scholarly journals Epithelioid and spindle-cell haemangioendothelioma in the brain of a dog: a case report

2018 ◽  
Vol 63 (No. 4) ◽  
pp. 193-197 ◽  
Author(s):  
T. Yaman ◽  
A. Uyar ◽  
OF Keles ◽  
Z. Yener

A 9.5-year-old male Belgian malinois dog died after showing clinical symptoms that included fatigue, anorexia and dyspnoea. Necropsy revealed macroscopic findings in the brain and other organs. A solitary, brown-red-coloured mass, approximately 0.5 cm thick and 1.5 × 2 cm in diameter, was detected on the right side of the medulla oblongata, pons and cerebellum. The cut surface showed no invasion of the brain parenchyma. Histologically, the neoplasm was characterised by proliferation of endothelial cells, which showed epithelioid and spindle cell features. Some tumour cells had intracytoplasmic lumen formations containing red blood cells. The nuclei of the tumour cells were large and vesicular. In immunohistochemical experiments the tumour cells stained positive for factor VIII-related antigen, CD31 and CD34. A description is provided of the features of this epithelioid and spindle-cell haemangioendothelioma (EHE) that originated from vessels of the meninges in the subarachnoid space.

Author(s):  
Taïssia Lelekov-Boissard ◽  
Guillemette Chapuisat ◽  
Jean-Pierre Boissel ◽  
Emmanuel Grenier ◽  
Marie-Aimée Dronne

The inflammatory process during stroke consists of activation of resident brain microglia and recruitment of leucocytes, namely neutrophils and monocytes/macrophages. During inflammation, microglial cells, neutrophils and macrophages secrete inflammatory cytokines and chemokines, and phagocytize dead cells. The recruitment of blood cells (neutrophils and macrophages) is mediated by the leucocyte–endothelium interactions and more specifically by cell adhesion molecules. A mathematical model is proposed to represent the dynamics of various brain cells and of immune cells (neutrophils and macrophages). This model is based on a set of six ordinary differential equations and explores the beneficial and deleterious effects of inflammation, respectively phagocytosis by immune cells and the release of pro-inflammatory mediators and nitric oxide (NO). The results of our simulations are qualitatively consistent with those observed in experiments in vivo and would suggest that the increase of phagocytosis could contribute to the increase of the percentage of living cells. The inhibition of the production of cytokines and NO and the blocking of neutrophil and macrophage infiltration into the brain parenchyma led also to the improvement of brain cell survival. This approach may help to explore the respective contributions of the beneficial and deleterious roles of the inflammatory process in stroke, and to study various therapeutic strategies in order to reduce stroke damage.


2019 ◽  
Vol 47 ◽  
Author(s):  
Viviane Motta dos Santos Moretto ◽  
Luciana Maria Curtio Soares ◽  
Esthefanie Nunes ◽  
Uiara Hanna Araújo Barreto ◽  
Valéria Régia Franco Sousa ◽  
...  

