Intracranial infections: clinical and imaging characteristics

Abstract

The radiologist plays a crucial role in identifying and narrowing the differential diagnosis of intracranial infections. A thorough understanding of the intracranial compartment anatomy and characteristic imaging findings of specific pathogens, as well incorporation of the clinical information, is essential to establish correct diagnosis. Specific types of infections have certain propensities for different anatomical regions within the brain. In addition, the imaging findings must be placed in the context of the clinical setting, particularly in immunocompromised and human immunodeficiency virus (HIV)-positive patients. This paper describes and depicts infections within the different compartments of the brain. Pathology-proven infectious cases are presented in both immunocompetent and immunocompromised patients, with a discussion of the characteristic findings of each pathogen. Magnetic resonance spectroscopy (MRS) characteristics for several infections are also discussed.

CT and MRI Findings in Cerebral Aspergilloma

“…Typical image patterns have been described for various intracranial infections, which help to discriminate between the types of infection. Differential diagnoses for the cases examined in this study are bacterial abscesses, which are characterized by a typical general diffusion restriction, as well as tuberculomas or toxoplasmosis [14]. Cerebral blood volume maps obtained by CT and MR perfusion are useful to identify primary brain tumors or lymphomas.…”

Freiburg Neuropathology Case Conference

“…On MRI fluid attenuated inversion recovery (FLAIR) images may present high signals in the subarachnoid space. According to Foerster et al the most important role of neuroimaging is to identify potential complications such as infarction, hydrocephalus, ventriculitis, brain empyema and sinus thrombosis [5]. Figure 2: immunohistochemical staining of sections from the lesion.…”

Neuroimaging in Secondary Headache Disorders

“…This can result from hematogenous dissemination, or local extension from a sinus, odontogenic, or otic source [46]. Headache is present in 69 % of patients along with fever and focal neurological signs.…”

“…The first stage is early cerebritis (1-4 days) followed by late cerebritis at 4-10 days. Capsule formation is divided into early (11 to 14 days) and late (>14 days) stages [46].…”