Primary central nervous system lymphoma: Imaging features and differential diagnosis.

Primary central nervous system lymphoma (PCNSL) represents 5% of malignant primary brain tumors. The clinical presentation typically includes focal neurological symptoms, increased intracranial pressure, seizures, and psychiatric symptoms. Although histological examination remains the gold standard for diagnostic confirmation, non-invasive imaging plays a crucial role for the diagnosis. In immunocompetent individuals, PCNSL usually appears as a single, well-defined, supratentorial lesion with a predilection for periventricular areas, iso- or hypointense on T1- and T2-weighted magnetic resonance imaging, with restricted diffusion, slightly increased perfusion, and homogenous gadolinium-enhancement. Differential diagnoses include high-grade glioma and pseudotumoral demyelinating disease. In immunocompromised patients, PCNSL may present as multiple lesions, with a higher likelihood of hemorrhage and necrosis and less restricted diffusion than immunocompetent individuals. Differential diagnoses include neurotoxoplasmosis, progressive multifocal leukoencephalopathy, and cerebral abscess. Atypical forms of lymphoma are characterized by extra-axial lymphoma, lymphomatosis cerebri, and intravascular lymphoma. Extra-axial lymphoma presents as single or multiple extra-axial dural lesions with diffuse leptomeningeal contrast-enhancement. Lymphomatosis cerebri appears as an infiltrative and symmetric lesion, primarily affecting deep white matter and basal ganglia, appearing hyperintense on T2-weighted imaging, without significant contrast-enhancement or perfusion changes. Intravascular lymphoma presents as multiple rounded or oval-shaped "infarct-like" lesions, located cortically or subcortically. This study aims to highlight the imaging characteristics of PCNSL, focusing on magnetic resonance imaging and its differential diagnosis.

Insights into Magnetic Resonance Imaging Findings in Central Nervous System Paracoccidioidomycosis: A Comprehensive Review.

Paracoccidioidomycosis (PCM) is a infection caused by the thermodimorphic fungus Paracoccidioides spp. (P. lutzii and, mainly, P. brasiliensis). This infection predominantly affects rural male workers aged between 30 and 50 years old who deal with soil on daily activities. Clinically, the disease is classified as acute/subacute phase, which evolves rapidly, secondary to dissemination of the fungus through to the phagocytic-mononuclear system, leading to fever, weight loss, and anorexia, associated with hepatosplenomegaly and lymphadenopathy, which can be complicated with suppuration and fistulization; and chronic phase, which corresponds to 74% to 95% of symptomatic cases, with a common pulmonary involvement. Central nervous system involvement is almost always a characteristic of the chronic form. Inhalation is the most common route of primary infection, usually affecting the lungs, forming the primary complex. From the primary complex, hematogenic dissemination can occur to any organ, including the brain and spinal cord. Although PCM of the central nervous system diagnosis is usually based on histopathological analysis and the imaging features are not specific for PCM, computed tomography and magnetic resonance imaging can demonstrate evidences of granuloma, abscess, meningitis, or a combination of these lesions, contributing to a preoperative diagnosis, especially when considered in conjunction with epidemiology. In this article, we review the pathophysiology, clinical manifestations and imaging aspects of neuro-PCM.

Imaging features of neurosyphilis.

Syphilis is an infectious disease caused by the spirochete Treponema pallidum, subspecies pallidum. Although its incidence has declined after the widespread availability of penicillin, it has recently re-emerged, especially in men who have sex with men and in people living with human immunodeficiency virus (HIV). The neurological manifestations of syphilis, generally known as neurosyphilis, may appear at any time during the infection, including the initial years after the primary infection. Neurosyphilis can be asymptomatic, only with cerebrospinal fluid abnormalities, or symptomatic, characterized by several different clinical syndromes, such as meningitis, gumma, meningovascular, brain parenchyma involvement, meningomyelitis, tabes dorsalis, and peripheral nervous system involvement. However, these syndromes may simulate several other diseases, making the diagnosis often a challenge. In addition, syphilis can also be vertically transmitted from mother to child during pregnancy, leading to neurological manifestations. Neuroimaging is essential to demonstrate abnormal brain or spinal cord findings in patients with neurosyphilis, aiding in the diagnosis, treatment, and follow-up of these patients. This article aims to review the imaging features of neurosyphilis, including the early and late stages of the infection.

The role of neuroimaging in the determination of brain death.

Brain death is the irreversible cessation of all brain function. Although protocols for its determination vary among countries, the concept of brain death is widely accepted, despite ethical and religious issues. The pathophysiology of brain death is related to hypoxia and ischemia in the setting of extensive brain injury. It is also related to the effects of brain edema, which increases intracranial pressure, leading to cerebral circulatory arrest. Although the diagnosis of brain death is based on clinical parameters, the use of neuroimaging to demonstrate diffuse brain injury as the cause of coma prior to definitive clinical examination is a prerequisite. Brain computed tomography (CT) and magnetic resonance imaging (MRI) demonstrate diffuse edema, as well as ventricular and sulcal effacement, together with brain herniation. Angiography (by CT or MRI) demonstrates the absence of intracranial arterial and venous flow. In some countries, electroencephalography, cerebral digital subtraction angiography, transcranial Doppler ultrasound, or scintigraphy/single-photon emission CT are currently used for the definitive diagnosis of brain death. Although the definition of brain death relies on clinical features, radiologists could play an important role in the early recognition of global hypoxic-ischemic injury and the absence of cerebral vascular perfusion.

A morte encefálica é a cessação irreversível de todas as funções cerebrais. Embora os protocolos para sua determinação variem entre os países, o conceito de morte encefálica é amplamente aceito, apesar de questões éticas e religiosas. A fisiopatologia da morte encefálica está relacionada a hipóxia e isquemia no cenário de uma lesão cerebral difusa. Também está relacionada aos efeitos do edema cerebral, que aumenta a pressão intracraniana, levando à parada da circulação cerebral. Embora o diagnóstico de morte encefálica seja baseado em parâmetros clínicos, o uso de neuroimagem para demonstrar lesão cerebral difusa como causa do coma antes do exame clínico definitivo é um pré-requisito. A tomografia computadorizada (TC) e a ressonância magnética (RM) de crânio demonstram edema difuso e apagamento de ventrículos e sulcos, associados a herniações transcompartimentais. A angio-TC e a angio-RM demonstram a ausência de fluxo arterial e venoso intracraniano. Em alguns países, a eletroencefalografia, a angiografia por subtração digital cerebral, a ultrassonografia transcraniana com Doppler ou a cintilografia/TC por emissão de fóton único são atualmente usadas para o diagnóstico definitivo de morte encefálica. Embora a definição de morte encefálica dependa de características clínicas, os radiologistas podem desempenhar papel importante no reconhecimento precoce da lesão hipóxico-isquêmica global e da ausência de perfusão vascular cerebral.