Case record...Multiple pyogenic brain abscesses
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Case record...Multiple pyogenic brain abscesses

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Case record...Multiple pyogenic brain abscesses

Case record...Multiple pyogenic brain abscesses
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Case record...Multiple pyogenic brain abscesses Case record...Multiple pyogenic brain abscesses Document Transcript

  • CASE OF THE WEEK PROFESSOR YASSER METWALLY CLINICAL PICTURE CLINICAL PICTURE: 60 years male diabetic patient presented clinically with fever, manifestations of increased intracranial pressure, and meningeal irritation signs. The patient was also suffering from chronic renal failure. RADIOLOGICAL FINDINGS RADIOLOGICAL FINDINGS: Figure 1. Postcontrast CT scan images showing multiple multilocular cerebral abscesses, with densely enhanced capsules. The abscesses are mainly situated at the gray/white matter junction and most probably they are of hematogenous origin. Also noted non-cystic hypodense areas, probably representing early cerebritis stage. Most of the abscesses are situated in the frontal lobe.
  • Figure 2. Postcontrast CT scan images showing multiple cerebral abscesses, with densely enhanced capsules. Notice absence of intracavitary mural nodules. The abscesses are mainly situated at the cortical/subcortical junction and most probably they are of hematogenous origin. Also noted non-cystic hypodense areas, probably representing cerebritis. Laboratory data revealed leucocytosis 18,500 cells/mm3 with 83% neutrophils. He was HIV negative. Blood cultures revealed Klebsiella infection. DIAGNOSIS: DIAGNOSIS: MULTIPLE PYOGENIC BRAIN ABSCESSES DISCUSSION DISCUSSION: A brain abscess implies encapsulated pus within the brain substance, usually secondary to an acute purulent infection. The advances made in surgery and antibiotic therapy in the past have not resulted in the anticipated reduction in mortality. The major causes of mortality and morbidity have been related to delay in diagnosis and ineffective localization of brain abscess. Advances in the treatment of bacterial infections have resulted in a decline in the incidence of bacterial infection of the CNS. The mortality rate has also decreased to 14%. 39 This decrease is primarily the result of the efficient use of antibiotics and good localization by imaging techniques. Brain abscesses may occur at any age but are most commonly encountered in the first 4 decades of life. 36 Males are more commonly affected. Recognition is important because chemotherapy should be started immediately without waiting for bacteriology. Ultimately, however, most brain abscesses are treated by drainage or excision. The source of infection may be local or blood-borne. The primary source of local infection is the result of the complications related to trauma or chronic suppurative otitis media or sinusitis. Blood-borne infection resulting in brain abscess is commonly the result of chronic suppurative intrathoracic infection, such as bronchiectasis, lung abscess, and empyema. In addition, intravenous drug abusers with infected injection sites and immunodeficient patients, including those with diabetes, are at greater risk for developing brain abscesses. 31
  • Figure 1. An early septic embolus, which is shown here, consists of clusters of fibrin, bacteria, and leukocytes plugging the lumen of small vessels with surrounding microinfarcts and dense collections of neurtrophils. Cerebritis and abscess formation in the temporal lobe or cerebellum commonly develops from chronic suppurative otitis media with Bacteroides, Streptococcus, and Enterobacter. 28,31 Adhesions between the petrous temporal bone and temporal lobe or cerebellum predispose to abscess formation at these sites. Septic thrombophlebitis of the emissary veins in the temporal lobe that drain into the intracranial venous sinuses and to the cortical veins may also result in abscess formation. Prolonged mastoid infections may have similar results. Figure 2. Brain abscess during the cerebritis Stage. The abscess is situated at the gray/white matter junction (blood bone infection) Chronic infections about the face and scalp may also lead to cerebritis and abscess formation; this is particularly true of chronic sinusitis of the frontal sinus with the presentation as a frontal lobe abscess. Untreated dural tears of the anterior cranial fossa may also present as a frontal lobe abscess. These abscesses commonly are associated with Streptococcus, Bacteroides, and Staphylococcus aureus. Cerebral abscesses as a result of dental sepsis often contain mixed mouth flora with a predominance of anaerobic bacteria. Their path of spread may result from local sepsis or bacteremia. 18 Infants and children have a unique set of predisposing factors in the setting of cerebritis and abscess. Congenital malformations are frequent pathways for infection, particularly meningomyelocele, encephalocele, ectodermal defects, and cyanotic congenital heart disease. Minor trauma also may result in indolent local infection with subsequent brain abscess. Conditions that result in neuroectodermal defects predispose to S. aureus abscess formation. Congenital heart disease may be a predisposing factor as a result of local reduction in resistance to infections. The rare familial disorder chronic granulomatous disease may result in staphylococcal cerebral abscess in children. Cerebral abscesses may occur anywhere in the brain, with the most common location in the frontal lobe. On encountering an abscess on an imaging study, one should search for a local cause, such as sinusitis, otitis media or mastoiditis, or ectodermal defect. The authors have identified a child with a cerebellar abscess as a result of a congenital dermoid. Abscess formation is preceded by cerebritis. On arrival of bacteria to the cortex or white matter, there is migration
