Skip to main content
NCBI home page
Medscape General Medicine logoLink to Medscape General Medicine
. 2006 Jan 5;8(1):3.

Case 11: A Young Woman With Ring-Enhancing Brain Lesions

Irene Cortese 1, Avindra Nath 2
PMCID: PMC1681925  PMID: 16915133

Presenting Complaint

A 35-year-old woman was referred to Johns Hopkins Hospital, Baltimore, Maryland, for a brain biopsy. The patient initially presented to a local community hospital following 5 days of blurred vision associated with headache and 2 days of left face, arm, and leg numbness. These symptoms had come on gradually, were becoming progressively worse, and were accompanied with generalized fatigue and anxiety. She also complained of a dry cough and dyspnea on exertion. She denied any fever, chills, night sweats, or weight loss. She reported no contacts with other sick individuals and no recent travel outside her hometown. She did not own any pets.

Past Medical History

The patient had diabetes mellitus type 2. She had undergone a hysterectomy a few years earlier for cervical cancer. She also had been diagnosed with pulmonary alveolar proteinosis (PAP).

Social History

She lived with her husband; they had no children. She reported a 20-year, 2-packs-per-day smoking history, but had recently cut down to 1 pack per day. She denied any alcohol or illicit drug use.

Family History

Multiple family members were known to have coronary artery disease, hypertension, and diabetes.

Physical Exam

The patient's initial physical exam from the local hospital was not available. She reported that she did not have a fever, and although her left side felt numb and heavy, she was able to walk.

Initial Laboratory Studies

White blood cell count: 9.7 × 103 cells/mm3.

Hematocrit: 43%.

Platelets: 256,000 cells/mL.

Na: 137 mEq/L.

K: 3.9 mEq/L.

BUN: 16 mg/dL.

Creatinine: .6 mg/dL.

Albumin: 3.6 g/dL.

Protein: 7 g/dL.

Alkaline phosphatase: 67 IU/L.

AST: 12 IU/L.

ALT: 36 IU/L.

Readers are encouraged to respond to George Lundberg, MD, Editor of MedGenMed, for the editor's eye only or for possible publication via email: glundberg@medscape.net

Imaging Studies

The patient underwent head computed tomography (CT) and magnetic resonance imaging (MRI) of the brain. These showed multiple, bilateral lesions with surrounding edema on fluid-attenuated inversion recovery (FLAIR) images (Figure 1), which appeared ring-enhancing on postgadolinium images (Figure 2).

  1. Which of the following would be the least likely cause of ring-enhancing brain lesions in an immunocompetent patient?
    1. Metastases
    2. Pyogenic abscess
    3. Toxoplasmosis
    4. Multiple sclerosis
  2. Which of the following would be the least likely cause of ring-enhancing brain lesions in an immunocompromised patient?
    1. Metastases
    2. Pyogenic abscess
    3. Toxoplasmosis
    4. Primary central nervous system (CNS) lymphoma
  3. According to the American Academy of Neurology (AAN) guidelines, what is the next best step for the management of ring-enhancing lesions in the immunocompromised host?
    1. Go directly to brain biopsy
    2. Treat empirically for toxoplasmosis
    3. Treat empirically for pyogenic abscess
    4. Treat empirically with steroids

Figure 1.

Figure 1

Open in a new tab

Fluid-attenuated inversion recovery (FLAIR) images reveal bilateral lesions with surrounding edema.

Figure 2.

Figure 2

Open in a new tab

Postgadolinium scan demonstrates ring enhancement of the lesions.

Differential Diagnosis of Ring-Enhancing Lesions

The mnemonic, MAGIC DR, can be used as a prompt for the etiologies of ring-enhancing lesions:

  • Metastases;

  • Abscess, including pyogenic abscess and abscess caused by atypical organisms, such as bacterial pathogens (Mycobacteria, Nocardia, Actinomyces, Rhodococcus, and Listeria); fungal pathogens (zygomycosis, Histoplasma, Coccidioides, Aspergillus, and Cryptococcus); and parasitic pathogens (neurocystircercosis, Echinococcus, and Entamoeba);

  • Glioma and other primary CNS neoplasms (eg, lymphoma);

  • Infarction;

  • Contusion;

  • Demyelination (multiple sclerosis, acute disseminated encephalomyelitis); and

  • Resolving hematoma/radionecrosis.

