scans may demonstrate normal findings or may show 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 irregular enhancing 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.
• 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 4 astrocytomas), 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 of Taenia solium. In most pyogenic abscesses, the ring is smooth and thin walled ( <5 mm). The medial margin is often thinner 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.

Degree of Confidence

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 of fever, 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 be inspected within the context of other known malignancies, which may be a source for cerebral metastatic disease, glioma, lymphoma, and multiple sclerosis.

False Positives/Negatives

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 ringlike lesions of the brain for an abscess. Ring-enhancing lesions must be placed into the differential diagnosis, which includes some primary brain tumors (eg, anaplastic 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 primary CNS lymphoma in patients with AIDS.

Magnetic Resonance Imaging

Findings

MRI findings of brain abscess vary with time.

• 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 areas within the isointense to mildly hypointense edematous region.
• Late cerebritis stage
  • During the late cerebritis stage, the central necrotic area is hyperintense to brain tissue on proton-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 hypointense on 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
  • 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 images demonstrate 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 (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 other normal brain metabolites are nearly absent.

Diffusion-weighted MR 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 DWI is related to the cellularity and viscosity of the contents 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 for acute cerebral infarction.

Degree of Confidence

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 T2 brightness 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 enhanced lesions 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 these lesions by evaluating their degree of vascularity through dynamic blood flow analysis studies.

False Positives/Negatives

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

Findings

On sonograms, cerebral abscess is depicted as a complex cystic pattern with an echogenic wall and a sonographically hypoechoic or mildly hyperechoic central zone 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 sonographic images obtained through the anterior fontanelle. Brain sonograms can reveal the size and number of abscesses 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 been performed with excellent overall results.

Degree of Confidence

Sonography cannot help differentiate a cystic neoplasm from an abscess. When seen in the neonate, periventricular and arachnoid cysts commonly are not abscesses.

False Positives/Negatives

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

Findings

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 brain neoplasms. 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 the abscess. 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, resolving hematoma, brain infarct, thrombosed vascular malformation, demyelinating disease, thrombosed aneurysm, and primary CNS lymphoma in patients with AIDS.

Degree of Confidence

²⁰¹ Tl brain SPECT imaging appears to be unreliable for differentiating primary lymphoma from nonmalignant brain lesions in patients with AIDS. Follow-up scans showing improvement may help further differentiate the lesions, but brain biopsy is necessary to establish a definitive diagnosis in questionable cases.

False Positives/Negatives

False-positive²⁰¹ Tl SPECT imaging in brain abscess may indicate focally increased intracranial²⁰¹ Tl uptake; however, such activity may be an abscess if positive tumor activity 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 not aid 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 with follow-up imaging is necessary in some patients before excluding the possibility of CNS lymphoma.

Angiography

Findings

Cerebral angiography is rarely performed to define an abscess; however, mycotic cerebral aneurysms 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.

Degree of Confidence

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

False Positives/Negatives

The beaded appearance of the blood vessels affected by active vasculitis may be mistaken for movement on the part of the patient.

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. Drainage of pleural effusions and aspiration of lung abscesses may help direct initial antibiotic selection.

Patient Education:

For excellent patient education resources, visit eMedicine's Infections Center and Brain and Nervous System Center. Also, see eMedicine's patient education articles Brain Infection and Antibiotics.

Medicolegal Pitfalls

• Because CNS abscesses may be the result of postoperative infections, every effort must be made to control iatrogenic infections.
• Paranasal sinus surgery can damage the ethmoid sinus walls, resulting in a leak of cerebrospinal fluid (CSF). CSF leaks can lead to secondary infections and abscess formation.

Special Concerns

• Presentation of cerebral abscess in patients who are immunocompromised may not follow the expected stages of development.
  • Impaired host response often alters the appearance of cerebral abscesses on MRI or CT examinations.
  • Steroid treatment reduces edema and mass effect.
  • Margins of the abscess are less well defined.
  • The capsule is thinner and enhances less intensely.
  • Patients with systemic diseases, such as lymphoma or leukemia, present with multiple abscesses, often with unusual opportunistic organisms.
  • Abscess morphology also varies in these patients. Lesions caused by unusual opportunistic organisms may have thick and irregular walls and may be difficult to differentiate from primary or metastatic neoplasms.
  • Patients with AIDS rarely develop pyogenic abscesses. AIDS often is associated with opportunistic infections and primary brain lymphoma.

Multimedia

Media file 1: 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.

Media file 2: 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 temporal lobe. The pattern is consistent with possible early cerebritis; however, glioma and infarct may have similar presentations.

Media file 3: Brain abscess. Axial CT scan with intravenous (IV) contrast enhancement in a patient with fever, headache, and a recent history of pneumonia. An area of ringlike enhancement (yellow arrow) is noted within a much larger pattern of edema (white arrow). The central core of the abscess (black arrow) does not enhance, which is consistent with central necrosis.

Media file 4: 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 to exclude a tumor. Following resection of the temporal lobe abscess, extracranial, subdural, and intracerebral abscesses developed (arrows).

Media file 5: Brain abscess. 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.

Media file 6: 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.

