Abstract:Primary Epstein-Barr virus (EBV) infection is the main cause of infectious mononucleosis (IM), which typically presents with a triad of fever, lymphadenopathy, and tonsillar pharyngitis in young adults. In contrast, neurological manifestations of IM are rare. We report on a 23-year-old man with subacute oculomotor nerve palsy followed by symptoms of IM 6 days later. Primary EBV infection was confirmed by PCR detection of EBV DNA in blood as well as by subsequent serology. High-resolution magnetic resonance ima… Show more
“…9 ), while Ramsay Hunt syndrome is caused by VZV reactivation [ 37 ]. A slightly different mechanism, probably related to a para-infectious condition rather than a direct viral infection, characterized EBV CN changes that may affect the CN III nerve with the peculiar "shooting star" sign due to the involvement of its root exit zone with adjacent pial enhancement and associated edematous changes in the ventral mesencephalon [ 41 ]. Fig.…”
Section: Pathogenesis: Why Can Cranial Nerve Enhancement Occur?mentioning
Cranial nerve enhancement is a common and challenging MRI finding that requires a meticulous and systematic evaluation to identify the correct diagnosis. Literature mainly describes the various pathologies with the associated clinic-radiological characteristics, while the radiologist often needs a reverse approach that starts from the radiological findings to reach the diagnosis. Therefore, our aim is to provide a new and practical pattern-based approach to cranial nerve enhancement, which starts from the radiological findings and follows pattern-driven pipelines to navigate through multiple differential diagnoses, guiding the radiologist to reach the proper diagnosis. Firstly, we reviewed the literature and identified four patterns to categorize the main pathologies presenting with cranial nerve enhancement: unilateral linear pattern, bilateral linear pattern, unilateral thickened pattern, and bilateral thickened pattern. For each pattern, we describe the underlying pathogenic origin, and the main radiological features are displayed through high-quality MRI images and illustrative panels. A suggested MRI protocol for studying cranial nerve enhancement is also provided. In conclusion, our approach for cranial nerve enhancement aims to be an easy tool immediately applicable to clinical practice for converting challenging findings into specific pathological patterns.
“…9 ), while Ramsay Hunt syndrome is caused by VZV reactivation [ 37 ]. A slightly different mechanism, probably related to a para-infectious condition rather than a direct viral infection, characterized EBV CN changes that may affect the CN III nerve with the peculiar "shooting star" sign due to the involvement of its root exit zone with adjacent pial enhancement and associated edematous changes in the ventral mesencephalon [ 41 ]. Fig.…”
Section: Pathogenesis: Why Can Cranial Nerve Enhancement Occur?mentioning
Cranial nerve enhancement is a common and challenging MRI finding that requires a meticulous and systematic evaluation to identify the correct diagnosis. Literature mainly describes the various pathologies with the associated clinic-radiological characteristics, while the radiologist often needs a reverse approach that starts from the radiological findings to reach the diagnosis. Therefore, our aim is to provide a new and practical pattern-based approach to cranial nerve enhancement, which starts from the radiological findings and follows pattern-driven pipelines to navigate through multiple differential diagnoses, guiding the radiologist to reach the proper diagnosis. Firstly, we reviewed the literature and identified four patterns to categorize the main pathologies presenting with cranial nerve enhancement: unilateral linear pattern, bilateral linear pattern, unilateral thickened pattern, and bilateral thickened pattern. For each pattern, we describe the underlying pathogenic origin, and the main radiological features are displayed through high-quality MRI images and illustrative panels. A suggested MRI protocol for studying cranial nerve enhancement is also provided. In conclusion, our approach for cranial nerve enhancement aims to be an easy tool immediately applicable to clinical practice for converting challenging findings into specific pathological patterns.
