Cerebral Invasion Research Articles

HIV-associated Burkitt lymphoma with bone marrow and cerebral invasion in a patient with history of Plasmodium falciparum infection

HIV infected patients are more likely to develop non-Hodgkin lymphoma (NHL). Burkitt lymphoma (BL) is a highly aggressive NHL, associated with immunosuppression, especially with HIV. According to WHO classification there are three clinical types of BL: endemic, sporadic and immunosuppression-associated. Sporadic lymphoma was described especially in children (40% of child lymphomas in USA and EU). Two cofactors seem to be associated with BL: Ebstein Barr virus (EBV) and Plasmodium falciparum (PF) infection. PF and EBV are well-known co-factors in the pathogenesis of BL, but the mechanisms of interaction remain unclear. We present a 51 year-old male, who developed lymphadenopathy, prolonged fever, weight loss, splenomegaly and seizure. The patient was admitted to a Hematology University Hospital. After lymph node biopsy he was diagnosed with BL. A specimen of bone marrow from the right iliac crest showed gross invasion by Burkitt tumor cells. The patient tested positive for HIV and he was referred to the National Institute of Infectious Diseases “Prof. Dr. Matei Bals”, Bucharest. According to CDC Classification System for HIV Infection the patient had AIDS (C3 stage with a CD4 count of 39/cmm) and a high HIV viral load (500,262 copies/mL). The patient’s medical history revealed Plasmodium falciparum malaria 4 years ago, while he was living in South America. Epidemiological data revealed more than 200 sexual partners in the last two years. At admission to our hospital he had pancytopenia: white blood cells 1400/cmm, with 600 neutrophils and 600 lymphocytes, hemoglobin 9.6 g/dL and platelet count 25,000/cmm. The patient was tested for EBV infection and high titer of anti-VCA antibodies was found. ART was initiated with TDF-FTC-lopinavir/r with good virological outcome (after 6 weeks of therapy the viral load was 383 copies/mL). Cerebral MRI showed diffuse lymphomatous invasion. After 3 weeks of ART the patient was referred to Hematology Hospital where chemotherapy was started. Post-chemotherapy the pancytopenia was more severe: white blood cells – 200/cmm with CD4 count – 10/cmm, platelets – 15,000/cmm and hemoglobin – 7.9 g/dL. The BL response after chemotherapy was poor and the patient died two months after the diagnosis, despite the good virological outcome. We present a rare case of NHL in a HIV-infected patient, with multiple co-factors for BL: HIV infection, EBV infection and Plasmodium falciparum infection. The prognostic in AIDS depends on the comorbidities’ outcome.

Rhino-orbito-cerebral mucormycosis in a child with diabetic ketoacidosis.

Sir, We read the article “Rhino-orbito-cerebral mucormycosis in a child with diabetic ketoacidosis (DKA)” by Kumar et al.[1] with interest. The author reported a 9-year-old girl with DKA and rhino-orbito-cerebral mucormycosis. We want to highlight certain issues regarding diagnosis and management of this child. The child was diagnosed with rhino-orbital-cerebral mucormycosis after 48 h of admission. Her initial computed tomography (CT) brain was found to be normal. It is not clear whether the CT brain was plain or contrast enhanced. We can understand due to sickness of the child, CT may have been preferred over magnetic resonance imaging (MRI). However in a clinical scenario where cerebral invasion is suspected along with rhinosinusitis, MRI is preferred over CT scan. Contrast enhanced T1-weighed images are helpful in delineating intracranial spread and identifying invasion of cavernous portion of internal carotid artery.[2,3] The sensitivity of initial CT and MRI in detecting sinusitis is 97% and 100% respectively. However, initial MRI is more sensitive in detecting disease beyond sinuses like extension to orbits, cranium.[4] Since, she developed ophthalmoplegia at 72 h of admission, cavernous sinus thrombosis should be strongly suspected. Involvement of brain stem could not be ruled out as she had right facial palsy with left hemiparesis. Authors have mentioned amphotericin B as the treatment of choice in mucormycosis, but the current literature suggests that combination antifungal therapy is better than monotherapy in mucormycosis. Reed et al. concluded from a retrospective study that combination of caspofungin-polyene therapy is superior to polyene monotherapy.[4] Addition of echinocandins to polyenes increases the efficiency of polyenes by following mechanisms: Disruption of β glucan linking on the cell wall of Rhizopus resulting in better delivery of polyenes Altered virulence of fungus by stunting filamentation or altering cell wall contents Enhanced host response to the fungus. The authors have reported mortality of 40% and 10% in mucormycosis with and without cerebral involvement. However, a systematic review showed that children with cerebral, gastrointestinal, disseminated, and cutaneous mucormycosis had mortality of 100%, 100%, 88%, and 0% respectively.[5]