  • of polymorphs from local capillaries. The endothelium of the local capillaries becomes swollen resulting in a suppurative cerebritis. Cerebritis is a localized but poorly demarcated area of parenchymal softening. 21 Pathologically, there is scattered necrosis, edema, petechial hemorrhage, vascular congestion, and perivascular inflammatory infiltrates. 21 Figure 3. A, Focal cerebritis. B that progressed into mature abscess formation. The infection is blood borne and that is why it is situated in the gray/white matter junction. The Collagen capsule is usually less well Progression of an area of cerebritis to abscess occurs when a central developed on the ventricular side than on the zone of necrosis becomes better defined and liquefied and encircled cortical side, likely related to differences in by a Collagen capsule. 21 A zone of gliosis surrounds the Collagen blood supply capsule. 21 This evolution from cerebritis to abscess has been previously categorized into four stages: early cerebritis, late cerebritis, early capsule formation, and late capsule formation. 10,21 The late capsule stage is defined by a complete ring with only a minimal region of cerebritis outside the capsule. The Collagen capsule is usually less well developed on the ventricular side than on the cortical side, likely related to differences in blood supply This feature can be used as a helpful differential feature on imaging studies when trying to decide between a necrotic neoplasm and abscess, although the sign is not pathognomonic. Figure 4. Brain abscess during the encapsulated Stage In abscesses formed from hematogenously Another differential but nonspecific feature between cerebral disseminated infection, the abscess is located at abscess and necrotic neoplasm is the thickness of the capsule, with the gray-white matter junction in the distribution abscess generally demonstrating a thinner, smoother wall. The time
  • of the anterior or middle cerebral artery most that is required to progress from cerebritis to mature abscess is commonly in the frontal and parietal lobes. highly variable, from 2 weeks to several months. 1,21 The rate of progression likely depends on several factors, including the aggressiveness of the organism and status of the host's immune system. Brain abscesses vary greatly in size, are usually oval in shape, and may be multilocular. In abscesses formed from hematogenously disseminated infection, the abscess is located at the gray-white matter junction in the distribution of the anterior or middle cerebral artery most commonly in the frontal and parietal lobes. 21 White matter edema around the abscess is usually widespread. The thickness of the collagenous capsule varies in different parts of the abscess and varies with the age and immunity of the patient. The thickness usually increases by 1 mm per month, but this is a rough guide and not reliable. Figure 5. Microabscesses, The infection is blood borne and that is why it is situated in the gray/white matter junction.   Table 1. Pathognomonic pathological features of brain abscess  Absence of Inner Nodularity. It is our experience that a fully mature bacterial abscess capsule rarely shows modulations projecting into the central low-density area. However, a metastatic ringlike lesion commonly shows an irregular thickness of its wall with modulations projecting into the central low-density component of the lesion. The degree of edema is not a differentiating feature between an abscess and a metastatic lesion.  Multilocularity. We have found that multiple ringlike metastatic lesions are commonly separate and easily identifiable. This is in contrast to multilocular abscesses in which daughter loculi appear to branch off from the medial aspect of the mother abscess, a phenomenon that correlates with the pathologically known observation that the ventricular aspect of the abscess capsule is usually less mature than the one facing the cortex.  The Collagen capsule. The capsule is usually less well developed on the ventricular side than on the cortical side, likely related to differences in blood supply This feature can be used as a helpful differential feature on imaging studies when trying to decide between a necrotic neoplasm and abscess, although the sign is not pathognomonic.  The thickness of the capsule. Another differential but nonspecific feature between cerebral abscess and necrotic neoplasm is the thickness of the capsule, with abscess generally demonstrating a thinner, smoother wall. The thickness of the collagenous capsule varies in different parts of the abscess and varies with the age and immunity of the patient. The thickness usually increases by 1 mm per month, but this is a rough guide and not reliable.  Hematogenously disseminated infection. In abscesses formed from hematogenously disseminated infection, the abscess is located at the gray-white matter junction in the distribution of the anterior or middle cerebral artery most commonly in the frontal and parietal lobes. 39 White matter edema around the abscess is usually widespread.
  •  Reactive Hyperemia. Because of the hyperaemia associated with an abscess (caused by disturbed autoregulation, accumulation of waste products, and low pH) the ipsilateral cerebral hemisphere may show a variable degree of relatively increased "gyral" enhancement. This type of hyperaemia is not expected in noninflammatory lesions. Table 2. PATHOLOGICAL STAGES OF BRAIN ABSCESS Stage Comment Earliest Cerebritis Stage In this stage, the lesion consists of a poorly demarcated area of "acute focal encephalitis". The brain is swollen and soft. Capillaries are congested, veins are   distended, and exudate may be present in the leptomeninges along the distended veins. Microscopically, there are multiple foci of acute suppuration, capillary proliferation, necrosis, varying amounts of edema, and degeneration of brain tissue. The duration of this stage varies, depending on the virulence of the specific organism and the host resistance; this stage usually lasts from 2 to 4 days. Encapsulated Stage At this stage there is liquefaction of the center of the lesion with the formation of a (Primary Delimitation and "wall." The central necrotic area consists of dead tissue cells and Fibrosis) polymorphonuclear (PMN) leukocytes. Enzymes such as protease, peptidase, and lipase released by dead granulocytes cause further lysis of the breakdown products.   The abscess wall has two layers: an inner mesenchymal layer derived from blood vessels and an external astroglial layer derived from the surrounding brain. The inner wall is considered the "capsule" of the abscess and consists of granulation tissue (proliferated capillaries, fibroblasts, lymphocytes, plasma cells, and collagen fibrils) that surrounds the central pus or dead polymorphs. There is a variable infiltration of granulocytes into the inner wall of granulation tissue. The astroglial layer that surrounds the inner wall is poorly defined at this stage. Well-developed Abscess This occurs in 2 to 4 weeks. The wall becomes thicker, more defined, and the number Wall of granulocytes decreases. This stage may last for months   Figure 6. A, Pathologically, the gross appearance of an abscess in its early stage is that of a poorly localized area of discoloration and softening. The inflammatory process at this stage is referred to as cerebritis. B, Hematogenous spread of infection into the CNS from a source such as bacterial endocarditis often produces multiple abscesses, which on gross examination present as widespread small hemorrhages as shown in B. Thus, the true nature of these lesions is usually not appreciated grossly.