Background: Cerebral cavernous hemangioma is a rare neoplasm of vascular origin in the brain, characterized by abnormally dilated vascular channels surrounded by endothelium without muscle or elastic fibers. Presumptive diagnosis is performed by magnetic resonance or computed tomography (CT) scanning and can be confirmed by histopathology. The prognosis of intracranial cavernous hemangioma is poor, with progression of clinical signs culminating in spontaneous death or euthanasia. The purpose of this paper is to report a case of cerebral cavernous hemangioma in a dog, presenting the clinical findings, tomographic changes, and pathological findings.Case: This case involved a 2-year-old medium sized mixed breed female dog presenting with apathy, hyporexia, ataxia, bradycardia, dyspnea, and seizure episodes for three days. Hemogram and serum biochemistry of renal and hepatic function and urinalysis did not reveal any visible changes. CT scanning was also performed. The scans revealed a hyperdense nodule of 15.9 x 14 mm, with well defined borders, and a hypodense halo without post-contrast enhancement and mass effect in the right parietal lobe was observed in both transverse and coronal sections. Based on the image presented in the CT scans, the nodule was defined as a hemorrhagic brain lesion. The animal died after a seizure. The right telencephalon was subjected to necropsy, which revealed a reddish-black wel-defined nodule 1.7 cm in diameter extending from the height of the piriform lobe to the olfactory trine at the groove level and extending towards the lateral ventricle, with slight compression and deformation of the thalamus but no other macroscopic alterations in the other organs. The histopathology indicated that this nodular area in the encephalus contained moderate, well-delimited but unencapsulated cellularity, composed of large vascular spaces paved with endothelial cells filled with erythrocytes, some containing eosinophilic fibrillar material (fibrin) and others with organized thrombus containing occasional neutrophil aggregates. The endothelial cells had cytoplasm with indistinct borders, elongated nuclei, scanty crust-like chromatin, and cellular pleomorphism ranging from discrete to moderate, without mitotic figures.Discussion: The histological findings characterized the morphological changes in the brain as cavernous hemangioma, and the growth and compression of this neoplasm were considered the cause of the clinical signs of this dog. The main complaint was seizures, although ataxia and lethargy were also noted. These clinical signs are often related to changes in the anterior brain and brainstem. The literature does not list computed tomography as a complementary diagnostic method in cases of cerebral cavernous hemangioma in dogs, but CT scanning was useful in confirming cerebral hemorrhage. The main differential diagnosis for cerebral cavernous hemangioma would be a hamartoma, but what differentiates them histologically is the presence of normal interstices between the blood vessels, since no intervening neural tissue occurs in the case of cerebral hemangioma. Therefore, even in the absence of immunohistochemistry to more confidently confirm a cavernous hemangioma, the clinical signs, CT scans and especially the pathological findings were consistent with a case of cerebral cavernous hemangioma, a benign neoplasm with a poor prognosis due to the severe neurological changes it causes and its difficult treatment.


Author(s):  
A Ghare ◽  
K Langdon ◽  
A Andrade ◽  
R Kiwan ◽  
A Ranger ◽  
...  

Background: Myeloid sarcoma (MS) is a rare solid tumour made of myeloblasts or immature myeloid cells in an extramedullary site or in bone, associated with systemic hematologic neoplasms. When they occur in the brain parenchyma, they can often be misdiagnosed. Methods: The authors report a case of a 4-year old boy 6 months out of remission from AML, presenting with a short history of headaches and vomiting, and found to have a heterogenous contrast-enhancing lesion in the right cerebellar hemisphere, with differential diagnosis of myeloid sarcoma, astrocytoma, medulloblastoma and ATRT. Preliminary diagnosis was made flow cytometry from an intraoperative biopsy. The patient had a long course of chemotherapy and radiation, but eventually died from the systemic burden of his AML. Results: The authors present a literature review on 178 published cases of CNS myeloid sarcomas, and their radiological presentation and the basis of immunohistochemical and pathological diagnosis is discussed. Conclusions: Diagnosis rests on a combination of immunohistochemistry and histopathology of biopsied tissue. Surgical resection is controversial, especially given the efficacy of chemotherapy and radiation, and prognosis remains unclear. As with all uncommon and rare clinical entities, further investigation is warranted to determine prognosis and optimal management of CNS myeloid sarcomas.


Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2891
Author(s):  
Francesca Cutruzzolà ◽  
Amani Bouzidi ◽  
Francesca Romana Liberati ◽  
Sharon Spizzichino ◽  
Giovanna Boumis ◽  
...  

Brain metastases are the most severe clinical manifestation of aggressive tumors. Melanoma, breast, and lung cancers are the types that prefer the brain as a site of metastasis formation, even if the reasons for this phenomenon still remain to be clarified. One of the main characteristics that makes a cancer cell able to form metastases in the brain is the ability to interact with the endothelial cells of the microvasculature, cross the blood–brain barrier, and metabolically adapt to the nutrients available in the new microenvironment. In this review, we analyzed what makes the brain a suitable site for the development of metastases and how this microenvironment, through the continuous release of neurotransmitters and amino acids in the extracellular milieu, is able to support the metabolic needs of metastasizing cells. We also suggested a possible role for amino acids released by the brain through the endothelial cells of the blood–brain barrier into the bloodstream in triggering the process of extravasation/invasion of the brain parenchyma.