Hospital Course

The patient was treated empirically with ceftriaxone and vancomycin as well as dexamethasone and phenytoin for presumptive pyogenic brain abscess and for seizure prophylaxis. The dexamethasone was included in the regimen to shrink the edema surrounding the lesions.

Further laboratory studies included:

  • Erythrocyte sedimentation rate (ESR), 11 mm/hour;

  • C-reactive protein (CRP), .9 mg/dL; and

  • Antinuclear antibody (ANA) titer, < 1:40 (negative).

The patient was HIV-negative. Toxoplasma immunoglobulin (Ig)M and IgG were negative. Routine blood cultures were negative.

Following lumbar puncture, a cerebrospinal fluid (CSF) analysis revealed 11 white blood cells, with 93% lymphocytes, 0 red blood cells, glucose of 65 mg/dL, and protein of 45 g/dL. All CSF cultures, including fungal, were negative. CSF VDRL test, cryptococcal antigen, and Lyme titer were negative. Viral polymerase chain reactions of the CSF were negative. No oligoclonal bands were detected and the IgG index was normal. Cytopathology of the CSF cells showed only reactive lymphocytes.

Magnetic resonance angiography (MRA) of the brain and neck was normal; a CT of the chest, abdomen, and pelvis showed evidence of PAP, but was otherwise negative; bilateral mammogram was negative, as was a breast ultrasound. Transesophageal echocardiogram was normal. An electroencephalogram (EEG) revealed slowing over the right temporoparietal region, but no epileptiform activity.

The antibiotics were discontinued, and the patient was discharged from the community hospital with a dexamethasone taper and a presumptive diagnosis of multiple sclerosis.

During the next 2 weeks, the patient developed worsening left-sided weakness. She suffered multiple falls and finally was unable to walk because of her weakness. Her headaches also worsened and were now associated with nausea. She was readmitted to the local hospital where she underwent another MRI.

The FLAIR images showed a significant increase in the size of the lesions and the surrounding edema (Figure 3). No new lesions were noted. The postgadolinium images showed the persistence of ring enhancement (Figure 4). Moreover, the lesions now had clear multiloculated appearance.

Figure 3.

Figure 3

Open in a new tab

Repeat fluid-attenuated inversion recovery (FLAIR) images show significantly enlarged lesions and surrounding edema.

Figure 4.

Figure 4

Open in a new tab

Postgadolinium scans reveal persistent ring enhancement of multiloculated lesions.

Because of the MRI results, the patient was prescribed empiric treatment with sulfadiazine-pyrimethamine, acyclovir, ceftriaxone, and high-dose steroids. She was transferred to Johns Hopkins Hospital for brain biopsy.

Johns Hopkins Hospital Course

On admission to Johns Hopkins Hospital, the patient was afebrile, with a blood pressure of 122/84 mm Hg and pulse of 90 beats/minute. She appeared anxious but in no acute distress. Cardiac exam revealed a regular rate and rhythm with no murmurs, rubs, or gallops. Her lungs were clear to auscultation, with reduced breath sounds at the bases. Her abdomen was soft and nontender. No clubbing, cyanosis, or edema was present in her extremities.

She was alert and oriented to date, time, and place, with intact language. Her pupils were equal, round, and reactive to light; fundoscopic exam was normal; the patient had a right visual field cut. Extraocular movements and facial sensation and movements were intact; tongue and uvula were midline.

The patient had normal bulk and tone of all muscle groups, with 5 of 5 strength throughout except the left deltoid, left hip flexion, and left ankle dorsiflexion, which were 4 of 5. She reported subjective reduction of sensation involving the left upper and lower extremities to all modalities. Coordination was intact to finger-nose-finger and heel-shin testing; rapid alternating movements were clumsy with the left hand. Her gait was cautious. Deep tendon reflexes were brisk on the left compared with the right, with an upgoing toe on the left.