Media file 7: Brain abscess. Sagittal T1 weighted unenhanced MRI of the brain in a patient with fever following head trauma. Osteomyelitis of the skull developed in this patient following cranial trauma (yellow arrow. An abscess of the brain (red arrow) developed by direct extension of the infection beyond the skull. The leading edge of the cerebritis is marked by the pattern of mass effect within the deeper margins of the left parietal lobe (white arrow).

Media file 8: Brain abscess. Sagittal diffusion weighted unenhanced MRI of the brain in a patient with fever following head trauma. Osteomyelitis of the skull developed in this patient following cranial trauma. An abscess of the brain (white arrows) developed by direct extension of the infection beyond the skull. Cerebral abscesses may present with an intermediate degree of signal brightness, as in this case, when evaluated by diffusion-weighted protocols.

Media file 9: Brain abscess. Coronal T1-weighted post–gadolinium-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 edge of the cerebritis is marked by the pattern of enhancement within the deeper margins of the left parietal lobe (white arrow).

Media file 10: 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.

Media file 11: Brain abscess. Axial contrast-enhanced CT scan in a patient who was treated surgically for a depressed 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).

Media file 12: 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).

Media file 13: Brain abscess. Axial T1-weighted MRI in a patient with a mature cerebral abscess of the right frontal lobe of the brain. Note the thick wall of the abscess with enhancement (black arrow). The central content of the abscess is dark on T1-weighted imaging with no enhancement (double white arrows.)

Media file 14: Brain abscess. Anterior view of a chest radiograph in a patient with thick-walled right lung abscess. The patient later developed a brain abscess.

Media file 15: Brain abscess. Axial fast spin-echo inversion recovery MRI in a patient with left orbital swelling. Orbital cellulitis may progress to intracranial abscess, as the infection spreads, by causing venous thrombosis and sepsis. Arrows indicate the nonfocal nature of the cellulitis in this patient.

Media file 16: Brain abscess. Axial contrast-enhanced CT scan in a patient with a 6-day history of right orbital pain and swelling. The optic nerve (black arrow) is displaced by an abscess that has formed posterior to the globe of the eye (white arrow). Such a mass may cause retro-orbital veins to clot, resulting in septic phlebothrombosis and the development of an intracranial abscess.

Media file 17: Brain abscess. Axial CT scan with intravenous (IV) contrast enhancement in a patient with fever 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).

Media file 18: Brain abscess. Gadolinium-enhanced coronal T1-weighted MRI in a patient who presented with headache, fever, and diplopia. The right frontal lobe of the 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.

Media file 19: 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 the infection arose. The medial superior right maxillary sinus has been destroyed (yellow arrow).

Media file 20: Brain abscess. Coronal T1-weighted gadolinium-enhanced MRI of the orbits and sinuses in a patient who presented with diplopia, headache, and fever. An abscess is noted within the medial inferior right orbit. The right maxillary sinus (double white arrows) contains infected secretions and mucus.

Media file 21: Brain abscess. Surface 3-dimensional model of a craniofacial CT scan in a patient with headache, orbital swelling, and diplopia of 48 hours' duration. Note the remarkable degree of right orbital swelling, which has resulted in the right lid being closed.

Media file 22: Brain abscess. Axial fluid-attenuated inversion recovery (FLAIR) MRI in a patient with Nocardia-related abscess of the cerebellar vermis (black arrow).

Media file 23: Brain abscess. Axial T2-weighted fast spin-echo MRI in a patient with a Nocardia-related abscess of the midline cerebellum. Note the large area of increased signal, both within the abscess and within the surrounding cerebellum (black arrow).

Media file 24: Brain abscess. Anteroposterior chest radiograph in a chronically ill patient who has diabetes and has had prior coronary surgery. Note the infiltrate in the right lower lobe (black arrow). Pneumonia resulting from Nocardia infection provided the source for an abscess of the midline cerebellum.

Media file 25: Brain abscess. Coronal T1-weighted spin-echo gadolinium-enhanced MRI demonstrates a central zone of enhancement within the abscess, with a zone of decreased brightness (edema, white arrow). Nocardia organisms were cultured from within the abscess cavity.

Media file 26: Brain abscess. Sagittal T1-weighted spin-echo gadolinium-enhanced MRI demonstrates an enhanced mass within the right medial cerebellum (yellow arrow). The thick-walled cystic mass was opened. Nocardia organisms were cultured from within the abscess.

Media file 27: Brain abscess. Nocardia organisms (black arrows) were identified on this microscopic slide of the aspirate from an abscess of the midline cerebellum (silver stain, original magnification X100).

Media file 28: Brain abscess. Axial fluid-attenuated inversion recovery (FLAIR) MRI of a left occipital-parietal brain abscess. The edema pattern (white arrows) surrounds the central abscess (A). A secondary (daughter) abscess is noted anterior to the primary abscess cavity.

Media file 29: Brain abscess. Axial diffusion weighted echo-planar MRI of a left occipital-parietal abscess. Both the primary and secondary (daughter) abscesses are demonstrated well (A). Fluid and necrotic tissue (bright area) are present within the abscess cavities, while edema surrounds the abscess cavities (black arrows).