  • Figure 7. A, With continued development, a capsule forms around the periphery of the abscess and its center becomes softened. B, In its late stage, an abscess is characterized by a densely fibro-gliotic capsular wall and pus filled center. APPLICATION OF NEUROIMAGING IN CEREBRAL ABSCESS Imaging studies reveal a focal area of edema on T2-weighted images or FLAIR images. Early comparisons with CT scan show the inherent sensitivity of proton density and T2-weighted images to alterations of the tissue water, enabling early detection of cerebritis compared with CT scan. 37 Tl- weighted images demonstrate areas that are slightly hypointense to adjacent brain associated with mass effect as manifested by sulcal effacement or ventricular compression. Subacute hemorrhage, if present, may be revealed as foci of hyperintense Tl signal interspersed in the edematous brain. Contrast enhancement is usually minimal and heterogeneous. CT SCAN IMAGING OF BRAIN ABSCESS  The CT findings faithfully reflect the basic pathologic stage of the brain abscess. In the early phases, CT can demonstrate only an In the cerebritis stage, there is a low-density area in the affected part inconstant subtle ring enhancement on postcontrast scans, of the brain. This area represents the edematous and necrotizing which becomes irregular and thicker in the subsequent component of the lesion, confined predominantly to the white matter. phases of cerebritis. Perilesional edema is usually present. Capsule formation is characterized by a thin, sharp, Owing to blood-brain barrier (BBB) breakdown, an irregular type of uniform, and continuous ring enhancement thicker toward contrast enhancement is present in this acute cerebritis stage. Even oxygen sources, usually cortical vessels. Upon resolution ringlike enhancement can be present, especially at the late cerebritis of the abscess The amount of edema diminishes first, then stage when the reticulin is laying down the framework for final the abscess cavity shrinks gradually. capsule formation. It should be stressed that ringlike contrast enhancement is not necessarily present only when the mature capsule has formed and the abscess has become "walled off." Rather, it is the so-called "filling in" of the ringlike lesion by contrast medium on the 30- to 60-minutes or later delayed CT scans that is the most important criterion for deciding whether or not the capsule has fully matured. Whereas the central part of the ring can "fill in" to a variable degree in delayed scans in the cerebritis stage, such central "filling in" is minimal or absent when the capsule has fully evolved. The capsule of the bacterial abscess is commonly regular and thin; it is not more than 4 to 8 mm in thickness.
  • Figure 8. Occipital lobe pyogenic abscess with ring enhancement. The capsule of the bacterial abscess is commonly regular and thin; it is not more than 4 to 8 mm in thickness, notice the smooth surface of the capsule with absence of inner nodularity, also notice the surrounding edema, and the mass effect. Although a number of different pathologic processes may assume a ringlike morphology on contrast CT scan, the main problem arises in differentiating an abscess from metastatic carcinoma. We feel that it may be possible to more correctly diagnose an abscess if the following three CT scan features are considered:  Absence of Inner Nodularity. It is our experience that a fully mature bacterial abscess capsule rarely shows modulations projecting into the central low-density area. However, a metastatic ringlike lesion commonly shows an irregular thickness of its wall with modulations projecting into the central low-density component of the lesion. The degree of edema is not a differentiating feature between an abscess and a metastatic lesion.  Multilocularity. We have found that multiple ringlike metastatic lesions are commonly separate and easily identifiable. This is in contrast to multilocular abscesses in which daughter loculi appear to branch off from the medial aspect of the mother abscess, a phenomenon that correlates with the pathologically known observation that the ventricular aspect of the abscess capsule is usually less mature than the one facing the cortex.  Reactive Hyperemia. Because of the hyperaemia associated with an abscess (caused by disturbed autoregulation, accumulation of waste products, and low pH) the ipsilateral cerebral hemisphere may show a variable degree of relatively increased "gyral" enhancement. This type of hyperaemia is not expected in noninflammatory lesions. Figure 9. Frontal abscess showing ring enhancement and multiloculations. The Collagen capsule is usually less well developed on the ventricular side than on the cortical side, likely related to differences in blood supply MRI IMAGING OF BRAIN ABSCESS WITH PATHOLOGICAL CORRELATION Cerebritis is an inflammatory-infectious process, caused by small septic emboli occluding small-sized arterial vessels or trespassing the vessel walls by contiguous spread. Brain response limiting the spread of the infection depends on a complex interaction between host and the infectious organism. Early cerebritis is a focal but not localized (capsulated) process. Congested vessels with perivascular polymorphonuclear cells and edema start the process. In the beginning, the inflammatory focus shows reduced rarefied infiltration and petechial hemorrhages.
  • Three to 5 days after, in the late cerebritis phase, necrotic liquefaction ensues. Vessels proliferate, and some neutrophilic granulocytes infiltrate the nervous tissue, with an external layer of granulation tissue, infiltrated with lymphocytes, plasma cells, and granulocytes. The surrounding tissue is edematous. In late cerebritis, macrophages and fibroblasts appear. The transformation of chronic cerebritis into a frank well-formed abscess is linked to fibrous capsule formation (early capsule stage, 2 weeks from the beginning of inflammation). Collagen and reticular fibers delineate the surrounding compressed parenchyma, which exhibits reactive gliosis. In the late capsule stage (weeks to months), the completely formed capsule presents an inner inflammatory layer of granulation tissue and macrophages, a middle collagenous layer, and an outer hyperplastic gliosis layer, surrounded by compressed (mass effect, edema) nervous tissue. Early stages of cerebritis show no enhancement on postcontrast scans. In the late stages of cerebritis, early abscess formation is suggested by a thin, ill-defined ring or ovoid zone of enhancement inside the edema. The ring-enhancing mass (surrounded by edema) of a formed abscess can be accompanied by smaller adjacent daughter rings, extending preferentially toward the white matter. The relative paucity of blood supply with respect to near gray-matter junction could explain a minor richness of the middle collagen layer in the early abscess capsule formation. Therapeutic success in the treatment of an abscess can be recognized by a decrease in edema and enhancement. Steroids, reversing the BBB damage, could lead to a decrease in enhancement falsely suggesting that the process has resolved. Therapeutic monitoring consists in repeating the MR imaging scans every 2 weeks or in every case of abrupt clinical worsening. Contrast enhancement persists for weeks or months after disease resolution. Figure 10. Brain abscesses with multiloculation and ring enhancement Figure 11. Brain abscess with ring enhancement MR imaging demonstrates an increase in water content on long T2-weighted images in early cerebritis, not frequently coinciding with postcontrast enhancement on Tl-weighted images. Enhancement helps to distinguish edema from inflammatory lesions in this phase. The high protein content at the center of the cerebritis explains the high proton density and T2 signal owing to alteration in BBB permeability with free passage of proteins and