The patient underwent an open brain biopsy. After the initial incision, a large amount of purulent material under pressure was rapidly exposed within 1 mm of the surface of the brain. The STAT gram stain showed light-to-moderate polymorphonucleated cells with heavy branching, gram-positive rods that were modified acid-fast positive (Figure 5). The pathogen was definitively diagnosed as Nocardia.

  • 4.
    What risk factor does this patient have for nocardial infection?
    1. History of smoking
    2. Obesity
    3. Immunocompromise
    4. PAP

Figure 5.

Figure 5

Open in a new tab

Gram stain reveals polymorphonucleated cells with gram-positive, modified acid-fast positive rods.

Discussion

The differential diagnosis of ring-enhancing lesions largely depends on the immune status of the patient. In the immunocompetent host, tumors – both primary and metastatic – and pyogenic abscesses remain the most likely diagnoses; abscesses caused by atypical organisms and demyelinating disease must also be considered. In the immunocompromised host, the leading diagnoses are toxoplasmosis and primary CNS lymphoma. Furthermore, these patients are at risk for abscesses, from both pyogenic and atypical organisms, and tumors. Tuberculous brain abscess should be considered in endemic regions in both immunocompetent and immunocompromised hosts.

Attempts have been made to identify distinctive radiologic characteristics of ring-enhancing lesions. In general, abscesses are said to possess a thin, uniform ring, which is thinner on the medial border, and a smoother outer margin; satellite lesions are often present.[1] By contrast, neoplasms are purported to have thicker, more irregular rims. Ring-enhancing lesions seen in demyelinating disease tend not to be perfect rings, but rather incomplete rings, hence the “open-ring sign.[2]” However, despite these attempts to correlate imaging features with specific underlying lesions, such lesions cannot be distinguished purely on the basis of the radiologic findings.

The different pathologies that can cause ring-enhancing lesions require very different treatment, the institution of which requires early diagnosis. This has led to the development of different strategies to permit noninvasive, early diagnosis.

Can Noninvasive Approaches Ensure an Accurate Diagnosis?

Positron emission tomography (PET) can provide dynamic information regarding the metabolism of a lesion, which may be useful for differentiating tumors from abscesses, with a specificity and sensitivity above 90%. Tumors typically show increased metabolic activity in the center of the lesion, whereas abscesses do not. However, in high-grade neoplasms that often hold a necrotic center, the reduced metabolic activity in the center of the tumor can make it difficult to differentiate from the pattern found in abscesses.[3,4]

Since the 1980s, numerous reports have suggested that thallium-201 single photon emission computed tomography (Th-SPECT) is able to grade tumor malignancy.[5–8] In 1994, Ruiz and colleagues[5] described 100% sensitivity and specificity of Th-SPECT in differentiating primary CNS lymphoma from toxoplasmosis. Despite initial enthusiasm, several studies since then have reported sensitivities and specificities as low as 60% and 71%.[6–9] Th-SPECT is still considered useful in this differentiation when in association with other tests, such as toxoplasmosis serology or CSF Epstein-Barr virus polymerase chain reaction.[6–9]

MR spectroscopy has led to identification of MR spectra patterns that appear specific to tumors and abscesses, and can help in the differentiation of these. Brain abscesses are characterized by reductions in choline, creatine, and N-acetyl-aspartate. Brain tumors, on the other hand, usually show elevated choline levels and reduced levels of creatine and N-acetyl-aspartate. These changes are not diagnostic, however. Abscesses also contain high lactate, succinate, acetate, alanine, valine, leucine, and isoleucine levels.[10–12] Amino acids and other small molecules, such as acetate, lactate, pyruvate, and succinate, are known metabolic end products of proteolysis of the microorganisms, or polymorphonuclear leukocytes in pus, or both. Among these, only lactate is a nonspecific marker, seen in many other neurologic diseases, including brain tumors. In fact, a succinate peak on MR spectroscopy, although not seen in all brain abscesses, is fairly specific for the diagnosis of intracranial infection rather than neoplasm because it was not seen in any brain tumors investigated. Acetate and pyruvate were only seen in conjunction with infection and not with tumors, as well.[13] Thus, studies suggest that MR spectroscopy could accurately distinguish between brain tumors and bacterial abscesses; however, MR spectroscopy does not appear helpful in distinguishing parasitic or fungal infections from tumors.[12]