2021 ◽  
Vol 11 ◽  
Author(s):  
Yiran Zhang ◽  
Yun Yang ◽  
Licheng Zhu ◽  
Qing Zhu ◽  
Yuxi Jia ◽  
...  

Background: Depression is a major psychiatric disorder and the leading cause of disability worldwide. Previous evidence suggested certain pattern of structural alterations were induced by major depression disorder (MDD) with heterogeneity due to patients' clinical characteristics and proposed that early impairment of fronto-limbic-striatal circuit was involved. Yet the hypothesis couldn't be replicated fully. Accordingly, this study aimed to validate this hypothesis in a new set of first-episode, drug naïve MDD patients and further explore the neuroimaging biomarker of illness severity using whole-brain voxel-based morphometry (VBM).Materials and Methods: A total of 93 participants, 30 patients with first-episode medication-naïve MDD, and 63 healthy controls were enrolled in the study. VBM was applied to analyze differences in the gray matter volume (GMV) between these two groups. The correlation between the GMV of the identified brain regions and the severity of clinical symptoms quantified by the Hamilton Depression Scale (HAMD) was further conducted in the post-hoc analysis to confirm the role of GMV structural alteration in clinical symptoms.Results: Our results revealed that the brain gray matter volume of the prefrontal lobe, limbic system, striatum, cerebellum, temporal lobe, and bilateral lingual gyri were significantly decreased in MDD patients compared with healthy controls. Besides, the HAMD scores were negatively correlated with GMV of the right insula and positively correlated with that of the right lingual gyrus.Conclusions: Our findings provide robust evidence that gray matter structural abnormalities within the prefronto-limbic-striatal circuit are implicated in the pathophysiology of MDD at an early stage without confounding influence of medication status. Besides, our data suggest that the cerebellum, lingual gyrus, and fusiform gyrus should also be integrated into the brain alterations in MDD. Future synthesis of individual neuroimaging studies and more advanced statistical analysis comparing subfields of the aforementioned regions are warranted to further shed light on the neurobiology of the disease and assist in the diagnosis of this burdensome disorder.


2020 ◽  
Vol 73 (11) ◽  
pp. 2555-2556
Author(s):  
Pavel A. Dyachenko ◽  
Anatoly G. Dyachenko

Ramsay Hunt syndrome (RHS) occurs due to reactivation of latent Varicella Zoster Virus (VZV) infection in the geniculate ganglion of the facial nerve. Major clinical symptoms include ipsilateral facial paralysis, otic pain, and herpetic vesicles (rashes) along the nerve with accompanying ear pain. Rarely clinical findings include retrograde transaxonal spread of the virus from the ganglion into the brain parenchyma with developing the encephalitis or multiple cranial nerve involvement. We describe here a patient with both RHS along with complicating brains


1995 ◽  
Vol 83 (6) ◽  
pp. 1045-1050 ◽  
Author(s):  
Kevin R. Lee ◽  
A. Lorris Betz ◽  
Richard F. Keep ◽  
Thomas L. Chenevert ◽  
Seoung Kim ◽  
...  

✓ Purified thrombin from an exogenous source is a hemostatic agent commonly used in neurosurgical procedures. The toxicity of thrombin in the brain, however, has not been examined. This study was performed to assess the effect of thrombin on brain parenchyma, using the formation of brain edema as an indicator of injury. Ten µl of test solution was infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later, and the extent of brain edema and ion content were measured. Concentrations of human thrombin as low as 1 U/µl resulted in a significant increase in brain water content. Rats receiving 10 U/µl had a mortality rate of 33% compared to no mortality in the groups receiving smaller doses. Thrombin-induced brain edema was inhibited by a specific and potent thrombin inhibitor, hirudin. A medical grade of bovine thrombin commonly used in surgery also caused brain edema when injected at a concentration of 2 U/µl. Edema formation was prevented by another highly specific thrombin inhibitor, Nα-(2-Naphthalenesulfonylglycyl)-4-dl-phenylalaninepiperidide (α-NAPAP). Thrombininduced brain edema was accompanied by increases in brain sodium and chloride contents and a decrease in brain potassium content. Changes in brain ions were inhibited by both hirudin and α-NAPAP, corresponding to the inhibition of brain water accumulation. This study shows that thrombin causes brain edema when infused into the brain at concentrations as low as 1 U/µl, an amount within the range of concentrations used for topical hemostasis in neurosurgery.


