L’imagerie dans la mucormycose rhinocérébrale

Mnif, N.; Hmaied, E.; Oueslati, S.; Rajhi, H.; Hamza, R.; Marrakchi, M.; Kaffel, N; Kooli, H.; Salah, Mohamed Ben; Ferjaoui, M.

doi:10.1016/s0221-0363(05)81485-4

Cited by 41 publications

(12 citation statements)

References 2 publications

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“…There are few cases of zygomycosis in the literature secondary to various type of cell-mediated immunodeficiency [3]. Cyst formation in zygomycosis is very rare and has been reported as orbital or brain abscess in the literature [4]. The role of T cells in mediating protection against abscess formation by some bacterial species has been described [5].…”

Section: Discussionmentioning

confidence: 99%

Rare Presentation of Rhino-Orbital-Cerebral Zygomycosis: Bilateral Facial Nerve Palsy

Mohebbi

Jahandideh

Harandi

2011

Case Reports in Medicine

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Rhino-orbital-cerebral zygomycosis afflicts primarily diabetics and immunocompromised individual, but can also occur in normal hosts rarely. We here presented an interesting case of facial nerve palsy and multiple cold abscesses of neck due to rhino-orbital-cerebral zygomycosis in an otherwise healthy man. Although some reports of facial nerve paralysis in conjunction with rhino-orbital-cerebral zygomycosis exist, no case of bilateral complete facial paralysis has been reported in the literature to date.

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Section: Discussionmentioning

confidence: 99%

Rare Presentation of Rhino-Orbital-Cerebral Zygomycosis: Bilateral Facial Nerve Palsy

Mohebbi

Jahandideh

Harandi

2011

Case Reports in Medicine

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“…Numerous agents have been reported (table 2) and include bacteria (Mycobacterium tuberculosis [101][102][103][104], Mycoplasma pneumoniae [105], Burkholderia pseudomallei [106], Fusobacterium necrophorum [107][108][109], and Salmonella paratyphi [110]), viruses (measles [111], varicella-zoster virus [112,113], hepatitis virus B and C [114][115][116], immunodeficiency virus [117][118][119], and cytomegalovirus [119]), spirochetae (Lepstospira interrogans [120], and Treponema pallidum [121]), parasitae (Plasmodium falciparum [122,123], and Trichinella spiralis [124,125]), and fungi (Rhizopus species [126][127][128], Aspergillus fumigatus [129][130][131][132][133][134], and Coccidioides immitis [135]). [16,76], endocarditis [76], typhoid [76], tuberculosis [101][102][103][104], Mycoplasma pneumoniae …”

Section: Infectionmentioning

confidence: 99%

Risk Factors of Cerebral Vein and Sinus Thrombosis

Freitas

Bogousslavsky

2007

Handbook on Cerebral Venous Thrombosis

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The risk factors for deep venous thrombosis (and for cerebral vein and sinus thrombosis, CVST) differ from those for arterial disease. The risk factors for venous thrombosis are linked to the Virchow triad of stasis of the blood, changes in the vessel wall, and changes in the composition of the blood, especially the first and third of these. Risk factors are usually divided into acquired (e.g. surgery, trauma, pregnancy, puerperium, lupus anticoagulant, malignant disease, and female hormones) and genetic (congenital thrombophilia). However, the separation of genetic and acquired risk factors is somewhat artificial, since they have additive effects and venous thrombosis is often multifactorial. In this review, we discuss acquired risk factors for CVST. These include hormonal changes (e.g. oral contraceptives use, hormone replacement therapy, pregnancy and puerperium), mechanical precipitants (e.g. head trauma, jugular catheterization, surgery, lumbar puncture), local and generalized infections, cancer, acquired prothrombotic states (e.g. hyperhomocysteinemia, nephrotic syndrome), inflammatory diseases (e.g. vaculitis, intestinal inflammatory disease), hematological disorders, neurological diseases (e.g. dural arteriovenous malformations, spontaneous intracranial hypotension), drugs and other situations. However, only some conditions are consistently present in case series, while many appear only in anecdotal reports. Thus, in most situations, a causal link cannot be established. Determining a cause-and-effect relationship is essential for developing preventive, diagnostic, and therapeutic strategies. Therefore, further multicentered, case-controlled studies are crucial for better understanding the pathogenesis of CVST.

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“…The physical examination may reveal hemiparesis or hemiplegia contralateral to the lesion with homolateral facial palsy, brachial monoplegia, auditory hallucinations, meningeal signs, or involvement of cranial pairs (VI, VII, VIII, IX, X, XI, XII). Other complications may be observed such as meningoencephalitis, brain abscess, thrombosis of the cavernous sinus or of the carotid, intracranial hypertension, or subdural or intracerebral hemorrhages [10,13,20,21]. In our patients, the cerebral involvement was peripheral for four patients, with involvement of cranial nerves, and central in three patients with consciousness disorders ( Table 1).…”

Section: Discussionmentioning

confidence: 67%

“…We observed radiological signs of sinus involvement in all patients, as well as radiological images of exophthalmia (patients 1 and 2) and images of cerebral extension such as thrombosis of the right lateral sinus (patient 4) or ventricular dilatation, or dilated cortical grooves (patient 3). The CT scan allows distinguishing between a tumor and local inflammation, and following the evolution under treatment [21]. Only two of our patients survived (patients 2 and 5) and underwent a control cerebral CT scan during and after the end of treatment for mucormycosis.…”

Section: Discussionmentioning

confidence: 99%