A Diagnostic Challenge of Ring-Enhancing Intracranial Lesions: A Case Report
Poster #: 052
Session/Time: A
Author:
Katherine Mary Horenstein, BS
Mentor:
James Wyant, MD
Research Type: Case Report
Abstract
INTRODUCTION:
Ring-enhancing lesions are a common neuroimaging abnormality with diverse etiologies including infection, malignancy, inflammation and vascular disease. Identification of the underlying cause is crucial as misdiagnosis can lead to worse outcomes. However, diagnosis is often challenging due to overlapping clinical presentations and imaging features. We present a patient with two intracranial ring-enhancing lesions and a cavitary pulmonary lesion.
CASE INFORMATION:
Our patient is a 65-year-old male with multiple chronic conditions whose clinical course began with identification of a cavitary lung lesion after a new onset productive cough. A biopsy was positive for Streptococcus intermedius, and he was treated outpatient for pneumonia. Months later, his symptoms persisted, and he developed worsening headaches prompting him to present to the hospital. Brain magnetic resonance imaging (MRI) revealed ring-enhancing lesions leading to admission. Physical exam was remarkable only for dental caries. Routine and fungal cultures/smears of serum, sputum and urine were negative. Cerebrospinal fluid (CSF) cytology showed elevated WBC, RBC, and protein, and normal glucose. Laboratory analysis was also unremarkable for opportunistic fungi (e.g., Cryptococcus, Coccidioides, Aspergillus, Blastomyces, Histoplasma), Strongyloides, Toxoplasma, Mycobacterium, syphilis, Human Immunodeficiency Virus, and Hepatitis. Immunoglobulin studies were significant for: IgA 195, IgG 497, IgM <25, IgE 1293. On hospital day 8, lumbar puncture was repeated for routine CSF serology (e.g., bacterial, fungal, mycobacterial) which was negative. The patient clinically worsened on day 15, with new fevers, chills, and encephalopathy. Brain MRI revealed interval ependymitis. Subsequently, brain biopsy was performed. Purulent intra-lesional material was aspirated and sent for basic serology which was unremarkable. On post-operative day 7 the patient had new onset confusion, agitation, and visual hallucinations. Repeat brain MRI showed new vasogenic edema. Standard serologic analysis was obtained with the addition of meningitis/encephalitis panel and serum bartonella panel. All were negative. On post-operative day 18 the patient was prepared for discharge to a skilled nursing facility for continued antibiotic treatment.
DISCUSSION:
Intracranial ring-enhancing lesions carry a broad differential, creating complex clinical scenarios. While intra-lesional diffusion restriction and smooth, evenly enhancing walls may suggest an abscess compared to other etiologies, these findings are not pathognomonic, and imaging cannot determine the causative organism. Ultimately, up to 25% of brain abscesses remain cryptogenic. This case presents unique complexity in the setting of a pulmonary lesion as a possible infectious source as S. intermediately, which is a recognized cause of brain abscess. Similarly, an odontogenic process also provided a possible unifying etiology. However, only the pulmonary lesion was responsive to antibiotic therapy. Additionally, the clinical picture was complicated by intermittent steroid exposure prior to this admission and an abnormal immunoglobulin profile, suggesting immune dysfunction. This highlights how individual factors can significantly complicate diagnostic reasoning for ring-enhancing lesions.
CONCLUSION:
We present an ambiguous ring-enhancing process with discordant extracranial-intracranial response and unclear etiology despite extensive laboratory testing, exposing limitations of current diagnostic approaches. This case may demonstrate a need for early escalation of care and caution against therapeutic inertia. We believe this case brings nuances to the management and diagnosis of ring-enhancing lesions.
Ring-enhancing lesions are a common neuroimaging abnormality with diverse etiologies including infection, malignancy, inflammation and vascular disease. Identification of the underlying cause is crucial as misdiagnosis can lead to worse outcomes. However, diagnosis is often challenging due to overlapping clinical presentations and imaging features. We present a patient with two intracranial ring-enhancing lesions and a cavitary pulmonary lesion.
CASE INFORMATION:
Our patient is a 65-year-old male with multiple chronic conditions whose clinical course began with identification of a cavitary lung lesion after a new onset productive cough. A biopsy was positive for Streptococcus intermedius, and he was treated outpatient for pneumonia. Months later, his symptoms persisted, and he developed worsening headaches prompting him to present to the hospital. Brain magnetic resonance imaging (MRI) revealed ring-enhancing lesions leading to admission. Physical exam was remarkable only for dental caries. Routine and fungal cultures/smears of serum, sputum and urine were negative. Cerebrospinal fluid (CSF) cytology showed elevated WBC, RBC, and protein, and normal glucose. Laboratory analysis was also unremarkable for opportunistic fungi (e.g., Cryptococcus, Coccidioides, Aspergillus, Blastomyces, Histoplasma), Strongyloides, Toxoplasma, Mycobacterium, syphilis, Human Immunodeficiency Virus, and Hepatitis. Immunoglobulin studies were significant for: IgA 195, IgG 497, IgM <25, IgE 1293. On hospital day 8, lumbar puncture was repeated for routine CSF serology (e.g., bacterial, fungal, mycobacterial) which was negative. The patient clinically worsened on day 15, with new fevers, chills, and encephalopathy. Brain MRI revealed interval ependymitis. Subsequently, brain biopsy was performed. Purulent intra-lesional material was aspirated and sent for basic serology which was unremarkable. On post-operative day 7 the patient had new onset confusion, agitation, and visual hallucinations. Repeat brain MRI showed new vasogenic edema. Standard serologic analysis was obtained with the addition of meningitis/encephalitis panel and serum bartonella panel. All were negative. On post-operative day 18 the patient was prepared for discharge to a skilled nursing facility for continued antibiotic treatment.
DISCUSSION:
Intracranial ring-enhancing lesions carry a broad differential, creating complex clinical scenarios. While intra-lesional diffusion restriction and smooth, evenly enhancing walls may suggest an abscess compared to other etiologies, these findings are not pathognomonic, and imaging cannot determine the causative organism. Ultimately, up to 25% of brain abscesses remain cryptogenic. This case presents unique complexity in the setting of a pulmonary lesion as a possible infectious source as S. intermediately, which is a recognized cause of brain abscess. Similarly, an odontogenic process also provided a possible unifying etiology. However, only the pulmonary lesion was responsive to antibiotic therapy. Additionally, the clinical picture was complicated by intermittent steroid exposure prior to this admission and an abnormal immunoglobulin profile, suggesting immune dysfunction. This highlights how individual factors can significantly complicate diagnostic reasoning for ring-enhancing lesions.
CONCLUSION:
We present an ambiguous ring-enhancing process with discordant extracranial-intracranial response and unclear etiology despite extensive laboratory testing, exposing limitations of current diagnostic approaches. This case may demonstrate a need for early escalation of care and caution against therapeutic inertia. We believe this case brings nuances to the management and diagnosis of ring-enhancing lesions.