Atypical Sino-Orbital Inflammatory Myofibroblastic Tumor with Bone and Cerebral Invasion Extending to the Orbit

To report the case of an atypical sino-orbital inflammatory myofibroblastic tumor. Case report. A 71-year-old man presented slowly progressive painless diplopia followed by unilateral proptosis of the left eye with slight edema of the upper eyelid. Visual acuity was 0.4 with a relative afferent pupillary defect (RAPD). Abduction and depression of the left eye were limited. Imaging showed a left sino-orbital tumor with mass effect on the medial rectus muscle resulting in proptosis. The lesion showed intracranial extension through the superior orbital fissure with bone erosion and sclerotic bone reaction. Endoscopic ethmoidal, maxillary, and orbital biopsies revealed an inflammatory myofibroblastic tumor. Full blood count showed an eosinophilia while antineutrophil cytoplasmic antibodies and C-reactive protein were negative. To date, 7 cases of orbital myofibroblastic tumor have been described, though none of the prior studies have described bone invasion. This erosive sino-orbital inflammatory myofibroblastic tumor is a novel finding mimicking a malignant tumor.

Mesenchymal stem cells induce T-cell tolerance and protect the preterm brain after global hypoxia-ischemia.

Hypoxic-ischemic encephalopathy (HIE) in preterm infants is a severe disease for which no curative treatment is available. Cerebral inflammation and invasion of activated peripheral immune cells have been shown to play a pivotal role in the etiology of white matter injury, which is the clinical hallmark of HIE in preterm infants. The objective of this study was to assess the neuroprotective and anti-inflammatory effects of intravenously delivered mesenchymal stem cells (MSC) in an ovine model of HIE. In this translational animal model, global hypoxia-ischemia (HI) was induced in instrumented preterm sheep by transient umbilical cord occlusion, which closely mimics the clinical insult. Intravenous administration of 2 x 106 MSC/kg reduced microglial proliferation, diminished loss of oligodendrocytes and reduced demyelination, as determined by histology and Diffusion Tensor Imaging (DTI), in the preterm brain after global HI. These anti-inflammatory and neuroprotective effects of MSC were paralleled by reduced electrographic seizure activity in the ischemic preterm brain. Furthermore, we showed that MSC induced persistent peripheral T-cell tolerance in vivo and reduced invasion of T-cells into the preterm brain following global HI. These findings show in a preclinical animal model that intravenously administered MSC reduced cerebral inflammation, protected against white matter injury and established functional improvement in the preterm brain following global HI. Moreover, we provide evidence that induction of T-cell tolerance by MSC might play an important role in the neuroprotective effects of MSC in HIE. This is the first study to describe a marked neuroprotective effect of MSC in a translational animal model of HIE.

Combined treatment of Aβ immunization with statin in a mouse model of Alzheimer's disease

We evaluated the therapeutic efficacy of combined treatment of Aβ-immunization with simvastatin in an Alzheimer mouse model at age 22months. DNA prime-adenovirus boost immunization induced modest anti-Aβ titers and simvastatin increased the seropositive rate. Aβ-KLH was additionally administered to boost the titers. Irrespective of simvastatin, the immunization did not decrease cerebral Aβ deposits but increased soluble Aβ and tended to exacerbate amyloid angiopathy in the hippocampus. The immunization increased cerebral invasion of leukocytes and simvastatin counteracted the increase. Thus, modest anti-Aβ titers can increase soluble Aβ and simvastatin may reduce inflammation associated with vaccination in aged Alzheimer mouse models.