Several reports have asserted that diffusion-weighted MRI imaging (DWI) can be helpful for distinguishing tumors and abscesses.[11,14,15] DWI is based on the random movement of water known as Brownian motion. Stationary water, unlike freely moving water, is depicted as high signal intensity on DWI, with a decreased signal on the corresponding apparent diffusion coefficient (ADC) maps. The more restricted the water motion is, the less is the value of the ADC. An abscess cavity usually demonstrates high signal on DWI with decreased ADC values, unlike necrotic tumor cavities, which demonstrate the opposite. The restricted diffusion is directly related to the presence of pus in the abscess cavity, likely associated with high cellularity and viscosity. Some studies have reported that abscesses are DWI bright/ADC dark, and that this is characteristic but not pathognomonic.[11,15]

MR perfusion is another technique that has been used in the noninvasive diagnosis of ring-enhancing lesions. The necrotic, avascular center of an abscess would be expected to have low flow, in contrast to a tumor, which is usually marked with hypervascularity and neovascularization. Several studies support the utility of this method, alone or in combination with others, for differentiating focal mass lesions.[16–18]

Notwithstanding these findings, the general consensus is that no noninvasive approach has emerged as being able to reliably discern whether a ring-enhancing lesion is tumor or abscess, and therefore early biopsy is generally considered essential for definitive diagnosis. The only exception to this rule is stated in the AAN guidelines for the management of patients with AIDS.[19] In this case, only an isolated ring-enhancing lesion in the setting of negative toxoplasmosis serology requires early biopsy. Otherwise, a trial of pyrimethamine and sulfadiazine is considered appropriate for treatment of presumptive toxoplasmosis.

Nocardial Abcess

In our patient, open biopsy led to the diagnosis of cerebral nocardiosis. Nocardia was first identified by Nocard in 1888 in bovine farcy.[1] The first human disease was described by Eppinger in 1890.[1] Nocardia is a gram-positive, branching, filamentous, weakly acid-fast bacterium. These organisms are not part of normal flora and are very rarely laboratory contaminants. Pathogenic Nocardia are members of the family Nocardiaceae, the aerobic Actinomycetes. Nocardia asteroides is the principal cause of nocardiosis in the United States (responsible for 80% of human infection). Nocardia is ubiquitous in the soil and decaying vegetables and is found worldwide.[1,20–22]

Roughly 500-1000 new Nocardia infections are diagnosed each year, and often in an opportunistic setting; up to 20% of patients with renal transplants develop nocardiosis.[1] The organism can cause pulmonary, extrapulmonary, CNS, or cutaneous disease[1]; CNS involvement is more common in the immunocompromised host. The route of infection is generally by inhalation or wound inoculation. Clinical manifestations can be acute, subacute, or chronic suppurative infections.

Nocardia is responsible for 2% of all brain abscesses; 15% to 45% of infected patients develop CNS involvement.[20] In 36% of patients, the abscesses are multiloculated, which may be of diagnostic significance when seen on MRI scans.[20] In all, 41% of patients have multiple abscesses, and an extraneural source is identified in 66%.[20] The diagnosis requires isolation and identification from the clinical specimen. Nocardia are gram-stain-positive and modified acid-fast stain-positive. Cultures can take 1-3 weeks to develop and speciation is difficult.[20]

Treatment

No prospective, randomized trials exist addressing the most appropriate treatment of these infections. For more than 50 years, the mainstay of treatment has been trimethoprim-sulfamethoxazole. Second-line agents include imipenem-cilastatin, amikacin, minocycline, ceftriaxone, and dapsone. Successful outcome has also been reported with meropenem,[23] a newer carbapenem with a spectrum of activity comparable to that of imipenem-cilastatin. Resistance to both sulfonamides and cephalosporins is most common among Nocardia farcinicia isolates. Duration of treatment is prolonged and may require up to 1 year of treatment. Generally, the maximum dose of medications is given for 6 weeks, followed by reduced-dose treatment for 6 months to 1 year.[1,20,24,25]