“…35 Occasionally, oculomotor nerve palsy may manifest as the presenting symptom of primary EBV infection, with imaging demonstrating focal edema and enhancement at the root exit zone of the affected nerve (shooting star sign). 36 Spinal Cord Involvement ATM is generally idiopathic or postinfectious immune-mediated demyelination, with EBV being a rare culprit. 4,37,38 EBV myelitis is characterized by T2 hyperintensity in the spinal cord that extends over $2 segments covering equal or more than two-thirds of the cord, with the thoracic cord being the most affected (Figs 2 and 3).…”
Epstein-Barr virus is a ubiquitous herpesvirus that may cause both infective (encephalitis, meningitis, and so forth) and postinfection inflammatory (such as Guillain-Barré syndrome, acute disseminated encephalomyelitis) manifestations in the CNS. Diagnosis of Epstein-Barr virus-related CNS pathologies is often complicated due to a nonspecific clinical presentation and overlap with other infectious and noninfectious causes, both clinically and on imaging. The Epstein-Barr virus is also implicated in several lymphoproliferative disorders in both immunocompromised and immunocompetent hosts. MR imaging is preferred for evaluating the extent of involvement and monitoring therapy response, given its high sensitivity and specificity, though imaging findings may be nonspecific. Herein, we review the imaging spectrum of Epstein-Barr virus-associated CNS disorders.ABBREVIATIONS: ADEM ¼ acute disseminated encephalomyelitis; ATM ¼ acute transverse myelitis; EBV ¼ Epstein-Barr virus; EBNA ¼ Epstein-Barr nuclear antigen; Ig ¼ immunoglobulin; LG ¼ lymphomatoid granulomatosis; LPD ¼ lymphoproliferative disorder; MOG ¼ myelin oligodendrocyte glycoprotein; PCNSL ¼ primary CNS lymphoma; PCR ¼ polymerase chain reaction; PTLD ¼ posttransplant lymphoproliferative disorder; SMT ¼ smooth-muscle tumor
Background:
Infectious mononucleosis is common among adolescents and young adults.
Although the majority of cases resolve spontaneously, life-threatening manifestations, and complications have been recognised.
Objective:
The purpose of this article is to familiarize clinicians with the clinical manifestations,
evaluation, diagnosis, and management of infectious mononucleosis.
Methods:
A search was conducted in October 2022 in PubMed Clinical Queries using the key terms
"infectious mononucleosis" OR “Epstein-Barr virus” OR “EBV”. The search strategy included all
clinical trials, observational studies, and reviews published within the past 10 years. Only papers
published in the English literature were included in this review. The information retrieved from the
aforementioned search was used in the compilation of the present article.
Results:
Infectious mononucleosis, caused by Epstein-Barr virus, most commonly affects adolescents and adults aged 15 to 24 years. Epstein-Barr virus is transmitted primarily in saliva. Infectious
mononucleosis is characterized by a triad of fever, tonsillar pharyngitis, and lymphadenopathy. Fatigue may be profound but tends to resolve within three months. Periorbital and/or palpebral edema,
typically bilateral, occurs in one-third of patients. Splenomegaly and hepatomegaly occur in approximately 50% and 10% of cases, respectively. A skin rash, which is usually widely scattered, erythematous, and maculopapular, occurs in approximately 10 to 45% of cases. Peripheral blood leukocytosis is observed in most patients; lymphocytes make up at least 50% of the white blood cell
differential count. Atypical lymphocytes constitute more than 10% of the total lymphocyte count.
The classic test for infectious mononucleosis is the demonstration of heterophile antibodies. The
monospot test is the most widely used method to detect the serum heterophile antibodies of infectious mononucleosis. When confirmation of the diagnosis of infectious mononucleosis is required in
patients with mononucleosis-like illness and a negative mono-spot test, serologic testing for antibodies to viral capsid antigens is recommended. Infectious mononucleosis is a risk factor for chronic fatigue syndrome. Spontaneous splenic rupture occurs in 0.1 to 0.5% of patients with infectious
mononucleosis and is potentially life-threatening. Treatment is mainly supportive. Reduction of activity and bed rest as tolerated are recommended. Patients should be advised to avoid contact sports
or strenuous exercise for 8 weeks or while splenomegaly is still present. Most patients have an uneventful recovery.
Conclusion:
Infectious mononucleosis is generally a benign and self-limited disease. Prompt diagnosis is essential to avoid unnecessary investigations and treatments and to minimize complications.
Splenic rupture is the most feared complication. As avoiding exposure to EBV is almost impossible,
the most effective way to prevent EBV infection and infectious mononucleosis is the development
of an effective, safe, and affordable EBV vaccine that can confer life-long immunity.
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