Érysipèle de la face révélant une mucormycose

Mucormycosis is an opportunistic fungal infection, typically affecting immunocompromised patients. Rhino-orbital location is the most frequent form with cerebral blood vessels invasion and a fatal outcome.An immunocompetent 38-year-old woman, with previous history of primary cutaneous mucormycosis, was admitted for a febrile erythemato-oedematous lesion of the face with well-demarcated edge evoking erysipelas. No cutaneous portal of entry was identified. Oral cavity examination found an ulceronecrotic lesion of the hard palate. Diagnosis of mucormycosis was retained after nasal endoscopy and histological findings. The patient was first treated for erysipelas, then by ascending dose of intravenous amphotericin B. A good outcome was observed despite the occurrence of nephrotoxicity which normalized by alkaline hyperhydratation. Healing was obtained after 1month of effective dose leaving cleft palate sequelae.Mucormycosis occurs rarely in immunocompetent, even more if it is a second episode. Affecting the face, it may simulate or be revealed by superficial skin infection. Within that, a meticulous otorhinolaryngeal examination is required when the portal of entry is not obvious.

Donor-derived adult T-cell leukaemia

In July, 2008, a 55-year-old woman was referred to us with a 2-month history of progressive aphasia after a febrile episode. She had been diagnosed with chronic adult T-cell leukaemia in June, 1999, and had had a nonmyeloablative peripheral-blood stem-cell transplant with conditioning of pentostatin and 2 Gy total body irradiation in March, 2002. The stem cells had been harvested from her brother, an asymptomatic carrier of human T-cell lymphotropic virus type 1 (HTLV-1). After treatment, she had complete remission. Ciclosporin was discontinued 6 months after the transplant ation because of graft-versus-host disease. Our patient had had no bacterial or viral infections. She had no skin lesions, lymphadenopathy, or splenomegaly. Her leucocyte count was 8·74×109/L with 2·5% adult T-cell leukaemia-like cells. The leukaemia was therefore con sidered to be in remission. CD3-positive cells in the peripheral blood were confi rmed as donor derived by XY-fl uorescence insitu hybridisation (XY-FISH). Serum IgG was 13·7 g/L, IgA was 2·82 g/L, and IgM was 1·16 g/L. Our patient was immunocompetent; absolute number of circulating cells positive for CD4 was 1·74×109/L, CD8 0·475×109/L, CD19 0·522×109/L, and CD56 0·326×109/L. Brain MRI showed hyperintense, non-enhancing lesions in the left temporoparietal lobe and right frontal lobe (fi gure A), which suggested encephalitis, progressive multiple leukoencephalopathy, demyelinating disorder, or lymphoma. Serum concentrations of calcium, lactate dehydro genase, soluble interleukin-2 receptor, and β-2 microglobulin were not raised. CSF examination, culture, and PCR, abdominal ultrasonography, endoscopy, and 18F-fl urodeoxyglucose (18F-FDG) PET were normal. Craniotomy and biopsy of the left temporal lobe was done in July, 2008. Histopathology showed perivascular accumulation and cerebral infi ltration by mononuclear tumour cells with large, indented nuclei (fi gure B). Tumour cells were positive for CD3, CD4, CD8, and CD45RO, but negative for B-cell markers (CD20 and CD79a), suggesting cerebral invasion by adult T-cell leukaemia cells (webappendix). XY-FISH showed an XY genotype of the tumour cells (fi gure C), suggesting that they had originated from the donated leucocytes. After whole brain irradiation and localised irradiation of the left temporoparietal lobe, our patient’s aphasia improved remarkably, and repeat MRI showed shrinkage of the brain lesions. In October, 2010, our patient was fully recovered. For patients with adult T-cell leukaemia, asymptomatic carriers of HTLV-1 have been widely considered acceptable as donors in allogeneic stem-cell transplantation. The immune system is thought to have an important role in leukaemia occurrence in HTLV-1-seropositive carriers. The only reported case of donor-derived adult T-cell leukaemia was in 2006, in an immunosuppressed recipient of a peripheral-blood stem-cell transplant. No cases of donorderived adult T-cell leukaemia have been reported in immunocompetent patients. The prognosis tends to be better for these patients than for those with CNS involvement subsequent to systemic adult T-cell leukaemia. Only two cases of isolated CNS involvement have been reported so far. The function of CD4-positive cells was not fully analysed, so there is a possibility of some functional defi cit in immune reconstitution. Our patient’s case suggests that the consent practices in patients who receive HTLV-1-positive cells should be re-evaluated.