  • macromolecules and degradation product debris. The periphery of late cerebritis is isointense to hyperintense on Tl-weighted images and hypointense on proton density weighted and T2- weighted images and enhances strongly after contrast medium administration. Such features are related to the increase in permeability of the preexisting inflamed vessels along with neovasculogenesis, with neovessels not having a mature BBB. The progressive diffusion of the contrast medium toward the center, with staining of the inflamed tissue, is the anatomic-pathologic basis of the filling in phenomenon observed and demonstrated on delayed scans during the phases of cerebritis. In the formed abscess, this phenomenon disappears because of the relative impermeability of the fibrous capsule surrounding necrotic centers. This phenomenon, frequently important in differentiating antibiotic permeable cerebritis from early abscess, is appreciable on CT, albeit better on MR imaging. In the mature forms, the center is filled with necrotic tissue which is purulent in the abscess. Such differences are related to the agent involved and to the host immune response. MR signals reflect the water content of the necrosis with long TI and long T2. The MR imaging features of brain abscesses are variable and change with the lesion stage. The collagenous capsule of the abscess can be seen on unenhanced scans as a thin-walled ring that is isointense to slightly hyperintense to brain on TI-weighted images and is hypointense on T2-weighted images. 14,32 The signal intensities of the rims seen with MR imaging have been attributed to various components of the rim, including Collagen, hemorrhage, or paramagnetic free radicals within phagocytosing macrophages. 14,32,37 Paramagnetic free radicals appear to be the most plausible explanation for the appearance of the abscess rim on unenhanced images. One report suggested that multiple concentric rims of hypointense T2 signal might be specific for infection in a patient with a Nocardia asteroides brain abscess. 22 This finding can likely be found with many different organisms. Important to the follow-up of abscess cavities is that the hypointense T2 rim resolves with successful surgical or medical treatment (or both) as phagocytic activity is reduced. Evaluation of the rim on T2-weighed images may be a better indicator of response to therapy because residual contrast enhancement can persist for months after successful therapy. 32,35 The mechanism of the capsule hypointensity on the T2 The capsule is formed by collagen produced by the fibroblasts weighted MRI scan is not certain. Proposals in this originating from the surrounding vessels and is sharp and easily respect include: identified also on nonenhanced MR imaging scans, being isointense or hyperintense on Tl- weighted images and hypointense on T2- 1-Relative lack of water in the fibrous capsule. weighted images. In immunocompetent hosts, capsule thickness can reach several millimeters. External to the collagen, a cerebritis zone 2-The presence of blood products in the abscess capsule persists, with macrophages devoted to the mobilization of debris. 3- The presence of paramagnetic free radicals within the This activity of phagocytosis releases free radicals for respiratory phagocytosing macrophages which are heterogeneously burst, inducing T2 shortening with the MR imaging appearance of a distributed in the periphery of the abscess, paramagnetic well-delineated but subtle ring of hypointensity on long TR, long TE free radicals induce T2 hypointensity. sequences. The T2 is so short that it is seen as a hypointense ring on Tl-weighted images obtained with a short TE, longer than the T2 of the middle layer of the capsule. Just around the outer layer, there is a zone of the neovessels or inflamed vessels, with a thick, regular ring of contrast enhancement. Figure 12 The activity of phagocytosis releases free radicals for respiratory burst which induces T2 shortening demonstrated as hypointense ring surrounding the brain abscess The appearance of the contrast-enhancing rim of an abscess capsule on postcontrast MR images is similar to that seen with postcontrast CT scans. 12,14 Postgadolinium Tl -weighted images are key in the diagnosis of brain abscess. T2-weighted images help determine the extent of edema and add specificity with the identification of a complete hypointense ring in the abscess wall. In a study of patients with various brain infections, Tsuchiya et al, 34 compared conventional Tl-weighted and T2- weighted images with FLAIR images and found that the FLAIR images provided no additional information in patients with brain abscess.
  • Figure 13. The activity of phagocytosis releases free radicals for respiratory burst which induces T2 shortening demonstrated as hypointense ring surrounding the brain abscess The enhancing rim is usually thin, measuring 5 mm or less, often with a thinner ventricular margin. The enhancing rim is also usually smooth when contrasted with a necrotic neoplasm, which typically has a nodular wall. Occasionally, daughter abscesses are encountered as adjacent smaller enhancing rings along the medial margin of the parent abscess. Typically the center of a mature abscess contains necrotic material slightly hyperintense to cerebrospinal fluid on Tl-weighted images with T2- weighted images approaching that of the cerebrospinal fluid and parenchymal edema. The signal within the central portion of the abscess cavity is variable and dependent on its contents as well as imaging parameters. Protein and other macromolecular components help to shorten Tl and increase the signal intensity within the cavity on Tl-weighted images. 30 The edema surrounding an abscessed cavity is usually quite extensive and may be greater in volume than the abscess itself. This associated mass effect, which is often significant, may ultimately lead to the demise of the patient if not immediately addressed. Intraventricular rupture associated with ependymitis may also lead to a poor outcome. 38 Figure 14. Mature, mixed anaerobic brain abscess. A, Contrast-enhanced axial CT scan with ring-enhancing mass in the right frontal lobe associated with vasogenic edema pattern, compression of ventricular system, subfalcine herniation, and effaced sulci. The abscess wall is thick and nodular and becomes thinned medially. CT appearance and lack of constitutional symptoms favor neoplasm over abscess. Subsequent MR imaging helped in the radiographic differential diagnosis. B, Axial Tl-weighted image reveals a thin, complete ringlike hyperintensity that is hypointense on T2-weighted image (C). Although not definitive, this complete ring is likely due to paramagnetic species and suggests a benign origin of the lesion. The MR signal emanating from the center of the lesion suggests an abundance of debris that is not pure fluid. D, Contrast-enhanced Tl -weighted axial image again reveals the thick nodular enhancing rim with a portion of the medial wall becoming thinner. Brain abscess was confirmed surgically.