Mortality is reported to be between 7% and 44% in the immunocompetent host and up to 85% in the immunocompromised host.[20] CNS disease carries a mortality of 20% in the immunocompetent host and 55% in the immunocompromised host. Using trimethoprim-sulfamethoxazole for suppressive treatment of Pneumocystis carinii pneumonia in the immunocompromised host probably also reduces the incidence of Nocardia. Similarly, the use of trimethoprim-sulfamethoxazole for empiric treatment of toxoplasmosis may lead to the underdiagnosis of cerebral nocardiosis in AIDS patients.[20]

Surgical treatment is often required. Mamelak and colleagues[20] assert that all abscesses greater than 2.5 cm in diameter should be aspirated, but that immunocompetent patients with documented extraneural Nocardia and small abscesses (< 2 cm) could be treated with antibiotics alone. If the abscess enlarges after 2 weeks of antibiotic treatment or fails to shrink after 4 weeks of treatment, craniotomy is needed for enucleation of the abscess. Based on 11 cases treated between 1971 and 1993 and a review of 120 cases reported since 1950, these investigators found that total excision was usually required.[20]

Lee and associates[21] reported a series of 11 patients between 1970 and 2001. They recommended that surgical aspiration be considered a suitable initial diagnostic treatment option, with aggressive surgical management reserved for the small proportion of patients who do not respond to the minimally invasive surgery.[21]

Thus, general recommendations suggest early biopsy for diagnosis followed by a trial of medical treatment. Low threshold for stereotactic aspiration or enucleation of the lesions is indicated if they are easily accessible.[20,21,26]

Nocardia and PAP

In the patient described in this case report, the risk factor for developing nocardiosis was PAP. This condition was first described by Rosen and colleagues[27] in 1958. PAP is characterized by intra-alveolar accumulation of lipid and proteinaceous PAS+ material and is clinically associated with increased work of breathing and derangement of gas exchange. It exists both as a primary and secondary condition (ie, in the setting of infection, malignancy, or inhalation). By 1998, an estimate of 332 patients with PAP had been described in the medical literature.[25] There is a strong male predominance (2:1-4:1), and the peak age of diagnosis is 20-50 years. Heavy smoking appears to be a risk factor.

The condition is caused by abnormal clearance of surfactant forming in the alveolar spaces and associated with macrophage dysfunction. The diagnosis is made by chest CT, pulmonary function tests, bronchoalveolar lavage, and biopsy. Treatment is with periodic whole lung lavage and administration of granulocyte-macrophage colony-stimulating factor (GM-CSF). Infectious complications associated with this disease are nocardiosis, Pneumocystis carinii pneumonia, and Mycobacterium avium-intracellulare. Recent data suggest a mortality between 0% and 8%.[25]

Patient Follow-up

We treated this patient with trimethoprim-sulfamethoxazole for 4 weeks. A follow-up MRI showed reductions in the size of the lesions and the surrounding edema. The patient's symptoms improved, and she was able to walk with assistance by the time of discharge. Of note, a comparison of the DWI images before treatment (Figure 6A,B) with after treatment (Figure 6C) showed that the initial restricted diffusion had resolved.

Figure 6.

Figure 6

Figure 6

Figure 6

Open in a new tab

(A,B) DWI before and (C) after treatment with trimethoprim-sulfamethoxazole.

Contributor Information

Irene Cortese, Clinical Neurophysiology, The Johns Hopkins University, Baltimore, Maryland.

Avindra Nath, Department of Neurology, The Johns Hopkins University, Baltimore, Maryland.