Inhibition of lymphocyte trafficking shields the brain against deleterious neuroinflammation after stroke

T lymphocytes are increasingly recognized as key modulators of detrimental inflammatory cascades in acute ischaemic stroke, but the potential of T cell-targeted therapy in brain ischaemia is largely unexplored. Here, we characterize the effect of inhibiting leukocyte very late antigen-4 and endothelial vascular cell adhesion molecule-1-mediated brain invasion-currently the most effective strategy in primary neuroinflammatory brain disease in murine ischaemic stroke models. Very late antigen-4 blockade by monoclonal antibodies improved outcome in models of moderate stroke lesions by inhibiting cerebral leukocyte invasion and neurotoxic cytokine production without increasing the susceptibility to bacterial infections. Gene silencing of the endothelial very late antigen-4 counterpart vascular cell adhesion molecule-1 by in vivo small interfering RNA injection resulted in an equally potent reduction of infarct volume and post-ischaemic neuroinflammation. Furthermore, very late antigen-4-inhibition effectively reduced the post-ischaemic vascular cell adhesion molecule-1 upregulation, suggesting an additional cross-signalling between invading leukocytes and the cerebral endothelium. Dissecting the specific impact of leukocyte subpopulations showed that invading T cells, via their humoral secretion (interferon-γ) and immediate cytotoxic mechanisms (perforin), were the principal pathways for delayed post-ischaemic tissue injury. Thus, targeting T lymphocyte-migration represents a promising therapeutic approach for ischaemic stroke.

Research development of the pathogenesis pathways for neuroschistosomiasis

The infection of the central nervous system (CNS) by schistosome may or may not have clinical manifestations. When symptomatic, neuroschistosomiasis (NS) is one of the most severe presentations of schistosome infection. Among the NS symptoms, cerebral invasion is mostly caused by Schistosoma japonicum (S. japonicum), and the spinal cord symptoms are mainly caused by S. mansoni or S. haematobium. There are 2 main pathways by which schistosomes cause NS: egg embolism and worm migration, via either artery or vein system, especially the valveless perivertebral Batson's plexus. The adult worm migrates anomalously through the above pathways to the CNS where they lay eggs. Due to the differences in species of schistosomes and stages of infection, mechanisms vary greatly. The portal hypertension with hepatosplenic schistosomiasis also plays an important role in the pathogenesis. Here the pathways through which NS occurs in the CNS were reviewed.

Capturing Changes in the Brain Microenvironment during Initial Tumor Cell Invasion.

Abstract Brain metastases occur mostly in patients with melanoma or primary tumors in the lung, breast or prostate. As therapies against primary tumors and extracranial metastases are improving and patients live longer, the incidence of brain metastases is increasing and brain lesions are seen in 20 to 40 % of patients with advanced metastatic disease. Unfortunately, no therapies are available to treat brain metastasis efficiently.Existing in vivo models of brain metastasis focus mainly on established macrometastases, while very little is known about the initial events of tumor cell brain colonization. In the present study, we used non-invasive bioluminescence imaging and detailed immunohistochemistry to capture the early events of tumor cell interaction with the cerebral microvasculature and invasion of the brain tissue. We used MDA-MB-435 metastatic cancer cells as a model because of their aggressive metastatic phenotype, and injected the cells into the internal carotid artery of immune deficient mice. Our results show that single cancer cells extravasate into the brain parenchyma 3 to 7 days after they arrest within brain capillaries and disrupt the vessel wall, bursting the microvasculature. Cancer cell arrest and extravasation occur exclusively in small vessels that are surrounded by pericytes and lack smooth-muscle cells. Early brain colonization consistently induces local activation of astrocytes, involving heterogeneous astrocyte populations. Reactive astrocytes express high levels of MMP-9 that may assist tumor cell invasion and provide first pro-angiogenic clues. Activated astrocytes consistently persist in the vicinity of growing metastases, and potentially contribute to metastatic proliferation. Occasionally, early host responses also include microglia with stellate or a reactive amoeboid morphology. Importantly, in addition to yielding actively proliferating macrometastases, tumor cell extravasation also leads to widespread single tumor cells dispersed throughout the brain tissue. The majority of these cells remains viable but stays quiescent and does not proliferate. We speculate that the diversity in early local responses of the brain microenvironment to initial cancer cell invasion contributes to the fate of extravasated tumor cells. An early involvement of diverse host cell types might provide distinct environmental clues and co-determine whether a single cell progresses to macrometastasis or remains dormant. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 4162.