  • Figure 15. Typical appearance of a brain abscess. A, Contrast-enhanced CT scan with thin rim-enhancing necrotic lesion of the left occipital lobe. Extensive vasogenic edema and mass effect is present. Just posterior to the mass is a vague area of enhancement suggestive of early daughter cyst formation. B, Axial T2-weighted FSE image reveals complete hypointense ring in several layers. Note similar hypointense ring of daughter abscess. C, Contrast- enhanced coronal view with smooth thin enhancing ring. Central pus is hyperintense to cerebrospinal fluid. Haemophilus aerophilus was the pathogen. Although contrast-enhanced MR imaging is extremely sensitive and better than contrast- enhanced CT scan in detecting brain abscesses, the identification of a ring-enhancing lesion within the brain is by no means diagnostic of an abscess. The differential diagnosis is extensive and includes primary brain tumors, metastasis, septic and aseptic infarction, resolving hematoma, thrombosed aneurysm, arteriovenous malformation, tumefactive multiple sclerosis, and lymphoma. 7,4,25 Although there may be helpful radiographic clues as outlined earlier and clinical findings that may point to the diagnosis of a cerebral abscess, they are not pathognomonic. A variety of primary and secondary tumors can have a similar appearance. There has been much work in trying to distinguish between a brain abscess and necrotic neoplasm with advanced MR imaging techniques, such as diffusion-weighted imaging and proton MR spectroscopy. The resolution of the process is based on the disappearance of the hypointense ring rather than on that of the enhanced ring because altered permeability lasts longer than macrophage activity. Daughter abscesses (due to extension of the infection or to coalescence of multiple lesions), ventriculitis-ependymitis (due to abscess rupture), choroid plexitis, and meningitis (also without abscess rupture) are common complications all shown on postcontrast Tl-weighted images by intense contrast enhancement. Immunocompromised patients have an impaired immune response and are not able to control the infection because of a reduced number of inflammatory cells such as neutrophils and macrophages, persistence of the microorganisms in the necrotic center, and delay in the formation of capsule because of a reduction in fibroblasts. On the neuroradiologic images, the capsule is less regular and less thick because of collagen formation dysfunction.   Figure 16. Brain abscess by proton MR spectroscopy. Axial CT scan demonstrates a faint ring-enhancing lesion of the left parietal lobe. There is minimal surrounding edema.   Diffusion-weighted MR imaging seems to indicate that an abscess cavity is present when depression of the apparent diffusion coefficient is encountered in the central portion of the abscess cavity, whereas tumor necrosis results in an increase in the apparent diffusion coefficient. 5,9,16,17,20,33 Diffusion-weighted images show corresponding increased signal intensity with brain abscess. There have been more studies of proton MR spectroscopy in the differential diagnosis between necrotic brain tumors and abscess. 2,3,6,15,19,23,24,26,29 It appears that abscess cavities often contain amino acids, succinate, and
  • acetate that are not present in necrotic tumors. 3,15,23,24,26 MR spectroscopy may also be of value in following the response to therapy. 2,6 More study, however, is necessary to determine the accuracy of diffusion- weighted imaging and MR spectroscopy in this differential diagnosis.   Figure 17. MRI T1 postcontrast showing cerebellar abscess, notice the ring enhancement and multiloculations   CONTRAST ENHANCEMENT IN CEREBRITIS AND BRAIN ABSCESS Pyogenic infections of the CNS usually arise from septic emboli transmitted hematogenously. Less frequently, transdural spread may occur from adjacent sinus infections (sphenoid, ethmoid, frontal, and mastoid air cells). After an initial unorganized inflammation or cerebritis, the successful immune response will include angiogenic neovascularity and collagen deposition (ie, a capsule of granulation tissue) and formation of an abscess. A layer of astrogliosis surrounds the granulation tissue. Ring enhancement in an abscess reflects the granulation tissue in its wall that has both increased vascularity and abnormally permeable capillaries. Collagen in the wall reinforces it to localize and confine the infected brain and pus. Preceding this organized abscess stage is cerebritis. Cerebritis is an acute inflammatory reaction with altered permeability of the native vessels but without angiogenesis or neovascularity. Before angiogenesis, the signal intensity and attenuation changes are directly caused by the inflammatory process, and perilesional vasogenic edema is variable and may be minimal. In the immunocompetent patient, cerebritis progresses to form an organized abscess. An intermediate stage of transition from cerebritis to an organized abscess may be suspected when the lesion does not have a sharp margin or a wall that is less discrete. On initial CT and MR images, cerebritis will appear as a ring-enhancing lesion. In cerebritis without a collagen capsule, images obtained over 20–40 minutes may show "fill-in" of the ring center. This "filling-in" does not occur in a well-organized abscess and suggests cerebritis. Cerebritis is often treated nonsurgically with high-dose antibiotics.
  • Figure 18. a. Smooth ring-enhancing pattern in late cerebritis and subsequent cerebral abscess. (a) Axial T2- weighted MR image shows a circular mass with extensive perilesional vasogenic edema that surrounds a dark rim (the abscess wall). Mild mass effect on the mid-line structures is seen. (b) On an axial gadolinium-enhanced T1-weighted MR image, the inner wall of the ring- enhancing lesion is smoother than the slightly irregular outer wall. This appearance reflects an earlier stage in the organization of the infection, as it makes the transition from cerebritis to abscess, since a more organized abscess will appear smoother. (c) Axial CT scan shows a sharply marginated, ringed lesion with surrounding perilesional vasogenic edema. (d) On an axial diffusion-weighted MR image, the lesion has markedly restricted diffusion (hyperintensity) due to the viscous pus and necrotic brain tissue in the abscess core. An abscess is the result of organization and partial neutralization of an infection. In the brain, an abscess may develop a well-formed capsule in 2–4 weeks. The organizing infection forms concentric zones or layers: (a) necrotic brain in the innermost layer, (b) reactive white cells (macrophages, monocytes) and fibroblasts, (c) capillary vascular proliferation and collagen capsule formation, (d) neovascularity and active cerebritis, and (e) reactive astrogliosis and vasogenic edema in the outer margin. Figure 19. Brain abscess. Photomicrograph (original magnification, x250; H-E stain) shows the microscopic layers from top to bottom: reactive gliosis and the brain margin, vascular proliferation with collagen formation (granulation tissue), migrating white blood cells (monocytes), and pus. polys = polymorphonuclear leukocytes The rim of reactive tissue is usually thin (2–7 mm), uniformly convex, and smooth on both the outer and inner aspects.