References

  • 1.Sabuncuoglu H, Cibali Acikgo ZZ, Caydere M, Ustun H, Semih Keskil I. Nocardia farcinica brain abscess: a case report and review of the literature. Neurocirugia. 2004;15:600–603. doi: 10.1016/s1130-1473(04)70453-4. [DOI] [PubMed] [Google Scholar]
  • 2.Masdeu JC, Quinto C, Olivera C, et al. Open-ring sign: highly specific for atypical brain demyelination. Neurology. 2000;54:1427–1433. doi: 10.1212/wnl.54.7.1427. [DOI] [PubMed] [Google Scholar]
  • 3.Floeth FW, Pauleit D, Wittsack HJ, et al. Multimodal metabolic imaging of cerebral gliomas: positron emission tomography with [18F]fluoroethyl-L-tyrosine and magnetic resonance spectroscopy. J Neurosurg. 2005;102:318–327. doi: 10.3171/jns.2005.102.2.0318. [DOI] [PubMed] [Google Scholar]
  • 4.Pauleit D, Floeth F, Hamacher K, et al. O-92-[18F]fuoroethyl0-L-tyrosine PET combined with MRI improves the diagnostic assessment of cerebral gliomas. Brain. 2005;128(pt3):678–687. doi: 10.1093/brain/awh399. [DOI] [PubMed] [Google Scholar]
  • 5.Ruiz A, Ganz WI, Post MJ, et al. Use of thallium-201 brain SPECT to differentiate cerebral lymphoma from toxoplasma encephalitis in AIDS patients. AJNR Am J Neuroradiol. 1996;15:1885–1894. [PMC free article] [PubMed] [Google Scholar]
  • 6.Licho R, Litofsky NS, Senitko M, George M. Inaccuracy of Tl-201 brain SPECT in distinguishing cerebral infections from lymphoma in patients with AIDS. Clin Nucl Med. 2002;27:81–86. doi: 10.1097/00003072-200202000-00001. [DOI] [PubMed] [Google Scholar]
  • 7.Skiest DJ, Erdman W, Chang WE, et al. SPECT thallium-201 combined with Toxoplasma serology for the presumptive diagnosis of focal central nervous system mass lesions in patients with AIDS. J Infect. 2000;40:274–281. doi: 10.1053/jinf.2000.0664. [DOI] [PubMed] [Google Scholar]
  • 8.Antinori A, De Rossi G, Ammassari A, et al. Value of combined approach with thallium-201 single-photon emission computed tomography and Epstein-Barr virus DNA polymerase chain reaction in CSF for the diagnosis of AIDS-related primary CNS lymphoma. J Clin Oncol. 1999;17:554–560. doi: 10.1200/JCO.1999.17.2.554. [DOI] [PubMed] [Google Scholar]
  • 9.Giancola ML, Rizzi EB, Schiavo R, et al. Reduced value of thallium-201 single-photon emission computed tomography in the management of HIV-related focal brain lesions in the era of highly active antiretroviral therapy. AIDS Res Hum Retroviruses. 2004;20:584–588. doi: 10.1089/0889222041217446. [DOI] [PubMed] [Google Scholar]
  • 10.Law M, Hamburger M, Johnson G, et al. Differentiating surgical from non-surgical lesions using perfusion MR imaging and proton MR spectroscopic imaging. Technol Cancer Res Treat. 2004;3:557–565. doi: 10.1177/153303460400300605. [DOI] [PubMed] [Google Scholar]
  • 11.Mishra AM, Gupta RK, Jaggi RS, et al. Role of diffusion-weighted imaging and in vivo magnetic resonance spectroscopy in the differential diagnosis of ring-enhancing intracranial cystic mass lesions. J Comput Assist Tomogr. 2004;28:540–547. doi: 10.1097/00004728-200407000-00017. [DOI] [PubMed] [Google Scholar]
  • 12.Grand S, Passaro G, Ziegler A, et al. Necrotic tumor versus brain abscess: importance of amino acids detected at 1H MR spectroscopy – initial results. Neuroradiology. 1999;213:785–793. doi: 10.1148/radiology.213.3.r99dc10785. [DOI] [PubMed] [Google Scholar]