Emerging therapeutic options in fulminant invasive rhinocerebral mucormycosis

Five cases of rhinocerebral mucormycosis (RCM) with different courses of illness and outcomes also due to different therapeutical strategies including Posaconazole as a new therapeutic option are described. Predisposing conditions for RCM are diabetes mellitus and immunosuppression. Diagnosis is often delayed because patients complain about nonspecific symptoms of acute rhinosinusitis, and initial CT imaging is unimpressive. Progressive disease, however, leads to early orbital and cerebral invasion. Due to the lack of typical clinical signs, diagnosis relies on histopathology. Therapy consists of the management of predisposing factors, radical surgical intervention and systemic antifungal therapy. We describe five cases of RCM with different comorbidities and outcomes. RCM remains a diagnostic and therapeutic challenge because it begins with nonspecific symptoms and ends as fulminant disease with high mortality. Here, systemic treatment with Posaconazole appears to be a more effective alternative to amphotericin. If a patient is suspected having RCM, improvement of predisposing diseases, radical surgical debridement and effective systemic antifungal therapy must be instituted immediately.

Papel de la difusión en la evaluación de los meningiomas: correlación radiopatológica

To study the behavior of meningiomas in diffusion-weighted sequences and the correlation of these findings with the histological findings. We prospectively included all patients operated on for meningiomas at our hospital during two years. We studied 30 meningiomas in 28 patients aged 31 to 85 years old. All patients underwent MRI prior to surgery, including diffusion-weighted sequences, in a 1.5 T scanner. We evaluated the signal intensity in T2-weighted images, diffusion-weighted images (b=1,000), and apparent diffusion coefficient (ADC) maps within the tumor and in the parietal white matter as a reference. In the histological study, cellularity, proliferation index, histological grade, and cerebral invasion were evaluated. Of the 30 meningiomas, 22 were World Health Organization (WHO) grade I and 8 were atypical or WHO grade II. The overall mean value of the ADC was 89.19+/-13.95x10(-3) mm2/s; the mean ADC value was 82+/-13.69x10(-3) mm2/s in the atypical group and 92.21+/-13.21x10(-3) mm2/s in the typical group. No statistically significant differences were found between the 2 groups. Two subtypes of typical meningiomas, secretory and angiomatous meningiomas, had the highest values in the ADC maps. In the histological analysis, there was a significant association between tumor cellularity and the signal in the ADC map. Meningiomas show moderately restricted diffusion. The signal on the ADC map is associated with tumor cellularity but we have not demonstrated its usefulness for predicting the histological grade.

Highly Invasive Intracranial Malignant Schwannoma in a Rat

A highly invasive intracranial malignant schwannoma containing several masses was detected in a 28-week-old male Crl:CD(SD) rat. Macroscopically, 3 masses were noted in the cranial cavity; one was present at the bottom of the cranial cavity and involved the trigeminal nerve, and the other two were in the parietal bone. Histologically, each mass consisted of fusiform cells with interlacing fascicular, wavy and nuclear pseudopalisading arrangements and round cells with cystic lesions. The tumor cells invaded not only the brain but also the parietal bone. In the brain, the tumor cells infiltrated diffusely into the leptomeningeal and perivascular spaces and parenchyma, in which the tumor cell morphology and invasive pattern closely resembled those of malignant astrocytoma and malignant reticulosis. Immunohistochemically, the tumor cells in the masses showed positive reactions for both S-100 protein and GFAP, while those in the cerebral invasion sites were negative for GFAP and less positive for S-100 protein. Electron microscopically, a single basal lamina layer and short intricate cell processes were confirmed in the tumor cells. From these results, the present tumor was diagnosed as a malignant schwannoma arising in the cranial cavity, probably originating from the trigeminal nerve. The present tumor is considered to be a relatively unique malignant schwannoma based on its growth and invasion patterns.

Identification and characterization of Paragonimus westermani leucine aminopeptidase

Paragonimus westermani is a tissue-invading trematode parasite that causes inflammatory lung disease as well as systemic infections including cerebral invasion in carnivorous mammals. While aminopeptidases play important roles in trematodes in the catabolism of host hemoglobin, an essential source of nutrient for the parasite, little is known about aminopeptidase in Paragonimus. Presently, we isolated a cDNA encoding a 58 kDa P. westermani leucine aminopeptidase (PwLAP). Deduced amino acid sequence of PwLAP exhibited significant sequence homology with LAP from Schistosoma spp. and Fasciola hepatica. Biochemical analysis of the recombinant PwLAP protein demonstrated preferential substrate specificity for Leu-NHMec and inhibition by EDTA, 1,10-phenanthroline, and bestatin, which are conserved characteristics of the M17 family of leucine aminopeptidase. PwLAP exhibited relatively higher enzyme activity in the presence of Mn 2+ compared to Schistosoma mansoni LAP. Based on the biochemical properties and immunohistochemical analysis, PwLAP is concluded to represent a leucine aminopeptidase. The enzyme is most likely responsible for the catabolism of host hemoglobin, and, hence, represents a potential target of Paragonimus chemotherapy.