  • Figure 20. Cerebral abscess in a patient with AIDS who died of multiple brain abscesses from Toxoplasma gondii. The ring-enhancing lesion of a cerebral abscess is classically described as having a smooth inner margin and a smooth outer margin. However, in some examples, especially during the transition from cerebritis to abscess, the outer rim of enhancement may resemble the corona of a solar eclipse. An abscess rim is typically hypointense on T2-weighted MR images, and a variety of explanations have been proposed, including dense collagen, blood products (hemosiderin), and paramagnetic free radicals (eg, atomic oxygen produced by leukocytes that are attacking the bacteria). Almost 90% of abscesses demonstrate a hypointense rim, and 75% form a continuous hypointense rim. The abscess wall often appears thicker on the gray matter or "oxygen side" of the ring and thinner along the white matter or ventricular side. The thinner margin of the deep or medial aspect of the lesion is predisposed to daughter abscess formation and deep rupture of the abscess into the ventricle (which leads to pyocephalus and high mortality). Occasionally, the outer perimeter of the abscess wall can appear irregular. The enhancement is both interstitial (from increased capillary permeability) and intravascular (from increased perfusion in the granulation tissue). The interstitial contrast material usually does not migrate into the center of an abscess cavity, even on delayed images, because of the viscosity of the pus and liquefaction necrosis. The viscosity of the necrotic center also explains its high signal intensity on diffusion-weighted images and corresponding reduced diffusion coefficient and therefore low signal intensity on the apparent diffusion coefficient maps. SUMMARY SUMMARY Advances in the treatment of bacterial infections have resulted in a decline in the incidence of bacterial infection of the CNS. The mortality rate has also decreased to 14%. This decrease is primarily the result of the efficient use of antibiotics and good localization by imaging techniques. Brain abscesses may occur at any age but are most commonly encountered in the first 4 decades of life. Males are more commonly affected. Recognition is important because chemotherapy should be started immediately without waiting for bacteriology. Ultimately, however, most brain abscesses are treated by drainage or excision.
  • The source of infection may be local or blood-borne. The primary source of local infection is the result of the complications related to trauma or chronic suppurative otitis media or sinusitis. Blood-borne infection resulting in brain abscess is commonly the result of chronic suppurative intrathoracic infection, such as bronchiectasis, lung abscess, and empyema. In addition, intravenous drug abusers with infected injection sites and immunodeficient patients, including those with diabetes, are at greater risk for developing brain abscesses. Cerebritis and abscess formation in the temporal lobe or cerebellum commonly develops from chronic suppurative otitis media with Bacteroides, Streptococcus, and Enterobacter. Adhesions between the petrous temporal bone and temporal lobe or cerebellum predispose to abscess formation at these sites. Septic thrombophlebitis of the emissary veins in the temporal lobe that drain into the intracranial venous sinuses and to the cortical veins may also result in abscess formation. Prolonged mastoid infections may have similar results. Chronic infections about the face and scalp may also lead to cerebritis and abscess formation; this is particularly true of chronic sinusitis of the frontal sinus with the presentation as a frontal lobe abscess. Untreated dural tears of the anterior cranial fossa may also present as a frontal lobe abscess. These abscesses commonly are associated with Streptococcus, Bacteroides, and Staphylococcus aureus. Cerebral abscesses as a result of dental sepsis often contain mixed mouth flora with a predominance of anaerobic bacteria. Their path of spread may result from local sepsis or bacteremia. Infants and children have a unique set of predisposing factors in the setting of cerebritis and abscess. Congenital malformations are frequent pathways for infection, particularly meningomyelocele, encephalocele, ectodermal defects, and cyanotic congenital heart disease. Minor trauma also may result in indolent local infection with subsequent brain abscess. Conditions that result in neuroectodermal defects predispose to S. aureus abscess formation. Congenital heart disease may be a predisposing factor as a result of local reduction in resistance to infections' The rare familial disorder chronic granulomatous disease may result in staphylococcal cerebral abscess in children. Cerebral abscesses may occur anywhere in the brain, with the most common location in the frontal lobe. On encountering an abscess on an imaging study, one should search for a local cause, such as sinusitis, otitis media or mastoiditis, or ectodermal defect. The authors have identified a child with a cerebellar abscess as a result of a congenital dermoid. Abscess formation is preceded by cerebritis. On arrival of bacteria to the cortex or white matter, there is migration of polymorphs from local capillaries. The endothelium of the local capillaries becomes swollen resulting in a suppurative cerebritis. Cerebritis is a localized but poorly demarcated area of parenchymal softening. Pathologically, there is scattered necrosis, edema, petechial hemorrhage, vascular congestion, and perivascular inflammatory infiltrates Imaging studies reveal a focal area of edema on T2-weighted images or FLAIR images. Early comparisons with CT scan show the inherent sensitivity of proton density and T2-weighted images to alterations of the tissue water, enabling early detection of cerebritis compared with CT scan. Tl- weighted images demonstrate areas that are slightly hypointense to adjacent brain associated with mass effect as manifested by sulcal effacement or ventricular compression. Subacute hemorrhage, if present, may be revealed as foci of hyperintense Tl signal interspersed in the edematous brain. Contrast enhancement is usually minimal and heterogeneous. Progression of an area of cerebritis to abscess occurs when a central zone of necrosis becomes better defined and liquefied and encircled by a Collagen capsule. A zone of gliosis surrounds the Collagen capsule. This evolution from cerebritis to abscess has been previously categorized into four stages: early cerebritis, late