The main route of entry of aspergillosis is airborn, the bronchopulmonary system is the first and most often involved, in healthy individuals. Inhaled spores are rejected by the mucociliary barrier or destroyed by alveolar macrophages. In the presence of a risk factor such as lack of efficient elimination, spores develop as mycelium [1].

In this case, the patient is not immunocompromised. He does not present any risk factor for invasive cerebral aspergillosis and a starting point of hematogenous dissemination is found. In fact, it was a case of pulmonary aspergillosis complicated by invasive cerebral aspergillosis in an immunocompetent subject. Cerebral aspergillosis is a rare condition, classically affecting immunocompromised patients, especially after bone marrow transplantation. Aspergillus spores usually enter the body by inhalation and colonize the lungs or facial sinuses, which may secondarily spread to other organs by hematogenous dissemination. The brain is a common site of dissemination, with an incidence of 10 to 40% of involvement during invasive aspergillosis [3]. The prognosis is very poor, with an estimated mortality rate of 85-100% in immunocompromised patients.

Unlike other microorganisms disseminated by the hematogenous route, aspergillary filaments are angioinvasive [12], which makes them responsible for specific cerebral lesions: aspergillary filaments infiltrate and destroy the wall of the large cerebral arteries, blocking the origin of the small perforating arteries, and causing areas of initially sterile infarction. In a second phase, aspergillary elements invade the infarcted area, which progresses to septic necrosis. The infarcted lesions may present a hemorrhagic component, which may orient the diagnosis. However, this aspect is described in only 25% of aspergillosis lesions [4]. One of the important signs classically described on imaging is the absence of enhancement of the lesions, due to the absence of an inflammatory reaction in immunocompromised patients or those undergoing corticosteroid therapy. However, peripheral contrast, corresponding to the formation of a capsule, may be present in 13 to 50% of cases [5], most often in the most immunocompetent patients and on the largest lesions. In our case, the patient's lesions show discrete peripheral enhancement, in a ring, despite the absence of major immunosuppression. The absence or presence of contrast enhancement is therefore not always a determining criterion for a positive diagnosis [6].

Diffusion imaging has rarely been described in the literature [7]. Most of the cases described concern lesions enhanced by contrast medium, showing a global decrease in water diffusion [8]. In our case, the two lesions do not present a homogeneous hypersignal on the diffusion sequences, in fact the diffusion hypersignal corresponds to infarcted parenchyma, as described by Miaux et al on the pathological analysis of autopsy specimens [9]. The main differential diagnoses are Toxoplasmosis, Cryptococcosis, Candidiasis and malignant lesions especially lymphoma [10] which have caracteristic morphological aspects that can be orientating, especially in diffusion sequence, bringing a precious help for the positive diagnosis of aspergillosis (global restriction of water diffusion or heterogeneous appearance in "target" [11]).