Neurosurgery ◽  
2011 ◽  
Vol 68 (1) ◽  
pp. E258-E262 ◽  
Author(s):  
Kyung-Jae. Park ◽  
Shin-Hyuk. Kang ◽  
Yang-Seok. Chae ◽  
Yong-Gu. Chung

abstract BACKGROUND AND IMPORTANCE: Arachnoid cysts have not been reported to be located within the brain parenchyma. We present a case of an arachnoid cyst that was contained entirely within the right frontal lobe devoid of communication with the subarachnoid space and ventricle. CLINICAL PRESENTATION: A 65-year-old woman presented with a 1-year history of progressive headache and nausea. Computed tomographic and magnetic resonance imagining scans showed a well-defined, nonenhancing mass measuring 5 × 5 × 3.5 cm in the right frontal lobe. The mass appeared to be contained entirely within the brain parenchyma. The patient underwent a right frontal craniotomy, at which time the cystic mass was identified in the brain parenchyma without any communication with the arachnoid space. The cyst contained a clear fluid, and its wall was excised. The fluid contents demonstrated a composition similar to that of normal cerebrospinal fluid. Histological and immunohistochemical examinations of the cyst wall were compatible with the diagnosis of an arachnoid cyst. Postoperatively, the symptoms of the patient resolved, and no recurrence was observed up to 6 months after removal. CONCLUSION: The present case showed an intraparenchymal arachnoid cyst arising in the frontal lobe. Although the etiology is not known, an arachnoid cyst should be included in the differential diagnosis of primary intracerebral cysts.


2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Anne-Eva van der Wijk ◽  
Theodosia Georgakopoulou ◽  
Jisca Majolée ◽  
Jan S. M. van Bezu ◽  
Miesje M. van der Stoel ◽  
...  

AbstractConsidering its intolerance to ischemia, it is of critical importance for the brain to efficiently process microvascular occlusions and maintain tissue perfusion. In addition to collateral microvascular flow and enzymatic degradation of emboli, the endothelium has the potential to engulf microparticles and thereby recanalize the vessel, through a process called angiophagy. Here, we set out to study the dynamics of angiophagy in relation to cytoskeletal remodeling in vitro and reperfusion in vivo. We show that polystyrene microspheres and fibrin clots are actively taken up by (brain) endothelial cells in vitro, and chart the dynamics of the actin cytoskeleton during this process using live cell imaging. Whereas microspheres were taken up through the formation of a cup structure by the apical endothelial membrane, fibrin clots were completely engulfed by the cells, marked by dense F-actin accumulation surrounding the clot. Both microspheres and fibrin clots were retained in the endothelial cells. Notably, fibrin clots were not degraded intracellularly. Using an in vivo microembolization rat model, in which microparticles are injected into the common carotid artery, we found that microspheres are transported by the endothelium from the microvasculature into the brain parenchyma. Microembolization with microspheres caused temporal opening of the blood–brain barrier and vascular nonperfusion, followed by microsphere extravasation and restoration of vessel perfusion over time. Taken together, angiophagy is accompanied by active cytoskeletal remodeling of the endothelium, and is an effective mechanism to restore perfusion of the occluded microvasculature in vivo.


2020 ◽  
Vol 81 (06) ◽  
pp. 575-578
Author(s):  
Hyukjoon Seo ◽  
Sang Hoon Kim ◽  
Jiwook Ryu ◽  
Sung Ho Lee

AbstractTension pneumocephalus is a treatable emergency that is usually caused by trauma or surgery. We present a rare case of spontaneous tension pneumocephalus. A 64-year-old woman presented with a severe aggravating headache. Computed tomography revealed a large air collection in the brain parenchyma of the right frontal lobe, both lateral ventricles, and the subarachnoid space. Emergent craniotomy was performed because her headache got progressively worse. We found that an abnormal bony protrusion connected the frontal sinus mucosa and the intraparenchymal pneumocephalus. After removal of the bony mass and repair of the defect, the patient immediately recovered and there was no recurrence.


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