cerebritis, early capsule formation, and late capsule formation. The late capsule stage is defined by a complete ring with only a minimal region of cerebritis outside the capsule. The Collagen capsule is usually less well developed on the ventricular side than on the cortical side, likely related to differences in blood supply This feature can be used as a helpful differential feature on imaging studies when trying to decide between a necrotic neoplasm and abscess, although the sign is not pathognomonic. Another differential but nonspecific feature between cerebral abscess and necrotic neoplasm is the thickness of the capsule, with abscess generally demonstrating a thinner, smoother wall. The time that is required to progress from cerebritis to mature abscess is highly variable, from 2 weeks to several months. The rate of progression likely depends on several factors, including the aggressiveness of the organism and status of the host's immune system. Brain abscesses vary greatly in size, are usually oval in shape, and may be multilocular. In abscesses formed from hematogenously disseminated infection, the abscess is located at the gray-white matter junction in the distribution of the anterior or middle cerebral artery most commonly in the frontal and parietal lobes. White matter edema around the abscess is usually widespread. The thickness of the collagenous capsule varies in different parts of the abscess and varies with the age and immunity of the patient. The thickness usually increases by 1 mm per month, but this is a rough guide and not reliable. The MR imaging features of brain abscesses are variable and change with the lesion stage. The collagenous capsule
  • of the abscess can be seen on unenhanced scans as a thin-walled ring that is isointense to slightly hyperintense to brain on TI-weighted images and is hypointense on T2-weighted images. The signal intensities of the rims seen with MR imaging have been attributed to various components of the rim, including Collagen, hemorrhage, or paramagnetic free radicals within phagocytosing macrophages. Paramagnetic free radicals appear to be the most plausible explanation for the appearance of the abscess rim on unenhanced images. Important to the follow-up of abscess cavities is that the hypointense T2 rim resolves with successful surgical or medical treatment (or both) as phagocytic activity is reduced. Evaluation of the rim on T2-weighed images may be a better indicator of response to therapy because residual contrast enhancement can persist for months after successful therapy. The appearance of the contrast-enhancing rim of an abscess capsule on postcontrast MR images is similar to that seen with postcontrast CT scans. Postgadolinium Tl -weighted images are key in the diagnosis of brain abscess. T2- weighted images help determine the extent of edema and add specificity with the identification of a complete hypointense ring in the abscess wall. In a study of patients with various brain infections, T The enhancing rim is usually thin, measuring 5 mm or less, often with a thinner ventricular margin. The enhancing rim is also usually smooth when contrasted with a necrotic neoplasm, which typically has a nodular wall. Occasionally, daughter abscesses are encountered as adjacent smaller enhancing rings along the medial margin of the parent abscess. Typically the center of a mature abscess contains necrotic material slightly hyperintense to cerebrospinal fluid on Tl-weighted images with T2- weighted images approaching that of the cerebrospinal fluid and parenchymal edema. The signal within the central portion of the abscess cavity is variable and dependent on its contents as well as imaging parameters. Protein and other macromolecular components help to shorten Tl and increase the signal intensity within the cavity on Tl-weighted images. The edema surrounding an abscessed cavity is usually quite extensive and may be greater in volume than the abscess itself. This associated mass effect, which is often significant, may ultimately lead to the demise of the patient if not immediately addressed. Intraventricular rupture associated with ependymitis may also lead to a poor outcome. Although contrast-enhanced MR imaging is extremely sensitive and better than contrast- enhanced CT scan in detecting brain abscesses, the identification of a ring-enhancing lesion within the brain is by no means diagnostic of an abscess. The differential diagnosis is extensive and includes primary brain tumors, metastasis, septic and aseptic infarction, resolving hematoma, thrombosed aneurysm, arteriovenous malformation, tumefactive multiple sclerosis, and lymphoma. Although there may be helpful radiographic clues as outlined earlier and clinical findings that may point to the diagnosis of a cerebral abscess, they are not pathognomonic. A variety of primary and secondary tumors can have a similar appearance. There has been much work in trying to distinguish between a brain abscess and necrotic neoplasm with advanced MR imaging techniques, such as diffusion-weighted imaging and proton MR spectroscopy. Diffusion-weighted MR imaging seems to indicate that an abscess cavity is present when depression of the apparent diffusion coefficient is encountered in the central portion of the abscess cavity, whereas tumor necrosis results in an increase in the apparent diffusion coefficient. Diffusion-weighted images show corresponding increased signal intensity with brain abscess. There have been more studies of proton MR spectroscopy in the differential diagnosis between necrotic brain tumors and abscess. It appears that abscess cavities often contain amino acids, succi More study, however, is necessary to determine the accuracy of diffusion- weighted imaging and MR spectroscopy in this differential diagnosis.  Addendum  A new version of this PDF file (with a new case) is uploaded in my web site every week (every Saturday and remains available till Friday.)  To download the current version follow the link "http://pdf.yassermetwally.com/case.pdf".  You can also download the current version from my web site at "http://yassermetwally.com".  To download the software version of the publication (crow.exe) follow the link: http://neurology.yassermetwally.com/crow.zip  The case is also presented as a short case in PDF format, to download the short case follow the link: http://pdf.yassermetwally.com/short.pdf  At the end of each year, all the publications are compiled on a single CD-ROM, please contact the author to know more details.
