You are in: eMedicine Specialties > Radiology > BRAIN/SPINE Brain, AbscessArticle Last Updated: Jan 24, 2007AUTHOR AND EDITOR INFORMATIONAuthor: 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 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 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 Editors: Lucien M Levy, MD, PhD, Director of Neuroradiology, Professor of Radiology, Department of Radiology, George Washington University Medical Center; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; 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; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; 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 Author and Editor Disclosure Synonyms and related 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 INTRODUCTIONBackgroundThe 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. PathophysiologyMost 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.
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. FrequencyUnited StatesIn 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%. InternationalIn 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/MorbidityEarly 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. RaceNo particular association exists between cerebral abscesses and race. SexNo particular predilection is noted in either sex. AgeBacterial 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. AnatomyCerebral 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. Clinical DetailsClinical 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 ExaminationThe 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 TechniquesPlain 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. DIFFERENTIALSArachnoiditis Astrocytoma, Brain Atrial Septal Defect Brain, Venous Sinus Thrombosis Cerebrospinal Fluid, Leak Cryptococcosis, CNS Cysticercosis, CNS Hemangioblastoma, Brain Leptomeningeal Carcinomatosis Meningitis, Bacterial Toxoplasmosis, CNS Ventricular Septal Defect
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| 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. | |
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| 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. | |
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| 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. | |
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| 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). | |
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| 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. | |
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| 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. | |
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| 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). | |
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| 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. | |
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| Media file 9: 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 edge of the cerebritis is marked by the pattern of enhancement within the deeper margins of the left parietal lobe (white arrow). | |
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| 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. | |
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| 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). | |
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| 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). | |
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| 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.) | |
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| 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. | |
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| 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. | |
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| 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. | |
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| 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). | |
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| 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. | |
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| 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). | |
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| 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. | |
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| 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. | |
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| 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). | |
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| 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). | |
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| 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. | |
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| 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. | |
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| 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. | |
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| 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). | |
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| 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. | |
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| 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). | |
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| 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). | |
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| 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. | |
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| 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. | |
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| 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. | |
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| 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. | |
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| 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). | |
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| Media file 36: Brain abscess. Axial nonenhanced CT scan demonstrates mass effect (white arrows). | |
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| 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. | |
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| 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. | |
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| 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). | |
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| 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. | |
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| 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. | |
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| 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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