Media file 30: Brain abscess. T1-weighted gadolinium-enhanced axial MRI of a primary abscess and a smaller daughter abscess (black arrows). Edema surrounding the abscess does not enhance (white arrows).

Media file 31: Brain abscess. Axial diffusion-weighted and T2-weighted echo-planar MRIs. A mildly increased signal brightness and mass effect are noted in the left thalamus and near the right caudate head. Analysis of a brain biopsy specimen demonstrated primary cerebral lymphoma.

Media file 32: Brain abscess. Axial T1-weighted gadolinium-enhanced MRI in a patient with multicentric brain lymphoma. Note the moderate mass effect on the left, with multiple areas of enhancement in both cerebral hemispheres (black arrows). This pattern is unlike the more geographic enhancement of a typical cerebral abscess.

Media file 33: Brain abscess. Coronal T2-weighted gradient-echo MRI in a patient with multicentric primary brain lymphoma. Mass effect, with associated surrounding edema in the left temporal lobe, is indicated by black arrows.

Media file 34: Brain abscess. Axial T2-weighted fast spin-echo MRI of the brain in a patient with multicentric brain lymphoma. Areas of intermediately increased brightness (black arrows) are noted lateral to the right thalamus and in the medial left temporal lobe.

Media file 35: Brain abscess. Thallous chloride Tl 201 single photon emission CT scans demonstrate a large focus of increased activity in the left thalamic and left periventricular region of the brain (black arrows).

Media file 36: Brain abscess. Axial nonenhanced CT scan demonstrates mass effect (white arrows).

Media file 37: Brain abscess. Axial T2-weighted fluid-attenuated inversion recovery (FLAIR) MRI demonstrates 2 areas of increased signal brightness that are noted in the left frontal and the left parietal brain (black arrows) in a patient with toxoplasmosis.

Media file 38: Brain abscess. Axial diffusion-weighted echo-planar MRI in a patient with toxoplasmosis. Mildly increased brightness suggests 2 areas of diffusion restriction in the left frontal and left parietal brain. Increased brightness is due primarily to a T2-weighted contribution rather than diffusion restriction.

Media file 39: Brain abscess. Coronal T1-weighted gadolinium-enhanced MRI in a patient with toxoplasmosis. The area of surrounding edema does not enhance (white arrows), while a nodule of enhancement is demonstrated within the ring lesion (yellow arrow).

Media file 40: Brain abscess. Sagittal T1-weighted gadolinium-enhanced MRI in a patient with toxoplasmosis. The area of surrounding edema does not enhance (white arrows), while a nodule of enhancement is demonstrated within the ring lesion (yellow arrow). The use of multiple images in several projections allows identification of additional lesions in patients with toxoplasmosis.

Media file 41: Brain abscess. Sagittal T1-weighted gadolinium-enhanced MRI in a patient with toxoplasmosis. Multiple small cystic areas of enhancement are noted in the periventricular region of the third ventricle.

Media file 42: Brain abscess. Thallous chloride Tl 201 single photon emission CT scan demonstrates a large focus of mildly increased activity in the left temporal and periventricular region of the brain (black arrows).

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Keywords

intracranial infection, pyogenic infection, pyogenic bacterial infection, tuberculous infection, fungal infection, parasitic infection, brain infection, cerebritis, purulent brain infection, cerebral abscess, cerebral infection, bacterial brain infection, central nervous system infection, CNS infection, Nocardia asteroides, Toxoplasma encephalitis, Listeria monocytogenes

Contributor Information and Disclosures

Author

Lennard A Nadalo, MD, Clinical Professor, Department of Radiology, University of Texas Southwestern Medical School; Consulting Staff, Envision Imaging of Allen and Radiological Consultants Association
Lennard A Nadalo, MD is a member of the following medical societies: American College of Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Radiological Society of North America, and Texas Radiological Society
Disclosure: Nothing to disclose.

Coauthor(s)

Leigh K Hunter, MD, FACP, Clinical Professor, Infectious Diseases Division, University of Texas Southwestern Medical School; Director, Internal Medicine Residency Program, Methodist Medical Center of Dallas
Leigh K Hunter, MD, FACP is a member of the following medical societies: American College of Physicians, American Society for Microbiology, and Association of Program Directors in Internal Medicine
Disclosure: Nothing to disclose.

Medical Editor

Lucien M Levy, MD, PhD, Director of Neuroradiology, Professor of Radiology, Department of Radiology, George Washington University Medical Center
Lucien M Levy, MD, PhD is a member of the following medical societies: American Cancer Society, American College of Radiology, American Heart Association, American Medical Association, American Roentgen Ray Society, American Society of Neuroradiology, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Val Runge, MD, Robert and Alma Moreton Centennial Chair in Radiology, Professor, Editor-in-Chief of Investigative Radiology, Department of Radiology, Scott and White Clinic and Hospital
Val Runge, MD is a member of the following medical societies: Society for Health and Human Values
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

James G Smirniotopoulos, MD, Professor of Radiology, Neurology, and Biomedical Informatics, Chairman, Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences
James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

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