  •  Screen resolution is better set at 1024*768 pixel screen area for optimum display.  For an archive of the previously reported cases go to www.yassermetwally.net, then under pages in the right panel, scroll down and click on the text entry "downloadable case records in PDF format"  Also to view a list of the previously published case records follow the following link (http://wordpress.com/tag/case-record/) or click on it if it appears as a link in your PDF reader REFERENCES References 1. Alford EC Jr, Shaw CM: Infectious anergic and demyelinating diseases of the nervous system. In Newton TH, Potts DG (eds): Radiology of the Skull and Brain: Anatomy and Pathology. St. Louis, CV Mosby 1977, pp 3088- 3172 2. Burtscher IM, Holtas S: In vivo proton MR spectroscopy of untreated and treated brain abscesses. AJNR Am j Neuroradiol 20:1049-1053, 1999 3. Chang KH, Song IC, Kim SH, et al: In vivo single- voxel proton MR spectroscopy in intracranial cystic masses. AJNR Am j Neuroradiol 19:401-405, 1998 4. Coularu CM, Seshul M, Donaldson J: Intracranial ring lesions: Can we differentiate by computed tomography? Invest Radiol 15:103-112, 1980 5. Desprechins B, Stadnik T, Koerts G, et al: Use of diffusion-weighted MR imaging in differential diagnosis between intracerebral necrotic tumors and cerebral abscesses. AJNR Am j Neuroradiol 20:1252- 1257,1999 6. Dev R, Gupta RK, Poptani H, et al: Role of in vivo proton magnetic resonance spectroscopy in the diagnosis and management of brain abscess. Neurosurgery 42:37-42, 1998 7. Dobkin JF, Healton EB, Dickson PC, et al: Nonspecificity of ring enhancement in "medically cured" brain abscess. Neurology 34:139-144, 1984 8. Dunn V, Ball Fj Jr, Zimmerman RA, et al: MRI in children with postinfectious disseminated encephalomyelitis. Magn Reson Imaging 4:25-32,1986 9. Ebisu T, Tanaka C, Umeda M, et al: Discrimination of brain abscess from necrotic or cystic tumors by diffusion- weighted echo planar imaging. Magn Reson Imaging 14:1113-1116,1996 10. Enzmann DR, Britt RH, Placone R: Staging of human brain abscess by computed tomography. Radiology 146:703-708 1983 11. Falcone S, Quencer RM, Bowen BC, et al: Creutzfeldt- Jakob disease: Focal symmetrical cortical involvement demonstrated by MR imaging. AJNR Am J Neuroradiol 12:403-406,1992 12. Grossman RI, Joseph PM, Wolf G, et al: Experimental intracranial septic infarction: Magnetic resonance enhancement. Radiology 155:649-653,1985 13. Grunwaldt F, Pohl C, Bender H, et al: 18 F-fluorodeoxyglucose-PET and Tc-bicisate-SPECT in Creutzfeldt- jakob disease. Ann Nucl Med 10:131-134,1996 14. Haimes AB, Zimmerman RD, Morgello S, et al: MR imaging of brain abscesses. AJR Am J Roentgenol 152:1073-1085, 1989 15. Kim SH, Chong KH, Song IC, et al: Brain abscess and brain tumor: Discrimination with in vivo H-1 MR spectroscopy. Radiology 204:239-245, 1997 16. Kim Yj, Chang KH, Song IC, et al: Brain abscess and necrotic or cystic brain tumor: Discrimination with signal intensity on diffusion-weighted MR imaging. AJR Am J Roentgenol 171:1487-1490, 1998 17. Krabbe K, Gidon P, Wong P, et al: MR diffusion imaging of human intracranial tumors. Neuroradiology 39:483-489,1997
  • 18. Leading article: Chemotherapy of brain abscess. Lancet 2:1081-1082, 1978 19. Martinez-Perez 1, Moreno A, Alonso J, et al: Diagnosis of brain abscess by magnetic resonance spectroscopy: Report of two cases. J Neurosurg 86:708- 713,1997 20. Noguchi K, Watanabe N, Nagayoshi T, et al: Role of diffusion-weighted echo-planar MRI in distinguishing between brain abscess and tumor: A preliminary report. Neuroradiology 41:171-174, 1999 21. Parker JC Jr, Dyer MC: Neurologic infections due to bacteria, fungi and parasites. In Doris RL, Robertson DM (eds): Textbook of Neuropathology. Baltimore, Williams & Wilkins, 1985, pp 632-703 22. Phytinen J, Paakko E, jartt P: Cerebral abscess with multiple rims of MRI. Neuroradiology 38:857-859, 1997 23. Poptani H, Gupta RK, Roy RR, et al: Characterization of intracranial mass lesions with in vivo proton MR spectroscopy. AJNR Am j Neuroradiol 16: 1593 - 1603,1995 24. Poptani H, Kaartinen J, Gupta RK, et al: Diagnostic assessment of brain tumors and non-neoplastic brain disorders in vivo using proton nuclear magnetic resonance spectroscopy and artificial neural networks. J Cancer Res Clin Oncol 125:343-349,1999 25. Post MJD, Hoffman TA: Cerebral inflammatory disease. In Rosenberg RN (ed): The Clinical Neurosciences: Neuroradiology. New York, Churchill Livingstone, 1984, pp 525-594 26. Remy C, Grond S, Lai ES, et al: IH MRS of human brain abscesses in vivo and in vitro. Magn Reson Med 34:508-514,1995 27. Saba PR, McDonald K, Hunn J, et al: Technetium-99m HMPAO labeled leukocytes as a primary diagnostic tool in a case of brain abscess. Clin Nucl Med 22:679- 682,1997 28. Saez-Llorens Xj, Umana MA, Odio CM, et al: Brain abscess in infants and children. Pediatr Infect Dis j 8:449- 458,1989 29. Schumacher DJ, Nelson TR, von Sonnenberg E, et al: Quantification of amino acids in human body fluids by H magnetic resonance spectroscopy: A specific test for the identification of abscess. Invest Radiol 27:999-1004,1992 30. Som PM, Dillon WP, Fullerton GD, et al: Chronically obstructed sinonasal secretions: Observations on Tl and T2 shortening. Radiology 172:515-520,1989 31. Strong Aj, Ingham HR: Brain abscess. Br J Hosp Med 30:396-403,1983 32. Sze G, Zimmerman RD: The magnetic resonance imaging of infections and inflammatory diseases. Radiol Clin North Am 26:839-859,1988 33. Tien RD, Felsberg Gj, Friedman H, et al: MR imaging of high grade cerebral gliomas: Value of diffusion- weighted echoplanar pulse sequences. AJR Am j Roentgenol 162:671-677,1994 34. Tsuchiya K, Inaoka S, Mizutani Y. Fast fluid-attenuated inversion recovery MR of intracranial infections. AJNR Am J Neuroradiol 18:909-913,1997 35. Whelan MA, Hilal SK: Computed tomography as a guide in the diagnosis and follow-up of brain abscesses. Radiology 135:633-671, 1980 36. Yang S: Brain abscess: A review of 400 cases. j Neurosurg 55:794-799, 1981 37. Zimmerman RA, Bilaniuk LT, Sze G: Intracranial infection. In Magnetic Resonance Imaging of the Central Nervous System. New York, Raven Press, 1987, pp 235-257 38. Lee SH: Infectious diseases. In Lee SH, Rao KCVG (eds): Cranial Computed Tomography. New York, McGraw-Hill, 1983, pp 505-546 39. Smith HP, Hendrick EB: Subdural empyema and epidural abscess in children. J Neurosurg 58:392-397, 1983 40. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD
  • agency for electronic publication, version 11.1a. January 2010