  • 13.Nath A, Crain B, Hammond D, Pomper Ml. Brain abscess. In: Joynt, Griggs, editors. Baker's Clinical Neurology. Philadelphia, Pa: Lippincott Williams & Wilkins; In press. [Google Scholar]
  • 14.Leuthardt EC, Wippold FJ, II, Oswood MC, Rich KM. Diffusion-weighted MR imaging in the preoperative assessment of brain abscesses. Surg Neurol. 2002;58:395–402. doi: 10.1016/s0090-3019(02)00929-1. [DOI] [PubMed] [Google Scholar]
  • 15.Hartmann M, Jansen O, Heiland S, et al. Restricted diffusion within ring enhancement is not pathognomonic for brain abscess. AJNR Am J Neuroradiol. 2001;22:1738–1742. [PMC free article] [PubMed] [Google Scholar]
  • 16.Ernst TM, Chang L, Witt MD, et al. Cerebral toxoplasmosis and lymphoma in AIDS: perfusion MR imaging experience in 13 patients. Radiology. 1998;208:663–669. doi: 10.1148/radiology.208.3.9722843. [DOI] [PubMed] [Google Scholar]
  • 17.Law M, Hamburger M, Johnson G, et al. Differentiating surgical from non-surgical lesions using perfusion MR imaging and proton MR spectroscopic imaging. Technol Cancer Res Treat. 2004;3:557–565. doi: 10.1177/153303460400300605. [DOI] [PubMed] [Google Scholar]
  • 18.Chan JH, Tsui EY, Chau LF, et al. Discrimination of an infected brain tumor from a cerebral abscess by combined MR perfusion and diffusion imaging. Comput Med Imaging Graph. 2002;26:19–23. doi: 10.1016/s0895-6111(01)00023-4. [DOI] [PubMed] [Google Scholar]
  • 19.AAN Practice Guidelines. Evaluation and management of intracranial mass lesions in AIDS. Report of the Quality Standards Subcommittee of the American Academy of Neurology. January 1998. Available at: http://aan.com/professionals/practice/guideline/index.cfm?fuseaction=home.welcome&Topics=21&Submit=Search Accessed July 14, 2005.
  • 20.Mamelak AN, Obana WG, Flaherty JF, Rosenblum ML. Nocardial brain abscess: treatment strategies and factors influencing outcome. Neurosurgery. 1994;35:622–631. doi: 10.1227/00006123-199410000-00007. [DOI] [PubMed] [Google Scholar]
  • 21.Lee GY, Daniel RT, Brophy BP, Reilly PL. Surgical treatment nocardial brain abscesses. Neurosurgery. 2002;51:668–671. [PubMed] [Google Scholar]
  • 22.Johann-Liang R. Nocardiosis. Updated July 1, 2003. Emedicine. Available at: http://www.emedicine.com/ped/topic1610.htm Accessed June 28, 2005.
  • 23.Malincarne L, Marroni M, Farina C, et al. Primary brain abscess with Nocardia farcinica in an immunocompetent patient. Clin Neurol Neurosurg. 2002;104:132–135. doi: 10.1016/s0303-8467(01)00201-3. [DOI] [PubMed] [Google Scholar]
  • 24.Loeffler JM, Bodmer T, Zimmerli W, Leib SL. Nocardial brain abscess: observation of treatment strategies and outcome in Switzerland from 1992 to 1999. Infection. 2001;29:337–341. doi: 10.1007/s15010-001-1147-1. [DOI] [PubMed] [Google Scholar]
  • 25.Trapnell BC, Whitsett JA, Nakata K. Pulmonary alveolar proteinosis. N Engl J Med. 2003;349:2527–2539. doi: 10.1056/NEJMra023226. [DOI] [PubMed] [Google Scholar]
  • 26.Valarezo J, Cohen JE, Valarezo L, et al. Nocardial cerebral abscess: report of three cases and review of the current neurosurgical management. Neurol Res. 2003;25:27–30. doi: 10.1179/016164103101201076. [DOI] [PubMed] [Google Scholar]
  • 27.Rosen SH, Castleman B, Liebow AA. Pulmonary alveolar proteinosis. N Engl J Med. 1958;258:1123–1142. doi: 10.1056/NEJM195806052582301. [DOI] [PubMed] [Google Scholar]

Articles from Medscape General Medicine are provided here courtesy of WebMD/Medscape Health Network

RESOURCES