Lambeaux locaux pour pertes de substance transfixiantes du scalp sur tumeurs évoluées. À propos d'une série de 21 patients

Subject The advanced tumors of the scalp can involve the calvarium, the dura and the cerebral tissue. The medium sized full thickness scalp defects secondary to the excision of such cutaneous malignancy can be successfully treated with local flaps coming from the remaining scalp if these flaps are large and including at least one major pedicle of the scalp. The cranioplasty can be done immediately or secondarily. Patients and methods From May 2001 to July 2006, 21 patients aged between 52 and 78 years old, suffering from advanced basal and squamous cell carcinomas with invasion of the calvarium in all cases, the dura in 1 case and the cerebral tissue in 2 cases have benefited from an excision of the scalp and calvarium with a margin between 1 and 3 cm. The secondary defects measured between 9 and 15 cm for the scalp and between 6 and 9 cm for the calvarium. In 1 case, the dura was resected and reconstructed with a fascia lata graft. The flaps used were: a single pedicled transposition flap based on one or two occipital pedicles in 10 cases — a bipedicled transposition flap based on the superficial temporal pedicles in 3 cases and on the frontal and occipital pedicles in 4 cases — a large rotation flap in 4 cases. These flaps were undermined under the galea without any galeotomies. Their donor sites were immediately grafted. The calvarium was reconstructed by a methylmetacrylate implant in 9 cases, simultaneously with these flaps in 4 cases and secondarily in 5 cases. Results There were no vascular problems in all these flaps — 3 cases of infection in the simultaneous reconstruction of the scalp and calvarium are reported. The two patients with cerebral invasion are deceased 1 year after the surgery. The other patients are still alive without any recurrence or metastasis with a mean follow-up of 36 months. Conclusion Such complex defects of the tumoral scalp can be reconstructed with large and axial local flaps of the remaining scalp with safety. The cranioplasty has to be delayed.

CT and MR Imaging in Choroid Plexus Carcinoma

This case report describes the CT and MR appearances of choroid plexus carcinomas in children less than two years of age. MR and CT imaging of this rare tumor revealed intensely enhancing mass lesions in an intraventricular location, the atrium of the lateral ventricle being the preferred site in children. The tumors were associated with hydrocephalus and cerebral parenchymal invasion.

Deep intracranial extension of squamous cell carcinoma of the scalp

We report a case of recurrent squamous cell carcinoma (SCC) of the scalp with deep cerebral invasion in a 15-year-old girl. Plain films and CT showed extensive, full thickness, and skull destruction at the vertex. Gadolinium-enhanced MRI revealed neoplastic invasion of the meninges and both cerebral hemispheres down to the lateral ventricle. This case represents an example of (SCC) imitating a primary brain tumor by exhibiting intracranial extension.

Giant basal cell carcinoma of the thoracic wall: a case report and review of the literature

Giant basal cell carcinoma is a rare skin tumour with aggressive biological behaviour, and deep invasion and metastasis have been reported. The authors describe a giant basal cell carcinoma involving the anterior chest wall. The lesion infiltrated the mediastinum, occluding the left brachiocephalic vein. Vascular invasion caused venous occlusion affecting the left upper limb. Neither surgical treatment nor radiotherapy were practicable.

Lethal basal cell carcinoma secondary to cerebral invasion

Intracranial invasion by a basal cell carcinoma on the scalp is extremely rare. We present an autopsy case of a 57-year-old woman who developed a large destructive basal cell carcinoma with extension through the calvarium and compression of the dura. We compare 7 similar cases reported in the literature and review the risks for development of these aggressive fatal basal cell carcinomas on the scalp.

Presentation and outcome of rhino-orbital-cerebral mucormycosis in patients with diabetes

Aim: To report presentation and outcome of rhino-orbital-cerebral mucormycosis (ROCM) exclusively in patients with diabetes mellitus. Methods: Retrospective, non-comparative, interventional analysis of the medical records of 35 patients with ROCM...